- - European weblog on food, health and environment
News - Week 25 - 2009
Rosemoor announces its Herbal
Medicine Week
RHS Garden Rosemoor is celebrating the
National Herbal Medicine Week from 20 - 27 June. A fascinating workshop on the wonderful
world of plant remedies is set to take place on Tuesday 23 June.
Early Detection of Osteoarthritis
in Dogs Could Open Doors for a Cure
Osteoarthritis is commonly diagnosed in the late and irreversible stages, when treatment
can only be expected to decrease pain and slow progression of disease. Because
osteoarthritis is a widespread problem in dogs, horses and humans, doctors and
veterinarians need a precise way to diagnose the disease early and accurately. Now,
University of Missouri researchers are investigating potential biomarkers in dogs for
early diagnosis of osteoarthritis, which could help identify patients at increased risk of
developing osteoarthritis. "By developing methods for earlier diagnosis of
osteoarthritis, prevention or even curative treatment strategies to manage the disease
become more realistic," said James Cook, professor of veterinary medicine and
surgery, and the William & Kathryn Allen Distinguished Professor in Orthopedic
Surgery. "Biomarkers could detect the disease before pain and swelling occurs, and
owners could take preventative measures, such as modifying activities or diet, helping
their pets lose weight and strengthen their joints, to reduce the likelihood of their dogs
developing osteoarthritis." In the study, researchers examined potential biomarkers
in synovial fluid. Synovial fluid, which is fluid that lubricates the joints, is known to
have sensitive and rapid responses to joint injury. Taking samples from dogs, researchers
found that synovial fluid quantity and quality were altered in injured stifle joints (the
joint in the hind limbs of dogs that is the equivalent joint to the human knee).
Charlotte Gerson and Howard Straus
Interview on "Healthy Planet, Healthy Me!"
Nobel Laureaute Dr. Albert Schweitzer
stated, "I see in Dr. Max Gerson one of the most eminent geniuses in the history of
medicine. He has achieved more than seemed possible under adverse conditions. Many of his
basic ideas have been adopted without having his name connected with them. He leaves a
legacy which commands attention and which will assure him his due place. Those whom he has
cured will attest to the truth of his ideas."
Dioxins in Food Chain Linked to
Breastfeeding Ills
Exposure to dioxins during pregnancy harms the cells in rapidly-changing breast tissue,
which may explain why some women have trouble breastfeeding or don’t produce enough
milk, according to a University of Rochester Medical Center study. Researchers believe
their findings, although only demonstrated in mice at this point, begin to address an area
of health that impacts millions of women but has received little attention in the
laboratory, said corresponding author B. Paige Lawrence, Ph.D., associate professor of
Environmental Medicine and of Microbiology and Immunology at URMC. “Estimates are
that three to six million mothers worldwide are either unable to initiate breastfeeding or
are unable to produce enough milk to nourish their infants,” Lawrence said. “But
the cause of this problem is unclear, though it has been suggested that environmental
contaminants might play a role. We showed definitively that a known and abundant pollutant
has an adverse effect on the way mammary glands develop during pregnancy.” Dioxins
are generated mostly by the incineration of municipal and medical waste, especially
certain plastics. Most people are exposed through diet. Dioxins get into the food supply
when air emissions settle on farm fields and where livestock graze. Fish also ingest
dioxins and related pollutants from contaminated waters. When humans take in dioxin –
most often through meat, dairy products, fish and shellfish – the toxin settles in
fatty tissues; natural elimination takes place very slowly. The typical human exposure is
a daily low dose, which has been linked to possible impairment of the immune system and
developing organs.
Natural hormone offers hope for
treatment of the metabolic syndrome
Angiotensin 1-7, a hormone in the body that has cardiovascular benefits, improves the
metabolic syndrome in rats, according to a new study. The results will be presented
Wednesday at The Endocrine Society's 91st Annual Meeting in Washington, D.C. "No
specific form of medical therapy for the metabolic syndrome presently exists," said
the study's lead author, Yonit Marcus, MD, a PhD student at the Weizmann Institute of
Science in Rehovot, Israel. "But an estimated 20 to 25 percent of the world's adult
population has the metabolic syndrome." The metabolic syndrome is a cluster of risk
factors that raise the risk of developing heart disease, stroke and diabetes. A diagnosis
of the metabolic syndrome comes from having at least three of the following: increased
waist circumference (abdominal obesity), low HDL ("good") cholesterol, high
triglycerides (fats in the blood), high blood pressure and high blood glucose (blood
sugar). The renin-angiotensin system and its key player, the hormone angiotensin II,
normally help control blood pressure, but when overactive, this hormone likely contributes
to the development of obesity and the metabolic syndrome. A product of angiotensin II
metabolism, a hormone called angiotensin 1-7, counteracts many of the negative effects of
excess angiotensin II, including high blood pressure, kidney disease, heart failure and
cardiac arrhythmia (abnormal heart rhythms), according to Marcus. With the other
researcheres, Marcus examined whether angiotensin 1-7 has a beneficial effect on the
metabolic syndrome, using an established model of the syndrome, "the fructose-fed
rat." In this model, rats are fed a diet heavy in fructose sweetener, and over time
they develop similar characteristics to the human metabolic syndrome.
Genetic pathway responsible for
link between body clock disturbance and worsening arthritis
The genes that regulate human circadian rhythm, or 'the body clock', are significantly
disturbed in individuals with arthritis, according to the results of a new study presented
today at EULAR 2009, the Annual Congress of the European League Against Rheumatism in
Copenhagen, Denmark. Notably, a specific genetic pathway has been identified as
responsible for interactions between the genes that regulate the body clock and those that
may worsen symptoms of arthritis. In a sample of 200 rheumatoid arthritis (RA) patients,
sleep was determined to be significantly disturbed in over 61%, as determined by a
Pittsburg Sleep Quality Index (PSQI) score of >5 (the PSQI global score was 8.55
±4.69). These values were shown to correlate with several measures of arthritis disease
activity, including levels of c-reactive protein, swollen joint count and DAS28*. A
further element of the study looked into the expression patterns of certain genes in mice
with arthritis. Here, researchers identified a novel biochemical pathway in which the
circadian regulatory gene CRY was found to up-regulate expression of a gene which promotes
the activation of TNF-alpha (tumour necrosis factor-alpha, a pro-inflammatory cytokine
used by the body to boost the immune system) by two fold, when comparing mice with the CRY
gene removed to those with a normal copy of the gene. Professor Shunichi Shiozawa of Kobe
University Graduate School of Medicine and University Hospital, Japan, who led the
research said: "Our study has shown that arthritis interferes with the genetics
behind an individual's circadian rhythm and, specifically, that certain body clock genes
may play a part in the activation of TNF-alpha, a signaling molecule that has an important
role in the inflammation commonly seen in a number of rheumatologic conditions. The
identification of this curious pathway may help to explain the 24-hour symptom cycle seen
by many patients who experience worsening of joint pain and stiffness in the mornings, and
lead to further research into new approaches for improving daily quality of life."
Parents key in new measure to
evaluate language in children with autism
New parent questionnaire, developed at the University of Waterloo, will help health
practitioners to more accurately gauge the acquisition of language skills in children with
autism. The pioneering Language Use Inventory (LUI) is among a set of measures for
evaluating spoken language development in children with autism spectrum disorders,
recommended by an expert panel. The experts' report, Defining Spoken Language Benchmarks
and Selecting Measures of Expressive Language Development for Young Children with Autism
Spectrum Disorders, appears in the June 2009 issue of the Journal of Speech, Language and
Hearing Research. The report was commissioned by the National Institute of Deafness and
Other Communication Disorders. "This is very exciting news," said UW professor
Daniela O'Neill, a developmental psychologist who created the LUI. "This report will
be of tremendous help to researchers, clinicians and speech-language professionals
involved in intervention with young children with autism and we are very proud to see the
LUI included among the measures recommended for evaluating the efficacy of interventions
that target spoken language." The LUI is a standardized questionnaire that asks
parents about their child's use of language in many different kinds of settings. Research
from the Centers for Disease Control suggests the prevalence of autism spectrum disorders
to be one in 150 children. "The LUI looks at pragmatic language development which has
do with how young children are able to use their language effectively and successfully in
everyday interactions with other people in ways that are age-appropriate and
typical," O'Neill explained. "For example, to ask for help, comment about
noticeable things, tease, tell stories and give others information they might need. The
pragmatics of language can be an area of great difficulty for children with autism."
Difficulty with learning language and communicating with others is often one of the first
things that parents become concerned about. Parents have much valuable information to
offer about their child's language use to professionals evaluating their child. "A
parent has had the most experience watching their child try to use their language in a
host of different settings and with many different people." The LUI provides
speech-language pathologists and researchers with a new tool to evaluate a young child's
broad pragmatic use of language. As many as 14 per cent of preschool-age children in
Canada and the U.S. may be at risk for language disorders.
Hormone therapy plus physical
activity reduce belly fat, body fat percentage after menopause
Older women who take hormone therapy to relieve menopausal symptoms may get the added
benefit of reduced body fat if they are physically active, according to a new study. The
results were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C.
The study provides new information on the health benefits of any type of physical
activity, not just exercise, said the presenting author Poli Mara Spritzer, MD, PhD, a
professor at the Federal University of Rio Grande do Sul in Porto Alegre, Brazil, and
chief of the Gynecological Endocrinology Unit at the university's Hospital de Clinicas de
Porto Alegre. After menopause, a woman's percentage of body fat tends to increase and
redistribute to the abdomen, Spritzer said. Excess belly fat is a risk factor for diabetes
and heart disease. Postmenopausal women who exercise have a lower percentage of body fat
than sedentary women, past research shows. However, Spritzer said less is known about the
influence on body fat composition of physical activity in women receiving hormone
replacement therapy, or HRT. Some data suggest that estrogen treatment may add to the
effect of exercise in reducing fat. Spritzer and her colleagues studied 34 healthy women
who had an average age of 51 years, had experienced menopause for less than 3 years and
sought HRT to relieve hot flashes, night sweats and vaginal dryness. They evaluated the
women's cholesterol levels, body mass index (BMI), waist circumference (a measure of
abdominal fat) and percentage of body fat before and after 4 months of HRT. The women
received estrogen plus progesterone therapy in either non-oral (nasal and vaginal) or
low-dose oral preparations. For 6 consecutive days before starting HRT and 6 days at the
end of HRT, women wore a pedometer to estimate their level of physical activity. The
device measured the steps they took, including walking, working, and doing house chores
and leisure activities. They were instructed to not change their usual activities. Most of
the women did not play sports or do any structured physical exercise, according to
Spritzer. Results showed that 24 of the women were physically active—defined as
taking 6,000 steps or more per day—and 10 were inactive (less than 6,000 steps a
day). For a woman who has a step, or stride, length of 2 feet (60 cm), 6,000 steps would
be around 2.25 miles (3.6 km), Spritzer estimated. For active women, the higher the number
of steps they took, the lower was their waist measurement and the better their level of
"good" (high-density-lipoprotein, or HDL) cholesterol, the authors reported. The
inactive women did not have any changes in body fat or cholesterol. However, when all 34
women were considered in the analysis, body fat still declined significantly after HRT.
Millions of British people are at risk of
developing serious health conditions because of low vitamin D levels declares a new
scientific review commissioned by the Health Supplements Information Service (HSIS).
Despite the proven health benefits of vitamin D, about three quarters of British *!*$@!
fail to reach even their basic requirements thanks to poor dietary intakes and a lack of
sun in this country.
Connection with Vitamin D and
Cancer
Can vitamin D help prevent certain cancers
and other diseases such as type 1 diabetes, cardiovascular disease, and certain autoimmune
and chronic diseases? To answer these questions and more, UCSD School of Medicine and
GrassrootsHealth bring you this innovative series on vitamin D deficiency. Join nationally
recognized experts as they discuss the latest research and its implications. In this
program, Donald Trump, MD, discusses what has been learned about vitamin D deficiency from
studying cancer patients.
Vitamin D and Diabetes-Can We
Prevent it?
Can vitamin D help prevent certain cancers
and other diseases such as type 1 diabetes, cardiovascular disease, and certain autoimmune
and chronic diseases? To answer these questions and more, UCSD School of Medicine and
GrassrootsHealth bring you this innovative series on vitamin D deficiency. Join nationally
recognized experts as they discuss the latest research and its implications. In this
program, Frank Garland, PhD, discusses vitamin D and the opportunity for prevention of
diabetes.
Brain molecule reduces food intake
Researchers at Imperial College London have identified a new appetite suppressant for
promoting weight loss that they say works in rodents and may one day be used to develop an
effective anti-obesity treatment. Results of the new study were presented at The Endocrine
Society's 91st Annual Meeting in Washington, D.C. The experimental treatment, prokineticin
2, is a recently discovered signaling molecule that occurs naturally in the part of the
brain that helps control hunger. Both lean and obese mice treated with PK2 for 5 days lost
almost 5 percent of their body weight, the authors reported. "This is a greater
weight loss than people achieve with current nonsurgical weight loss therapies," said
study co-author Waljit Dhillo, a clinical senior lecturer at Imperial College London. The
researchers first dissolved a commercially available form of PK2 (from PeproTech Ltd.) in
saline and injected it into the brain of 12 rats, which were allowed to eat as much as
they wanted for 24 hours. Compared with 12 control rats that received only saline
injections, the treated rats ate much less food; in the first hour alone, their food
intake was 86 percent less. PK2 did not affect movement, behavior or the ability to burn
off calories, the authors reported.
Our exposure to controversial
chemical may be greater than dose considered safe
People are likely being exposed to the commonly used chemical bisphenol A (BPA) at levels
much higher than the recommended safe daily dose, according to a new study in monkeys. The
results will be presented Thursday at The Endocrine Society's 91st Annual Meeting in
Washington, D.C. "BPA is now known to be a potent estrogen," said Frederick vom
Saal, PhD, a co-author of the new study and a professor of biological sciences at the
University of Missouri-Columbia. "Human and animal studies indicate it could be
related to diabetes, heart disease, liver abnormalities, miscarriage and other
reproductive abnormalities, as well as prostate and breast cancer." The U.S. Food and
Drug Administration (FDA) declared BPA is safe based on estimates that people consume only
small amounts each day from food. However, recent research indicated that U.S. adults are
exposed to more BPA from multiple sources than previously thought, vom Saal said. BPA is
found in polycarbonate plastic food and beverage containers, such as water and infant
bottles, as well as in the epoxy resin lining of cans and other sources. The chemical can
leach into food and beverages, according to the National Institutes of Health, which
funded the study by vom Saal and colleagues. "Between 8 and 9 billion pounds of BPA
are used in products every year," vom Saal said.
Bisphenol A exposure increases risk
of abnormal heart rhythms in female rodents
The chemical bisphenol A, commonly found in many plastic household items, has been linked
to yet another health problem in animals—an increased frequency of arrhythmias, or
heartbeat irregularities, a new study found. The results, seen only in females, will be
presented Saturday at The Endocrine Society's 91st Annual Meeting in Washington, D.C. Past
animal studies show that bisphenol A, or BPA, can have harmful effects on the
reproductive, nervous and immune systems. Also, a study in humans reported last year found
an increased prevalence of cardiovascular disease in people with high levels of BPA in the
urine. However, the effects of BPA on the heart are unknown, said study co-author Scott
Belcher, PhD, associate professor in the University of Cincinnati's Department of
Pharmacology and Cell Biophysics. In the new study, funded by the National Institutes of
Health, the University of Cincinnati researchers found that low-dose BPA and estrogen can
act alone or in combination to increase harmful arrhythmias in female rats and mice.
Because BPA has properties similar to the main female hormone estrogen, it is considered
an "environmental estrogen." Mice and rats in the study had normal heart rhythms
at baseline, before administration of BPA or estrogen (estradiol), Belcher said. The
investigators studied heart rhythms in both the working heart and in cultured heart muscle
cells. In both models, exposure to BPA increased the frequency of arrhythmias, compared to
baseline, in females but not in male animals, the authors found. Administration of
estrogen alone also increased the frequency of arrhythmias in females. Arrhythmias were
most frequent in the female rats and mice when they received both BPA and estrogen, at
levels normally found in female humans.
Bisphenol A exposure in pregnant
mice permanently changes DNA of offspring
Exposure during pregnancy to the chemical bisphenol A, or BPA, found in many common
plastic household items, is known to cause a fertility defect in the mother's offspring in
animal studies, and now researchers have found how the defect occurs. The results of the
new study will be presented Saturday at The Endocrine Society's 91st Annual Meeting in
Washington, D.C. The study, funded partly by the National Institutes of Health, joins a
growing body of animal research showing the toxic health effects of BPA, including
reproductive and developmental problems. Last August the U.S. Food and Drug Administration
found BPA to be safe as currently used but later said more research on its safety is
needed. BPA is used to make hard polycarbonate plastic, such as for baby bottles,
refillable water bottles and food containers, as well as to make the linings of metal food
cans.BPA has estrogen-like properties and in pregnant animals has been linked to female
infertility. "The big mystery is how does exposure to this estrogen-like substance
during a brief period in pregnancy lead to a change in uterine function," said study
co-author Hugh Taylor, MD, professor and chief of the reproductive endocrinology section
at Yale University School of Medicine.
Specific genetic cause of fetal
alcohol-related developmental disorders found
Alcohol consumption by pregnant women hinders brain development in their children by
interfering with the genetic processes that control thyroid hormone levels in the fetal
brain, a new animal study found. Results will be presented Wednesday at The Endocrine
Society's 91st Annual Meeting in Washington, D.C. Fetal alcohol exposure—even from
moderate drinking during pregnancy—can cause neurodevelopmental disorders, such as
emotional behavioral disorders and deficits in learning, memory and speech. There is
currently no treatment for these problems, said the author who will present the study
results, Laura Sittig, a student at Northwestern University Feinberg School of Medicine.
Past animal research shows that some of these lasting cognitive impairments occur because
alcohol consumption during pregnancy decreases the level of maternal thyroid hormones and,
therefore, fetal thyroid hormones. "Specific concentrations of thyroid hormones must
be available in the fetal brain to support normal neurological development," Sittig
said. One of the enzymes that control thyroid hormone levels in the fetal brain is the
iodothyronine deiodinase type III, or Dio3, she explained. Sittig and her colleagues
hypothesized that alcohol exposure in the womb leads to cognitive impairments by inducing
epigenetic alterations—changes to DNA that do not alter the actual DNA
sequence—of developmental genes like Dio3 in the fetal brain. To investigate this
hypothesis, they used rats to model moderate alcohol consumption during pregnancy. The
study, which was funded by the National Institutes of Health, demonstrated that fetal
alcohol exposure disrupts the epigenetic "imprinting" of Dio3. In this process,
Dio3 normally originates from the father's gene, while the maternal gene is silenced by
epigenetic control. But alcohol exposure changes the paternal-maternal dosage of Dio3,
which increases the amount of the enzyme present in specific brain regions of the fetus,
the authors found.
Evolution can occur in less than 10
years
How fast can evolution take place? In just a few years, according to a new study on
guppies led by UC Riverside's Swanne Gordon, a graduate student in biology. Gordon and her
colleagues studied guppies — small fresh-water fish biologists have studied for long
— from the Yarra River, Trinidad. They introduced the guppies into the nearby Damier
River, in a section above a barrier waterfall that excluded all predators. The guppies and
their descendents also colonized the lower portion of the stream, below the barrier
waterfall, that contained natural predators. Eight years later (less than 30 guppy
generations), the researchers found that the guppies in the low-predation environment
above the barrier waterfall had adapted to their new environment by producing larger and
fewer offspring with each reproductive cycle. No such adaptation was seen in the guppies
that colonized the high-predation environment below the barrier waterfall.
"High-predation females invest more resources into current reproduction because a
high rate of mortality, driven by predators, means these females may not get another
chance to reproduce," explained Gordon, who works in the lab of David Reznick, a
professor of biology. "Low-predation females, on the other hand, produce larger
embryos because the larger babies are more competitive in the resource-limited
environments typical of low-predation sites. Moreover, low-predation females produce fewer
embryos not only because they have larger embryos but also because they invest fewer
resources in current reproduction." Study results appear in the July issue of The
American Naturalist.
Cool plasma packs heat against
biofilms
Though it looks like a tiny purple blowtorch, a pencil-sized plume of plasma on the tip of
a small probe remains at room temperature as it swiftly dismantles tough bacterial
colonies deep inside a human tooth. But it's not another futuristic product of George
Lucas' imagination. It's the exciting work of USC School of Dentistry and Viterbi School
of Engineering researchers looking for new ways to safely fight tenacious biofilm
infections in patients – and it could revolutionize many facets of medicine. Two of
the study's authors are Chunqi Jiang, a research assistant professor in the Ming Hsieh
Department of Electrical Engineering-Electrophysics, and Parish Sedghizadeh, assistant
professor of clinical dentistry and Director of the USC Center for Biofilms.
"Nanosecond Pulsed Plasma Dental Probe" appears in the June 2009 issue of Plasma
Processes and Polymers. Sedghizadeh explained that biofilms are complex colonies of
bacteria suspended in a slimy matrix that grants them added protection from conventional
antibiotics. Biofilms are responsible for many hard-to-fight infections in the mouth and
elsewhere. But in the study, biofilms cultivated in the root canal of extracted human
teeth were easily destroyed with the plasma dental probe, as evidenced by scanning
electron microscope images of near-pristine tooth surfaces after plasma treatment. Plasma,
the fourth state of matter, consists of electrons, ions, and neutral species and is the
most common form found in space, stars, and lightning, Jiang said. But while many natural
plasmas are hot, or thermal, the probe developed for the study is a non-thermal, room
temperature plasma that's safe to touch. The researchers placed temperature sensors on the
extracted teeth before treatment and found that the temperature of the tooth increased for
just five degrees after 10 minutes of exposure to the plasma, Jiang said. The cooler
nature of the experimental plasma comes from its pulsed power supply. Instead of employing
a steady stream of energy to the probe, the pulsed power supply sends 100-nanosecond
pulses of several kilovolts to the probe once every millisecond, with an average power
less than 2 Watts, Jiang said.
HIV-1's 'hijacking mechanism'
pinpointed by McGill/JGH researchers
Researchers at McGill University and the affiliated Lady Davis Institute for Medical
Research at Montreal's Jewish General Hospital – along with colleagues at the
University of Manitoba and the University of British Columbia – may have found a
chink in the armour of the human immunodeficiency virus type 1 (HIV-1), the microorganism
which causes AIDS. They have pinpointed the key cellular machinery co-opted by HIV-1 to
hijack the human cell for its own benefit. Their study was published in May in the Journal
of Biological Chemistry. Once a cell is infected with HIV-1, activation of the virus's
gene generates a large HIV-1 RNA molecule known as the RNA genome. This is then
transported from the cell nucleus to the inner surface of the plasma membrane. The RNA
genome can produce both structural proteins and enzymes, but once it arrives at the plasma
membrane it can also assemble into new copies of the virus that actually bud out of the
cell. Dr. Andrew J. Mouland and his colleagues have discovered how the RNA genome gets
transported – or trafficked – from the nucleus to the plasma membrane.
"There is a highway inside the human cell," explained Dr. Mouland, Associate
Professor at McGill's Departments of Medicine and Microbiology and Immunology and head of
the HIV-1 RNA Trafficking Laboratory at the Lady Davis Institute. "When you drive
your car to Toronto you're 'trafficking' the items in your trunk. Similarly, what we have
shown is that HIV-1 commandeers the host cell's endosomal machinery to traffic its
structural proteins and RNA genome. Imagine that it's essentially jumping on board for the
ride and directing it to where it needs to go. This trafficking can occur very fast in
cells; so this is how these key components of HIV-1 so efficiently get to the plasma
membrane, where the virus can begin to assemble.
Report on US tobacco control
policies and use finds stark contrasts in progress among states
The United States is becoming a nation of haves and have-nots when it comes to tobacco
control, according to a comprehensive publication on cigarette smoking prevalence and
policies in the U.S. that was released today. The new report, "Cigarette Smoking
Prevalence and Policies in the 50 States: An Era of Change -- the Robert Wood Johnson
Foundation ImpacTeen Tobacco Chart Book," was presented today at the National
Conference on Tobacco or Health meeting in Phoenix. It was prepared for the Robert Wood
Johnson Foundation by researchers in the University at Buffalo Department of Health
Behavior in UB's School of Public Health and Health Professions and at the Roswell Park
Cancer Institute. Researchers from eight other institutions also contributed, including
the University of Illinois at Chicago, the National Cancer Institute and the Robert Wood
Johnson Foundation. The report includes individualized data on smoking behaviors for all
50 states as well as a discussion of national trends revealed by the data. "States
can reduce death and disease by reducing smoking prevalence," said Gary G. Giovino,
Ph.D., professor and chair of the Department of Health Behavior in the UB School of Public
Health and Health Professions and principal investigator on the report. "It's that
simple." "States should feel morally obligated to use a higher proportion of the
revenues they receive from cigarette excise taxes and settlement payments to prevent
smoking initiation, protect nonsmokers and help people who smoke to quit. Strong tobacco
control programs save lives," he added. The report points out that even after four
decades of tobacco control efforts, one-fifth of American adults still smoke and
prevalence is especially high among populations with lower levels of education and income,
Native Americans and those with psychiatric and substance abuse problems.
