News 2 juli 2009
Study Provides Greater
Understanding of Lyme Disease-Causing Bacteria
Lyme disease in theU.S. is caused by the tick-borne bacteria Borrelia burgdorferi and
usually begins with a skin lesion, after which the bacteria spread throughout the body to
the nervous system, heart or joints. About 60 percent of untreated individuals develop
arthritis, which affects the knees in particular. Lyme disease usually responds well to
antibiotic therapy, but in rare cases arthritis can persist for months or years after
treatment, a rare condition known as antibiotic-refractory Lyme arthritis. Joint fluid
usually tests negative for B burgdorferi after treatment, indicating that joint
inflammation may persist even after the bacteria has been eradicated. Two genetic marker
systems are used to correlate the variation of this bacterial strain with clinical
outcomes: OspC typing divides B burgdorferi strains into 21 types, while the ribosomal RNA
intergenic spacer type (RST) system divides them into just three groups, with certain RST
groups corresponding uniquely to specific OspC types. A new study led by Allen Steere of
Massachusetts General Hospital and Harvard Medical School analyzed joint fluid samples
from 124 patients with Lyme arthritis who were seen over a 30-year period. It identified
B. burgdorferi strains in the joints of patients with Lyme arthritis and found that the
genotype frequencies in joints reflected those in skin lesions. However, RST1 strains were
the most frequent in patients with antibiotic-refractory arthritis. The study was
published in the July issue of Arthritis & Rheumatism
Parkinson's Disease Alters
Patient's Ability to Learn from Rewards while Treatment Affects Ability to Learn from
Negative Outcomes
A new neuropsychological memory test is helping to uncover how Parkinson's disease can
alter people's ability to learn about the consequences of the choices they make. The test
was developed by Dr. Mark Gluck, professor of neuroscience at the Center for Molecular and
Behavioral Neuroscience at Rutgers University, Newark, working with co-researchers at
Rutgers, New York University, and in Hungary. As reported in a forthcoming article in the
journal Brain (advanced access published May 4, 2009 -- doi:10.1093/brain/awp094), Gluck
and co-researchers Nikoletta Bodi and Szabolcs Keri of Semmelweis University, Hungary,
found that non-medicated patients in the early stages of Parkinson’s were selectively
impaired at learning from reward. Brain Image ThumbnailPatients in Hungary were tested
using a novel feedback-learning task developed by Gluck and his colleagues: Catherine E.
Myers, research professor, Rutgers University, Newark; and Nathaniel Daw, assistant
professor, New York University. The research was supported by a Dekker Foundation Award
from the Bachman-Strauss Dystonia and Parkinson Foundation.
Vitamin D deficiency is widespread
and on the increase
A new report issued by the International Osteoporosis Foundation (IOF) and published in
the scientific journal Osteoporosis International1, shows that populations across the
globe are suffering from the impact of low levels of vitamin D. The problem is widespread
and on the increase, with potentially severe repercussions for overall health and fracture
rates.Compiled by IOF’s expert working group on nutrition, the report reviews the
scope and causes of low vitamin D levels in six regions: Asia, Europe, Latin America,
Middle East and Africa, North America and Oceania. Regional reports are available on the
IOF website Vitamin D is mainly produced in the skin upon exposure to sunlight, and, to a
lesser extent, is derived from nutritional sources. It plays an important role, through
its influence on calcium levels, in the maintenance of organ systems, and is needed for
normal bone mineralization and growth. Suboptimal levels of vitamin D may lead to
increased risk of osteoporosis and hip fracture and, in severe cases, to the development
of rickets, a softening of bones in children that can lead to skeletal fractures and
deformity. Although there is ongoing debate as to what constitutes the optimal level of
vitamin D, the report shows that regardless of whether it is defined at 50nmol/L or
75nmol/L, vitamin D status is seriously inadequate in large proportions of the population
across the globe.
