Dr. Jeffrey Wigand testifies about his experience as a whistleblower at a Workforce
Protections subcommittee hearing on whistleblower protections on May 15, 2007.
Study finds genetic link between
sleep disorders and depression in young children
A study in the Feb. 1 issue of the journal SLEEP was the first to use twin data to examine
the longitudinal link between sleep problems and depression. Results of this study
demonstrate that sleep problems predict later depression; the converse association was not
found. These findings are consistent with the theory that early treatment of sleep
problems may protect children from the development of depression. Results of the study
indicate that the stability of sleep problems across time is mainly caused by genetic
factors (46 percent of the genetic influences on sleep at age 10 were the same as those
that influenced a child at age 8). The stability of depression is mainly caused by
non-shared environmental influences (19 percent of the non-shared environmental influence
on depression at age 10 remained the same from the age of eight). According to lead author
Alice M. Gregory, senior lecturer in the department of psychology at Goldsmiths College in
London, the most surprising result of the study concerned the reasons why there may be
links between sleep problems and depression at different points in a young person's life.
"We reported in a study previously, that genes were the most important factor in
explaining the association between sleep problems and depression in eight year olds,"
said Gregory. "However, when we examined this issue at age 10, we found that genes
were less important in explaining the association and that environmental influences had
become more important. This could be because environmental experiences are becoming more
relevant as children grow older and could therefore play a role in both sleep problems and
depression." The process thought to underlie the associations between sleep and
depression reflects abnormalities that are known to be influenced by genetic variations. A
longitudinal twin study was used in order to distinguish shared and non-shared
environmental influences. Shared environmental influences create similarities among
individual family members, and can therefore be estimated by calculating the similarity
between identical twins that is not due to genetic influences. Non-shared environmental
influences individualize family members, and can therefore be estimated by examining the
associations between monozygotic (MZ) twin pairs; if there is not a perfect correlation
between MZ twins, it can be assumed that non-shared environmental influence are playing a
role.
Study suggests that inflammation
may be the link between extreme sleep durations and poor health
A study in the Feb. 1 issue of the journal SLEEP shows that sleep duration is associated
with changes in the levels of specific cytokines that are important in regulating
inflammation. The results suggest that inflammation may be the pathway linking extreme
sleep durations to an increased risk for disease. Each additional hour of self-reported
sleep duration was associated with an eight-percent increase in C-reactive protein (CRP)
levels and a seven-percent increase in interleukin-6 (IL-6), which are two inflammatory
mediators. In contrast, each hour of reduction in sleep measured objectively by
polysomnography was associated with an eight-percent increase in tumor necrosis factor
alpha, another pro-inflammatory cytokine. "The most surprising finding was that we
found different relationships based on how sleep was measured," said lead author Dr.
Sanjay R. Patel, assistant professor of medicine at Case Western Reserve University in
Cleveland, Ohio. According to the authors, research has linked both short and long sleep
durations with an increased risk for mortality, coronary heart disease, diabetes and
obesity. Chronic elevations in cytokines such as CRP and IL-6 also are associated with an
increased risk of problems such as diabetes and heart disease. The study involved 614
individuals from the Cleveland Family Study, a longitudinal family-based epidemiological
cohort designed to study the genetics of obstructive sleep apnea (OSA). Participants
completed questionnaires about sleep habits and underwent one night of polysomnography. In
the morning a fasting blood sample was collected, and it was analyzed for five
inflammatory cytokines.
Pregnancy-related hormonal changes
linked to increased risk of restless legs syndrome
A study in the Feb. 1 issue of the journal Sleep shows that the elevation in estradiol
levels that occurs during pregnancy is more pronounced in pregnant women with restless
legs syndrome (RLS) than in controls. During the last trimester of pregnancy, levels of
the estrogenic steroid hormone estradiol were 34,211 pg/mL in women with RLS and 25,475
pg/mL in healthy controls. At three months postpartum, estradiol levels had dropped to
30.73 pg/mL in the RLS group and 94.92 pg/mL in controls. Other hormone levels did not
differ significantly between the study groups. According to the authors the data strongly
suggest that estrogens play an important role in RLS during pregnancy. The study also
supports previous reports of high RLS incidence in the last trimester of pregnancy when
estradiol is maximally elevated. "Our findings strongly support the concept that
neuroactive hormones play a relevant pathophysiological role in RLS," said principal
investigator Thomas Pollmacher, MD, director of the Center for Medical Health at Klinikum
Ingolstadt and professor of psychiatry at Ludwig Maximilians University in Munich,
Germany. "This information will increase the understanding of RLS in pregnancy and
will assist in the development of specific therapeutic approaches." The American
Academy of Sleep Medicine describes RLS as a sleep-related movement disorder that involves
an almost irresistible urge to move the legs at night. This urge tends to be accompanied
by unusual feelings or sensations, called "paresthesias," that occur deep in the
legs. These uncomfortable sensations often are described as a burning, tingling, prickling
or jittery feeling. RLS can profoundly disturb a person's ability to go to sleep or return
to sleep after an awakening.The AASM reports that RLS occurs 1.5 to two times more often
in women than in men. Eighty percent to 90 percent of people with RLS also experience
periodic limb movements (PLMs) during sleep, which are involuntary jerking or twitching
movements of the feet or legs.
Making A Killing - A $330 billion
psychiatric industry
Psychotropic drugs. It's the story of big money--drugs that fuel a $330 billion
psychiatric industry, without a single cure. The cost in human terms is even
greater--these drugs now kill an estimated 42,000 people every year. And the death count
keeps rising. Containing more than 175 interviews with lawyers, mental health experts, the
families of victims and the survivors themselves, this riveting documentary rips the mask
off psychotropic drugging and exposes a brutal but well-entrenched money-making machine.
Researchers disrupt biochemical
system involved in cancer, degenerative disease
Screening a chemical library of 200,000 compounds, researchers at UT Southwestern Medical
Center have identified two new classes that can be used to study and possibly manipulate a
cellular pathway involved in many types of cancer and degenerative diseases. “The
identification of these chemicals and their targets within this cellular pathway
represents an important step in developing therapeutic agents,” said Dr. Lawrence
Lum, assistant professor of cell biology and senior author of the study, available at
Nature Chemical Biology. The researchers studied biochemical reactions within cells
controlled by a class of proteins called Wnt (pronounced “wint”). Wnt proteins
help control embryonic development in many animals, including humans. In adults, these
proteins also sustain the vital supply of stem cells that replenish various body tissues.
Misregulation of cellular responses to Wnt proteins, however, is associated with a broad
range of diseases including Alzheimer’s and polycystic kidney disease, cancer and
type 2 diabetes. In the current study, the researchers used cultured mouse cells that were
engineered to glow green when Wnt-controlled pathways were active. A robotic device then
tested 200,000 compounds to measure their effects on the cells.
Stanford study prevents pancreatic
tumor growth in mice by inhibiting key protein
Researchers at Stanford University School of Medicine have identified a protein critical
for the growth of pancreatic cancer. Blocking the expression of the protein slowed or
prevented tumor growth in mice and made cultured cancer cells vulnerable to the conditions
of low oxygen that occur in solid tumors. "This research clearly shows that
inhibiting the protein inhibits the tumor's ability to grow," said cancer biologist
Amato Giaccia, PhD. "Ultimately, we'd like to be able to specifically knock out the
expression of this protein in pancreatic tumors in humans." Pancreatic cancer is a
highly aggressive and deadly disease that accounts for more than 30,000 deaths in the
United States annually, and current therapies are largely ineffective. "Right now, we
have very little to offer these patients," said Giaccia. He is the Jack, Lulu and Sam
Willson Professor and professor of radiation oncology and the senior author of the
research, which will be published Feb. 1 in the journal Cancer Research. Giaccia is also a
member of the Stanford Cancer Center. The researchers studied a protein called connective
tissue growth factor, or CTGF. Also known as CCN2, the protein is involved in the abnormal
growth of connective tissue in response to injury or disease. It was also thought to be
involved in pancreatic tumor progression, although the exact role it played was unknown.
Giaccia and his collaborators found that human pancreatic cancer cells expressing high
levels of CCN2 grew robustly when injected under the skin of mice. In fact, in the
developing tumor these cells soon out-competed others that expressed lower levels of the
protein. Conversely, pancreatic cancer cells in which CCN2 expression was suppressed were
either less likely or unable to form tumors when injected into mice.The researchers
observed similar effects when the cancer cells were injected directly into the animals'
pancreases. Cancer cells expressing high levels of CCN2 formed tumors that grew more
rapidly and metastasized more aggressively than did those expressing lower levels, and the
mice died sooner than others injected with cancer cells expressing less CCN2.
Mesh-like Network of Arteries
Adjusts to Restore Blood Flow to Stroke-Injured Brain
A grid of small arteries at the surface of the brain redirects flow and widens at critical
points to restore blood supply to tissue starved of nutrients and oxygen following a
stroke, a study published this week has found.“This is optimistic news,” said
David Kleinfeld, a physics professor at the University of California, San Diego, whose
group studies blood flow in animal models of stroke. Damage from stroke can continue for
hours or even days as compromised brain tissue surrounding the core injury succumbs to
deprivation of oxygen and nutrients. “This is the area doctors are trying to protect
after a stroke,” said Andy Shih, a postdoctoral fellow in Kleinfeld’s group who
conducted the experiments. “Those neurons are teetering on the edge of death and
survival.”
Scientists say they have discovered a missing link in the way cells protect themselves
against cancer. They have uncovered how cells switch a gene called p53, which can block
the development of tumours, on and off.
LSUSHC researchers find potential
new target for hypertension treatment
Huijing Xia, PhD, a postdoctoral research associate in the lab of Eric Lazartigues, PhD,
Assistant Professor of Pharmacology at LSU Health Sciences Center New Orleans, is the lead
author on a paper reporting that a recently identified enzyme in the brain plays a
critically important role in the central regulation of blood pressure. The LSUHSC research
team showed that Angiotensin-converting enzyme 2 (ACE2) helps preserve the function of a
key spontaneous reflex involved in blood pressure regulation and confirms its potential as
a target for the prevention or treatment of High Blood Pressure. The research is published
in the February 1, 2009 issue of the peer reviewed journal, Hypertension, and the cover of
the issue features images of ACE2 expression from the Lazartigues laboratory at LSU Health
Sciences Center New Orleans. The LSUHSC researchers had previously identified ACE2 in the
mouse brain in areas involved in the central regulation of cardiovascular function. In
this study, they wanted to clarify the role it plays. Beat-to-beat short term regulation
of blood pressure is provided by a spontaneous reflex called the baroreceptor reflex.
Receptors in the arteries sense blood pressure and relay the information to the central
nervous system where a network of brain stem cells adjust vascular resistance and heart
rate. Action of a hypertensive hormone – Angiotensin II – is known to interfere
with that process. First, the researchers demonstrated that chronically hypertensive mice
showed dramatically decreased baroreceptor reflex sensitivity and ACE2 activity. Following
treatment with compounds to block both Angiotensin II receptors, the researchers found
that by blocking one of these receptors – AT1Rs – ACE2 activity increased. In
order to determine the relationship between AT1Rs blockade and ACE2, as well as the
significance of ACE2, the LSUHSC researchers generated a triple-transgenic mouse model
with increased ACE2 on a background of chronic hypertension. In this model, they observed
that the impaired baroreceptor reflex and other critical functions normalized, as did
blood pressure. "We now have evidence that brain ACE2 plays a critical role in
baroreceptor reflex function and , consequently, in the prevention of hypertension,"
says Dr. Xia.