Pre-pregnancy depressed mood may
heighten risk for premature birth
Researchers trying to uncover why premature birth is a growing problem in the United
States and one that disproportionately affects black women have found that pre-pregnancy
depressive mood appears to be a risk factor in preterm birth among both blacks and whites.
Black women, however, have nearly two times the odds of having a preterm birth compared to
white women, according to Amelia Gavin, a University of Washington assistant professor of
social work and lead author of a new study that appears online in the June issue of the
Journal of Women's Health. "Preterm births are one of the most significant health
disparities in the United States and the overall number of these births increased from
10.6 percent in 2000 to 12.8 percent in 2005," she said. While there appears to be
some sort of link between giving birth prematurely and depressed mood, the study found no
cause and effect, said Gavin, who studies health disparities. She believes the higher
preterm birth rate among blacks may be the result of declining health over time among
black women. For this study, premature birth referred to any child born after less than 37
weeks of gestation. Normal gestation ranges from 38 to 42 weeks. Data for the study was
drawn from a larger longitudinal investigation looking at the risks for cardiovascular
disease among more than 5,000 young adults in four metropolitan areas. The Coronary Artery
Risk Development in Young Adults Study also collected information about mental health and
pregnancy outcomes. Between 1990 and 1996, 555 women in the larger study gave birth. These
women were the subjects in the depression-premature birth study. "At this point we
can't say that pre-pregnancy depressive mood is a cause of preterm birth or how race
effects this association," said Gavin. "But it seems to be a risk factor in
giving birth prematurely and higher pre-pregnancy depressive mood among black women
compared to white women may indirectly contribute to the greater odds of preterm birth
found among black women."
Experts Launch Think Tank for
Mystery Disease
Ten leading scientists in Europe have
formed a Think Tank for ME and will hold their first meeting on the 13th of June. They
want to initiate an effective research effort to find the secret behind the mystery
disease that cripples an increasing number of lives. Myalgic Encephalomyelitis, often
referred to as Chronic Fatigue Syndrome (CFS), is a disease which affects at least one
million individuals in the US, and an even greater number in Europe. Despite the large
number of people affected, there is a lack of serious large-scale research initiatives
focused on the disease. The number of patients is rapidly increasing but healthcare
personnel lack knowledge about existing research and possible treatments.
Last year's winner of the Nobel Prize in
Medicine, Professor Luc Montagnier of France, says, "Scientists have already
uncovered a lot about ME, but this information does not reach professional healthcare
personnel, and the disease is still not taken seriously. It is about time this
changes.” Montagnier, one of the discoverers of the HIV-virus, is a supporter of the
Think Tank, but is unable to join the first meeting due to his demanding schedule.
Treatable Disease
Ten internationally recognized scientists, many of them prominent leaders in their
respective fields of research, have decided to do something about it. They have come
together in a Think Tank to promote cooperation among scientists from various disciplines
and to stimulate intense focus on innovative and creative research. The first meeting is
set in Stavanger, Norway on the 13th of June.
“There are more than 5000 research
papers which show that ME has an organic basis with abnormalities in the immune, nervous
and gastrointestinal systems and that it is influenced by genetic and environmental
factors,” states Professor Kenny De Meirleir of Belgium. “Despite these
findings, it has been close to impossible to initiate large-scale research to verify these
facts and observations. We will never be able to treat ME properly if we do not initiate
this type of research.” Using new biotechnological techniques, much of the
underlying pathophysiology of the disease has been unmasked. Several treatable clinical
entities have been discovered, but this information does not reach healthcare personnel.
The result is that patients remain undiagnosed and untreated for years with something that
might be fully treatable. This is a huge drain on the economy, as the estimated
socio-economic costs for Europe are estimated to be €20 billion annually.
Educate Professionals
An important part of the Think Tank’s mission is to spread knowledge about the
disease. The incidence of ME and the impact on public health are actually higher than that
of other better researched conditions like Multiple Sclerosis and HIV. Research shows that
ME can be a very disabling chronic disorder which often diminishes patients’ quality
of life to levels lower than that of cancer, MS, HIV and lupus. Professor Ola Didrik
Saugstad of Norway states, “There is a total lack of knowledge and understanding
about this disease in the healthcare system. We wish to use our knowledge to educate and
train
doctors, therapists and other healthcare personnel so they can better understand how to
manage an ME-patient.”
New in ME
The Think Tank meetings are the brainchild of a new organization, European Society for ME
(ESME). This society will focus on organizing research and educating professionals in the
field of ME. “Until now ME organizations have been patient-based and only focused on
the needs of the patients, so this is something completely new and unique. We are a group
of professionals who want to stimulate new research in the field of ME and to help doctors
and healthcare personnel to stay informed about the latest developments in diagnosing and
treating ME-patients,” says ESME board member Mrs. Catherine Miller-Duhen.
Researchers test nanoparticle to
treat cardiovascular disease in mice
Scientists and engineers at UC Santa Barbara and other researchers have developed a
nanoparticle that can attack plaque –– a major cause of cardiovascular disease.
The new development is described in a recent issue of the Proceedings of the National
Academy of Sciences. The treatment is promising for the eventual development of therapies
for cardiovascular disease, which is blamed for one third of the deaths in the United
States each year. Atherosclerosis, which was the focus of this study, is one of the
leading causes of cardiovascular disease. In atherosclerosis, plaque builds up on the
walls of arteries and can cause heart attack and stroke."The purpose of our grant is
to develop targeted nanoparticles that specifically detect atherosclerotic plaques,"
said Erkki Ruoslahti, distinguished professor at the Burnham Institute for Medical
Research at the University of California, Santa Barbara. "We now have at least one
peptide, described in the paper, that is capable of directing nanoparticles to the
plaques."The nanoparticles in this study are lipid-based collections of molecules
that form a sphere called a micelle. The micelle has a peptide, a piece of protein, on its
surface, and that peptide binds to the surface of the plaque. Co-author Matthew Tirrell,
The Richard A. Auhll Professor and dean of UCSB's College of Engineering, specializes in
lipid-based micelles. "This turned out to be a perfect fit with our targeting
technology," said Ruoslahti.
Illegal fishing harming present and
future New England groundfish fisheries
Weak enforcement combined with fishermen facing serious economic hardships are leading to
widespread violations of fisheries regulations along the Northeastern United States coast.
This pattern of noncompliance threatens the success of new fisheries management measures
put in place to protect and restore fish stocks, according to a new study published online
this week in the journal Marine Policy. Among their findings, environmental economists Dr.
Dennis King of the University of Maryland Center for Environmental Science and Dr. Jon
Sutinen of the University of Rhode Island detail nearly a doubling of the percent of total
harvest taken illegally over the last two decades in the Northeast multispecies groundfish
fishery (NEGF). The study estimates the annual illegal harvest to be 12 to 24 percent,
significantly higher than estimates of 6 to 14 percent in the 1980s. The study, supported
by the Lenfest Ocean Program, is based on the results of an extensive 2007 survey of
fishermen, managers, scientists and enforcement officials involved in the Northeast
multispecies groundfish fishery, and analysis of enforcement data from the NOAA Office of
Law Enforcement and NOAA National Marine Fisheries Service. "The one-two punch of
weak enforcement and deteriorating economic conditions combined with declining faith in
the competency and legitimacy of fisheries management is encouraging more and more
fisherman to press their luck and fish illegally," said Dr. King. "To many
fishermen, the current situation has reached an economic and moral tipping point where the
potential economic gains from illegal fishing far outweigh the expected cost of getting
caught." In the article, the authors outline how the existing enforcement system in
the NEGF fishery does not significantly deter illegal fishing because economic gains from
violating fishing regulations are nearly five times the economic value of expected
penalties. The study finds that only one-third of violators are caught, and only one-third
of those are actually prosecuted.
Association Found Between
Parkinson's Disease and Pesticide Exposure in French Farm Workers
The cause of Parkinson’s disease (PD), the second most frequent neurodegenerative
disease after Alzheimer’s disease, is unknown, but in most cases it is believed to
involve a combination of environmental risk factors and genetic susceptibility. Laboratory
studies in rats have shown that injecting the insecticide rotenone leads to an animal
model of PD and several epidemiological studies have shown an association between
pesticides and PD, but most have not identified specific pesticides or studied the amount
of exposure relating to the association. A new epidemiological study involving the
exposure of French farm workers to pesticides found that professional exposure is
associated with PD, especially for organochlorine insecticides. The study is published in
Annals of Neurology, the official journal of the American Neurological Association. Led by
Alexis Elbaz M.D., Ph.D., of Inserm, the national French institute for health research in
Paris, and University Pierre et Marie Curie (UPMC, Paris 6), the study involved
individuals affiliated with the French health insurance organization for agricultural
workers who were frequently exposed to pesticides in the course of their work.
Occupational health physicians constructed a detailed lifetime exposure history to
pesticides by interviewing participants, visiting farms, and collecting a large amount of
data on pesticide exposure. These included farm size, type of crops, animal breeding,
which pesticides were used, time period of use, frequency and duration of exposure per
year, and spraying method. The study found that PD patients had been exposed to pesticides
through their work more frequently and for a greater number of years/hours than those
without PD. Among the three main classes of pesticides (insecticides, herbicides,
fungicides), researchers found the largest difference for insecticides: men who had used
insecticides had a two-fold increase in the risk of PD.
Study gives clues to how adrenal
cancer forms
At the ends of chromosome are special pieces of DNA called telomeres. Think of it as the
little tip that caps off a shoelace. The telomeres send signals to the cells to let them
know it’s the end point, not a break that should be repaired. Over time, as cells
reproduce, the telomeres become shorter and eventually no longer do their job. The cells
then have a higher risk of mutating into cancer. But, a new study finds, if the telomere
becomes dysfunctional at any point – regardless of shortening – it can trigger a
cancer event. The study, by researchers at the University of Michigan Comprehensive Cancer
Center, was done in mice generally prone to develop cancer. The mice that also had
dysfunctional telomeres were particularly prone to develop the usually ultra-rare
adrenocortical cancer. This is the first mouse model to specifically address this rare but
lethal type of cancer.
One in four nursing home residents
carries MRSA
MRSA is a major problem in nursing homes with one in four residents carrying the bacteria,
a study by Queen’s University Belfast and Antrim Area Hospital has found. Its authors
say that the findings, which have been published in the Journal of the American Geriatrics
Society, highlight the need for infection control strategies to be given a higher priority
in nursing homes. The study, thought to be the largest of its kind studying MRSA in
private nursing homes in the UK, took nose swabs from 1,111 residents and 553 staff in 45
nursing homes in the former Northern Board area of Northern Ireland. Twenty-four per cent
of residents and 7 per cent of staff were found to be colonised with MRSA, meaning they
were carrying the bacteria but not necessarily showing signs of infection or illness.
'Shock and kill' research gives new
hope for HIV-1 eradication
Latent HIV genes can be 'smoked out' of human cells. The so-called 'shock and kill'
technique, described in a preclinical study in BioMed Central's open access journal
Retrovirology, might represent a new milestone along the way to the discovery of a cure
for HIV/AIDS. Dr. Enrico Garaci, president of the Istituto Superiore di Sanitŕ (the
Italian Institute of Health) and Dr. Andrea Savarino, a retrovirologist working at the
institution, worked with a team of researchers to study the so-called "barrier of
latency" which has been the main obstacle to HIV eradication from the body. Cells
harbouring a quiescent HIV genome are responsible for HIV persistence during therapy. In
other words, HIV-1 genes become pieces of the human organism, and many scientists have
simply thought there is nothing we can do. Dr Savarino's team aimed to 'smoke out' the
virus in order to render the latently infected cells targetable by the immune system or
artificial means. They write, "This can be achieved using inhibitors of histone
deacetylases (HDACs), which are a class of enzymes that maintain HIV latency. However,
their effects on HIV are evident only when used in toxic quantities".
Brain irradiation in lung cancer
A national Radiation Therapy Oncology Group (RTOG) study led by a Medical College of
Wisconsin Cancer Center physician at Froedtert Hospital in Milwaukee has found that a
course of radiation therapy to the brain after treatment for locally advanced non-small
cell lung cancer reduced the risk of metastases to the brain within the first year after
treatment. The study was presented at the American Society of Clinical Oncology annual
meeting in Orlando, June 1. "With improved treatments for non-small cell lung cancer,
patients are living longer and we are seeing more brain metastases," says study
author Elizabeth Gore, M.D. "This study compared the efficacy of prophylactic
(preventive) cranial irradiation (PCI) vs. observation in these patients, and found that
those not receiving cranial irradiation were two and one-half times more likely to develop
brain metastasis than those who did." The study analyzed 356 patients. While the
results did not show a statistically significant difference in survival between the two
groups, it did show that PCI significantly decreased the incidence of brain metastases
during the first year post-treatment. Dr. Gore anticipates that additional study of the
impact of PCI --on neuro-psychological function and quality of life in these patients--
will help determine if use of PCI should become standard care.
Ballerinas & Female Athletes
Share Quadruple Health Threat Important Prevention Tips for Young Female Athletes
A study led by sports medicine researcher Anne Hoch, DO, at The Medical College of
Wisconsin in Milwaukee has revealed that young female professional dancers face the same
health risks as young female athletes when they don’t eat enough to offset the energy
they spend, and stop menstruating as a consequence. “These two components of the
female athlete tetrad put them at higher risk for the other two; the cardiovascular and
bone density deficits of much older, postmenopausal women,” according to Dr. Hoch,
associate professor of orthopaedic surgery and director of the Froedtert & the Medical
College Women’s Sports Medicine Center. The researchers studied 22 professional
ballerinas, all members of the Milwaukee Ballet Company, to determine the prevalence of
disordered eating, amenorrhea (lack of menstruation), abnormal vascular function and low
bone density. Study findings were presented at the American College of Sports Medicine
meeting in Seattle, May 30. The dancers completed questionnaires on their menstrual
patterns and eating habits, and underwent a blood test for hormonal levels. Thirty-six
percent of the group had disordered eating habits and 77 percent were in a calorie
deficit. Twenty-seven percent were currently amenorrheic, 23 percent had low bone mass
density and nine percent were taking birth control. Arterial ultrasound measurements
revealed that 64 percent had abnormal artery dilation in response to blood flow.
Scientists discover new genetic
immune disorder in children
Your immune system plays an important function in your health—it protects you against
viruses, bacteria, and other toxins that can cause disease. In autoinflammatory diseases,
however, the immune system goes awry, causing unprovoked and dangerous inflammation. Now,
researchers from the National Institute of Arthritis and Musculoskeletal and Skin Diseases
(NIAMS), part of the National Institutes of Health, and other institutions have discovered
a new autoinflammatory syndrome, a rare genetic condition that affects children around the
time of birth. The findings appear in the current issue of the New England Journal of
Medicine. The scientists have termed the new autoinflammatory syndrome DIRA (deficiency of
the interleukin-1 receptor antagonist). Children with the disorder display a constellation
of serious and potentially fatal symptoms that include swelling of bone tissue; bone pain
and deformity; inflammation of the periosteum (a layer of connective tissue around bone);
and a rash that can span from small individual pustules to extensive pustulosis that
covers most of the patient's body. Most of the children begin to have symptoms from birth
to 2 weeks of age. "The beauty of this discovery is that the symptoms of this
devastating disease can now be treated," said NIAMS director and immunodermatologist,
Stephen I. Katz, M.D., Ph.D. "The abnormal inflammatory pathways seen in this disease
may also help us understand other common diseases that share clinical features, such as
psoriasis, as well as other autoinflammatory disorders." "We knew when we saw
these children that we were dealing with a previously unrecognized autoinflammatory
syndrome. The clinical characteristics were distinct from other diseases we had seen
before," said NIAMS researcher and lead author Raphaela Goldbach-Mansky, M.D., M.H.S.
When her colleague, Dr. Ivona Aksentijevich, tested the first patient for genetic
abnormalities, their suspicions were confirmed, and ultimately abnormalities were found in
a number of other cases. All the children had inherited mutations in IL1RN, a gene that
encodes a protein known as interleukin-1 receptor antagonist (IL-1Ra). IL-1Ra binds to the
same cell receptors as the inflammatory protein interleukin-1, and acts as a brake on this
inflammatory protein. Without IL-1Ra, the children's bodies cannot control systemic
inflammation that can be caused by interleukin-1.
The End of the Line Trailer
The End of the Line is a powerful film
about one of the world's most disturbing problems - over-fishing. Advances in fishing
technology mean whole species of wild fish are under threat and the most important stocks
we eat are predicted to be in a state of collapse by 2050. The film points the finger at
those most to blame, including celebrity chefs, and shows what we can do about it. This is
not just a film, it is also a campaign - for sustainable consumption of fish, for marine
protected areas to allow the sea to recover, and for a new ethic of responsible fishing.
Underwater Wilderness: Creating
Marine Protected Areas
The waters off the coast of California are
some of the richest in the world. But declines in fish species have led state leaders to
begin creating large protected areas, or "no fishing zones," similar to
wilderness areas on land. Although controversial with some fishing groups, the idea is to
protect entire ecosystems instead of single species. The hope is that a statewide network
may help bring back fish, birds and marine mammals that are currently on the brink.
Autoinflammatory disease model
reveals role for innate, not adaptive, immunity
Researchers at the University of California, San Diego School of Medicine have developed
the first mouse model for auto-inflammatory diseases, disorders that involve the
over-activation of the body's innate, primitive immune system. Their study, published
early on-line in Cell Immunity on June 4, suggests that the innate – not adaptive
– immune system drives auto-inflammatory diseases. The findings could open new
therapeutic directions for research into disorders such as gout or inflammatory bowel
disease. "Auto-inflammatory diseases are a relatively new classification of diseases
that are different from autoimmune diseases or allergies," said Hal Hoffman, MD,
associate professor of medicine at UC San Diego School of Medicine. Hoffman studies a
group of rare, inherited auto-inflammatory conditions called Cryopyrin-Associated Periodic
Syndromes (CAPS), which includes Familial Cold Auto-inflammatory Syndrome (FCAS) and
Muckle-Wells Syndrome (MWS). Autoimmune diseases arise from an overactive response of the
body's adaptive, or acquired, immune system against substances and tissues normally
present in the body. Allergies are also a product of the adaptive immune system, but in
response to environmental substances. Both involve the action of lymphocytes such as B
cells and T cells. The older innate immune system, on the other hand, recruits immune
cells to sites of infection and inflammation, but doesn't confer long-time protection.
Pathogens evoke an inappropriate response that doesn't involve antibodies or lymphocytes.
With CAPS, Hoffman had earlier discovered that mutations of the NLRP3 gene caused the
auto-inflammatory disease symptoms because the gene causes alterations in the protein
called cryopyrin. Cryopyrin regulates the release of interleukin-1, an important mediator
of fever and systemic inflammation during the body's innate immune response, and
alterations in cryopyrin lead to over-production of Il-1. Mutations in the NLRP3 gene are
thought to result in inappropriate activation of a multi-protein complex called an
inflammasome, leading to excessive Il-1? release and manifestation of CAPS disease
symptoms. Treatment with Il-1? inhibitors reduces the inflammation and symptoms in
auto-inflammatory diseases; however, NLRP3 may have other effects in addition to increased
Il-1?. "Patients treated with the Il-1? inhibitors got much better, but still
exhibited some symptoms," said Hoffman.
Study shows animal mating choices
more complex than once thought
When female tiger salamanders choose a mate, it turns out that size does matter - tail
size that is - and that's not the only factor they weigh. Findings of a Purdue University
study show that animals make more complex decisions about choosing mates than once
thought. The results of Andrew DeWoody's study, released Monday (June 8) in the journal
Molecular Ecology, refute a theory that animals use major histocompatibility complex (MHC)
genes as the sole basis for mate choice. Immunologists have long known that MHC genes play
key roles in the immune response, but more recently behavioral ecologists have postulated
that animal mate choice is often based on MHC-type because of the function of those genes.
Health risks begin in overweight
range, BMI doesn’t tell whole story
Being overweight is a health concern, and using only body mass index (BMI) to determine
weight classification may not give an accurate picture of a person’s health,
according to an advisory published in Circulation: Journal of the American Heart
Association. About one-third of the U.S. population is overweight — the middle range
between normal weight and obesity. Overweight in adults is a BMI of 25.0 to 29.9. BMI is a
numerical value of weight in relation to height. Studies that examined the relationship
between overweight (as measured by BMI) and risk of death from all causes (often referred
to as total mortality) have had contradictory results. However, considering death from all
causes overlooks the role that overweight may play in the development of risk factors for
cardiovascular diseases. Even among the young, overweight is related to the development of
serious risk factors for cardiovascular disease, such as high blood pressure, obesity,
elevated levels of cholesterol and type 2 diabetes.
Diabetes patients should have
regular exercise, weight training
To reduce their cardiovascular risk, people with type 2 diabetes should do at least
two-and-a-half hours per week of moderate-intensity or one-and-a-half hours per week of
vigorous-intensity aerobic exercises, plus some weight training, according to an American
Heart Association scientific statement published in Circulation: Journal of the American
Heart Association. The global increase in overweight and obesity has led to an
“unprecedented epidemic” in type 2 diabetes (when the body is unable to use
insulin efficiently to help turn glucose, or blood sugar, into energy for the body’s
cells). In 2007, type 2 diabetes in the United States cost an estimated $174 billion in
direct medical costs and indirect costs such as disability, lost productivity and
premature death. That amount represents a 30 percent increase from the $132 billion
estimated in 2002, according to the statement. Furthermore, heart and blood vessel disease
is responsible for nearly 70 percent of deaths in people with type 2 diabetes.
Self-regulation game predicts
kindergarten achievement
Early childhood development researchers have discovered that a simple, five-minute
self-regulation game not only can predict end-of-year achievement in math, literacy and
vocabulary, but also was associated with the equivalent of several months of additional
learning in kindergarten. Claire Ponitz from the University of Virginia and Megan
McClelland of Oregon State University assessed the effectiveness of a game called the
Head-Toes-Knees-Shoulders (HTKS) task, which is a new version of the Head-to-Toes task
developed by researchers at the University of Michigan. Both tasks have proved effective
at predicting academic skills among preschool age children. Their results were published
in the newest issue of the journal, Developmental Psychology.The researchers assessed a
group of 343 kindergarteners from Oregon and Michigan. Their self-regulation, or ability
to control behavior, was measured with the Head-Toes-Knees-Shoulders task, a structured
observation requiring children to perform the opposite of a response to four different
oral commands. For example, children were instructed to touch their toes if told to touch
their head, and vice versa. They found that students who performed well on his behavior
task in the fall achieved strong scores in reading, vocabulary and math in the spring,
compared to students who had low performance on the task. In addition, the research showed
that the children who performed well on the task scored 3.4 months ahead of peers who
performed at average levels on mathematics learning. "It's amazing that this game
works as well as it does," McClelland said. "It is simple to administer, fun for
the kids, and predicts children's academic achievement." One area where the task did
not make a difference was assessing children's interpersonal skills. McClelland explained
that the game is not "emotion-oriented," meaning it is not set up to trigger an
emotional response. Instead, the Head-Toes-Knees-Shoulders task tests children on
important classroom-related behavior such as listening, following directions and
remembering instructions.
4 risk factors raise probability of
developing precursor of heart failure
Four well-known risk factors for heart attack significantly increased the size of the
heart's left ventricle, a key precursor of heart failure, according to a study in
Circulation: Journal of the American Heart Association. High blood pressure, excessive
weight, smoking and diabetes were strongly correlated with greater size of the heart's
left ventricle over the short term (four years) and the long term (16 years) in a study of
more than 4,217 people. "Left ventricular mass has been associated in multiple
studies with risk of cardiovascular disease, including risk of developing heart failure.
We identified four risk factors that promote greater cardiac mass over the adult life
course. These factors can be directly targeted for prevention and lowering these risk
factors, therefore, could potentially lower the burden of heart failure." said
Ramachandran S. Vasan, M.D., the study's senior author, a senior investigator at the
Framingham Heart Study, and professor of medicine and the chief of the section of
Preventive Medicine at Boston University School of Medicine. Researchers assessed the
effect of risk factors on left ventricular (LV) mass by analyzing longitudinal data from
the Framingham (Mass.) Offspring Study. The participants averaged 45 years of age at study
entry. Fifty-three percent were women. The Framingham Offspring Study enrolled children of
participants of the original Framingham Heart Study, which began in 1948. Researchers used
data obtained at an initial exam in the 1970s and data from follow-up exams conducted at
four-year intervals through the late 1990s, and evaluated short-term associations of LV
mass using data from 2,605 of the participants. Study members were divided into three
groups: low, intermediate and high numbers of risk factors. High blood pressure, excessive
weight, smoking and diabetes strongly correlated with greater left ventricular mass; age,
and gender were also associated with heart muscle thickening, researchers said.
