News 3 juli 2009
Blood stem cell growth factor
reverses memory decline in mice
A human growth factor that stimulates blood stem cells to proliferate in the bone marrow
reverses memory impairment in mice genetically altered to develop Alzheimer's disease,
researchers at the University of South Florida and James A. Haley Hospital found. The
granulocyte-colony stimulating factor (GCSF) significantly reduced levels of the
brain-clogging protein beta amyloid deposited in excess in the brains of the Alzheimer's
mice, increased the production of new neurons and promoted nerve cell connections. The
findings are reported online in Neuroscience and are scheduled to appear in the journal's
print edition in August. GCSF is a blood stem cell growth factor or hormone routinely
administered to cancer patients whose blood stem cells and white blood cells have been
depleted following chemotherapy or radiation. GCSF stimulates the bone marrow to produce
more white blood cells needed to fight infection. It is also used to boost the numbers of
stem cells circulating in the blood of donors before the cells are harvested for bone
marrow transplants. Advanced clinical trials are now investigating the effectiveness of
GCSF to treat stroke, and the compound was safe and well tolerated in early clinical
studies of ischemic stroke patients. "GCSF has been used and studied clinically for a
long time, but we're the first group to apply it to Alzheimer's disease," said USF
neuroscientist Juan Sanchez-Ramos, MD, PhD, the study's lead author. "This growth
factor could potentially provide a powerful new therapy for Alzheimer's disease – one
that may actually reverse disease, not just alleviate symptoms like currently available
drugs." The researchers showed that injections under the skin of filgrastim
(Neupogen®) -- one of three commercially available GCSF compounds -- mobilized blood stem
cells in the bone marrow and neural stem cells within the brain and both of these actions
led to improved memory and learning behavior in the Alzheimer's mice. "The beauty in
this less invasive approach is that it obviates the need for neurosurgery to transplant
stem cells into the brain," Dr. Sanchez-Ramos said.
Study Examines Dietary Influences
Of Liver Disease
Diets high in protein and cholesterol are associated with a higher risk of hospitalization
or death due to cirrhosis or liver cancer, while diets high in carbohydrates are
associated with a lower risk. These findings are in the July issue of Hepatology, a
journal published by John Wiley & Sons on behalf of the American Association for the
Study of Liver Diseases (AASLD). The article is also available online at Wiley
Interscience. There are many reasons to suspect that dietary factors influence the
development of hepatic steatosis and its progression to more severe liver disease. First,
poor diet may lead to obesity, insulin resistance and diabetes, which are the most
important known risk factors for hepatic steatosis. Also, dietary lipids may directly
affect fat in the liver. Furthermore, a high cholesterol diet has been shown to induce
serious steatosis in animal studies.Researchers, led by George Ioannou of Veterans Affairs
Puget Sound Health Care System in Seattle, investigated whether dietary nutrient
composition was associated with the subsequent development of cirrhosis or liver cancer in
a representative sample of the U.S. population. They utilized data from 9,221 participants
in the National Health Examination Survey who had completed a 24-hour dietary recall
questionnaire. Participants were excluded if they suffered from cirrhosis or liver cancer
at the start of the study, or received a diagnosis within five years. During the follow-up
period, an average of 13.3 years, 123 participants received a new diagnosis of cirrhosis
(118 people) or liver cancer (5 people) according to hospitalization records and death
certificates. These individuals were more likely to be older, more obese with more central
fat distribution. They had lower educational attainment and higher alcohol consumption,
and were more likely to be male, diabetic and non-white.
Exercise Helps Patients with
Non-Alcoholic Fatty Liver Disease
Counseling patients with non-alcoholic fatty liver disease (NAFLD) on how to increase
physical activity leads to health benefits that are independent of changes in weight.
These findings are in a new study in the July issue of Hepatology, a journal published by
John Wiley & Sons on behalf of the American Association for the Study of Liver
Diseases (AASLD). The article is also available online at Wiley Interscience. NAFLD is the
most common form of chronic liver disease in developed countries. It is associated with
the metabolic syndrome, which also includes obesity, insulin resistance and type 2
diabetes, and is characterized by elevated liver enzymes. Currently, patients with NAFLD
are encouraged to alter their lifestyles, however the focus has been on weight loss
through dietary changes. The effects of increasing physical activity alone have not been
thoroughly investigated.Researchers led by Jacob George of Sydney West Area Health Service
in Australia, examined the health outcomes of patients who were counseled on how to
increase physical activity. They prospectively enrolled 141 patients with NAFLD from the
Sydney West Area Health Service. The participants were divided into a control group, a
low-intensity lifestyle intervention group, and a moderate-intensity lifestyle
intervention group. The patients in the intervention arms worked with exercise scientists
who provided individually tailored counseling on how to increase both planned and
incidental physical activity. Walking was the main type of exercise discussed and patients
were encouraged to be active for at least 150 minutes per week.
New Treatment for Receding Gums: No
Pain, Lots of Gain Tufts Dental Researchers Show Tissue Regeneration Application
Tufts dental researchers conducted a three-year follow-up study that examined the
stability of a treatment option for receding gums and found that complete root coverage
— the goal of the surgery — had been maintained. This specific tissue
regeneration application, developed at Tufts, reduces the considerable pain and recovery
time of gum grafting surgery. The case study of six patients is published in the July 2009
issue of the Journal of Periodontology. "Patients have a less invasive treatment
option for receding gums and we now have evidence to support the stability of this
relatively painless procedure. Instead of leaving the dental office with stitches in the
roof of their mouth, a patient leaves with a small bandage on the arm that can be removed
in an hour,” said Terrence Griffin, DMD, associate professor, chair of the department
of periodontology, and director of postdoctoral periodontology at Tufts University School
of Dental Medicine in Boston.“One of our previous research studies showed that all of
the post-operative bleeding and most of the post-operative pain were related to the gum
tissue removed from the roof of the mouth for use as a graft,” he continued.
Lack of sleep could be more
dangerous for women than men
Women who get less than the recommended eight hours sleep a night are at higher risk of
heart disease and heart-related problems than men with the same sleeping patterns.
Research by the University of Warwick and University College London has found that levels
of inflammatory markers vary significantly with sleep duration in women, but not men. The
study, published today (Weds) in the American journal SLEEP, found levels of Interleukin-6
(IL-6), a marker related to coronary heart disease, were significantly lower in women who
reported sleeping eight hours as compared with 7hours. A second marker, High-sensitivity
C-reactive protein (hs-CRP), is predictive of future cardiovascular morbidity. Levels of
hs-CRP were significantly higher in women who reported sleeping five hours or less. Lead
author of the study, Associate Professor of Biochemical Medicine at Warwick Medical School
Michelle Miller said short-term sleep deprivation studies have shown that inflammatory
markers are elevated in sleep-deprived individuals, suggesting that inflammatory
mechanisms may play a role in the cardiovascular risk associated with sleep deprivation.