Queen's chemist sheds light on
health benefits of garlic
A Queen's-led team has discovered the reason why garlic is so good for us. Researchers
have widely believed that the organic compound, allicin – which gives garlic its
aroma and flavour – acts as the world's most powerful antioxidant. But until now it
hasn't been clear how allicin works, or how it stacks up compared to more common
antioxidants such as Vitamin E and coenzyme Q10, which stop the damaging effects of
radicals. "We didn't understand how garlic could contain such an efficient
antioxidant, since it didn't have a substantial amount of the types of compounds usually
responsible for high antioxidant activity in plants, such as the flavanoids found in green
tea or grapes," says Chemistry professor Derek Pratt, who led the study. "If
allicin was indeed responsible for this activity in garlic, we wanted to find out how it
worked." The research team questioned the ability of allicin to trap damaging
radicals so effectively, and considered the possibility that a decomposition product of
allicin may instead be responsible. Through experiments with synthetically-produced
allicin, they found that an acid produced when the compound decomposes rapidly reacts with
radicals. Their findings are published in the January 2009 issue of the international
chemistry journal Angewandte Chemie. "Basically the allicin compound has to decompose
in order to generate a potent antioxidant," explains Dr. Pratt, who is Canada
Research Chair in Free Radical Chemistry. "The reaction between the sulfenic acid and
radicals is as fast as it can get, limited only by the time it takes for the two molecules
to come into contact. No one has ever seen compounds, natural or synthetic, react this
quickly as antioxidants."
Researchers at the UCLA School of Public Health have found the first evidence that
perfluorinated chemicals, or PFCs — chemicals that are widely used in everyday items
such as food packaging, pesticides, clothing, upholstery, carpets and personal care
products — may be associated with infertility in women. Published online in Human
Reproduction, Europe's leading reproductive medicine journal, the study found that women
who had higher levels of perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) in
their blood took longer to become pregnant than women with lower levels. The UCLA
researchers used data from the Danish National Birth Cohort to assess whether levels of
PFOS and PFOA in pregnant women's plasma were associated with a longer time to pregnancy.
A total of 1,240 women were included in their analyses. Blood samples were first taken
between 4 and 14 weeks into the pregnancy so that concentrations of PFOS and PFOA could be
measured. The researchers also interviewed the women at around the 12th week of pregnancy
to find out whether the pregnancy was planned or not and how long it took them to become
pregnant. Infertility was defined as a time to pregnancy of longer than 12 months or a
situation in which infertility treatments were used to establish the pregnancy, and the
results were adjusted for potential confounding factors such as age, lifestyle and
socioeconomic status. The level of PFOS in the women's plasma ranged from 6.4 nanograms
per milliliter (ng/ml) to 106.7 ng/ml, and from less than 1 ng/ml to 41.5 ng/ml for PFOA.
The researchers divided the women's levels of PFOS/PFOA into four quartiles and found
that, compared with women with the lowest levels of exposure, the likelihood of
infertility increased by 70 to 134 percent for women in the higher three quartiles of PFOS
exposure and by 60 to 154 percent for women in the higher three quartiles of PFOA
exposure. "Perfluorooctanoate and perfluorooctane sulfonate were considered to be
biologically inactive, but recently, animal studies have shown that these chemicals may
have a variety of toxic effects on the liver, immune system and developmental and
reproductive organs," said UCLA researcher Chunyuan Fei, the study's first author.
"Very few human studies have been done, but one of our earlier studies showed that
PFOA, although not PFOS, may impair the growth of babies in the womb, and another two
epidemiological studies linked PFOA and PFOS to impaired fetal growth."
Mayo Clinic study finds younger men
with erectile dysfunction at double risk of heart disease
Men who experience erectile dysfunction between the ages of 40 and 49 are twice as likely
to develop heart disease than men without dysfunction, according to a new Mayo Clinic
study. Researchers also found that men with erectile dysfunction have an 80 percent higher
risk of heart disease. "The highest risk for coronary heart disease was in younger
men," says researcher Jennifer St. Sauver, Ph.D. The study was published in the
February 2009 issue of Mayo Clinic Proceedings. The results suggest that younger men and
their doctors may need to consider erectile dysfunction a harbinger of future risk of
coronary heart disease -- and take appropriate steps to prevent it, says Dr. St. Sauver.
"The importance of the study cannot be overstated," writes Martin Miner, M.D.,
in an editorial in the same issue of Mayo Clinic Proceedings. The results "raise the
possibility of a 'window of curability,' in which progression of cardiac disease might be
slowed or halted by medical intervention," writes Dr. Miner, who practices at the
Men's Health Center, Miriam Hospital, Providence, R.I. Erectile dysfunction is common, and
prevalence increases with age. It affects 5 to 10 percent of men at age 40. By age 70,
from 40 to 60 percent of men have the condition. Dr. St. Sauver says researchers wanted to
learn more about the connections between age, cardiovascular disease and erectile
dysfunction. Two previous studies, both published in 2005, laid groundwork for the Mayo
Clinic study. One found that erectile dysfunction predicted an increased risk of heart
disease, but the erectile dysfunction of the study participants was not assessed with an
externally validated questionnaire and cardiac events were not subjected to standardized
review for diagnostic accuracy [Thompson et al, JAMA, 2005]. The second predicted that
future cardiovascular disease would be higher in younger men with erectile dysfunction,
but wasn't able to follow the men to determine if heart disease developed [Ponholzer et
al, Eur Urol, 2005]. For the Mayo Clinic study, the investigators identified 1,402 men who
lived in Olmsted County, Minn., in 1996 and did not have heart disease. Every two years
for 10 years, these men were assessed for urological and sexual health.
Director: Michael Mann Cast: Al Pacino, Russell Crowe, Christopher Plummer, Diane
Venora, Philip Baker Hall Plot: Based on a true story about a CBS 60 Minutes-episode in
1994 on malpractices in the tobacco industry, that was not aired because CBS parent
company Westinghouse objected. Pacino plays the 60 Minutes producer.
Study identifies potential 'safe
period' for hormone replacement use
A new study makes important new findings on the role of hormone use on the risk of breast
cancer, confirming that the use of estrogen plus progesterone increases the risk of both
ductal and lobular breast cancer far more than estrogen-only; suggesting a two-year
"safe" period for the use of estrogen and progesterone; and finding that the
increased risk for ductal cancers observed in long-term past users of hormone replacement
therapy drops off substantially two years after hormone use is stopped. The study appears
in CANCER, a peer-reviewed journal of the American Cancer Society. Previous studies have
shown that hormone replacement therapy after menopause increases the risk of breast cancer
and that use of a regimen that includes both estrogen and progesterone is more detrimental
for the breast than the use of estrogen alone. But more data from large prospective
studies are needed to fully characterize the impact of exogenous hormones on breast cancer
incidence by type of hormone preparation and histology of the cancer. To investigate the
association in more detail, American Cancer Society epidemiologists led by Eugenia E.
Calle, PhD, did a prospective study of 68,369 postmenopausal women who were cancer-free at
baseline in 1992. They examined the use of estrogen-only and estrogen and progesterone in
current and former users of varying duration, and the subsequent risk of developing
invasive ductal and lobular carcinoma of the breast. They also looked at whether the risk
for each type of breast cancer and each type of hormone regimen varied by body mass index
(BMI), stage of disease at diagnosis, and estrogen receptor (ER) and progesterone receptor
(PR) status. For the present study, the follow-up period ended on June 30, 2005.
New technique images tumor vessel
leakiness to predict breast cancer chemotherapy outcome
Chemotherapy is an integral part of modern cancer treatment, but it's not always
effective. Successful chemotherapy depends on the ability of anticancer drugs to escape
from the bloodstream through the leaky blood vessels that often surround tumors.
Predicting chemotherapy's efficacy could save thousands of individuals from unnecessary
toxicity and the often difficult side effects of the treatments. In a study published in
the February issue of the journal Radiology, researchers describe a technique for
determining the "leakiness" of tumor blood vessels using a simple digital
mammography unit. The researchers designed nanometer-sized capsules containing a contrast
agent that could only leak into tumors with blood vessels that were growing and therefore
leaky. The digital mammography-based quantification of "leakiness" is closely
correlated to the ability of a clinically approved chemotherapy agent to enter the tumor,
allowing the researchers to predict the agent's therapeutic efficacy. We developed a
quantitative way to measure the leakiness of the blood vessels, which is directly linked
to the amount of drug that gets to the cancer and in turn determines effectiveness,"
said Ravi Bellamkonda, a professor in the Wallace H. Coulter Department of Biomedical
Engineering at Georgia Tech and Emory University. "By simply measuring how much
contrast agent reaches the tumor, we can predict how much of a clinically approved
chemotherapeutic will reach the tumor, allowing physicians to personalize the dose and
predict effectiveness."In some cases, one chemotherapy drug may not be effective in
treating the tumor, but this new technique allows oncologists to investigate other drugs
sooner since they know the drug is reaching the tumor. Studies are currently underway to
determine if mammography can predict the optimal dose of a wide range of breast cancer
chemotherapeutics.
Penn study finds link between
Parkinson's disease genes and manganese poisoning
A connection between genetic and environmental causes of Parkinson's disease has been
discovered by a research team led by Aaron D. Gitler, PhD, Assistant Professor in the
Department of Cell and Developmental Biology at the University of Pennsylvania School of
Medicine. Gitler and colleagues found a genetic interaction between two Parkinson's
disease genes (alpha-synuclein and PARK9) and determined that the PARK9 protein can
protect cells from manganese poisoning, which is an environmental risk factor for a
Parkinson's disease-like syndrome. The findings appear online this week in Nature
Genetics. Manganism, or manganese poisoning, is prevalent in such occupations as mining,
welding, and steel manufacturing. It is caused by exposure to excessive levels of the
metal manganese, which attacks the central nervous system, producing motor and dementia
symptoms that resemble Parkinson's disease. In Parkinson's patients, the alpha-synuclein
protein normally found in the brain misfolds, forming clumps. Yeast cells, the model
system in which Gitler studies disease proteins, also form clumps and die when this
protein is expressed at high levels. These are the same yeast cells that bakers and
brewers use to make bread, beer, and wine. As a postdoctoral fellow at the Whitehead
Institute in Cambridge, Massachusetts, Gitler and colleagues started looking for genes
that could prevent the cell death caused by mis-folded alpha-synuclein in yeast.
Eventually they found a few genes to test in animal models and some were able to protect
neurons from the toxic effects of alpha-synuclein. "One of the genes that we found
was a previously uncharacterized yeast gene called YOR291W. No one knew what it did back
in 2006," he recalls.
New technology discovery at Mount
Sinai Hospital holds promise for improved breast cancer treatment
In a study published by Nature Biotechnology online on February 1, 2009, Mount Sinai
Hospital researchers have unveiled a new technology tool that analyzes breast cancer
tumours to determine a patient's best treatment options. The tool can predict with more
than 80 per cent accuracy a patient's chance of recovering from breast cancer.
