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Week 43
Elderly immune system needs a boost
Elderly cancer patients need a combination of treatments tailor-made to their specific
needs to successfully combat the disease. The challenge is to boost their immune response
to cancer vaccines, because like the rest of our organs, our immune system ages and
gradually becomes less efficient as we get older. Dr. Joseph Lustgarten, from the Mayo
Clinic College of Medicine in the US, reviews the effects of aging on the immune system
and strategies used to activate a stronger antitumor immune response in the elderly,
including genetic modifications in animal models. His findings1 have just been published
in the latest issue of Springer’s journal Cancer Immunology, Immunotherapy.
Reversing Brain Drain
A battered U.S. economy has sent many of the country's leading minds packing for
"greener" shores. America is losing thousands of top scientists, academics and
biotech executives to cities like Singapore, which offer more lucrative salaries. Now, an
Israeli specialist is sharing a proven formula for wooing the expatriates back home. It
worked in Israel, and he says it could rebuild America's innovation edge as well.
Medication effective for acute
liver failure in early stages of disease
The antidote for acute liver failure caused by acetaminophen poisoning also can treat
acute liver failure due to most other causes if given before severe injury occurs, UT
Southwestern Medical Center researchers and their colleagues at 21 other institutions have
found. Acute liver failure occurs when cells in the liver die quickly, resulting in toxins
being released into the bloodstream and brain. Patients often end up in a hepatic coma as
a result of toxins not being cleared by the failing liver. Known causes of acute liver
failure include autoimmune hepatitis, drug-induced liver injury, hepatitis A and B, and
acetaminophen poisoning. In a study published in the September issue of Gastroenterology,
researchers found that acute liver failure patients in early stages of hepatic comas, when
treated with the medicine N-acetylcysteine (NAC), were nearly 2.5 times more likely to
survive than those treated only with a placebo.
OU Part of International Study on
Genetic Impact of Radiation
Researchers at the University of Oklahoma Health Sciences Center are helping to lead a
massive international study on the possible genetic effects of radiation and cancer drug
exposures on future generations. The study’s principal investigators are meeting this
week at the OU Health Sciences Center to discuss their recent findings, which will be
presented at an upcoming meeting of the American Society of Human Genetics. The study,
which combines cancer survivors in the United States and Scandinavia, is looking at
potential genetic consequences of reproductive organs exposed to curative therapy by drugs
or radiation. Scientists want to determine whether radiation and chemotherapy before
conception increases the occurrence of birth defects, stillbirths and specific conditions
such as Down syndrome. They also want to know if radiation treatment leads to cancer or
DNA damage in the patients’ offspring. It is the first and largest study of its kind.
In Denmark and Finland, researchers have been able to identify all cancer survivors since
1943 and 1952, respectively, who had cancer before age 35. They also documented the nearly
20,000 children produced by the survivors. Scientists now want to compare their findings
with patients in the United States.
Countries slow to use lifesaving
diarrhea treatments for children
Despite evidence that low-cost diarrhea treatments such as lower osmolarity oral
rehydration salts (ORS) and zinc supplements could drastically reduce the number of deaths
among children, little progress has been made in implementing these life-saving
techniques, according to researchers at the Johns Hopkins Bloomberg School of Public
Health. They examined the implementation of current treatment guidelines and found that
few countries are equipped to quickly adapt policies, and many struggle to develop and
maintain the recommended supplies. The analysis is featured in the October issue of
Bulletin of the World Health Organization. "Low osmolarity ORS and zinc are
inexpensive, safe and easy to use and have the potential to dramatically lower diarrhea
morbidity and mortality," said Robert Black, MD, MPH, co-author of the article, chair
and Edgar Berman Professor of International Health at the Bloomberg School. "Many
countries have changed diarrhea management policies to include low osmolarity ORS and
zinc, but there is a significant gap between policy change and effective program
implementation, leaving few children treated appropriately. In many countries, adopting
child health policies is complex and the registration and importation of zinc supplements
requires input from drug regulatory agencies and procurement officials, making it
difficult to secure these necessary supplies." Diarrhea remains the second leading
cause of death among children globally, accounting for 18 percent of childhood deaths and
13 percent of all disability-adjusted life years. In 2004 the World Health Organization
(WHO) and UNICEF released a joint statement recommending countries switch to a lower
osmolarity formulation ORS and introduce zinc supplements for 10 to 14 days to decrease
diarrhea deaths among children. The recommendation came after scientific consensus that
this treatment has the potential to reduce more than three quarters of all diarrhea
associated deaths. Large scale programs in Bangladesh and India have demonstrated that
together they can decrease unnecessary use of antibiotics and reinvigorate community
management of diarrhea while keeping costs low and saving lives.
Last time carbon dioxide levels
were this high - 15 million years ago, scientists report
You would have to go back at least 15 million years to find carbon dioxide levels on Earth
as high as they are today, a UCLA scientist and colleagues report Oct. 8 in the online
edition of the journal Science. "The last time carbon dioxide levels were apparently
as high as they are today — and were sustained at those levels — global
temperatures were 5 to 10 degrees Fahrenheit higher than they are today, the sea level was
approximately 75 to 120 feet higher than today, there was no permanent sea ice cap in the
Arctic and very little ice on Antarctica and Greenland," said the paper's lead
author, Aradhna Tripati, a UCLA assistant professor in the department of Earth and space
sciences and the department of atmospheric and oceanic sciences. "Carbon dioxide is a
potent greenhouse gas, and geological observations that we now have for the last 20
million years lend strong support to the idea that carbon dioxide is an important agent
for driving climate change throughout Earth's history," she said. By analyzing the
chemistry of bubbles of ancient air trapped in Antarctic ice, scientists have been able to
determine the composition of Earth's atmosphere going back as far as 800,000 years, and
they have developed a good understanding of how carbon dioxide levels have varied in the
atmosphere since that time. But there has been little agreement before this study on how
to reconstruct carbon dioxide levels prior to 800,000 years ago. Tripati, before joining
UCLA's faculty, was part of a research team at England's University of Cambridge that
developed a new technique to assess carbon dioxide levels in the much more distant past
— by studying the ratio of the chemical element boron to calcium in the shells of
ancient single-celled marine algae. Tripati has now used this method to determine the
amount of carbon dioxide in Earth's atmosphere as far back as 20 million years ago.
"We are able, for the first time, to accurately reproduce the ice-core record for the
last 800,000 years — the record of atmospheric C02 based on measurements of carbon
dioxide in gas bubbles in ice," Tripati said. "This suggests that the technique
we are using is valid.
Gluten-free diet reduces bone
problems in children with celiac disease
Celiac disease (CD) is an inherited intestinal disorder characterized by life-long
intolerance to the ingestion of gluten, a protein found in wheat, rye, and barley.
Although CD can be diagnosed at any age, it commonly occurs during early childhood
(between 9 and 24 months). Reduced bone mineral density is often found in individuals with
CD. A new article in the journal Nutrition Reviews examines the literature on the topic
and reveals that a gluten-free diet can affect children's recoveryMetabolic bone disease
remains a significant and common complication of CD. Reduced bone mineral density can lead
to the inability to develop optimal bone mass in children and the loss of bone in adults,
both of which increase the risk of osteoporosis. There also exists an additional risk of
fracture in people with CD. However, evidence suggests that a gluten-free diet (GFD)
promotes a rapid increase in bone mineral density that leads to complete recovery of bone
mineralization in children. A GFD improves, although rarely normalizes, bone mineral
density in adults. Children may attain normal peak bone mass if the diagnosis is made and
treatment is given before puberty, thereby preventing osteoporosis in later life. Also,
nutritional supplements consisting of calcium and vitamin D seem to increase the bone
mineral density of children and adolescents with CD. "Our findings reinforce the
importance of a strict gluten-free diet, which remains the only scientific proven
treatment for celiac disease to date," the authors conclude. "Early diagnosis
and therapy are critical in preventing celiac disease complications, like reduced bone
mineral density."
Exercise improves body image for
fit and unfit alike
Attention weekend warriors - the simple act of exercise and not fitness itself can
convince you that you look better, a new University of Florida study finds.People who
don't achieve workout milestones such as losing fat, gaining strength or boosting
cardiovascular fitness feel just as good about their bodies as their more athletic
counterparts, said Heather Hausenblas, a UF exercise psychologist. Her study is published
in the September issue of the Journal of Health Psychology."You would think that if
you become more fit that you would experience greater improvements in terms of body image,
but that's not what we found," she said. "It may be that the requirements to
receive the psychological benefits of exercise, including those relating to body image,
differ substantially from the physical benefits." The study by Hausenblas and
graduate student Anna Campbell is the first to systematically analyze the wide-ranging
effects of exercise on body image by examining all intervention studies on the subject
until June 2008. From the 57 publications, the researchers found conclusively that
exercise buffed up the way people see their bodies regardless of the actual benefits, but
the results varied. Negative body image has grown to almost epidemic proportions in the
past 20 years, with as many as 60 percent of adults in national studies saying they don't
like the way their bodies look, Hausenblas said. Americans spend billions of dollars a
year for products designed to change their body size and shape, including diet pills and
various cosmetic procedures, she said. "Body dissatisfaction is a huge problem in our
society and is related to all sorts of negative behavior including yo-yo dieting, smoking,
taking steroids and undergoing cosmetic surgery," she said. "It affects men and
women and all ages, starting with kids who are as young as five years old saying they
don't like how their bodies look."
Toward better solar cells -
Chemists gain control of light-harvesting paths
University of Florida chemists have pioneered a method to tease out promising molecular
structures for capturing energy, a step that could speed the development of more
efficient, cheaper solar cells.“This gives us a new way of studying light-matter
interactions,” said Valeria Kleiman, a UF associate professor of chemistry. “It
enables us to study not just how the molecule reacts, but actually to change how it
reacts, so we can test different energy transfer pathways and find the most efficient
one.” Kleiman is the principal investigator in the research featured in a paper set
to appear Friday in the journal Science. Her work focuses on molecules known as dendrimers
whose many branching units make them good energy absorbers. The amount of energy the
synthetic molecules can amass and transfer depends on which path the energy takes as it
moves through the molecule. Kleiman and three co-authors are the first to gain control of
this process in real time. The team demonstrated that it could use phased tailored laser
pulses — light whose constituent colors travel at different speeds — to prompt
the energy to travel down different paths. “What we see is that we control where the
energy goes by encoding different information in the excitation pulses,” Kleiman
said.
Simple tool can boost motivation,
improve health in older adults
Researchers from Boston University School of Medicine (BUSM) have identified a tool, the
"Getting-Out-of-Bed (GoB) measure" to assess motivation and life outlook in
older adults. The study, which appears in the October issue of the Journal of Psychosocial
Oncology, shows that the tool has the potential to be an easy-to-use measure to bolster
motivation and thus, improve health behaviors and outcomes in the growing population of
older adults. The demographics of aging in the United States continues to change
dramatically. In 2006, 37 million Americans, 12 percent of the population were 65 years or
older. By 2030, those 65 years and older are projected to number 71.5 million representing
nearly 20 percent of the US population. Furthermore, between 1992 and 2004 average
inflation-adjusted health care costs for older Americans increased from $8,644 to $13,052
and are expected to continue to rise considerably. According to the researchers, such
numbers underscore the importance of understanding common diseases and health behaviors of
older adults, because many conditions can be prevented and/or modified with behavioral
interventions. "Motivation and life outlook play an important part in an older
adult's ability to recover from illness or disabling events and to maintain and/or adopt
health-promoting behaviors," said lead author Kerri Clough-Gorr, DSc, MPH, from the
Section of Geriatrics at BUSM. The researchers conducted telephone interviews on a sample
of 660 women with breast cancer from four geographic regions of the country at three and
six months intervals. Motivation and life outlook was assessed using GoB questions. Women
with GoB scores ?50 (representing higher motivation) at baseline were statistically
significantly more likely at 6 months to have good health-related quality of life, good
self-perceived health and report regular exercise than those with scores <50, indicating good predictive ability.
Scans show learning 'sculpts' the
brain's connections
Spontaneous brain activity formerly thought to be "white noise" measurably
changes after a person learns a new task, researchers at Washington University School of
Medicine in St. Louis and the University of Chieti, Italy, have shown. Scientists also
report that the degree of change reflects how well subjects have learned to perform the
task. Their study is published online this week in the Proceedings of the National Academy
of Sciences. "Recent studies have shown that in the absence of any overt behavior,
and even during sleep or anesthesia, the brain's spontaneous activity is not random, but
organized in patterns of correlated activity that occur in anatomically and functionally
connected regions," says senior author Maurizio Corbetta, M.D., Norman J. Stupp
Professor of Neurology. "The reasons behind the spontaneous activity patterns remain
mysterious, but we have now shown that learning causes small changes in those patterns,
and that these changes are behaviorally important." At the start of the experiment,
Corbetta, graduate students Chris Lewis and Antonello Baldassarre and their colleagues in
Italy used functional connectivity magnetic resonance imaging to scan the spontaneous
brain activity of 14 volunteers as they sat quietly. Next, researchers scanned the
subjects as they spent one to two hours a day for five to seven days learning to watch a
display inside the MRI scanner for the brief presence of an inverted "T" in a
specific part of the screen. Two sets of brain areas were particularly active during the
task: part of the visual cortex that corresponded to the portion of the visual field where
subjects were looking for the "T", and areas in the dorsal part of the brain
involved in directing attention to the location on the screen.
Developing enzymes to clean up
pollution by explosives
Scientists at the University of York have uncovered the structure of an unusual enzyme
which can be used to reverse the contamination of land by explosives. The discovery, by
scientists in the York Structural Biology Laboratory and the Centre for Novel Agricultural
Products, will support the development of plants that can help tackle pollution caused by
royal demolition explosive, also known as RDX.
