- - European weblog on food, health and environment
News - Week 37 - 2008
TGen and Washington University
Researchers Discover New Approach to Treating Endometrial Cancer
Researchers at the Translational Genomics Research Institute (TGen) today announced a new
approach to treating endometrial cancer patients that not only stops the growth of tumors,
but kills the cancer cells. In a potentially major breakthrough, TGen scientists and
collaborators at Washington University School of Medicine in St. Louis discovered that
introducing a particular inhibitor drug can turn "off" receptors responsible for
the growth of tumors in a significant number of patients with endometrial cancer. And,
they found that the inhibitor drug proved effective even in cancer tumors containing a
commonly occurring mutant gene, PTEN, previously associated with resistance to drug
treatment. TGen’s findings appear today in a paper published as a priority report by
Cancer Research, a Philadelphia-based peer-reviewed journal dedicated to original cancer
research. A clinical trial based on the TGen study will start within the next year. Dr.
Pamela Pollock, an associate investigator in TGen’s Cancer and Cell Biology Division
and the paper’s senior author, led a team that used the latest genome-scanning
technology to sequence 116 endometrioid endometrial tumor samples. This work was done in
association with Dr. Paul Goodfellow, an expert in endometrial cancer and a professor in
the departments of Surgery and of Obstetrics and Gynecology at Washington University.
Pollock and colleagues in May 2007 announced that they had discovered previously
unrecognized alterations in the fibroblast growth factor receptor 2 (FGFR2) gene. The
altered FGFR2 is present in the cancer cells of nearly 15 percent of women with
endometrioid endometrial tumors. These kinds of tumors represent 80 percent of all
endometrial cancers. By introducing a commercially available inhibitor drug, PD173074,
TGen researchers showed that they could stop the growth of tumors, and even kill cancer
cells, in cases where the tumors contained the altered FGFR2 gene. The altered gene causes
the receptors to get stuck in the "on" position and signal the endometrial cells
to grow out of control. "These findings could accelerate the development of new
treatments for endometrial cancer because there are already drugs in clinical trials that
inhibit FGFR2 function," Pollock said.
Noninvasive test accurately
identifies advanced liver disease without biopsy
Non-invasively measuring liver stiffness with transient elastography accurately diagnoses
patients with late-stage liver disease, reports a new study in Clinical Gastroenterology
and Hepatology, the official journal of the American Gastroenterological Association (AGA)
Institute. Liver biopsy has been the gold standard for assessing liver disease. However,
it is limited by invasiveness, risk of complications, patient discomfort and the
availability of expertise. Liver stiffness measurement (LSM) has been shown to be a
reliable tool to detect liver cirrhosis, and transient elastography is a rapid,
non-invasive and reproducible new technique being employed to measure liver stiffness.
"Research has shown that LSM has the potential to become a non-invasive way to
diagnose severe liver disease," said Henry LY Chan, MD, with Prince of Wales Hospital
in Hong Kong. "We wanted to take a closer look at its potential, evaluating its
accuracy in relation to traditional biopsy. Comparing the results of transient
elastography with biopsy reports enables us to determine just how precise this technique
can be." In the study, Dr. Chan and colleagues evaluated the accuracy of LSM to
detect severe liver fibrosis in 133 patients suffering from chronic liver diseases. The
research team recruited adult patients with chronic liver diseases who were clinically
indicated for liver biopsy examination in a twelve-month window. Chronic drinkers or those
with decompensated liver disease, complications of liver cirrhosis, previous liver surgery
or liver transplantation were excluded. LSM was performed within four weeks of the liver
biopsy examination. Study results showed that LSM is most accurate when diagnosing liver
disease in patients with advanced, or pericellular, fibrosis, revealing a high correlation
(r=0.43) between LSM and pericellular disease. In addition, the correlation of LSM and
pericellular fibrosis was stronger in patients with severe fibrosis than in those with
mild disease. Though not statistically significant, LSM also provided a better prediction
of cirrhosis than did bridging fibrosis, which is an earlier stage of liver disease.
Brain Imaging Links Chronic
Insomnia to Reversible Cognitive Deficits, but Behavioral Performance May not Suffer
neuroimaging study in the Sept. 1 issue of the journal Sleep is the first to find that
cognitive processes related to verbal fluency are compromised in people with insomnia
despite the absence of a behavioral deficit. These specific brain function alterations can
be reversed, however, through non-pharmacological treatment with sleep therapy. Results of
functional magnetic resonance imaging (fMRI) scanning during verbal fluency tasks show
that people with insomnia have less activation than controls in the left medial prefrontal
cortex and the left interior frontal gyrus, two fluency-specific brain regions. However,
participants with insomnia generated more words than controls on both the category fluency
task (46.4 words compared with 38.7 words) and the letter fluency task (40.1 words
compared with 32.7 words). “It was surprising to see that the patients performed at a
higher level than the control group, but showed reduced brain activation in their fMRI
results,” said principal investigator Ysbrand Der Werf, PhD, of the Netherlands
Institute for Neuroscience in Amsterdam. “The success during the task may reflect a
conscious effort to counteract the effect of poor sleep.”Results from post-treatment
neuroimaging shows that cognitive abnormalities recovered for insomnia patients who
received sleep therapy, but not for those assigned to a wait-list group. Participants in
the sleep therapy group also generated more words on the verbal fluency tasks after
treatment than members of the wait-list group, although the results did not achieve
statistical significance.
Akansas fights against the Flu
Shots Merck Gardisil Lies!!!
Watch this report about the lies and the courageous people that are fighting the Drug
companies that lie to you and won't disclose what is in vaccinations. It is making people
sick and they are attacking our children. WAKE UP AMERICA and FIGHT BACK against Gardasil
and Merck and the Flu shots that contain Thimerosal!
Study Shows that Subjective
Sensitivity to Changes in Skin Temperature is Decreased in Older Adults with Insomnia
A study in the Sept. 1 issue of the journal Sleep shows that the subjective interpretation
of temperature change is decreased in older adults, particularly those who suffer from
insomnia.The study is the first to find pronounced attenuation of subjective
thermosensitivity in elderly insomniacs within the small range of normal bed temperatures.
Researchers manipulated core body temperature, proximal skin temperature and distal skin
temperature in order to observe the effect on sleep-onset latency. All temperature
increases were seen as discomforting by the elderly with no sleep complaints, but none
were discomforting to elderly insomniacs.This inability to adequately feel how warm or
cold the body is could contribute to the poor sleep of elderly insomniacs. Surprisingly,
results indicate that warming the skin of elderly people may facilitate sleep onset
despite the diminished ability to detect changes in temperature. Core body cooling also
accelerates sleep onset in elderly insomniacs.
More Daytime Sleeping Predicts Less
Recovery during Rehabilitation for Older Adults
A study in the Sept. 1 issue of the journal Sleep shows that daytime sleeping during a
rehabilitation stay predicts less functional recovery for older adults, with effects
lasting as long as three months. Results show that a higher percentage of daytime sleep
during rehabilitation was significantly associated with less functional recovery from
admission to discharge even after adjusting for other predictors such as mental status,
hours of therapy received and reason for admission. More daytime sleeping during rehab
remained a significant predictor of less functional recovery at a three-month follow-up.
“We were surprised that the results suggested that it was the excessive daytime
sleeping in the rehabilitation facility which was associated with less improvement in
their physical functioning,” said principal investigator Cathy A. Alessi, MD, of the
VA Greater Los Angeles Healthcare System and the UCLA David Geffen School of Medicine.
“We were also surprised by how long this effect lasted. For up to three months later,
more sleeping during the daytime while they were in the rehabilitation facility was still
related to their physical functioning after being discharged.”The authors suggest
that these findings are particularly significant because sleep disturbances may be a
modifiable predictor of rehabilitation outcomes. In contrast, many other predictors of
rehabilitation outcomes such as cognitive functioning or hospital readmission are
difficult or impossible to change. Interventions to improve sleep patterns of older people
during rehabilitation, and in particular to reduce daytime sleeping, may promote
functional recovery. The study involved 245 adults with an average age of 80.6 years. Each
participant had been admitted at one of two study sites for in-patient
“post-acute” rehabilitation related to conditions such as an orthopedic problem,
a heart problem or a stroke. According to the study, older people who are admitted to the
hospital due to an illness or injury sometimes are unable to return home immediately.
Instead, elderly patients may require a period of therapy and recovery in a rehabilitation
facility such as a nursing home.
'Superbug' breast infections
controllable in nursing mothers, researchers find
Many nursing mothers who have been hospitalized for breast abscesses are afflicted with
the “superbug” methicillin-resistant Staphylococcus aureus, or MRSA, but
according to new research by UT Southwestern Medical Center physicians, conservative
treatment can deal with the problem. The study focused on hospitalized women with
mastitis, and showed that MRSA was much more likely to be found in those who had both
mastitis (an inflammation of the milk glands) and abscesses (pockets of infection).
“The take-home message is that a patient with mastitis does not necessarily need an
antibiotic against MRSA,” said Dr. George Wendel, professor of obstetrics and
gynecology and senior author of the study, which appears in the September issue of the
journal Obstetrics and Gynecology. “She will improve with a less specific antibiotic
as long as she also empties her breasts, either through feeding or pumping, and if
there’s an abscess, gets it treated.” The study also showed that if a nursing
mother has an abscess, she does not immediately need antibiotics against MRSA, but can be
switched to them if tests reveal she has MRSA.
New research led by University of
Leicester into why men are more prone to heart disease
Men are more prone to – and likely to die of - heart disease compared with women of a
similar age – and sex hormones are to blame, according to a new University of
Leicester led study The findings of a study by Dr Maciej Tomaszewski, New Blood Lecturer
in Cardiovascular Medicine in the Department of Cardiovascular Sciences at the University
of Leicester, suggest that this “male disadvantage” may be related to the
sex-specific effects of naturally occurring sex hormones. The research by Dr Tomaszewski
and his colleagues, which has been published on line in the journal Atherosclerosis,
involved 933 men aged, on average, 19 years, from the Young Men Cardiovascular Association
study. The study was supported by an NIH Fogarty International Research Collaboration
Award. The researchers looked at ways that the sex hormones - estradiol, estrone,
testosterone and androstenedione - interacted with three major risk factors of heart
disease (cholesterol, blood pressure and weight). They found that two of these sex
hormones (estradiol and estrone, called together estrogens) are linked to increased levels
of bad cholesterol (LDL-cholesterol) and low levels of good cholesterol (HDL-cholesterol)
in men. This suggests that certain sex hormones may be important risk factors of heart
disease in men, even before they present symptoms of coronary artery disease or stroke. Dr
Tomaszewski commented “We hypothesised that circulating concentrations of sex
hormones were associated with cardiovascular disease risk factors in men long before any
apparent manifestations of cardiovascular disease such as stroke or myocardial
infarction”. “We examined association of circulating estrogens (estradiol and
estrone) as well as androgens (testosterone and androstenedione) with major cardiovascular
risk factors (lipids, blood pressure, body mass) in 933 young (median age – 19
years), apparently healthy men.“Our studies showed that one of the sex hormones -
estradiol - was associated positively with total cholesterol and negatively with
HDL-cholesterol. Circulating concentrations of another sex hormone - estrone - showed
strong positive associations with both total cholesterol and LDL-cholesterol. “Thus,
men with the highest concentrations of estrone and estradiol may have the highest level of
cardiovascular risk as their levels of detrimental LDL-cholesterol are high whilst their
cardio-protective HDL-cholesterol is low. “Most importantly, the demonstrated
associations between cholesterol and estrogens were independent of other sex hormones
(testosterone and androstenedione), age, body weight, blood pressure and other potential
confounding factors. “Our data suggest that higher levels of estrogens may have
negative influence on lipid profile in men early in life, before the apparent onset of
cardiovascular disease.