"Breast cancer is the most common cancer in Canadian women," said Dr. Jeff
Wrana, Senior Investigator and the Mary Janigan Research Chair in Molecular Cancer
Therapeutics at the Samuel Lunenfeld Research Institute of Mount Sinai Hospital, and an
International Scholar of the Howard Hughes Medical Institute. "Our hope with this
technology is to eventually provide individualized analysis to breast cancer patients and
their oncologists so that they are better informed and empowered to select a treatment
best suited to them." The technology, called 'DyNeMo' analyzes networks of proteins
in cancer cells. Analysis of more than 350 patients found that those who survive breast
cancer have a different organization of the network of proteins within the tumour cells,
compared with patients who succumbed to the illness. DyNeMo can be used to predict the
outcome in a newly diagnosed breast cancer patient and then assist clinicians and patients
in making informed decisions on treatment. The study was led by the Mount Sinai Hospital
team and co-authored by researchers at the University of Toronto and London, England's The
Institute for Cancer Research. In the future, this tool may be used to analyze other types
of cancer and could be used to predict an individual's response to particular drugs.
Quantum dots may be toxic to cells,
environment under certain conditions
Researchers in Texas are reporting that quantum dots (QDs) — a product of the
revolution in nanotechnology increasingly used in electronics, solar cells, and medical
imaging devices — may be toxic to cells under acidic or alkaline conditions. Their
study, the first to report on how different pH levels may affect the safety of QDs,
appears in the Jan.15 issue of ACS' Environmental Science & Technology, a semi-monthly
journal. In the new study, Pedro Alvarez, Shaily Mahendra, and colleagues note that QDs
are semiconductor nanocrystals composed of a metal core surrounded by a shell composed of
zinc or cadmium sulfide. Scientists are increasingly concerned that these submicroscopic
dots, about 1/50,000th the width of a human hair, could decompose during normal use or
after disposal. That decomposition could release toxic metals into the environment, posing
a health risk to humans and animals. To explore this concern, the scientists exposed two
common types of bacteria that serve as models of cell toxicity and indicators of
environmental health to QDs under different conditions of acidity and alkalinity. At near
neutral pH levels, bacteria exposed to QDs experienced decreased rates of growth, but did
not die. However, at moderately acidic or alkaline conditions, many of the QD-exposed
bacteria died as QDs shells decomposed, releasing their content of toxic metals. However,
proteins and natural organic matter may be able to mitigate toxicity by complexing metal
ions or coating particles. The study cautions, "the release of toxic inorganic
constituents during their weathering under acidic or alkaline conditions in the human body
or the environment may cause unintended harm that might be difficult to predict with
short-term toxicity tests."
The findings, to be published this winter in the journal Environmental Research, suggest
that from 1953 to 2003, the fall and rise of the average SAT math and verbal score has
tracked the rise and fall of blood lead levels so closely that half of the change in
scores over 50 years, and possibly more, probably is the result of lead, says economist
Rick Nevin.
Insulin is a Possible New Treatment
for Alzheimer’s
A Northwestern University-led research team reports that insulin, by shielding
memory-forming synapses from harm, may slow or prevent the damage and memory loss caused
by toxic proteins in Alzheimer’s disease. The findings, which provide additional new
evidence that Alzheimer’s could be due to a novel third form of diabetes, will be
published online the week of Feb. 2 by the Proceedings of the National Academy of Sciences
(PNAS). In a study of neurons taken from the hippocampus, one of the brain’s crucial
memory centers, the scientists treated cells with insulin and the insulin-sensitizing drug
rosiglitazone, which has been used to treat type 2 diabetes. (Isolated hippocampal cells
are used by scientists to study memory chemistry; the cells are susceptible to damage
caused by ADDLs, toxic proteins that build up in persons with Alzheimer’s disease.)
The researchers discovered that damage to neurons exposed to ADDLs was blocked by insulin,
which kept ADDLs from attaching to the cells. They also found that protection by low
levels of insulin was enhanced by rosiglitazone. ADDLs (short for “amyloid
beta-derived diffusible ligands”) were discovered at Northwestern and are known to
attack memory-forming synapses. After ADDL binding, synapses lose their capacity to
respond to incoming information, resulting in memory loss.
Medical historian Allan Brandt discusses the history of conflict between health
researchers and the American tobacco industry.
Adrenal Fatigue
A self-help lifesaver for everyone who suffers from any of the above symptoms along with
many others described in the book. Adrenal Fatigue is also related to several other
chronic health conditions including: frequent infections, chemical sensitivities,
allergies, autoimmune diseases, fibromyalgia, rheumatoid arthritis, menopause, Hashimoto's
thyroiditis, chronic fatigue syndrome, PMS, difficult menopause, loss of libido, chronic
anxiety, and mild depression.All of these common problems and more can result from stress.
It's estimated that over 80% of North Americans suffer from some form of stress-related
Adrenal Fatigue. Although many people realize that stress is a problem in their lives, few
understand the actual physical ways stress acts on their bodies and minds through the
Adrenal glands, or more importantly, what they can do about it. Unfortunately even most
doctors still do not recognize the common health conditions produced by Adrenal Fatigue.
This leaves a lot of people suffering without anywhere to turn for help. That's where
Adrenal Fatigue: The 21st Century Stress Syndrome comes in.
Hypersensitivity to perfumes is the most common contact allergy in adults. Research at the
University of Gothenburg has demonstrated that even natural aromatic oils, which many deem
harmless compared to synthetic perfumes, may cause allergic reactions. Roughly one in five
adults in northern Europe is believed to suffer from contact allergy to one or more
chemicals. The most common is nickel allergy, but many people also suffer from contact
allergy to perfumes – even perfume substances that at first glance appear to be
harmless can cause allergic reactions. New eczema-provoking allergens are formed by
reaction with acid in the ambient air (known as autoxidation) or with skin enzymes. Modern
society commonly regards anything that comes from nature as being healthier and less
dangerous. Where it concerns natural aromas, known as essential oils, many manufacturers
believe that natural antioxidants in these oils offer protection against autoxidation thus
making them safer and longer lasting than artificial perfumes. Research at the University
of Gothenburg shows this is not the case. Lina Hagvall, a researcher at the University of
Gothenburg's Department of Chemistry, has examined natural lavender oil in her thesis. Her
results show that essential oils do not prevent the formation of allergenic substances
through reactions with acid; something which had not previously been possible to confirm.
Hagvall's thesis also examines geraniol, a common constituent of perfumes such as rose
oil. The study shows geraniol by itself to be only slightly allergenic. However through
autoxidation and reaction with skin enzymes, the substance is activated and becomes the
closely related allergen geranial. This is the first time these activation pathways have
been demonstrated for the substance. It is important to investigate how perfumes react
with air or on skin. Lina Hagvall's thesis concludes that such risks must be factored into
health risk assessments of chemicals relating to contact allergy. The thesis also
demonstrates that more perfumes than previously believed can be activated into allergens,
and that more studies should be done to increase knowledge within the field and thus
reduce the number of eczema cases.
Zen meditation – a centuries-old practice that can provide mental, physical and
emotional balance – may reduce pain according to Université de Montréal
researchers. A new study in the January edition of Psychosomatic Medicine reports that Zen
meditators have lower pain sensitivity both in and out of a meditative state compared to
non-meditators. Joshua A. Grant, a doctoral student in the Department of Physiology,
co-authored the paper with Pierre Rainville, a professor and researcher at the Université
de Montréal and it's affiliated Institut universitaire de gériatrie de Montréal. The
main goal of their study was to examine whether trained meditators perceived pain
differently than non-meditators. "While previous studies have shown that teaching
chronic pain patients to meditate is beneficial, very few studies have looked at pain
processing in healthy, highly trained meditators. This study was a first step in
determining how or why meditation might influence pain perception." says Grant.
HOPKINS TRANSPLANT SURGEONS REMOVE
HEALTHY KIDNEY THROUGH DONOR’S VAGINA
In what is believed to be a first-ever procedure, surgeons at Johns Hopkins have
successfully removed a healthy donor kidney through a small incision in the back of the
donor’s vagina. “The kidney was successfully removed and transplanted into the
donor’s niece, and both patients are doing fine,” says Robert Montgomery, M.D.,
Ph.D., chief of the transplant division at Johns Hopkins University School of Medicine who
led the team that performed the historic operation.The transvaginal donor kidney
extraction, performed Jan. 29 on a 48-year-old woman from Lexington Park, Md., eliminated
the need for a 5-to-6-inch abdominal incision and left only three pea-size scars on her
abdomen, one of which is hidden in her navel.
Women who have higher levels of a hormone produced by the placenta midway through
pregnancy appear more likely to develop postpartum depression, a study authored by a UC
Irvine researcher finds. The discovery could help identify and treat women at risk for
postpartum depression long before the onset of symptoms. Ilona Yim, psychology and social
behavior assistant professor, and colleagues found that women whose levels of
corticotrophin-releasing hormone started to increase more rapidly around 25 weeks of
gestation had a higher incidence of postpartum depression. Normally secreted in very small
amounts by the hypothalamus, this hormone regulates the body's response to stress. During
pregnancy, large amounts are produced in the placenta and are associated with
delivery."The hormone we studied plays an important part in pregnancy and has been
linked to depression," Yim said. "Many factors may cause some women's bodies to
produce more of this hormone during pregnancy. Evidence suggests that stress early in
pregnancy could play a role."
2 immune-system proteins linked to
colitis-associated cancer
Recent research from the laboratory of Michael Karin, PhD, at the University of
California, San Diego School of Medicine – the first researcher to demonstrate a
molecular link between inflammation and cancer – has identified two potential targets
for the prevention and treatment of colitis-associated cancer (CAC), the most serious
complication of inflammatory bowel disease. Karin, Distinguished Professor of Pharmacology
and Pathology and member of the Moores UCSD Cancer Center, and his team used genetic tools
to demonstrate in mice that a cytokine called Interleukin 6 (IL-6), is an important
regulator of tumor production during CAC development, and that its molecular effects are
largely mediated by the transcription factor STAT3 in cancer cells. Their latest study
– which is also the first to establish the cancer-promoting function of STAT3 in a
validated mouse model of human cancer – will be published in the February 3 on-line
edition of the journal Cancer Cell. Recurrent inflammation and chronic infections
contribute to a large number of different cancers including CAC which occurs in people
suffering from chronic colitis, a common inflammatory bowel disease, putting them at very
high risk for cancer. Cytokines – small proteins released by immune-system cells
– have been suggested to drive early tumor growth by stimulating the growth and
survival of pre-malignant cells. In previous work, Karin's team showed that activation of
a pro-inflammatory protein called NF-kB stimulates the proliferation of premalignant
epithelial cells in CAC, giving rise to malignant growths in the colon. Interestingly,
NF-kB in colonic epithelial cells promotes the development of cancer, not through
inflammation, but through inhibition of apoptosis or cell death. On the other hand, NF-kB
in the immune cells promotes cancer by enhancing inflammation, mostly by controlling the
expression of pro-inflammatory cytokine expression. One of these cytokines was thought to
be IL-6. "IL-6 fosters chronic inflammation and malignant cell survival and growth by
regulating the survival of T cells, white blood cells that direct the body's immune
system," Karin said.
New strategies to tackle medical
ghostwriting are debated
Better strategies to tackle ghostwriting in the medical literature are the subject of a
debate by leading authors in next week's issue of the open-access journal PLoS Medicine.