Nanotechnology may increase
longevity of dental fillings
Tooth-colored fillings may be more attractive than silver ones, but the bonds between the
white filling and the tooth quickly age and degrade. A Medical College of Georgia
researcher hopes a new nanotechnology technique will extend the fillings' longevity.
"Dentin adhesives bond well initially, but then the hybrid layer between the adhesive
and the dentin begins to break down in as little as one year," says Dr. Franklin Tay,
associate professor of endodontics in the MCG School of Dentistry. "When that
happens, the restoration will eventually fail and come off the tooth." Half of all
tooth-colored restorations, which are made of composite resin, fail within 10 years, and
about 60 percent of all operative dentistry involves replacing them, according to research
in the Journal of the American Dental Association. "Our adhesives are not as good as
we thought they were, and that causes problems for the bonds," Dr. Tay says.
UCLA collaboration identifies
immune system link to schizophrenia
Schizophrenia is a devastating mental disease, thought to be caused by the interaction of
both genetic and environmental factors. Because there is no biochemical test that can
identify the disorder, physicians rely upon the recognition of its symptoms — which
can include auditory hallucinations and paranoia — in order to make their diagnosis.
Now following on their earlier work that identified three gene locations that may be
implicated in schizophrenia, researchers at UCLA and colleagues from around the world
have, for the first time, identified additional genes that confirm what scientists have
long suspected — that the immune system may play a role in the development of the
disorder. Further, they have also identified genetic anomalies that disrupt the cellular
pathways involved in brain development, memory and cognition, all markers of
schizophrenia. The research appears in the July 1 online edition of the journal Nature.
Roel Ophoff, the co-lead author and an assistant professor at the Center for
Neurobehavioral Genetics at the UCLA Semel Institute for Neuroscience and Human Behavior,
and his collaborators from nearly 50 institutions worldwide, performed a genome-wide scan
of 2,663 people diagnosed with schizophrenia and 13,498 controls from eight European
locations. They were looking for single nucleotide polymorphisms (SNP), genetic variations
that are commonly present in the general population but more often present in those
suffering from the disorder. In total, nearly 314,000 SNPs were included in their
analysis. They found significant associations with genetic markers on the Major
Histocompatibility Complex (MHC), a group of genes that controls several aspects of the
immune response. Further, they discovered additional variations in two other genes, called
NRGN and TCF4, which points to perturbation of pathways involved in brain development,
memory and cognition.
Newly appreciated membrane estrogen
receptor important therapeutic target for breast cancer
New research at Rhode Island Hospital has uncovered the biological effects of a novel
membrane estrogen receptor, a finding that has potential implications for hormonal therapy
for breast cancer. The study is published in the July edition of the journal Molecular
Endocrinology. This new study by Edward Filardo, MD, and his research team further
supports earlier published work by the group that linked the transmembrane receptor,
GPR30/GPER-1, to specific estrogen binding, rapid estrogen signaling and breast cancer
metastasis. "What is exciting about this new work," says Filardo, "is that
it provides some insight into the influence of GPR30 at the cellular level. It shows that
estrogen action through GPR30 allows for breast tumor cell survival, and not breast tumor
cell proliferation." Prior studies by Filardo's group showed that estrogen acts
through GPR30 to promote the rapid release of preformed growth factors that are tethered
to the surface of breast cancer cells. Their latest study was conducted in an effort to
better understand the mechanism by which GPR30 triggered the release of epidermal growth
factor (EGF) polypeptides from the surface of breast cancer cells.The investigator's found
that the "growth factors" did not promote cellular growth, which by itself is
not a novel finding. It has long been appreciated that EGF-related factors are also
important in other cellular activities such as cellular survival. Filardo and the research
team, however, found that estrogen action through GPR30 had a more profound effect on
tumor cell survival. They found that GPR30 promoted the assembly of what is called a
"provisional extracellular matrix" -- a crucial event in cellular survival. More
specifically, they found that release of growth factor by GPR30 required the activation of
a latent adhesion receptor (known as integrin a5b1). Filardo says, "Activation of
integrin a5b1 by GPR30 is a significant event because it provides a way for invading cells
to gain hold once they metastasize to tissues distant to the primary breast cancer. This
happens because activated integrin a5b1 can convert soluble plasma protein fibronectin
into an insoluble cage. The breast cancer cells can use this to adapt to a new
environment."
Both good/bad movie characters who
smoke influence teens to do the same
Dartmouth researchers have determined that movie characters who smoke, regardless of
whether they are "good guys" or "bad guys," influence teens to try
smoking. The study, published in the July 2009 issue of the journal Pediatrics, is titled
"Adolescent Smoking: Who Matters More, Good Guys or Bad Guys?" "Previous
studies have confirmed a link between smoking in movies and the initiation of smoking by
adolescents, and we wanted to dig deeper into the data to see if the type of character who
is smoking matters. Is it 'good guys' or 'bad guys' that have more of an influence?"
said Susanne Tanski, the lead author on the study, and an assistant professor of
pediatrics at Dartmouth Medical School. "It's true that 'bad guys' are more often
smokers in the movies, but there really are not that many 'bad guys' compared to 'good
guys'. Episode for episode, youth who saw negative character smoking were more likely to
start smoking, but since overall there is so much more exposure to 'good guy' smoking, the
net effect is similar." The survey also revealed that low-risk teens, based on
sensation-seeking behavior, are more strongly influenced by "bad guy" movie
smoking. "This suggests that it's alluring for 'good' kids to emulate the 'bad'
characters on the movie screen," said Tanksi. Tanski is part of a team of researchers
at Dartmouth College and Dartmouth Medical School (DMS) who have been studying the
connections between popular culture and risky behavior in adolescents. They have published
numerous journal articles that document the link between exposure to smoking and drinking
alcohol in movies and teens using tobacco and alcohol. In May 2009, two members of this
team, James Sargent and Todd Heatherton, published a research letter in the Journal of the
American Medical Association that reported declining trends in both occurrences of smoking
in movies and in smoking among U.S. eight graders between 1996 and 2007. In that letter,
the authors state, "[M]ovie smoking represents only one of several factors that
contribute to youth smoking trends, including the marketing of tobacco, price of
cigarettes, restrictions imposed by the Master Settlement Agreement in 1999, and state
prevention programs. … Nonetheless, the downward trend in movie smoking is consistent
with an influence on downward trends in adolescent smoking." Sargent is a professor
of pediatrics and the co-director of the Cancer Control Research Program at DMS's Norris
Cotton Cancer Center at Dartmouth-Hitchcock Medical Center, Heatherton is a professor of
psychological and brain sciences at Dartmouth College. Tanski acknowledges that, although
there is a downward trend, smoking still occurs in many movies that teens watch,
particularly given the popularity of movie channels and video rentals providing access to
older films. "Parents should limit movie viewing and specifically restrict access to
R-rated movies, which tend to contain more smoking," she said. "When teens do
see movies or TV shows that contain smoking, parents should talk with them in an effort to
discourage initiation of smoking."