New master switch found in the
brain that regulates appetite and reproduction
Body weight and fertility have long known to be related to each other – women who are
too thin, for example, can have trouble becoming pregnant. Now, a master switch has been
found in the brain of mice that controls both, and researchers at the Salk Institute for
Biological Studies say it may work the same way in humans.Findings from the study,
published ahead of print in the Aug. 31 online edition of Nature Medicine, suggest that
variations in the gene that produces this master switch, known as TORC1, could contribute
a genetic component to obesity and infertility, and might be regulated with a novel drug.
"This gene is crucial to the daisy chain of signals that run between body fat and the
brain," says Marc Montminy, Ph.D., a professor in the Clayton Foundation Laboratories
for Peptide Biology, who led the study. "It likely plays a pivotal role in how much
we, as humans, eat and whether we have offspring."It is just as important as leptin,
the well-known star regulator of appetite, Montminy says, because leptin turns on TORC1,
which in turn activates a number of genes known to help control feeding and fertility.
Judith Altarejos Ph.D., first author on this study, had been trying to understand human
energy balance, and what can go awry to promote obesity, diabetes and other metabolic
syndromes. In this study, she looked at the signals that travel from body fat to the
brain, informing the brain of how well fed the body is. The primary hormone that performs
that function is leptin, which travels through the bloodstream to the hypothalamus in the
brain (the appetite center), keeping the brain aware of the body's nutritional status.
"Leptin tells the brain that times are good, your body is full, and that it is not
necessary to eat more at the moment," Montminy says. The hormone also is known to
play a role in reproduction - although, until this study, no one understood what is was.
(Very thin women often do not have periods.) "Controlling appetite and reproduction
together provides a big evolutionary advantage," Montminy says. "If there is no
food, the brain believes the body should not reproduce because without body fat, a baby's
growth in the womb could be stunted, and without food to replenish the body's energy
reserves, there will be nothing to feed the offspring." "Leptin works remarkably
well to give the brain a good indication of how much food has been eaten; 99.9 percent of
the time it balances food intake with energy use," he says. "The problem is that
no machine works 100 percent of the time, and that slight bit of inefficiency can lead to
extra body weight." Obesity results when the brain becomes "deaf" to the
leptin signal, so one goal of Montminy's research is to "try to make a way to make
sure the brain signals are being heard." But to do that, he and his research team
first have to understand all of the signals involved in the satiety pathway. Through years
of research, they have uncovered a family of genes that act as energy switches, turning
other genes on or off. One gene, TORC2, acts like a fasting switch that flips on the
production of glucose in the liver when blood glucose levels run low, usually during
sleep. During the day, the hormone insulin normally shuts down TORC2, ensuring that blood
sugar levels don't rise too high. Problems along the pathway, however, can help lead to
diabetes.
Clem Bezold on Preventing and Reversing Diabetes and Obesity
Clem Bezold, co-founder of the Institute of Alternative Futures and author of more than
ten books about the future, discusses preventing and reversing diabetes and obesity in the
future. His comments were made during What's in Store, a food and nutrition event hosted
by Fleishman-Hillard on June 6, 2008 in New York.
Noted Toxicologist Discusses TCE
Contamination at El Toro - 15 min
Lethally toxic chemicals were dumped into the groundwater over the decades at the now
closed El Toro Marine Corps Air Station in Irvine, Cal...all » Lethally toxic chemicals
were dumped into the groundwater over the decades at the now closed El Toro Marine Corps
Air Station in Irvine, California. Marines and their family members have become sick over
the years and the health problems can be passed on generationally. TCE,
(Trichloroethylene) is known to cause liver failure, several types of cancer, mutations
and intestinal disorders.
China will be drilling for oil off
our coast - 19 min
Idaho Senator Larry Craig delivers a speech on the floor of the United States Senate
exposing the fact that China is developing oil resources in Cuban waters 50 miles from the
U.S coast.
Drawing The Line: A Look at US Oil
Dependency and ANWR - 13 min
This video makes the clear economic argument that drilling in the Arctic National
Wildlife Refuge is a bad move for the country. Instead, renewable energy sources need to
be developed to keep us prosperous, competitive and safe.
New genes found for inflammatory
bowel disease in children
Researchers have discovered two new genes that increase the risk of developing
inflammatory bowel disease (IBD) in childhood. While further study is needed to identify
the specific disease-causing mutations in these new genes, the researchers say the genes
are particularly strong candidates to be added to the list of genes already known to
affect IBD. "As we continue to find genes that interact with each other and with
environmental influences in this complex, chronic disease, we are building the foundation
for personalized treatments tailored to a patient's genetic profile," said co-first
author Robert N. Baldassano, M.D., director of the Center for Pediatric Inflammatory Bowel
Disease at The Children's Hospital of Philadelphia. "We will resequence the gene
regions we have identified to pinpoint the causative mutations in these genes," added
study leader Hakon Hakonarson, M.D., Ph.D., director of the Center for Applied Genomics at
Children's Hospital. "We strongly suspect one gene will provide a compelling target
for drug development, given what's known about its biology." Both authors direct
research programs at Children's Hospital and are also faculty members of the University of
Pennsylvania School of Medicine. Their study, performed in collaboration with researchers
from the Medical College of Wisconsin, The University of Utah, Cincinnati Children's
Hospital and two research hospitals in Italy, appears in advance online publication Aug.
31 in Nature Genetics. IBD is a painful, chronic inflammation of the gastrointestinal
tract, affecting about two million children and adults in the United States. Of that
number, about half suffer from Crohn's disease, which can affect any part of the
gastrointestinal tract, and half have ulcerative colitis, which is limited to the large
intestine. IBD that begins in childhood tends to be more severe than adult-onset disease,
and is more likely to affect the colon than other areas of the GI tract. Those age-related
differences in IBD spurred the current research team to do their gene hunting in
childhood-onset disease. "Although the gene variants we found may have a stronger
signal in pediatric IBD than in adult-onset IBD, we do not believe them to be limited to
varieties of the disease that begin in childhood," said Baldassano. The researchers
performed a genome-wide association study, searching for genetic variations in DNA samples
from 1,000 patients with childhood-onset IBD, compared to samples from 4,250 healthy
subjects. Both patients and controls were of European ancestry.
Neurogenesis in the adult brain -
The association with stress and depression
The brain is the key organ in the response to stress. It reacts in a complex, orchestrated
manner that is related to the activation and inhibition of neural structures involved in
sensory, motor, autonomic, cognitive and emotional processes. It is the brain which
finally determines what in the world is threatening and might be stressful for us, and
which regulates the stress responses that can be either adaptive or maladaptive. Chronic
stress can affect the brain and lead into depression: Environmental stressors (e.g. job
and family situation, neighborhood) and especially stressful life events such as trauma or
abuse are amongst the most potent factors to induce depression. Since the development of
novel approaches to antidepressant treatment is based upon an improved neurobiological
understanding of this condition, new information about the cellular changes that take
place in the brain is required. Depression is a chronic, recurring, multifactorial, and
life-threatening disorder, which represents a collection of psychological, neuroendocrine,
physiological and behavioural symptoms. Chronicity and frequency of these symptoms
constitute the clinical condition. Depressive disorders affect up to 20% of people at some
time in their life. In primary care, an estimated 20??% of patients suffer from
depression, but often are not diagnosed correctly (Wittchen, 2000).Depressive disorders
are among the most prevalent illnesses worldwide, producing significant public health and
socioeconomic problems (WHO, 2001). The immense costs of depression account for
approximately 1% of the gross domestic product in Europe (approximately 100 billion Euro).
Depression is affecting more than 120 million people globally, and is set to rise to
become one of the leading causes of disability, second only to cardiovascular disease, by
the year 2015. The areas of the brain that are most affected by the changes caused by
depression are the prefrontal cortex, amygdala and hippocampus, which are central to
emotion, memory and learning. Structural and functional changes as a consequence of stress
and/or major depression are a reduction in volume, neuronal size and density, associated
with changes in cerebral blood flow and glucose metabolism (see figure 1). In addition,
there is a reduced density of glial support cells that are instrumental in the
communication between nerve cells, which is particularly relevant to the reduced volume of
the prefrontal cortex and the hippocampus. The shrinkage might explain some of the
emotional changes observed in people with depression.
Landmark study opens door to new
cancer, aging treatments
Researchers at The Wistar Institute have deciphered the structure of the active region of
telomerase, an enzyme that plays a major role in the development of nearly all human
cancers. The landmark achievement opens the door to the creation of new, broadly effective
cancer drugs, as well as anti-aging therapies. Researchers have attempted for more than a
decade to find drugs that shut down telomerase—widely considered the No. 1 target for
the development of new cancer treatments—but have been hampered in large part by a
lack of knowledge of the enzyme's structure. The findings, published online August 31 in
Nature, should help researchers in their efforts to design effective telomerase
inhibitors, says Emmanuel Skordalakes, Ph.D., assistant professor in Wistar's Gene
Expression and Regulation Program, who led the study. "Telomerase is an ideal target
for chemotherapy because it is active in almost all human tumors, but inactive in most
normal cells," Skordalakes says. "That means a drug that deactivates telomerase
would likely work against all cancers, with few side effects." The study elucidates
the active region of telomerase and provides the first full-length view of the telomerase
molecule's critical protein component. It reveals surprising details, at the atomic level,
of the enzyme's configuration and how it works to replicate the ends of chromosomes—a
process critical to both tumor development and the aging process.
Issues on Cholesterol - Diet,
Statins and Genetics
Genetic lipoprotein disorders are frequently seen in patients with premature coronary
artery disease (CAD). An example of strong genetic predisposition is the disorder:
familial hypercholesterolemia, where a single gene defect (the low density lipoprotein
receptor) contributes to most of the familial expression of CAD. Conversely, lifestyle,
diabetes, dyslipidemia, cigarette smoking and hypertension contribute to most of the
population-attributable risk in the large, international INTERHEART study of acute
myocardial infarction (heart attacks). The identification of single gene disorders may
pave the way to a better understanding of complex metabolic pathways. Understanding the
genes that regulate high density lipoprotein (HDL) metabolism may lead to novel
therapeutic approaches.
Does Treatment of Depression
Improve Prognosis After Heart Attack?
epression and heart disease are the two leading disorders with the strongest contributions
to the global burden of disease. Depression and heart disease are also intertwined. In
recent years, much attention has been given to depression following heart attack and its
effects on prognosis. Several large scale studies have been undertaken (ENRICHD, SADHART,
MIND-IT, CREATE) in which depression was targeted. Although we hoped that treating
depression would result in an improved prognosis, these studies have not provided much
evidence to support this position: effects on depression itself have been minor and did
not translate into cardiovascular benefits. One of the reasons for these findings may be
the heterogeneity of depression following heart attack, with some depression types being
cardiotoxic and responding to treatment, and others not.
Pharma Not in Business of Health,
Healing, Cures, Wellness
Ex-Pharma Sales Reps Speaks Out - Pharma Not in Business of Health, Healing, Cures,
Wellness. Gwen Olsen spent fifteen years as a pharmaceutical sales rep working for such
healthcare giants as Johnson & Johnson, Bristol-Myers Squibb, and Abbott Laboratories.