Top notch decisions in the
developing airways bring insights into lung disease
In the normal lung, the airways are lined by a balanced mixture of ciliated, secretory and
neuroendocrine cells which perform functions as diverse as air humidification,
detoxification, and clearance of environmental particles. This balance can be altered
dramatically by faulty adaptation responses of the lung to cigarette smoke or allergens in
patients with Chronic Obstructive Pulmonary Disease (COPD) and asthma. How these different
cell types emerge from lung progenitor cells and how these fates are balanced in
developing airways, remain an open question. A study from a research team led by
Wellington Cardoso, MD, a professor at the Pulmonary Center Boston University School of
Medicine and Director of the Program in Lung Development and Progenitor Cell Biology,
sheds light into this problem. The Notch pathway is a major regulator of cell fate
decisions in developing cells from fruit flies to humans. Using mouse genetic models, the
BU researchers inactivated Notch signaling in the lung and discovered that airways no
longer formed secretory cells. Instead they became populated almost exclusively by
ciliated cells. The researchers showed that this imbalance seems to result from the loss
of a mechanism of cell fate choice triggered by the Notch called lateral inhibition.
"When you lose Notch signaling, you lose the ability to generate secretory cells that
make the lining fluid critical for protection and integrity of airway, and the other fate,
of ciliated cells is de-repressed" said Dr. Cardoso.
Common chemotherapy drug triggers
fatal allergic reactions
A chemotherapy drug that is supposed to help save cancer patients' lives, instead resulted
in life-threatening and sometimes fatal allergic reactions. A new study from the Research
on Adverse Drug Events and Reports (RADAR) pharmacovigilance program at Northwestern
University Feinberg School of Medicine identified 287 unique cases of hypersensitivity
reactions submitted to the FDA's Adverse Event Report System between 1997 and 2007 with
109 (38 percent) deaths in patients who received Cremophor-based paclitaxel, a
solvent-administered taxane chemotherapy. Adverse event reports generally only represent
from 1 to 10 percent of actual incidence, so the number of hypersensitivity reactions and
deaths is likely significantly higher. The severe allergic reactions are believed to be
caused by Cremophor, the chemical solvent - a derivative of castor oil -- that is used to
dissolve some insoluble drugs before they can be injected into the blood stream.Two
patients who died from an allergic reaction had early-stage breast cancer, which had been
surgically removed, and were being treated with Cremophor-containing paclitaxel to prevent
the cancer from coming back. Both of these patients had received medications before the
chemotherapy to reduce the risk of hypersensitivity reactions. The study was led by
Charles Bennett, M.D., RADAR program coordinator and a professor of hematology/oncology at
Northwestern's Feinberg School, and Dennis Raisch, a professor of pharmacy at the
University of New Mexico."The deaths of women with early-stage breast cancer are
particularly disturbing because without the adverse reaction, they could have likely had
40 years of life ahead of them," Bennett said. RADAR investigators also found that 22
percent of all fatalities occurred in patients despite patients having received
premedication to prevent hypersensitivity reactions, while another 15 percent of such
patients experienced life-threatening respiratory arrest.
Horse whisperers, lion tamers not
needed - Scientists find genetic regions that soothe savage beasts
In what could be a breakthrough in animal breeding, a team of scientists from Germany,
Russia and Sweden have discovered a set of genetic regions responsible for animal
tameness. This discovery, published in the June 2009 issue of the journal GENETICS
(http://www.genetics.org), should help animal breeders, farmers, zoologists, and anyone
else who handles and raises animals to more fully understand what makes some animals
interact with humans better than do others. It may also lead to more precise breeding
strategies designed to pass specific genes from one generation to the next as a way to
produce tame animals. "I hope our study will ultimately lead to a detailed
understanding of the genetics and biology of tameness," said Frank Albert, a
scientist from the Max Planck Institute for Evolutionary Anthropology in Germany and the
first author of the research report. "Maybe we'll then be able to domesticate a few
of those species where humans have historically not been successful like the wild African
Buffalo." The roots of this study date back to 1972 when researchers in Novosibirsk,
USSR (now Russia), caught a large group of rats in the wilderness around the city. After
bringing them into the laboratory, the researchers divided them into two groups. The first
group included the most "friendly" rats – those that were not aggressive
toward people. The second group included only the most aggressive rats – those that
screamed, attacked and bit the researchers. Since then, these rats have been bred with one
another, and now, the two groups of rats act very differently toward people. The tame rats
tolerate being touched and picked up, and never attack. The aggressive rats scream, run
away, or attack and bite. For this research study, the scientists mated the tame with the
aggressive rats and identified regions in the rat genome that cause a rat to be tamer or
more aggressive. "For thousands of years, humans have domesticated animals,"
said Mark Johnston, Editor-in-Chief of the journal GENETICS, "and all during this
time, much folklore and mythology has surrounded the process. But of course genetics plays
a large role in the process, and this research provides a solid scientific explanation of
this phenomenon, and offers clues about how genomes can be manipulated to breed tame
animals of species once believed to be untamable."
More Ontario children are getting
diagnosed with diabetes
Ontario children are more likely to get diagnosed with diabetes than their American
counterparts. A study out of the Institute for Clinical Evaluative Sciences (ICES) has
found a 3 per cent increase per year in the rate of diabetes in Ontario children from 1994
to 2004. Childhood diabetes is a chronic disease that can cause major health problems.
Most children with diabetes have Type 1, where their pancreas does not make insulin. But a
growing number of children are getting diagnosed with Type 2 diabetes, in which the body
produces enough insulin but is resistant to its effect, usually because of genetic
disposition and obesity. "It is concerning that we are seeing more children in
Ontario diagnosed with this serious chronic disease - we need to better understand why
this happening and ensure that adequate healthcare resources are available to diagnose and
treat these children and youth," says principal investigator and ICES Scientist, Dr.
Astrid Guttmann.
Vaporized viral vector shows
promise in anti-cancer gene therapy
A new lung cancer therapy employing a vaporized viral vector to deliver a
cancer-inhibiting molecule directly to lung tissue shows early promise in mouse trials,
according to researchers at the Ministry of Education, Science and Technology in Korea.
Gene therapy is an area of great promise, but delivery mechanisms, which have included
intravenous injection and intratracheal instillation, have proven problematic for
effective delivery of genetic therapy to lung tissues. "Aerosol delivery targets the
lungs specifically and represents a noninvasive alternative for targeting genes to the
lung," wrote Myung-Haing Cho, D.V.M., Ph.D., professor at Seoul National University
and principal investigator of the study. "The delivery of genes via aerosol holds
promise for the treatment of a broad spectrum of pulmonary disorders and offers numerous
advantages over more invasive modes of delivery." The results of Dr. Cho's promising
research will be published in the June 15 issue of the American Journal of Respiratory and
Critical Care Medicine. Lung cancer is the most common cause of cancer deaths worldwide,
killing more people each year than breast, prostate and colon cancers combined. It costs
the U.S. alone more than $9 billion a year, according to the Centers for Disease Control
and Prevention. Most available therapies—surgery, radiation and
chemotherapy—offer transient relief at best and are typically ineffective in advanced
stages of the disease. For this reason, novel therapies for lung cancer are of great
interest. Dr. Cho and colleagues targeted the Akt signaling pathway, which has been shown
to be an important regulator of cell proliferation and cancer progression. A recent report
found that 90 percent of non-small cell lung carcinomas were associated with the
activation of the Akt signaling pathway. They chose a lentiviral vector, derived from a
retrovirus and known for its ability to infect nondividing cells and effect persistent
genetic changes. They transfected the lentiviral vector with a negative regulator of Akt
signaling, carboxyl-terminal modulator protein (CTMP), which would theoretically inhibit
Akt signaling, thus suppressing cancer cell proliferation and tumor growth. Using a mouse
model of lung cancer, the researchers designed a double-control study, exposing one-third
of the mice to the aerosolized CTMP vector, one-third to the vector alone and one third
were untreated.
Defeating nicotine's double role in
lung cancer
A lung cancer treatment that inhibits nicotine receptors was shown to double survival time
in mice, according to Italian researchers. The results of the early phase animal model
study were reported in the June 15 issue of the American Journal of Respiratory and
Critical Care Medicine. Changes in genes encoding nicotine receptors are strongly
associated not only with the tendency to smoke, but with susceptibility to lung cancer.
Nicotine exposure also heightens the expression of the nicotine receptors, which leads to
increased cell proliferation and inhibition of apoptosis, further setting the stage for
cancer. Patrizia Russo, Ph.D. and Laura Paleari, Ph.D. of the Lung Cancer Unit of the
National Cancer Research Institute in Genoa, Italy and colleagues from San Raffaele Pisana
Scientific Institute for Research, Hospitalization and Health Care (IRCCS), Catholic
University, Campus Biomedico University in Rome, Mario Negri Institute in Milan and CEA
Gyf sur Yvette in France showed in past research that an antagonist of nicotine
acetylcholine receptors (nAChRs), may serve as an anticancer agent. The antagonist, called
d-tubocurarine/?-Cobratoxin (?-CbT), specifically targeted the ?7 subunit of nAChRs, the
area primarily associated with increased cell proliferation. In this study, the authors
took the research a step further and showed that ?-CbT could inhibit non-small cell lung
carcinoma (NSCLC) growth and prolong life in non-obese/severe combined immunodeficient
(NOD/SCID) mice that had human NSCLC grafted to their lungs. This study attempted to mimic
human cancer conditions more closely by delaying treatment until the tumors were
well-established. In addition to control mice that were untreated, the researchers
randomized one third of the mice to receive standard chemotherapy. They found that
NOD/SCID mice treated with the standard chemotherapy agent, cisplatin, had a 16 percent
longer median survival time than untreated mice (p= 0.05). Mice treated with ?-CbT,
however, had an increased median survival time of 1.7-fold over the cisplatin-treated mice
and 2.1-fold over the no-treatment controls (p=0.0005). "The results of this study
show that ?-CbT, a powerful, high-affinity ?-7-nAChR inhibitor, induces antitumor activity
against NSCLC by triggering apoptosis," wrote Dr. Russo. "The prolonged survival
of ?-CbT-treated animals in our mouse model of NSCLC is most likely the result of several
mechanisms, including various antiproliferative and antiangiogenic effects."
Researchers shed light on trading
behavior in animals -- and humans
Humans, from ancient exchanges of food to modern day home mortgages, have bartered or
traded to receive something that they couldn't achieve on their own. It's the basis of the
economy, and it requires a leap of faith to believe that each party will receive a payoff
in return for taking a risk. When confidence breaks down, such as what happened during the
recent collapse of the housing market, the economy slows. The willingness to take risk is
based at least in part on the reputation of trading partners and may be unique among
humans. Our closest evolutionary relatives, chimpanzees, aren't very good at it, according
to new research by scientists at Georgia State University's Language Research Center.
Georgia State's Sarah Brosnan, assistant professor of psychology, and research scientist
Michael Beran conducted a study to see if chimpanzees spontaneously bartered foods among
each other, using tokens which represented those foods. While results indicated that the
animals were cognitively able to understand trade, without enforcement from human
experimenters, trade disappeared. Chimpanzees are known to trade services, such as
grooming for food, but the ability does not seem to extend to trading commodities.Most of
the trading of services seems to occur between partners who interact a lot, and so are
familiar with each others' behavior. The chimpanzees thus know whether the risk is likely
to pay off, and most of the time, what's being traded is a relatively inexpensive
commodity. "If I spend five minutes grooming you, but you don't groom back, I haven't
lost very much," Brosnan said. "But I might not want to trade a food that
represents 10 or 20 percent of my calories for the day if I risk getting noting in return.
If you don't complete the trade, I've lost a lot."
Study says colorectal cancer
increasing in young adults
A new study finds that in sharp contrast to the overall declining rates of colorectal
cancer in the United States, incidence rates among adults younger than age 50 years are
increasing. The authors theorize that these increases may be related to rising rates of
obesity and changes in dietary patterns, including increased consumption of fast food. The
study, which appears in the June 2009 issue of Cancer Epidemiology Biomarkers and
Prevention, says further studies are necessary to elucidate causes for this trend and to
identify potential prevention and early detection strategies. Overall incidence rates for
colorectal cancer in the United States have been on the decline since the mid-1980s, with
the drop accelerating in the most recent time period. Rates are now dropping 2.8 percent
per year in men and 2.2 percent per year in women, largely due to an increase in
screening, particularly colonoscopy, among individuals ages 50 years and older. Screening
can reduce colorectal cancer incidence by detecting and removing polyps before they become
cancerous. But recent incidence trends among adults younger than 50 years, for whom
routine screening is not recommended, have not been analyzed thoroughly. A previous study
did find an increase in incidence from 1973 to 1999 for all races combined, but that study
did not include 40 to 49 year-olds, who represent 73 percent of colorectal cancer patients
under age 50. In a new analysis, American Cancer Society researchers led by Rebecca L.
Siegel, M.P.H., looked at trends in colorectal cancer incidence rates between 1992 and
2005 among young adults (ages 20 to 49) by sex, race/ethnicity, age, stage at diagnosis,
and anatomic subsite. The study found that among individuals ages 20 to 49, incidence
rates of colorectal cancer increased 1.5 percent per year in men and 1.6 percent per year
in women from 1992 to 2005. Among non-Hispanic Whites, rates increased for both men and
women in each 10-year age grouping (20-29, 30-39, and 40-49 years) and for every stage of
diagnosis. They found the largest annual percent increase in colorectal cancer incidence
was in the youngest age group (20-29 years), in whom incidence rates rose by 5.2% per year
in men and 5.6% per year in women. They say the rises are due to an increase in left-sided
tumors, particularly in the rectum.
University of Saskatchewan and
Canadian Synchrotron researchers shed light on esophageal disease
Canadian Light Source (CLS) staff scientist Luca Quaroni and Dr. Alan Casson, Head of the
Department of Surgery at the University of Saskatchewan (U of S) used the synchrotron's
infrared microscope to identify tissue afflicted with a condition known as Barrett's
Esophagus from chemical fingerprints associated with the disease, which can lead to
esophageal cancer. The finding is published in the June, 2009 issue of the Royal Society
of Chemistry journal, The Analyst. "The advantage to using microscopes with
synchrotron light is that it allows us to identify chemical biomarkers inside specific
cells," says Dr. Quaroni, who conducted the synchrotron analysis. "Often the
differences between healthy and malignant tissue can be quite small, but the differences
seen here were quite striking. This is a good proof of concept for developing a traceable
technique that matches what can be seen at the macroscopic scale using microscopic
samples." The team analyzed preserved samples of healthy and diseased tissue that Dr.
Casson had collected during esophageal biopsies. Using a technique known as Fourier
Transform Infrared Microscopy, Quaroni and Casson identified specific chemicals –
known as biomarkers - within the individual cells that make up the tissue. It was found
that increased concentrations of particular biomarkers such as glycoproteins were
associated with the Barrett's tissue.
LSUHSC researchers first to
document early signs for diabetes in kids as young as 7
Research conducted under the direction of Melinda Sothern, PhD, Professor and Director of
Health Promotion at the LSU Health Sciences Center New Orleans School of Public Health,
showing early signs of diabetes in healthy children as young as seven years old will be
presented at the American Diabetes Association 2009 Annual Scientific Session Meeting in
New Orleans. Dr. Sothern's group is the first to document previously unknown markers for
obesity, heart disease and diabetes, collectively called the Metabolic Syndrome, in
children this young. Posters will be presented on Saturday, June 6, 2009, and Brian
Bennett, a Research Associate in Dr. Melinda Sothern's laboratory will make the oral
presentation, Early Markers for the Metabolic Syndrome in Youth, on Monday, June 8, 2009
at 9:30 a.m. at the Ernest N. Morial Convention Center, Room 343. Dr. Sothern will be
there for the presentation. Data reported are from 118 healthy children, age 7 - 9 years
old, enrolled in LSUHSC's ongoing Study of Insulin-sensitivity in Louisiana
Low-birth-weight Youth (SILLY). LSUHSC's Dr. Sothern is the principal investigator of the
NIH-funded study which is investigating the importance of birth weight to diabetes. The
increasing prevalence of type 2 diabetes mellitus in children parallels the pediatric
obesity epidemic. According to the American Academy of Pediatrics, over the past two
decades, the prevalence of children who are obese has doubled, while the number of
adolescents who are obese has tripled. And according to the National Health and Nutrition
Examination Survey, 31.9% of children and adolescents were overweight (BMI at or above the
85th percentile) and 16.3% were obese (BMI at or above 95th percentile). Insulin
resistance/poor insulin sensitivity is closely associated with increased total body fat
and may precede development of the metabolic syndrome and type 2 diabetes. Indicators of
impaired insulin sensitivity have yet to be clearly identified in children prior to
puberty.
Boys with intermittent eye
deviation appear more likely to develop mental illness
Children and especially boys diagnosed with intermittent exotropia, a condition in which
the eye turns outward (away from the nose) only some of the time, appear more likely to
develop mental illness by young adulthood than children without strabismus (when the eyes
deviate or are misaligned when looking at an object), according to a report in the June
issue of Archives of Ophthalmology, one of the JAMA/Archives journals. "Intermittent
exotropia occurs in approximately 1 percent of developmentally healthy children in the
United States and, given its predominance over esodeviations [when the eye turns in] among
Asian populations, it may be the most prevalent form of strabismus worldwide," the
authors write as background information in the article. Jeff A. McKenzie, B.A., and
colleagues at Mayo Clinic, Rochester, Minn., analyzed the medical records of 183 children
younger than 19 in Olmsted County, Minn., who were diagnosed with intermittent exotropia
between 1975 and 1994. For each patient, the researchers identified one control child who
was the same age but did not have a diagnosis of any type of strabismus. Both groups were
followed to an average age of 22. During the 20-year study period, 97 of the children with
intermittent exotropia (53 percent) were diagnosed with a mental health disorder, compared
with 55 controls (30.1 percent)—meaning that patients with the condition had an
increased risk of developing a psychiatric illness. Mental health disorders were diagnosed
in 63 percent of boys (41 of 65) and 47 percent of girls (56 of 118) with intermittent
exotropia, compared with 33 percent of boys (22 of 66) and 28 percent of girls (33 of 117)
in the control group."Additionally, males with intermittent exotropia had a greater
use of psychotropic medication, psychiatric emergency department visits, psychiatric
hospital admissions, suicide attempts and suicidal ideation than controls, and females
with intermittent exotropia had more suicidal ideation than controls," the authors
write.
Embryology Study Offers Clues to
Birth Defects
Gregg Duester, Ph.D., professor of developmental biology at Burnham Institute for Medical
Research (Burnham), along with Xianling Zhao, Ph.D., and colleagues, have clarified the
role that retinoic acid plays in limb development. The study showed that retinoic acid
controls the development (or budding) of forelimbs, but not hindlimbs, and that retinoic
acid is not responsible for patterning (or differentiation of the parts) of limbs. This
research corrects longstanding misconceptions about limb development and provides new
insights into congenital limb defects. The study was published online in the journal
Current Biology on May 21.
Hypertension among lower-status
employees lingers well into retirement
Retirement from some occupations may not provide relief from the potentially devastating
health effects of work-related hypertension, according to a new study from UC Davis.
Published in the June issue of the Journal of Occupational and Environmental Medicine, the
study is the first to show that retirement-aged Americans who held higher-status jobs
— such as chief executives, financial managers and management analysts — tend to
have the lowest rates of hypertension, while those who had lower-status jobs tend to have
the highest rates. Hypertension is diagnosed when blood pressure on the artery walls is
consistently too high. This condition can eventually damage cells of the arteries' inner
lining, leading to angina, heart attack, stroke, aneurysm, kidney failure and other
serious health problems. "People's occupations during their working years can clearly
be a risk for hypertension after they retire," said senior study author Paul Leigh, a
professor with the Center for Healthcare Policy and Research and the Department of Public
Health Sciences at UC Davis. "The body seems to have built up a stress reaction that
takes years to ramp down and may last well beyond age 75." While one European study
correlated pre-retirement jobs with heart disease among seniors, most similar research has
focused on working people between the ages of 25 and 65. Consequently, Leigh said,
"it's been an open question whether occupations could influence hypertension after
retirement, and we wanted to help close that gap in the research." Leigh, an expert
in economics and occupational illnesses, and study co-author Juan Du, who recently
received her Ph.D. from UC Davis and is now an assistant professor in the School of
Business at The College of New Jersey, based their research on data compiled by the
University of Michigan Health and Retirement Study. Funded by the National Institute on
Aging, the study surveys more than 22,000 non-institutionalized Americans over the age of
50 every two years and includes detailed information on job history, health status,
lifestyle and socioeconomic factors. Using data collected between March 2004 and February
2005, Leigh and Du looked at 7,289 men and women over the age of 65. Their occupations
during working years ran the gamut — from managers and white-collar professionals to
clerical and blue-collar workers. Just a small percentage was still working at the time
the data was collected — 10 percent of 65-year-olds and 2 percent of 75-year-olds.
UC Davis to collaborate on nation's
most comprehensive study of autism early risk factors
A network of leading autism researchers from three regions across the country today
launched one of the largest research studies of its kind to investigate early risk factors
for Autism Spectrum Disorders (ASD). The network, called the Early Autism Risk
Longitudinal Investigation (EARLI) study, will follow up to 1,200 pregnant women who
already have a child with autism. The study is considered one of the best-equipped to
discover biological markers and environmental risk factors for autism, due to its elevated
autism-risk pregnancy cohort, wide-ranging data collection with extensive bio-sampling,
lengthy follow-up of pregnant women and their babies, and multidisciplinary team of expert
investigators. Under the study, researchers at four network field sites around the
country, including UC Davis, will study possible environmental risk factors and their
interplay with genetic susceptibility during the prenatal, neonatal and early postnatal
periods. The project will also investigate early biological indicators of autism. The
EARLI study is one of 11 National Institutes of Health Autism Centers of Excellence
projects nationwide.
Researchers identify new risk
factor gene for rheumatoid arthritis
Scientists at The Feinstein Institute for Medical Research and a team of collaborators
from across the country have identified a new risk factor gene for rheumatoid arthritis.
The paper will be published in Nature Genetics and the finding brings light to the nature
of the disease. The gene, dubbed REL, is a member of the NF-?B family, important
transcription factors that have many roles in the body. The NF-?B family seems to have a
big hand in regulating the body's immune response as well. "The NF-?B is a key
switching point for many cellular activities," said Peter K. Gregersen, MD, head of
the Robert S. Boas Center for Genomics and Human Genetics at the Feinstein Institute and
lead author of the study. Dr. Gregersen is part of a nationwide consortium of
investigators seeking to identify risk genes for rheumatoid arthritis (RA). The hope is to
figure out the genetic triggers and identify treatments that block this autoimmune
process. In theory, such advances can point the way to understanding other autoimmune
disorders. About one percent of the population will develop rheumatoid arthritis, which
can be crippling. REL is a key regulator of CD40, which works through the NF-?B pathway.
"This paper represents the latest in a series of important publications chronicling
an exceptionally productive collaboration between extramural and intramural scientists
through the North American Rheumatoid Arthritis Consortium," said Daniel Kastner, MD,
PhD, clinical director of the National Institute of Arthritis and Musculoskeletal and Skin
Diseases. "In describing yet another gene in the CD40 signaling pathway that is
involved in rheumatoid arthritis susceptibility, this paper reinforces the possibility of
targeting this pathway in selected patients with this debilitating illness." The
consortium has helped identify many genes involved in rheumatoid arthritis but this
genetic finding is significant because of its key role in immune system regulation. It did
not reveal itself in previous genetic studies because the sample size was just not large
enough. In previous studies, genetic samples from about 2,000 patients were used to
identify markers associated with risk for RA. In the latest study, the scientists analyzed
samples from 4,000 RA patients and controls. According to Dr. Gregersen, this particular
genetic variant is rather common, found in about a third of people in North America. That
means that it must confer an important survival advantage. That said, scientists need to
figure out its role in increasing the risk for RA. Next on the research agenda is to see
if they can measure how the gene is regulated under specific conditions that set the stage
for RA. "There are a huge number of unknowns," said Dr. Gregersen. "These
findings are clear – this pathway is involved – but there is a lot of work to be
done." Genetic differences between individuals help scientists understand many
diseases. But this is just the beginning, added Dr. Gregersen. Today, most markers that
are used to identify genes represent variants that occur in more than five percent of the
population. The next wave in genetic screening will have to include the variants that
occur in less than one percent of the population.