ADA releases updated position paper
on vegetarian diet
The American Dietetic Association has released an updated position paper on vegetarian
diets that concludes such diets, if well-planned, are healthful and nutritious for adults,
infants, children and adolescents and can help prevent and treat chronic diseases
including heart disease, cancer, obesity and diabetes. ADA's position, published in the
July issue of the Journal of the American Dietetic Association, represents the
Association's official stance on vegetarian diets "It is the position of the American
Dietetic Association that appropriately planned vegetarian diets, including total
vegetarian or vegan diets, are healthful, nutritionally adequate and may provide health
benefits in the prevention and treatment of certain diseases. Well-planned vegetarian
diets are appropriate for individuals during all stages of the life-cycle including
pregnancy, lactation, infancy, childhood and adolescence and for athletes."ADA's
position and accompanying paper were written by Winston Craig, PhD, MPH, RD, professor and
chair of the department of nutrition and wellness at Andrews University; and Reed Mangels,
PhD, RD, nutrition advisor at the Vegetarian Resource Group, Baltimore, Md. The revised
position paper incorporates new topics and additional information on key nutrients for
vegetarians, vegetarian diets in the life cycle and the use of vegetarian diets in
prevention and treatment of chronic diseases. "Vegetarian diets are appropriate for
all stages of the life cycle," according to ADA's position. "There are many
reasons for the rising interest in vegetarian diets. The number of vegetarians in the
United States is expected to increase over the next decade." Vegetarian diets are
often associated with health advantages including lower blood cholesterol levels, lower
risk of heart disease, lower blood pressure levels and lower risk of hypertension and type
2 diabetes, according to ADA's position. "Vegetarians tend to have a lower body mass
index and lower overall cancer rates. Vegetarian diets tend to be lower in saturated fat
and cholesterol and have higher levels of dietary fiber, magnesium and potassium, vitamins
C and E, folate, carotenoids, flavonoids and other phytochemicals. These nutritional
differences may explain some of the health advantages of those following a varied,
balanced vegetarian diet." The position paper draws on results from ADA's evidence
analysis process and information from the ADA Evidence Analysis Library to show vegetarian
diets can be nutritionally adequate in pregnancy and result in positive maternal and
infant health outcomes. Additionally, an evidence-based review showed a vegetarian diet is
associated with a lower risk of death from ischemic heart disease.
Genetically engineered mice yield
clues to 'knocking out' cancer
Deleting two genes in mice responsible for repairing DNA strands damaged by oxidation
leads to several types of tumors, providing additional evidence that such stress
contributes to the development of cancer. That's the conclusion of a recent study* in DNA
Repair by researchers at the National Institute of Standards and Technology (NIST), Oregon
Health and Science University (OHSU) and the New York University School of Medicine
(NYUSM). Although all cells need oxygen to survive, the element also can be stressful to
cells and their components—particularly DNA—as part of "reactive
species" in the environment, such as free radicals and peroxides. The damage levied
on DNA by these compounds can include lesions, breaks, cross-links and deletions—errors
in our normal genetic codes that, if left unchecked, may accelerate the aging process and
increase susceptibility to several disease states. In humans, DNA repair genes produce
enzymes called DNA glycosylases that excise sections of DNA strands already modified by
oxidative stress, and thus protect the genetic material.One of these repair genes, neil1,
was identified and characterized in 2002 by Sankar Mitra and his team at the University of
Texas Medical Branch in collaboration with NIST researchers Miral Dizdaroglu and Pawel
Jaruga. The gene produces a DNA repair protein, NEIL1 that is nearly identical in humans
and mice. Therefore, a mouse serves a perfect model for studying the biological function
of the neil1 gene in both species. To do this, OHSU researchers under R. Stephen Lloyd
genetically engineered mice without the neil1 gene (known as neil1 knockout mice). During
their first 6-10 months of life, the majority of male mice developed severe obesity,
dyslipidemia (abnormal levels of lipids in the blood), fatty liver disease and
hyperinsulinemia (excess levels of circulating insulin in the blood). In humans, these
disorders are collectively known as metabolic syndrome, a condition that affects more than
40 million persons in the United States.
New clue into how brain stem cells
develop into cells which repair damaged tissue
The joint research, funded by the National Multiple Sclerosis Society and the UK MS
Society as well as the National Institutes of Health and Howard Hughes Medical Institute,
was conducted by scientists at the University of California San Francisco (UCSF) and
University of Cambridge and was published today (01 July) in the journal Genes and
Development. Multiple sclerosis is an autoimmune disease which is caused by the body's
immune system attacking nerve fibres and their protective insulation, the myelin sheath,
in the central nervous system. This damage prevents the nerves from 'firing' properly, and
then leads to their destruction, resulting in physical and intellectual disabilities. It
is currently thought that two components determine clinical outcomes in MS. First, it is
important to stop ongoing damage (mainly achieved by controlling inflammation in the
central nervous system). The second is to repair the damage that has occurred to the
protective myelin sheaths surrounding the nerve fibres (this involves a regenerative
process called remyelination in which new myelin sheaths are restored to nerve fibres).
While there exist several effective treatments to reduce inflammatory damage, no
treatments are available to augment remyelination to repair the damage to nerve fibres.
Critical to the development of such repair therapies is to understand how the brain's own
stem cells can replace the myelin forming cells (oligodendrocytes) lost in the disease.
During early stages of the disease the brains own stem cells are surprisingly good at
repairing damage in MS. However, for reasons that until now have not been well explained,
they become less efficient as the disease progresses. In this study the researchers have
identified the Wnt pathway, which plays an active role in the maintenance and
proliferation of stem cells, as a crucial determinant of whether oligodendrocytes can
efficiently make myelin. Their studies demonstrate that if the Wnt pathway is abnormally
active, then the process is inhibited. This opens up the exciting possibility that the
repair can be enhanced in MS patients by drugs that block the Wnt pathway.