She enjoyed a successful, fast-paced career until several conscious-altering experiences
began awakening her to the dangers lurking in every American medicine cabinet. Her most
poignant lessons, however, came as both victim and survivor of life-threatening adverse
drug reactions. After leaving pharmaceutical sales in 2000, Gwen worked in the natural
foods industry first as an Account Manager for Nature's Way, and then as a Regional Sales
Manager for Gaia Herbs. She is currently a writer, speaker, and natural health consultant.
The United States health care system is killing Americans at an alarming rate, even though
we spend over fifteen percent of the Gross National Product (GNP) on health care.
According to the Journal of the American Medical Association, our health care outcomes
ranked only fifteenth among twenty-five industrialized nations worldwide. Adverse effects
from prescription drugs have become the third-leading killer of Americans. Only heart
disease and cancer claim more lives. We trust our doctors to inform us and our government
to protect us from medical malfeasance that may put profits ahead of consumer health and
safety. But the fine line walked by the FDA between the interests of the pharmaceutical
manufacturers and the American public has continually been crossed. The result is the
unleashing of an unprecedented number of lethal drugs on the U.S. market! Gwen Olsen
learned firsthand the danger that lurks in every American's medicine cabinet, working in
the pharmaceutical industry. But her most poignant education would come as a victim and,
ultimately, as a survivor.
Despite the fact that our nation spends more money on health care than any other nation
in the world, we experience the worst overall health that many other industrialized
country's.
Mark Schapiro, Exposing a Toxic
U.S. Policy - 40 min
Investigative reporter Mark Schapiro explains in a new book that toxic chemicals exist
in many of the products we handle every day — agents that can cause cancer, genetic
damage and birth defects, lacing everything from our gadgets to our toys to our beauty
products. And unlike the European Union, the U.S. doesn't require businesses to minimize
them — or even to list them, so consumers can evaluate the risks. Schapiro argues
that that policy isn't just bad for public health: In an increasingly green economy, he
says, American businesses stand to get shut out of a huge market. Schapiro, editorial
director of the nonprofit Center for Investigative Reporting, has written for Harper's,
The Nation, Mother Jones and The Atlantic Monthly. His book is called Exposed: The Toxic
Chemistry of Everyday Products, and What's at Stake for American Power.
The Katrina Myth; the Truth about a
thoroughly unnatural disaster
Few people understand what really happened in New Orleans or what caused it. Fewer
still realize that they too may be living under a similar or an even greater threat. This
video exposes the key myths and misunderstandings about the New Orleans flood.
Effects of n-3 PUFA in patients
with symptomatic chronic heart failure
Researchers involved in the GISSI trial, concluded that simple, safe and cheap treatment
with n-3 PUFA can provide a moderate beneficial advantage in terms of mortality and
admission to hospital for cardiovascular reasons in patients with chronic heart failure,
in a context of usual careSeveral epidemiological and experimental studies suggested that
n-3 PUFA could exert favourable effects on the atherotrombotic cardiovascular disease
including arrhythmias. The GISSI team investigated whether n-3 PUFA could improve
morbidity and mortality in a large population of patients with symptomatic heart failure
of any cause. The GISSI researchers undertook a randomised, double blind, placebo
controlled trial in 357 cardiology sites in Italy. They enrolled 6 975 patients with
chronic heart failure of New York Heart Association class II-IV, assigned to n-3 PUFA 1 g
daily or placebo. Patients were followed up for a median of 3•9 years. Primary
end-points were time to death and time to death or admission to hospital for
cardiovascular reasons. Analysis was by intention-to-treat population. Among the GISSI
findings - 955 (27%) patients died from any cause in the n-3 PUFA group and 1014 (29%) in
the placebo group (relative risk reduction 9%, p=0•041). 1981 (57%) patients in the
n-3 PUFA group and 2053 (59%) in the placebo group died or were admitted to hospital for
cardiovascular reasons (relative risk reduction 8%, p=0•009). In absolute terms, 56
patients needed to be treated for 3.9 years to avoid one death or 44 to avoid one event
like death or admission to hospital for cardiovascular reasons. In a per-protocol analysis
performed in about 5000 full complier patients, the relative risk of death was reduced by
14% (p 0.004). Safety was excellent.
Blood vessel cells are instructed
to form tube-like structures
How do blood vessel cells understand that they should organise themselves in tubes and not
in layers? A research group from Uppsala University shows for the first time that a
special type of “instructor” molecule is needed to accomplish this. These
findings, published in the scientific journal Blood, might be an important step towards
using stem cells to build new organs. In order for a body to develop and function the
cells in the body must be able to organise themselves in relation to each other. The way
in which cells are arranged depends on the organ where they are located. Blood vessel
cells need to form three-dimensional, tube-like structures that can transport blood. But
how do blood vessel cells know that they should do that? An important part of the
communication between cells and their environment is the use of growth factors. These are
proteins that bind to receptors on the surface of the cell that receives the information.
When the receptor in turn forms a complex with other proteins, on the inside of the cell,
the read-out from the DNA can be altered. The information has “arrived”.
Why Strawberry Jam is More
Regulated than Cigarettes
While jams and other consumer products are strictly regulated and are required to pass
stringent tests before they can be sold, tobacco has no restrictions and manufacturers
can, and do, add anything they want into the product. Published in Respirology by
Wiley-Blackwell, the invited editorial “Regulation of Consumer Products: The Bizarre
Case of Strawberry Jam and Cigarettes” discusses the issues surrounding tobacco
regulations and how the industry could be more effectively governed. “The
establishment of regulation is a political process and occurs slowly. However, with the
gradual but prolonged and massive epidemic of tobacco-related diseases, regulation of the
industry’s products – specifically the constituents of tobacco smoke – has
to begin now”, says author Dr. Nigel Gray, member of the World Health
Organization’s (WHO) Tobacco Regulation Study Group.* Despite the complexities of
regulating cigarette manufacturing, the Tobacco Regulation Study Group, or TobReg, has
proposed practical means to begin the progressive process of tobacco regulation. As a
first step, it has suggested setting mandatory levels for some of the major carcinogens
and toxicants in cigarettes. In addition, regular reviews must also be conducted as
initial toxin levels are considered generous by industry standards for many countries.
“There is no need for an expensive bureaucracy to oversee this regulation. Countries
can simply mandate TobReg’s recommendations and publicize them as advice from the
world’s central public health board. Countries without cigarette manufacturing
facilities can simply refuse to import cigarette that do not meet these standards”,
says Dr. Gray. He adds, “International standards are highly desirable as large
amounts of cigarettes are traded between countries with differing national standards. It
is timely for WHO to set standards and offer world leadership – particularly as their
Framework Convention on Tobacco Control is now in its implementation process, albeit much
slower than most public health advocates would desire. Singapore, Australia and New
Zealand are ideally placed to pioneer the introduction of these measures.”
The inflammatory responses of
salmon may be influenced by new types of feed
With the aquaculture industry showing strong growth, future increases in production will
demand the use of alternative feeds. The availability of marine feedstuffs on the world
market is today limited, and the hunt for alternatives to both fish meal as a protein
source, and to fish oil, has been going on for a long time. An important question in this
regard is whether alternative feed sources affect fish immune defence systems and health.
In his doctorate, Haugland investigated whether components in some of these alternative
feed sources can influence the inflammatory reaction of salmon. An alternative to the fish
meal currently used in feed is soya protein. The results of the work showed that an
extract from the soya plant, Glycine tomentella, reduces the level of one of the central
chemical messengers in inflammation, none other than TNF-a. Fish oil is a scarce resource
that in fish feed is being replaced by rapeseed oil. Haugland's studies have shown that
this replacement leads to significant changes in the fatty acid composition of salmon
tissues, but that neither the degree of inflammation nor the bacteria-killing abilities
appear to be affected.
New study assesses the impact of
soft drink availability in elementary schools on consumption
The consumption of soft drinks is generally considered to be a contributing factor in
childhood obesity. Because children spend a substantial amount of time at school, the
school food environment plays a central part in shaping eating behaviors. While the
availability of soft drinks in middle and high schools has been investigated previously, a
study published in the September 2008 issue of the Journal of the American Dietetic
Association systematically assesses how the availability of soft drinks in elementary
schools across the United States relates to school-based and overall consumption. A
broader question raised by this investigation is how limiting soft drink availability at
an early age may alter eating behaviors over time.While the National School Breakfast and
Lunch Programs are federally regulated, no similar standards exist for "competitive
foods," that is foods and beverages sold through a la carte lines, vending machines,
school stores and school fund raisers. Guidelines and legislation to fill this gap have
been developing in private schools as well as at the school district- and state-level.
Voluntary sales restrictions are another new development, such as the agreement reached
between the Alliance for a Healthier Generation and the American Beverage Association;
Cadbury Schweppes; Coca-Cola and PepsiCo in May 2006. As a result, some school districts
and even the states of California and Connecticut have already banned soft drink sales in
public elementary schools.Meenakshi M Fernandes, Pardee RAND Graduate School, Santa
Monica, CA, analyzed data from the Early Childhood Longitudinal Study from close to 11,000
fifth graders in 2,303 schools in 40 states. The study investigated socio-demographic
differences in how availability of soft drinks at elementary schools relates to
consumption of soft drinks at school and overall. Fernandes found that limiting
availability of soft drinks at school is associated with a 4% decrease in the rate of any
consumption overall.
If there’s one thing that everyone knows about newborn babies, it’s that they
don’t sleep through the night, and neither do their parents. But in fact, those first
six months of life are crucial to developing the regular sleeping and waking patterns,
known as circadian rhythms, that a child will need for a healthy future. Some children may
start life with the sleep odds stacked against them, though, say University of Michigan
sleep experts who study the issue. They will present data from their study next week at
the European Sleep Research Society meeting in Glasgow, Scotland. Babies whose mothers
experienced depression any time before they became pregnant, or developed mood problems
while they were pregnant, are much more prone to having chaotic sleep patterns in the
first half-year of life than babies born to non-depressed moms, the team has found.
Study finds B-vitamin deficiency
may cause vascular cognitive impairment
A deficiency of B-vitamins may cause vascular cognitive impairment, according to a new
study. Researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA)
at Tufts University used an experimental model to examine the metabolic, cognitive, and
microvascular effects of dietary B-vitamin deficiency. Their findings appear in the August
26, 2008 issue of Proceedings of the National Academy of Sciences (PNAS). "Metabolic
impairments induced by a diet deficient in three B-vitamins -folate, B12 and B6- caused
cognitive dysfunction and reductions in brain capillary length and density in our mouse
model," says Aron Troen, PhD, the study's lead author. "The vascular changes
occurred in the absence of neurotoxic or degenerative changes." Troen, who is an
assistant professor at Tufts University's Friedman School of Nutrition Science and Policy,
explains, "Mice fed a diet deficient in folate and vitamins B12 and B6 demonstrated
significant deficits in spatial learning and memory compared with normal mice." Troen
and colleagues observed similar but less pronounced differences between normal mice and a
third group of mice that were fed a diet enriched with methionine. "The
B-vitamin-deficient mice also developed plasma homocysteine concentrations that were
seven-fold higher than the concentrations observed in mice fed a normal diet," adds
Troen. Homocysteine is produced by the breakdown of a dietary protein called methionine.
B-vitamins, including folate, vitamin B12, and vitamin B6, are required to convert
homocysteine back to methionine, thereby reducing the blood concentration of homocysteine.
Studies have linked elevations in plasma homocysteine with an increased risk for cognitive
impairment. "However," Troen says, "it has not been determined that
homocysteine is directly responsible. Based on the findings of our study, we theorize that
a deficiency of B-vitamins induces a metabolic disorder that manifests with high
homocysteine, as well as cerebral microvascular dysfunction."