Vitamin D status in Europe
The vitamin D status within different European countries shows a high variation [1]. A
serum 25(OH)D lower than 25nmol/l was found in 2 to 30% of adults, but this percentage may
increase to 75% or more in older persons in institutions. It can be concluded that vitamin
D deficiency (serum 25(OH)D <25nmol/l) is more common in southern than in northern
Europe. Risk groups are the elderly (especially the institutionalised and house-bound),
adolescents, and non-western immigrants. Dependent on the required serum 25(OH)D level,
either 50 or 75nmol/l, the percentage of the population with vitamin D insufficiency
is high or very high in most European countries.
Peer pressure plays major role in
environmental behavior
People are more likely to enroll in conservation programs if their neighbors do – a
tendency that should be exploited when it comes to protecting the environment, according
to a pioneering study from Michigan State University. The research, published in the
Proceedings of the National Academy of Sciences, is the first to focus on the phenomenon
of social norms in the context of China’s conservation efforts, said Jianguo “Jack”
Liu, University Distinguished Professor and study co-author. The study focused on a
mammoth government initiative called Grain to Green that pays Chinese farmers to convert
cropland back to forest. While money is a key factor in whether people sign up for the
voluntary program, peer pressure also plays a surprisingly large role, Liu said.“That’s
the power of social norms,” Liu said. “It’s like recycling. If you see your
neighbors doing it, you’re more likely to do it.”
OJ Worse for Teeth than Whitening,
Says Eastman Institute for Oral Health Researchers
With the increasing popularity of whitening one’s teeth, researchers at the Eastman
Institute for Oral Health, part of the University of Rochester Medical Center, set out to
learn if there are negative effects on the tooth from using whitening products. Eastman
Institute’s YanFang Ren, DDS, PhD, and his team determined that the effects of 6
percent hydrogen peroxide, the common ingredient in professional and over-the-counter
whitening products, are insignificant compared to acidic fruit juices. Orange juice
markedly decreased hardness and increased roughness of tooth enamel. Unlike ever before,
researchers were able to see extensive surface detail thanks to a new focus-variation
vertical scanning microscope. “The acid is so strong that the tooth is literally
washed away,” said Ren, whose findings were recently published in Journal of
Dentistry. “The orange juice decreased enamel hardness by 84 percent.” No
significant change in hardness or surface enamel was found from whitening.
Discovery may provide new
treatments for alcohol dependence
Researchers at the Sahlgrenska Academy, Gothenburg, have discovered a new brain mechanism
involved in alcohol addiction involving the stomach hormone ghrelin. When ghrelin’s
actions in the brain are blocked, alcohol’s effects on the reward system are reduced.
It is an important discovery that could lead to new therapies for addictions such as
alcohol dependence. The results will be published in the renowned American scientific
journal Proceedings of the National Academy of Sciences (PNAS). Ghrelin is a hormone
produced by the stomach and, by signalling in the brain, increases hunger. The new
finding, that it is also involved in alcohol addiction, highlights the reward system of
the brain as a key target for ghrelin’s effects. "Ghrelin’s actions in the
brain may be of importance for all kinds of addictions, including chemical drugs such as
alcohol and even food" says Suzanne Dickson, Professor of Physiology, a leading
expert in appetite regulation.
Risk of tuberculosis from arthritis
medication examined
Treatment with anti-tumor necrosis factor (TNF) agents is recognized as a risk factor for
tuberculosis (TB) in patients with immune-mediated inflammatory diseases such as
rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, psoriatic arthritis and
psoriasis. Most TB cases develop as a result of reactivation of a latent TB infection, and
health authorities worldwide recommend screening for latent TB and treating patients
before initiating anti-TNF treatment. A new study examined cases of TB associated with
anti-TNF therapy and found that the risk of TB is higher for patients receiving anti-TNF
monoclonal antibody therapy (infliximab or adalimumab) than for those receiving soluble
TNF receptor therapy (etanercept). The study is published in the July issue of Arthritis
& Rheumatism (http://www3.interscience.wiley.com/journal/76509746/home). Led by Xavier
Mariette of the Université Paris-Sud, researchers set up a national registry in France to
collect all cases of TB occurring during a three-year period in patients receiving
anti-TNF therapy for any reason. Researchers collected data on 69 cases of TB, assessing
risk factors for TB before anti-TNF therapy began and anti-TNF treatment history.