Physiological response may explain
why some severely obese patients overeat
Don't feel like you are getting full when eating a large meal? New research from The
Miriam Hospital suggests that a physiological response may partially explain why severely
obese individuals may not feel satisfied after eating and often have difficulty
controlling the amount of food they consume during a meal. Researchers led by Dale Bond,
PhD, of The Miriam Hospital's Weight Control and Diabetes Research Center focused on
habituation, or the idea that continual exposure to a specific food decreases one's
physical response to that food. Habituation theory suggests that if one habituates, or
adjusts, slowly to food cues, they are less likely to feel satisfied with that particular
food and can consume more of it. In the study, published online in Obesity Surgery, the
research team looked at saliva production following repeated exposure to lemon juice. They
compared the responses of two groups – severely obese patients preparing for
bariatric surgery and normal weight individuals – and found that the bariatric
surgery candidates continued to salivate at a consistent rate throughout the tastings,
indicating that very little habituation occurred. Meanwhile, the salivation rate of the
normal weight controls decreased with successive exposures to the lemon juice. "The
failure of bariatric surgery candidates to habituate suggests that satiation, or the
feeling of fullness while eating, is impaired in this population. This could play a role
in the inability of some severely obese individuals to regulate or control the amount of
food that they eat during a meal," says Bond. He adds that the findings make a case
for the use of habituation as a model to study why some patients who have undergone
bariatric surgery continue to engage in problematic behaviors, such as binge eating, which
contributes to poorer weight loss outcomes. The study included 34 severely obese bariatric
surgery candidates and 18 individuals of normal weight. Saliva was collected from cotton
balls positioned in each participant's mouth during two baseline water trials and ten
lemon juice trials. Participants also completed questionnaires to assess the level of
conscious control over eating as well as the frequency of binge eating episodes during the
previous 28 days.
Study finds colorectal cancer rates
increasing worldwide
A new study finds colorectal cancer incidence rates for both males and females increased
in 27 of 51 countries worldwide between 1983 and 2002, and points to increasing
Westernization as being a likely culprit. The rise was seen primarily in economically
transitioning countries including Eastern European countries, most parts of Asia, and some
countries of South America. The study is the first in a peer-reviewed journal to present
colorectal cancer incidence trends across all five continents. It appears in the June 2009
issue of Cancer Epidemiology Biomarkers and Prevention. An accompanying editorial says the
rise points toward a failed early detection and prevention strategy as well as failure to
address lifestyle and dietary challenges of urbanization that affect most of the globe.
Colorectal cancer is the fourth most common cancer in men and the third most common cancer
in women worldwide. Previous studies have reported rapid increases in colorectal cancer
incidence rates in economically transitioning countries in many parts of the world, likely
reflecting changing dietary and physical activity patterns. However, those studies used
old data and examined regional or country-specific trends. The new study, led by American
Cancer Society epidemiologist Melissa Center, MPH, reviewed colorectal cancer incidence
data from 51 cancer registries worldwide with long-term incidence data from the Cancer
Incidence in Five Continents (CI5) databases created by the International Agency for
Research on Cancer (IARC). Researchers analyzed the change in incidence rates over the
past 20 years; 1983-87 through 1998-2002. They found colorectal cancer incidence rates for
both males and females increased for 27 of 51 cancer registries considered in the analysis
between 1983-87 and 1998-2002. The increases were more prominent for men than for women.
Some of the increases were dramatic. For example, in Slovenia, colorectal cancer incidence
increased 70 percent among men and 28 percent among women. In Miyagi, Japan, rates rose 92
percent among men and 47 percent among women. The researchers also observed substantial
regional and ethnic variations in colorectal cancer incidence trends within countries such
as Japan, Israel, and Singapore. The United States was the only country where colorectal
cancer incidence rates declined in both males and females.
Colon Cancer Screening Technique
Shows Continued Promise in New Study
Recent clinical trials show that a new colon cancer screening technique created by
Northwestern University researchers has a high enough sensitivity that it could
potentially be as or more successful than a colonoscopy in screening for colon cancer. The
technique uses optical technology, called low-coherence enhanced backscattering (LEBS)
spectroscopy, to analyze tissue samples taken from the base of the rectum. Light shines on
the tissue, scatters, and some of that light bounces back to sensors in the probe. A
computer analyzes the pattern of light scattering, looking for the "fingerprint"
of carcinogenesis in the nanoarchitecture of the cells. Researchers led by Vadim Backman,
professor of biomedical engineering at the McCormick School of Engineering and Applied
Science, obtained biopsies from patients undergoing colonoscopies and found that LEBS
could detect the presence of growths elsewhere in the colon even though it just analyzed
tissue from the base of the rectum. The results were recently published in the journal
Cancer Research. Clinical trials have been conducted in collaboration with Hemant Roy,
M.D., director of gastroenterology research at NorthShore University HealthSystem. The
study is a step toward clinical application of the technology, since it used tissue
samples near the location where doctors may ultimately use a probe to test technology.
Black Hole Is Biggest Ever
Discovered
The most massive black hole yet weighed
lurks at the heart of the relatively nearby giant galaxy M87. The supermassive black hole
is two to three times heftier than previously thought, a new model showed, weighing in at
a whopping 6.4 billion times the mass of the sun. The new measure suggests that other
black holes in nearby large galaxies could also be much heftier More.. than current
measurements suggest, and it could help astronomers solve a longstanding puzzle about
galaxy developmen "We did not expect it at all," said team member Karl Gebhardt
of the University of Texas at Austin. The discovery was announced here today at the 214th
meeting of the American Astronomical Society.
CNN's Lou Dobbs Myths of Corn
Ethanol
CNN's Lou Dobbs says three new studies
raise serious important new questions about the benefits and the efficiency of producing
corn ethanol. Corn ethanol has the full backing of President Obama, the federal government
and has been touted as the clean, renewable fuel of the future. There is some evidence
that corn ethanol may not be as less -- as clean and as less costly as its backers claim
-- according to this CNN report.
Is Fast Food as Addictive as
Tobacco?
Is Fast Food as Addictive as Tobacco? | Is
the obesity crisis the result of a lack of personal responsibility?
UNC scientists identify growth
factor as possible cancer drug target
To grow and spread, tumors need new blood vessels, a process called angiogenesis. One
growth factor that causes angiogenesis has been identified - vascular endothelial growth
factor or VEGF - and drugs to inhibit VEGF are already in use. But not all tumors respond
to the therapy initially or over the long term. Thus new growth factors need to be
identified to aid in developing the next generation of angiogenesis inhibitors. Scientists
at the UNC Lineberger Comprehensive Cancer Center report finding a new angiogenesis
protein, SFRP2, found in the blood vessels of numerous tumor sites, including breast,
prostate, lung, pancreas, ovarian, colon, kidney tumors, and angiosarcomas. The scientists
found that SFRP2 is a potent stimulator of angiogenesis. This protein may be a favorable
target for inhibiting angiogenesis which would then “starve” the tumor of its
blood supply, thus destroying the cancer. “The discovery that SFRP2 stimulates
angiogenesis and is present in blood vessels of a wide variety of tumors provides us with
a new target for drug design,” said Nancy Klauber-DeMore, M.D., senior author. The
study was published online in the journal Cancer Research. Klauber-DeMore is associate
professor of surgery and a member of UNC Lineberger Comprehensive Cancer Center. Based on
the UNC-led team’s understanding of how this protein works in the blood vessels,
scientists successfully utilized a drug, tacrolimus, which is commonly used to prevent
organ transplant rejection, to inhibit the growth of angiosarcoma in pre-clinical studies.
Angiosarcoma is a highly aggressive cancer that begins in the cells lining the blood or
lymph vessels for which options for therapy are limited.
New antibiotics could come from a
DNA binding compound that kills bacteria in 2 minutes
A synthetic DNA binding compound has proved surprisingly effective at binding to the DNA
of bacteria and killing all the bacteria it touched within two minutes. The DNA binding
properties of the compound were first discovered in the Department of Chemistry at the
University of Warwick by Professor Mike Hannon and Professor Alison Rodger (Professor Mike
Hannon is now at the University of Birmingham). However the strength of its antibiotic
powers have now made it a compound of high interest for University of Warwick researchers
working on the development of novel antibiotics.Dr Adair Richards from the University of
Warwick said ; "This research will assist the design of new compounds that can attack
bacteria in a highly effective way which gets around the methods bacteria have developed
to resist our current antibacterial drugs. As this antibiotic compound operates by
targeting DNA, it should avoid all current resistance mechanisms of multi-resistant
bacteria such as MRSA." The compound [Fe2L3]4+ is an iron triple helicate with three
organic strands wrapped around two iron centres to give a helix which looks cylindrical in
shape and neatly fits within the major groove of a DNA helix. It is about the same size as
the parts of a protein that recognise and bind with particular sequences of DNA. The high
positive charge of the compound enhances its ability to bind to DNA which is negatively
charged.
MU Study Finds Connection Between
Evolution, Classroom Learning
Over thousands of years, humans have evolved to naturally understand things like facial
expressions and social interactions. But a University of Missouri researcher has found
there is an ever-widening gap between what humans can naturally learn and what they need
to learn to be successful adults in today's modern society. Schools have traditionally
helped bridge the gap between evolution and new knowledge, but in the U.S. more may need
to be done. "Schools need to push children to learn things that they do not do
naturally, which is more important as our knowledge of the world continues to
expand," said David Geary, Curators' Professor of Psychological Sciences in the MU
College of Arts and Science. "Learning is not always going to be fun and children
should not expect it to be. Attempting to engage children by making activities fun, causes
those activities to become more similar to what students are already doing naturally and
can limit new learning."
New accurate diagnostic test for
swine H1N1 influenza using RT-PCR technology
A new, easy-to-perform method for detecting both seasonal influenza A virus and the
emerging H1N1 swine-derived influenza A virus in human clinical samples offers a fast,
sensitive, and cost-effective diagnostic test that runs on standard laboratory equipment.
This timely and broadly applicable molecular technique is described in an article
published online ahead of print in Vector-Borne and Zoonotic Diseases, a peer-reviewed
journal published by Mary Ann Liebert, Inc. (www.liebertpub.com). The article is available
free online at www.liebertpub.com/vbzThe recent emergence and global spread of a new swine
flu virus highlights the urgent need for a reliable diagnostic test that can discriminate
the H1N1 influenza virus from other strains and can be readily implemented in clinical
testing laboratories. The molecular strategy described in the article in Vector-Borne and
Zoonotic Diseases is based on proven and widely used Real-Time, Polymerase Chain Reaction
(RT-PCR) technology. The authors of the report entitled "A Simple Method for
Molecular Detection of Swine-Origin and Human-Origin Influenza A Virus" describe the
development of a new molecular probe that improves on the existing PCR assay used to
diagnose seasonal influenza and enables detection of both the seasonal and H1N1 influenza
A viruses in the same patient sample using a simple test protocol. Laetitia Ninove and
colleagues from Université de la Méditerranée and Institut de Recherche pour le
Développement (Marseille, France), Hôpitaux de Marseille, CEH Oxford (UK), and EHESP
School of Public Health (Rennes, France) provide data to support the sensitivity and
effectiveness of the SYBR Green RT-PCR one-step assay used for screening clinical samples
to detect the presence of influenza A virus. In positive samples this is followed by the
addition of two probes that are able to discriminate between the seasonal and swine H1N1
viruses to yield a definitive diagnosis.Early, accurate identification of infected
individuals will expedite appropriate antiviral therapy and enhance control and
containment efforts. Furthermore, this new molecular test specifically amplifies and
characterizes the viral genetic material, enabling rapid detection of new viral strains as
they evolve. Using these genetic sequence data and making minor alterations to the PCR
primers used in the assay, the test could be easily modified to detect newly emerging
viral variants, including avian influenza strains.
Immune cells ameliorate
hypertension-induced cardiac damage in mice
Researchers in Berlin, Germany have found that a specific type of immune cell, the
regulatory T lymphocyte (Treg) plays an important role in hypertension-induced cardiac
damage. The injected Treg that they harvested from donor mice into recipient mice were
infused with angiotensin II, a blood pressure-raising peptide. The Tregs had no influence
on the blood pressure response to angiotensin II. Nonetheless, cardiac enlargement,
fibrosis, and inflammation was sharply reduced by Treg treatment. Furthermore, the
tendency to develop abnormal heart rhythms that could lead to sudden cardiac death was
also reduced. Dr. Heda Kvakan and Dr. Dominik N. Müller at the Experimental and Clinical
Research Center at the Max Delbrück Center do not intend Treg as a therapy. However, a
better understanding of how the immune system fits into hypertension-induced organ damage
could result from these studies (Circulation, Vol. 119, No. 22, June 9, 2009, 2904-2912
).*The researchers transferred Treg cells into mice. These cells normally keep the immune
system in balance. If the number of Treg cells is reduced or their function impaired, the
immune system gets out of balance and, rather than recognizing and destroying bacteria or
viruses, the immune cells attack body tissue or organs instead. Autoimmune diseases, such
as diabetes type I or Multiple sclerosis, result from the malfunctioning of the immune
system. Aside from its physiological role in maintaining blood pressure, it has long been
known that the hormone angiotensin II plays a pivotal role in the onset of hypertension
and in subsequnt hypertensive organ damage, e.g. cardiac hypertrophy. Angiotensin II also
has proinflammatory properties and actives the cells of the immune system. The activation
of these cells also seems to have a major part in Angiotension II-induced target organ
damage. The researchers wanted to know if the suppression of activated immune cells by
Treg cells could reduce cardiac damage. And indeed, hypertensive mice that had received
Treg cells, exhibited less cardiac damage. "Hypertrophy and the thickening of the
cardiac walls were reduced, also fibrosis and arrhythmia", Dr. Kvakan explains. The
Treg cells had brought the immune cells under their control.
Researchers estimate risk of
transmission of Huntington's disease to offspring among male carriers
Researchers from Boston University School of Medicine (BUSM) have quantified the
probability of a male who carries a "high normal" variant of the Huntington's
Disease (HD) gene having a child who develops the disease. Although thought to be a very
rare event, the probability has never been estimated using current information and disease
guidelines. The findings, appear on-line in the American Journal of Medical Genetics, may
be useful during prenatal genetic counseling. Huntington disease (HD) is a hereditary
neurodegenerative disorder that arises from expansion of a CAG trinucleotide repeat on
chromosome 4. Individuals with a variant of at least 36 CAG repeats will likely develop HD
in their lifetime. Most individuals have a variant below 27 CAG repeats and are not at
risk for the disease nor are they at risk of passing on the disease to their children.
However, although individuals with a variant between 27 and 35 CAG repeats (called high
normal) are not at risk of developing HD, males may pass an expanded CAG repeat onto their
children making the child at risk of developing HD. While several studies suggest that
male carriers of high normal alleles have a low probability of transmitting an expanded HD
allele in the penetrant range, few studies have attempted to estimate this probability.
The researchers estimated the conditional probability of an offspring inheriting an
expanded allele from a father with a high normal allele by applying probability
definitions and rules to estimates of HD incidence, paternal birth rate, frequency of no
family history of HD, and frequency of high normal alleles in the general population.
"The estimated probability that a male high normal allele carrier will have an
offspring who develops HD ranges from 1/6,241 to 1/951," said lead author Audrey
Hendricks, a research assistant and biostatistics doctoral student at BUSM and Boston
University School of Public Health.
Pregnancy and the flu - A link to
schizophrenia
When mothers become infected with influenza during their pregnancy, it may increase the
risk for schizophrenia in their offspring. Influenza is a very common virus and so there
has been substantial concern about this association. A new study in the June 15th issue of
Biological Psychiatry, published by Elsevier suggests that the observed association
depends upon a pre-existing vulnerability in the fetus. Specifically, Dr. Lauren Ellman
and colleagues determined that fetal exposure to influenza leads to cognitive problems at
age 7 among children who later develop a psychotic disorder in adulthood, but fetal
exposure to influenza does not lead to cognitive problems among children who do not later
develop a psychotic disorder. It is important to note that these results were dependent
upon the type of influenza, with this association present only after fetal exposure to
influenza B as opposed to influenza A. This research was conducted as part of the
Collaborative Perinatal Project, which followed pregnant women and their offspring in the
1950's and 60's, collecting blood throughout pregnancies for later analyses. A series of
cognitive assessments were conducted with the children of study participants and then
psychotic diagnoses were determined in adulthood. The findings from this study suggest
that a genetic and/or an additional environmental factor associated with psychosis likely
is necessary for the fetal brain to be vulnerable to the effects of influenza, given that
decreases in cognitive performance were only observed in influenza-exposed children who
developed a psychotic disorder in adulthood. "The good news is that most fetuses
exposed to influenza virus while in the womb will not go on to develop schizophrenia. The
bad news is that the prior association between influenza infection and later development
of psychotic disorders was supported," comments John Krystal, M.D., the editor of
Biological Psychiatry. This finding has the potential to influence efforts to develop
prevention, early intervention and treatment strategies, such as taking steps to maintain
careful hygiene and, if clinically appropriate, administration of the influenza
vaccination to reduce infection among women prior to pregnancy. Dr. Krystal notes,
"It also raises an important unanswered question: How does influenza virus affect the
vulnerable developing brain and how can we prevent or reverse the consequence of fetal
influenza infection in vulnerable individuals before they develop schizophrenia?"
More research is needed to elicit answers to these vital issues.
Gene activity reveals dynamic
stroma microenvironment in prostate cancer
As stroma – the supportive framework of the prostate gland – react to prostate
cancer, changes in the expression of genes occur that induce the formation of new
structures such as blood vessels, nerves and parts of nerves, said researchers at Baylor
College of Medicine in a report that appears in the current issue of the journal Clinical
Cancer Research. In this study, using special techniques and gene chips that allowed them
to sample the entire genome, the researchers found changes in 1,141 genes. They were
either upregulated – meaning that there was more of the protein with which they were
associated than expected – or downregulated, which meant the opposite, said Dr.
Michael Ittmann, professor of pathology at BCM and a senior author of the report. These
gene changes may explain why men with reactive stroma face a more aggressive disease, said
Ittmann and Dr. Gustavo Ayala, professor in the departments of pathology and urology at
BCM and another senior author. "Often in prostate cancer, you don't see much change
in the stromal cells," said Ittmann. "However, in this subgroup of patients (in
which the stroma become visibly reactive), you see a histologically recognizable change in
the appearance of the stroma. Dr. Ayala has shown previously that this correlates with a
bad prognosis. We know the stroma are doing something to promote bad behavior in cancer
cells." "These findings are very important as this is the first step in
discovering pathways and mechanisms in the tumor microenvironment that could be targeted
as a novel therapeutic approach to treat prostate cancer by treating the cancer
microenvironment niche", said Dr. David Rowley, professor of molecular and cellular
biology and urology at BCM, and another author. Dr. Chad Creighton, an assistant professor
in the Dan L. Duncan Cancer Center at BCM, searched the scientific literature to determine
the biological processes with which the genes with changes had been linked in prior
studies. "We found that the top terms linked to the genes were related to
neurogenesis (the growth of neurons or nerve cells)," said Ittmann. "This
independently supported Dr. Ayala's previous finding that prostate cancer prompts the
growth of new nerve cells, which is linked to poor prognosis." Other genes were
linked to axongenesis, which refers to new axons, the slender projection that conducts
nerve impulses away from the body of a nerve cell.
Computer-related injuries on the
rise
While back pain, blurred vision and mouse-related injuries are now well-documented hazards
of long-term computer use, the number of acute injuries connected to computers is rising
rapidly. According to a study published in the July 2009 issue of the American Journal of
Preventive Medicine, researchers from the Center for Injury Research and Policy and The
Research Institute at Nationwide Children's Hospital; and The Ohio State University
College of Medicine, Columbus have found a more-than-sevenfold increase in
computer-related injuries due to tripping over computer equipment, head injuries due to
computer monitor falls and other physical incidents. According to data from the National
Electronic Injury Surveillance System database, over 78,000 cases of acute
computer-related injuries were treated in U.S. emergency departments from 1994 through
2006. Approximately 93% of injuries occurred at home. The number of acute computer-related
injuries increased by 732% over the 13-year study period, which is more than double the
increase in household computer ownership (309%). Injury mechanisms included hitting
against or catching on computer equipment; tripping or falling over computer equipment;
computer equipment falling on top of the patient; and the straining of muscles or joints.
The computer part most often associated with injuries was the monitor. The percentage of
monitor-related cases increased significantly, from 11.6% in 1994 to a peak of 37.1% in
2003. By 2006, it had decreased to 25.1%. The decrease since 2003 corresponds to the
replacement of heavier cathode ray tube (CRT) monitors with smaller and easier-to-lift
liquid crystal display (LCD) monitors.
Study links primary insomnia to a
neurochemical abnormality
A research abstract that will be presented on Tuesday, June 9, at SLEEP 2009, the 23rd
Annual Meeting of the Associated Professional Sleep Societies, is the first demonstration
of a specific neurochemical abnormality in adults with primary insomnia (PI), providing
greater insight to the limited understanding of the condition's pathology. Results
indicate that gamma-aminobutyric acid (GABA), the most common inhibitory transmitter in
the brain, is reduced by nearly 30 percent in individuals who suffer from primary insomnia
for more than six months. These findings suggest that primary insomnia is a manifestation
of a neurobiological state of hyperarousal, which is present during both waking and sleep
at physiological and cognitive levels. According to principal investigator Dr. John
Winkelman of Brigham and Women's Hospital, at Harvard Medical School in Boston, Mass., the
recognition that primary insomnia is associated with a specific neurochemical deficiency
helps validate the often misunderstood complaint of insomnia. "Recognition that
insomnia has manifestations in the brain may increase the legitimacy of those who have
insomnia and report substantial daytime consequences," he said. "Insomnia is not
just a phenomenon observed at night, but has daytime consequences for energy,
concentration and mood." The study included 16 non-medicated individuals (eight of
whom were women) with PI and 16 individuals (seven women) who were deemed normal sleepers.
Global brain GABA levels were measured in both groups. PI was established through clinical
interviews, sleep diary, actigraphy use and polysomnograpy.
Nightmares predict elevated
suicidal symptoms
Self-reported nightmares among patients seeking emergency psychiatric evaluation uniquely
predicted elevated suicidal symptoms, according to a research abstract that will be
presented on Tuesday, June 9, at SLEEP 2009, the 23rd Annual Meeting of the Associated
Professional Sleep Societies. Results indicate that severe nightmares were independently
associated with elevated suicidal symptoms after accounting for the influence of
depression, whereas symptoms of insomnia were not. These findings suggest that nightmares
stand alone as a suicide risk factor. The sample included 82 men and women between the
ages of 18 and 66, who were in a community mental health hospital admissions unit awaiting
an emergency psychiatric evaluation. Evaluations determined eligibility for crisis
stabilization inpatient admittance. Patients' nightmares, insomnia, depression and
suicidal tendencies were assessed through several questionnaires, including the Disturbing
Dreams and Nightmare Severity Index, Insomnia Severity Index (ISI), Beck Depression
Inventory (BDI), and the Beck Scale for Suicide Ideation (BSS). According to principal
investigator, Rebecca Bernert, doctoral candidate in clinical psychology at Florida State
University, findings of the study emphasize the need for a more thorough assessment of
sleep among acutely-ill patients, as it may be an important opportunity for intervention.
Meditation may be an effective
treatment for insomnia
Meditation may be an effective behavioral intervention in the treatment of insomnia,
according to a research abstract that will be presented on Tuesday, June 9, at SLEEP 2009,
the 23rd Annual Meeting of the Associated Professional Sleep Societies Results indicate
that patients saw improvements in subjective sleep quality and sleep diary parameters
while practicing meditation. Sleep latency, total sleep time, total wake time, wake after
sleep onset, sleep efficiency, sleep quality and depression improved in patients who used
meditation.According to principal investigator Ramadevi Gourineni, MD, director of the
insomnia program at Northwestern Memorial Hospital in Evanston, Ill., insomnia is believed
to be a 24-hour problem of hyperarousal, and elevated measures of arousals are seen
throughout the day. "Results of the study show that teaching deep relaxation
techniques during the daytime can help improve sleep at night," said Gourineni.
Later parental-mandated bedtimes
for teens linked to depression and suicidal thoughts
Earlier parental-mandated bedtimes could help protect teens from depression and suicidal
thoughts by lengthening sleep duration, according to a research abstract that will be
presented on Tuesday, June 9, at SLEEP 2009, the 23rd Annual Meeting of the Associated
Professional Sleep Societies. The study by James Gangwisch, PhD, of Columbia University in
New York, examined data from 15,659 adolescents. A total of 1,143 teens (7.3 percent)
suffered from depression and 2,038 (13 percent) had suicidal thoughts. Adolescents with
parental-mandated bedtimes at midnight or later were 25 percent more likely to suffer from
depression and 20 percent more likely to have suicidal ideation compared with adolescents
who had parental-mandated bedtimes of 10 p.m. or earlier."It is a common perception
and societal expectation that adolescents do not need as much sleep as preadolescents, yet
studies suggests that adolescents may actually require more sleep," said Gangwisch.
"Studies have found that adolescents do not go to bed early enough to compensate for
earlier school start times, and transitions to earlier school start times have been shown
to be associated with significant sleep deprivation." According to Gangwisch, the
study supports the argument that inadequate sleep could lead to depression.