Amyotrophic lateral sclerosis may
involve a form of sudden, rapid aging of the immune system
Premature aging of the immune system appears to play a role in the development of
amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease, according to research
scientists from the Maxine Dunitz Neurosurgical Institute at Cedars-Sinai Medical Center,
the Weizmann Institute of Science in Israel, and Sheba Medical Center in Israel. A study
published in the Journal of Cellular and Molecular Medicine shows that CD4+ T cells, which
grow and mature in the thymus before entering the bloodstream, are reduced in number in
patients who have ALS as the thymus shrinks and malfunctions. Theoretically, devising
therapies to support or replace these cells could be a strategy in treating the disease.
The research was led by Michal Schwartz, Ph.D., a visiting professor at the Center of
Neuroimmunology and Neurogenesis in the Department of Neurosurgery at Cedars-Sinai and
professor of neuroimmunology at the Weizmann Institute in Rehovot, Israel. The findings
are consistent with evidence collected over a decade by Schwartz's group suggesting that a
well-functioning immune system plays a pivotal role in maintaining, protecting and
repairing cells of the central nervous system. Studies conducted in animals have shown
that boosting immune T-cell levels may reduce symptoms and slow progression of certain
neurodegenerative diseases. Results from the current study suggest that premature aging of
the immune system and thus a decrease in protection from immune T cells could contribute
to the aggressive and rapid progression of amyotrophic lateral sclerosis, which attacks
motor neurons – nerve cells responsible for muscle strength and voluntary movements.
The researchers found that thymic malfunction occurs simultaneously with motor neuron
dysfunction, both in laboratory mice bred to mimic amyotrophic lateral sclerosis and in
humans suffering from the disease.
Lessons learned from H1N1 virus
pandemic
A comprehensive study has revealed, for the first time, the impact of swine flu on the
health of the general public in Australia and New Zealand. The lessons learned in
Intensive Care Units (ICUs) across the two countries on the impact of the H1N1 (swine flu)
virus are being shared with countries in the Northern Hemisphere to help them prepare for
their upcoming flu season. The three-month study, conducted at the height of the pandemic
between June and August, reveals that 722 patients were admitted to ICUs and that at the
peak of the epidemic up to 20 per cent of ICU beds were occupied by patients with swine
flu infection. The study was co-coordinated by the Monash University-based Australian and
New Zealand Intensive Care Research Centre (ANZIC-RC). The study involved all ICUs in
Australia and New Zealand with the affected patients being treated in 109 of these units.
The study was conducted utilising the resources of the Australian and New Zealand
Intensive Care Society Clinical Trials Group (ANZICS CTG). Dr Ian Seppelt, a specialist in
Intensive Care Medicine and based at Sydney's Nepean Hospital, said the impact of the
virus on ICUs across Australia and New Zealand was dramatic. "Intensive Care Units
specialise in the management of patients with life-threatening illness and the surge of
patients with H1N1 placed substantial strain on staff and resources. The most severely
affected patients had pneumonia affecting both lungs that was caused by the virus. The
number of patients admitted to ICUs with this complication represented a 600 per cent
increase compared to previous years," Dr Seppelt said.
Increased levels of
Muellerian-inhibiting substance could mean greater breast cancer risk
Women with increased levels of Müllerian inhibiting substance (MIS), best known for
regulating in utero sexual differentiation in boys, may be at a greater risk for breast
cancer, according to a new study published online October 9 in the . To determine whether
MIS levels were associated with breast cancer risk, Joanne F. Dorgan, Ph.D., MPH, of the
Fox Chase Cancer Center in Philadelphia, and colleagues conducted a prospective
case-control study of 309 participants who were registered in the Columbia, Missouri Serum
Bank. Blood samples were donated by women with in situ or invasive breast cancer who, at
the time of donation, were free of cancer. Each of 105 breast cancer patients was matched
to two control subjects. MIS was measured in serum using an enzyme-linked immunosorbent
assay. Researchers found that increasing MIS serum concentrations were associated with
increased breast cancer risk in this population. "Additional research is needed,
including confirmatory epidemiological studies on the association of serum MIS with breast
cancer and studies aimed at identifying the biological mechanism underlying the
association," the authors write.
Researchers identify mechanism that
helps bacteria avoid destruction in cells
Infectious diseases currently cause about one-third of all human deaths worldwide, more
than all forms of cancer combined. Advances in cell biology and microbial genetics have
greatly enhanced understanding of the cause and mechanisms of infectious diseases.
Researchers from Thomas Jefferson University, the Pasteur Institute in Paris, and Yale
University reported in PLoS ONE, a way in which intracellular pathogens exploit the
biological attributes of their hosts in order to escape destruction.Intracellular
pathogens include Chlamydia, which causes infertility in women, and Legionella, which
causes Legionnaire's disease. These pathogens are able to escape destruction and remain in
the cells. Until now, it was unclear how they were able avoid the destruction process. The
team of researchers, led by Fabienne Paumet, Ph.D., assistant professor of Microbiology
and Immunology at Jefferson Medical College of Thomas Jefferson University, found that it
appears to be due to SNARE-like proteins expressed by the pathogen. SNARE proteins are
necessary for eukaryotic cells to fuse to their intracellular compartments. These
proteins, which are present on the surface of almost all intracellular compartments,
interact to form a stable complex, triggering fusion of the membranes. Intracellular
pathogens, like Chlamydia and Legionella, must contend with vesicular trafficking and
membrane fusion in the host cell. But they manage to bypass the lysosome, where other
pathogens would normally be destroyed. The researchers tested the hypothesis that
SNARE-like proteins expressed by the bacteria themselves were capable to interact with the
eukaryotic SNAREs and alter membrane fusion to their advantage. The Chlamydia bacteria
expressed a SNARE-like protein called IncA and the Legionella expressed a SNARE-like
protein called IcmG/DotF, both of which inhibit SNARE-protein-mediated fusion.
Receptor activated exclusively by
glutamate discovered on tongue
One hundred years ago, Kikunae Ikeda discovered the flavour-giving properties of
glutamate, a non essential amino acid traditionally used to enhance the taste of many
fermented or ripe foods, such as ripe tomatoes or cheese. New research now reveals that
the tongue has a receptor that is exclusively activated by glutamate. "Although other
receptors have been found on the tongue that are also aroused by glutamate, they are not
specific. That is, they need to be in contact with nucleotides and many other amino acids
to be activated. Our study reveals the first receptor on the tongue exclusively for
glutamate," Ana San Gabriel, the main author of the article and a scientist belonging
to the Spanish Network of Researchers Abroad, based at the Institute of Life Sciences in
Ajinomoto, Kawasaki (Japan), explained to SINC. According to the study, which was
published in the latest issue of the American Journal of Clinical Nutrition, glutamate is
a non essential amino acid that is used commercially as glutamate sodium salt, monosodium
glutamate (MSG) E-621, because it is stable and easy to dissolve. This added glutamate,
identical to the 'natural glutamate', is sometimes used to reduce cooking and meal
preparation time and to provide more flavour. MSG is also used to reduce the sodium in
meals: table salt contains 40% sodium, whereas MSG contains 13%. Many fermented or ripe
foods are rich in natural MSG, such as ripe tomatoes (250-300 mg/100g), parmesan cheese
(1600 mg/100g), Roquefort cheese (1600 mg/100g) and Gouda cheese (580 mg/100g). Manchego
cheese and Iberian cured ham have a similar taste.
Rising sea levels are increasing
the risk of flooding along the south coast of England
A new study by researchers at the University of Southampton has found that sea levels have
been rising across the south coast of England over the past century, substantially
increasing the risk of flooding during storms.The team has conducted a major data
collection exercise, bringing together computer and paper-based records from across the
south of England, from the Scilly Isles to Sheerness, to form a single data set of south
coast sea levels across the years. Their work has added collectively about 150 years worth
of historic data to the existing record of English Channel sea-level change and extended
the data along the south coast. Their findings are published in the latest edition of the
journal Continental Shelf Research. The data shows that both average sea levels and
extreme sea levels have been rising at a similar rate through the 20th Century. The rate
of rise is in the range 1.2 to 2.2 mm per year, with 1.3 mm per year recorded at
Southampton.
Suppressing a gene in mice prevents
heart from aging, preserves its function
Scientists prevented age-related changes in the hearts of mice and preserved heart
function by suppressing a form of the PI3K gene, in a study reported in Circulation:
Journal of the American Heart Association. “The study provides evidence that delaying
or preventing heart failure in humans may be possible,” said Tetsuo Shioi, M.D.,
Ph.D., senior author of the study and assistant professor of medicine at Kyoto University
Graduate School of Medicine in Kyoto, Japan. “Advanced age is a major risk factor for
heart failure. One reason is that aging increases the chance of exposure to cardiovascular
risk factors. However, natural changes due to aging may also compromise the cardiovascular
system.” According to the American Heart Association, 5.7 million Americans have
heart failure, and nearly 10 out of every 1,000 people over age 65 suffer heart failure
every year.
Scientists encouraged by new mouse
model's similarities to human ALS
A new mouse model of amyotrophic lateral sclerosis (ALS) closely resembles humans with the
paralyzing disorder, researchers at Washington University School of Medicine in St. Louis
report. Like humans with ALS, the new genetically engineered mouse develops progressive
paralysis; loses muscle mass and specific types of motor neurons, which are nerve cells
that control muscles; and dies of the disorder, which is currently fatal in humans.
"As far as we know, this is the first mouse model that recapitulates 'typical' ALS to
be produced in more than a decade," says senior author Robert Baloh, M.D., Ph.D.,
assistant professor of neurology. "That could make it very helpful for our efforts to
better understand and identify treatments for this terrible disorder." Scientists
report the details of the new mouse model online this week in Proceedings of the National
Academy of Sciences. Baloh's work with the mice was made possible in part by the Hope
Center for Neurological Disorders, a collaboration between the School of Medicine and Hope
Happens, a non-profit foundation that raises funds for research into neurodegenerative
disorders such as ALS. The foundation was established by Christopher Hobler, a St. Louisan
who died of ALS, and his family. The mouse model has a point mutation or single letter of
erroneous DNA code in the gene for a protein called TDP-43. Researchers at the University
of Pennsylvania linked TDP-43 to inherited forms of ALS in 2006. Washington University
scientists Nigel Cairns, Ph.D., and Alison Goate, Ph.D., sequenced a point mutation in the
TDP-43 gene of a St. Louis family with an inherited form of ALS, and Baloh's lab created a
mouse line with the family's mutation. "Ten percent of all ALS cases are inherited,
but only a small portion of the known inherited forms of the disorder are clinically
indistinguishable from sporadic ALS," Baloh says. "TDP-43 is only the second
gene to be linked to an inherited form of ALS that appears clinically identical to
sporadic ALS, and it's very promising that this similarity allows the symptoms of sporadic
ALS to be accurately modeled in mice."
Rochester-led Parkinson's study
pays off again, 2 decades later
Parkinson disease progresses more slowly in patients who have higher levels of urate, a
chemical that at very high level is associated with gout, scientists have found. While
it's unknown whether the high levels actually somehow protect patients or simply serve as
a marker of protection, the finding supports the idea that patients and doctors may one
day be able to better predict the course of the illness. The study, led by scientists at
Massachusetts General Hospital and the Harvard School of Public Health and including
physicians at the University of Rochester Medical Center, was published online in the
Archives of Neurology. The new findings are based on biological samples, primarily blood
and cerebrospinal fluid, collected from people with Parkinson disease who participated in
a landmark study known as DATATOP, which was conducted two decades ago. DATATOP, conceived
and led by Rochester neurologist Ira Shoulson, M.D., is best known for shifting the
landscape of neurology clinical research. Shoulson convinced dozens of investigators
around the world to work together, pooling their resources to ask questions about
potential new treatments for the disease – big questions that could be answered only
with participation by hundreds of people with the disease. Beginning in 1987, Shoulson and
colleagues studied 800 people with Parkinson disease, looking at whether the drug deprenyl
(selegiline), vitamin E, or a combination might slow the progression of the disease. The
answer was a definitive "no" for vitamin E, while deprenyl provided patients
with some relief.But the scale and scope of the study proved to be useful beyond the
specific questions it was designed to answer. The mountain of information collected on the
800 participants over eight years provided one of the great repositories of data about
Parkinson disease ever assembled: thousands of blood, urine, and cerebrospinal fluid
samples, as well as notes from more than 16,000 physical examinations of patients by
doctors and nurses. The data was central to the new study, which was led by Michael A.
Schwarzschild, M.D., Ph.D., of Massachusetts General Hospital, and Alberto Ascherio, M.D.
of the Harvard School of Public Health, who have been studying a possible role for urate
in protecting patients against the effects of Parkinson disease. They found that the
disease progressed more slowly in participants with the highest levels of urate than in
people with the lowest levels.