Colorectal cancer
Previously, only a few genes had been associated with the formation of metastases in
colorectal cancer. Now, researchers of the Max Delbrück Center for Molecular Medicine
(MDC) Berlin-Buch and Charité – University Medicine Berlin, Germany, have identified
115 genes that are disregulated both in the primary tumor and in its metastases. In the
future, their findings may help identify patients with aggressive tumors at an earlier
stage (Gastroenterology 2009, doi:10.1053/j.gastro.2009.03.041).* The National Cancer
Institute estimates that, alone in the United States, 106,100 cases of colon cancer will
occur and 49,920 patients will die both from colon and rectal cancer in 2009. Beginning in
glands in the bowel lining, colorectal cancer often remains undiscovered initially.
"However, the main problem is not the primary tumor," explained the surgeon and
clinical researcher Dr. Johannes Fritzmann, "but the dangerous metastases."
Metastases arise when single cells break off from the primary tumor and spread to other
body regions via the blood vessels or the lymphatic system. In colorectal cancer, these
cells usually settle in the liver, lungs, or lymph nodes. Since the affected patient
seldom feels pain or shows other symptoms, the tumor is frequently not discovered until it
has already formed metastases.
MS study offers theory for why
repair of brain's wiring fails
Scientists have uncovered new evidence suggesting that damage to nerve cells in people
with multiple sclerosis accumulates because the body's natural mechanism for repair of the
nerve coating called "myelin" stalls out. The study, published today, July 1,
2009, in the print edition of "Genes & Development," was conducted by
scientists at the University of California, San Francisco and University of Cambridge. The
research was led by co-senior investigator David Rowitch, MD, PhD, a Howard Hughes Medical
Institute investigator at UCSF. The investigation, conducted in mice and in human tissue,
showed that repair of nerve fibers is hampered by biochemical signals that inhibit the
development of cells known as oligodendrocytes, which function as repair workers in the
brain. Oligodendrocytes form a protective sheath, known as myelin, that insulates the
fibrous cables, or axons, radiating from nerve cells. In multiple sclerosis, the immune
system's T cells and B cells attack oligodendrocytes, ultimately damaging the myelin
sheath to the point that the electrical signals transmitted by the axons beneath it are
disrupted. Remarkably, the brain generally is able to recruit fresh, immature
oligodendrocytes to the myelin sheath to repair the damage, for a time. This explains why,
in the most common form of the disease, known as relapsing remitting MS, the symptoms --
which range from tingling and numbness in the limbs to loss of vision and paralysis --
disappear or are greatly reduced, for some times months or years at a time. Ultimately,
however, the repair process falters and the disease progresses. In their study, the team
set out to see if they could determine what was slowing down myelin repair. They lesioned
a small region of white matter in healthy mice, then monitored the repair process,
examining the tissue after five, 10, and 14 days. To find out which genes were
contributing to three key stages in the repair process – the recruitment of
oligodendrocyte precursors to the site of injury, the maturation of those cells into
functional oligodendrocytes, and the formation of a new myelin sheath -- they measured the
activity of 1,040 genes. All of the genes they studied encode transcription factors, which
regulate the activity of other genes. Their experiments showed that 50 transcription
factors are working during key steps in myelin repair. The team then honed in on a gene
called Tcf4, because its expression was strong in damaged areas where repair attempts were
under way.
Sugar Is a Poison, Says UCSF
Obesity Expert
The rise of obesity is usually blamed on too much eating and not enough exercising, but
Robert Lustig, MD, a UCSF pediatric neuroendocrinologist, asks us to look beyond the
obvious. Yes, more Americans are overweight today than 30 years ago. Kids are still
getting heavier, compared with prior generations of kids. That leads some UCSF researchers
to warn that heart disease and other health problems will grow in future decades.
Joint replacement patients with
diabetes greatly benefit from controlled glucose
Diabetics undergoing total joint replacement often are at a higher risk of experiencing
complications after surgery due to various pre-existing health conditions. According to a
new study published in the July 2009 issue of The Journal of Bone and Joint Surgery
(JBJS), those complications are less likely to occur when a diabetic patient has glucose
levels under control. "We found that controlled glucose levels really do make a
difference for the patient," said study co-author Milford Marchant Jr., MD, an
orthopaedic surgeon who conducted the study with colleagues of the Adult Reconstruction
Section at Duke University Medical Center. The study found that patients with uncontrolled
glucose levels were more than 3 times as likely to experience a stroke or death after
joint replacement surgery and about twice as likely to experience post-operative bleeding
and infection.
Infants Should Be Screened For Hip
Trouble
Developmental hip dysplasia is the most common congenital defect in newborns. The
condition occurs when a hip joint is shallow, unstable or when the joint is dislocated.
Infants with the condition are often at risk of developing arthritis of the hip as a young
adult. A new study published in the July 2009 issue of The Journal of Bone and Joint
Surgery (JBJS) finds that screening all infants for hip dysplasia can significantly
decrease their chance of developing early arthritis. “This study systematically
evaluated what we know about hip dysplasia to determine the best screening strategy for
newborns,” said study author Susan Mahan, MD, Pediatric Orthopaedic Surgeon with
Children’s Hospital in Boston and instructor in orthopaedic surgery at Harvard
Medical School. “Our study confirms that pediatricians need to continue their current
screening strategies for hip dysplasia. However, our findings refute a recent report from
The United States Preventive Services Task Force that was unable to recommend screening
strategies.”
Stanford discovery pinpoints new
connection between cancer cells, stem cells
A molecule called telomerase, best known for enabling unlimited cell division of stem
cells and cancer cells, has a surprising additional role in the expression of genes in an
important stem cell regulatory pathway, say researchers at the Stanford University School
of Medicine. The unexpected finding may lead to new anticancer therapies and a greater
understanding of how adult and embryonic stem cells divide and specialize.
"Telomerase is the factor that accounts for the unlimited division of cancer
cells," said Steven Artandi, MD, PhD, associate professor of hematology, "and
we're very excited about what this connection might mean in human disease." Artandi
is the senior author of the research, which will be published in the July 2 issue of the
journal Nature. He is also a member of Stanford's Cancer Center. In many ways, telomerase
is the quintessential molecule of mystery — hugely important and yet difficult to pin
down. Telomerase was known to stabilize telomeres, special caps that protect the ends of
chromosomes. It stitches short pieces of DNA on these chromosome ends in stem cells and
some immune cells, conferring a capacity for unlimited cell division denied to most of the
body's other cells. Its importance is highlighted by the fact that it is inappropriately
activated in more than 90 percent of cancer cells, suggesting that drugs or treatments
that block telomerase activity may be effective anticancer therapies. However, its vast
size, many components and relative rarity — it is not expressed in most of the body's
cells — hinder attempts to learn more about it. Artandi and his lab have spent many
years identifying and studying the components of the telomerase complex. In this most
recent study, they were following up on a previous finding suggesting that one part, a
protein called TERT, was involved in more than just maintaining telomeres. They had
discovered that overexpressing TERT in the skin of mice stimulated formerly resting adult
stem cells to divide — even in the absence of other telomerase components. "This
was a pretty clear hint that TERT was involved in something more than just telomere
maintenance," he said. Artandi and his colleagues recognized that the cells' response
to TERT mimicked that seen when another protein, beta-catenin, was overexpressed in mouse
skin. Beta-catenin is a component of a vital signaling cascade known as the Wnt pathway,
which is important in development, stem cell maintenance and stem cell activation.