"Adolescents with later parental-mandated bedtimes went to bed later, got less sleep,
and were less likely to get enough sleep. Short sleep duration explained the relationship
between parental-mandated bedtimes and depression, functioning as a risk factor for
depression and suicidal ideation."
Stopping diabetes damage with
vitamin C
Researchers at the Harold Hamm Oklahoma Diabetes Center have found a way to stop the
damage caused by Type 1 diabetes with the combination of insulin and a common vitamin
found in most medicine cabinets. While neither therapy produced desired results when used
alone, the combination of insulin to control blood sugar together with the use of Vitamin
C, stopped blood vessel damage caused by the disease in patients with poor glucose
control. The findings appear this week in the Journal of Clinical Endocrinology and
Metabolism. "We had tested this theory on research models, but this is the first time
anyone has shown the therapy's effectiveness in people," said Michael Ihnat, Ph.D.,
principal investigator and a pharmacologist at the OU College of Medicine Department of
Cell Biology. Ihnat said they are now studying the therapy in patients with Type 2
diabetes. The goal of the work being done by Ihnat and British scientists from the
University of Warwick led by Dr. Antonio Ceriello is to find a way to stop the damage to
blood vessels that is caused by diabetes. The damage, known as endothelial dysfunction, is
associated with most forms of cardiovascular disease such as hypertension, coronary artery
disease, chronic heart failure, peripheral artery disease, diabetes and chronic renal
failure. By reducing or stopping the damage, patients with diabetes could avoid some of
the painful and fatal consequences of the disease that include heart disease, reduced
circulation and amputation, kidney disease and diabetic retinopathy, which can lead to
blindness. Insulin and many other drugs have long been used to control blood sugar, but
Ihnat – in an earlier project with scientists in Italy and Hungary – found that
cells have a "memory" that causes damage to continue even when blood sugar is
controlled. By adding antioxidants like Vitamin C, Ihnat found that cell
"memory" disappeared and cell function and oxidation stress were normalized.
Scripps research scientists uncover
a novel mechanism controlling tumor growth in the brain
As survival rates among some patients with cancer continue to rise, so does the spread of
these cancers to the brain – as much as 40 percent of all diagnosed brain cancers are
considered metastatic, having spread from a primary cancer elsewhere in the body. Now,
scientists from The Scripps Research Institute have discovered a molecular mechanism that
plays a pivotal role in controlling cancer growth in the brain. The discovery could
provide a basis for potentially effective therapies for the treatment of brain metastasis.
The study was published in an online Early Edition of the journal Proceedings of the
National Academy of Sciences (PNAS) the week of June 8, 2009. "Our study could have a
broad impact because it explains at a molecular level how metastatic lesions thrive in the
brain," said Scripps Research Associate Professor Brunhilde Felding-Habermann, who
led the research. "This offers a potential target for inhibiting the growing problem
of brain metastasis." For tumor cells that have invaded the brain, Felding-Habermann
and her colleagues found that when activated, a tumor cell receptor known as integrin ?v?3
increased the supply of a growth factor involved in the development of new blood vessels
("angiogenesis") necessary for tumor expansion within the brain tissue. In
contrast, the same receptor did not influence tumor growth at the primary cancer site, in
this case, the breast. "The fact that we uncovered a link between activated ?v?3 and
angiogenesis is quite striking," said Senior Research Associate Mihaela Lorger, the
first author of the study. "In addition, our study showed that that the ability of
tumor cell ?v?3 to enhance angiogenesis depends very much on the microenvironment."
This receptor's varying effects on tumor cells depending on their location in the body
reinforces a principle that the Felding-Habermann lab uncovered a few years ago.
Fatal brain disease at work well
before symptoms appear
University of Florida scientists have discovered why a paralyzing brain disorder speeds
along more rapidly in some patients than others — a finding that may finally give
researchers an entry point toward an effective treatment for amyotrophic lateral
sclerosis, often referred to as ALS or Lou Gehrig's disease. Of more than 100 possible
mutations of a single gene inherited by people with familial ALS, the mutations most
inclined to produce clumps of problematic cellular debris known as "protein
aggregates" appear to be associated with quicker progress of the disease, according
to researchers with the University of Florida's McKnight Brain Institute writing online
this week in Human Molecular Genetics. Meanwhile, in a separate study recently online in
the Proceedings of the National Academy of Sciences, scientists describe how these protein
clumps — long considered a defining characteristic of ALS — do not cause the
disease, but appear later on, increasing in number between onset of weakness and paralysis
in patients. Together, these findings suggest that the deadly course of the disease is
linked to the formation of these protein clumps, even though the sickness may have been
well under way. "Blocking aggregation of these proteins could be a therapeutic target
for individuals with this genetic mutation," said David Borchelt, Ph.D., a professor
of neuroscience and director of the SantaFe HealthCare Alzheimer's Disease Research Center
at UF's McKnight Brain Institute. "Right now, there is little that can be done to
help these patients." ALS involves the death of nerve cells that stretch from the
brain to the spinal cord, and from the spinal cord to muscles. It strikes people between
the ages of 40 and 70, according to the ALS Association. An estimated 30,000 Americans
have the disease at any given time. Patients usually have a life expectancy of two to five
years, with some notable exceptions, such as Cambridge University scientist and author
Stephen Hawking, who has survived for more than 40 years since his diagnosis. The cause of
ALS is unknown in about 80 percent of cases, but 10 percent to 20 percent of ALS cases can
be traced to an inherited genetic defect. No matter the cause, scientists believe that a
basic cellular process in which amino acids are folded into proteins goes wrong in ALS.
The misfolded proteins cannot perform their intended function. Instead, they form the
troublesome protein aggregates.
Enzyme necessary for DNA synthesis
can also erase DNA
In this week's edition of Proceedings of the National Academy of Sciences, PNAS, Uppsala
University scientists describe a new mechanism behind an important process that causes a
rapid reduction of DNA in the chromosomes of bacteria. The findings advance our knowledge
of how DNA content has been reduced, which is something that has occurred in bacteria that
live as parasites inside the cells of other organisms. The amount of DNA in the
chromosomes of bacteria can change rapidly, either by increasing, so-called gene
amplification, or by decreasing, so-called gene deletion. These processes are
evolutionarily very important, and the discovery of a new mechanism that is involved when
DNA disappears is of fundamental importance to our understanding what influences the
stability of chromosomes and why the amount of DNA can decrease in certain types of
bacteria. "How rapidly and by what mechanisms DNA can disappear from the chromosome
is a central genetic and evolutionary question," says Professor Dan I Andersson, the
lead author of the study. Previously these types of large gene deletions, have mostly been
studied in artificial model systems with two long identical and neighboring DNA sequences.
Normal spontaneous deletions, on the other hand, are often remote from each other and lack
sequence identity.In the current study, the PhD student Sanna Koskiniemi has carried out
comprehensive genetic analyses of Salmonella mutants and her results show that a special
type of DNA-synthesizing enzymes are necessary if spontaneous deletions are to be formed
in the bacteria. This new function has never before been described in these enzymes. By
genetically inactivating or overproducing these enzymes, the researchers were able to show
that the deletion rates decreased or increased by up to 30 times.
Nutrition Expert's New Book Debunks
Calcium as a Means to Prevent Osteoporosis
For years, doctors and scientists have told the public to drink milk, eat dairy products
and take calcium supplements to improve bone health and prevent osteoporosis. The problem
is they're wrong, according to a new book co-authored by a University of North Carolina at
Asheville researcher. Amy Lanou, UNC Asheville assistant professor of health and wellness,
and noted health writer Michael Castleman’s new book, "Building Bone Vitality: A
Revolutionary Plan to Prevent Bone Loss and Reverse Osteoporosis," dispels the
calcium myth using the latest clinical studies and medical information. Published by
McGraw Hill, the book hits shelves this month. "Building Bone Vitality" provides
readers with practical advice to strengthen bones, reduce the risk of fractures and
prevent osteoporosis. Readers will also learn why there's no proof of dairy's usefulness
in bone health, despite what doctors say, and why eating low-acid foods and taking daily
walks are the most effective ways to prevent bone loss.The authors' suggested eating plan
includes six to nine daily servings of fruits and vegetables and no more than one or two
servings of high-protein foods such as meat, dairy and eggs daily. Why? Because protein is
composed of amino acids. As the body digests high-protein foods, the blood becomes more
acidic, leaching calcium from the bones. For example, have you ever taken Tums for acid
indigestion? Its active ingredient, calcium carbonate, neutralizes stomach acid because
it's highly alkaline. To neutralize excess acid in the bloodstream, the body draws the
same compound from bone. A high-protein diet of meat, dairy and eggs draws calcium from
bone and eventually causes osteoporosis, the authors say. Of course, fruits and vegetables
also contain some protein, but much less than meat, dairy and eggs. Fruits and vegetables
also contain a great deal of alkaline material. When you eat these foods, only a small
amount of acid enters the bloodstream along with a great deal of alkaline material, which
neutralizes the acid. Therefore, the body does not have to draw calcium compounds out of
bone. "Fruits and vegetables keep calcium in bone where it belongs," said Lanou.
To further back up their theory, Lanou and Castleman pored over completed human clinical
trials and found that they also refute the calcium claim. Since 1975, 140 clinical trials
have explored calcium's effects on osteoporotic fracture risk. Two-thirds of these studies
show no benefit from high calcium intake. Overall, the clinical trials dealing with
fracture prevention run two-to-one against calcium, the authors noted. Finally, the
authors reviewed research on the impact of exercise on bone health. They found that the
consensus of research shows that just 30 to 60 minutes of daily walking is enough exercise
to build strong bones. "The good news is that you don't have to join a gym or sweat
buckets," said Castleman. "But you do have to walk every day."
Natural Therapeutic Treatments for
Arthritis
New natural treatments may help improve the quality of life for more than 21 million
osteoarthritis (OA) sufferers, according to new research presented at the 2009 Institute
of Food Technologists (IFT) Annual Meeting and Food Expo®. Studies show that a novel,
natural chicken derivative is more effective and longer-lasting than traditional
chondroitin and glucosamine treatments. OA causes localized joint inflammation, often with
crippling effects. Conventional medicines used to treat OA include non-steroidal
anti-inflammatory drugs, such as ibuprofen, which can cause gastric injury. Alternatives
such as rofecoxib and valdecoxib increase the rise of cardiovascular dysfunctions,
including stroke. The new natural arthritis treatments do not have these side effects,
making them more appealing to those with arthritis symptoms. Studies show that UC-II, a
novel undenatured type II collagen derived from chicken sternum cartilage, decreased
arthritis pain scores by 33 percent, compared to 14 percent in groups treated with
glucosamine and chondroitin. "In addition, the UC-II continued to work even after the
glucosamine-chondroitin results plateaued, making it more effective over time," said
Manashi Bagchi, Ph.D., of Interhealth Nutraceuticals, Inc., Benicia, CA. In studies with
arthritic dogs and horses, daily treatment with UC-II markedly alleviated arthritis
symptom as well. The natural supplements were tolerated well with no adverse effects.
Oxidative stress may be to blame
for Down's symptoms
A paper published today in the Proceedings of the National Academy of Sciences by
researchers at Tufts Medical Center and Tufts University reports that amniotic fluid
surrounding Down syndrome fetuses shows oxidative stress, a condition that could harm
fetal cells and potentially play a role in affected individuals. The results suggest there
are secondary adverse consequences of Down syndrome that are evident by the second
trimester of pregnancy, leading to pathways to explore potential novel prenatal therapies
for diagnosed fetuses. Diana Bianchi, M.D., Vice Chair for research in the Department of
Pediatrics at Floating Hospital for Children at Tufts Medical Center, and Donna Slonim,
Ph.D., associate professor of computer science at Tufts University’s School of
Engineering, conducted an analysis of the human genome from cell-free fetal messenger RNA
floating in the amniotic fluid that surrounds fetuses with Down syndrome and normal
fetuses. The researchers identified significant molecular changes that were evident in the
Down syndrome fetuses as early as the fourth month of pregnancy.Down syndrome occurs when
an individual has three copies of chromosome 21 instead of the usual two copies. The
longstanding assumption about Down syndrome has been that extra proteins produced by the
additional copy of chromosome 21 were almost exclusively responsible for the abnormal
development and function associated with the syndrome. A surprising aspect of the findings
was that the molecular abnormalities observed were predominantly produced by genes on the
other chromosomes, in addition to more modest changes in expression of the genes on
chromosome 21. As a next step, the researchers are examining amniotic cells to determine
if they show similar genomic profiles to the cell-free material in the fluid. If that is
the case, they will begin to look at the effectiveness of anti-oxidant compounds in
laboratory tests.“While more research is needed, this study illuminates a possible
pathway to treating some aspects of Down syndrome in the womb,” Bianchi said.
“While we do not know the extent to which the developing fetus is affected by
oxidative stress, we know that this abnormal environment is not conducive to optimal
development.”
Ground-breaking Alzheimer's
findings reveal new treatment strategy
Alzheimer’s disease affects the major two types of brain cells, neurones and
neuroglia. For a long time glial cells have been thought to have a purely supportive role.
However, recent work and more specifically ongoing studies at the University of Manchester
are probing a much more relevant functional role including new treatment opportunities,
for neurodegenerative processes such as Alzheimer’s disease. Dr José J. Rodríguez
Arellano and Professor Alexei Verkhratsky believe that, contrary to popular belief,
neuroglial cells (astrocytes) in the brain shrink during Alzheimer’s disease.
Astrocytes are vital in providing for generation and maintenance of synapses and therefore
diminished astroglial support alters synaptic connectivity thus redusing brain cognitive
power. They say that probably the new strategies aimed at protection and support of
neuroglia may help to combat brain degeneration in Alzheimer disease. Dr
Rodriguez-Arellano, whose work was funded by the Alzheimer’s Research Trust, says:
“These are amazing findings and totally unexpected. We have found that model animals
(transgenic mice) with Alzheimer’s pathology have problems with glial cells as well
as with the neurones in the brain. “Everybody thought that glial cells grew bigger in
response to the disease but we have found that some of them actually shrink and this
causes serious problems. Glial cells are not merely supportive; they have an active role
in maintaining synapses so the imbalance of these cells can have a serious negative
effect.”
Breastfeeding associated with a
reduced risk of relapse in women with multiple sclerosis
Women with multiple sclerosis who breastfeed exclusively for at least two months appear
less likely to experience a relapse within a year after their baby's birth, according to a
report posted online today that will appear in the August print issue of Archives of
Neurology, one of the JAMA/Archives journals. "Multiple sclerosis (MS) is a chronic
inflammatory disease of the central nervous system that predominantly affects women in
their childbearing years," the authors write as background information in the
article. "It is well known that women with MS have fewer relapses during pregnancy
and a high risk of relapse in the postpartum period." Medications used to treat MS by
modifying the immune system—including interferon beta and natalizumab—are not
recommended for use during pregnancy or breastfeeding. Therefore, women with MS who give
birth must choose between nursing and resuming MS treatment. Annette Langer-Gould, M.D.,
Ph.D., then of Stanford University School of Medicine, Stanford, Calif., and now of Kaiser
Permanente Southern California, Pasadena, and colleagues studied 32 pregnant women with MS
and 29 pregnant women without MS who were the same age. The participants were interviewed
about clinical, menstrual and breastfeeding history during each trimester and again two,
four, six, nine and 12 months after they gave birth. In addition, neurological examination
findings were collected from the physicians of women with MS. More healthy women than
women with MS breastfed (96 percent vs. 69 percent), and among those who did breastfeed,
women with MS were more likely to begin daily formula feedings within two months after
birth (30 percent compared with 18 percent). "Of the 52 percent of women with MS who
did not breastfeed or began regular supplemental feedings within two months postpartum [15
women], 87 percent [13 women] had a postpartum relapse, compared with 36 percent [five
women] of the women with MS who breastfed exclusively for at least two months postpartum
[14 women]," the authors write. "Women with MS and healthy women who breastfed
exclusively had significantly prolonged lactational amenorrhea [absence of menstruation],
which was associated with a decreased risk of relapse in women with MS."
Study redefines roles of alcohol,
smoking in risk for pancreatitis
Although alcohol consumption is known to be associated with chronic pancreatitis, new
evidence indicates that a threshold of five or more drinks per day is required to
significantly raise risk; however, most patients with chronic pancreatitis do not drink
this amount, according to a report in the June 8 issue of Archives of Internal Medicine,
one of the JAMA/Archives journals. In addition, smoking is an independent, dose-dependent
risk factor. "Chronic pancreatitis is an inflammatory syndrome of the pancreas
characterized by progressive parenchymal fibrosis [scarring of the organ], maldigestion,
diabetes mellitus and pain," the authors write as background information in the
article. "Recurrent acute pancreatitis [acute pancreatitis that occurs on two or more
occasions and may become chronic] and chronic pancreatitis are associated with alcohol
consumption and cigarette smoking. The etiology of recurrent acute pancreatitis and
chronic pancreatitis is complex, and effects of alcohol and smoking may be limited to
specific patient subsets." Dhiraj Yadav, M.D., M.P.H., of the University of
Pittsburgh, and colleagues in the North American Pancreatic Study Group examined the
current prevalence of alcohol use and smoking and their association with pancreatitis in
patients evaluated at U.S. referral centers. Between 2000 and 2006, 1,000 patients (540
with chronic pancreatitis and 460 with recurrent acute pancreatitis) were enrolled in the
North American Pancreatitis Study 2 (NAPS2), as were 695 healthy controls. All
participants (average age 49.7) reported their alcohol consumption and smoking habits.
About one-fourth of both controls and patients were lifetime abstainers. Among those with
chronic pancreatitis, 38.4 percent of men and 11 percent of women were very heavy drinkers
(five or more drinks per day), compared with 16.9 percent of men and 5.5 percent of women
with recurrent acute pancreatitis and 10 percent of men and 3.6 percent of women in the
control group. "We found the threshold drinking amount for association between
alcohol use and chronic pancreatitis to be five or more drinks per day," the authors
write. Compared with abstaining and light drinking (half a drink per day or less), very
heavy drinking was associated with approximately triple the odds of developing chronic
pancreatitis. However, fewer patients with chronic pancreatitis than expected (about
one-fourth) drank at this level. Other factors, including genetic mutations, also
contribute to pancreatitis risk.
Less sleep associated with high,
worsening blood pressure in middle age
Middle-aged adults who sleep fewer hours appear more likely to have high blood pressure
and to experience adverse changes in blood pressure over time, according to a report in
the June 8 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Almost one-third of Americans have hypertension or high blood pressure, a condition that
contributes to 7 million deaths worldwide each year, according to background information
in the article. "Identifying a novel lifestyle risk factor for high blood pressure
could lead to new interventions to prevent or reduce high blood pressure," the
authors write. "Laboratory studies of short-term sleep deprivation have suggested
potential mechanisms for a causal link between sleep loss and hypertension." Sleep
deprivation is associated with increased activity in the sympathetic nervous system, which
controls the body's stress response. Over time, this activation could contribute to high
blood pressure. Kristen L. Knutson, Ph.D., of the University of Chicago, and colleagues
studied 578 adults who first had their blood pressure and other clinical, demographic and
health variables measured between 2000 and 2001. In 2003 and 2005, sleep duration was
measured using surveys and wrist actigraphy, in which a sensor is worn on the wrist to
record periods of rest and activity. Blood pressure, demographic and self-reported sleep
information were measured again in 2005 and 2006.Participants (average age 40.1) slept an
average of six hours per night; only seven (1 percent) averaged eight or more hours of
sleep. After excluding patients taking medication for high blood pressure and controlling
for age, race and sex, the researchers found that individuals who slept fewer hours were
significantly more likely to have higher systolic (top number) and diastolic (bottom
number) blood pressure.
Plant-based, low-carb diet may
promote weight loss and improve cholesterol levels
Overweight individuals who ate a low-calorie, low-carbohydrate diet high in plant-based
proteins for four weeks lost weight and experienced improvements in blood cholesterol
levels and other heart disease risk factors, according to a report in the June 8 issue of
Archives of Internal Medicine, one of the JAMA/Archives journals. A high-carbohydrate,
low-fat vegetarian diet also resulted in weight loss but without the additional
cardiovascular benefits. "There is a dilemma relating to the proportion and source of
fat, protein and carbohydrate that constitutes the optimal weight loss and
cholesterol-lowering diet," the authors write as background information in the
article. Newer dietary approaches for the prevention and treatment of chronic disease
emphasize increased fruit and vegetable intake and reduced meat consumption. However,
low-carbohydrate diets with increased meat consumption have also been promoted for body
weight reduction and the prevention and treatment of diabetes and coronary heart disease.
These diets have been shown to be effective in inducing weight loss, reducing insulin
resistance, lowering blood fats known as triglycerides and raising high-density
lipoprotein cholesterol (HDL-C, or "good" cholesterol) levels, but have tended
to increase low-density lipoprotein cholesterol (LDL-C, or "bad" cholesterol)
levels. "This lack of a benefit for LDL-C control is a major disadvantage in using
this dietary strategy in those already at increased risk of coronary heart disease,"
the authors write. David J.A. Jenkins, M.D., of St. Michael's Hospital and the University
of Toronto, Ontario, Canada, and colleagues tested the effects of a low-carbohydrate diet
high in vegetable proteins from gluten, soy, nuts, fruits, vegetables, cereals and
vegetable oils among overweight men and women with high LDL cholesterol levels. A total of
25 participants were randomly assigned to consume this diet—the
"Eco-Atkins" diet—for four weeks, while an additional 25 participants ate a
control diet that was high-carbohydrate, lacto-ovo vegetarian and based on low-fat dairy
and whole grain products. Study food was provided to participants at 60 percent of their
estimated calorie requirements. Of the 47 participants who began the study, 44 (22 in each
group) completed the four-week period. Weight loss was similar—about 4 kilograms or
8.8 pounds—in both groups. However, reductions in LDL-C levels and improvements in
the ratios between total cholesterol and HDL-C were greater for the low-carbohydrate diet
compared with the high-carbohydrate diet. The low-carbohydrate diet also appeared to
produce beneficial changes in levels and ratios of apolipoproteins, proteins that bind to
fats. In addition, small but significantly greater reductions were seen in both systolic
(top number) and diastolic (bottom number) blood pressure for the low-carbohydrate vs. the
high-carbohydrate group.Pending answers to important questions, including whether further
reducing carbohydrate intake would produce additional benefits, "a plant-based
low-carbohydrate diet high in vegetable proteins and oils may be an effective option in
treating those with dyslipidemia for whom both weight loss and lower LDL-C concentrations
are treatment goals," the authors conclude.
Food, Inc Trailer HD 1080p
Bentonite Clay is AMAAZZING-
Tutorial
This tutorial shows how I mix apply and
overall use bentonite clay....I also use it on my skin but will show that another day..I
soo love this treatment and so does my hair, hope you like it !! What is it?
Bentonite, also referred to as
Montmorillonite, is one of the most effective and powerful healing clays used to treat
both internal and external maladies. Bentonite can be used externally as a clay poultice,
mud pack or in the bath and, in skin care recipes. Internally it can be added to water or
glazed upon food to help those with sensitive palates. A good quality Bentonite should be
a grey/cream color and anything bordering "pure white" is suspect. It has a very
fine, velveteen feel and is odorless and non-staining.
How does it work?
Bentonite is very unusual in the fact that once it becomes hydrated, the electrical and
molecular components of the clay rapidly change and produce an "electrical
charge". Its highest power lies in the ability to absorb toxins, impurities, heavy
metals and other internal contaminants. Bentonite clay's structure assists it in
attracting and soaking up poisons on its exterior wall and then slowly draw them into the
interior center of the clay where it is held in a sort of repository.
Television watching before bedtime
can lead to sleep debt
According to a research abstract that will be presented on Monday, June 8, at SLEEP 2009,
the 23rd Annual Meeting of the Associated Professional Sleep Societies, television
watching may be an important determinant of bedtime, and may contribute to chronic sleep
debt. The study included data from 21,475 people aged 15 or older who completed the
American Time Use Survey between the years 2003 and 2006. The study examined the
activities participants undertook two hours before and after bed time. It found that
television viewing was by far and away the dominant pre-sleep activity, accounting for
almost 50% of pre-bed time. According to the authors of the study, Mathias Basner, MD, MS,
MSc, and David F. Dinges, PhD, of the University of Pennsylvania School of Medicine in
Philadelphia, they were surprised to find that watching television seemed to be the most
important time cue for the beginning of the sleep period, rather than hours past sunset or
other more biological factors. So, in fact, TV may make people stay up late, while alarm
clocks make them get up early, potentially reducing sleep time below what is
physiologically needed. Sleeping less than 7-8 hours daily impairs alertness and is
associated with increased obesity, morbidity and mortality. Despite this fact, up to 40
percent of Americans sleep for less than the recommended time per night.
Sleep Restriction Results in Weight
Gain Despite Decreases in Appetite, Food Cravings and Consumption
According to a research abstract that will be presented on Monday, June 8 at SLEEP 2009,
the 23rd Annual Meeting of the Associated Professional Sleep Societies, in the presence of
free access to food, sleep restricted subjects reported decrease in appetite, food
cravings and food consumption; however, they gained weight over the course of the study.