Most H1N1 patients with respiratory
failure treated with oxygenating system survive illness
Despite the severity of disease and the intensity of treatment, most patients in Australia
and New Zealand who experienced respiratory failure as a result of 2009 influenza A(H1N1)
and were treated with a system that adds oxygen to the patient's blood survived the
disease, according to a study to appear in the November 4 issue of JAMA. This study is
being published early online because of its public health importance.The influenza A(H1N1)
pandemic affected Australia and New Zealand during the 2009 southern hemisphere winter,
causing an epidemic of critical illness. Some patients developed severe acute respiratory
distress syndrome (ARDS) and were treated with extracorporeal membrane oxygenation (ECMO),
according to background information in the article. ARDS is a lung condition that leads to
respiratory failure due to the rapid accumulation of fluid in the lungs. ECMO is a type of
life support that circulates blood through a system that adds oxygen. ECMO was used for
the patients in this study because they developed very low blood oxygen levels that
developed rapidly despite standard ventilator (or respirator) settings. ECMO is generally
used for a limited time because of the risks of bleeding, clotting, infection, and organ
failure. The Australia and New Zealand Extracorporeal Membrane Oxygenation (ANZ ECMO)
Influenza Investigators in collaboration with the Australian and New Zealand Intensive
Care Research Centre at Monash University in Melbourne, conducted an observational study
of patients with 2009 influenza A(H1N1)-associated ARDS treated with ECMO in 15 intensive
care units (ICUs) in Australia and New Zealand between June 1 and August 31, 2009. The
researchers looked at incidence, clinical features, the degree of lung dysfunction,
technical characteristics, the duration of ECMO, complications, and survival. The study
found that 68 patients with severe influenza-associated ARDS were treated with ECMO,
including 53 with confirmed 2009 influenza A(H1N1). An additional 133 patients with
influenza A received mechanical ventilation, but not ECMO, in the same ICUs. The 68
patients who received ECMO had a median (midpoint) age of 34.4 years and half were men.
Breast tenderness during hormone
replacement therapy linked to elevated cancer risk
Women who developed new-onset breast tenderness after starting estrogen plus progestin
hormone replacement therapy were at significantly higher risk for developing breast cancer
than women on the combination therapy who didn't experience such tenderness, according to
a new UCLA study. The research, published in the Oct. 12 issue of the Archives of Internal
Medicine, is based on data from more than 16,000 participants in the Women's Health
Initiative estrogen-plus- progestin clinical trial. This trial was abruptly halted in July
2002 when researchers found that healthy menopausal women on the combination therapy had
an elevated risk for invasive breast cancer. Researchers do not know why breast tenderness
indicates increased cancer risk among women on the combination therapy, said the new
study's lead researcher, Dr. Carolyn J. Crandall, a clinical professor of general internal
medicine and health services research at the David Geffen School of Medicine at UCLA.
"Is it because the hormone therapy is causing breast-tissue cells to multiply more
rapidly, which causes breast tenderness and at the same time indicates increased cancer
risk? We need to figure out what makes certain women more susceptible to developing breast
tenderness during hormone therapy than other women," Crandall said.This study
compared the daily use of oral conjugated equine estrogens (0.625 mg) plus
medroxyprogesterone acetate (2.5 mg), or CEE+MPA, with the daily use of a placebo pill. Of
the participants in the trial, 8,506 took estrogen plus progestin and 8,102 were given
placebos. Participants underwent mammography and clinical breast exams at the start of the
trial and annually thereafter. Self-reported breast tenderness was assessed at the
beginning of the trial and one year later, and invasive breast cancer over the next 5.6
years was confirmed by medical record review.
Gene mingling increases sudden
death risk
A multi-national research team has discovered that two genetic factors converge to
increase the risk of sudden cardiac death. The investigators – from the United
States, Italy and South Africa – report in the journal Circulation that variations in
the gene NOS1AP increase the risk of cardiac symptoms and sudden death in patients who
have an inherited cardiac disease called congenital long-QT syndrome.The findings will
help in assessing the risk of sudden death – and assigning therapy – in patients
with this syndrome, said senior author Alfred George Jr., M.D., director of the Division
of Genetic Medicine at Vanderbilt University Medical Center. Congenital long-QT syndrome
affects the electrical activity of the heart ("QT" refers to a time measure on
the electrocardiogram – it is longer than normal in patients with the syndrome).
Long-QT syndrome makes patients susceptible to potentially fatal disorders of heart
rhythm. It is a known cause of sudden death, especially in young adults and children, and
has recently been estimated to affect about one in 2,200 individuals. But not all people
who have gene mutations that cause congenital long-QT syndrome have symptoms (fainting,
cardiac arrest, sudden death). The big question mark, George said, is how to manage a
patient who has a long-QT gene mutation, but doesn't have any symptoms. "The concern
of course is that the first symptom could be sudden death," he said. "And
everything needs to be done to try to prevent that. "But does every mutation carrier
need an implantable defibrillator? Pharmacological therapies? Or should they just be
watched?"The variability in symptoms suggests that other factors play a role –
either to promote or prevent symptoms.
Study supports possible role of
urate in slowing Parkinson's disease progression
By examining data from a 20-year-old clinical trial, a research team based at the
MassGeneral Institute for Neurodegenerative Diseases (MGH-MIND) and Harvard School of
Public Health (HSPH), has found evidence supporting the findings of their 2008 study
– that elevated levels of the antioxidant urate may slow the progression of
Parkinson's disease. The report – which will appear in the December 2009 Archives of
Neurology and has been released online – analyzed blood and cerebrospinal fluid
samples from participants in a 1980s trail of potential Parkinson's medications,
confirming the previous study's findings in a totally different group of patients.
"These results were critically important. Only now we can be reasonably sure that the
slower rate of progression in patients with higher concentrations of urate is real and not
a chance occurrence," says Alberto Ascherio, MD, DrPh, of HSPH, the new study's lead
author. Parkinson's disease – characterized by tremors, rigidity, difficulty walking
and other symptoms – is caused by destruction of brain cells that produce the
neurotransmitter dopamine. The 2008 study, which investigated the observation that healthy
people with elevated but still normal urate levels have a reduced risk of developing
Parkinson's, found an association between higher blood urate levels and slower disease
progression in 800 participants from a previous clinical trial. To follow up that finding,
the current study reviewed information from a much earlier trial that had investigated
whether the drug deprenyl, now an established treatment for Parkinson's, or doses of
vitamin E would slow disease progression. The researchers analyzed samples of both blood
and cerebrospinal fluid from 800 participants in the DATATOP study, conducted by the
Parkinson's Study Group at centers across the U.S. and Canada, to find any association of
urate levels with how quickly recently diagnosed patients progressed to the point where
they needed to begin standard drug therapy. Confirming the results of the 2008 study, they
found that participants with the highest blood urate levels had a 36 percent less chance
of needing to begin treatment during the two-year study period than did those with the
lowest urate levels. Similar results were seen for urate levels in the cerebrospinal
fluid. Also echoing last year's results, the association of urate levels with risk was
robust in men but less clear in women, which may reflect the fact that few women have the
high natural urate levels associated with risk reduction.
Children can greatly reduce
abdominal pain by using their imagination
Children with functional abdominal pain who used audio recordings of guided imagery at
home in addition to standard medical treatment were almost three times as likely to
improve their pain problem, compared to children who received standard treatment alone.
And those benefits were maintained six months after treatment ended, a new study by
University of North Carolina at Chapel Hill and Duke University Medical Center researchers
has found. The study is published in the November 2009 issue of the journal Pediatrics.
The lead author is Miranda van Tilburg, Ph.D., assistant professor in the Division of
Gastroenterology and Hepatology in the UNC School of Medicine and a member of the UNC
Center for Functional GI & Motility Disorders. "What is especially exciting about
our study is that children can clearly reduce their abdominal pain a lot on their own with
guidance from audio recordings, and they get much better results that way than from
medical care alone," said van Tilburg. "Such self-administered treatment is, of
course, very inexpensive and can be used in addition to other treatments, which
potentially opens the door for easily enhancing treatment outcomes for a lot of children
suffering from frequent stomach aches."
More infants surviving pre-term
births results in higher rates of eye problems
As more extremely pre-term infants survive in Sweden, an increasing number of babies are
experiencing vision problems caused by abnormalities involving the retina, according to a
report in the October issue of Archives of Ophthalmology, one of the JAMA/Archives
journals. "Retinopathy of prematurity [abnormal development of blood vessels in the
retina] remains an important cause of childhood blindness and visual impairment throughout
the world," the authors write as background information in the article. "During
the last decade, neonatal care has changed with an increase in centralization,
implementation of new therapies and provision of intensive care for infants of extremely
low gestational age. These changes have contributed to an increasing population of
survivors in neonatal intensive care units today. The incidence of retinopathy of
prematurity in these extremely preterm infants is, therefore, unknown." Dordi
Austeng, M.D., of University Hospital, Uppsala, Sweden, and Trondheim University Hospital,
Trondheim, Norway, and colleagues studied Swedish infants born before 27 weeks' gestation
between 2004 and 2007. Infants were screened for retinopathy of prematurity beginning at
five weeks after birth and were treated for the condition according to established
guidelines. During the study, 506 of 707 infants survived until the first eye examination.
Of these, 368 (72.7 percent) had retinopathy of prematurity, including 37.9 percent with
mild cases and 34.8 percent whose condition was severe. A total of 99 (19.6 percent) were
treated.
Impaired foetal growth increases
risk of asthma
A new study from Karolinska Institutet shows that children born with low birth weight are
at a higher risk of developing asthma later in life. The study, which is published in the
journal Pediatrics, is based on data on the incidence of asthma in 10,918 twins from the
Swedish Twin Registry. Questionnaire data on asthma in 9- and 12- year old twins was
linked to the national Swedish Medical Birth Registry which records, amongst other data,
birth weight and gestational age (i.e. how long into the pregnancy the baby is born).
Since twins have the same gestational age and share DNA, uterine environment and
conditions of early infancy, twin studies are an excellent way to examine the relationship
between foetal growth and childhood disease. "Our study shows that there's a distinct
correlation between foetal growth and asthma that's independent of gestational age and
environmental or genetic factors," says Catarina Almqvist Malmros, paediatrician and
Assistant professor at the Department of medical epidemiology and biostatistics,
Karolinska Institutet. According to the WHO some 300 million people currently suffer from
asthma. It is the most common chronic disease among children, and the number of children
with the condition has risen steadily during the last decades. At the same time, an
increasing number of children are being born with a low birth weight, a possible symptom
of malnutrition in the womb. The study suggests that impaired foetal growth affects lung
development.
Like humans, monkeys fall into the
'uncanny valley'
Princeton University researchers have come up with a new twist on the mysterious visual
phenomenon experienced by humans known as the "uncanny valley." The scientists
have found that monkeys sense it too. The uncanny valley, a phrase coined by a Japanese
researcher nearly three decades ago, describes that disquieting feeling that occurs when
viewers look at representations designed to be as human-like as possible -- whether
computer animations or androids -- but somehow fall short. Movie-goers may not be familiar
with the term, but they understand that it is far easier to love the out-of-proportion
cartoon figures in the "The Incredibles," for example, than it is to embrace the
more realistic-looking characters in "The Polar Express." Viewers, to many a
Hollywood director's consternation, are emotionally unsettled by images of artificial
humans that look both realistic and unrealistic at the same time. In an attempt to add to
the emerging scientific literature on the subject and answer deeper questions about the
evolutionary basis of communication, Princeton University researchers have found that
macaque monkeys also fall into the uncanny valley, exhibiting this reaction when looking
at computer-generated images of monkeys that are close but less than perfect
representations.
New cancer gene discovered
A new cancer gene has been discovered by a research group at the Sahlgrenska Academy. The
gene causes an insidious form of glandular cancer usually in the head and neck and in
women also in the breast. The discovery could lead to quicker and better diagnosis and
more effective treatment.The study is published today in the prestigious scientific
journal Proceedings of the National Academy of Sciences (PNAS). The cancer caused by this
new cancer gene is called adenoid cystic carcinoma and is a slow-growing but deadly form
of cancer. The research group can now show that the gene is found in 100% of these
tumours, which means that a genetic test can easily be used to make a correct diagnosis.
“Now that we know what the cancer is down to, we can also develop new and more
effective treatments for this often highly malignant and insidious form of cancer,”
says professor Göran Stenman, who heads the research group at the Lundberg Laboratory for
Cancer Research at the Sahlgrenska Academy. “One possibility might be to develop a
drug that quite simply turns off this gene.”The newly discovered cancer gene is what
is known as a fusion gene, created when two healthy genes join together as a result of a
chromosome change. “Previously it was thought that fusion genes pretty much only
caused leukaemia, but our group can now show that this type of cancer gene is also common
in glandular cancer,” says Stenman.
Silence of the Genes
The molecular architecture of a protein complex that helps determine the fate of human
cells has been imaged for the first time by researchers with the U.S. Department of
Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab). Known as a human
RISC-loading complex, this structure consists of snippets of ribonucleic acid (RNA) that
control whether genetic messages are silenced or expressed.From these new images, the
research team, led by biochemist Jennifer Doudna and biophysicist Eva Nogales, has been
able to propose a model of how RISC and other so-called “small RNA molecules”
are able to target specific messenger RNA molecules for gene silencing and/or destruction.
Their results have been published in the journal Nature Structure and Molecular Biology in
a paper entitled: “Structural insights into RNA Processing by the Human RISC-Loading
Complex.” RISC stands for RNA-Induced Silencing Complex. Doudna and Nogales both hold
joint appointments with Berkeley Lab, the University of California (UC) Berkeley, and the
Howard Hughes Medical Institute (HHMI). Co-authoring the paper with them were Hong-Wei
Wang, Cameron Noland, Bunpote Siridechadilok, David Taylor, Enbo Ma and Karin Felderer.
“We now know how the three main components of the RISC machinery - the Dicer and
Argonaute enzymes and the TRBP binding protein - are arranged, and how they interact with
one another and are likely to interact as a complex with messenger RNA,” says Doudna,
an authority on RNA molecular structures. “Our work should help others in the design
of mutants to test the mechanisms of the RNA binding and processing used by the
gene-silencing RNA machinery in humans.”