Stanford developmental biologist and professor Roeland Nusse, PhD, a collaborator on the
current study, identified the first Wnt molecule in 1982.
Mayo Clinic study finds celiac
disease 4 times more common than in 1950s
Celiac disease, (http://www.mayoclinic.org/celiac-disease/) an immune system reaction to
gluten in the diet, is over four times more common today than it was 50 years ago,
according to findings of a Mayo Clinic study published this month in the journal
Gastroenterology (http://www.gastrojournal.org/). The study also found that subjects who
did not know they had celiac disease were nearly four times more likely than celiac-free
subjects to have died during the 45 years of follow-up. "Celiac disease has become
much more common in the last 50 years, and we don't know why," says Joseph Murray,
M.D., (http://www.mayoclinic.org/bio/13032852.html) the Mayo Clinic gastroenterologist who
led the study. "It now affects about one in a hundred people. We also have shown that
undiagnosed or 'silent' celiac disease may have a significant impact on survival. The
increasing prevalence, combined with the mortality impact, suggests celiac disease could
be a significant public health issue." In patients with celiac disease, the presence
of a protein called gluten from wheat, barley or rye triggers an immune system attack,
damaging the villi in the small intestine. Villi are fingerlike projections that increase
the intestine's surface area for nutrient absorption. Celiac disease symptoms may include
diarrhea, abdominal discomfort, weight loss, anemia, unexplained infertility, loss of
teeth or even premature or severe osteoporosis. The Mayo Clinic research team tested blood
samples gathered at Warren Air Force Base (AFB) in Wyoming between 1948 and 1954 for the
antibody that people with celiac disease produce in reaction to gluten. They compared
those blood test results with those from two recently collected sets from Olmsted County,
Minn. One matched the ages of those from the 1948 testing at the time of the blood draw,
and the other matched their birth years. Researchers found that young people today are 4.5
times more likely to have celiac disease than young people were in the 1950s, while those
whose birth years matched the Warren AFB participants were four times more likely to have
celiac disease.
Acid-reducing medicines may lead to
dependency
Treatment with proton pump inhibitors (PPIs) for eight weeks induces acid-related symptoms
like heartburn, acid regurgitation and dyspepsia once treatment is withdrawn in healthy
individuals, according to a new study in Gastroenterology, the official journal of the
American Gastroenterological Association (AGA) Institute. "The observation that more
than 40 percent of healthy volunteers, who have never been bothered by heartburn, acid
regurgitation or dyspepsia, develop such symptoms in the weeks after cessation of PPIs is
remarkable and has potentially important clinical and economic implications," said
Christina Reimer, MD, of Copenhagen University and lead author of the study. "This
study indicates unrecognized aspects of PPI withdrawal and is a very strong indication of
a clinically significant acid rebound phenomenon that needs to be investigated in proper
patient populations." The use of PPIs for acid-related symptoms and disorders is
extensive and rapidly escalating. While the incidence of new patients being treated with
PPIs remains stable, the prevalence of long-term treatment is rising, the reasons for
which are not fully known. Studies have shown that up to 33 percent of patients who
initiate PPI treatment continue to refill their prescriptions without an obvious
indication for maintenance therapy. Rebound acid hypersecretion, defined as an increase in
gastric acid secretion above pre-treatment levels following antisecretory therapy, is
observed within two weeks after withdrawal of treatment and could theoretically lead to
acid-related symptoms such as heartburn, acid regurgitation or dyspepsia that might result
in resumption of therapy. In a randomized double-blind placebo-controlled trial,
researchers aimed to determine the clinical relevance of rebound acid hypersecretion in
order to establish if long-term treatment with a PPI creates a need for continuous
treatment. A total of 120 healthy participants were randomized to 12 weeks of placebo or
eight weeks of esomeprazole (40 mg per day) followed by four weeks with placebo. The
Gastrointestinal Symptom Rating Scale (GSRS) was filled out weekly. The symptoms observed
in this trial caused mild to moderate discomfort and appeared for the majority of subjects
in the first two weeks after withdrawal of therapy. While there were no significant
differences between the groups in GSRS scores at baseline, GSRS scores for acid-related
symptoms were significantly higher in the PPI group in weeks 10, 11 and 12. Of those
randomized to PPIs, 44 percent reported at least one relevant acid-related symptom in
weeks nine through 12 compared to 15 percent in the placebo group. The proportion
reporting dyspepsia, heartburn or acid regurgitation in the PPI group was 22 percent in
week 10, 22 percent in week 11 and 21 percent in week 12. Corresponding figures in the
placebo group were 7 percent, 5 percent and 2 percent. "We find it highly likely that
the symptoms observed in this trial are caused by rebound acid hypersecretion and that
this phenomenon is equally relevant in patients treated long term with PPIs. If rebound
acid hypersecretion induces acid-related symptoms, this might lead to PPI dependency. Our
results justify the speculation that PPI dependency could be one of the explanations for
the rapidly and continuously increasing use of PPIs," Dr. Reimer added.
Obesity Predicts Inadequate Bowel
Prep at Colonoscopy
Obesity is an independent predictor of inadequate bowel preparation at colonoscopy, and
the presence of additional risk factors further increases the likelihood of a poorly
cleansed colon, according to a new study in Clinical Gastroenterology and Hepatology, the
official journal of the American Gastroenterological Association (AGA) Institute. Obesity
has become an epidemic in the present era, both in the U.S. and in other developed
nations. Abnormal elevation of body mass index (BMI) is associated with several
gastrointestinal diagnoses, including diverticular disease, gastroesophageal reflux
disease, colon polyps and colon cancer. Since the majority of colon cancers arise from
adenomatous (benign) colon polyps, proper screening becomes crucial while performing
colonoscopy on obese patients. An inadequately cleansed colon can jeopardize the
effectiveness of screening or surveillance colonoscopy, exposing these patients at higher
risk for colorectal tumors to the dangers of missed lesions and higher cost of repeat
colonoscopy. “The implications of our findings are profound. Since over a quarter of
all patients had an inadequate examination, identification of a patient profile with a
high risk for poor colon preparation will be helpful in capturing those who would benefit
from an initial individualized designer preparation regimen,” said Brian Borg, MD, of
Washington University in St. Louis, MO, and lead author of the study. “Our results
suggest that the obese patient should at least be subject to more precise instructions and
possibly a more rigorous bowel preparation regimen. In addition, as the number of risk
factors for an inadequate bowel preparation increase, the need for early repeat
colonoscopy escalates.”