Thus, the finding suggests that energy intake exceeded energy expenditure during the sleep
restriction Results indicate that people whose sleep was restricted experienced an average
weight gain of 1.31 kilograms over the 11 days of the study. Of the subjects with
restricted sleep who reported a change in their appetite and food consumption, more than
70 percent said that it decreased by day 5 of the study. A group of well rested control
subjects did not experience the weight gain. According to lead investigator Siobhan Banks,
PhD, a research fellow at the University of South Australia and former assistant research
professor at the University of Pennsylvania School of Medicine, it was surprising that
participants did not crave foods rich in carbohydrates after sleep restriction, as
previous research suggested they might. Results indicate that even though physiologically
the desire to eat was not increased by sleep loss in participants, other factors such as
the sedentary environment of the laboratory and the ability to snack for longer due to
reduction in time spent asleep might have influenced the weight gain.
Relationship Found between Napping,
Hyperactivity, Depression and Anxiety
Napping may have a significant influence on young children’s daytime functioning,
according to a research abstract that will be presented on Monday, June 8 at SLEEP 2009,
the 23rd Annual Meeting of the Associated Professional Sleep Societies Results indicate
that children between the ages of 4 and 5 who did not take daytime naps were reported by
their parents to exhibit higher levels of hyperactivity, anxiety and depression than
children who continued to nap at this age. According to lead author Brian Crosby, PhD,
postdoctoral fellow of psychology at Pennsylvania State University, previous studies have
shown that poor or inadequate sleep is linked with symptoms of hyperactivity, anxiety and
depression; researchers involved in this study were happy to demonstrate the potential
importance of napping for optimal daytime functioning in young children, as napping is
often overlooked in favor of nighttime or total sleep. “There is a lot of individual
variability in when children are ready to give up naps. I would encourage parents to
include a quiet ‘rest’ time in their daily schedule that would allow children to
nap if necessary.”
Long and Short Sleep Durations Are
Associated with Increased Risk for Diabetes
According to a research abstract that will be presented on Monday, June 8, at SLEEP 2009,
the 23rd Annual Meeting of the Associated Professional Sleep Societies, both long and
short sleepers are at greater risk for diabetes. Individuals sleeping for more than eight
hours per night may be particularly vulnerable. Results indicate that the adjusted odds
ratio was 1.24 for diabetes associated with short sleep (five hours per night or less) and
1.48 for diabetes associated with long sleep (nine or more hours per night). The
prevalence of diabetes was 12 percent for blacks and 8 percent for whites, and the
prevalence of obesity (body mass index of 30 kg/m2 or greater) was 52 percent for blacks
and 38 percent for whites. According to lead author Girardin Jean-Louis, PhD, associate
professor at the SUNY Downstate Medical Center at the Brooklyn Health Disparities Research
Center in New York, findings suggest that both patients who have excessive or insufficient
sleep time have increased risk for developing diabetes, a serious health condition.
“Both blacks and whites who were obese tended to have short sleep time. These
findings suggest that race significantly influenced the risk of obesity conferred by short
sleep duration,” said Jean-Louis. “As obesity is associated with diabetes and
sleep apnea, it may be that more blacks are at risk for sleep apnea and diabetes, which
are both linked to cardiovascular disease.”
Researchers solve 'bloodcurdling'
mystery
By applying cutting-edge techniques in single-molecule manipulation, researchers at
Harvard University have uncovered a fundamental feedback mechanism that the body uses to
regulate the clotting of blood. The finding, which could lead to a new physical,
quantitative, and predictive model of how the body works to respond to injury, has
implications for the treatment of bleeding disorders. A team, co-led by Timothy A.
Springer, Latham Family Professor of Pathology at Harvard Medical School and Children's
Hospital Boston, and Wesley P. Wong, Rowland Junior Fellow and a Principal Investigator at
the Rowland Institute at Harvard, reported its discovery about the molecular basis for the
feedback loop responsible for hemostasis in the June 5th issue of Science. "The human
body has an incredible ability to heal from life's scrapes and bruises," explains
Wong. "A central aspect of this response to damage is the ability to bring bleeding
to end, a process known as hemostasis. Yet regulating hemostasis is a complex balancing
act." Too much hemostatic activity can lead to an excess of blood clots, resulting in
a potentially deadly condition known as thrombosis. If too little hemostatic activity
occurs in the body, a person may bleed to death. To achieve the proper balance, the body
relies on a largely mechanical feedback system that relies on the miniscule forces applied
by the circulation system on a molecular "force sensor" known as the A2 domain
of the blood clotting protein von Willebrand factor (VWF). By manipulating single
molecules of this A2 domain, the researchers found that the A2 domain acts as a highly
sensitive force sensor, responding to very weak tensile forces by unfolding, and losing
much of its complex three-dimensional organization. This unfolding event allows the
cutting of the molecule by an enzyme known as ADAMTS13. "In the body, these cutting
events decrease hemostatic potential and also enable blood clots to be trimmed in size.
The system is so finely tuned that the A2 shear sensor is able to regulate the size of VWF
within the blood stream, maintaining the optimal size for responding properly to
traumas," says Wong.
Investigation finds that cigarette
smoking does not affect everyone in same way
Cigarette smoking induced COPD, or chronic obstructive pulmonary disease, is a disease
that results in severe breathing difficulty. According to World Health Organization (WHO)
it is the fourth leading killer worldwide. However the mechanisms responsible for some
smokers developing COPD and others evading the disease have not been well
understood.Dr.Manuel Cosio from the McGill University Health Centre, in collaboration with
Italian and Spanish scientists, reports in the New England Journal of Medicine that an
autoimmune mechanism, compounded by genetic predisposition in COPD, would explain the
progression of the disease in some smokers and the evasion in others. COPD has a family
connection and next of kin of patients with COPD have a much higher chance of developing
the disease, a characteristic of autoimmune diseases. Although smoking is the primary risk
factor for COPD in the western world, open fire pollutant cooking and heating fuels in the
home is an important risk factor for the development of COPD in women in developing
nations. "Smoke can play an important role in autoimmune diseases such as COPD, and
other diseases like rheumatoid arthritis, because it accentuates genetic predispositions
to the disease," warns Dr. Cosio. Yet contrary to previous scientific beliefs, COPD
does not progress in the same way in all smokers. The authors describe three steps in the
potential progression to COPD in smokers: "COPD does not go from stage one, two and
three in all people," Dr. Cosio says. "Depending on their personal balance
between immune response and immune control some people would stop at stage one, others at
stage two, and some will progress to stage three, full autoimmunity and lung
destruction." "Hopefully investigators will now see the disease in a totally
different way," Dr Cosio stresses. "Our hope is that our research will open the
door for a different investigation on COPD, where scientists learn more about the
immunological processes and how these processes could be controlled and modulated to
eventually provide the right treatment."
Penn study demonstrates new way to
boost immune memory
After a vaccination or an infection, the human immune system remembers to keep protecting
against invaders it has already encountered, with the aid of specialized B-cells and
T-cells. Immunological memory has long been the subject of intense study, but the
underlying cellular mechanisms regulating the generation and persistence of long-lived
memory T cells remain largely undefined. Now, University of Pennsylvania School of
Medicine researchers have found that a common anti-diabetic drug might enhance the
effectiveness of vaccines. The findings are described this week in an advanced online
publication of Nature. In this study, an experimental preventive vaccine was made more
efficacious by boosting numbers of cancer fighting T cells with the anti-diabetic drug
metformin. This resulted in a larger population of memory immune cells that were able to
fight off a tumor at a later time. "We serendipitously discovered that the
metabolizing, or burning, of fatty acids by T cells following the peak of infection is
critical to establishing memory in those T cells," says senior author Yongwon Choi,
PhD, Professor of Pathology and Laboratory Medicine. "As a consequence, we used the
widely prescribed anti-diabetic drug metformin, which is known to operate on fatty-acid
metabolism, to enhance this process." "We have shown experimentally in mice that
metformin increases T-cell memory as well as the ensuing protective immunity of an
experimental anti-cancer vaccine," notes postdoctoral fellow and first author Erika
Pearce, PhD. "These findings were unanticipated, but are potentially extremely
important and could revolutionize current strategies for both therapeutic and prophylactic
vaccines," says Choi.
Promising antimicrobial attacks
virus, stimulates immune system
A promising antimicrobial agent already known to kill bacteria can also kill viruses and
stimulate the innate immune system, according to researchers at National Jewish Health. In
a paper appearing online June 4 in the Journal of Investigative Dermatology, Michael
Howell, PhD, Assistant Professor of Pediatrics, and his colleagues demonstrated that the
synthetic compound CSA-13 can kill vaccinia virus in cell cultures and in mice.
Additionally, they showed that CSA-13 stimulates cells to produce their own antimicrobial
proteins. "This compound is demonstrating broad effectiveness," said Dr. Howell.
"While our experiments were designed to test its ability to attack the vaccinia
virus, its immune-stimulating ability was a surprising observation." CSA-13 is one of
a class of compounds known as ceragenins, which were developed by Brigham Young University
Professor Paul Savage to mimic antimicrobial proteins that occur naturally in the body.
The ceragenins are smaller than antimicrobial proteins, and are not as vulnerable to
degradation in the body. They have previously been shown to be effective against a variety
of bacterial species. Dr. Howell and his colleagues wanted to learn if CSA-13 could fight
vaccinia virus infections. Vaccinia virus is closely related to the organism that causes
smallpox and is used in smallpox vaccines. However, millions of people in the United
States who have had eczema are susceptible to a serious and potentially fatal complication
of the vaccination, known as eczema vaccinatum, which occurs when the vaccinia virus
infects the skin. Dr. Howell is part of a team, led by Professor of Allergy and Clinical
Immunology Donald Leung, MD, PhD, that is seeking protection against this complication so
that eczema patients could receive the vaccination in case of a bioterrorist attack with
smallpox.
Sleuths follow lung stem cells for
generations to shed light on healing
More than one kind of stem cell is required to support the upkeep and repair of the lungs,
according to a new study published in the journal Cell Stem Cell. Scientists at Duke
University Medical Center painstakingly followed and counted genetically labeled cells in
the mouse lung for over a year, under differing conditions, to learn more about natural
renewal and healing processes. This information may shed light on what goes wrong in
conditions like lung cancer, chronic bronchitis and asthma. "We are learning the
exact processes that maintain the various regions of the lung in tip-top condition and
what happens when things go wrong," said Brigid Hogan, Ph.D., chair of the Duke
Department of Cell Biology and senior author of the study. "Normally, the lung is
beautifully organized, with the exact proportion of secretory and ciliated cells lined up
next to each other to get their jobs done." The secretory cells lubricate and
protect, while the hair-like projections of the ciliated cells waft the secretions up and
out of the lungs. In humans, under conditions of heavy smoking, or infection or
inflammation due to asthma or cystic fibrosis, repeated cycles of damage and repair lead
to a messy arrangement, she said. "You can get patches of cells building up in a
stacked, flattened formation like skin cells. Some cells multiply too fast; others may
make too much mucus." The team tagged secretory cells, called Clara cells, found in
both the trachea and bronchioles, the airway branches inside the lung. They followed them
in normal mice and during the amazingly efficient repairs after damage by too much oxygen
or other environmental stresses. They tested the theory that there are BASCs
(bronchioalveolar stem cells). These purportedly are on the border between the bronchioles
and alveoli, which are the small air sacs where gas exchange takes place. BASCs were
thought to replenish both regions of the lung.
Protein may be strongest indicator
of rare lung disease, study shows
Researchers at the University of Cincinnati (UC) have discovered a protein in the lungs
that can help in determining progression of the rare lung disease Idiopathic Pulmonary
Fibrosis (IPF). Researchers say the protein—Serum surfactant protein A—is
superior to other IPF predictors and could lead to better decisions about treatment and
timing of lung transplantation. The study, led by Brent Kinder, MD, is published in the
June 4 edition of the journal Chest. Surfactant proteins are lipoproteins that allow the
lungs to stretch and function. These have previously been investigated by UC pulmonary
researchers Frank McCormack, MD, and Jeffrey Whitsett, MD. Kinder and colleagues report
that Serum surfactant protein A is the strongest predictor of a patient's survival in the
first year after diagnosis with IPF. "A simple blood test may give us the information
we need to help determine the short term risk of death in a patient with IPF," says
Kinder, an assistant professor of medicine at the UC College of Medicine and pulmonologist
with UC Physicians. "This protein is a stronger predictor of the severity of illness
than age, symptoms or prognostic data, like breathing tests." IPF is scarring of the
lung. As the disease progresses, air sacs in the lungs become replaced by fibrotic scar
tissue. Lung tissue becomes thicker where the scarring forms, causing an irreversible loss
of the tissue's ability to carry oxygen into the bloodstream.
Ottawa scientists discover new way
to enhance stem cells to stimulate muscle regeneration
Scientists at the Ottawa Hospital Research Institute (OHRI) and the University of Ottawa
have discovered a powerful new way to stimulate muscle regeneration, paving the way for
new treatments for debilitating conditions such as muscular dystrophy. The research, to be
published in the June 5 issue of Cell Stem Cell, shows for the first time that a protein
called Wnt7a increases the number of stem cells in muscle tissue, leading to accelerated
growth and repair of skeletal muscle. "This discovery shows us that by targeting stem
cells to boost their numbers, we can improve the body's ability to repair muscle
tissue," said senior author Dr. Michael Rudnicki. Dr. Rudnicki is the Scientific
Director of Canada's Stem Cell Network and a Senior Scientist at OHRI and Director of
OHRI's Sprott Centre for Stem Cell Research, as well as a Professor of Medicine at the
University of Ottawa. Stem cells give rise to every tissue and organ in the body.
Satellite stem cells are specialized muscle stem cells that live in adult skeletal muscle
tissue and have the ability to both replicate and differentiate into various types of
muscle cells. Dr. Rudnicki's team found that the Wnt7a protein, when introduced into mouse
muscle tissue, significantly increased the population of these satellite stem cells and
fueled the regeneration process, creating bigger and stronger muscles. Muscle tissue mass
was increased by nearly 20 per cent in the study.
Tiny protein-activator responsible
for brain cell damage in Huntington disease
Johns Hopkins brain scientists have figured out why a faulty protein accumulates in cells
everywhere in the bodies of people with Huntington's disease (HD), but only kills cells in
the part of the brain that controls movement, causing negligible damage to tissues
elsewhere. The answer, reported this week in Science, lies in one tiny protein called
"Rhes" that's found only in the part of the brain that controls movement. The
findings, according to the Hopkins scientists, explain the unique pattern of brain damage
in HD and its symptoms, as well as offer a strategy for new therapy. HD itself is caused
by a genetic defect that produces a mutant version of the protein "huntingtin"
that gathers in all cells of the body, but only seems to affect the brain. Passed from
parent to child through an alteration of a normal gene, HD over time causes irreversible
uncontrolled movement, loss of intellectual function, emotional disturbances and death.
"It's always been a mystery why, if the protein made by the HD gene is seen in all
cells of the body, only the brain, and only a particular part of the brain, the corpus
striatum, deteriorates," says Solomon H. Snyder, M.D., professor of neuroscience at
Johns Hopkins. "By finding the basic culprit, the potential is there to develop drugs
that target it and either prevent symptoms or slow them down." Curious about the
huntingtin protein's striatal-specific effect, Snyder's research team, led by Srinivasa
Subramaniam, Ph.D., a postdoctoral fellow, searched for proteins that interacted locally,
specifically and exclusively with huntingtin in the corpus striatum, guessing that the
molecular answer to the mystery most likely would be found there. The protein Rhes caught
their attention because they already were studying a related protein for other reasons.
Rhes was known to be found almost exclusively in the corpus striatum.
Link unraveled between chromosomal
instability and centrosome defects in cancer cells
In a new study, Dana-Farber Cancer Institute scientists disprove a century-old theory
about why cancer cells often have too many or too few chromosomes, and show that the
actual reason may hold the key to a novel approach to cancer therapy. Since the late 19th
century, scientists have attributed the surplus or shortage of intact chromosomes in
cancer cells to a kind of fragmentation in cell division: instead of dividing neatly into
two identical daughter cells, as normal cells do, cancer cells were thought to frequently
split into three or four cells, each with a motley assortment of chromosomes. This
explosive division was thought to occur because many cancer cells have extra centrosomes,
tiny circular structures that help pairs of chromosomes line up in preparation for cell
division. When study lead author Neil Ganem, PhD, of Dana-Farber used newly developed
microscope equipment to watch living cancer cells for a week or more, he found that not
only were such abnormal divisions quite rare, but the resulting daughter cells were so
discombobulated by their chromosomal quirks, they generally survived for only a few days
– far too briefly to deliver abnormal chromosome content to a tumor. The way that
extra centrosomes do cause chromosome instability, Ganem and his colleagues have
discovered, is by setting up a tug-of-war for chromosomes that are eventually caught
between newly forming daughter cells of a dividing cancer cell. In normal cells, which
have two centrosomes, division occurs as the pairs of chromosomes split neatly apart, like
halves of a zipper, each set moving into one of the daughter cells. The extra centrosomes
in cancer cells exert an unequal pull on some chromosomes, causing the daughter cells to
inherit an irregular number of them – explaining, in part, why tumors are often
filled with cells of varying quantities of chromosomes. Their findings are reported in the
journal Nature as an advanced online publication. "Chromosome instability is a
hallmark of most cancer cells, arising when chromosomes are missegregated into daughter
cells during division," said Ganem, who led the study with senior author David
Pellman, MD, and co-author Susana Godinho, PhD, of Dana-Farber. "Such instability may
be a double-edged sword. It may confer a survival benefit on cancer cells by enabling them
to adapt to a stressful environment in the body or by helping them become resistant to
chemotherapy drugs. But it may also have deleterious effects that could make tumor cells
susceptible to therapeutic attack.""Although centrosome defects have been
recognized in tumors for a long time," Pellman said, "it has been a tough
problem to rigorously study. Neil and Susana have made a significant advance by developing
useful methods to create comparable cells that carry or don't carry extra
centrosomes."
Routine diabetes screenings could
cut health-care costs
Screening adults for diabetes could result in significant cost-savings for health care
systems compared to the costs of not screening individuals at all. Emory University
researchers will present the findings of their diabetes screening cost analysis today at
the annual meeting of the American Diabetes Association in New Orleans. "The economic
costs of diabetes threaten the financial integrity of our health care systems," says
study co-author Lawrence S. Phillips, MD, Emory University School of Medicine Professor of
Medicine, Division of Endocrinology. "We asked whether there is economic
justification for screening for prediabetes and unrecognized diabetes since early
treatment could help prevent or delay development of diabetes and its complications and
reduce associated costs." Phillips and his research team screened 1,259 adults who
had never been diagnosed with diabetes. The volunteer participants underwent four
screening tests, including random plasma and capillary glucose, and a 50g oral glucose
challenge test (without a prior fast, at different times of the day) with plasma and
capillary glucose measured one hour after the glucose drink. All participants also had a
definitive 75g oral glucose tolerance test (OGTT) performed in the morning after an
overnight fast. The researchers found that 24 percent of the adults screened had either
diabetes or prediabetes. In addition, they concluded that costs for screening and three
years of treatment with metformin, or change in lifestyle for individuals found to have
prediabetes or previously unrecognized diabetes, would be lower than costs for not
screening. The costs of two-step screening (only positive screens would have the OGTT)
were projected to include the costs of testing, costs for false negatives (in individuals
where the diagnosis would be missed), and costs for treatment of true positives (people
found to have diabetes or prediabetes, treated with metformin, or change in lifestyle).
A lethal cancer knocked down by
one-two drug punch
In the battle against cancer, allies can come from unexpected sources. Research at The
Jackson Laboratory has yielded a new approach to treating leukemia, one that targets
leukemia-proliferating cells with drugs that are already on the market. Jackson Adjunct
Professor Shaoguang Li, M.D., Ph.D., who now has a laboratory at the University of
Massachusetts Medical School in Worcester, led a research team that identified a gene
involved with the inflammatory response that could hold the key to treating or even
preventing chronic myeloid leukemia (CML), a lethal cancer. In research published in the
journal Nature Genetics, the researchers also showed that an asthma medication for human
patients is an effective treatment for CML in mice. The gene, Alox5, processes essential
fatty acids to leukotrienes, which are important agents in the inflammatory response. But
according to the researchers, Alox5 has a more sinister side. It is vital to the
development and maintenance of cancer stem cells. Cancer stem cells are slow-dividing
cells that are thought to give rise to a variety of cancers, including leukemia, and to be
critical for maintaining them. Researchers theorize that cancer stem cells must be
targeted for effective treatment of many cancers, but direct evidence is still lacking.
The researchers found that CML did not develop in mice without Alox5 because of impaired
function of leukemia stem cells. Also, Alox5 deficiency did not affect normal stem cell
function, providing the first clear differentiation between normal and cancer stem cells.
Li also treated mice with CML with Zileuton, an asthma medication that inhibits the Alox5
inflammation pathway, as well imatinib, commonly known as Gleevec, the most effective
current leukemia medication. Imatinib effectively treated CML, but Zileuton was more
effective. The two drugs combined provided an even better therapeutic effect.The Jackson
Laboratory is seeking patent protection on the novel approach to treat CML that Li and
colleagues have demonstrated.
Recruitment of reproductive
features into other cell types may underlie extended lifespan in animals
In the sense that organisms existing today are connected through a chain of life –
through their parents, grandparents and other ancestors – almost a billion years back
to the first animals of the pre-Cambrian era, an animal's reproductive cells can be
considered to be immortal. These germline cells generate their offspring's somatic cells
– other cells involved in all aspects of growth, metabolism and behavior, which have
a set lifespan – and new germline cells that continue on, generation after
generation. Now in a dramatic finding, researchers from the Massachusetts General Hospital
(MGH) Department of Molecular Biology have found that certain genetic mutations known to
extend the lifespan of the C. elegans roundworm induce 'mortal' somatic cells to express
some of the genes that allow the 'immortality' of reproductive germline cells. Their
report will appear in the journal Nature and is receiving advance online release. "C.
elegans mutants with extreme longevity accomplish this feat, in part, by adopting genetic
programs normally restricted to the germline into somatic cells," says Sean Curran,
PhD, of MGH Molecular Biology, the study's lead author. "We know that germline cells
are more stable than somatic cells – they live longer and are more resistant to
stresses that damage other cells – and understanding the molecular pathways involved
in that stability may someday allow us to devise therapies protective against age-related
decline in other tissues." Curran is a research fellow in the laboratory of MGH
investigator Gary Ruvkun, PhD, whose work focuses on the development, longevity and
metabolism of C. elegans, a tiny worm broadly used as a model for studying basic
biological systems. Ruvkun and other researchers discovered that simple mutations in
genetic pathways conserved throughout evolution can double or triple the lifespan of C.
elegans, and that similar mutations in the corresponding pathways also dramatically extend
mammalian lifespan.
Researchers develop the first
climate-based model to predict Dengue fever outbreaks
Dengue Fever (DF) and Dengue Hemorrhagic Fever (DHF) are the most important vector-borne
viral diseases in the World. Around 50-100 million cases appear each year putting 2.5
billion people at risk of suffering this debilitating and sometimes fatal disease. Dengue
Fever is prevalent in the Tropics. For that reason, an interdisciplinary team of
researchers from the University of Miami (UM) and the University of Costa Rica have used
global climatological data and vegetation indices from Costa Rica, to predict Dengue
outbreaks in the region. The new model can predict Dengue Fever epidemics with 83%
accuracy, up to 40 weeks in advance of an outbreak and provide information on the
magnitude of future epidemics. The model can be expanded to include the broader region of
Latin America and the Caribbean, where incidence and spread of the disease has increased
dramatically over the past 25 years. An early warning system to prevent and mitigate the
spread of the disease can potentially be developed using this model, explained Douglas O.
Fuller, associate professor and chair of the department of Geography and Regional Studies
in the UM College of Arts and Sciences and principal investigator of this project.
"Such a tool will provide sufficient time for public health authorities to mobilize
resources to step up vector control measures, alert at-risk populations to impending
conditions and help health professionals plan for increased case loads," Fuller said.
Vector-born diseases, such DF and DHF, are ones in which the disease is transmitted from
an infected individual to another by a biological agent. In the case of Dengue, one of
four closely related Dengue viruses is transmitted to humans by the Aedes aegypti or more
rarely the Aedes albopictus mosquito, sometimes with other animals serving as intermediary
hosts. Most of the world's population infected by Dengue (also known as "breakbone
fever") is located in tropical and subtropical areas of the globe, where the weather
is dominated by rainfall.