Link found between history of
periodontitis and cerebrovascular disease in men
The potential role of periodontitis, an inflammatory disease of the gums, in the risk of
cardiovascular disease, particularly ischemic stroke, has received growing attention
during the last decade. A new study is the first prospective cohort study to use clinical
measures of periodontitis to evaluate the association between this disease and the risk of
cerebrovascular disease. The study is published in Annals of Neurology, the official
journal of the American Neurological Association Led by Thomas Dietrich of the University
of Birmingham School of Dentistry, and Elizabeth Krall of the Boston VA and the Boston
University School of Dental Medicine, the study analyzed data from 1,137 men in the VA
Normative Aging and Dental Longitudinal Study, an ongoing study begun in the 1960s with
healthy male volunteers from the greater Boston area. A trained periodontist conducted
dental exams every three years that included full mouth X-rays and periodontal probing at
each tooth. Cerebrovascular disease was defined as a stroke or transient ischemic attack
(TIA) and follow-up lasted an average of 24 years. The results showed a significant
association between periodontal bone loss and the incidence of stroke or TIA, independent
of cardiovascular risk factors. This association was much stronger among men younger than
65 years old. There are several possible pathways that could explain the association found
in the study. There could be direct or indirect effects of the periodontal infection and
the inflammatory response, or some people may have an increased pro-inflammatory
susceptibility that could contribute to both cerebrovascular disease and periodontal
disease. The study found that only periodontal bone loss, which would indicate a history
of periodontal disease, not probing depth, which would indicate current inflammation, was
associated with the incidence of cerebrovascular disease. Also, the stronger association
in younger men seen in this and other studies may indicate a pro-inflammatory
susceptibility in some men that is reflected in periodontal destruction at a younger age.
The authors note that if periodontitis caused cerebrovascular disease, it could be an
important risk factor, given its relatively high prevalence and the strength of the
association in younger men. It is also possible that people with periodontitis may pay
less attention to health in general (e.g., they may not take medications as regularly).
The authors conclude: "Large epidemiologic studies using molecular and genetic
approaches in various populations are necessary to determine the strength of the
association between periodontitis and cerebrovascular disease and to elucidate its
biologic basis."
Current search for heart disease
treatment may not be fruitful
A protein used by doctors to indicate a patient's risk of coronary heart disease may have
drug developers barking up the wrong treatment tree, according to the authors of a study
published today in the Journal of the American Medical Association (JAMA). Their research
suggests that C-reactive protein, an enticing target for scientists working on new
treatments for coronary heart disease, may not have a role in causing the disease, even
though it is a predictive marker. Coronary heart disease is the leading cause of death
worldwide and is particularly common in Western countries, including the UK, where it is
responsible for over 100,000 deaths per year. It is caused by atherosclerosis, where
plaques and fatty acids build up in the walls of the arteries. The progression of the
disease from early to later, sometimes fatal, stages involves inflammation. There is
strong interest in measuring levels of C-reactive protein in a patient's blood, because it
is a marker of inflammation. Previously, scientists had not known whether C-reactive
protein causes coronary heart disease, even though a number of studies over the past 12
years have indicated that it is a risk indicator. Today's study, by researchers from
Imperial College London and 12 other universities and institutes in Europe and North
America, looks at the genes that control C-reactive protein levels in blood and their
effect on the risk of coronary heart disease. Variations in the gene that codes for
C-reactive protein were not associated with risk of coronary heart disease, which the
authors say argues against C-reactive protein being directly involved in causing the
disease. However, interest still remains in whether C-reactive protein is a useful marker
of disease risk. In the same study, the authors identified genetic variations in three
other genes associated with C-reactive protein, which according to the authors, may also
be associated with a person's risk of coronary heart disease.