Schizophrenia linked for first time
to chromosome region in study led by Stanford scientists
Stanford University School of Medicine scientists have played a major role in an
international effort that has shown, for the first time, that modern genetic technologies
can solve the riddle of how gene variations lead to schizophrenia. Researchers at Stanford
and 14 other institutions carried out a study of common DNA variations throughout the
genome, and then combined forces with two independent studies to complete a pooled
analysis of 27,000 individuals. The largest genetic differences between the study
participants with and without schizophrenia were found on a stretch of chromosome 6
containing numerous genes associated with immune response (and some with other roles).
This raises the possibility that immune function plays a role in schizophrenia. Stanford's
Jianxin Shi, PhD, and Douglas Levinson, MD, are first and second authors of one of three
linked papers to be published online together in Nature on July 1. Their paper reports on
the Molecular Genetics of Schizophrenia Project. This undertaking implicated a region of
the human genome not previously suspected as a risk factor for schizophrenia. That finding
was bolstered by another of the simultaneously published papers, which showed an even
stronger association when the number of subjects was increased to almost 48,000, and
identified significant association in two additional genes. The third paper shows that
there are likely to be many common gene variations, perhaps hundreds or more, that have
small effects in the risk of schizophrenia. Taken together, "the papers present the
first highly significant findings of gene regions associated with schizophrenia
risk," said Levinson, professor of psychiatry and behavioral sciences, director of
that department's Program on the Genetics of Brain Function, and the Walter E. Nichols,
MD, Professor in the School of Medicine. It is already known that schizophrenia —
which strikes close to one in every 100 people — has a very strong genetic component,
probably accounting for at least 80 percent of risk for this disease. However, unlike
sickle-cell anemia or Huntington's disease, in which a defect at a single genetic location
is responsible, most cases of schizophrenia are believed to involve interactions among a
multitude of genes, with a variant of any single gene contributing only a tiny bit to a
person's risk. "That makes it hard to tease out, in a statistically significant way,
any of these schizophrenia-associated genes," said Levinson. But it is feasible with
very large numbers of subjects, he said. Finding genes involved in a multigenic trait can,
at least in theory, be accomplished by means of so-called genome-wide association studies,
in which DNA variations are measured in two large groups of people, one with a common
pathology and the other without it.
Schizophrenia and bipolar disorder
share genetic roots
A trio of genome-wide studies – collectively the largest to date – has
pinpointed a vast array of genetic variation that cumulatively may account for at least
one third of the genetic risk for schizophrenia. One of the studies traced schizophrenia
and bipolar disorder, in part, to the same chromosomal neighborhoods. "These new
results recommend a fresh look at our diagnostic categories," said Thomas R. Insel,
M.D., director of the National Institute of Mental Health (NIMH), part of the National
Institutes of Health. "If some of the same genetic risks underlie schizophrenia and
bipolar disorder, perhaps these disorders originate from some common vulnerability in
brain development." Three schizophrenia genetics research consortia, each funded in
part by NIMH, report separately on their genome-wide association studies online July 1,
2009, in the journal Nature. However, the SGENE, International Schizophrenia (ISC) and
Molecular Genetics of Schizophrenia (MGS) consortia shared their results – making
possible meta-analyses of a combined sample totaling 8,014 cases and 19,090 controls. All
three studies implicate an area of Chromosome 6 (6p22.1), which is known to harbor genes
involved in immunity and controlling how and when genes turn on and off. This hotspot of
association might help to explain how environmental factors affect risk for schizophrenia.
For example, there are hints of autoimmune involvement in schizophrenia, such as evidence
that offspring of mothers with influenza while pregnant have a higher risk of developing
the illness. "Our study was unique in employing a new way of detecting the molecular
signatures of genetic variations with very small effects on potential schizophrenia
risk," explained Pamela Sklar, M.D., Ph.D., of Harvard University and the Stanley
Center for Psychiatric Research, who co-led the ISC team with Harvard's Shaun Purcell,
Ph.D. "Individually, these common variants' effects do not all rise to statistical
significance, but cumulatively they play a major role, accounting for at least one third
– and probably much more – of disease risk," said Purcell.
Much Touted “Depression Risk
Gene” May Not Add to Risk After All
Stressful life events are strongly associated with a person's risk for major depression,
but a certain gene variation long thought to increase risk in conjunction with stressful
life events actually may have no effect, according to researchers funded by the National
Institute of Mental Health (NIMH), part of the National Institutes of Health. The study,
published in the June 17, 2009, issue of the Journal of the American Medical Association,
challenges a widely accepted approach to studying risk factors for depression.
"Rigorous re-evaluations of published studies provide the checks and balances
necessary for scientific progress," said Thomas R. Insel, M.D., director of NIMH.
"We are still in the early days of understanding how genes and environment interact
to increase the risk for depression." Most mental disorders are thought to be caused
by a combination of many genetic risk factors interacting with environmental triggers.
However, finding the exact combinations continues to present significant challenges to
research. Advances in scientific understanding and technologies during the past decade
have led to powerful tools for studying how genetic and environmental factors can affect a
person's risk for disease. Such advances allowed mental health researchers in 2003 to show
that a gene involved in serotonin activity increased the risk of major depression in
people who had a number of stressful life events over a five-year period (see "More
About the Science" below for more information about this gene and serotonin). Coming
at a time of heightened research interest in these gene-environment interactions and the
relative lack of progress in the field for mental disorders, this study received wide
acclaim and had a far-reaching influence. Not only have considerable resources been
invested in subsequent studies that built on this finding, but also some researchers have
proposed marketing the gene test to the public, claiming to be able to predict a person's
risk for depression. However, efforts to replicate the 2003 study's findings—a key
step in scientific progress that helps show whether a particular finding was a chance
event—have had inconsistent results.
Cost-effectiveness of HPV
vaccination in the Netherlands
Even under favorable assumptions, including lifelong protection against 70% of all
cervical cancers and no side effects, vaccination against the human papillomavirus (HPV)
is not cost-effective in the Netherlands, according to a study published online July 1 in
the Journal of the National Cancer Institute.Researchers conducted the study because the
cost effectiveness of HPV vaccination may be limited by the low number of cervical cancer
cases and deaths in the region associated with the current Dutch cervical cancer screening
program. In the study, Inge M.C.M. de Kok of the Department of Public Health at Erasmus
MC, University Medical Center in Rotterdam, the Netherlands, and colleagues estimated the
costs and effects of adding HPV vaccination to the current program (screening only) using
a microsimulation screening analysis model. They found that adding HPV vaccination was not
cost-effective, even under favorable assumptions. "To become cost-effective, the
vaccine price would have to be decreased considerably, depending on the effectiveness of
the vaccine," the authors write.