Truth and Consequences and
Enrollment in Clinical Trials
Knowing about financial relationships between medical researchers and the companies that
sponsor their studies has little effect on most patients considering enrolling in a
clinical trial, according to a new study from the Duke Clinical Research Institute.
"The patients in our study were very clear - They told us they care about these
relationships and want to be fully informed about them. But at the same time, the
information didn't substantially affect their decision to enter a trial," says Dr.
Kevin Weinfurt, a medical psychologist at Duke and the lead author of the study. What
seemed to be more important in the decision-making process was the patients' pre-existing
level of trust in medical research in general, Weinfurt says. The findings, appearing
online in American Heart Journal, reveal that patients are astute enough to draw
distinctions between various types of financial arrangements, finding some reasonable, and
others, less so. Researchers from Duke University Medical Center, Johns Hopkins Berman
Institute of Bioethics and Wake Forest University conducted a telephone survey of 470
patients diagnosed with coronary artery disease who agreed to go through a consent process
involving enrollment in a hypothetical clinical trial. Investigators first assessed the
patients' overall level of trust in medical research through a four-item questionnaire and
then randomized them into one of three disclosure groups. Patients who were told that the
doctor leading the study also held stock in the company sponsoring the research were the
least willing to participate in the study. They also spontaneously offered three times the
number of negative comments about the relationship than participants in the other groups,
using words like, "disingenuous," "unacceptable," and
"unethical." Ten members of this group also spontaneously said they would not
take part in a trial where the lead investigator held stock in the company sponsoring the
trial. Patients who were told that the sponsoring company covered the cost of the trial,
including the physician's salary, were generally accepting of such a financial
relationship, saying, "OK, that sounds more appropriate. So there's no payment to
him, but through the university. OK, I'm good."
Post-marketing studies finding
adverse events in drugs used in children
The Food and Drug Administration Modernization Act (FDAMA, 1997), designed to stimulate
more drug safety studies in children, has resulted in more than 130 label changes since
its inception nearly six years ago, according to researchers at Duke Children's
Hospital.Their analysis appears in the September issue of Pediatrics. Under this and
subsequent renewal of this legislation, pharmaceutical companies were given a six-month
extension of their exclusive marketing rights on a drug if they performed clinical trials
requested by the FDA to determine the drugs' safety, dosing, and efficacy in children.
According to P. Brian Smith, MD, an assistant professor in Duke's department of
pediatrics, many safety concerns cannot be detected until after the introduction of a
product to a larger and more diverse population. The Best Pharmaceuticals for Children Act
(2002) required the FDA to review and report to a public expert panel the adverse events
occurring after granting pediatric exclusivity. That effort was needed because pediatric
clinical trials are notoriously small, making it more likely that some safety concerns
would not be detected until after the drug is used in a larger pediatric population. Using
MedWatch, the FDA's computerized information database for collecting reports of adverse
events, the FDA's Pediatric Advisory Committee reviewed 67 drugs granted the extension.
"This is a voluntary, cost-effective reporting system that can identify adverse
events that may never have been seen in a clinical trial," Smith said."Just
because a drug goes through testing and clinical trials does not mean its entire safety
profile is known," says Danny Benjamin, MD, a co-author of the study and pediatrician
at Duke Children's Hospital. "Before this incentive, there was no systematic, focused
pediatric review of the data provided to the FDA's adverse event reporting system. Now,
field experts in pediatrics are evaluating the data. That's what's so unique about this
effort." The majority of the 67 drugs studied (65.7 percent) did not appear to cause
enough adverse events to require continued pediatric monitoring. However, nearly one in
five drugs studied required label changes consisting of additional warnings and cautions
for use in children, and several of the adverse events revealed during this process were
considered life threatening.
Biomarkers for ischaemia and
necrosis -- simple blood tests to detect myocardial infarction
In conjunction with clinical assessment and the ECG, simple and rapid blood tests have
become the standard for the detection of myocardial infarction. Starting in the year 2000,
recommendations by the European Society of Cardiology and other major cardiology societies
worldwide have begun to state uniformly that a rise in cardiac troponins -- sensitive and
specific markers for dying cells in the heart -- is a prerequisite for the clinical
diagnosis of myocardial infarction.
Antiangiogenic and
anti-inflammatory drugs - Are they safe?
Since rofecoxib was withdrawn from the worldwide market based on the safety findings of
the APPROVe study, the uncertainty around the cardiovascular safety of NSAIDs and COX-2
inhibitors remains and leaves practitioners with difficult management decisions for the
hundreds of millions of patients worldwide who continue to require pain-relieving therapy
to maintain an acceptable quality of life.
Hospitals provide formula sample
packs while medical organizations encourage breastfeeding
A majority of US hospitals on the East coast distribute formula sample packs to new
mothers, contrary to recommendations from most major medical organizations concerned about
the potential for distributing these packs to reduce breastfeeding rates, according to a
report in the September issue of Archives of Pediatrics & Adolescent Medicine, one of
the JAMA/Archives journals. However, the practice is changing significantly.
At the 21st Congress of the ECNP 2008 in Barcelona, professor Marion Leboyer, University
of Paris, France, presented the compelling neurobiological story of discovering the first
autism genes. Thereby she highlighted new findings on the role of gene mutations, their
association with synapse abnormalities, and -- surprisingly -- a connection between
circadian rhythms and autism risk. These insights will nurture applied projects on the
development of new therapeutic strategies.
Herzinfarkt - Hormon-Schutz versagt
bei Raucherinnen
„Es gibt einen Geschlechter-Unterschied bei der Auswirkung des Rauchens auf die
Herzkranz-Gefäße, Raucherinnen haben ein signifikantes zusätzliches
Herzinfarkt-Risiko", berichten Wissenschaftler auf dem Europäischen
Kardiologenkongress (ESC) in München. In harten Zahlen: Während nichtrauchende
Herzinfarkt-Patientinnen ihren ersten Infarkt durchschnittlich im Alter von 80,7 Jahren
bekommen, trifft es Raucherinnen bereits mit 66,2 Jahren, also 14,4 Jahre früher.
„Berücksichtigt man weitere Risikofaktoren wie hohe Blutdruck- oder Blutfettwerte,
so ist allein das Rauchen für 13,7 Jahre des frühzeitiger auftretenden Herzinfarkt
verantwortlich", so die Autoren der Studie aus Lillehammer (Norwegen), bei der 1.784
Patientendaten ausgewertet wurden.Zum Vergleich - Nichtrauchende männliche
Herzinfarkt-Patienten sind bei ihrem ersten Infarkt im Schnitt 72,2 Jahre alt, Raucher
63,9 Jahre. Der zeitliche Abstand bei Männern beträgt 8,3 Jahre, wovon das Rauchen für
6,2 Jahre verantwortlich ist – also für weniger als die Hälfte als bei
Frauen.„Die Rauchergewohnheiten haben sich in den vergangenen Jahren in Richtung
weniger Raucher und mehr Raucherinnen entwickelt, wobei das Einstiegsalter zunehmend
niedriger wird", so Prof. Eckart Fleck (Deutsches Herzzentrum Berlin), Pressesprecher
der Deutschen Gesellschaft für Kardiologie (DGK). „Deshalb bekommen rauchende Frauen
häufig bereits vor der Menopause einen Herzinfarkt. Rauchen ist ein derart potenter
Herzinfarkt-Risikofaktor, dass selbst der Schutz durch den natürlichen Hormonstoffwechsel
nicht ausreicht, der Nichtraucherinnen in der Regel bis zur Menopause vor einem Infarkt
schützt."
Loss of Sleep, Even For A Single
Night, Increases Inflammation in the Body
Loss of sleep, even for a few short hours during the night, can prompt one’s immune
system to turn against healthy tissue and organs. A new article in the September 15th
issue of Biological Psychiatry, by the UCLA Cousins Center research team, reports that
losing sleep for even part of one night can trigger the key cellular pathway that produces
tissue-damaging inflammation. The findings suggest a good night’s sleep can ease the
risk of both heart disease and autoimmune disorders such as rheumatoid arthritis.
Specifically, the researchers measured the levels of nuclear factor (NF)-?B, a
transcription factor that serves a vital role in the body’s inflammatory signaling,
in healthy adults. These measurements were repeatedly assessed, including in the morning
after baseline (or normal) sleep, after partial sleep deprivation (where the volunteers
were awake from 11 pm to 3:00 am), and after recovery sleep. In the morning after sleep
loss, they discovered that activation of (NF)-?B signaling was significantly greater than
after baseline or recovery sleep. It’s important to note that they found this
increase in inflammatory response in only the female subjects. These data close an
important gap in understanding the cellular mechanisms by which sleep loss enhances
inflammatory biology in humans, with implications for understanding the association
between sleep disturbance and risk of a wide spectrum of medical conditions including
cardiovascular disease, arthritis, diabetes, certain cancers, and obesity. John H.
Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University
School of Medicine and the VA Connecticut Healthcare System, comments: “The closer
that we look at sleep, the more that we learn about the benefits of sleeping. In this
case, Irwin and colleagues provide evidence that sleep deprivation is associated with
enhancement of pro-inflammatory processes in the body.”
How friendly bacteria avoids immune
attack to live happily in the gut
For a long time scientists have been puzzled by the fact that the immune system in the gut
is capable of fighting toxic bacterial infection while staying, at the same time, tolerant
to its resident “friendly” bacteria. But an article now published in the journal
Cell Host & Microbe1 is starting to open the door to this mystery by revealing how a
recently discovered gene - pims – is activated by the gut immune response against
friendly bacteria to rapidly suppress it, effectively creating tolerance to the gut
microbiota. In the same way pims is also shown to control the magnitude of immune
responses against toxic bacteria by suppressing immuno-reactivity when a certain
activation threshold is achieved, assuring, in this way, that the response stays
restricted to the infection site and is proportional to the extent of the infection. These
results suggest that the balance tolerance/immuno-reaction in the gut is achieved through
self-regulatory cycles where suppression by negative regulators, such as pims, is
triggered as soon as a specific threshold of immuno activation is reached. This work has
implications in the understanding of diseases in which the normal gut immune response is
disrupted - such as Crohn's disease and ulcerative colitis – but, potentially, also
in oral tolerance. In fact, oral tolerance vaccines - in which the molecule we want
immuno-tolerated is ingested - have been tentatively used for the treatment of several
autoimmune diseases (where the immune system abnormally attacks parts of the body) with
mixed results and the new research, by elucidating the players in gut immuno-tolerance,
might help to understand why.Multicellular animals live peacefully in close contact with a
multitude of microorganisms that inhabit their bodies. Humans, for example, have more
microorganisms within the body than cells, with just the intestine containing up to 100
trillion microbes, a number about 10 times greater that all our cells. Still, although we
remain fully immune competent - so capable of responding to infection by pathogenic
microorganisms - we do not react against these “friendly” bacteria. But how do
these two opposite immune responses against bacteria so similar exist simultaneously?