Important defence against stomach
ulcer bacterium identified
A special protein in the lining of the stomach has been shown to be an important part of
the body’s defence against the stomach ulcer bacterium Helicobacter pylori in a new
study from the Sahlgrenska Academy. The discovery may explain why the bacterium makes some
people more ill than others. The study was conducted in collaboration with researchers at
universities in Brisbane and Melbourne and has been published in the scientific journal
Public Library of Science Pathogens. “Half of all people carry Helicobacter pylori in
their bodies,” says Sara Lindén from the Sahlgrenska Academy, one of the researchers
behind the study. “Many don’t even notice that they have the bacterium, but some
develop stomach ulcers, and in some cases the inflammation leads to stomach cancer. Our
discovery may partially explain why the bacterium affects people so differently. ”The
research team has shown that a protein called MUC1 found in the lining of the stomach is
important for the body’s defence against the bacterium. Greatly magnified, MUC1 looks
like a tree growing out of low bushes on the surface of the stomach. As MUC1 is taller
than the other structures on the cell surface, Helicobacter pylori readily becomes
attached to the protein and then rarely gets to infect the cell.“You could say that
MUC1 acts as a decoy which prevents the bacterium from coming into close contact with the
cell surface,” says Lindén. “Genetic variations between people mean that our
MUC1 molecules vary in length, and this may be part of the reason why Helicobacter pylori
makes some people more ill than others.”
Current safety equipment may not be
adequate for nanoprotection
Writing in a forthcoming issue of the International Journal of Nanotechnology, Canadian
engineers suggest that research is needed into the risks associated with the growing field
of nanotechnology manufacture so that appropriate protective equipment can be developed
urgently. Patricia Dolez of the Department of Mechanical Engineering, at the École de
technologie supérieure, in Montréal and colleagues point out that skin is not an
impervious membrane. This is the reason that protective clothing and gloves, in addition
to respirators, are often an essential and common sight in the chemical industry. However,
they wonder if standard protection against chemical risks is enough for workers who are
handling nanomaterials. According to the most recent estimates from the U.S. National
Science Foundation, the nanotechnology market could reach as much as $1 trillion by
2011/2012. This, says Dolez, corresponds to about 2 million workers involved in
nano-related activities. She adds that it has already been shown that nanoparticles may
affect biological activity through oxidative stress at the cellular and molecular levels,
although these effects are yet to be manifest as health problems among workers. The
anticipated hazards associated with this incredibly diverse range of substances falling
under the general and broad tag of "nanomaterials" remain largely unknown. And,
some scientists have suggested that we are vigilant to emerging health problems associated
with nanomaterials. The U.S. government recently updated its National Nanotechnology
Initiative strategic plan to highlight the need for an assessment of nanomaterials
toxicity before production begins.
Bioluminescence imaging used for
eye cancer detection
At the moment, doctors rely on biopsy analysis to determine the progression of eye cancer.
However, researchers now believe that a new technology, bioluminescence imaging (BLI),
will allow doctors to detect tumors earlier and quickly choose a method of treatment that
doesn't necessarily involve eye surgery. BLI is a new technology that uses the making and
giving off of light by an organism to map diseases in a non-invasive way. Scientists have
harnessed this technology to delicately detect and monitor various diseases, including eye
cancer. BLI has several advantages over biopsy analysis, including in vivo monitoring,
higher sensitivity, easier use and an overall more accurate correlation between cell
numbers detected and tumor growth. A study detailed in the Association for Research in
Vision and Ophthalmology's peer-reviewed Investigative Ophthalmology & Visual Science
("Non-invasive visualization of retinoblastoma growth and metastasis via
bioluminescence imaging") shows how the researchers, led by Qian Huang, MD, PhD, of
the First People's Hospital in Shanghai, China, were able to effectively create human eye
tumors in mice using particular genes to label eye cancer. BLI was then performed on the
mice using the NightOwl LB 981 Molecular Imaging System to monitor the growth and
succession of these created tumors. "BLI allowed sensitive and quantitative
localization and monitoring of intraocular and metastatic tumor growth in vivo and thus
might be a useful tool to study cancer biology as well as anti-cancer therapies,"
said Huang.
Absent pheromones turn flies into
lusty lotharios
When Professor Joel Levine's team genetically tweaked fruit flies so that they didn't
produce certain pheromones, they triggered a sexual tsunami in their University of Toronto
Mississauga laboratory. In fact, they produced bugs so irresistible that normal male fruit
flies attempted to mate with pheromone-free males and even females from a different
species-generally a no-no in the fruit fly dating scene. The study, published in the Oct.
15 issue of Nature, points to a link between sex, species recognition and a specific
chemical mechanism, and is part of Levine's larger research into the genetic basis of
social behaviour. "This is important not only from the point of view of understanding
social dynamics, but it's also fundamental biology, because these pheromones provide
recognition cues that facilitate reproductive behaviour," says Levine, an assistant
professor of biology. "Lacking these chemical signals (pheromones) eliminated
barriers to mating. It turned out that males of other species were attracted to females
who didn't have these signals, so that seemed to eliminate the species barrier."
U-M researchers find those with
severe H1N1 at risk for pulmonary emboli
University of Michigan researchers have found that patients with severe cases of the H1N1
virus are at risk for developing severe complications, including pulmonary emboli,
according to a study published today in the American Journal of Roentgenology.A pulmonary
embolism occurs when one or more arteries in the lungs become blocked. The condition can
be life-threatening. However, if treated aggressively, blood thinners can reduce the risk
of death. “The high incidence of pulmonary embolism is important. Radiologists have
to be aware to look closely for the risks of pulmonary embolism in severely sick
patients,” said Prachi P. Agarwal, M.D., assistant professor of radiology at the U-M
Medical School and lead author of the study.
'Beneficial' Effects of Alcohol
According a new study of over 3,000 adults aged 70-79, the apparent association between
light-to-moderate alcohol consumption and reduced risk of functional decline over time did
not hold up after adjustments were made for characteristics related to lifestyle, in
particular physical activity, body weight, education, and income.The authors of the study,
publishing today in the Journal of the American Geriatrics Society, say this suggests that
life-style related characteristics may be the real determinant of the reported beneficial
effects of alcohol and functional decline. “In recent years the relationship between
alcohol intake and health outcomes has gained growing attention, but while there is now
considerable consensus that consuming alcohol at moderate levels has a specific beneficial
effect on the risk of cardiovascular disease, the benefit of alcohol intake on other
health-related outcomes is less convincing,” said study author Cinzia Maraldi, M.D.,
of the University of Ferrara, Italy. “We wanted to evaluate this question over a
long-term follow-up and with a prospective design, which most previous studies have not
used.” During a follow-up time of six and a half years, the researchers found that
participants consuming moderate levels of alcohol had the lowest incidence of mobility
limitation and disability. After adjusting for demographic characteristics, moderate
alcohol intake was still associated with reduced risk compared to never or occasional
consumption, but adjusting for life-style related variables substantially reduced the
strength of the associations. Adjustment for diseases and health status indicators did not
affect the strength of the associations, which led the authors to conclude that life-style
is the most important factor in confounding this relationship.
Bosses who feel inadequate can turn
into bullies
Bosses who are in over their heads are more likely to bully subordinates. That's because
feelings of inadequacy trigger them to lash out at those around them, according to new
research from the University of California, Berkeley, and the University of Southern
California. In a new twist on the adage "power corrupts," researchers at UC
Berkeley and USC have found a direct link among supervisors and upper management between
self-perceived incompetence and aggression. The findings, gleaned from four separate
studies, are published in the November issue of the journal Psychological Science. With
more than one-third of American workers reporting that their bosses have sabotaged, yelled
at or belittled them, the new study challenges previous assumptions that abusive bosses
are solely driven by ambition and the need to hold onto their power. "By showing when
and why power leads to aggression, these findings are highly relevant as abusive
supervision is such a pervasive problem in society," said Nathanael Fast, assistant
professor of management and organization at USC and lead author of the study. During
role-playing sessions, study participants who felt their egos were under threat would go
so far as to needlessly sabotage an underling's chances of winning money. In another test,
participants who felt inadequate would request that a subordinate who gave a wrong answer
to a test be notified by a loud obnoxious horn, even though they had the option of
choosing silence or a quiet sound.
Cell death occurs in the same way
in plants, animals and humans
Research has previously assumed that animals and plants developed different genetic
programs for cell death. Now an international constellation of research teams, including
one at the Swedish University of Agricultural Sciences, has shown that parts of the
genetic programs that determine programmed cell death in plants and animals are actually
evolutionarily related and moreover function in a similar way. The findings were published
in Nature Cell Biology October 11. For plants and animals, and for humans as well, it is
important that cells both can develop and die under controlled forms. The process where
cells die under such forms is called programmed cell death. Disruptions of this process
can lead to various diseases such as cancer, when too few cells die, or neurological
disorders such as Parkinson's, when too many cell die. The findings are published jointly
by research teams at SLU (Swedish University of Agricultural Sciences) and the Karolinska
Institute, the universities of Durham (UK), Tampere (Finland), and Malaga (Spain) under
the direction of Peter Bozhkov, who works at SLU in Uppsala, Sweden. The research findings
are published in the prestigious scientific journal Nature Cell Biology. The scientists
have performed comparative studies of an evolutionarily conserved protein called TUDOR-SN
in cell lines from mice and humans and in the plants norway spruce and mouse-ear cress. In
both plant and animal cells that undergo programmed cell death, TUDOR-SN is degraded by
specific proteins, so-called proteases. The proteases in animal cells belong to a family
of proteins called caspases, which are enzymes. Plants do not have caspases – instead
TUDOR-SN is broken down by so-called meta-caspases, which are assumed to be ancestral to
the caspases found in animal cells. For the first time, these scientists have been able to
demonstrate that a protein, TUDOR-SN, is degraded by similar proteases in both plant and
animal cells and that the cleavage of TUDOR-SN abrogate its pro-survival function. The
scientists have thereby discovered a further connection between the plant and animal
kingdoms. The results now in print will therefore play a major role in future studies of
this important protein family.
People who work after retiring
enjoy better health, according to national study
Retirees who transition from full-time work into a temporary or part-time job experience
fewer major diseases and are able to function better day-to-day than people who stop
working altogether, according to a national study. And the findings were significant even
after controlling for people's physical and mental health before retirement. The study's
authors refer to this transition between career and complete retirement as "bridge
employment," which can be a part-time job, self-employment or a temporary job. The
findings are reported in the October issue of the Journal of Occupational Health
Psychology, published by the American Psychological Association. "Given the economic
recession, we will probably see more people considering post-retirement employment,"
said co-author Mo Wang, PhD, of the University of Maryland. "These findings highlight
bridge employment's potential benefits." For this study, Wang and his fellow
researchers looked at the national Health and Retirement Study, which is sponsored by the
National Institute on Aging. They used data from 12,189 participants who were between the
ages of 51 and 61 at the beginning of the study. The participants were interviewed every
two years over a six-year period beginning in 1992 about their health, finances,
employment history and work or retirement life.In order to measure the respondents' health
over the course of the study, the researchers considered only physician-diagnosed health
problems, such as high blood pressure, diabetes, cancer, lung disease, heart disease,
stroke and pschiatric problems. They controlled not only for baseline physical and mental
health but also for age, sex, education level, and total financial wealth. The results
showed the retirees who continued to work in a bridge job experienced fewer major diseases
and fewer functional limitations than those who fully retired.
Study questions need for routine
intervention in patients with renovascular disease
Some invasive procedures that are becoming increasingly common as a first line of
treatment for patients diagnosed with narrowed arteries in and around the kidneys may not
be necessary, according to a new study by researchers at Wake Forest University Baptist
Medical Center. The study shows that the condition, known as renal artery stenosis, only
progresses to a dangerous blockage in a very small percentage of cases and does not always
necessitate a surgical or even minimally-invasive procedure, such as angioplasty and
stenting, both of which are becoming more and more common as technology makes the
narrowing easier to detect. The finding is especially timely because the number of these
procedures has risen so dramatically in recent years that the federal Centers for Medicare
and Medicaid Services has questioned whether such procedures are, in fact, necessary for
all patients with renal artery stenosis – and whether the government should pay for
them. Renal artery stenosis is the narrowing of blood vessels in and around the kidneys
that can lead to declining kidney function or hypertension that is difficult to control.
There is an ongoing debate about how best to treat patients with this condition. Current
management options include treatment with medicine, surgical bypass of the stenosis, or
approaches such as angioplasty and stenting, where a wire mesh tube is placed over a
balloon and threaded through the blood vessels via a needle puncture of the skin to the
area of narrowing. When the balloon is inflated, the stent expands, locks in place and
forms a scaffold, permanently holding the artery open to increase blood flow. "We
think these interventions are beneficial for a group of patients," said study
co-author, Ross P. Davis, M.D., a vascular surgery fellow in the Department of Vascular
and Endovascular Surgery. "But as physicians, we need to be careful about reserving
those interventions for specific indications, not just for all patients whose ultrasound
reports confirm the presence of artery narrowing. There need to be other indicators of
progressive renovascular disease present to consider subjecting patients to the risks and
costs of these procedures."
Dysfunctional protein dynamics
behind neurological disease?
Researchers at Lund University, Sweden, have taken a snapshot of proteins changing shape,
sticking together and creating structures that are believed to trigger deadly processes in
the nervous system. The discovery opens the possibility of designing drugs for a
devastating neurological disease, ALS. Research indicates that ALS, in common with other
neurological disorders, such as Alzheimer's and Parkinson's disease, is caused by our own
proteins, which form aberrant aggregates that are fatally toxic to our nerve cells.