Key to evolutionary fitness - Cut
the calories
Charles Darwin and his contemporaries postulated that food consumption in birds and
mammals was limited by resource levels, that is, animals would eat as much as they could
while food was plentiful and produce as many offspring as this would allow them to.
However, recent research has shown that, even when food is abundant, energy intake reaches
a limit, even in animals with high nutrient demands, such as lactating females. Scientists
at the Research Institute of Wildlife Ecology in Vienna suggest that this is due to active
control of maternal investment in offspring in order to maintain long-term reproductive
fitness. The research, to be presented by Dr Teresa Valencak at the Society for
Experimental Biology Annual Meeting in Glasgow has shown that, when their energy reserves
are low or when their offspring are kept in cooler temperatures, Brown hares are able to
increase their energy turnover and rate of milk production above that normally observed.
This indicates that, ordinarily, the hares are operating at below their maximum capacity
and shows that this is not due to any kind of physiological constraint, such as length of
digestive tract or maximum capacity of mammary glands. Also, as the hares were provided
with plentiful food, there could be no limitation of energy turnover due to food
availability. The way that females regulated their energy expenditure according to pup
demand and their own fat reserves but did not exceed certain levels fitted with the
group's theory that using energy at close to the maximum rate has costs for animals which
may compromise their ability to successfully reproduce in the future. If a hare puts most
of its energy into a litter of pups then it will have little left over for growth and body
repairs for example, which may shorten its life or make it less able to produce or care
for young in the future. By actively limiting the rate of energy turnover, a mother can
prevent this and maintain a higher level of reproductive success over her lifetime.
Poor sleep is independently
associated with depression in postpartum women
A study in the July 1 issue of the journal SLEEP suggests that postpartum depression may
aggravate an already impaired sleep quality, as experiencing difficulties with sleep is a
symptom of depression. Twenty-one percent of depressed postpartum women included in the
study reported having also been depressed during pregnancy and 46 percent reported at
least one previous depressive episode prior to conception, suggesting that new mothers
diagnosed with postpartum depression are not merely reporting symptoms of chronic sleep
deprivation. Results indicate that two months after delivery, poor sleep was associated
with depression when adjusted for other significant risk factors, such as poor partner
relationship, previous depression, depression during pregnancy and stressful life events.
Sleep disturbances and subjective sleep quality were the aspects of sleep most strongly
associated with depression. Overall, nearly 60 percent of the postpartum women experienced
poor global sleep quality, and 16.5 percent had depressive symptoms. According to lead
author Karen Dørheim, MD, PhD, psychiatrist at Stavanger University Hospital in Norway,
depression after delivery is often not identified by new mothers, whereas tiredness and
lack of sleep are common complaints. These symptoms may be attributed to poor sleep, but
the tiredness could also be caused by depression. "It is important to ask a new
mother suffering from tiredness about how poor sleep affects her daytime functioning and
whether there are other factors in her life that may contribute to her lack of
energy," said Dørhei. "There are also helpful depression screening
questionnaires that can be completed during a consultation. Doctors and other health
workers should provide an opportunity for postpartum women to discuss difficult
feelings."
Sleep duration is associated with
variations in levels of inflammatory markers in women
A study in the July 1 issue of the journal SLEEP demonstrates that levels of inflammatory
markers varied significantly with self-reported sleep duration in women but not men. The
study found that both interleukin-6 (IL-6) and high-sensitivity C-reactive protein
(hs-CRP) levels varied with sleep duration in women following multiple adjustments for a
number of confounding factors. Compared with women who reported sleeping seven hours on an
average weekday, IL-6 levels were significantly lower in women who reported sleeping eight
hours. Levels of hs-CRP were significantly higher in women who reported sleeping 5 hours
or less. In contrast, adjusted results show no significant variations in inflammatory
markers with sleep duration in men. The study reports that hs-CRP, a nonspecific marker of
acute-phase inflammatory response, is predictive of future cardiovascular morbidity, and
the relationship of IL-6 to coronary heart disease is similar to that of CRP. According to
lead author Michelle A Miller, PhD, associate professor (reader) of biochemical medicine
at the University of Warwick Medical School in the U.K., short-term sleep deprivation
studies have shown that inflammatory markers are elevated in sleep-deprived individuals,
suggesting that inflammatory mechanisms may play a role in the cardiovascular risk
associated with sleep deprivation. “Our study may provide some insight into a
potential mechanism for the observation in previous studies which indicates an increased
risk of death from cardiovascular disease in individuals who have less than five hours
sleep per night and increased risk of non-cardiovascular death in long sleepers,”
said Miller.
Microalgae as a source of
alternative energy
The great controversy over the use of agricultural crops as a source of energy is well
known – fundamentally due to its possible competition with crops for food. The use of
sources of an organic nature for the production of biofuels, different from the
traditional use for crops, could be the solution to the social debate that has arisen in
this sector. As a consequence, it has been necessary to turn to alternative resources to
traditional crops, such as lignocellulosic biomass and/or microorganisms, amongst these
being microalgae. In concrete, the mass production of microalgae could meet this demand
given that it does not compete with the food sector, does not require large surface areas
nor fertile terrain and maximises water savings (closed cycle) for their production. At
the same time, it contributes to environmental enhancement with CO2 capture and can be
integrated into the use of saline industrial effluents. The Energy Unit at TECNALIA is
researching the potential of mass production of microalgae as a crop, working on the
selection of stocks, the optimisation of crop production systems (open, closed and mixed),
as well as the optimisation of various operation variables in the harvesting and final
treatment of the microalgae for their transformation into energy. At the same time, the
synergic aspects of the process are being studied, such a the capture of CO2 as a nutrient
for the algae, the use of saline industrial effluents and the valuation of sub-products.
Food for thought - report published
into the UK's health
Medical scientists from Southampton have contributed to a major new report published
today, setting out plans to enhance the nation's health by improving diet, increasing
physical activity and cutting harmful drinking. Professor David Coggon and Dr Nick Sheron
of the University of Southampton's School of Medicine, are among a panel of experts from
health charities, consumer organisations, academia and the food and drink industry,
commissioned to explore how business and government can work together to promote public
health. The report found that deaths from alcohol have doubled in the last 15 years as
consumption has increased and in two decades obesity has tripled, while just 1 in 4 women
and 4 in 10 men do the recommended amount of exercise. Dr Sheron, a hepatologist at the
University of Southampton and one of the UK's leading experts on alcohol misuse explains:
"Alcohol-related liver deaths in the UK have outstripped France, Spain and Italy.