Ghostwriting is scientific misconduct, argues Peter Gøtzsche, Director of the Nordic
Cochrane Centre, Copenhagen, Denmark, because it is dishonest and often does not allow for
proper accountability of the role of authors and study sponsors in the publication
process. "Court cases that allowed access to industry files have shown that ghost and
guest authorship are common," says Dr. Gøtzsche, citing a recent example involving
the anti-inflammatory drug rofecoxib (Vioxx) in the Journal of the American Medical
Association (JAMA). But Jerome Kassirer, former editor-in-chief of the New England Journal
of Medicine, disagrees. He states that while ghostwriting "debases the fundamental
tenets of the medical profession" and can jeopardize patient care, we still do not
have enough evidence of its existence. "We must be careful not to impose excessive
regulations to solve problems that may not be threatening," argues Dr. Kassirer. A
third perspective on ghostwriting comes from an international group of professional
medical writers who argue that so long as their contribution to publication is explicitly
disclosed, "the communication expertise and health care knowledge" of
professional medical writers can be an untapped resource to help researchers publish and
disseminate their research. They propose a new checklist for authors using medical writers
that can be included with manuscript submission and encourages appropriate disclosure of
writing assistance.
While chronic inflammation is widely believed to be a predisposing factor for colon
cancer, the exact mechanisms linking these conditions have remained elusive. Scientists at
the Melbourne Branch of the international Ludwig Institute for Cancer Research (LICR) and
the Technical University Munich have jointly discovered a new piece of this puzzle by
demonstrating how the Stat3 protein links inflammation to tumor development, a discovery
that may well lead to the identification of new therapeutic targets for colon cancer.
Aberrant activation of the intracellular signaling protein, Stat3, has been associated
with inflammation and several cancers, including those of the gastrointestinal tract. The
results published on-line today in the journal Cancer Cell provide the first direct
evidence confirming the role for Stat3 in inflammation-associated tumorigenesis. Using an
inflammation-associated cancer model in genetically manipulated mice, the team identified
a relationship between epithelial cell Stat3 activity and colonic tumor incidence, as well
as tumor growth. They also determined that stimulation of Stat3 by the cytokines IL-6 and
IL-11, chemicals produced by inflammatory and other tumor-associated cells, promotes both
cell survival and growth of tumor cells.The collaboration was sparked by discussions
between Professors Matthias Ernst (LICR) and Florian Greten (Technical University Munich)
at a scientific meeting, when they discovered they were both individually pursuing the
mechanism by which Stat3 links inflammation to gastrointestinal cancers. Rather than
compete, the two decided to join forces to discover the Stat3 connection between
inflammation and colon cancer.
Zinc supplements during pregnancy
may counteract damage from early alcohol exposure
Animal research has shown that binge drinking – even just once – during early
pregnancy can cause numerous problems for the fetus, including early postnatal death.
Fetal zinc deficiency may explain some of the birth defects and neurodevelopmental
abnormalities associated with alcohol exposure. New rodent findings are the first to show
that dietary zinc supplements throughout pregnancy can reduce some alcohol-related birth
defects. Results will be published in the April issue of Alcoholism: Clinical &
Experimental Research and are currently available at Early View. "Alcohol's damage to
the fetus depends not only on the amount and duration of alcohol exposure, but also on the
timing of the exposure relative to the development stage of the cells and tissues
involved," said Peter Coyle, associate professor at the Hanson Institute in Adelaide,
and corresponding author for the study. "Earlier work had shown that prenatal
alcohol, as well as other toxins, can result in fetal zinc deficiency and teratogenicity
by inducing the zinc-binding protein, metallothionein, in the mother's liver. Since then,
our group has confirmed the importance of metallothionein in alcohol-mediated birth
defects." Coyle and his colleagues injected pregnant mice with either saline or a
25-percent solution of alcohol on gestational day (GD) eight; all mice received either a
regular or zinc-supplemented diet from GD zero to 18. On GD 18, fetuses from all four
groups – saline, saline plus zinc, alcohol, alcohol plus zinc – were assessed
for external birth abnormalities. In addition, from birth to day 60, researchers examined
the growth of survivors from all four groups. "There were three key findings,"
said Coyle. "One, fetal abnormalities caused by acute alcohol exposure in early
pregnancy can be prevented by dietary zinc supplementation. Two, dietary zinc
supplementation throughout pregnancy can protect against post-natal death caused by acute
alcohol exposure in early pregnancy. Three, dietary zinc supplementation increases the
mother's blood zinc to overwhelm the transient drop in zinc caused by alcohol, which we
believe prevents the fetal zinc deficiency and subsequent fetal damage."
Inflammation in colon may get
doused before fueling cancer development
A tiny molecule found in most plant-based foods douses the flames before damaging lesions
can form in the colon, according to a study by Texas AgriLife Research scientist Dr. Nancy
Turner. Even better, the compound can be obtained easily by eating vegetables and fruit
rather than by taking expensive prescriptions or supplements, Turner said. The molecule is
quercetin. Tiny but potent, quercetin gets into the body through onions, peppers, tomatoes
and most other common produce but also in "fun things like wine," she said.
"Just about any plant-based food in the human diet has some level of quercetin."
Previous studies showed quercetin was effective in reducing the rate of colon cancer in
laboratory tests, but Turner's latest research, published in the Journal of Nutrition,
shows how the compound works. That means researchers may now begin to understand how
quercetin could help other inflammatory bowel diseases such as Crohn's and celiac disease.
"The nice thing is that albeit high relative to what you see in the American diet,
the level used in this study is actually similar to what can be achieved in diets around
the world such as in, say, the Mediterranean-style diets," she said. "So it's
not an unachievable goal for us good ol' Americans if we do the right thing with our food
consumption." For this study, Turner's team examined the response of
quercetin-supplement diets in lab rats -- some in the early stages of colon cancer
formation and others without cancer. "Early lesions in a colon are some of the first
true changes in the colon that can be observed visually," she said. "This in not
just something you see in our animal model. You see it in human patients as well."
Vitamin D tied to muscle power in
adolescent girls
Vitamin D is significantly associated with muscle power and force in adolescent girls,
according to a new study accepted for publication in The Endocrine Society's Journal of
Clinical Endocrinology & Metabolism (JCEM). Although vitamin D is naturally produced
in the body through exposure to direct sunlight, vitamin D deficiency has become widely
common in the United States. Vitamin D deficiency has been shown to have a significant
negative impact on muscle and bone health, and can lead to conditions including
osteoporosis and rickets. "We know vitamin D deficiency can weaken the muscular and
skeletal systems, but until now, little was known about the relationship of vitamin D with
muscle power and force," said Dr. Kate Ward, Ph.D., of the University of Manchester
in the U.K., and lead author of the study. "Our study found that vitamin D is
positively related to muscle power, force, velocity and jump height in adolescent
girls." For this study, researchers followed 99 adolescent girls between the ages of
12 and 14 years. Dr. Ward and her colleagues took blood samples to measure the girls'
serum levels of vitamin D. Many of these girls were found to have low levels of vitamin D
despite not presenting any symptoms.
Research finds new cause of ozone
wheezing and potential treatments
Researchers at the National Institute of Environmental Health Sciences (NIEHS), part of
the National Institutes of Health, and Duke University have discovered a cause of airway
irritation and wheezing after exposure to ozone, a common urban air pollutant. Using an
animal model, the researchers were also able to identify several ways to stop the airways
from narrowing. These findings help identify potential new targets for drugs which may
eventually help physicians better treat emergency room patients suffering from wheezing,
coughing and shortness of breath. "We found that it is not the ozone itself that
causes the body to wheeze, but the way the lungs respond to ozone," said Stavros
Garantziotis, M.D., principal investigator in the NIEHS Laboratory of Respiratory Biology
and lead author of the paper published online this week in the Journal of Biological
Chemistry. "Animals exposed to ozone produced and released high amounts of a sugar
known as hyaluronan," said John Hollingsworth, M.D., a pulmonologist who is an
assistant professor in the Department of Medicine at Duke University Medical Center and
senior author of the paper. "We found hyaluronan to be directly responsible for
causing the airways to narrow and become irritated. We believe this may contribute to
asthma symptoms in humans as well." The researchers found several proteins which can
mediate the hyaluronan effect and can be used as treatment targets. They were also able to
block the airway responsiveness by binding the native hyaluronan away, as well as by
administering a slightly modified form of hyaluronan. "Although more research is
needed before these findings can be translated to humans, we are optimistic these
treatment options could prove beneficial to patients," said Hollingsworth.
A variation in the gene FOXO3A has a positive effect on the life expectancy of humans, and
is found much more often in people living to 100 and beyond – moreover, this appears
to be true worldwide. A research group in the Faculty of Medicine at the
Christian-Albrechts-University in Kiel (CAU) has now confirmed this assumption by
comparing DNA samples taken from 388 German centenarians with those from 731 younger
people. The results of the study appear this week in the prestigious American scientific
journal Proceedings of the National Academy of Sciences ("PNAS").
Don’t go changing - New
chemical keeps stem cells young
Scientists at the Universities of Bath and Leeds have discovered a chemical that stops
stem cells from turning into other cell types, allowing researchers to use these cells to
develop new medical treatments more easily. Stem cells have the ability to develop into
many other cell types in the body, and scientists believe they have huge potential to
treat diseases or injuries that don’t currently have a cure. Professor Melanie
Welham’s team at the University of Bath’s Department of Pharmacy &
Pharmacology, collaborating with Professor Adam Nelson at the University of Leeds, have
discovered a chemical that can be added to embryonic stem cells grown in the lab, allowing
them to multiply without changing into other cell types.
Road traffic noise in residential
areas can increase the risk of heart attack
People living in environments with high levels of road traffic noise might be more likely
to suffer myocardial infarction than people in quieter areas. This according to a new
study from the Swedish medical university Karolinska Institutet carried out in the
Stockholm area. The study compared 1,571 people from Stockholm County who had suffered a
myocardial infarction between 1992 and 1994 with controls from the same area. In order to
ascertain whether traffic noise in residential areas increases the risk of myocardial
infarction, the addresses of all individuals over the past 20 years were identified, and a
level of noise estimated. Similarly, exposure to air pollution was charted and information
on different risk factors for myocardial infarction was gathered using questionnaires and
interviews. No clear correlation between noise exposure and myocardial infarction was
found in the entire study population. However, once people with impaired hearing or
exposure to other sources of noise had been eliminated from the study, it was found that
there was a 40 per cent higher risk of myocardial infarction in people exposed to road
traffic noise exceeding 50 decibels. This relationship applied independently of other
known risk factors for myocardial infarction, such as exposure to air pollutants.
BPA Blocks Effects of Breast Cancer
Chemotherapy Drugs
Widespread human exposure to the chemical bisphenol A (BPA) has resulted from its use in a
diverse array of consumer products. Research on the potential health effects of BPA has
focused on the chemical’s ability to mimic or block natural estrogen. In animal
studies, prenatal exposure to BPA increased susceptibility to mammary cancer in adulthood.
However, studies of adult animals and cell cultures have had mixed results, and even less
certain is how BPA might influence established breast cancer and its treatment. A new cell
culture study is the first to show that BPA, at concentrations comparable to those found
in the general population, reduces the efficacy of chemotherapy drugs in breast cancer
cells, apparently by altering expression of proteins involved in apoptosis, or programmed
cell death
Phthalates in Prescription Drugs
Some Medications Deliver High Doses
Until recently, most of the concern surrounding the health risks of phthalates has focused
on the use of these plasticizers in toys, personal care products, food packaging, and
medical equipment such as intravenous tubing. A case report in 2004 raised the possibility
that certain prescription medications may also be a source of phthalate exposure for some
people [EHP 112:751–753 (2004)]. That finding prompted a systematic investigation
that links phthalate-containing medications with high internal exposure to these chemicals
[EHP 117-185–189; Hernández-Díaz et al.].