However, it has not been known what causes these proteins to aggregate. Researchers at
Lund University have now revealed what happens with proteins during the very first,
critical step towards forming larger aggregates. It turns out that the protein superoxide
dismutase interchanges between its normal structure and a misfolded form. During a brief
moment the structure becomes partially misfolded to expose sticky patches that normally
are hidden in the interior. These patches cause two or several protein molecules to stick
together, thereby forming the cornerstone of the larger structures that are believed to
underlie ALS. The research team headed by Mikael Akke at the Center for Molecular Protein
Science of Lund University used NMR spectroscopy to create a snapshot of the misfolded
structure, which had not previously been seen. Knowledge of the misfolded protein
structure potentially makes possible future efforts to rationally design drugs that
prevent the misfolding event and hence the development of ALS.
Blood ties -- younger generation
more willing to donate blood
Youth may not bring wisdom but, according to a new study from Canada, it does bring
generosity as young adults are found to be the most likely to donate blood. The research,
published in BioMed Central's open access International Journal of Health Geographics,
looked at what factors had an impact on donating blood. 'Like other countries, Canada's
population is aging, and the implications of this demographic change need to be better
understood from the perspective of blood supply' says Antonio Páez who carried out the
research with a team from McMaster University, Canada. Thus, while younger people are more
likely to donate, they are also a declining share of Canada's population. The research,
supported by Canada's Social Sciences and Humanities Research Council, Canada Blood
Services, and Environics Analytics,is prompted by the importance of creating a sustained
and reliable donor base. Currently, despite the fact that almost everyone will need to use
donor blood at some point in their life, less than 4% of eligible donors give blood. By
examining the records from the Canadian Blood Services, several patterns were observed.
Firstly, the 15-24 age group showed the strongest likelihood to be donors, whilst those of
working age (25-54) were the least likely to be donors. The authors predict that due to an
ageing population this reliance on the younger generation will be unsustainable. The study
also showed positive ties between level of education and ability to speak English with
donation likelihood, whilst immigrants and the wealthy were less likely to donate. The
paper shows that those living in a big city were much less likely to donate blood than
those living in smaller cities or towns, coining the phrase "the stingy big-city
effect". According to Páez, "The fact that those who possessed a higher level
of education were more likely to donate lends weight to the assertion that, with 25% of
Canadians thinking there are some risks in donating blood, educating the public would help
expand the donor database". "Blood products are an essential component of modern
medicine and necessary to support many life-saving and life-prolonging procedures,"
states Páez, who concludes "To achieve the target levels of donations, there need to
be targeted campaigns designed to encourage a greater number of Canadians to consider
blood donation".
Loss of tumor supressor gene
essential to transforming benign nerve tumors into cancers
Researchers at UCLA's Jonsson Comprehensive Cancer Center showed for the first time that
the loss or decreased expression of the tumor suppressor gene PTEN plays a central role in
the malignant transformation of benign nerve tumors called neurofibromas into a malignant
and extremely deadly form of sarcoma.The work, a collaboration between the Institute for
Molecular Medicine, the Department of Molecular and Medical Pharmacology and the cancer
center's Sarcoma Program, could lead to the development of new therapies that target the
cell signaling pathway regulated by PTEN. A novel mouse model of neurofibromatosis type 1
(NF1) developed at UCLA first illustrated the importance of PTEN tumor suppressor in
malignant transformation and this finding was validated in human malignant peripheral
nerve sheath tumors, the deadly sarcomas.The study will be published this week in the
early online edition of the peer-reviewed journal Proceedings of the National Academy of
Sciences. "The loss of expression of PTEN in the human sarcomas we studied mirrored
the loss of PTEN in mice, and we anticipate being able to target this pathway abnormality
for the development of new methods of diagnosis and treatment" said Dr. Fritz Eilber,
director of the Sarcoma Program and an assistant professor of surgical oncology.
"Within the sarcoma world, malignant peripheral nerve sheath tumors are one of the
most lethal sub-types, so this is a significant finding and may lead to new and more
effective treatments."NF1 is one of the most common genetically inherited disorders,
with an incidence of about 1 in every 2,500 births, said, Dr. Hong Wu, associate director
of the molecular medicine institute, a Jonsson Cancer Center researcher and senior author
of the study. "Patients with NF1 have an about 10 percent lifetime risk of developing
this lethal sarcoma sub-type," Wu said. The study also showed that Positron Emission
Tomography (PET) scanning with the glucose analogue FDG - both in the mice and in humans -
is a highly accurate way to distinguish between the benign tumors and the malignant ones,
indicating that this non-invasive imaging technology is valuable in assessing therapeutic
response to new treatments.
UF researchers find triggers in
cells' transition from colitis to cancer
University of Florida researchers have grown tumors in mice using cells from inflamed but
noncancerous colon tissue taken from human patients, a finding that sheds new light on
colon cancer and how it might be prevented. Scientists observed that cancer stem cells
taken from the gastrointestinal system in patients with a chronic digestive disease called
ulcerative colitis will transform into cancerous tumors in mice. The finding, now online
and to be featured on the cover of the Thursday (Oct. 15) issue of Cancer Research, may
help explain why patients with colitis have up to a 30-fold risk of developing colon
cancer compared with people without the disease.New understanding of the link between
colitis and cancer could lead to diagnostic tests that would evaluate tissue taken from
patients with colitis for signs of cancer stem cell development, thereby identifying
patients who may be at greater risk for cancer. "Ultimately it would be great if we
could prevent colitis or treat colitis so it never gets to the cancerous stage," said
UF colorectal surgeon Emina Huang, M.D., who is a member of the Program in Stem Cell
Biology and Regenerative Medicine at UF's McKnight Brain Institute and the UF College of
Medicine. Although colonoscopy is very effective in screening and preventing colon cancer
for most people, for patients with colitis no diagnostic tests work well because the
inflamed tissue makes identification of precancerous changes difficult. According to the
Crohn's and Colitis Foundation of America, approximately 700,000 people have colitis in
the United States. The National Cancer Institute estimates that cancer of the colon and
rectum will claim the lives of about 50,000 people this year. UF scientists gathered
colitic tissue from humans and chemically screened it for colon cancer stem cells, also
called tumor initiating cells. These cells were then isolated and monitored in mice to see
if tumors would grow.
No such thing as 'junk RNA,' say
Pitt researchers
Tiny strands of RNA previously dismissed as cellular junk are actually very stable
molecules that may play significant roles in cellular processes, according to researchers
at the University of Pittsburgh School of Medicine and the University of Pittsburgh Cancer
Institute (UPCI). The findings, published last week in the online version of the Journal
of Virology, represent the first examination of very small RNA products termed unusually
small RNAs (usRNAs). Further study of these usRNAs, which are present in the thousands but
until now have been neglected, could lead to new types of biomarkers for diagnosis and
prognosis, and new therapeutic targets. In recent years, scientists have recognized the
importance of small RNAs that generally contain more than 20 molecular units called
nucleotides, said senior author Bino John, Ph.D., assistant professor, Department of
Computational Biology, Pitt School of Medicine. "But until we did our experiments, we
didn't realize that RNAs as small as 15 nucleotides, which we thought were simply cell
waste, are surprisingly stable, and are repeatedly, reproducibly, and accurately produced
across different tissue types." Dr. John said. "We have dubbed these as usRNAs,
and we have identified thousands of them, present in a diversity that far exceeds all
other longer RNAs found in our study." The team's experiments began with the
observation that the Kaposi sarcoma-associated herpesvirus produces a usRNA that can
control the production of a human protein. Detailed studies using both computational and
experimental tools revealed a surprisingly large world of approximately 15 nucleotide-long
usRNAs with intriguing characteristics. Many usRNAs interact with proteins already known
to be involved in small RNA regulatory pathways. Some also share highly specific
nucleotide patterns at one end. The researchers wrote that the existence of several
different patterns in usRNAs reflects the diverse pathways in which the RNAs participate.
A high fat diet during pregnancy
can lead to severe liver disease in offspring
Scientists have discovered a previously unknown link between a mother's diet in pregnancy
and a severe form of liver disease in her child. In a study, published in the journal
Hepatology today, researchers at the University of Southampton found that a high fat diet
during a woman's pregnancy makes her offspring more likely to develop a severe form of
fatty liver disease when they reach adulthood. The findings are another piece in the
jigsaw for scientists who believe diets containing too high levels of saturated fat may
have an adverse effect on our health. Non-alcoholic fatty liver disease (NAFLD) is a
condition associated with obesity and caused by the build up of fat in the liver. The
condition advances in some people and it is important to understand the factors that
contribute to disease progression. Until recently, NAFLD was considered rare and
relatively harmless but now it is one of the most common forms of liver disease that may
progress to cirrhosis a serious life threatening chronic liver disease. Professor
Christopher Byrne, with colleagues Dr Felino Cagampang and Dr Kim Bruce, of the
University's School of Medicine and researchers at King's College London, conducted the
study, funded by the BBSRC. Prof Byrne explained: "This research shows that too much
saturated fat in a mother's diet can affect the developing liver of a fetus, making it
more susceptible to developing fatty liver disease later in life. An unhealthy saturated
fat-enriched diet in the child and young adult compounds the problem further causing a
severe form of the fatty liver disease later in adult life." The next stage of this
research, also funded by the BBSRC, will be to understand, more precisely, the reason why
fatty liver disease develops and to intervene to prevent the fatty liver disease
occurring.
Teen smoking-cessation trial first
to achieve significant quit rates
For the first time, researchers at Fred Hutchinson Cancer Research Center have
demonstrated that it is possible to successfully recruit and retain a large number of
adolescent smokers from the general population into a smoking intervention study and,
through personalized, proactive telephone counseling, significantly impact rates of
six-month continuous quitting. These findings, by Arthur V. Peterson Jr., Ph.D., Kathleen
A. Kealey and colleagues, are reported in a pair of papers in the Oct. 12 "Advance
Access" online edition of the Journal of the National Cancer Institute. "When
this study started, despite decades of research and dozens of intervention trials, there
was no proven way to reach teens from the general population and recruit them into smoking
cessation programs, and there was no proven way to help these teens quit," said
Peterson, a member of the Hutchinson Center's Public Health Sciences Division and lead
author of the paper that reported the results of the Hutchinson Study of High School
Smoking, the largest randomized trial of teen smoking cessation ever conducted. The trial,
funded by the National Institutes of Health, involved 2,151 teenage smokers from 50 high
schools in Washington. Half of the schools were randomly assigned to the experimental
intervention; teens in these schools were invited to take part in confidential,
personalized telephone counseling designed to help motivate them to quit. The remaining 25
schools served as a comparison group; teen smokers from these schools did not participate
in the telephone intervention. The study also included 745 nonsmokers to ensure that
contacting students for participation in the trial would not reveal a participant's
smoking status.Study recruitment was robust; in the experimental group 65.3 percent of the
smokers were eligible and participated in the telephone intervention. Recruitment took
place in their junior year and the counseling intervention took place during their senior
year. "The literature says it is very difficult to recruit kids to teen smoking
programs. People have tried. The field has encountered great obstacles in recruiting teens
to smoking cessation programs. And so we took that as a challenge," Peterson said.
The study found that a proactive strategy of reaching out to teens and offering them the
opportunity to receive up to nine personalized, confidential telephone counseling sessions
effectively helped many of them to kick the habit. In addition, by proactively identifying
and recruiting teen smokers (with parental consent for those under age 18), two-thirds of
all identified smokers participated in the telephone counseling and nearly half completed
all of their scheduled counseling calls.
Researchers discover RNA repair
system in bacteria
In new papers appearing this month in Science and the Proceedings of the National Academy
of Sciences, University of Illinois biochemistry professor Raven H. Huang and his
colleagues describe the first RNA repair system to be discovered in bacteria. This is only
the second RNA repair system discovered to date (with two proteins from T4 phage, a virus
that attacks bacteria, as the first). The novelty of the newly discovered bacterial RNA
repair system is that, before the damaged RNA is sealed, a methyl group is added to the
two-prime hydroxyl group at the cleavage site of the damaged RNA, making it impossible to
cleave the site again. Thus, the repaired RNA is "better than new." This
discovery has implications for protecting cells against ribotoxins, a class of toxins that
kills cells by cleaving essential RNAs involved in protein translation. Because the enzyme
responsible for methylation in the newly-discovered RNA repair system is the Hen1 homolog
in bacteria, the finding has also implications for the understanding of RNA interference
and gene expression in plants, animals, and other eukaryotes. The eukaryotic Hen1 is one
of three enzymes (along with Dicer and Argonaute) essential for the generation of small
noncoding RNAs of 19-30 nucleotides in RNA interference. While the Science paper describes
the mechanism of the entire RNA repair process, the article in PNAS focuses on the
chemistry of the methylation reaction, specifically the crystal structure of the
methyltransferase domain of bacterial Hen1. Because the eukaryotic Hen1 carries out the
same chemical reaction, the study should further understanding of RNA interference in
eukaryotic organisms.
Effects of aspirin and folic acid
on inflammation markers for colorectal adenomas
Unexpectedly, inflammation markers do not appear to be involved with the chemopreventative
effect of aspirin on colorectal adenomas, according to a brief communication published
online October 12 in the Journal of the National Cancer Institute. Aspirin has been shown
to prevent the recurrence of colorectal polyps, but it's not clear how it works. One
hypothesis is that it may affect the levels of substances, such as C-reactive protein and
others, that are markers of inflammation. To study this, Gloria Y.F. Ho, Ph.D., of the
department of Epidemiology & Population Health, at Albert Einstein College of Medicine
in Bronx, N.Y., and colleagues examined changes in plasma levels of five inflammation
markers—C-reactive protein, interleukin 6, tumor necrosis factor, soluble TNF
receptor type II, and IL-1 receptor antagonist—at baseline and at year 3 of 884
subjects. The trial had three aspirin groups (including an aspirin placebo group) and two
folic acid groups (including a folate placebo group). Changes in levels of all five
inflammation markers were not associated with adenoma recurrence. For those who did not
receive folic acid, C-reactive protein levels in those in the 325 mg/d aspirin group
changed very little, whereas it was statistically significantly increased in the placebo
group. For subjects who received folic acid, the reverse association was observed.