New discovery about growth factor
can be breakthrough for cancer research
A research team at the Ludwig Institute and Uppsala University has discovered an entirely
new signal path for a growth factor that is of crucial importance for the survival and
growth of cancer cells. This discovery, published in today’s issue of Nature Cell
Biology, opens up an entirely new landscape for research on breast and prostate cancer,
among other types. Our cells’ ability to understand signals from various growth
factors is critical for normal fetal development. The aggressiveness and capacity for
survival in cancer cells are also governed by a number of growth factors, with
transforming growth factor b (TGF-b) playing a prominent role. In the present study,
researchers at the Ludwig Institute for Cancer Research and the Department of Genetics and
Pathology, Uppsala University, have identified an entirely new signal path that is
regulated by TGF-b. “This discovery is of tremendous importance for our ability to
identify what signal paths TGF-b uses to inhibit the growth of cells, or to stimulate the
ability of cancer cells to survive and metastasize,” says Marene Landström, who
directed the study. TGF-b conveys its signal to the inside of the cell via receptors bound
to the cell membrane in a way that is similar in the great majority of animals. Just over
ten years ago, scientists discovered so-called Smad proteins, which serve as unique
messengers for the active TGF-b signal. These proteins are activated when phosphate groups
bind to them in a manner that is dependent on enzyme activity (of serine-threonine
kinases) in the TGF-b receptors. The new signal path that the research team has now
identified is regulated quite independently of this serine-threonine kinase activity,
which makes the discovery published in the article extremely interesting. The study shows
that the receptors are used instead to activate another enzyme, TRAF6, which binds to the
complex of receptors. TRAF6 is a so-called ubiquitin-ligase, which, when activated, places
short little protein chains on itself and other proteins. TRAF6 therefore functions as a
switch that can determine what signals should be turned on in the cell. TRAF6 is used by
TGF- to be specifically able to activate a kinase called TAK1, which subsequently
activates other so-called stress-activated kinases, leading to cell death.
A higher intake of trans fat means a higher risk of colon cancer risk, according to a new
study published in the August 1 2008 issue of the American Journal of Epidemiology. The
study showed people ate highest amounts of trans fat were more likely to have
pre-cancerous lesions or polyps in their colons than those who consumed the least.
Americans' Attitudes Toward
Breastfeeding Are Making Our Kids Sick
A nameless woman at a mall was somehow the one to find the insult that I could not toss
onto the neat pile of words that would never hurt me. It did hurt. And, these attitudes
toward breastfeeding are making our children sick, especially African-American children,
who are the least likely to get the benefit of mothers' milk.
International team reveals first
prognosticator of survival in aggressive cancer
The tumor suppressor gene pRb2/p130 may provide the first independent prognostic biomarker
in cases of soft tissue sarcoma (STS), according to an international collaboration of
researchers, including scientists at the Sbarro Institute for Cancer Research and
Molecular Medicine at the College of Science and Technology at Temple University in
Philadelphia, PA, the Department of Human Pathology and Oncology, University of Siena and
the Center of Oncological Research of Mercogliano (CROM) in Avellino, Italy. The research
appears in the latest issue of Clinical Cancer Research (www.aacrjournals.org). The
findings show that a reduction in the expression of pRb2/p130 can mean a higher risk of
recurrence and death from STSs. The gene pRb2/p130, a member of the retinoblastoma family
of genes, regulates a portion of the cell cycle. Clinicians have long sought a prognostic
test for the disease, which can be highly aggressive and unpredictable, making it
difficult to determine the most beneficial course of chemotherapy and/or radiation
treatments following surgery. A prognostic indicator will help doctors determine which
patients have a higher risk of recurrence of the disease and who might benefit from a more
aggressive adjuvant therapy. In the study, researchers examined specimens taken from 41
patients with STS. In a subset of 31 cases of nonmetastatic cancers, they found a direct
relationship between pRb2/p130 expression and the clinical outcome of patients."We
found that pRb2/p130 expression was lost or decreased and significantly correlated with
recurrence of disease and poor survival rates in the subset of patients with nonmetastatic
tumors," said Valeria Masciullo, M.D., Ph.D., lead author of the study.
Obese people with asthma have
nearly 5 times greater risk of hospitalization for asthma
Obese people who have asthma are nearly five times more likely to be hospitalized for the
condition than non-obese people with asthma, according to a Kaiser Permanente study
published in the September issue of the Journal of Allergy and Clinical Immunology. This
is the first study to control for the risk factors – smoking, use of oral or inhaled
corticosteroid medications, gastroesophageal reflux disorder, and demographics – that
might explain the obesity-asthma association. Previous studies have shown that obese
people are more likely to suffer asthma than non-obese people, and that obese patients
often have more severe asthma than their non-obese counterparts. More than 20 million
Americans have been diagnosed with asthma. Nearly a third of adults with asthma are also
obese, according to researchers. The Centers for Disease Control and Prevention defines
obesity as having a Body Mass Index of 30 or higher
(http://www.cdc.gov/nccdphp/dnpa/obesity/defining.htm) Researchers at Kaiser Permanente
Center for Health Research in Portland, Ore., and the Kaiser Permanente Institute for
Health Research in Denver surveyed 1,113 patients in Oregon, Washington, and Colorado, age
35 and older, who have persistent asthma. The researchers asked the patients about their
weight, height, smoking habits, other illnesses, treatment and their asthma-specific
quality of life, asthma control and asthma-related hospitalizations. "The big finding
here is that even after adjusting for risk factors, obese adults were nearly five times
more likely to be hospitalized for their asthma," said study lead author David M.
Mosen, Ph.D., MPH, of the Kaiser Permanente Center for Health Research. "Given that
nearly 30 percent of our country is obese, this study is yet another example of the
long-term dangers of obesity, along with heart disease, diabetes, stroke and
dementia." The study uncovered these findings - * Obese people with asthma had
significantly worse asthma control, lower asthma-related quality of life, and had 4.6
times higher risk for asthma-related hospitalizations than non-obese asthmatics * Obese
people with asthma were younger and less educated than non-obese people with asthma* Obese
people with asthma used more oral corticosteroids * Obese people with asthma had a higher
incidence of gastroesophageal reflux disorder.
UTMB’s Dr. Michael H. Malloy has published a study on how Cesarean section seems to
improve the survival of most infants delivered prematurely (at 22 to 25 weeks of
pregnancy, instead of 40 weeks). “Although the choice of cesarean section for the
most immature of these infants may offer survival advantages, consideration of the
neurodevelopmental risks associated with survival at this early age and consideration of
the maternal costs of cesarean section also must be taken into account.”
University of Texas Medical Branch at Galveston researchers have discovered a key
biochemical link in the process by which the Ebola Zaire virus infects cells — a
critical step to finding a way to treat the deadly disease produced by the virus. Ebola
produces severe and often fatal hemorrhagic fever in its victims and inflicts mortality
rates close to 90 percent in some outbreaks. No vaccine or antiviral therapy has been
developed against the virus, and it is considered a high-risk agent for bioterrorism. In
addition, recent devastating outbreaks hit in Uganda in 2008 and the Democratic Republic
of the Congo in 2007. The UTMB group tied Ebola's cellular invasion mechanism to a series
of biochemical reactions called the phophoinositide-3 kinase pathway (named for an enzyme
found in the cell membrane). By activating the PI3 kinase pathway, they found, an Ebola
virus particle tricks the cell into drawing it into a bubble-like compartment known as an
endosome, which is pulled, together with the virus, into the cell. Then – at a
critical point — the virus bursts free from the endosome and begins to reproduce
itself.However, if the PI3 kinase pathway is shut down — as the UTMB team did with a
drug designed for that purpose — Ebola virus particles can't escape from the
endosome, and the disease process comes to a halt. "The nice part about identifying
entry mechanisms is you can prevent the virus from infecting the cell," said UTMB
microbiology and immunology associate professor Robert Davey, senior author of a paper on
the investigation appearing online in the current issue of the journal PloS Pathogens.
"You can stop the whole show before it even gets started." The researchers did
some of their work using the Ebola Zaire virus itself, working in UTMB's Robert E. Shope,
MD, Biosafety Level 4 laboratory to ensure their safety. They also conducted experiments
using harmless, hollow, virus-like particles coated with the critical envelope proteins
that activate the PI3 kinase pathway. Using a unique test created at UTMB that adds a
light-emitting molecular beacon, called luciferase, to Ebola viruses and the virus-like
particles, the investigators were able to determine exactly when and where each broke out
of its bubble, and track its progress.
M. D. Anderson-Prevention Poll
Finds Women Who Are Close to Someone With Breast Cancer Have Greater Sense of Risk
Women whose lives have been touched by the breast cancer experience of a friend or
relative are more acutely attuned to their own risk for the disease and are taking action
to protect themselves, according to a new national opinion poll by The University of Texas
M. D. Anderson Cancer Center and Prevention magazine. Yet against a backdrop of
unprecedented public awareness and despite the fact that an estimated 40,000 America women
will lose their lives to breast cancer this year, 69 percent are largely unaware that
regular exercise provides protection against the disease and 61 percent do not realize
that being overweight or obese increases breast cancer risk. Most women (84 percent) do
know, however, that taking hormone therapy increases risk even as it relieves symptoms of
menopause. Prevention editor-in-chief Liz Vaccariello said, “We were very surprised
to find such low level concern about getting breast cancer. It may be that women feel
confident of their ability to beat the disease due to advances in early detection and
treatment.”
M. D. Anderson Study Finds Change
in HER2 Status After Treatment With Herceptin
Researchers at The University of Texas M. D. Anderson Cancer Center have discovered that
when treated with Herceptin prior to surgery, 50 percent of HER2 positive, breast cancer
patients showed no signs of disease at the time of surgery. However, of those women who
had residual disease, about one-third had tumors that converted from HER2 positive to HER
2 negative status —possibly indicating a resistance to the targeted therapy. The
study will be presented today in advance of the American Society for Clinical Oncology
Breast Cancer Symposium. Approximately 30 percent of breast cancer cells have an excess
amount of the HER2 protein on their surface, which makes the cancer more aggressive.
Herceptin, also known as trastuzumab, is a monoclonal antibody that latches on to these
proteins and inhibits tumor growth. It was approved in 1998 for women whose advanced,
metastatic breast cancer is HER2-positive; it was approved in 2006 for use in the early
setting. It’s known that a small percentage of HER2 positive patients develop a
resistance to Herceptin during treatment, and there have been several described mechanisms
for Herceptin resistance, said Elizabeth Mittendorf, M.D., assistant professor in M. D.
Anderson’s Department of Surgical Oncology.
K-State professor's research
suggests that cigarettes' power may not be in nicotine itself
There may be a very good reason why coffee and cigarettes often seem to go hand in hand. A
Kansas State University psychology professor's research suggests that nicotine's power may
be in how it enhances other experiences. For a smoker who enjoys drinking coffee, the
nicotine may make a cup of joe even better. And that may explain why smoking is so hard to
quit. "People have very regimented things they do when they smoke," said Matthew
Palmatier, assistant professor of psychology at K-State. "If you think about where
people smoke or who they smoke with, you realize that it occurs in very specific places,
often with a specific group of people. Maybe it's a reason why nicotine is so addictive
— if you get used to having that extra satisfaction from things you normally enjoy,
not having nicotine could reduce the enjoyment in a given activity. "People may not
be smoking to obtain a pleasurable drug state. They may be smoking in order to regulate
their mood, and that effect could make nicotine more addictive than other drugs."
Palmatier said much previous research on nicotine addiction has looked at the drug itself
rather than the other factors he is studying. "The approach we're taking is out of
left field," he said. "But it seems to be one of the best explanations as to why
people smoke." Palmatier has a grant from the National Institute on Drug Abuse to
understand how this phenomenon can be used to better design tobacco addiction treatments,
usually offered in patches and pills. He began psychological research in addiction as a
graduate student and later began researching the reinforcing effects of nicotine.
"The big picture is trying to figure out why people smoke," Palmatier said.