Quantitative Approach for
Incorporating Methylmercury Risks and Omega-3 Fatty Acid Benefits in Developing
Species-Specific Fish Consumption Advice
Estimated omega-3 FA benefits outweigh MeHg risks for some species (e.g., farmed salmon,
herring, trout) ; however, the opposite was true for others (swordfish, shark) . Other
species were associated with a small net benefit (e.g., flounder, canned light tuna) or a
small net risk (e.g., canned white tuna, halibut) . These results were used to place fish
into one of four meal frequency categories, with the advice tentative because of
limitations in the underlying dose–response information. Separate advice appears
warranted for the neurodevelopmental risk group versus the cardiovascular risk group
because we found a greater net benefit from fish consumption for the cardiovascular risk
group.
Occupational Exposure to
Polychlorinated Biphenyls and Risk of Breast Cancer
Overall, the breast cancer SIR was 0.81 (95% confidence interval, 0.72–0.92 ; n =
257) , and regression modeling showed little effect of employment duration or cumulative
exposure. However, for the 362 women of questionnaire-identified races other than white,
we observed positive, statistically significant associations with employment duration and
cumulative exposure ; only smoking, birth cohort, and self- or proxy questionnaire
completion had statistically significant explanatory power when added to models with
exposure metrics.
Endocrine Disruptors in the
Workplace, Hair Spray, Folate Supplementation, and Risk of Hypospadias
Excess risks of hypospadias associated with occupational exposures to phthalates and hair
spray suggest that antiandrogenic EDCs may play a role in hypospadias. Folate
supplementation in early pregnancy may be protective.
USC study finds that green tea
blocks benefits of cancer drug
ontrary to popular assumptions about the health benefits of green tea, researchers at the
University of Southern California (USC) have found that the widely used supplement renders
a cancer drug used to treat multiple myeloma and mantle cell lymphoma completely
ineffective in treating cancer. The study, which found that a component of green tea
extract (GTE) called EGCG destroys any anticancer activity of the drug Velcade in
tumor-bearing mice, will be published in a future print edition of the journal, Blood. It
is now available online at the journal's pre-publication First Edition website. "Our
finding that GTE or EGCG blocked the therapeutic action of Velcade was completely
unexpected," says lead author Axel H. Schönthal, PhD, associate professor in the
Department of Microbiology and Immunology at the Keck School of Medicine of USC. "Our
hypothesis was that GTE or EGCG would enhance the anti-tumor effects of Velcade, and that
a combination of GTE with Velcade (or EGCG with Velcade) would turn out to be a superior
cancer treatment as compared to treatment with Velcade alone." Herbal remedies,
including green tea, have become a popular remedy for cancer patients dealing with side
effects of chemotherapy. However, these supplements are unregulated and, for most, their
beneficial and/or detrimental effects have not been qualified through research. Using
preclinical models and tumor-bearing mice, the researchers found that the unusually
effective blockage of Velcade's therapeutic activity was based on the chemical interaction
between molecules. The EGCG molecule and the Velcade molecule were able to form chemical
bonds, meaning that the Velcade molecule could no longer bind to its intended target
inside the tumor cells.Clincal trials to verify these results in humans would be highly
unethical to conduct, because of the predictably unfavorable outcome. Nevertheless, the
researchers expect the results of the study to be applicable to cancer patients.
Researchers Disprove 15-year-old
Theory about the Nervous System
A delay in traffic may cause a headache, but a delay in the nervous system can cause much
more. University of Missouri researchers have uncovered clues identifying which proteins
are involved in the development of the nervous system and found that the proteins
previously thought to play a significant role, in fact, do not. Understanding how the
nervous system develops will give researchers a better understanding of neurological
diseases, such as multiple sclerosis and Charcot-Marie-Tooth disorders. “Speed is the
key to the nervous system,” said Michael Garcia, investigator in the Christopher S.
Bond Life Sciences Center and assistant professor of biological sciences in the MU College
of Arts and Science. “The peripheral nervous system ‘talks’ to muscles
through nerve impulses in response to external stimuli. When babies are born, they do not
have fully developed nervous systems, and their systems run slower. Eventually, the
nervous system matures. Our study tried to understand that maturation process.”
Mayo Clinic Researchers Suspect a
Novel Gene is Causing Restless Legs Syndrome in a Large Family
In 2005, a woman who had trouble sleeping asked Siong-Chi Lin, M.D., for help. Dr. Lin, a
sleep disorders specialist at the Mayo Clinic campus in Florida, diagnosed restless legs
syndrome. This common neurologic disorder interrupts sleep because of unpleasant
sensations in the legs at rest, especially in the evening, that are temporarily relieved
by movement. Restless legs syndrome affects between 5 and 11 percent of the population in
North America and Europe, says Dr. Lin. The cause may be a number of clinical factors,
such as iron deficiency, but it has a strong genetic component as well. "In most
people, it is likely due to a number of different causes, but genes are very likely the
most important factor in affected families," he says. Medications, especially agents
that increase transmission of dopamine in brain neurons, are effective in many people and
worked for his new patient, says Dr. Lin. "The syndrome may appear as a nuisance for
most people, however it can also seriously affect some people's quality of life," he
says.
Tobacco Smoke and Alcohol Harm
Liver Worse as Combo
Exposure to second-hand smoke and alcohol significantly raises the risk of liver disease,
according to researchers at the University of Alabama at Birmingham (UAB). The finding
adds to mounting evidence that tobacco smoke and alcohol are worse for health as a
combination, beyond the individual exposure risks, said Shannon Bailey, Ph.D., an
associate professor in the UAB Department of Environmental Health Sciences and a co-lead
author on the study. "This new data is a significant finding considering the combined
effect of alcohol and cigarette smoke exposures, and the implications for public
health," Bailey said. The researchers reported on mice exposed to smoky air in a
laboratory enclosure and fed a liquid diet containing ethanol, the intoxicating ingredient
in alcohol drinks. Mice exposed to second-hand smoke and who drank ethanol had 110 percent
more liver fibrosis proteins than mice who breathed filtered air. Additionally, the
twice-exposed mice had 65 percent more liver fibrosis proteins than mice who breathed
smoky air but did not drink ethanol. Fibrosis is scar-like tissue in the liver that can
lead to cirrhosis.
Could Carbon Dioxide Replace
Antibiotics in Surgery?
The paper explains that wound infection is a serious surgical complication leading to
longer stays in hospital and greater risk of death. Problems include bacterial
contamination of the wound, drying of body tissues and heat loss. The authors suggest that
a wound could continuously be flooded with carbon dioxide gas (CO2) during surgery. Carbon
dioxide could prevent airborne bacteria from reaching the wound and would also suffocate
germs. CO2 is already used for this purpose in the food packaging business. Humidified CO2
would also keep the wound warm and moist, which should reduce tissue damage and speed-up
healing. The authors have already tested their idea in the laboratory, and the next step
should be a proper clinical trial in humans.
A team of Vanderbilt University Medical Center investigators has developed a group of
chemical compounds that could represent a new class of drugs for treating cancer. The
compounds are the first selective inhibitors of the protein phospholipase D (PLD), an
enzyme that has been implicated in multiple human cancers including breast, renal, gastric
and colorectal. The new inhibitors, reported in the February issue of Nature Chemical
Biology, block the invasive migration of breast cancer cells, supporting their further
development as antimetastatic agents. They will also be useful tools for understanding the
complex roles of PLD in cellular physiology, said H. Alex Brown, Ph.D., professor of
Pharmacology and one of the team leaders. "PLD is associated with many fundamental
cellular processes like secretion, migration, growth and proliferation. But the absence of
selective inhibitors has really interfered with the ability of biologists to study this
important enzyme," Brown said. There are two related "isoforms" of PLD:
PLD1 and PLD2. Both PLD enzymes produce phosphatidic acid, a key lipid metabolic and
signaling molecule. But whether the two PLDs have different roles is an open question, one
that the new isoform-selective inhibitors can now be used to address. Brown and colleagues
had discovered that PLD was important to the invasive migration of breast cancer cells in
culture using a genetic tool called small interfering RNA (siRNA). "When we had
evidence from siRNA and other methods that blocking PLD resulted in dramatic effects of
blocking metastatic invasion of breast cancer cells, we were highly motivated to attempt
to make isoform-selective inhibitors," Brown said.
Johns Hopkins researchers discover
new schizophrenia gene
Researchers at the Johns Hopkins University School of Medicine are one gene closer to
understanding schizophrenia and related disorders. Reporting in the Jan. 9 issue of the
American Journal of Human Genetics, the team describes how a variation in the neuregulin 3
gene influences delusions associated with schizophrenia. "Neuregulin 3 is clearly one
more gene to add to the few currently known to contribute to schizophrenia," says
David Valle, M.D., director of the McKusick-Nathans Institute of Genetic Medicine at
Hopkins. "There's much more to do, but we're making progress." Schizophrenia is
a varied condition with a number of symptoms not shared by all affected. This could be one
reason why it's been difficult to identify genes that contribute to the condition. To
address this, the team first rigorously separated the 73 different symptoms into nine
distinct factors associated with the condition—prodromal, negative, delusion,
affective, scholastic, adolescent sociability, disorganization, disability, hallucination.
Then, using genetic samples from more than 450 people with schizophrenia and their parents
as well as unrelated non-affected people for comparison, the team focused on one region of
chromosome 10 that previously had been implicated to contain genes that contribute to the
condition. They analyzed more than 1,400 single nucleotide polymorphisms, or SNPs for
short, to see if any particular SNPs were more frequently carried by schizophrenia
patients than unaffected people.
Tinkering with the circadian clock
can suppress cancer growth
Researchers at the University of North Carolina at Chapel Hill have shown that disruption
of the circadian clock – the internal time-keeping mechanism that keeps the body
running on a 24-hour cycle – can slow the progression of cancer. The study disputes
some of the most recent research in the field indicating that alteration of this daily
cycle predisposes humans and mice to cancer. The UNC researchers found that genetically
altering one of four essential "clock" genes actually suppressed cancer growth
in a mouse model commonly used to investigate cancer. The findings could enable clinicians
to reset the internal clock of each cancer cell to render it more vulnerable to attack
with chemotherapeutic drugs. "Adjusting the clock in this way could certainly be a
new target for cancer treatment," said senior study author Aziz Sancar, M.D., Ph.D.,
a member of the UNC Lineberger Comprehensive Cancer Center and Sarah Graham Kenan
Professor of Biochemistry and Biophysics in the UNC School of Medicine. Sancar is also a
member of the National Academy of Sciences, the Turkish Academy of Sciences and the
American Academy of Arts and Sciences. "Our study indicates that interfering with the
function of these clock genes in cancer tissue may be an effective way to kill cancer
cells and could be a way to improve upon traditional chemotherapy," Sancar said. His
findings appear February 2, 2009 in the online early edition of the Proceedings of the
National Academy of Sciences. Previous research has shown that the disruption of the
body's natural circadian rhythms affects people's health. One of the largest
epidemiological studies ever performed, the Nurses' Health Study, found that nurses who
worked the night shift had a higher incidence of breast cancer than those who worked days.
Another study of flight attendants whose internal biological clocks had been wrecked by
travel on transatlantic flights produced similar findings. Yet when scientists, including
Sancar, began to tinker with the molecular mechanisms within the internal clocks of animal
models, they did not always see such an effect. Circadian rhythms in humans and in mice
are controlled by "clock genes," four of which are absolutely essential. In a
study four years ago, Sancar found that deleting the clock gene cryptochrome in mice did
not increase the incidence of cancer as had previously been expected.