"Our data suggest that low dose aspirin has modest effects on stabilizing [C-reactive
protein], which may be abrogated by a high level of folate," the authors write.
"However, such beneficial effects do not appear to confer protection against
colorectal neoplasia. Inflammation markers do not mediate the previously observed effects
of aspirin and folic acid on colorectal adenomas."
New guidelines identify best
treatments to help ALS patients live longer, easier
New guidelines from the American Academy of Neurology identify the most effective
treatments for amyotrophic lateral sclerosis (ALS), often called Lou Gehrig's disease. The
guidelines are published in the October 13, 2009, issue of Neurology®, the medical
journal of the American Academy of Neurology. "While we are waiting for a cure,
people need to know that a lot can be done to make life easier and longer for people with
ALS," said lead guidelines author Robert G. Miller, MD, with the Department of
Neurology at California Pacific Medical Center in San Francisco and Fellow of the American
Academy of Neurology. ALS is a rapidly progressive and fatal neurologic disease that
attacks the nerve cells that control voluntary muscles. Eventually people with ALS are not
able to stand or walk, or use their hands and arms, and they have difficulty breathing and
swallowing. Most people with ALS die within three to five years from the onset of
symptoms. However, about 10 percent survive for 10 or more years. According to the
guidelines, the drug riluzole should be offered to people with ALS to slow the rate at
which the disease progresses. Riluzole is the only drug approved by the U.S. Food and Drug
Administration to treat ALS and has a modest effect on prolonging survival. The guidelines
also state that life expectancy will likely increase and quality of life may increase for
people with ALS who use an assisted-breathing device. Longer life expectancy is also
likely for people with ALS who use a feeding tube known as a PEG tube, since nutrition
plays a critical role in prolonging survival. The guidelines also recommend doctors
consider offering their patients botulinum toxin B to treat sialorrhea, also known as
drooling, if oral medications do not help. Moreover, doctors should consider screening
their patients for behavioral or thinking problems because studies show many people with
ALS have these problems. Such problems might affect some patients' willingness to accept
suggested treatments.
Radio waves 'see' through walls
University of Utah engineers showed that a wireless network of radio transmitters can
track people moving behind solid walls. The system could help police, firefighters and
others nab intruders, and rescue hostages, fire victims and elderly people who fall in
their homes. It also might help retail marketing and border control. "By showing the
locations of people within a building during hostage situations, fires or other
emergencies, radio tomography can help law enforcement and emergency responders to know
where they should focus their attention," Joey Wilson and Neal Patwari wrote in one
of two new studies of the method. Both researchers are in the university's Department of
Electrical and Computer Engineering – Patwari as an assistant professor and Wilson as
a doctoral student. Their method uses radio tomographic imaging (RTI), which can
"see," locate and track moving people or objects in an area surrounded by
inexpensive radio transceivers that send and receive signals. People don't need to wear
radio-transmitting ID tags. One of the studies – which outlines the method and tests
it in an indoor atrium and a grassy area with trees – is awaiting publication soon in
IEEE Transactions on Mobile Computing, a journal of the Institute of Electrical and
Electronics Engineers. The study involved placing a wireless network of 28 inexpensive
radio transceivers – called nodes – around a square-shaped portion of the atrium
and a similar part of the lawn. In the atrium, each side of the square was almost 14 feet
long and had eight nodes spaced 2 feet apart. On the lawn, the square was about 21 feet on
each side and nodes were 3 feet apart. The transceivers were placed on 4-foot-tall stands
made of plastic pipe so they would make measurements at human torso level.
Ironing out the genetic cause of
hemoglobin problems
A gene with a significant effect on regulating hemoglobin in the body has been identified
as part of a genome-wide association study, which looked at the link between genes and
hemoglobin level in 16,000 people. The research was carried out by scientists from
Imperial College London and published in Nature Genetics today. It shows a strong
association between a gene known as TMPRSS6 and the regulation of hemoglobin. Hemoglobin
is contained within red blood cells and is essential for transporting oxygen around the
body. Problems with hemoglobin production cause common diseases, such as anaemia, which
comes from low levels of hemoglobin and is found in 25% of the world's population.
"This new finding is critical: understanding how hemoglobin levels are controlled at
a genetic level has significant public health implications for people of all ages in
developing and developed countries", explains Dr John Chambers, from the Department
of Epidemiology and Public Health at Imperial College London and one of the lead authors
of the study. "Abnormally high or low levels are associated with a range of serious
health problems, such as poor growth (low levels) and increased risk of stroke (high
levels). Changes in hemoglobin levels can also affect our susceptibility to diseases like
malaria, which infect the red blood cells" says Professor Kooner, from the National
Heart and Lung Institute at Imperial College London and the study's chief investigator.The
new research adds to our understanding of the multiple causes of problems with hemoglobin
levels, which include an iron-deficient diet, chronic diseases such as cancer, and genetic
associations, such as the one described in this paper. In the future, the finding could
lead to new treatments for people suffering from chronic problems with hemoglobin levels
not linked to iron in the diet. "The enzyme protein produced by the TMPRSS6 gene is a
good target for drug development. Designing a drug that enhances TMPRSS6 activity could
augment hemoglobin in people such as cancer and kidney failure patients, who suffer from
chronically low levels. A different drug that blocked TMPRSS6 enzyme production might
bring down high hemoglobin levels", adds Dr Chambers.
Blood counts are clues to human
disease
A new genome-wide association study published today in Nature Genetics begins to uncover
the basis of genetic variations in eight blood measurements and the impact those variants
can have on common human diseases. Blood measurements, including the number and volume of
cells in the blood, are routinely used to diagnose a wide range of disorders, including
anaemia, infection and blood cell cancers. An international team of scientists measured
haemoglobin concentration, the count and volume of red and white cells and the sticky
cells that prevent bleeding - platelets, in over 14,000 individuals from the UK and
Germany. They uncovered 22 regions of the human genome implicated in the development of
these blood cells. Of the 22 regions, 15 had not previously been identified. The study
represents the first genome-wide association of blood measurements to be completed in
cohorts with large sample sizes. "This study has been made possible by a great
collaboration of scientists from the UK and Germany, and the contribution of clinical
colleagues working in the field of heart disease, diabetes and coeliac disease in the UK,
Germany and the United States," explains Dr Nicole Soranzo, group leader at the
Wellcome Trust Sanger Institute and co-lead of the HaemGen consortium. "This unique
collaboration has allowed us to discover novel genetic determinants of blood cell
parameters, providing important insights into novel biological mechanisms underlying the
formation of blood cells by the blood stem cells and their role in disease. "This
study highlights the importance of studying large collections of samples from healthy
individuals where many different traits are measured."
New strategy for mending broken
hearts?
By mimicking the way embryonic stem cells develop into heart muscle in a lab, Duke
University bioengineers believe they have taken an important first step toward growing a
living "heart patch" to repair heart tissue damaged by disease. In a series of
experiments using mouse embryonic stem cells, the bioengineers used a novel mold of their
own design to fashion a three-dimensional "patch" made up of heart muscle cells,
known as cardiomyocytes. The new tissue exhibited the two most important attributes of
heart muscle cells -– the ability to contract and to conduct electrical impulses. The
mold looks much like a piece of Chex cereal in which researchers varied the shape and
length of the pores to control the direction and orientation of the growing cells. The
researchers grew the cells in an environment much like that found in natural tissues. They
encapsulated the cells within a gel composed of the blood-clotting protein fibrin, which
provided mechanical support to the cells, allowing them to form a three-dimensional
structure. They also found that the cardiomyocytes flourished only in the presence of a
class of "helper" cells known as cardiac fibroblasts, which comprise as much as
60 percent of all cells present in a human heart.
Mediterranean diet associated with
reduced risk of depression
Individuals who follow the Mediterranean dietary pattern -rich in vegetables, fruits,
nuts, whole grains and fish- appear less likely to develop depression, according to a
report of the University of Navarra, published in the October issue of Archives of General
Psychiatry.The lifetime prevalence of mental disorders has been found to be lower in
Mediterranean than Northern European countries, according to background information in the
article. One plausible explanation is that the diet commonly followed in the region may be
protective against depression. Previous research has suggested that the monounsaturated
fatty acids in olive oil -used abundantly in the Mediterranean diet- may be associated
with a lower risk of severe depressive symptoms.The researchers studied 10,094 healthy
Spanish participants who completed an initial questionnaire between 1999 and 2005.
Participants reported their dietary intake on a food frequency questionnaire, and the
researchers calculated their adherence to the Mediterranean diet based on nine components
(high ratio of monounsaturated fatty acids to saturated fatty acids; moderate intake of
alcohol and dairy products; low intake of meat; and high intake of legumes, fruit and
nuts, cereals, vegetables and fish).
Cancer drug is no different in
effectiveness as gold standard treatment for macular degeneration
Investigators from Boston University School of Medicine (BUSM) and the VA Boston
Healthcare System have shown, at 6 months in a small group of patients, that there is no
difference in efficacy between Bevacizumab (Avastin) and Ranibizumab (Lucentis) for the
treatment of age-related macular degeneration (AMD). The study, which appears currently
on-line in the American Journal of Ophthalmology, is the first to report early outcomes of
a prospective, double-masked, randomized, controlled trial comparing Bevacizumab to
Ranibizumab for the treatment of exudative (wet) age-related macular degeneration. AMD is
the leading cause of blindness over the age of 50 in developed Western countries. It can
present in 2 forms, exudative (wet) or nonexudative (dry). While dry AMD can lead to
severe vision loss, wet AMD is often more visually devastating with a higher risk of
blindness. The gold standard of treatment is ranibizumab (Lucentis, Genentech Inc.), which
was FDA approved for AMD in 2006. Bevacizumab (Avastin, Genentech Inc.) was FDA approved
for colo-rectal cancer in 2004, and has since been used worldwide as an off-label, local
intravitreal treatment for wet AMD. Both have shown to be efficacious in the treatment of
AMD, however, it is unknown which one is more effective.
Researchers report benefits of new
standard treatment study for rare pediatric brain cancer
A team of researchers led by The University of Texas M. D. Anderson Cancer Center unveiled
results today from the largest-ever collaborative study addressing the treatment of a rare
pediatric brain tumor. The findings suggest a new standard protocol could improve survival
nearly two-fold for pediatric patients with choroid plexus tumors, as reported at the 41st
Annual Meeting of the International Society of Pediatric Oncology (SIOP). Johannes Wolff,
M.D., professor in the Children's Cancer Hospital at M. D. Anderson Cancer Center and lead
investigator on the study, revealed that the protocol, consisting of three chemotherapy
agents and radiation, had projected overall survival rates of 93 percent at one year, 82
percent at five years, and 78 percent at eight years. "This SIOP 2000 study started
10 years ago and has grown to include more than 100 institutions from more than 20
countries," said Wolff. "With the data we have, we can tell which patients are
prone to do better and which ones have a poor prognosis. In addition, we've established a
promising standard protocol for these patients." Choroid plexus carcinomas are
malignant brain tumors that originate in the choroid plexus epithelium, which is the gland
that produces cerebrospinal fluid. Often the tumors may block the flow of cerebrospinal
fluid causing pressure to build in the brain and possibly enlarge the skull. It is a very
rare tumor affecting approximately 1,500 children worldwide each year, occurring more
often in infants. Due to the rarity of the disease, there is no standard treatment
protocol for the disease, but Wolff and other international researchers hope to change
that through their studies. They also developed an innovative statistical module for
institutions to use that will ensure quality and efficient data coming out of the study.
KEAP1 Keeps Major Cancer-Promoting
Protein at Bay
A tumor-suppressing protein snatches up an important cancer-promoting enzyme and tags it
with molecules that condemn it to destruction, a research team led by scientists at The
University of Texas M. D. Anderson Cancer Center reports this week in the journal
Molecular Cell. “KEAP1 is a recently discovered tumor suppressor, but how it works
has not been known. IKKß is a known oncoprotein that promotes cancer in at least two
different ways, but we did not know how it was regulated. We think we’ve answered
both questions with this research,” said senior author Mien-Chie Hung, Ph.D.,
professor and chair of M. D. Anderson’s Department of Molecular and Cellular
Oncology. The researchers showed that KEAP1, short for the tongue-twisting Kelch-like
ECH-associated protein 1, binds to IKKß and attaches molecules known as ubiquitins to the
oncoprotein, which targets it for dissolution by the cell’s proteasome complex.They
also showed that underexpression of KEAP1 is associated with poor survival among breast
cancer patients, and that it’s mutated and inactivated in some breast, liver, lung
and colon tumors.
Study Finds No Relationship Between
PCR Rate and Race in Women with Breast Cancer
Locally advanced breast cancer patients who received the same class of neoadjuvant
chemotherapy were found to have no evidence of disease at the time of their surgery, or
achieved pathological complete response, at the same rate regardless of race, according to
researchers at The University of Texas M. D. Anderson Cancer Center. The study, presented
in a poster discussion session at the 2009 Breast Cancer Symposium in San Francisco, is
the largest in a homogenous group of breast cancer patients evaluating pathological
complete response (pCR) according to race. Only one other study, also conducted at M. D.