"There are a lot of health risks, and the majority of smokers already know what they
are. They want to quit but can't. It's not because nicotine is a potent drug; it doesn't
induce significant amounts of pleasure or euphoria. Yet, it's just as difficult if not
more difficult to quit than other drugs." At K-State, Palmatier studies rats that are
allowed to self-administer nicotine by pushing a lever. The main source of light in their
testing environment shuts off when the rats earn a dose of nicotine. After about a minute,
the light comes back on to signal that more nicotine is available. By manipulating this
signal, Palmatier and his colleagues found that the rats weren't really that interested in
nicotine by itself.
New nano device detects immune
system cell signaling
Scientists have detected previously unnoticed chemical signals that individual cells in
the immune system use to communicate with each other over short distances. The signals the
researchers detected originated in dendritic cells – the sentinels of the immune
system that do the initial detection of microscopic invaders – and were received by
nearby T-cells, which play a number of crucial roles in the immune system, including
coordination of attacks on agents that cause disease or infection. The chemical signals
cells exchange when they come into contact have been studied extensively. But it has not
been possible to detect chemical messages that travel between cells that are nearby but
not in contact – called paracrine signals – because they are highly localized
and they are produced in concentrations that have been below detection levels. A new
technology, called a multi-trap nanophysiometer, was required to demonstrate the existence
of non-contact signaling. This is one of the first microfluidic devices that has been
applied successfully to the study of cell-to-cell signaling in the immune system.A
detailed description of the multi-trap nanophysiometer (MTN) and how it enabled the
accidental discovery of paracrine signaling has been published online by the Lab on a Chip
journal. The new device was developed by a team of researchers at the Vanderbilt Institute
for Integrative Biosystems Research and Education headed by John P. Wikswo, the Gordon A.
Cain University Professor at Vanderbilt. "This is an important advance and
potentially very useful technology," says co-author Derya Unutmaz, now an associate
professor of microbiology at New York University's School of Medicine. "The ability
to study the behavior of single cells may not be as critical if you are studying the heart
or muscles, which are mostly formed by uniform cells, but it is crucial for understanding
how the immune system functions. The wide surveillance of the body that it conducts
requires extensive communication between dozens of different kinds of immune cells."
The reason for this is that the dendritic cells, T-cells and B-cells in the immune system,
which tend to concentrate in the lymph nodes spread throughout the body, function as
individual, unattached cells. If dendritic cells detect invaders in the body, they rapidly
migrate to lymph nodes and have to find the appropriate T-cells to alert them. But how
dendritic cells attract the right T-cells among millions of cells within the lymph nodes
remains an immunological puzzle.
New methods identify and manipulate
'newborn' cells in animal model of Parkinson's disease
When cells in the brain are lost through disease or injury, neighboring cells begin to
divide and multiply, but only a few areas in the brain are able to produce new neurons.
Patients with Parkinson's disease suffer degeneration of certain neurons that reside in an
area of the brain called the substantia nigra and project into the striatum. Many of the
newborn cells in these areas have not been well described because of limitations of
methods used to characterize them.A research team from Cedars-Sinai Medical Center's
Maxine Dunitz Neurosurgical Institute and Lund University in Sweden used an engineered
virus to deliver a protein that glows green when exposed to blue light (green fluorescent
protein) into newborn cells of the striatum in an animal model (rats) of Parkinson's
disease. This revealed that no neurons are formed; most of the cells appear to be glial
(structural) cells.To determine if the newborn cells could be manipulated to generate
neurons, the researchers delivered into the cells two genes (neurogenin2 and noggin) that
are involved in the genesis of neurons. Neither gene had any effect on the ability of
newborn striatal cells to form new neurons, but the insertion of noggin greatly increased
the number of oligodendrocytes, cells that support neurons.
Acupuncture may hold promise for
women with hormone disorder
Getting pregnant with her first child was difficult, but when Rebecca Killmeyer of
Charlottesville, Va., experienced a miscarriage during her second pregnancy, she wasn't
sure if she would ever have another baby. When she decided to enter a study testing the
impact of acupuncture on women with polycystic ovary syndrome at the University of
Virginia Health System, she came out with a miracle.
Yerkes researchers create animal
model of chronic stress
In an effort to better understand how chronic stress affects the human body, researchers
at the Yerkes National Primate Research Center and the Department of Psychiatry and
Behavioral Sciences, Emory University, have created an animal model that shows how chronic
stress affects behavior, physiology and reproduction. Developing the animal model better
positions the researchers to understand the neurohormonal causes of such stress and the
body reaction in order to develop more effective treatment options for humans. The study
is available in the current online edition of Molecular Psychiatry. According to lead
researcher Mark Wilson, PhD, chief of the Division of Psychobiology at Yerkes,
"Chronic stress can lead to a number of behavioral changes and physical health
problems, including anxiety, depression and infertility." Via the animal model, the
researchers found corticotropin releasing factor (CRF) is a key neurohormone involved in
stress response. Wilson explains, "CRF is located in several different brain regions,
serving different functions. Its release is important for our ability to adapt to every
day stressors and to maintain our physical and emotional health." In response to
stress, CRF levels rise; CRF levels decrease when the stressor no longer is present.
Chronic stress, however, increases the length and volume of expression of CRF in areas of
the brain associated with fear and emotion, including the amygdala. Such chronic stress
changes the body's response, and the resulting increased expression of CRF is thought to
be the cause of such health-related stress problems including anxiety, depression and
infertility.
Scientists produce nanoscale
droplets with cancer-fighting implications
UCLA scientists have succeeded in making unique nanoscale droplets that are much smaller
than a human cell and can potentially be used to deliver pharmaceuticals. "What we
found that was unexpected was within each oil droplet there was also a water droplet
— a double emulsion," said Timothy Deming, professor and chair of the UCLA
Department of Bioengineering and a member of both the California NanoSystems Institute
(CNSI) at UCLA and UCLA's Jonsson Cancer Center. "We have a water droplet inside of
an oil droplet, in water." "The big challenge," Deming added, "was to
make these double-emulsion droplets in the sub-100-nanometer size range with these
properties and have them be stable. We have demonstrated we can make these emulsions that
are stable in this size range, which no one has ever been able to do before. These double
nanoemulsions are generally hard to form and very unstable, but ours are very
stable."
Serum microRNAs (miRNAs) can serve as biomarkers for the detection of diseases including
cancer and diabetes, according to research published online this week in Cell Research.
The findings pave the way for a revolutionary non-invasive diagnostic tool. miRNAs are a
class of naturally occurring small non-coding RNAs that have been linked with cancer
development. Recent studies reporting individual miRNAs as diagnostic biomarkers of
specific cancers were unable to rule out the possibility that these miRNAs appeared as a
result of contamination. Chen-Yu Zhang and colleagues are the first to comprehensively
characterize entire blood miRNA profiles of healthy subjects and patients with lung
cancer, colorectal cancer and diabetes, ruling out contamination. They propose that the
specific serum miRNA expression profiles they identified constitute
‘fingerprints’ for cancer and disease.
Arteries from distinct regions of
the body have unique immune functions
Human arteries play distinct roles in the immune system depending on their anatomical
location, researchers at Emory University School of Medicine have discovered. Their
findings explain why vascular diseases affect different parts of the arterial network and
could help doctors fine-tune the treatment of such diseases as atherosclerosis and
vasculitis. Atherosclerosis causes heart attacks and strokes because it occurs
preferentially in arteries supplying the heart and the brain. The results were published
online this week by the journal Circulation. Arteries can play an active role in sensing
foreign invasion and bodily injury, because cells embedded in the arterial walls called
dendritic cells act like smoke-sensing fire alarms for the immune system, says senior
author Cornelia Weyand, MD. PhD, co-director of the Kathleen B. and Mason I. Lowance
Center for Human Immunology at Emory University. "All of our major arteries have this
alarm system," she says. "To our surprise, we found that the arteries of the
neck, the arms, the abdomen and the legs are triggered by different infectious organisms.
Thus, each artery functions in a specialized way." Some vascular diseases attack
arteries only in the abdomen or in the neck and upper extremities, and this selectivity
has puzzled doctors for years, Weyand says. To probe the differences among arteries,
Weyand and her co-workers examined the activity of genes that encode Toll-like receptors
in blood vessels from human donors. Toll-like receptors are a cornerstone of the
"innate" immune system, which can be activated by common features of
infection-causing invaders. The capture of bacterial or viral fragments through Toll-like
receptors alerts the immune system early during an infectious attack. Toll-like receptors
can respond to whip-like antennas on bacteria called flagellae, parts of bacterial cell
walls, or DNA and RNA that leaks from viruses or bacteria.
Research engineers and sleep medicine specialists from two Michigan universities have
joined technical and clinical hands to put innovative quantitative analysis,
signal-processing technology and computer algorithms to work in the sleep lab. One of
their recent findings is that a new approach to analyzing sleep fragmentation appears to
distinguish fibromyalgia patients from healthy controls.
Study shows pine bark naturally
reduces knee osteoarthritis
According to the Center for Disease Control (CDC), osteoarthritis, the most common type of
arthritis, is on the rise. A new study published in the August journal of Phytotherapy
Research, reveals Pycnogenol, bark extract from the French maritime pine tree, reduced
overall knee osteoarthritis (OA) symptoms by 20.9 percent and lowered pain by 40.3
percent. To date, this is the third clinical trial on osteoarthritis treatment with
Pycnogenol. This study investigated what happens to joint symptoms after treatment with
Pycnogenol is terminated and the results show that no relapse occurred after two weeks.
Pycnogenol acts as potent anti-inflammatory and the lasting effects found in this study
suggest that Pycnogenol may help the joints to recover.With osteoarthritis cases on the
rise, many are seeking non-traditional medication to help ease the pain and reduce the
amount of traditional medication taken. The CDC estimates osteoarthritis affects 34
percent of all adults over the age of 65. In 2005, an estimated 26.9 million adults in the
U.S. had osteoarthritis, which was up from 21 million in 1990. While there's no known cure
for osteoarthritis, treatments such as nonsteroidal anti-inflammatory drugs (NSAIDs) or
analgesics can help reduce pain and also maintain joint movement, to help the quality of
life for people living with the disease. In more severe cases, cortisone shots and joint
replacement surgery are used to treat OA.
A landmark government study suggests nearly one in two people (46 percent) will develop
painful knee osteoarthritis over their lifetime, with the highest risk among those who are
obese. According to the Arthritis Foundation, the study underscores the immediate need for
the public to understand what they can do to reduce the tremendous pain, disability and
cost associated with arthritis.
Gynecological screening tests for cervical cancer have been available to all women in
Sweden for almost four decades. Despite this, many immigrant women have a higher risk of
developing the disease than Swedish-born women, according to a new study from the medical
university Karolinska Institutet.
Oxidative stress - Mechanism of
cell death clarified
Dr. Marcus Conrad of the Institute of Clinical Molecular Biology and Tumor Genetics at the
Helmholtz Zentrum München has decrypted the molecular mechanism through which the death
of cells is caused by oxidative stress. This knowledge opens novel perspectives to
systematically explore the benefit of targeted therapeutic interventions in the cure of
ageing and stress-related degenerative diseases.
Substance Found In Fruits And
Vegetables Reduces Likelihood Of The Flu
Mice given quercetin, a naturally occurring substance found in fruits and vegetables, were
less likely to contract the flu, according to a study published by The American
Physiological Society. The study also found that stressful exercise increased the
susceptibility of mice to the flu, but quercetin canceled out that negative
effect.Quercetin, a close chemical relative of resveratrol, is present in a variety of
fruits and vegetables, including red onions, grapes, blueberries, tea, broccoli and red
wine. It has been shown to have anti-viral properties in cell culture experiments and some
animal studies, but none of these studies has looked specifically at the flu.The study,
“Quercetin reduces susceptibility to influenza infection following stressful
exercise,” was carried out by J. Mark Davis, E.A. Murphy, J.L. McClellan, and M.D.