Vitamin D acts like a hormone in the human body. It is essential for promoting calcium
absorption in the gut and maintaining adequate blood levels of calcium and phosphate
levels to allow muscles to work properly. It's needed for bone growth in infants and
children (prevention of rickets) and protects older adults from osteoporosis (which leads
to greater risk of bone fracture).
APHA Lists Vitamin D Deficiency as
Top Public Health Issue
Researchers have estimated that nearly half (40-50 percent) of adults and more than 30
percent of children in the United States are at risk of vitamin D deficiency.
Early Research Shows What Your
Mother Did When She Was a Child May Have an Effect On Your Memory and Learning Ability
A new study by researchers from Rush University Medical Center and Tufts University School
of Medicine using mice indicate that a child’s memory and the severity of learning
disorders may be affected by what his or her mother did when she was a child. Findings
from the study will be published in the February 4th issue of The Journal of Neuroscience.
Neuroscience researchers studied the brain function of pre-adolescent mice that have a
genetically-created defect in memory. When these young mice were given an enriched
environment, which is exposure to stimulatory objects, enhanced social interaction and
voluntary exercise for two weeks, the memory defect, caused by inhibiting the formation of
Ras-GRF1 and Ras-GRF2 proteins, was reversed. After a few months, the same mice were
fertilized and they gave birth to offspring that had the same genetic mutation. However,
the offspring had no indications of the memory defect even though the offspring were never
exposed to an enriched environment like their mothers.
Fermented Soy is Only Soy Food Fit
for Human Consumption
Writings about the soybean date back to 3000 B.C., when the Emperor of China listed the
virtues of soybean plants for regenerating the soil for future crops. His praises centered
on the root of the plant, not the bean. These ancient writing suggested that the Chinese
recognized the unfitness of soybeans for human consumption in their natural form.
The drug, which was said to have been administered on many diabetic victims, has been
found to be very safe and highly effective. It was also said to have corrected erective
dysfunctions noticed in those victims.
Hope for preventative treatment for
cystic fibrosis lung disease
Early inhalation of amiloride prevents chronic lung disease in a mouse model / Heidelberg
researchers publish in the “American Journal of Respiratory and Critical Care
Medicine” Heidelberg researchers have succeeded in preventing cystic fibrosis lung
disease in an animal model by spraying amiloride into the lungs of young mice. This is the
first therapy to successfully attack the root cause of the widespread hereditary disease
in a living organism. When mice are given inhalation treatment with the drug in the first
days of life, no thick mucus forms in the lungs and airway inflammation and chronic lung
damage can be prevented. The researchers at Department of Pediatrics at Heidelberg
University Hospital have demonstrated for the first time that preventative therapy of lung
disease is possible for cystic fibrosis. Their study was published in the ”American
Journal of Respiratory and Critical Care Medicine”.
Spanish scientists confirm extra
virgin olive oil helps to combat breast cancer
UGR News Researchers of the Catalonian Institute of Oncology (Spain) and the University of
Granada (Spain) have discovered that extra virgin olive oil may help to combat breast
cancer, according to a paper published in the last issue of the renowned scientific
journal ‘BMC Cancer’. The scientists have confirmed the bioactivity of
polyphenols (this is, natural antioxidants) present in olive oil in breast cancer cell
lines. The study has proved the anti-HER2 effect of fractions of phenolic compounds
directly extracted of extra virgin olive oil in breast cancer cell lines. They have used
solid-phase extraction methods of semi-preparative liquid chromatography to isolate
fractions of commercial oils and, later, separation techniques (capillary electrophoresis
and liquid chromatography connected to mass spectrometry) to check the purity and
composition of the fractions. Such fractions were tested in their anti-cancer capacity
both against positive HER2 and negative HER2 breast cancers, using in Vitro models and
evaluating the effect of polyphenolic fractions in the expression and activation of HER2
oncoprotein through ELISA specific methods for HER2. Fractions containing polyphonels such
as hydroxitirosol, tirosol, elenolic acid, lignans, pinoresinol and acetopinoresinol, and
secoiridoids, diacetox oleuropein aglycone, ligustrosid aglycone and oleuropein aglycone
were able to induce important tumoricid effects in a range of micromolar and in a
selective way against HER2 oncogene.
Immunological tests for more
accurate detection of cancer precursors
A large portion of the almost 73,000 colorectal cancers diagnosed in Germany each year
could be avoided. If precancerous lesions – growths of the intestinal mucosa called
adenomas – are detected and removed at an early stage, there is a great chance that
cancer will not develop at all. Therefore, statutory health insurances in Germany offer a
fecal occult blood test free of charge for all insured persons from the age of 50. This
test can detect precursors of colorectal cancer. In addition, persons from the age of 55
are entitled to receive an endoscopic examination of the colon (colonoscopy) once every 10
years. A colonoscopy identifies precancerous lesions with a certainty of over 90 percent.
Nevertheless, due to reluctance to take the examination, only about 30 percent of those
entitled to it actually do so (extrapolated to the 10-year period between the two
colonoscopies covered by the health insurance). "Therefore, the simple laboratory
tests for occult blood in the stool are still important in order to reach those who do not
wish to receive a colonoscopy," explains Professor Hermann Brenner, who heads the
Division of Clinical Epidemiology and Aging Research at DKFZ. However, the widely used
HaemOccult test which is covered by the health insurances has substantial disadvantages:
It is less sensitive and the test result, which is based on enzymatic detection of
hemoglobin, can be falsified by the patient's diet such as red meat or vitamin C
supplements. By contrast, immunological detection methods are based on a very specific
identification of blood components by antibodies. In order to compare the accuracy of
available tests, Brenner's team carried out a large-scale study. The epidemiologists
screened stool samples of 1,319 individuals before their scheduled regular screening
colonoscopy. All samples were tested with the HaemOccult method as well as with six
different immunochemical tests. All methods investigated are so-called quick tests whose
results can be obtained directly at any doctor's office. The test results were then
compared with the results of the colonoscopies.
Pharmaceuticals sold in Sweden
cause serious environmental harm in India
Many of the substances in our most common medicines are manufactured in India and China.
Some of these factories release large quantities of antibiotics and other pharmaceutical
substances to the environment. There is an obvious risk of these releases leading to
resistant bacteria. Research from the Sahlgrenska Academy at University of Gothenburg,
Sweden, shows that Sweden is a major consumer of pharmaceutical substances from factories
that fail to adequately treat their wastewater. As it is difficult to find out where the
pharmaceutical substances are manufactured and how much is released, it is impossible at
present for consumers to avoid contributing to this environmental harm. These findings are
presented in the medical journal Regulatory Toxicology and Pharmacology and are
highlighted today in a news article in Nature. Last week the research of the Swedish group
became headline news in New York Times, Washington Post and Times of India. "We used
to think that pharmaceuticals that ended up in the environment mostly came from the use of
the medicines and that the substances were dispersed through wastewater. We now know that
certain factories that manufacture substances release very large quantities of active
substances," says associate professor Joakim Larsson of the Sahlgrenska Academy in
Gothenburg,Sweden, one of the research scientists behind the studies.
A Texas AgriLife Research scientist and fellow researchers have discovered that arginine,
an amino acid, reduces fat mass in diet-induced obese rats and could help fight human
obesity. "Given the current epidemic of obesity in the U.S. and worldwide, our
finding is very important,” said Dr. Guoyao Wu, an AgriLife Research animal
nutritionist in College Station and Senior Faculty Fellow in the department of animal
science at Texas A&M University. The research found dietary arginine supplementation
shifts nutrient partitioning to promote skeletal-muscle gain, according to the
researchers. The findings were published recently in the Journal of Nutrition
(http://jn.nutrition.org). In laboratory experiments, rats were fed both low-and high-fat
diets. They found that arginine supplementation for a 12-week period decreased the body
fat gains of low-fat and high-fat fed rats by 65 percent and 63 percent, respectively. The
long-term arginine treatment did not have any adverse effects on either group. “This
finding could be directly translated into fighting human obesity,” Wu said. “At
this time, arginine has not been incorporated into our food (but could in the
future).”
A recent study published in Crop Science of the anticancer benefits of dry beans shows
that different market classes of beans contain varying levels of antioxidants and other
cancer reducing contents.As the world seeks new ways to prevent and treat chronic diseases
such as diabetes, heart disease and cancer, more research continues to be conducted on the
benefits of certain foods in reducing people’s risk of contracting these ailments.
Legumes in particular are often cited as being high in antioxidants, which have the
property of being able to fight off free radical cells within the body, reducing the risk
of cancer and other chronic diseases. A recent study further investigated these
connections, as researchers focused on the benefits of one type of legume, dry beans, in
reducing the risk of mammary cancer. To address whether dry bean consumption is associated
with a reduction in mammary cancer, scientists at Colorado State University studied the
anticancer activity of six market classes of bean including; small red, great northern,
navy, black, dark red and white kidney bean in the diet of laboratory animals. They also
evaluated whether the level of antioxidants or seed coat pigments in the bean were related
to mammary cancer. The study was funded by a grant from the Beans for Health Alliance, and
the Colorado Agricultural Experiment Station with assistance from Archer Daniels Midland
Co. and Bush Brothers Inc. Results from the study were published in the January-February
2009 issue of the journal Crop Science.
Molecule that suppresses immune
response under study in type 1 diabetes
The idea is to teach the immune system of children at high risk for type 1 diabetes not to
attack the insulin-producing cells of the pancreas. "We want to create a no-go
zone," said Dr. Andrew Mellor, immunologist who directs the Medical College of
Georgia Immunotherapy Center. Type 1 diabetes is classified as an autoimmune disease
because the immune system targets healthy islet cells for destruction, leaving young
patients unable to use glucose, a major fuel source for the body. MCG researchers think
they may be able to delay or even prevent that destruction by boosting the body's levels
of an enzyme fetuses uses to escape the mother's immune response or by packaging islet
cell antigens, which get the immune system's attention, with this suppressor. T-cells are
immune cells that decide whether to attack or ignore an antigen. Dr. Mellor believes
they'll ignore insulin-producing cells if they see them for the first time with
indoleomine 2,3-dioxegenase, or IDO, a powerful immune system inhibitor. "We are
going to be in a situation, in the not too distant future where you can identify an
individual at risk, such as a 5-year-old child who has a 90 percent chance of becoming a
type 1 diabetic within 10 years," he said. "Once you know that information the
onus is on medicine to do something about reducing that risk."
Discovery by Brown researchers
could lead to new autism treatment
A Brown University research team has discovered something in the brain that could serve as
a target for future autism and mental retardation treatments.Discovery of the novel
Fragile X granule is detailed in the Feb. 4, 2009, issue of the Journal of Neuroscience.
This finding opens a new line of research about potential treatments for autism, a
neurological disorder that strikes young children and can impair development of social
interaction and communication. “If you are going to treat the disease you need to be
able to target the defective elements,” said Justin Fallon, professor of neuroscience
at Brown. “The Fragile X granule offers such a target.” Fallon is senior author
of the paper titled “The FXG: A presynaptic Fragile X granule expressed in a subset
of developing brain circuits.” Two postdoctoral students at Brown served as lead
authors: Sean Christie and Michael Atkins. James Schwob, a researcher from Tufts
University Medical School, also participated. Autism affects as many as 1.5 million
Americans, and the number is increasing, according to the Autism Society of America. It is
estimated that 1 in 150 births involve children with some form of autism. Autism can be
caused by a variety of genetic factors, but Fallon’s lab focused on one particular
area — the Fragile X protein. If that protein is mutated, it leads to Fragile X
syndrome, which causes mental retardation and is often accompanied by autism.There is
growing recognition in the field that autism and mental retardation are diseases of the
synapse, the basic unit of information exchange and storage in the brain. Many groups have
extensively studied the role of the Fragile X protein in the post-synaptic, or receiving
side of synaptic connections. This was a starting point for the research conducted by
Fallon’s team in their study of the Fragile X protein and synaptic connections in
healthy mice.