Patients with moderate to severe
periodontitis need evaluation for heart disease risk
Additional research is called for and patients with moderate to severe periodontitis
should receive evaluation and possible treatment to reduce their risk of atherosclerotic
cardiovascular disease (CVD), according to a special consensus paper by editors of The
American Journal of Cardiology and Journal of Peridontology in the July 1, 2009 issue of
The American Journal of Cardiology (http://www.ajconline.org), published by Elsevier.
Periodontitis, a bacterially-induced, localized, chronic inflammatory disease, destroys
connective tissue and bone that support the teeth. Periodontitis is common, with mild to
moderate forms affecting 30 to 50% of adults and the severe generalized form affecting 5
to 15% of all adults in the USA. In addition, there is now strong evidence that people
with periodontitis are at increased risk of atherosclerotic CVD — the accumulation of
lipid products within the arterial vascular wall. The explanation for the link between
periodontitis and atherosclerotic CVD is not yet clear, but a leading candidate is
inflammation caused by the immune system. In recent years the inflammation is now
recognized as a significant active participant in many chronic diseases. Other
explanations for periodontitis and atherosclerotic CVD are common risk factors such as
smoking, diabetes mellitus, genetics, mental anxiety, depression, obesity, and physical
inactivity. Regardless of the cause, the expert panel believes that the current evidence
is strong enough to recommend that doctors assess atherosclerotic CVD in their patients
with periodontitis. The research recommends that patients with moderate to severe
periodontitis should be informed that there may be an increased risk of atherosclerotic
CVD associated with periodontitis, and those patients with one or more known major risk
factor for atherosclerotic CVD should consider a medical evaluation if they have not done
so in the past 12 months. "This consensus paper is important because it will draw
attention to the fact that patients with periodontitis, especially moderate and severe
forms of the disease, can have increased risk for coronary disease," commented to
David Dionne, Executive Publisher of The American Journal of Cardiology.
Metabolic factors may play a role
in risk for breast cancer
Physiological changes associated with the metabolic syndrome may play a role in the risk
of postmenopausal breast cancer, according to study results published in Cancer
Epidemiology, Biomarkers & Prevention, a journal of the American Association for
Cancer Research. The metabolic syndrome, or insulin resistance syndrome, consists of a
constellation of factors including abdominal obesity, high blood glucose levels, impaired
glucose tolerance, abnormal lipid levels and high blood pressure. Affecting roughly 47
million Americans, the metabolic syndrome is also associated with poor diet and lack of
physical activity. It can also increase the risk for diabetes and heart disease. The
metabolic syndrome is characterized by elevated insulin levels, and in recent years
scientists have proposed that insulin may contribute directly or indirectly to the
development of breast cancer. Researchers suspect that the metabolic syndrome could
influence the risk for breast cancer by affecting interrelated hormones, such as insulin,
estrogen, cytokines and growth factors. "This study suggests that having the
metabolic syndrome itself or some of its components may increase a woman's risk of
postmenopausal breast cancer. However, much more work is needed to understand the role of
these metabolic factors and their interplay with better established breast cancer risk
factors, such as reproductive and hormonal factors," said researcher Geoffrey C.
Kabat, Ph.D., senior epidemiologist in the department of epidemiology and population
health at Albert Einstein College of Medicine, New York. Studies to date have evaluated
individual components of the metabolic syndrome and breast cancer, with inconsistent
results, according to Kabat. For the first time, Kabat and colleagues assessed whether
women who met the criteria of having the metabolic syndrome were at greater risk for
postmenopausal breast cancer.
Scripps research scientists find
key culprits in lupus
The more than 1.5 million Americans with systemic lupus erythematosus (or lupus) suffer
from a variety of symptoms that flare and subside, often including painful or swollen
joints, extreme fatigue, skin rashes, fever, and kidney problems. Researchers at The
Scripps Research Institute have now identified the main trigger for the development of
this disease. Lupus is one of several autoimmune diseases in which the immune system turns
against parts of the body, destroying the very cells and tissues it is meant to protect.