Anderson but limited to triple negative breast cancer patients (estrogen and progesterone
receptor negative, HER2 negative), has analyzed the relationship between the two."Our
findings confirm pathological complete response is a strong prognostic indicator and a
surrogate for good survival, despite a patient's race, and that it's vital we continue to
strive towards achieving this milestone for all women with breast cancer," said
Mariana Chavez MacGregor, M.D., a medical oncology fellow at M. D. Anderson. "The
study also mandates that we continue to research the differences across races in breast
cancer."
Although more older women receive
breast-conserving therapy, gaps in treatment exist
According to a new study published in the October issue of the Journal of the American
College of Surgeons, although breast-conserving surgery (BCS), commonly known as
lumpectomy, is increasingly being used to treat older women with nonmetastatic invasive
breast cancer, there are still significant socioeconomic and geographic disparities in the
use of this type of therapy. For example, women in the Northeast and Pacific West are
significantly more likely to receive BCS than those in the South and parts of the Midwest.
In BCS, only a part of the affected breast is removed, whereas a mastectomy involves
removing all of the breast tissue, sometimes along with other nearby tissues. Combined
with radiotherapy, BCS is as effective as a mastectomy for treatment of early invasive
breast cancer. Yet despite the large body of evidence supporting the efficacy of BCS,
studies conducted in the last two decades reported that less than half of all surgically
treated patients with nonmetastatic invasive disease received BCS. "Treatment of
nonmetastatic invasive breast cancer has improved significantly over the past several
decades, but we continue to fall short of the goal to treat every woman with the highest
quality care," said Grace L. Smith, MD, PhD, Postdoctoral Fellow, Department of
Radiation Oncology, The University of Texas M. D. Anderson Cancer Center. "Our study
suggests that barriers exist that may prevent many women with breast cancer –
especially those in poorer areas, areas with low education levels, rural communities and
counties with few radiation oncologists – from being offered every treatment option
that should be available to them."
Common herbicides and fibrates
block nutrient-sensing receptor found in gut and pancreas
According to new research from the Monell Center and the Mount Sinai School of Medicine,
certain common herbicides and lipid-lowering fibrate drugs act in humans to block T1R3, a
nutrient-sensing taste receptor also present in intestine and pancreas. Commonly used in
agriculture and medicine, these chemical compounds were not previously known to act on the
T1R3 receptor. The T1R3 receptor is a critical component of both the sweet taste receptor
and the umami (amino acid) taste receptor. First identified on the tongue, emerging
evidence indicates that T1R3 and related taste receptors also are located on
hormone-producing cells in the intestine and pancreas. These internal taste receptors
detect nutrients in the gut and trigger the release of hormones involved in the regulation
of glucose homeostasis and energy metabolism. "Compounds that either activate or
block T1R3 receptors could have significant metabolic effects, potentially influencing
diseases such as obesity, type II diabetes and metabolic syndrome," noted Monell
geneticist and study leader Bedrich Mosinger, M.D., Ph.D. In the study, published online
in the Journal of Medicinal Chemistry, researchers tested the ability of two classes of
chemical compounds to block the T1R3 receptor. The compounds – fibrates and
phenoxy-herbicides – were selected based on their strong structural similarity to
lactisole, a sweet taste inhibitor that exerts its taste effects by blocking T1R3.
Fibrates are a class of drugs frequently used to treat lipid disorders such as high blood
cholesterol and triglycerides. Phenoxy-herbicides are used in agriculture to control
broad-leaf weeds; the best known, 2,4-D, is one of the most extensively used herbicides
worldwide. Using an in vitro preparation, the researchers found that both classes of
compounds potently blocked activation of the human sweet taste receptor, acting at
micromolar concentrations to inhibit binding of sugars to the T1R3 component of the
receptor. Additional testing revealed that the inhibitory effect of both fibrates and
phenoxy-herbicides on the T1R3 receptor is specific to humans. That is, the ability of
these compounds to block the receptor did not generalize across species to the rodent form
of the receptor.
UCSD researchers pave the way for
effective liver treatments
A combination of bioengineering and medical research at the University of California, San
Diego has led to a new discovery that could pave the way for more effective treatments for
liver disease. In this work, the researchers have utilized an array system that can
identify the biological components that can lead to or alleviate liver disease. The
technology works by controlling the range of environments surrounding star-shaped liver
cells called hepatic tellate cells (HSCs). HSCs are the major cell type involved in liver
fibrosis, which is the formation of scar tissue in response to liver damage. The activated
stellate cell is responsible for secreting collagen that produces a fibrous scar, which
can lead to cirrhosis. Current approaches to identify the factors affecting HSC biology
typically focus on each factor individually, ignoring the complex cross-talk between the
many components acting on the cells. The high-throughput cellular array technology
developed by UCSD researchers systematically assesses and probes the complex relationships
between hepatic stellate cells and components of their microenvironment. By doing this,
they found that certain proteins are critical in regulating HSC activation and that the
proteins influence one another's actions on the cells. The findings were published in a
paper entitled "Investigating the role of the extracellular environment in modulating
hepatic stellate cell biology with array combinatorial microenvironments" in the
September 2009 issue of Integrative Biology.
Key new ingredient in climate model
refines global predictions
For the first time, climate scientists from across the country have successfully
incorporated the nitrogen cycle into global simulations for climate change, questioning
previous assumptions regarding carbon feedback and potentially helping to refine model
forecasts about global warming. The results of the experiment at the Department of
Energy's Oak Ridge National Laboratory and at the National Center for Atmospheric Research
are published in the current issue of Biogeosciences. They illustrate the complexity of
climate modeling by demonstrating how natural processes still have a strong effect on the
carbon cycle and climate simulations. In this case, scientists found that the rate of
climate change over the next century could be higher than previously anticipated when the
requirement of plant nutrients are included in the climate model. ORNL's Peter Thornton,
lead author of the paper, describes the inclusion of these processes as a necessary step
to improve the accuracy of climate change assessments. "We've shown that if all of
the global modeling groups were to include some kind of nutrient dynamics, the range of
model predictions would shrink because of the constraining effects of the carbon nutrient
limitations, even though it's a more complex model." To date, climate models ignored
the nutrient requirements for new vegetation growth, assuming that all plants on earth had
access to as much "plant food" as they needed. But by taking the natural demand
for nutrients into account, the authors have shown that the stimulation of plant growth
over the coming century may be two to three times smaller than previously predicted. Since
less growth implies less CO2 absorbed by vegetation, the CO2 concentrations in the
atmosphere are expected to increase. However, this reduction in growth is partially offset
by another effect on the nitrogen cycle: an increase in the availability of nutrients
resulting from an accelerated rate of decomposition – the rotting of dead plants and
other organic matter – that occurs with a rise in temperature.Combining these two
effects, the authors discovered that the increased availability of nutrients from more
rapid decomposition did not counterbalance the reduced level of plant growth calculated by
natural nutrient limitations; therefore less new growth and higher atmospheric CO¬2
concentrations are expected. The study's author list, which consists of scientists from
eight different institutions around the U.S. including ORNL, the National Center for
Atmospheric Research, the National Oceanic and Atmospheric Administration Earth System
Research Laboratory, and several research universities, exemplifies the broad expertise
required to engage in the multidisciplinary field that is global climate modeling.
Hyper-SAGE boosts remote MRI
sensitivity
A new technique in Magnetic Resonance Imaging dubbed "Hyper-SAGE" has the
potential to detect ultra low concentrations of clincal targets, such as lung and other
cancers. Development of Hyper-SAGE was led by one of the world's foremost authorities on
MRI technology, Alexander Pines, a chemist who holds joint appointments with the Lawrence
Berkeley National Laboratory (Berkeley Lab) and the University of California, Berkeley.
The key to this technique is xenon gas that has been zapped with laser light to
"hyperpolarize" the spins of its atomic nuclei so that most are pointing in the
same direction. "By detecting the MRI signal of dissolved hyperpolarized xenon after
the xenon has been extracted back into the gas phase, we can boost the signal's strength
up to 10,000 times," Pines says. "It is absolutely amazing because we're looking
at pure gas and can reconstruct the whole image of our target. With this degree of
sensitivity, Hyper-SAGE becomes a highly promising tool for in vivo diagnostics and
molecular imaging." MRI is a painless and radiation-free means of obtaining high
quality three-dimensional tomographical images of internal tissue and organs. It is
especially valuable for optically opaque samples, such as blood. However, the application
of MRI to biomedical samples has been limited by sensitivity issues. For the past three
decades, Pines has led an on-going effort to find ways of enhancing the sensitivity of MRI
and its sister technology, nuclear magnetic resonance (NMR) spectroscopy. Hyper-SAGE, the
latest development, represents a significant new advance for both technologies, according
to Xin Zhou, a member of Pines' research group.
Ashok Gadgil's inexpensive
inventions address big problems of world's poor
EarthSky spoke with environmental scientist Ashok Gadgil of the Lawrence Berkeley National
Laboratory. Dr Gadgil has spent decades applying science to improve the lives of the
world’s poor. Ashok Gadgil: When it comes to issues that are desperate problems for
the bottom half, economically, the bottom half of humanity, problems could be very
serious, regarding shelter and access to safe drinking water, access to energy, and even
adequate food supplies going forward. And science could make a huge difference there. Dr.
Gadgil has a long list of inexpensive inventions he’s developed that address big
problems, including a simple cook stove for families in Darfur that’s three times as
efficient traditional ones. And he developed a water purifier that uses ultraviolet light
to produce clean water for 1,000 people each day.
Breast cancer patients with high
risk gene diagnosed 6 years earlier than generation before
Women with a deleterious gene mutation are diagnosed with breast cancer six years earlier
than relatives of the previous generation who also had the disease and/or ovarian cancer,
according to new research from The University of Texas M. D. Anderson Cancer Center. The
findings, presented in a poster session at the 2009 Breast Cancer Symposium, could have an
impact on how women at highest risk for the disease are counseled and even screened in the
future, explained Jennifer Litton, M.D., assistant professor in M. D. Anderson's
Department of Breast Medical Oncology. "In our practice, we've noticed that women
with a known deleterious BRCA gene mutation are being diagnosed earlier with the disease
than their moms or aunts," said Litton, M.D., the study's first author. "With
this study, we looked at women who had been both treated and had their BRCA testing at M.
D. Anderson to determine if what we were seeing anecdotally was consistent
scientifically." It's estimated that five to 10 percent of all breast cancers are
associated with either the BRCA1 or 2 mutation, both of which are associated with an
increased risk for breast and ovarian cancers. According to the American Cancer Society
(ACS), women with BRCA1 or 2 have a 60 percent lifetime risk of developing breast cancer,
compared to a 12 percent risk for women in the general population. Given their greater
risk, women with known BRCA mutations and/or whose mothers and/or aunts from either side
of the family have the mutation are screened beginning at age 25. In 2007, as a complement
to mammography, ACS guidelines added Magnetic Resonance Imaging (MRI) in the surveillance
of these women at highest risk, as MRI is thought to catch smaller tumors even earlier.
Consideration of prophylactic mastectomies is also a component of their surveillance, said
Litton. "Currently, BRCA positive women are counseled that they won't need to worry
about breast cancer until a certain age. However, our findings show that we may actually
start seeing the disease even earlier in future generations. We need to make changes
accordingly in order to best advise and care for these women at greatest risk,"
Litton said.
Child safety seat education needs
an extra boost
Motor vehicle crashes are a leading cause of death among children despite the widespread
availability of effective child passenger restraint systems (CPRSs) such as child safety
seats. However, even when provided with free CPRSs and education about how to use them
properly, many caregivers do not make them a part of their daily routine, according to the
authors of a new study published in the Wisconsin Medical Journal (Vol. 108, No. 7).
Researchers from The Medical College of Wisconsin in Milwaukee conducted a community-based
study in which a certified car seat technician educated caregivers of more than 100
low-income, minority and urban children about how to choose and install the appropriate
CPRS based on their child's age, height and weight. In addition to this training, each
caregiver was given a CPRS for their child at no cost. While the rate of appropriate
restraint soared to 85 percent soon after receiving the free CPRS and 30-minute training
session with a technician, it declined to 65 percent over the next nine months. Older
children were less likely to be restrained properly than younger children, suggesting that
interventions focused on reaching families with children before it is time to transition
them into a booster seat might be most effective. The underlying reasons why caregivers do
not use CPRS in daily routines are not clear, but factors such as difficulties in having
multiple caregivers transport the same child in multiple vehicles may play a part. A
better understanding of these reasons is important in developing interventions to increase
appropriate use of CPRS.
Owners should count calories for
obese pets, consider several factors for good health
You might watch your daily calorie intake or glance over nutritional information on food
packages, but do you do the same for your pet? Dr. Susan Nelson, a veterinarian and
assistant professor of clinical sciences at Kansas State University, said there are
several guidelines to follow when feeding your pet to ensure that it maintains good
health. Just like human food packages, many cat and dog food packages contain nutritional
information, Nelson said. Packages often list the kilocalories, protein, fat,
carbohydrates and fiber per cup. In recent years, manufacturers started listing some
nutritional information, including calorie content, for dog and cat treats. "In the
past, we didn't know how many calories were in various treats," Nelson said.