This report highlights the need for proper funding of alcohol services and makes the point
that the Government needs to think about both minimum pricing and fiscal measures that can
reduce alcohol consumption. "We have reached the stage where hazardous and harmful
drinkers are now drinking three-quarters of all the alcohol sold in the UK."
Chromosomal problems affect nearly
all human embryos; discovery may explain low fertility rates in humans
For the first time, scientists have shown that chromosomal abnormalities are present in
more than 90% of IVF embryos, even those produced by young, fertile couples. Ms Evelyne
Vanneste, a PhD student in the Centre for Human Genetics and the University Fertility
Center, Leuven University, Belgium, told the 25th annual conference of the European
Society of Human Reproduction and Embryology today (Wednesday July 1), that the surprising
finding meant that current techniques used in preimplantation genetic screening (PGS),
where embryos are screened genetically in order to select the best embryo for transfer, do
nothing to improve pregnancy and live birth rates. Indeed, it can lead to potentially
viable embryos being discarded, she said. Ms Vanneste and her team studied each cell from
23 three or four day-old IVF embryos from young (less than 35 years old), fertile couples
who had asked for preimplantation genetic diagnosis (PGD). PGD is carried out where one or
both parents have a known genetic abnormality, in this case an X-linked disorder or the
microdeletions (loss of a tiny piece of a chromosome) that can cause such disorders as the
cancer predisposition syndrome neurofibromatosis type 1. The embryos are screened to avoid
the implantation of one carrying that abnormality. Such embryos are the most
representative of normal human embryogenesis, the process that begins once an egg has been
fertilised. Using new technologies that can detect chromosomal aberrations in the whole
genome (all human chromosomes) of a single cell, the team was able to screen embryonic
cells at a much higher resolution than previously, and hence identify more chromosomal
abnormalities than has been possible using the current technique, fluorescent in situ
hybridisation (FISH), which can only analyse ten of the approximately 32,000 genetic
regions at the same time.
Newly discovered gene regulates
balance of 'bad' cholesterol
In an article in Science, Noam Zelcer from the LACDR describes a previously unknown
mechanism for regulating the amount of LDL cholesterol. This offers opportunities for
supplementing and improving the effect of so-called statins: medicines that remove 'bad'
cholesterol from the bloodstream. Cholesterol is not water-soluble. In order to be
transported in the blood, it therefore forms fat globules, called lipoproteins, together
with other fats. The two most familiar are known as HDL (high density lipoprotein) or
‘good’ cholesterol, and LDL (low density lipoprotein) or ‘bad' cholesterol.
Too much LDL in the blood can contribute to the development of cardiovascular diseases. A
group of substances, known as statins, is often used as a medication to reduce the LDL
level in the blood. They achieve this by on the one hand blocking the production of
cholesterol and on the other hand by raising the number of receptors for LDL on the cells
of the liver. This allows the cells to absorb more LDL from the blood, so that the blood
becomes 'cleaner'. Statins are currently the most frequently sold medicines. However, they
are not perfect.
Researchers show new antioxidant
could help treat cardiovascular disease
Researchers at the University of Glasgow believe they have found a potential new treatment
for cardiovascular disease which reduces blood pressure. Scientists at the British Heart
Foundation Glasgow Cardiovascular Research Centre (BHF GCRC) used a recently-developed
antioxidant called MitoQ10 to prevent damage to the mitochondria of cells in an
experimental model of hypertension and stroke. The researchers found that MitoQ10 improved
the function of the endothelial cells which line blood vessels and play an important part
in controlling blood pressure, as well as reducing thickening of the heart muscle (cardiac
hypertrophy) which results from high blood pressure (hypertension). Lead researcher
Professor Anna Dominiczak, Head of the BHF GCRC and BHF Chair of Cardiovascular Medicine,
said: “We have shown that this particular type of antioxidant can substantially
reduce the damage caused by oxidising molecules. “Given the apparent role that
mitochondrial damage plays in cardiovascular disease, this research opens up new
possibilities for novel treatments which will reduce high blood pressure in patients with
this condition.” Mitochondria are sub-units within a cell which provide energy to the
cell, help control cell metabolism and play a part in cell signalling, which if damaged
can result in a wide range of diseases, including cardiovascular disease.
Inflammatory markers in the blood
identify higher risk of fatal heart attacks, suggests study
The presence of inflammatory markers in the blood of elderly people at risk of
cardiovascular disease can identify individuals at higher risk of a fatal heart attack or
stroke, a study has found. Inflammation is an immune response to injury but is also
believed to play a part in cardiovascular disease with previous studies indicating a link
between high levels of markers of inflammation in the circulation with a higher risk of
heart attack or stroke. Researchers at the University of Glasgow hope the discovery will
result in further investigation into how inflammatory markers might predict the risk of
death from heart disease and whether treatments which reduce inflammation might reduce
mortality. The study, led by Prof Naveed Sattar in the British Heart Foundation Glasgow
Cardiovascular Research Centre (BHF GCRC) and Prof David Stott, David Cargill Chair of
Geriatric Medicine in the Department of Cardiovascular and Medical Sciences, analysed data
from an existing trial known as PROSPER (the Prospective Study of Pravastatin in the
Elderly at Risk). The PROSPER trial involved participants aged between 70 and 82 who had
or were at risk of cardiovascular disease. Three inflammatory markers were examined –
interleukin-6 (IL-6), C-reactive protein (CRP) and fibrinogen – and each was shown to
be more strongly associated with fatal cardiovascular events than with non-fatal
cardiovascular events over a three-year period.
Team Develops Anti-Infection
Technology
Combat-related injuries have long plagued the military in part because of
multidrug-resistant bacteria. Imagine being able to spray a compound fracture with
microcapsules that deliver a drug to bolster the immune system, stopping infection before
it starts. That technology might be around the corner, says Bingyun Li, Ph.D., of the West
Virginia University Department of Orthopaedics and director of the WVU Biomaterials,
Bioengineering & Nanotechnology Laboratory. Li’s team has developed a
drug-delivery technology involving microcapsules – and a second technique,
nanocoating – that have been shown to work in animal studies.Results of the team’s
research involving the drug interleukin-12, a drug currently in anti-cancer clinical
trials, has been published in the May issue of the journal Biomaterials. A deeper
explanation of the approach, which could develop into an alternative to antibiotic
therapy, is scheduled to be published in an upcoming issue of the Journal of Orthopaedic
Research.“These pioneering techniques could be important to the United States because
of the wars in Iraq and Afghanistan,” Li says. “The treatment of battlefield
casualties is expensive, and the infection rate runs from 2 percent to 15 percent. In some
cases, because the organisms have developed resistance, antibiotics don’t work.”
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