Genetic study shows direct link
between vitamin D and MS susceptibility 'gene'
Researchers have found evidence that a direct interaction between vitamin D and a common
genetic variant alters the risk of developing multiple sclerosis (MS). The research,
published on 6 February in the open-access journal PLoS Genetics, suggests that vitamin D
deficiency during pregnancy and the early years may increase the risk of the offspring
developing MS later in life. MS is the most common disabling neurological condition
affecting young adults. More than 85,000 people in the UK and 2.5 million worldwide are
thought to suffer from the condition, which results from the loss of nerve fibres and
their protective myelin sheath in the brain and spinal cord, causing neurological damage.
The causes of MS are unclear, but it has become evident that both environmental and
genetic factors play a role. Previous studies have shown that populations from Northern
Europe have increased MS risk if they live in areas receiving less sunshine. This supports
a direct link between deficiency in vitamin D, which is produced in the body through the
action of sunlight, and increased risk of developing the disease. The largest genetic
effect by far comes from the region on chromosome six containing the gene variant known as
DRB1*1501 and from adjacent DNA sequences. Whilst one in 1,000 people in the UK are likely
to develop MS, this number rises to around one in 300 amongst those carrying a single copy
of the variant and one in 100 of those carrying two copies. Now, in a study funded by the
UK's MS Society, the MS Society of Canada, the Wellcome Trust and the Medical Research
Council, researchers at the University of Oxford and the University of British Columbia
have established a direct relationship between DRB1*1501 and vitamin D.
Statin therapy ineffective in
breast cancer prevention
Laboratory work in animals showed limited activity when statins were given to prevent
breast cancer, according to a report in the February issue of Cancer Prevention Research,
a journal of the American Association for Cancer Research. Statins, sold under brand names
like Lipitor and Zocor, are primarily given to lower cholesterol and prevent heart
disease, and prominent cardiologists almost universally agree that their use has changed
the landscape. The use of these drugs in cancer prevention has been more controversial.
Results of epidemiology studies, which rely on looking backward rather than forward and
thus are subject to confounding factors, have yielded mixed results when examining breast
cancer. Scientists under the auspices of the NCI, including Ronald Lubet, Ph.D., an NCI
program director, and Clinton Grubbs, Ph.D., director of the Chemoprevention Center at the
University of Alabama at Birmingham conducted laboratory work in animals to determine if
statins actually prevent both ER-positive and ER-negative breast cancer.
Possible drug target for obesity
treatment a no-brainer
Scientists at the University of North Carolina at Chapel Hill School of Medicine have
discovered a gene that when mutated causes obesity by dampening the body's ability to burn
energy while leaving appetite unaffected. The new research could potentially lead to new
pharmacologic approaches to treating obesity in humans that do not target the brain,
according to study senior author Yi Zhang, Ph.D., Howard Hughes Medical Institute
investigator and professor of biochemistry and biophysics in the UNC School of Medicine.
Zhang is also a member of the UNC Lineberger Comprehensive Cancer Center. The findings
also add new knowledge to the burgeoning field of epigenetics, in which heritable changes
in gene expression or physical appearance are caused by mechanisms besides changes in the
underlying DNA. The gene in question encodes for a specific epigenetic factor, an enzyme
called Jhdm2a. In 2006, Zhang showed that Jhdm2a was able to demethylate, or remove, a
methyl group from one of four histone proteins bound to all genes. Because they are so
intimately associated with DNA, even slight chemical alterations of histones can have
profound effects on nearby genes. The new study focused on a line of so-called
"knockout" mice that lacked the Jhdm2a gene. Zhang found impairment in two
molecular signaling pathways important for normal function in brown fat tissue and muscle
cells. Both pathways exert a major influence on metabolism, the body's conversion of food
to energy. Without the enzyme, the mice had reduced metabolisms, becoming visibly obese.
To Zhang's knowledge, this is the first mouse model to exhibit obese traits that do not
resulting from an alteration in appetite, which is largely a brain function. "Given
that this gene is not expressed in the brain, any drug that targets this gene would not
have an effect on brain function," he said. "Therefore, we are really looking
for a pure effect on metabolism."
New evidence of hormone therapy
causing breast cancer, Stanford professor says
Postmenopausal women who take combined estrogen plus progestin menopausal hormone therapy
for at least five years double their annual risk of breast cancer, according to new
analyses from a major study that clearly establishes a link between hormone use and breast
cancer, Stanford researchers say. The multi-center study also found that women on hormones
can quickly reduce their risks of cancer simply by stopping the therapy. The study is a
follow-up to the landmark Women's Health Initiative report of 2002, which found that
postmenopausal women taking estrogen plus progestin were at far greater risk of developing
breast cancer and other serious conditions than women on placebo. After publication of the
WHI data, use of hormone therapy plummeted in the United States - from 60 million
prescriptions in 2001 to 20 million in 2005. Breast cancer rates also declined
significantly within the year, suggesting a strong link between hormone use and cancer
risk. But some scientists still questioned the connection, saying the dip in breast cancer
rates could not have occurred so rapidly and may have been related to patterns of
mammogram use. The latest study, however, should put those questions to rest, said Marcia
Stefanick, PhD, professor of medicine at Stanford University School of Medicine and a
co-author of the study. "This is very strong evidence that estrogen plus progestin
causes breast cancer," said Stefanick, chair of the WHI executive committee.
"You start women on hormones and within five years, their risk for breast cancer is
clearly elevated. You stop the hormones and within one year, their risk is essentially
back to normal. It's reasonably convincing cause-and-effect data." The results, she
cautioned, do not apply to women taking estrogen alone. The large WHI trial of
estrogen-only did not find an increase in breast cancer for the majority of women assigned
to estrogen-only therapy.
Source of cancer stem cells'
resistance to radiation discovered at Stanford
Much to the dismay of patients and physicians, cancer stem cells — tiny powerhouses
that generate and maintain tumor growth in many types of cancers — are relatively
resistant to the ionizing radiation often used as therapy for these conditions. Part of
the reason, say researchers at Stanford University School of Medicine, is the presence of
a protective pathway meant to shield normal stem cells from DNA damage. When the
researchers blocked this pathway, the cells became more susceptible to radiation.
Researchers at the Centenary Institute in Sydney have discovered a molecule on the surface
of immune cells which plays a critical role in cancer rejection. Using advanced
multi-photon microscopy, the scientists have tracked the migration of immune cells called
T cells within tumours in experimental models, and found that the surface molecule (CD44)
directly impacts whether a tumour progresses or is rejected by T cells. Professor Wolfgang
Weninger, Head of the Immune Imaging program at Centenary, says this discovery advances
our knowledge of the immune processes at play in cancer. "The immune system and
cancer were first linked in the 1900s but it wasn't until the 1980s that interactions
between the immune system and cancer cells became a focus for medical researchers,"
says Professor Weninger. "We know that migration of T cells within tumours is very
important for rejection but we didn't know about how it worked. We found that this
particular molecule regulates the navigation of T cells in tumours. In its absence, T
cells are inhibited in migration and show a defect in their ability to reject a
tumour." Understanding how tumours avoid the natural processes of the immune system
is one of the biggest questions in cancer. Finding the answer could significantly improve
cancer treatment. Professor Weninger explains - "By understanding how the immune
system fights tumours, we may be able to optimise cancer therapies in the future. It may
provide the opportunity to design treatments that mimic certain aspects of immune
responses and cellular processes, making cancer treatments less hit and miss and reducing
the toll on patients."
Bone fractures can double or triple
mortality for up to 10 years
A new study shows that osteoporotic fractures increase a person’s risk of dying, even
after relatively minor fractures if that person is elderly. With hip fractures, there is
double the risk of death for women, three times the risk for men. The premature mortality
lasts for about 5 years post-fracture, except for hip fractures when it lasts for around
10 years. It then declines towards the background population level. If there’s a
subsequent fracture, mortality risk will rise again for the next 5 years. These facts
underline the importance of preventing and treating osteoporosis, a potentially
devastating condition that affects roughly 2 million Australians. Someone is admitted to
hospital with an osteoporotic fracture every 5-6 minutes, averaging 262 hospitalisations
each day.
Low-GI diet better than eating more
fibre if you have diabetes
Foods that release energy slowly, like nuts, beans and lentils, help people control
diabetes better than a diet rich in high-fibre foods like wholemeal bread and potatoes. In
a new study, eating a low-GI diet that gave a slow, steady supply of energy helped
diabetics have healthier blood sugar and cholesterol levels.
Bicarbonate from fruit and
vegetables may protect bones
Fruit and vegetables produce a chemical called bicarbonate when they're digested.
Researchers have found that bicarbonate supplements help people's bodies retain larger
amounts of calcium, which plays an important part in keeping bones healthy.
Considering Anemia when Treating
Rheumatoid Arthritis Patients
“Since anemia afflicts such a large proportion of patients with RA, it should be an
important consideration in clinical assessment and management,” stated Dr. Daniel
Furst, a rheumatologist and Professor at the UCLA David Geffen School of Medicine.
Researchers at the University of Minnesota found antibiotic residues in corn, potatoes,
green onions, cabbage and lettuce after only six weeks of greenhouse propagation with
manure from treated livestock says Environmental Health Service--much less time than the
typical growing season.
Losing weight can cure obstructive
sleep apnea in overweight patients
For sufferers of obstructive sleep apnea (OSA), a new study shows that losing weight is
perhaps the single most effective way to reduce OSA symptoms and associated disorders,
according to a new study in the American Journal of Respiratory and Critical Care
Medicine, one of the American Thoracic Society's three peer-reviewed journals. Weight loss
may not be a new miracle pill or a fancy high-tech treatment, but it is an exciting
therapy for sufferers of OSA both because of its short- and long-term effectiveness and
for its relatively modest price tag. Surgery doesn't last, continuous positive airway
pressure (CPAP) machines are only as effective as the patient's adherence, and most other
devices have had disappointing outcomes, in addition to being expensive, unwieldy and
having poor patient compliance. Furthermore, OSA is generally only treated when it has
progressed to a moderate to severe state. "Very low calorie diet (VLCD) combined with
active lifestyle counseling resulting in marked weight reduction is a feasible and
effective treatment for the majority of patients with mild OSA, and the achieved
beneficial outcomes are maintained at 1-year follow-up," wrote Henri P.I. Tuomilehto,
M.D., Ph.D., of the department of Otorhinolaryngology at the Kuopio University Hospital in
Finland. The prospective, randomized trial found that, in 81 patients with mild OSA, the
40 patients who were in the intervention arm underwent a diet that strictly limited
caloric intake combined with lifestyle counseling lost more than 20 pounds on average in a
year—and kept it off, resulting in markedly lower symptoms of OSA. The 41 patients in
the control arm, who only received lifestyle counseling and lost on average less than 6
pounds, and were much less likely to see improvements in their OSA.