"Now that's becoming more available, and that's because more pets are becoming obese
and their owners are asking for that information. Pets are overeating and underexercising,
and they're eating too many high-fat foods and treats." Nelson said these plumper
pets are not only benefitting from improvements in pet food quality, but also from the
increased calorie content caused by the higher fat content of many premium diets. But does
that call for owners to start counting calories for their pets? "It's important to
count calories if the pet is overweight, but it's probably not necessary if you have a pet
that is of normal weight," Nelson said. "If it starts to get pudgy, you need to
take a look at how much exercise it is getting, how much food you are feeding it, and how
many treats you're giving it." Calories from treats should be no more than 10 percent
of your pet's diet. If owners want to count their pet's calories, Nelson said,
veterinarians can make diet calculations for dogs and cats. The overall recommendation for
the amount of food to feed your pet is based on several factors, including the type of
food you are feeding your pet, your pet's metabolism and how much exercise it gets.
Too much of a good thing?
Scientists explain cellular effects of vitamin A overdose and deficiency
If a little vitamin A is good, more must be better, right? Wrong! New research published
online in the FASEB Journal shows that vitamin A plays a crucial role in energy production
within cells, explaining why too much or too little has a complex negative effect on our
bodies. This is particularly important as combinations of foods, drinks, creams, and
nutritional supplements containing added vitamin A make an overdose more possible than
ever before."Our work illuminates the value and potential harm of vitamin A use in
cosmetic creams and nutritional supplements," said Ulrich Hammerling, co-author of
the study, from the Sloan-Kettering Institute for Cancer Research in New York.
"Although vitamin A deficiency is not very common in our society, over-use of this
vitamin could cause significant disregulation of energy production impacting cell growth
and cell death." Although the importance of vitamin A to human nutrition and fetal
development is well-known, it has been unclear why vitamin A deficiencies and overdoses
cause such widespread and profound harm to our organs, until now. The discovery by
Hammerling and colleagues explains why these effects occur, while also providing insight
into vitamin A's anti-cancer effects. The scientists used cultures from both human and
mice cells containing specific genetic modifications of the chemical pathways involved in
mitochondrial energy production. The cells were then grown with and without vitamin A, and
scientists examined the impact on the various steps of energy production. Results showed
that retinol, the key component of vitamin A, is essential for the metabolic fitness of
mitochondria and acts as a nutritional sensor for the creation of energy in cells. When
there is too much or too little vitamin A, mitochondria do not function properly, wreaking
havoc on our organs. "Beauty might be only skin deep, but vitamin A isn't. It goes to
the nucleus of our cells and can affect our health for better or worse," said Gerald
Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "Using too many products
enriched with vitamin A could lead to negative, even fatal, consequences."
U-M discovery about biological
clocks overturns long-held theory
University of Michigan mathematicians and their British colleagues say they have
identified the signal that the brain sends to the rest of the body to control biological
rhythms, a finding that overturns a long-held theory about our internal clock.
Understanding how the human biological clock works is an essential step toward correcting
sleep problems like insomnia and jet lag. New insights about the body's central pacemaker
might also, someday, advance efforts to treat diseases influenced by the internal clock,
including cancer, Alzheimer's disease and mood disorders, said University of Michigan
mathematician Daniel Forger. "Knowing what the signal is will help us learn how to
adjust it, in order to help people," said Forger, an associate professor of
mathematics and a member of the U-M's Center for Computational Medicine and
Bioinformatics. "We have cracked the code, and the information could have a
tremendous impact on all sorts of diseases that are affected by the clock." The
body's main time-keeper resides in a region of the central brain called the
suprachiasmatic nuclei, or SCN. For decades, researchers have believed that it is the rate
at which SCN cells fire electrical pulses---fast during the day and slow at night---that
controls time-keeping throughout the body. Imagine a metronome in the brain that ticks
quickly throughout the day, then slows its pace at night. The rest of the body hears the
ticking and adjusts its daily rhythms, also known as circadian rhythms, accordingly.
That's the idea that has prevailed for more than two decades. But new evidence compiled by
Forger and his colleagues shows that "the old model is, frankly, wrong," Forger
said.
Study pinpoints key mechanism in
brain development, raising question about use of antiseizure drug
Researchers at the Stanford University School of Medicine have identified a key molecular
player in guiding the formation of synapses — the all-important connections between
nerve cells — in the brain. This discovery, based on experiments in cell culture and
in mice, could advance scientists' understanding of how young children's brains develop as
well as point to new approaches toward countering brain disorders in adults. The new work
also pinpoints, for the first time, the biochemical mechanism by which the widely
prescribed drug gabapentin (also marketed under the trade name Neurontin) works. "We
have solved the longstanding mystery of how this blockbuster drug acts," said Ben
Barres, MD, PhD, professor and chair of neurobiology. The study shows that gabapentin
halts the formation of new synapses, possibly explaining its therapeutic value in
mitigating epileptic seizures and chronic pain. This insight, however, may lead physicians
to reconsider the circumstances in which the drug should be prescribed to pregnant women.
The paper, to be published online Oct. 8 in the journal Cell, looks at the interaction
between neurons — the extensively researched nerve cells that account for 10 percent
of the cells in the brain — and the less-studied but much more common brain cells
called astrocytes. Much work has been done on how neurons transmit electrical signals to
each other through synapses — the nanoscale electrochemical contact points between
neurons. It is the brain's circuitry of some 100 trillion of these synapses that allow us
to think, feel, remember and move. It is commonly agreed that the precise placement and
strength of each person's trillions of synaptic connections closely maps with that
person's cognitive, emotional and behavioral makeup. But exactly why a particular synapse
is formed in a certain place at a certain time has largely remained a mystery. In 2005,
Barres took a big step toward explaining this process when he and his colleagues
discovered that a protein astrocytes secrete, called thrombospondin, is essential to the
formation of this complex brain circuitry. Still, no one knew the precise mechanism by
which thrombospondin induced synapse formation.
Being overweight super-sizes both
risk and consequences of sleep-disordered breathing
Overweight individuals are not just at greater risk of having sleep-disordered-breathing
(SDB), they are also likely to suffer greater consequences, according to new research.
According to the study, to be published in the October 15 issue of the American Journal of
Respiratory and Critical Care Medicine, an official publication of the American Thoracic
Society, excess weight increased the severity of oxygen desaturation in the blood of
individuals with SDB during and after apneas and hypopneas. "We knew that excess body
weight is strongly related to more frequent breathing events—apneas and
hypopneas—in persons with SDB," said lead author Paul E. Peppard, Ph.D.,
assistant professor of population health sciences at the University of Wisconsin-Madison.
"In this study, we wanted to go a step further and measure how much the excess weight
contributes to the severity of individual breathing events." Dr. Peppard and
colleagues recruited 750 adults from the Wisconsin Sleep Cohort study, an ongoing
epidemiological investigation into the natural history of SDB, to have their breathing,
blood-oxygen levels and sleep analyzed. Participants were also evaluated on several
measures of physique—body mass index (BMI), neck -circumference and waist-to-hip
ratio. Among the participants in the overnight study, 40 percent of whom were obese, there
were more than 37,000 SDB events. The researchers found that a number of factors
influenced the severity of blood oxygen desaturation associated with these events,
including age, gender, body position and sleep phase (REM or non-REM sleep). However, even
after these other factors were accounted for, the researchers found that BMI predicted the
degree to which the body's tissues were "starved" of oxygen during apneas and
hypopneas. In fact, each 10-point increase in BMI predicted a 10 percent increase in the
severity of oxygen depletion associated with SDB events.
Will giving coffee to babies keep
them awake as adults?
An F1000 evaluation looks at a Canadian study on how giving caffeine to newborn rats has a
long-lasting and detrimental effect on sleep and breathing in adulthood Breathing problems
are the leading causes of hospitalisation and death in premature babies. These babies are
therefore often given caffeine because of its qualities as a respiratory stimulant. Until
recently, the long-term effects of this treatment in humans have not been examined.
However, Gaspard Montandon and colleagues showed in the Journal of Physiology that the use
of caffeine in neonates can cause serious alterations in the sleeping patterns of adult
rats as a result of its effect on the developing respiratory system. Sleep abnormality is
a significant indicator for ill health and reduced life span.When the caffeine-treated
rats reached adulthood, their sleeping time was reduced, the length of time they took to
reach the first stage of sleep was increased, and their non-REM sleep was fragmented.
Breathing at rest was higher than in rats not treated with caffeine. In his review of the
study, F1000 Faculty Member James Duffin of the University of Toronto says the results
"raise concerns about the long-term consequences of neonatal caffeine administration
on brain development and behaviour."
Discovery of genetic defect may
lead to better treatments for common gut diseases
New findings related to an uncommon genetic disorder may impact the diagnosis and
treatment of inflammatory bowel disease (IBD), the most common chronic gastrointestinal
illness in children and teens. Two million Americans have IBD which involves inflammation
of the gastrointestinal tract. Researchers from the United States and Canada have
identified a genetic defect not previously known to be a cause of chronic granulomatous
disease (CGD), an inherited disorder with recurrent bacterial and fungal infections. Some
patients also develop gastrointestinal inflammation, as occurred in the patient in whom
the new gene defect was discovered. CGD, which occurs in 1 in 200,000, is usually
diagnosed in childhood. In addition to providing insight into CGD, a condition in which an
enzyme defect prevents white blood cells in the body from killing invading bacteria, the
new findings highlight how abnormal white blood cell function can predispose individuals
to IBD, and may help provide insight into why IBD develops. Crohn's disease and ulcerative
colitis are the most common forms of IBD. The research was led by Mary Dinauer, M.D.,
Ph.D., of the Herman B Wells Center for Pediatric Research at the Indiana University
School of Medicine and Riley Hospital for Children, Nicola Wright, M.D., and colleagues at
the Alberta Children's Hospital and the University of Calgary, and William Nauseef, M.D.,
of the University of Iowa. The new findings are reported in the October 8 print edition of
the journal Blood.
Protective Role for Copper in
Alzheimer’s Disease
New research has shown that there could be a protective role for copper in
Alzheimer’s disease. Previous research has shown that copper is one component of the
amyloid beta plaques which are found in the brains of people of Alzheimer’s disease.
A central tenet of the Amyloid Cascade Hypothesis of Alzheimer’s disease is the
aberrant deposition in the brain of A?42 in ?-sheets in neuritic or senile plaques. The
Keele team have shown in previous research in JAD (House et al., (2004) JAD 6, 291-301)
that copper (Cu(II)) prevents the deposition of A?42 in ?-sheets while in the current
research they show that Cu(II) abolishes the ?-sheet structure of preformed amyloid
fibrils of A?42. A similar finding was made by the group of Jiang for the other form of
beta amyloid, A?40, and together these observations strongly suggest that copper prevents
both the formation and the accumulation of plaques in the brain. Coincident with the
copper-catalysed dissolution of ?-sheets of A?42, Exley’s group made the first
observation of the in vitro formation of spherulites of this peptide. These spherical
globules of amyloid have only previously been observed in vitro for the other
amyloid-forming proteins insulin and ?-lactoglobulin. Copper appeared to have a role in
the formation of spherulites of A?42 and this will be investigated in future research. The
role of metals in the formation, deposition and metabolism of A? in Alzheimer’s
disease is much debated and these new findings highlight a potential protective role for
copper in Alzheimer’s disease.
Discovery of genetic defect may
lead to better treatments for common gut diseases
New findings related to an uncommon genetic disorder may impact the diagnosis and
treatment of inflammatory bowel disease (IBD), the most common chronic gastrointestinal
illness in children and teens. Two million Americans have IBD which involves inflammation
of the gastrointestinal tract. Researchers from the United States and Canada have
identified a genetic defect not previously known to be a cause of chronic granulomatous
disease (CGD), an inherited disorder with recurrent bacterial and fungal infections. Some
patients also develop gastrointestinal inflammation, as occurred in the patient in whom
the new gene defect was discovered. CGD, which occurs in 1 in 200,000, is usually
diagnosed in childhood. In addition to providing insight into CGD, a condition in which an
enzyme defect prevents white blood cells in the body from killing invading bacteria, the
new findings highlight how abnormal white blood cell function can predispose individuals
to IBD, and may help provide insight into why IBD develops. Crohn's disease and ulcerative
colitis are the most common forms of IBD.
Liver cells grown from patients'
skin cells
Scientists at The Medical College of Wisconsin in Milwaukee have successfully produced
liver cells from patients' skin cells opening the possibility of treating a wide range of
diseases that affect liver function. The study was led by Stephen A. Duncan, D. Phil.,
Marcus Professor in Human and Molecular Genetics, and professor of cell biology,
neurobiology and anatomy, along with postdoctoral fellow Karim Si-Tayeb, Ph.D., and
graduate student Ms. Fallon Noto. "This is a crucial step forward towards developing
therapies that can potentially replace the need for scarce liver transplants, currently
the only treatment for most advanced liver disease," says Dr. Duncan. Liver disease
is the fourth leading cause of death among middle aged adults in the United States. Loss
of liver function can be caused by several factors, including genetic mutations,
infections with hepatitis viruses, by excessive alcohol consumption, or chronic use of
some prescription drugs. When liver function goes awry it can result in a wide variety of
disorders including diabetes and atherosclerosis and in many cases is fatal. The Medical
College research team generated patient–specific liver cells by first repeating the
work of James Thomson and colleagues at University of Wisconsin-Madison who showed that
skin cells can be reprogrammed to become cells that resemble embryonic stem cells. They
then tricked the skin–derived pluripotent stem cells into forming liver cells by
mimicking the normal processes through which liver cells are made during embryonic
development. Pluripotent stem cells are so named because of their capacity to develop into
any one of eh more than 200 cell types in the human body. At the end of this process, the
researchers found that they were able to very easily produce large numbers of relatively
pure liver cells in laboratory culture dishes. "We were excited to discover that the
liver cells produced from human skin cells were able to perform many of the activities
associated with healthy adult liver function and that the cells could be injected into
mouse livers where they integrated and were capable of making human liver proteins,"
says Dr. Duncan.
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