Carmichael, of the University of South Carolina and J.D. Gangemi of Clemson University.
The study appears in the current issue of the American Journal of Physiology-Regulatory,
Integrative and Comparative Physiology.The study was conducted using mice, but if
quercetin provides a similar benefit for humans, it could help endurance athletes,
soldiers and others undergoing difficult training regimens, as well as people under
psychological stress, according to Davis.
New study reveals higher protein
breakfast may help dieters stay on track
A new study published online today in the British Journal of Nutrition found that timing
of dietary protein intake affects feelings of fullness throughout the day. The study
concluded that when people ate high-quality protein foods, from sources such as eggs and
lean Canadian bacon, for breakfast they had a greater sense of sustained fullness
throughout the day compared to when more protein was eaten at lunch or dinner. "There
is a growing body of research which supports eating high-quality protein foods when
dieting to maintain a sense of fullness," said Wayne W. Campbell, PhD, study author
and professor of Foods and Nutrition at Purdue University. "This study is
particularly unique in that it looked at the timing of protein intake and reveals that
when you consume more protein may be a critical piece of the equation." The study
included overweight or obese men who ate a reduced calorie diet. The diet consisted of two
variations of protein intakes, both which were within federal nutrition recommendations:
normal protein intake (11-14 percent of calories) or increased protein (18-25 percent of
calories). The researchers tested the effect of consuming the additional protein at
specific meals – breakfast, lunch or dinner – or spaced evenly throughout the
day. Purdue researchers found that the feeling of fullness was greatest and most sustained
throughout the day when the additional protein, from eggs and lean Canadian bacon, was
eaten at breakfast – versus lunch or dinner.
Height Linked to Risk of Prostate
Cancer Development and Progression
A man's height is a modest marker for risk of prostate cancer development, but is more
strongly linked to progression of the cancer, say British researchers who conducted their
own study on the connection and also reviewed 58 published studies. In the September issue
of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association
for Cancer Research, 12 researchers at four universities in England studied more than
9,000 men with and without prostate cancer and estimated that the risk of developing the
disease rises by about six percent for every 10 centimeters (3.9 inches) in height a man
is over the shortest group of men in the study. That means a man who is one foot taller
than the shortest person in the study would have a 19 percent increased risk of developing
the disease. Still, these increases in risk are a lot less than those linked with other
established risk factors, such as age, family history of the disease, and race. Because of
that, the researchers do not suggest that taller men be screened more often than is
typical, or that their cancer treatment be altered.
Fatal protein interactions may
explain neurological diseases
In a collaborative study at the University of California, San Diego, investigators from
neurosciences, chemistry and medicine, as well as the San Diego Supercomputer Center
(SDSC) have investigated how proteins involved in neurodegenerative diseases such as
Alzheimer's and Parkinson's disease interact to form unique complexes. Their findings
explain why Alzheimer's patients might develop Parkinson's, and vice versa. The new and
unique molecular structures they discovered can now be used to model and develop new drugs
for these devastating neurological diseases. Their findings will be published in the
September 3 issue of Public Library of Science (PLoS) ONE on September 4, 2008. The team,
led by Eliezer Masliah, M.D., professor of neurosciences and pathology in the UC San Diego
School of Medicine, found that "fatal" or abnormal interactions among the
a-synuclein protein (a-syn, involved in Parkinson's disease) and Abeta amyloid (Aß, which
leads to the plaques associated with Alzheimer's disease) interact and form unique
"hybrid" complexes. These hybrid abnormal protein interactions result in
combined neurodegenerative diseases. "Clinically, we knew that having one
neurological disease, such as Alzheimer's, put patients at risk for another neurological
disease in combination with it, for example, Parkinson's disease or frontotemporal
dementia. But as doctors and scientists, we didn't understand why this occurred until
now," Masliah said. Through computer modeling, they discovered that when the Aß and
a-syn interacted they formed a new hybrid protein with a small hole called a
"nanopore" that alters neuronal activity. Masliah described the model of the
hybrid complex as being "like looking at a boat with holes in it. Because we can now
see the holes, we can learn how to stop the leak." Misfolding and aggregation of
neuronal proteins has been proposed to play a critical role in the development of
neurodegenerative disorders, including the leading disorders in the aging population
– Alzheimer's disease and Parkinson's disease – which result in dementia and
movement disorders. More than five million Americans live with such neurological
conditions, and it is estimated that this country alone will see a 50 percent increase in
Alzheimer's and Parkinson's disease alone by the year 2025.
Too much calcium in blood may
increase risk of fatal prostate cancer
Men who have too much calcium in their bloodstreams may have an increased risk of fatal
prostate cancer, according to a new analysis from Wake Forest University School of
Medicine and the University of Wisconsin. "We show that men in upper range of the
normal distribution of serum calcium subsequently have an almost three-fold increased risk
for fatal prostate cancer," said Gary G. Schwartz, Ph.D., associate professor of
cancer biology and of epidemiology and prevention at Wake Forest, a part of Wake Forest
University Baptist Medical Center. Such excess calcium can be lowered, he said. The
research appears in the September issue of Cancer Epidemiology, Biomarkers &
Prevention, a journal of the American Association for Cancer Research. Co-author Halcyon
G. Skinner of the School of Medicine and Public Health at the University of Wisconsin
stressed there is "little relationship between calcium in the diet and calcium in
serum. So men needn't be concerned about reducing their ordinary dietary intakes of
calcium." Schwartz and Skinner analyzed the results of 2,814 men who participated in
the National Health and Nutrition Examination Survey (NHANES-1). Measurement of the amount
of calcium in the bloodstreams was determined an average of 9.9 years before prostate
cancer was diagnosed. The researchers focused on the 85 cases of prostate cancer and 25
prostate cancer deaths among the 2,814 men and divided the group into thirds, based on the
serum calcium level. "Comparing men in the top third with men in the bottom third, we
found a significantly increased hazard for fatal prostate cancer. "To our knowledge,
this is the first study to examine prostate cancer risk in relation to serum
calcium," Schwartz and Skinner wrote. "These results support the hypothesis that
high serum calcium, or a factor strongly associated with it, such as high serum
parathyroid hormone, increases the risk for fatal prostate cancer." In an interview,
Schwartz said that if the relationship between serum calcium and prostate cancer
"turns out to be causal, it suggests a means for potentially reducing the risk of
fatal disease through medicines that reduce serum levels of calcium and/or parathyroid
hormone."
Deep brain stimulation, a surgical technique often viewed as a last resort for people with
Parkinson’s disease, halts the progression of dopamine-cell loss in animal models,
according to preliminary research by scientists at the Neuroscience Institute at the
University of Cincinnati (UC) and University Hospital. The scientists also discovered
clues to why the technique works. The act of stimulating neurons with electrodes boosted
the amount of an important protein in animals’ brains. The protein, a trophic factor
known as BDNF (brain-derived neurotrophic factor), is a nurturing, growth-promoting
chemical. Parkinson’s disease is a degenerative neurological disorder involving the
death of dopamine-producing brain cells, or neurons.
Innate immune system targets
asthma-linked fungus for destruction
A new study shows that the innate immune system of humans is capable of killing a fungus
linked to airway inflammation, chronic rhinosinusitis and bronchial asthma. Researchers at
Mayo Clinic and the Virginia Bioinformatics Institute (VBI) have revealed that
eosinophils, a particular type of white blood cell, exert a strong immune response against
the environmental fungus Alternaria alternata. The groundbreaking findings, which shed
light on some of the early events involved in the recognition of A. alternata by the human
immune system, were published recently in the Journal of Immunology.* Eosinophils
typically combat parasitic invaders of the human body larger than bacteria or viruses,
such as flukes or parasitic worms (collectively known as helminths). Evidence from
different experimental approaches suggests that asthma and chronic sinusitis can arise
when the body perceives that it has encountered a disease-causing organism. Environmental
fungi such as Alternaria do not typically cause invasive infections like parasites but for
some reason, in certain people, the body responds as if it is being attacked and chronic
inflammation can result from the ensuing cascade of immune-related events. Principal
Investigator Hirohito Kita, M.D., from Mayo Clinic, remarked: "Our results strongly
demonstrate that eosinophils have the capacity to recognize and exert immunological
responses to certain fungi such as Alternaria. We have shown that CD11b receptors on the
surface of eosinophils recognize and adhere to beta-glucan, a major cell wall component of
the fungus. This in turn sets in motion the release of toxic granule proteins by the white
blood cells, leading to extensive damage and ultimate destruction of the fungus. To the
best of our knowledge, this is the first time that live eosinophils and not just the
intracellular components have been shown to target and destroy a fungus."
affecting eight percent of America’s population, diabetes can lead to blindness,
kidney failure, strokes and heart disease. Thanks to Tel Aviv University researchers, a
new cure -- based on advances in cell therapy -- may be within reach.Prof. Shimon Efrat
from TAU’s Sackler Faculty of Medicine, whose research group is among world leaders
in beta cell expansion, has developed a way to cultivate cells derived from
insulin-producing beta cells from human tissue in the laboratory. It may be possible to
implant these new healthy cells into patients with type 1 diabetes.If successful, this
method, which artificially replicates the insulin cells people need, could ensure that
fewer people will die while waiting for a life-saving pancreas and kidney. Prof.
Efrat’s research paves the way for new and alternative forms of treatment in cases in
which organ transplantation is not an option. And one day, the procedure may be as simple
as a blood transfusion.
Researchers Offer First Direct
Proof of How Arthritis Destroys Cartilage
A team of orthopaedic researchers has found definitive, genetic proof of how the most
common form of arthritis destroys joint cartilage in nearly 21 million aging Americans,
according to a study published today onlinein the Journal of Bone and Mineral Research.
The findings serve as an important foundation for the design of new treatments for
osteoarthritis (OA), researchers said. OA gradually destroys all cartilage in joints while
forming scar tissue and painful bony growths. Advanced cases bring deformity and severe
pain as patients loose the protective cushion between bones in weight-bearing joints like
knees and hips. Until the late 1980s, OA was regarded as part of growing old. Since then,
studies have revealed that biochemical changes contribute to the disease that might be
reversed by drugs. Current medications, NSAIDs and Cox 2 inhibitors, are used to reduce
symptoms in patients with mild cases, and joint replacement surgery for severe cases. Few
options exist for those in between. Going into the current study, little was known about
the cellular and molecular events that cause cartilage to break down in osteoarthritic
joints. Past studies had suggested that higher levels of a key signaling protein,
beta-catenin, were connected to osteoarthritis, but there was no direct evidence to
confirm it, or to suggest its role. The current study provides both.
Early onset gene for inflammatory
bowel diseases identified
A study of Crohn's disease and ulcerative colitis in children has identified a gene that
influences whether children get these diseases early in life, and points to a potential
new target for treatment. The findings of the international team that performed the study
were published online this week by the journal Nature Genetics. Crohn's disease and
ulcerative colitis are chronic inflammatory diseases that affect the intestines, resulting
in pain, severe diarrhea, intestinal bleeding, weight loss and fever. In ulcerative
colitis, the inner lining of the colon is inflamed, while in Crohn's disease the
inflammation extends deeper into the intestinal wall and can involve both the small and
large intestine. While several genes that influence susceptibility to the two diseases
have been found previously, this study is the first to focus on inflammatory bowel disease
(IBD) with childhood onset, says co-first author Subra Kugathasan, MD. Kugathasan recently
was recruited to Emory University School of Medicine's Department of Pediatrics from the
Medical College of Wisconsin to head the Pediatric Inflammatory Bowel Disease program. Dr
Kugathasan's future research will focus on discovery of additional IBD genes and in depth
study of how these genes influence disease onset and progression. "Our novel
candidate gene is in the same inflammatory pathway as some other susceptibility genes, so
it may represent an accessible target for treatment," Kugathasan says.