International researchers tackle
stillbirth taboo
Every year there are more than 3 million stillbirths. Yet despite advances and, at times,
information overload in the medical world, stillbirths remain underreported and either are
not found in data records or are not recognised in national policymaking, which suggests
that stillbirths are a taboo subject. In a BMC-published journal, researchers from around
the globe examined the problem, in an attempt to improve knowledge and help put a stop to
the problem. Data show that more than 3 million stillbirths occur worldwide, and 98% of
those are found in low- to middle-income countries. Intrapartum stillbirths, which are
stillbirths that occur during labour, stand at around 1 million and are also usually found
in low- and middle-income countries. Experts say stillbirth cases number more than
malaria-based child deaths worldwide. Stillbirth cases are 3 to 4 per 1 000 full-term
births in western European countries, while the US reports 7 per 1 000 full-term births.
A new lead for autoimmune disease
A drug derived from the hydrangea root, used for centuries in traditional Chinese
medicine, shows promise in treating autoimmune disorders, report researchers from the
Program in Cellular and Molecular Medicine and the Immune Disease Institute at Children's
Hospital Boston (PCMM/IDI), along with the Harvard School of Dental Medicine. In the June
5 edition of Science, they show that a small-molecule compound known as halofuginone
inhibits the development of Th17 cells, immune cells recently recognized as important
players in autoimmune disease, without altering other kinds of T cells involved in normal
immune function. They further demonstrate that halofuginone reduces disease pathology in a
mouse model of autoimmunity. Currently there is no good treatment for autoimmune
disorders; the challenge has been suppressing inflammatory attacks by the immune system on
body tissues without generally suppressing immune function (thereby increasing risk of
infections). The main treatment is antibodies that neutralize cytokines, chemical
messengers produced by T cells that regulate immune function and inflammatory responses.
However, antibodies are expensive, must be given intravenously and don't address the root
cause of disease, simply sopping up cytokines rather than stopping their production;
patients must therefore receive frequent intravenous infusions to keep inflammation in
check. Powerful immune-suppressing drugs are sometimes used as a last resort, but patients
are left at risk for life-threatening infections and other serious side effects. Through a
series of experiments, the researchers show that halofuginone prevents the development of
Th17 cells in both mice and humans, halts the disease process they trigger, and is
selective in its effects. It also has the potential to be taken orally. "This is
really the first description of a small molecule that interferes with autoimmune pathology
but is not a general immune suppressant," says Mark Sundrud, PhD, of the PCMM/IDI,
the study's first author.
From oxygen transport to melanin
formation - Activation mechanism of key enzymes explained
Pandinus imperator, the emperor scorpion, is not only popular as a pet, but is also of
interest for research purposes. The reason for this is its blue blood, which transports
oxygen and distributes it throughout the body. Like tyrosinase, the key enzyme in melanin
synthesis, the blue blood pigment hemocyanin found in the emperor scorpion and other
arthropods belongs to a group of special molecules that occur in all organisms and that
have many different functions: coloring the skin, hair and eyes, immune response, wound
healing or the brown discoloration of fruit. "When these enzymes mutate, this may
result in albinism, or in birth marks when production of the pigment melanin increases, as
often seen in melanoma," explains Professor Heinz Decker of Johannes Gutenberg
University Mainz. The biophysicist has been studying hemocyanins and the associated
tyrosinases for the past 20 years. In cooperation with researchers, Dr. Cong and Dr. Chiu,
from the Baylor College of Medicine in Houston he has now been able to show for the first
time exactly how the enzymes become active, thereby fulfilling their various functions.
This work was published in the journal Structure on 13 May.
Discovery of new proteins may lead
to more effective treatment of endocarditis and infections associated with implants
A research team at the Faculty of Odontology at Malmö University in Sweden has discovered
two new proteins that are of importance to the survival of bacteria and their colonization
of the human body. Besides enhancing our knowledge of the ability of bacteria to spread,
the findings may also lead to more effective treatment of endocarditis and infections
associated with implants. Each year some 500 people in Sweden develop endocarditis,
inflammation of the heart valves. The condition can be life-threatening, and one of the
bacteria that cause the disease is Streptococcus gordonii, a bacterium that exists in the
mouth. "It's part of the natural flora of bacteria there, but sometimes it gets into
the bloodstream, and then it can lead to infective endocarditis. The bacteria have also
been found in infections surrounding various kinds of implants," says Associate
Professor Julia Davies, who directed the research team at the Faculty of Odontology. To
survive in the oral cavity the bacteria must be able to attach to a surface, such as the
mucous membrane. This is done with the help of proteins. In the mid 1990s one of these
proteins from the bacterium S. gordonii was identified by a research team in England.
Advanced image analysis can provide
better risk assessment in hardening of the arteries
Ultrasound examination of the carotid artery is a patient-friendly and inexpensive method
for assessing atherosclerosis and thereby predicting the risk of cardiovascular diseases.
Peter Holdfeldt, who recently defended his doctoral thesis at Chalmers University of
Technology in Sweden, has developed new analytical methods for ultrasound images that can
provide more reliable and more exact assessments of atherosclerosis. Cardiovascular
diseases brought on by hardening of the arteries are the most common cause of death in the
Western world. Hardening of the arteries means a thickening of the walls of blood vessels
and the appearance of so-called atherosclerotic plaque, which consist of stored fat, among
other things. With the aid of ultrasound images, it is possible to find individuals who
are at risk by measuring the thickness of the walls in the carotid artery. Another
ultrasound method is to analyze whether the character of various types of plaque can
predict the risk of cardiovascular diseases. Peter Holdfeldt has developed new and more
refined methods of image analysis that are based on dynamic programming.
"Measurements of the thickness of the walls of the carotid require the detection of
boundaries between different layers of tissue in the blood vessel," he says.
"Previously dynamic programming has been used to automatically detect boundaries in
still images. But the new method uses dynamic programming for detection in image sequences
of one and the same blood vessel instead."
Help for the silent sufferers
A unique research project into the highly sensitive problem of domestic violence towards
older women is being carried out by researchers from The University of Nottingham’s
Division of Nursing. 12 participants have already taken part since the project started
last year for this valuable study aimed at helping those who have experienced abuse and
health professionals deal with the problem.One participant who has already been
interviewed, Ann aged 63, told the researchers - "A lot of older women stay in the
abusive partnership, and remain in it, because they don’t know there is any support
out there. A lot of women never talk about it. I think it is the 'hiddenness' of it that
is the problem actually, and I think that needs to stop. I think we’ve got to give
permission to women, to get people to realise that it is very wrong that they have been
abused." Leading the study, Dr Julie McGarry, says: “Older women who suffer
domestic abuse are historically a silent section of our society. This research aims to
give them a voice and break the taboo surrounding the problem. We are finding older women
may be too ashamed to come forward but we can reassure them that our work with them will
be completely confidential and they can even contact us anonymously to help our
study.” Domestic abuse is not just about physical violence. Verbal abuse such as
belittling, malicious ridicule, shouting and unreasonable demands also have adverse
effects on women’s mental health and physical wellbeing. Up to now, there has been
little research into the experiences of older women because most domestic violence surveys
tend to exclude women over 59.
Stopping fatty change in heart
cells
Heart failure is one of the world's most frequent causes of death - caused by conditions
such as diabetes and obesity. With people who are overweight, the heart has to do more
work in order to pump the blood through the circulatory system and this causes an increase
in blood pressure. The heart itself becomes enlarged as the myocardial muscle cells
increase in mass. To enable the heart to grow there also has to be an increased supply of
energy and oxygen. However, the myocardial muscle cells suffer from a lack of oxygen and
energy until such time as there are enough blood vessels to support the tissue. This is
the critical moment in which the cells convert their metabolism. A healthy heart burns
fat. But the abnormally enlarged heart cells burn sugar in the form of glucose because
this form of energy is quickly available. The protein HIF1-alpha is responsible for this
conversion to sugar combustion. This has been demonstrated in research work done by Jaya
Krishnan from the group of Wilhelm Krek, Professor of Cell Biology at ETH Zurich. His
research has just been published in the online journal "Cell Metabolism".
Asthma rates and where you live
Neighborhoods with restaurants, entertainment, cultural facilities and ethnic diversity
have lower asthma rates in the city of Chicago than neighborhoods where residents are less
likely to move, and where there are more churches and not-for-profit facilities. Published
in the spring 2009 issue of the Journal of Allergy and Clinical Immunology, the two-year
study led by Ruchi Gupta, MD, MPH, a researcher at Children's Memorial Hospital and
associate professor of pediatrics at Northwestern University Feinberg School of Medicine,
showed that neighborhoods with more community vitality, specifically economic potential,
community amenities and social capital had lower asthma rates. The study focused on 287
Chicago neighborhoods, where nearly 50,000 children grades K-8 were screened for asthma.
Asthma is the leading chronic childhood illness, affecting more than 9 million children
nationwide. Chicago has twice the national average asthma mortality rate. "Previous
studies showed that neighborhoods right next to each other with similar racial makeup had
very different asthma rates; we wanted to see what else was going on in each neighborhood
to cause such a disparity," said Gupta. "So we looked at specific factors in
each neighborhood." Ethnically diverse communities with greater potential for
economic development that were civically engaged, meaning that there were high percentages
of registered voters had low asthma rates while stable communities, defined as communities
where residents were less likely to move, with more social interaction had higher asthma
rates. Although it is not entirely clear how these factors affect health outcomes,
previous research has shown that asthma and other chronic illnesses of childhood are
associated with poverty, which may explain why communities with low asthma rates had a
greater capacity for economic growth. Researchers suspect that the association between
neighborhood stability and asthma may indicate that homes in which residents are less
likely to move receive less frequent and thorough cleanings, leading to an accumulation of
indoor pollutants known to trigger asthma. Similarly, the association of higher
interaction potential and increased asthma may signify overcrowding, which also leads to
increased indoor pollutants.
Fatty foods -- not empty stomach --
fire up hunger hormone
New research led by the University of Cincinnati (UC) suggests that the hunger hormone
ghrelin is activated by fats from the foods we eat—not those made in the body—in
order to optimize nutrient metabolism and promote the storage of body fat. The findings,
the study's author says, turn the current model about ghrelin on its head and point to a
novel stomach enzyme (GOAT) responsible for the ghrelin activation process that could be
targeted in future treatments for metabolic diseases. The laboratory study, led by
Matthias Tschöp, MD, UC associate professor of psychiatry and internal medicine, is
published online ahead of print Friday, June 5, 2009, in the journal Nature Medicine.
Ghrelin is a hormone that was believed to accumulate during periods of fasting and is
found in the body in high concentrations just before meals. It is dubbed the "hunger
hormone" because it has been shown that administration of pharmacological doses acts
in the brain to stimulate hunger and increase food intake in animal models and humans. The
ghrelin hormone is unique in that it requires acylation (the addition of a fatty acid) by
a specific enzyme (ghrelin O-acyl transferase, or GOAT) for activation. Originally it was
assumed that the fatty acids attached to ghrelin by GOAT were produced by the body during
fasting.The new data by Tschöp and his team suggests that the fatty acids needed for
ghrelin activation actually come directly from ingested dietary fats. In a departure from
an earlier model that was upheld for nearly a decade, Tschöp says, it appears that the
ghrelin system is a lipid sensor in the stomach that informs the brain when calories are
available—giving the green light to other calorie-consuming processes such as
growing. Tschöp and his team used mouse models to test the effects of over expressing the
GOAT enzyme, or "knocking it out." They found that, when exposed to a lipid-rich
diet, mice without GOAT accumulated less fat than normal mice, while those with
over-expressed GOAT accumulated more fat mass than normal mice. "When exposed to
certain fatty foods, mice with more GOAT gain more fat," says Tschöp. "Mice
without GOAT gain less fat since their brain does not receive the 'fats are here, store
them' signal."
FSU study links 'warrior gene' to
gang membership, weapon use
Boys who carry a particular variation of the gene Monoamine oxidase A (MAOA), sometimes
called the "warrior gene," are more likely not only to join gangs but also to be
among the most violent members and to use weapons, according to a new study from The
Florida State University that is the first to confirm an MAOA link specifically to gangs
and guns.Findings apply only to males. Girls with the same variant of the MAOA gene seem
resistant to its potentially violent effects on gang membership and weapon use. Led by
noted biosocial criminologist Kevin M. Beaver at FSU's College of Criminology and Criminal
Justice, the study sheds new light on the interplay of genetics and environment that
produces some of society's most serious violent offenders."While gangs typically have
been regarded as a sociological phenomenon, our investigation shows that variants of a
specific MAOA gene, known as a 'low-activity 3-repeat allele,' play a significant
role," said Beaver, an award-winning researcher who has co-authored more than 50
published papers on the biosocial underpinnings of criminal behavior. "Previous
research has linked low-activity MAOA variants to a wide range of antisocial, even
violent, behavior, but our study confirms that these variants can predict gang
membership," he said. "Moreover, we found that variants of this gene could
distinguish gang members who were markedly more likely to behave violently and use weapons
from members who were less likely to do either." The MAOA gene affects levels of
neurotransmitters such as dopamine and serotonin that are related to mood and behavior,
and those variants that are related to violence are hereditary. Some previous studies have
found the "warrior gene" to be more prevalent in cultures that are typified by
warfare and aggression.
Fatigue common after myocardial
infarction
Half of all patients who undergo myocardial infarction are experiencing onerous fatigue
four months after the infarction. The patients who are most fatigued are those who
perceive the infarction as a sign of chronic illness, those who experience the illness as
difficult to control, and those who believe that the illness has a large impact on their
life. These are the conclusions of a thesis presented at the Sahlgrenska Academy. Just
over 200 persons completed a questionnaire one week after they had experienced an
infarction and again four months later. Many of the patients were also interviewed. Around
half of the patients stated that they felt onerous fatigue four months after the
infarction. One third of the patients exhibited expressed fatigue, while one fifth also
exhibited symptoms of depression."Many people experienced the fatigue as new, and
different. It was not related to physical effort or a lack of rest; it occurred
unpredictably and could not be attributed to any definite cause", says nurse Pia
Alsén, author of the thesis.
Brominated Flame Retardants in
Children’s Toys
Brominated flame retardants (BFRs), including polybrominated diphenyl ethers (PBDEs),
1,2-bis(2,4,6-tribromophenoxy)ethane (BTBPE), decabromodiphenyl ethane (DBDPE), and
polybrominated biphenyls (PBBs) were found in children’s toys purchased from South
China. The median BFR concentrations in the hard plastic toys were 53000, 5540 ng/g, 101.1
ng/g, and 27.9 ng/g, for total PBDEs, DBDPE, BTBPE, and PBBs, respectively, which were
notably higher than values in other toys. The PBDE concentrations were below the threshold
limit (1000 ppm) required by the European Commission’s Restriction of Hazardous
Substances (RoHS) and Waste Electrical and Electronic Equipment (WEEE) directives in all
of the toys, except for one hard plastic toy with a total PBDE concentration of 5344000
ng/g. The BFR profiles in the toys were consistent with the patterns of their current
production and consumption in China, where PBDEs, specifically decaBDE product, were the
dominant BFR, followed by the emerging DBDPE. The relatively high concentrations of octa-
and nonaBDEs in the foam toys and the results of principal component analysis (PCA) may
suggest the decomposition of highly brominated BDEs during the manufacturing processes of
the toys. Daily total PBDE exposures associated with toys via inhalation, mouthing, dermal
contact, and oral ingestion ranged from 82.6 to 8992 pg/kg bw-day for children of 3 months
to 14 years of age. Higher exposures, predominantly contributed through the mouthing
pathway, were observed for infants and toddlers than for the other subgroups. In most
cases, children’s BFR exposure via the toys likely accounts for a small proportion of
their daily BFR exposure, and the hazard quotients for noncancer risk evaluation were far
below 1. To the author’s knowledge, this is the first study to examine the
concentrations of BFRs in toys, and the potential exposures to children.
Advanced image analysis can provide
better risk assessment in hardening of the arteries
Ultrasound examination of the carotid artery is a patient-friendly and inexpensive method
for assessing atherosclerosis and thereby predicting the risk of cardiovascular diseases.
Peter Holdfeldt, who recently defended his doctoral thesis at Chalmers University of
Technology in Sweden, has developed new analytical methods for ultrasound images that can
provide more reliable and more exact assessments of atherosclerosis. Cardiovascular
diseases brought on by hardening of the arteries are the most common cause of death in the
Western world. Hardening of the arteries means a thickening of the walls of blood vessels
and the appearance of so-called atherosclerotic plaque, which consist of stored fat, among
other things. With the aid of ultrasound images, it is possible to find individuals who
are at risk by measuring the thickness of the walls in the carotid artery. Another
ultrasound method is to analyze whether the character of various types of plaque can
predict the risk of cardiovascular diseases. Peter Holdfeldt has developed new and more
refined methods of image analysis that are based on dynamic programming.
Drinking water from air humidity
Not a plant to be seen, the desert ground is too dry. But the air contains water, and
research scientists have found a way of obtaining drinking water from air humidity. The
system is based completely on renewable energy and is therefore autonomous. Cracks
permeate the dried-out desert ground, the landscape bears testimony to the lack of water.
But even here, where there are no lakes, rivers or groundwater, considerable quantities of
water are stored in the air. In the Negev desert in Israel, for example, annual average
relative air humidity is 64 percent – in every cubic meter of air there are 11.5
milliliters of water. Research scientists at the Fraunhofer Institute for Interfacial
Engineering and Biotechnology IGB in Stuttgart working in conjunction with their
colleagues from the company Logos Innovationen have found a way of converting this air
humidity autonomously and decentrally into drinkable water. “The process we have
developed is based exclusively on renewable energy sources such as thermal solar
collectors and photovoltaic cells, which makes this method completely energy-autonomous.
It will therefore function in regions where there is no electrical infrastructure,”
says Siegfried Egner, head of department at the IGB. The principle of the process is as
follows: hygroscopic brine – saline solution which absorbs moisture – runs down
a tower-shaped unit and absorbs water from the air. It is then sucked into a tank a few
meters off the ground in which a vacuum prevails. Energy from solar collectors heats up
the brine, which is diluted by the water it has absorbed. Because of the vacuum, the
boiling point of the liquid is lower than it would be under normal atmospheric pressure.
This effect is known from the mountains: as the atmospheric pressure there is lower than
in the valley, water boils at temperatures distinctly below 100 degrees Celsius. The
evaporated, non-saline water is condensed and runs down through a completely filled tube
in a controlled manner. The gravity of this water column continuously produces the vacuum
and so a vacuum pump is not needed. The reconcentrated brine runs down the tower surface
again to absorb moisture from the air. “The concept is suitable for various sizes of
installation. Single-person units and plants supplying water to entire hotels are
conceivable,” says Egner. Prototypes have been built for both system components
– air moisture absorption and vacuum evaporation – and the research scientists
have already tested their interplay on a laboratory scale. In a further step the
researchers intend to develop a demonstration facility.
New imaging technique: toward
spinal cord regeneration?
The axon is a part of the neuron through which nerve impulses are transmitted, and at the
end of which is located the synapse, which connects it to another neuron. In the event of
a lesion, the axon is the component which must be regenerated in order to restore the
connections between the different neurons and re-form the nerve. The regeneration capacity
of axons within the central nervous system, of which the spinal cord is part, has until
now been much debated. Axons can regenerate toward the muscles, whereas in the opposite
direction inhibiting factors prevent regrowth toward the nerve centers. The observation
made by Genevičve Rougon's team at IBDML shows that the axons also regrow in the
direction of the spinal cord within a short lapse of time after the injury. Moreover, this
regrowth is encouraged by post-traumatic angiogenesis, in other words by the process of
formation of new blood vessels in the damaged tissue. After injury to a mouse's spinal
cord, extensive and extremely active angiogenesis is observed, peaking in intensity one
week after the lesion. At the same time, regrowth of the axons takes place preferentially
and more rapidly in the vicinity of the blood vessels. These observations suggest that
stimulating and prolonging angiogenesis could open up new prospects for treatment and
encourage functional recovery after, for instance, lesion of the spinal cord.
Jellyfish Shed Fluorescent Light On
How The Brain Works
New research offers prospect of watching the brain as it learns. Scientists at the
University of Leicester are developing new ways of studying how brain cells work -thanks
to jellyfish! Professor of Neuroscience at the University of Leicester, Nicholas Hartell,
is leading a research group examining the connections between brain cells, called
synapses. And thanks to fluorescent protein sensors derived from proteins originally
discovered in jellyfish, the researchers can watch synapses as they transmit and store
information. Professor Hartell, of the Department of Cell Physiology and Pharmacology,
will be explaining his research at an inaugural public lecture to be held on Tuesday 9
June at 5.30pm in Lecture Theatre 1, Ken Edwards Building. It is open to the public and
free. He said "Changes in the strength of signalling between excitable cells in the
brain provide a mechanism for information storage in the brain. In this lecture, I will
discuss how synapses, the specialised connections formed between brain cells, can change
their properties and so contribute to the learning and the formation of memory. "In
particular, I will introduce recent work that aims to develop methods of visualising
synaptic transmission during learning. I will also consider the application of technology
originally developed for televisions, projectors and the telecommunications industry to
high speed visualisation of neurones and neural networks."
Researchers develop an intelligent
chip which regulates diabetes
Scientists of the Electronic Technology group of the University of Seville (US), led by
Professor José Manuel Quero, have completed the first phase of Mireia, a research project
financed by the Plan Nacional del Ministerio de Ciencia e Innovación (National Plan of
the Spanish Science and Innovation Ministry), whose aim is to develop an intelligent chip
to regulate diabetes in any kind of patients suffering this disease. With this research,
the idea is to extract the interstitial liquid with micro needles that are 200 microns
long (the double than a hair's thickness). This painless process is carried out with
sensors and micro fluidics and patients are informed every now and again in their mobiles
of their level of glucose. 'There are many devices in the glucose field that do work, but
the novelty of our research work is that we can use the same technology to extract liquid
and to inject it', José Manuel Quero says. He does not hesitate to stress that the
following stage would consist of providing insulin almost automatically, and always under
medical supervision. This could be also applied to many other medicaments.
Key to blood clotting discovered
By applying cutting-edge techniques in single-molecule manipulation, researchers at
Harvard University have uncovered a fundamental feedback mechanism that the body uses to
regulate the clotting of blood. The finding, which could lead to a new physical,
quantitative, and predictive model of how the body works to respond to injury, has
implications for the treatment of bleeding disorders.A team, co-led by Timothy A.
Springer, Latham Family Professor of Pathology at Harvard Medical School and Children's
Hospital Boston, and Wesley P. Wong, Rowland Junior Fellow and a principal investigator at
the Rowland Institute at Harvard, reports its discovery about the molecular basis for the
feedback loop responsible for hemostasis in the June 5 issue of Science. "The human
body has an incredible ability to heal from life's scrapes and bruises," explains
Wong. "A central aspect of this response to damage is the ability to bring bleeding
to an end, a process known as hemostasis
Shining light on leptin’s role
in brain
In investigating the complex neurocircuitry behind weight gain and glucose control,
scientists have known that the hormone leptin plays a key role in the process. But within
the myriad twists and turns of the brain’s intricate landscape, the exact pathways
that the hormone travels to exert its influence have remained a mystery.Now, a study led
by Harvard investigators at Beth Israel Deaconess Medical Center (BIDMC) sheds further
light on the subject. Reported in the journal Cell Metabolism, the findings demonstrate
that when leptin sensitivity is restored to a tiny area of neurons in the brain’s
hypothalamus, a group of mice deficient in the leptin receptor are cured of severe
diabetes – and also spontaneously double their activity levels – independent of
any change in weight or eating habits.
Health, life insurers hold billions
in tobacco stocks
More than a decade after Harvard Medical School researchers first revealed that life and
health insurance companies were major investors in tobacco stocks – prompting calls
upon them to divest – the insurance industry has yet to kick the habit, they say.A
letter about insurance company holdings, published in the June 4 issue of the New England
Journal of Medicine, shows that U.S., Canadian, and U.K. insurance firms hold at least
$4.4 billion of investments in companies whose subsidiaries manufacture cigarettes,
cigars, chewing tobacco, and related products.Tobacco products currently contribute to the
deaths of 5.4 million people worldwide annually, according to the World Health
Organization. Tobacco use is a major risk factor for stroke, heart attack, lung disease,
and cancer.“Despite calls upon the insurance industry to get out of the tobacco
business by physicians and others, insurers continue to put their profits above
people’s health,” said J. Wesley Boyd, lead author of the letter, an assistant
clinical professor of psychiatry at Harvard Medical School, and an attending psychiatrist
at Cambridge Health Alliance. “It’s clear their top priority is making money,
not safeguarding people’s well-being.”
People with Intellectual or
Developmental Disabilities Particularly Vulnerable to Effects of Tobacco Use and
Dependence
While tobacco use is an ongoing health hazard for the entire population, its consequences
for people with developmental or intellectual disabilities can be especially severe. And
the medical community often tends to overlook the tobacco-related burdens these people
face. An extensive review of published research on this topic appears in the June edition
of the journal Intellectual and Developmental Disabilities. “This is too important an
issue to ignore,” said Dr. Marc L. Steinberg, an assistant professor of psychiatry at
the UMDNJ-Robert Wood Johnson Medical School and the article’s lead author.
“Health care professionals often do not ask these individuals about tobacco use or
exposure.”