Effects of smoking linked to
accelerated aging protein
A University of Iowa study is apparently the first to make a connection between a rare,
hereditary premature aging disease and cell damage that comes from smoking. The study
results point to possible therapeutic targets for smoking-related diseases. The
investigation found that a key protein that is lost in Werner's syndrome is decreased in
smokers with emphysema, and this decrease harms lung cells that normally heal wounds. The
findings appear in the Feb. 6 issue of the American Journal of Respiratory and Critical
Care Medicine. While people know that smoking is bad for health, not all the mechanisms by
which smoke damages the body are fully understood, said Toru Nyunoya, M.D., assistant
professor of internal medicine at the University of Iowa Carver College of Medicine and a
pulmonologist with University of Iowa Hospitals and Clinics. "Smoking can accelerate
the aging process and shorten the lifespan by an average of more than 10 years. We focused
on what happens within the lungs because of the similar aging effects, including
atherosclerotic diseases and cancer, seen in people with Werner's syndrome and people who
smoke," said Nyunoya, whose study was based in the lab of senior author Gary
Hunninghake, M.D., University of Iowa professor of internal medicine and a researcher with
the Iowa City Veterans Affairs Medical Center.
Scientists at Melbourne's Burnet Institute have developed a potential new treatment for
patients with prostate cancer. An article, which described the invention, has recently
been published in the prestigious international journal The Journal of Clinical
Investigation. Head of the Burnet Institute's Cancer Immunotherapy Laboratory, Associate
Professor Pei Xiang Xing said his group has produced a monoclonal antibody to a unique
tumour marker for the treatment of prostate cancer. The monoclonal antibody is directed at
cancer-producing cells carrying the specific molecule known as PIM-1, which is responsible
for cell survival, proliferation and differentiation. Over-expression of PIM-1 plays a
critical role in the development, progression and metastasis of prostate cancer and other
cancers such as leukaemia. The monoclonal antibody significantly inhibited cancer cell
growth when used in laboratory models of prostate cancer. Professor Xing's group
demonstrated that the monoclonal antibody binds to PIM-1 present in cancer cells and
creates a chain of events leading to the death of the cells. In particular, the
therapeutic effect was improved by combination of the antibody with other drugs currently
used to treat prostate cancer.
Maintaining Healthy Teeth and Gums
Is a Wise Investment
Faced with plummeting investments and an unsteady job market, many Americans are feeling
the effects of the recent economic crisis. In fact, a recent study by the American
Psychological Association found that over 80 percent of Americans rank money and the
economy as significant causes of stress. And while chronic stress can lead to a host of
health problems, including a weakened immune system and increased blood pressure, it can
also take its toll on periodontal health. If left untreated, periodontal disease may
result in even more serious, and potentially expensive, overall health complications.
It's not uncommon for students to consume energy drinks to increase their concentration as
they study throughout the night. "Energy drinks are the coffee of a new
generation," says Stéphanie Côté, nutritionist with Extenso, a Université de
Montréal health and nutrition think-tank. "These drinks are made up of sugar and
caffeine and can have a negative impact on health." According to a 2008 report by
Agriculture and Agri-Food Canada, 1.5 billion cans of Red Bull were sold in the United
States in 2004. Consumption in Canada is said to be comparable and it is a growing trend
for 18-to 24-year-olds. This market segment is broadening as younger children are
beginning to consume these drinks before doing physical activity. But these drinks aren't
recommended to either athletes or children under the age of 12. "Energy drinks don't
hydrate the body efficiently," says Côté. "Because they have too much sugar.
And caffeine doesn't necessarily improve physical performance. In high quantities it can
increase the risks of fatigue and dehydration." Several studies have demonstrated
that strong doses of caffeine can increase hypertension, cause heart palpitations, provoke
irritability and anxiety as well as cause headaches and insomnia. Health Canada does not
recommend consuming more than two cans per day.
GEN reports on strategies to
overcome blood-brain barrier
The blood-brain barrier (BBB) remains a major obstacle to the successful delivery of drugs
to treat central nervous system (CNS) disorders, reports Genetic Engineering and
Biotechnology News (GEN). Researchers are exploring a variety of approaches to preserve
the ability of the BBB to block harmful and toxic substances from entering the brain and
to permit the passage of effective medicines for the treatment of CNS diseases, according
to the February 1 issue of GEN (http://www.genengnews.com/articles/chitem.aspx?aid=2778).
"The blood-brain barrier issue probably serves as the most significant roadblock to
the treatment of central nervous system diseases," says John Sterling, Editor in
Chief of GEN. "The key challenge is to treat people suffering from CNS disorders
while trying to stay true to the physician's oath, 'First do no harm'." One
technology for enabling active transport of small molecule drugs across the BBB involves
targeting endogenous nutrient transporters. These transporters are members of the solute
carrier (SLC) transporter superfamily. Transport of small molecules across the BBB by
these membrane proteins is known as carrier-mediated transport (CMT). In order to design
drugs that utilize CMT to cross the BBB, researchers modify their chemical structures so
that they resemble nutrients that are transported across the BBB by specific SLCs. The
prototypical drug that uses this strategy (which was developed long before mechanisms of
CMT were known) is L-DOPA, the major current drug for Parkinson's disease. L-DOPA is used
to replace dopamine that is lost due to degeneration of dopaminergic neurons in the
substantia nigra of the brain.
Isolongifolenone, a natural compound found in the Tauroniro tree (Humiria balsamifera) of
South America, has been found to effectively deter biting of mosquitoes and to repel
ticks, both of which are known spreaders of diseases such as malaria, West Nile virus, and
Lyme disease. Derivatives of isolongifolenone have been widely and safely used as
fragrances in cosmetics, perfumes, deodorants, and paper products, and new processing
methods may make it as cheap to produce as DEET.
Georgia State researchers shed
light on fat burning
Researchers at Georgia State University have found that fat cells give feedback to the
brain in order to regulate fat burning much the same way a thermostat regulates
temperature inside a house. With an increase in obesity threatening the health and life
expectancies of people across the world, the research may help scientists better
understand how weight is shed. C. Kay Song and Tim Bartness of Georgia State, along with
Gary J. Schwartz of the Albert Einstein College of Medicine, found that during the process
of burning fat — called lipolysis — fat cells use sensory nerves to feed
information to the brain. Using viruses to trace communications in the nerves of Siberian
hamsters, they found that the brain uses part of the nervous system used to regulate body
functions, called the sympathetic nervous system, to in turn communicate back to the cells
to initiate, continue or stop the fat burning depending upon the information the brain
receives from the fat. "The brain can trigger lipid burning by fat cells and through
these sensory nerves, the fat cell can give the brain feedback," Bartness explained.
"This is a really important concept in biology, as it can regulate the process of
lipolysis much like how a thermostat regulates temperature in your house, using input from
the air and output to a furnace or heating unit. "The presence and function of the
sensory nerves has been completely ignored and the areas in the brain that receive this
sensory information were unknown until we did these studies," he said. When the body
has a low amount of a type of readily available fuel, a carbohydrate called glycogen, the
body starts lipolysis to release energy stored in fats. At the end nerves which are part
of the sympathetic nervous system, a chemical called norepinephrine is released to trigger
the breakdown of fat.
Columbia research shows novel
benefits of fatty acids in arteries
New research from Columbia University Medical Center continues to shed light on the
benefits of making fish a staple of any diet. Fish are generally rich in omega-3 fatty
acids, which have shown benefit in many health areas such as helping to prevent mental
illness and delaying some of the disabilities associated with aging. Eating tuna,
sardines, salmon and other so-called cold water fish appears to protect people against
clogged arteries. Omega-3 fatty acids can also lower triglycerides, a type of fat often
found in the bloodstream. Now, a CUMC research team led by Richard J. Deckelbaum, M.D.,
Director of the Columbia Institute of Human Nutrition, has found that a diet rich in fish
oils can prevent the accumulation of fat in the aorta, the main artery leaving the heart.
The beneficial actions of fish oil that block cholesterol buildup in arteries are even
found at high fat intakes. The study was conducted in three separate populations of mice:
one that was fed a balanced diet, one that was fed a diet resembling a "Western"
diet high in saturated fat, and a third that was fed a high fish fat diet rich in omega-3
fatty acids. Researchers in Dr. Deckelbaum's laboratory, including Chuchun Liz Chang, a
Ph.D. student in nutritional and metabolic biology, found that the fatty acids contained
in fish oil markedly inhibit the entry of "bad," or LDL, cholesterol into
arteries and, as a result, much less cholesterol collects in these vessels. They found
that this is related to the ability of those fatty acids to markedly decrease lipoprotein
lipase, a molecule that traps LDL in the arterial wall. This will likely prove to be
important as a new mechanism which helps explain benefits of omega-3 fatty acids on heart
health. Dr. Deckelbaum advises those interested in increasing omega-3 intakes do so by
either increasing fish intake or by using supplements that contain the
"long-chain" fatty acids, EPA and DHA, which are found in cold water fish.
UCSB scientists make headway in
understanding Alzheimer's disease
Scientists at UC Santa Barbara have discovered that a protein called BAG2 is important for
understanding Alzheimer's disease and may open up new targets for drug discovery. They are
ready to move from studying these proteins in culture to finding out how they work with
mice. In a paper published this week in the Journal of Neuroscience, the scientists
describe important activities of BAG2 in cleaning up brain cells. The protein tau is
normally found in brain cells, but scientists don't know why it clumps into tangles in
people with Alzheimer's disease. Senior author Kenneth S. Kosik, co-director of UCSB's
Neuroscience Research Institute, and Harriman Chair in Neuroscience, has been involved in
the study of neurons that develop neurofibrillary tangles, one of the hallmarks of the
disease, since he was a postdoctoral fellow. "Early on in my career, we were one of
several labs to discover that tau was in the neurofibrillary tangles," said Kosik.
Kosik's team recently started to work on BAG2 to find out how it may be involved in the
removal of tangled tau. "It turns out that when you put this protein into the cell,
it clears away the damaged tau very nicely," said Kosik. It doesn't clear away all
the tau; it goes for the damaged tau protein and removes it.
A team of Danish medical researchers has published a paper arguing that women are not
being properly informed about the potential harms of breast cancer screening.
More and more research is uncovering the beneficial qualities of fatty or oily fish as a
healthy food. A recent study in Sweden has added to this databank of knowledge, having
found that Swedish women who consumed such fish at least once every week had a markedly
lower risk of developing kidney cancer, as compared to those who did not eat fish or who
ate lean fish.
FDA Warns Risk of Muscle Injury
Linked to Simvastatin
The FDA has issued a warning that the popular cholesterol-lowering drug simvastatin, when
mixed with the anti-arrhythmia drug amiodarone, can cause a rare muscle injury that can
lead to kidney failure or even death.
It is found that mixture of Honey and Cinnamon can be used in helping to remove the
symptoms of the various diseases. Honey is produced in most of the countries of the world.
Ayurvedic as well as Yunani medicine have been using honey as a vital medicine for
centuries. Scientists of today also accept honey as a "Ram Ban" (very effective)
medicine for all kinds of diseases. Honey can be used without any side effects for any
kind of diseases. Today's science says that even though honey is sweet, if taken in the
right dosage as a medicine, it does not harm diabetic patients. A famous magazine named
Weekly World News published in Canada dated 17 January, 95 has given a list of diseases
that can be cured by Honey and Cinnamon as researched by western scientists.
Ashley was an active, healthy teenager. Since receiving the Gardasil vaccine to prevent
cervical cancer, however, Ashley has suffered seizures, headaches, nausea, dizziness and
paralysis.