Unsuccessful drug against anxiety
opens a novel gateway for the treatment of cancer
According a new study, unsatisfying drug for anxiety reveals scientists a promising novel
anti-cancer drug target. Cancer cells have multiple ways to avoid apoptosis, programmed
cell death the means by which organisms deal with defective cells. One defense is to
produce quantities of phosphatic acid, a phospholipid constituent of cellular membranes.
Unlike other phospholipids, phosphatidic acid also acts as a signaling molecule for cells
promoting cellular growth and preventing apoptosis. Finnish and Danish researchers have
now shown that phosphatidic acid may well be a target molecule for novel anti-cancer
drugs.
EU directive on laboratory animals
expected this autumn
This autumn a proposal will be presented for new EU regulations regarding how animals may
be used in research. A key issue is how and whether apes should be used as laboratory
animals. 'There is constant progress regarding laboratory animals. Many animal experiments
have been replaced by animal-free methods. But when it comes to developing vaccines
against HIV/AIDS and research on brain diseases, there are no alternatives to using apes,'
says Håkan Billig of the Swedish Research Council.
Consumption of fruit and berries is
inversely associated with carotid atherosclerosis in elderly men
The difference of 348 g of fruit and berries per d between the lowest and highest quartile
of intake was associated with a 5.5 % adjusted difference in mean IMT. These findings
suggest that consumption of fruit and berries may be protective against carotid
atherosclerosis in elderly men at high risk of CVD
Tooth cavities are usually closed with plastic fillings. However, the initially soft
plastic shrinks as it hardens. The tension can cause gaps to appear between the tooth and
the filling, encouraging more caries to form. For the first time, researchers have
simulated this process. The patient’s hands are clasped firmly around the armrests as
the dentist drills away the caries-stricken sections of the tooth. Once the drilling is
over, most toothache sufferers can begin to relax. All the doctor now has to do is to
slightly etch the cavity, apply an adhesive film, and fill it with a special type of
plastic. The plastic is soft at first, so that the doctor can easily press it into the
cavity. It only solidifies afterwards under the light of a small lamp. However, the
material tends to shrink slightly as it hardens, occasionally producing tension that can
cause tiny gaps to form between the plastic filling and the tooth. Bits of food can get
caught in these gaps and lead to more caries. Manufacturers of filling materials therefore
offer a variety of plastics to choose from. But which filling is best suited to which
shape of cavity?
Nutritionists of the UGR suggest
diet improvements during Ramadan
Researchers from the UGR have analysed the diet followed by thirty students aged between
19 and 27 during Ramadan. They tested that the diet led to an increase in corporal fat and
a reduction in muscular mass. They suggest modifications in diet to reduce fat and
increase proteins and carbohydrates, according to the nutritional needs of this population
group.
Linseed is said to protect against cancer – but not everybody likes the taste.
Researchers have now isolated the valuable components of the flax seeds. Incorporated in
bread, cakes or dressings, they support the human organism without leaving an unpleasant
aftertaste.
A new study found that trained sexologists could infer a woman's history of vaginal orgasm
by observing the way she walks. The study is published in the September 2008 issue of The
Journal of Sexual Medicine, the official journal of the International Society for Sexual
Medicine and the International Society for the Study of Women's Sexual Health.Led by
Stuart Brody of the University of the West of Scotland in collaboration with colleagues in
Belgium, the study involved 16 female Belgian university students. Subjects completed a
questionnaire on their sexual behavior and were then videotaped from a distance while
walking in a public place. The videotapes were rated by two professors of sexology and two
research assistants trained in the functional-sexological approach to sexology, who were
not aware of the women's orgasmic history.The results showed that the appropriately
trained sexologists were able to correctly infer vaginal orgasm through watching the way
the women walked over 80 percent of the time. Further analysis revealed that the sum of
stride length and vertebral rotation was greater for the vaginally orgasmic women.
"This could reflect the free, unblocked energetic flow from the legs through the
pelvis to the spine," the authors note.There are several plausible explanations for
the results shown by this study. One possibility is that a woman's anatomical features may
predispose her to greater or lesser tendency to experience vaginal orgasm. According to
Brody, "Blocked pelvic muscles, which might be associated with psychosexual
impairments, could both impair vaginal orgasmic response and gait." In addition,
vaginally orgasmic women may feel more confident about their sexuality, which might be
reflected in their gait. "Such confidence might also be related to the
relationship(s) that a woman has had, given the finding that specifically penile-vaginal
orgasm is associated with indices of better relationship quality," the authors state.
Research has linked vaginal orgasm to better mental health.
A light bulb and a few chemicals -
Scientists find a way to help make new reactions
Princeton scientists have discovered a way of stimulating organic molecules that they
expect will prompt researchers to create materials from new kinds of chemical reactions.
The method of catalysis, when used, could lead to groundbreaking kinds of drugs and
agricultural chemicals and will provide a shortcut to standard multi-step methods of
chemical production. The work, conducted by David MacMillan, the A. Barton Hepburn
Professor of Organic Chemistry at Princeton, and David Nicewicz, a postdoctoral fellow,
will appear in a special online edition of Science on Sept. 4. The method is disarmingly
easy to perform but deeply complex in terms of the science behind it. At its simplest, the
process involves using a weak source of light -- like a household light bulb -- to
catalyze or propel a reaction in a flask of fluid containing two different classes of
chemicals. Like magic or even a child's tabletop science experiment, the chemicals in the
container start to selectively react with each other when exposed to the light.
Bisphenol A linked to metabolic
syndrome in human tissue
New research from the University of Cincinnati (UC) implicates the primary chemical used
to produce hard plastics—bisphenol A (BPA)—as a risk factor for metabolic
syndrome and its consequences. In a laboratory study, using fresh human fat tissues, the
UC team found that BPA suppresses a key hormone, adiponectin, which is responsible for
regulating insulin sensitivity in the body and puts people at a substantially higher risk
for metabolic syndrome. Metabolic syndrome is a combination of risk factors that include
lower responsiveness to insulin and higher blood levels of sugar and lipids. According to
the American Heart Association, about 25 percent of Americans have metabolic syndrome.
Left untreated, the disorder can lead to life-threatening health problems such as coronary
artery disease, stroke and type 2 diabetes. Nira Ben-Jonathan, PhD, and her team are the
first to report scientific evidence on the health effects of BPA at environmentally
relevant doses equal to "average" human exposure. Previous studies have
primarily focused on animal studies and high doses of BPA. They report their findings in
the Aug. 14, 2008, online edition of the journal Environmental Health Perspectives. This
scientific data comes just before a key Federal Drug Administration meeting about the
safety of the chemical in consumer products scheduled for Sept. 16, 2008. "People
have serious concerns about the potential health effects of BPA. As the scientific
evidence continues to mount against the chemical, it should be given serious attention to
minimize future harm," says Ben-Jonathan, a professor of cancer and cell biology at
UC who has studied BPA for more than 10 years.
Study Reveals Promising Method for
Reducing MRSA Infections
Doctors at the University of Virginia Health System have significantly reduced MRSA
infections among surgical intensive care patients by using antibiotic cycling, a method of
rotating drugs at regular intervals. In a study published in the September 3, 2008 issue
of Surgical Infections, UVA researchers report that switching between two antibiotics,
linezolid and vancomycin, every three months in the surgical ICU decreased the MRSA
infection rate from 1.9 to 1.4 patients per 100 admissions. In-hospital mortality from
surgical ICU-acquired MRSA infections fell from 3.8 patients per year to none. Study data
spanned six years, including the period before cycling began (1997 to 2001) and the period
after it was instituted (2002 to 2003). The study's key focus was resistant gram-positive
cocci, a subgroup defined as MRSA (which stands for methicillin-resistant Staphylococcus
aureus) and VRE (which is an acronym for vancomycin-resistant Enterococcus). "Before
we began cycling, 67 percent of the Staphylococcus aureus infections in our surgical ICU
were caused by MRSA," notes the study's lead author, Dr. Robert Sawyer, a professor
of surgery and co-director of UVA's Surgical Trauma Intensive Care Unit. "Cycling
reduced MRSA cases to 36 percent of that total."
Potential remedy for the
‘mental fog’ in cancer patients
Cancer patients have complained for years about the mental fog known as chemobrain. Now in
animal studies at West Virginia University (WVU), researchers have discovered that
injections of N-acetyl cysteine (NAC), an antioxidant, can prevent the memory loss that
breast cancer chemotherapy drugs sometimes induce. The WVU researchers’ study has
just been published in the September issue of the Springer journal Metabolic Brain
Disease.
Intellectual work induces excessive
calorie intake
A Université Laval research team has demonstrated that intellectual work induces a
substantial increase in calorie intake. The details of this discovery, which could go some
way to explaining the current obesity epidemic, are published in the most recent issue of
Psychosomatic Medicine. The research team, supervised by Dr. Angelo Tremblay, measured the
spontaneous food intake of 14 students after each of three tasks: relaxing in a sitting
position, reading and summarizing a text, and completing a series of memory, attention,
and vigilance tests on the computer. After 45 minutes at each activity, participants were
invited to eat as much as they wanted from a buffet. The researchers had already shown
that each session of intellectual work requires only three calories more than the rest
period. However, despite the low energy cost of mental work, the students spontaneously
consumed 203 more calories after summarizing a text and 253 more calories after the
computer tests. This represents a 23.6% and 29.4 % increase, respectively, compared with
the rest period.
Studies Spot Numerous Undiscovered
Gene Alterations In Pancreatic and Brain Cancers
HHMI investigators have detected a multitude of broken, missing, and overactive genes in
pancreatic and brain tumors, in the most detailed genetic survey yet of any human tumor.
Some of these genetic changes were previously unknown and could provide new leads for
improved diagnosis and therapy for these devastating cancers.
Gladstone scientists identify
genetic link that may neutralize HIV
Scientists from the Gladstone Institute of Virology and Immunology (GIVI) and the National
Institutes of Allergy and Infectious Diseases (NIAID) have identified a gene that may
influence the production of antibodies that neutralize HIV. This new information will
likely spur a new approach for making an HIV vaccine that elicits neutralizing antibodies.
Neutralizing antibodies, once produced in the host, can attack and checkmate an infecting
virus. The research was reported in the September 5 issue of Science. Scientists have been
striving in vain to stimulate strong protective antibodies with an HIV vaccine for years
because these antibodies hold great promise for controlling HIV infection in humans. HIV
is a type of virus called a "retrovirus," which copies its RNA genetic material
into DNA and incorporates it into the DNA of its host. In 1978, researchers at the
National Institutes of Health (NIH) studying a similar retrovirus in mice discovered a
gene called Rfv3 that influenced the production of neutralizing antibodies that allowed
the animals to recover. By 1999, they had narrowed the location of Rfv3 to a relatively
small region on mouse chromosome 15, but that region contained more than 60 genes. The
laboratory of GIVI Director Warner C. Greene and a team of scientists from NIAID now
demonstrate that Rfv3 is Apobec3, an innate immunity gene with antiretroviral activity.
"This newfound link between Apobec3 and the production of neutralizing antibodies
came as a complete surprise," said Dr. Greene, senior author on the paper.