Researchers identify four new
targets for breast cancer
Four suspects often found at the scene of the crime in cancer are guilty of the initiation
and progression of breast cancer in mice that are resistant to the disease, a team led by
scientists at The University of Texas M. D. Anderson Cancer Center reports in the June
edition of Cancer Cell."We have a smoking gun" that shows it's no coincidence
the three protein receptors and the enzyme that makes them are abnormally expressed in
many types of cancer, said Gordon Mills, M.D., Ph.D., professor and chair of M. D.
Anderson's Department of Systems Biology and senior author of the paper. "We've
compiled lots of evidence that they are associated with cancer, what's been missing is
proof that they could cause cancer," Mills said. "There are no questions left,
they should be targeted." The four are three lysophosphatidic acid (LPA) receptors
(LPA1, LPA2, and LPA3) and the LPA-producing enzyme, autotaxin. "Lysophosphatidic
acid", Mills said, "is the single most potent known cellular survival
factor." LPA binds to a series of G protein-coupled receptors to spark normal cell
proliferation, viability, production of growth factors and survival. The Cancer Cell paper
shows this powerful network is hijacked to initiate breast cancer and fuel tumor growth,
invasion and metastasis. The team took a strain of mice that is highly resistant to breast
cancer and then created four transgenic strains, each strain expressing one of the
receptors or autotaxin. At 24 months, none of the 44 original cancer-resistant mice
developed mammary gland cancer. Only one case of inflammation and two cases of a
potentially precancerous accumulation of cells known as hyperplasia were noted.
Tracking down the causes of
multiple sclerosis
Over 100,000 people suffer from multiple sclerosis in Germany alone. Despite intensive
research, the factors that trigger the disease and influence its progress remain unclear.
Scientists from the Max Planck Institute of Neurobiology in Martinsried and an
international research team have succeeded in attaining three important new insights into
the disease. It would appear that B cells play an unexpected role in the spontaneous
development of multiple sclerosis and that particularly aggressive T cells are activated
by different proteins. Furthermore, a new animal model is helping the scientists to
understand the emergence of the most common form of the disease in Germany. (Nature
Medicine, May 31, 2009 & Journal of Experimental Medicine, June 1, 2009) Multiple
Sclerosis (MS) poses enormous problems for both patients and doctors: it is the most
common inflammatory disease of the central nervous system in our part of the world and
often strikes patients at a relatively young age. In some patients it leads to severe
disability. Moreover, despite decades of research on MS, the causes and course of the
disease are still largely unclear. There is much evidence to support the fact that MS is
triggered by an autoimmune reaction: immune cells that should actually protect the body
against threats like viruses, bacteria and tumours, attack the body's own brain tissue.
New treatments now available can attenuate the harmful immune reaction and thus delay the
progress of the disease. However, the more effective the treatment, the more serious its
side effects. Therefore, it is a matter of extreme urgency that new forms of treatment be
developed which can differentiate in a targeted way between the immune cells that cause
the disease and those that should be protected. A better understanding of the disease is
required in order to achieve this.
Team led by Scripps research
scientists finds new way that cells fix damage to DNA
A team of researchers at The Scripps Research Institute and other institutions has
discovered a new way by which DNA repairs itself, a process that is critical to the
protection of the genome, and integral to prevention of cancer development. Scientists who
study the repair of the DNA bases, which make up the information in the human genome, had
known of only one type of method that cells use to fix a specific kind of damage to their
DNA, but in the June 11, 2009 issue of Nature, the team found a novel way—one that
combines elements from the known mechanisms and an unrelated second method that was
previously not known to play a role in this type of DNA repair. "We found a
connection between the known DNA repair processes that people did not know was
there," says Professor John Tainer, a member of the Skaggs Institute for Chemical
Biology at Scripps Research, who led the study with Geoffrey P. Margison of the University
of Manchester (United Kingdom) and Anthony E. Pegg of the Pennsylvania State University
College of Medicine. "This changes the game, and gives us something important to look
for in cancers that are resistant to chemotherapy." This new mechanism is controlled
by alkyltransferase-like proteins (ATLs), whose structure and function had been unknown
and which had been identified only in bacteria and yeast. In addition to describing the
function of ATLs, in the new study the scientists showed that ATLs exist in a
multicellular organism, the sea anemone, which suggests this protein or its cousins in
terms of repair activity also exist in other species, including humans.
BPA may cause heart disease in
women, research shows
New research by a team of scientists at the University of Cincinnati (UC) shows that
bisphenol A (BPA) may be harmful for the heart, particularly in women. Results of several
studies are being presented in Washington, D.C., at ENDO 09, the Endocrine Society's
annual meeting, June 10-13. A research team lead by Scott Belcher, PhD, Hong Sheng Wang,
PhD, and Jo El Schultz, PhD, in the department of pharmacology and cell biophysics, found
that exposure to BPA and/or estrogen causes abnormal activity in hearts of female rats and
mice. In addition, these researchers found that estrogen receptors are responsible for
this affect in heart muscle cells. "There is broad exposure to bisphenol A, despite
recognition that BPA can have harmful effects," Belcher says. "We had reason to
believe that harmful cardiovascular affects can be added to the list." BPA, an
environmental pollutant with estrogen activity, is used to make hard, clear plastic and is
common in many food product containers. It has been linked to neurological defects,
diabetes and breast and prostate cancer.
Radiation Seeds Effective Against
Single Metastatic Brain Tumors
A study led by specialists at the Brain Tumor Center at the University of Cincinnati (UC)
Neuroscience Institute affirms the benefits and safety of aggressive, localized treatment
for patients with a single brain metastasis. The retrospective study of 72 patients,
published in the May issue of the Journal of Neuro-Oncology, demonstrates that the
implantation of radioactive seeds following the surgical removal of a single brain
metastasis is as effective as the standard treatment of radiating the entire brain
following surgery. Radiation seeds are titanium casings about the size of a grain of rice
that are filled with low-level, I-125 radioactivity. The standard treatment, known as
whole-brain radiation therapy (WBRT), effectively kills microscopic and undetectable
cancer cells not only around the tumor but also in other parts of the brain where they
have not yet been detected with MRI scans. But it can cause long-term radiation toxicity
and can result in cognitive problems in up to 10 percent of patients. “The potential
adverse affects of WBRT are of concern,” says Ronald Warnick, MD, professor of
neurosurgery and radiation oncology at UC, director of the Brain Tumor Center and the
study’s principal investigator. “These include acute effects, such as fatigue
and hair loss, but also delayed, cognitive effects, including memory loss and personality
changes. These cognitive side effects can compromise the benefit that WBRT
provides.”The risk of cognitive impairment is especially undesirable because patients
with a single brain metastasis can survive longer than one to two years.
Researchers find how a common
genetic mutation makes cancer radiation resistant
Many cancerous tumors possess a genetic mutation that disables a tumor suppressor called
PTEN. Now researchers at Washington University School of Medicine in St. Louis have shown
why inactivation of PTEN allows tumors to resist radiation therapy. The PTEN gene produces
a protein found in almost all tissues in the body. This protein acts as a tumor suppressor
by preventing cells from growing and dividing too rapidly. Mutations in PTEN are
frequently found in prostate cancer and endometrial cancer, melanoma and certain
aggressive brain tumors. Tumors with PTEN mutations are often resistant to radiation
therapy, and Tej K. Pandita, Ph.D., a researcher with the Siteman Cancer Center at
Washington University School of Medicine and Barnes-Jewish Hospital, and his colleagues
have been trying to find out why. That information could enable researchers to develop
drugs that overcome that resistance and increase the effectiveness of radiation
treatments.In an article to be published July 15, 2009, in the journal Cell Cycle and now
available online, they demonstrate that PTEN-deficient cells have defective checkpoints.
As cells grow and divide, they pass through several phases. Checkpoints operate during
each phase and assess whether a cell is healthy enough to continue growing and dividing.
If not - for example, if there is damage to genetic material resulting from radiation
treatments — signals from checkpoints should tell the cell to wait until repairs are
made or should induce the cell to die. The finding that checkpoints are affected in
PTEN-deficient cells is contrary to some previous research, which had suggested instead
that cells with PTEN mutations had defective DNA repair mechanisms. But Pandita showed
that DNA repair is independent of PTEN function in tumor cells grown in the laboratory.
That indicated that defective DNA repair is not the cause of the unstable genomes
frequently seen in PTEN-deficient tumor cells and not the explanation for radiation
resistance in these tumors.
Sight for sore eyes
In a world-first breakthrough, University of New South Wales (UNSW) medical researchers
have used stem cells cultured on a simple contact lens to restore sight to sufferers of
blinding corneal disease.Sight was significantly improved within weeks of the procedure,
which is simple, inexpensive and requires a minimal hospital stay. The research team from
UNSW's School of Medical Sciences harvested stem cells from patients' own eyes to
rehabilitate the damaged cornea. The stem cells were cultured on a common therapeutic
contact lens which was then placed onto the damaged cornea for 10 days, during which the
cells were able to re-colonise the damaged eye surface. While the novel procedure was used
to rehabilitate damaged corneas, the researchers say it offers hope to people with a range
of blinding eye conditions and could have applications in other organs. A paper detailing
the breakthrough appears in the high-impact journal Transplantation this week. The trial
was conducted on three patients; two with extensive corneal damage resulting from multiple
surgeries to remove ocular melanomas, and one with the genetic eye condition aniridia.
Other causes of cornea damage can include chemical or thermal burns, bacterial infection
and chemotherapy. "The procedure is totally simple and cheap," said lead author
of the study, UNSW's Dr Nick Di Girolamo. "Unlike other techniques, it requires no
foreign human or animal products, only the patient's own serum, and is completely
non-invasive. "There's no suturing, there is no major operation: all that's involved
is harvesting a minute amount – less than a millimeter – of tissue from the
ocular surface," Dr Di Girolamo said.
Rheumatoid arthritis is associated
with poor sleep in women
According to a research abstract that will be presented on Wednesday, June 10, at SLEEP
2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies, symptoms of
Rheumatoid Arthritis (RA) negatively affect women's sleep. Sleep is further impaired by
pain, depression and poor adherence to RA medications. Results indicate that length of
time since RA diagnosis, RA disease activity, level of pain, depression symptoms and
adherence to medications for RA may cause women suffering from the disease to have poor
sleep quality. According to lead author Faith Luyster, PhD, of the University of
Pittsburgh, Pa., findings emphasize the need for further research concerning poor RA
medication adherence and sleep quality. "Treating depression in women with RA may not
only improve sleep but may also improve pain and adherence to medications," said
Luyster. The study involved 133 women with RA; their average age was 56 years, and they
were primarily Caucasian, married, had at least a high school education, were not
depressed and had RA for 14.76 years. A majority of participants (71 percent) reported
poor sleep quality. Pain and depression were measured through subjective reports, and
medication adherence was measured objectively with an electronic medication monitor on
medication bottle caps. Sleep disturbances and depression are more prevalent in women in
the general population. According to the American Academy of Sleep Medicine (AASM), women
face many challenges that interfere with their sleep quality and duration.
First-Time Moms’ Exhaustion
May Be Caused by Sleep Fragmentation, Rather than Timing of Sleep
Contrary to popular belief, the timing of sleep in new mothers is preserved after giving
birth, according to a research abstract that will be presented on Wednesday, June 10, at
SLEEP 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies.
Researchers state that while postpartum mothers did experience sleep disruption and
daytime consequences, their sleep/wake times remained aligned with self-reported preferred
sleep/wake times. The exception was mothers with multiple children; these women’s
actual awakening times were earlier than desired. The study, authored by Megan
Clegg-Kraynok, M.S., and Hawley Montgomery-Downs, PhD, of West Virginia University in
Morgantown, W. Va., involved 24 women with an average age of 30.5 years and average yearly
income of $65,808. Of the participants, 92 percent were white, 96 percent were
married/cohabitating, 50 percent were first-time mothers and 67 percent were
breastfeeding. According to Montgomery-Downs, postpartum moms may not suffer sleep
deprivation at all. Findings of the study support the hypothesis that the exhaustion new
moms experience is likely due to sleep fragmentation, rather than not sleeping enough or
sleeping at the wrong times. “We found that although our participants are quite
fatigued, and their sleep at night is highly interrupted, first-time mothers of newborns
go to sleep at night and awaken in the morning at the times they report are their
preferred sleep and wake times,” said Clegg-Kraynok. “Mothers of newborns who
have other children also fell asleep at their preferred time but awoke for the day earlier
than their preferred time. We expect this is because they are awakened by the older
child.”
Wistar Institute team finds key
target of aging regulator
Researchers at The Wistar Institute have defined a key target of an evolutionarily
conserved protein that regulates the process of aging. The study, published June 11 in
Nature, provides fundamental knowledge about key mechanisms of aging that could point
toward new anti-aging strategies and cancer therapies. Scientists have long known that a
class of proteins called sirtuins promotes fitness and longevity in most organisms ranging
from single-celled yeast to mammals. At the cellular level, sirtuins protect genome
integrity, enhance resistance to adverse stresses, and antagonize senescence. However, the
underlying molecular mechanisms have remained poorly understood. The team, led by senior
author Shelley Berger, Ph.D., Hilary Koprowski Professor at The Wistar Institute,
demonstrated for the first time a molecular target for a member of this class, Sir2, in
regulation of aging in yeast cells. Sir2 removes an acetyl group attached to a specific
site (lysine at position 16 or K16) on histone H4—histones are proteins that package
and organize the long strands of DNA within the nucleus and also are central regulators in
turning genes on and off. The study reveals that removal of this acetyl group by Sir2 near
the chromosome ends—the telomeres—is important for yeast cells to maintain the
ability to replicate. Researchers found that Sir2 levels decline as cells age, and there
is a concomitant accumulation of the acetylation mark along with disrupted histone
organization at telomeres. Deacetylation of H4K16 by Sir2 and consequent telomere
stability play a major role in maintaining long lifespan in yeast. Since sirtuins
deacetylate many different proteins, these results clarify a key role of Sir2 protein in
control of lifespan. "Some modifications on histones, like this acetylation on
histone H4 lysine 16, are persistent and are maintained through generations of cell
divisions. This DNA-independent inheritance is called epigenetics," Berger says.
"Characteristic epigenetic features have been discovered for various developmental
processes in recent years. Understanding epigenetic changes associated with aging is a
hugely exciting direction in aging research. It will provide insights and ideas not only
for new therapies to regulate cells that have lost control of proliferation, such as
'immortal' cells found in cancers, but also for new strategies to maintain health and
fitness." "We plan to continue to search for new targets of Sir2 and other aging
regulators," says lead author Weiwei Dang, Ph.D., a postdoctoral scientist working
with Berger. "We are designing unbiased screens for other aging targets and
mechanisms in chromatin. Using yeast as our aging model enables us to do many discovery
screens that are impossible with other, more complex organisms. Yet it is remarkable that
many of these chromatin mechanisms associated with yeast could turn out to be relevant
even for aging human cells."
Stable marriage is linked with
better sleep in women
Being stably married or gaining a partner is associated with better sleep in women than
being unmarried or losing a partner, according to a research abstract that will be
presented on Wednesday, June 10, at SLEEP 2009, the 23rd Annual Meeting of the Associated
Professional Sleep Societies. Results show that women who were stably married or who had
gained a partner during the eight years of the study had better sleep than women who were
unmarried or who had lost a partner over the course of the study follow-up. According to
the study's lead author, Wendy Troxel, PhD, Assistant Professor at the University of
Pittsburgh School of Medicine, women who were stably married had the highest quality sleep
measured objectively and subjectively, and these results persisted even after controlling
for other known risk factors for sleep, including age, ethnicity, socioeconomic status,
and depressive symptoms. "Women who had 'gained' a partner over the eight years of
the study had similar subjective sleep quality as compared to the stably married women;
however, after looking at specific objective sleep measurements we discovered that these
women had more restless sleep than the always married women," said Troxel. "We
speculate that these findings may reflect a 'newlywed effect' or simply the fact that
these women may be less adjusted to sleeping with their partner than the 'stably married'
women."
Sleep May Be Important in
Regulating Emotional Responses
According to a research abstract that will be presented on Thursday, June11, at SLEEP
2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies, sleep
selectively preservers memories that are emotionally salient and relevant to future goals
when sleep follows soon after learning. Effects persist for as long as four months after
the memory is created. Results indicate that the sleeping brain seems to calculate what is
most important about an experience and selects only what is adaptive for consolidation and
long-term storage. Across long delays of 24 hours, or even three–to-four months,
sleeping soon after learning preserved the trade-off (compared to waiting an entire day
before going to sleep).According to lead author Jessica Payne, PhD, of Harvard Medical
School in Boston, Mass., it was surprising that in addition to seeing the enhancement of
negative memories over neutral scenes, there was also selectivity within the emotional
scenes themselves, with sleep only consolidating what is most relevant, adaptive and
useful about the scenes. It was even more surprising that this selectivity lasted for a
full day and even months later if sleep came soon after learning. “It may be that the
chemical and physiological aspects of sleep underlying memory consolidation are more
effective if a particular memory is ‘tagged’ shortly prior to sleeping,”
said Payne.
Extended and Shortened Sleep
Durations Linked to Weight Gain
Body mass index (BMI) varies as a function of habitual sleep duration, according to a
research abstract that will be presented on Thursday, June 11, at SLEEP 2009, the 23rd
Annual Meeting of the Associated Professional Sleep Societies. Results indicate that twins
who slept between 7 and 8.9 hours each night had a lower mean BMI (25.0 kg/m2) compared to
those who regularly slept either more (25.2 kg/m2) or less (26.4 kg/m2) per night. The
relationship between sleep duration and BMI remained significant after controlling for
genetics and shared environment. According to lead author Nathaniel Watson, MD,
co-director at the University of Washington Sleep Institute in Seattle, sleep habits have
a significant impact on weight and BMI. “Findings of the study point towards an
environmental cause of the relationship between sleep duration and BMI,” said Watson.
“Results were robust enough to be present when the sample was limited to identical
twins.” The study involved data from 1,797 twins, including 634 twin pairs (437
monozygotic, 150 dizygotic and 47 indeterminate pairs) and 529 individual twins with a
mean age of 36.8 years. Habitual sleep duration was obtained by self-reported length of
sleep per night, and BMI was calculated by self-reported height and weight. Of the sample,
68.3 percent was female, and 88.2 percent was Caucasian. Results persisted in a co-twin
control analysis of within twin pair differences in sleep duration and BMI.
Fifty-one genes predict breast
cancer survival
It may be possible in the future to use a specimen from the tumour to determine which
patients with breast cancer have a good chance of overcoming the disease, and which
patients should be given more intensive treatments. Fifty-one genes may together provide
information about the prognosis for an individual patient. These are the conclusions of a
thesis presented at the Sahlgrenska Academy, University of Gothenburg, Sweden.The research
group has analysed specimens from a number of breast tumours, both from patients that died
from the disease and from patients surviving at least 10 years from diagnosis. The levels
of expression of 51 genes differed between the two groups. It should be possible to use
the differences in order to classify the patients into one of two groups: a favourable
prognosis group and a poor prognosis group. "Many breast cancer patients are
currently overtreated, while some are undertreated. If it was possible to identify
patients with poor prognosis, it would be possible to use greater treatment resources on
these patients. At the same time, patients with a favourable prognosis could avoid
unnecessary treatment", says Elin Karlsson who successfully defended her thesis on
June 5.
Muscular Dystrophy - New Drug
Promises Benefit Without Risk OfInfection
A new drug being studied for the treatment of muscle degenerating diseases has shown
promising results. According to a study published today in the British Journal of
Pharmacology, Debio 025 is as effective as current drugs but, crucially, does not cause
unwanted immunosuppressive effects. Bethlem Myopathy and Ullrich Congenital Muscular
Dystrophy (UCMD) are muscle wasting diseases caused by deficiencies in collagen VI, a
component of connective tissue. Patients are usually diagnosed at birth and suffer from
muscle weakness that worsens over time. UCMD patients often also suffer respiratory
failure, which is complicated by lung infections. Although the drug cyclosporin A (CsA)
offers some benefit for these patients, its long term use may be undesirable because it
interacts with calcineurin, an important immunoregulatory protein.
From oxygen transport to melanin
formation - Activation mechanism of key enzymes explained
Pandinus imperator, the emperor scorpion, is not only popular as a pet, but is also of
interest for research purposes. The reason for this is its blue blood, which transports
oxygen and distributes it throughout the body. Like tyrosinase, the key enzyme in melanin
synthesis, the blue blood pigment hemocyanin found in the emperor scorpion and other
arthropods belongs to a group of special molecules that occur in all organisms and that
have many different functions: coloring the skin, hair and eyes, immune response, wound
healing or the brown discoloration of fruit. "When these enzymes mutate, this may
result in albinism, or in birth marks when production of the pigment melanin increases, as
often seen in melanoma," explains Professor Heinz Decker of Johannes Gutenberg
University Mainz. The biophysicist has been studying hemocyanins and the associated
tyrosinases for the past 20 years. In cooperation with researchers, Dr. Cong and Dr. Chiu,
from the Baylor College of Medicine in Houston he has now been able to show for the first
time exactly how the enzymes become active, thereby fulfilling their various functions.
This work was published in the journal Structure on 13 May.
What Causes Irritability In
Menopause?
Irritability is frequently the main presenting complaint of perimenopausal and
postmenopausal women; yet, studies specifically researching on irritability in this
population are lacking.As it remains controversial whether mood symptoms related to
menopause are independently associated with hormonal changes or whether they are secondary
to vasomotor or other bothersome symptoms of menopause, such as insomnia. This study aims
to assess irritability in either perimenopausal or postmenopausal women, to look for
possible associations with vasomotor symptoms, insomnia and chronic disease, and to
explore possible hormonal links with sex steroids, gonadotrophins, prolactin and thyroid
hormones. A total of 163 peri- and postmenopausal women, non-hormonal therapy or tibolone
users, attending a menopause clinic were included in this cross-sectional study.The
subjects completed the Irritability, Depression, Anxiety Scale, which is an 18-item
self-report scale that assesses irritability as a temporary psychological state.
Irritability is divided into ‘outwardly directed’ if it is expressed toward
others and ‘inwardly directed’ if it is directed toward oneself. Climacteric
symptoms were evaluated by Greene’s scale, which provides subscores for vasomotor
symptoms. Insomnia was measured by the Athens Insomnia Scale. Chronic disease refers to
the existence of hypertension, cardiac disease, diabetes mellitus or thyroid disease.
Can Light Therapy Improve Your
Sexual Functioning? New Promising Data
Although we are still far from knowing exactly where and how the pineal suppressive role
is exerted, the fact that the gland exerts an inhibitory function on the reproductive axis
is widely accepted. In fact, the pineal seems to exert its hormonal effect at different
levels of the reproductive axis, both at the hypothalamic-pituitary level and at the
gonadal level, where melatonin receptors have also been found. Furthermore, melatonin
appears to increase prolactin secretion, which may contribute to sexual dysfunction. Based
on the observations mentioned above a group of italian investigators hypothesized that an
inhibition of pineal gland activity via a treatment with bright light could favorably
influence sexual function and pilottested the usefulness of bright light therapy in a
small sample of 9 male patients with nonorganic sexual dysfunction. Subjects (age
39–60) were consecutively recruited in the outpatient clinic of the Urology
Department of the University of Siena Medical Center on the basis of a diagnosis of
primary (i.e. not due to another illness or to a medication or a drug of abuse) hypoactive
sexual desire disorder (HSDD, n = 2), sexual arousal disorder (SAD, n = 6), and orgasmic
disorder (OD, n = 1) and the absence of a mood disorder, as assessed via the Mini
International Neuropsychiatric Interview. Subjects were randomly assigned to active light
treatment (ALT) or placebo light treatment (L-PBO) and assessed at baseline and after 2
weeks of ALT/L-PBO treatment via the Structured Clinical Interview for DSM-IV-Sexual
Disorders (SCID-S) and via a sexual satisfaction self-report, which asked them to rate on
a scale from 1 to 10 their level of sexual satisfaction.
Can Omega-3 Fatty Acids Prevent
Depression In Coronary Heart Disease?
Depression is an established risk factor for the development of coronary heart disease
(CHD) in healthy patients and for adverse cardiovascular outcomes in patients with
existing CHD. Dietary factors resulting in lower levels of omega–3 fatty acids not
only increase CHD risk, but may also be involved in the pathophysiology of depression. The
investigators measured red blood cell levels of two omega–3 fatty acids,
docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), and assessed depressive
symptoms in a cross-sectional study of 987 adults with CHD. Omega –3 fatty acids were
blindly measured in fasting venous blood samples using capillary gas chromatography to
measure the fatty acid composition of red blood cell membranes. Red blood cell levels of
EPA and DHA are presented as a percentage composition of total fatty acid methyl esters.
The investigators assessed current depression using the 9-item Patient Health
Questionnaire. They evaluated the association between omega –3 fatty acid levels and
depressive symptoms as continuous variables using linear regression.