In a study published in the Early Edition of the Proceedings of the National Academy of
Sciences (PNAS) the week of June 29, 2009, Scripps Research Professor of Immunology and
Microbial Science Dwight Kono and colleagues demonstrate that three proteins, called
Toll-like receptors (TLRs), are necessary for this autodestruction to occur. TLRs may thus
provide effective targets for the development of new treatments for lupus, as well as
other autoimmune diseases. In response to infection, a healthy immune system produces
antibodies—proteins that fight and destroy invading pathogens such as viruses,
bacteria, and other foreign substances. But in lupus something goes awry with the chain of
events leading to antibody production. As a result, the immune system produces
"autoantibodies" against some of the body's own molecules, cells and tissues.
TLRs are proteins found in immune cells that normally help stimulate the initial response
of the immune system to foreign pathogens. Humans have 10 different types of TLRs. Some of
them sit on the surface of immune cells and seek out molecules that appear on the coating
of bacteria and viruses. Other TLRs—TLR 3, TLR7, (TLR 8 in humans, but not mice), and
TLR 9—reside inside immune cells, in a compartment known as the endolysosome, where
bits of foreign substances usually end up. When bacteria or viruses enter the body, some
are engulfed by immune cells and degraded in the endolysosome. Inside this compartment,
resident TLRs come across the bacterial and viral debris. These TLRs specifically detect
the genetic material of pathogens—viral DNA, viral RNA, and bacterial DNA—and
stimulate immune cells to produce antibodies against these molecules. But the production
of antibodies against foreign DNA and RNA seems to be particularly prone to error. The
most common types of autoantibodies found in lupus patients are ones to the body's own
genetic material—the DNA and RNA that resides inside the cell's command center, or
nucleus. As a result, doctors often test for the presence of "antinuclear"
antibodies to diagnose lupus. "That's the Achilles heel," says Kono. "These
endolysosomal TLRs are needed for viral and bacterial immunity, but they open the
possibility of self reactivity."
Early heart attack therapy with
bone marrow extract improves cardiac function
A UCSF study for the treatment of heart failure after heart attack found that the extract
derived from bone marrow cells is as effective as therapy using bone marrow stem cells for
improving cardiac function, decreasing the formation of scar tissue and improving cardiac
pumping capacity after heart attack. Findings were published online and in the July 2009
issue of the Journal of Molecular Therapy. The cover of the journal features a microscope
image of cells from the UCSF study. The studies were done in mice using a novel stem cell
delivery method developed by UCSF researchers to show that the extract from bone marrow
cells is as beneficial to cardiac function as are intact, whole cells. Both the cell and
cell extract therapies resulted in the presence of more blood vessels and less cardiac
cell death, or apoptosis, than no therapy. The study also showed that heart function
benefitted despite the finding that few of the injected cells remained in the heart at one
month after therapy. "Peer-reviewed medical literature is controversial as to whether
bone marrow cells differentiate into cardiomyocytes, or cardiac muscle cells, but there is
general agreement that stem cell therapy with these cells results in some level of
functional improvement after a heart attack. The exact mechanism for this is not yet
clear. Our results confirm that whole cells are not necessarily required in order to see
the beneficial effects of bone marrow cell therapy," said Yerem Yeghiazarians, MD,
study author, cardiologist and director of UCSF's Translational Cardiac Stem Cell
Development Program. UCSF researchers are investigating these new therapies to improve
cardiac function after heart attack in an effort to prevent heart failure. Heart failure
occurs when cardiac muscle is damaged and scar tissue replaces beating cardiomyocytes. As
scar replaces healthy tissue, it causes the heart to enlarge and lose its pumping
capacity. When the pumping capacity decreases, the heart fills with fluid, which moves to
the lungs and can lead to organ failure and death. "Current therapies improve
symptoms but do not replace scar tissue. Our hope is to use stem cells to decrease the
scar, minimize the loss of cardiac muscle and maintain or even improve the cardiac
function after a heart attack," Yeghiazarians said. Using a novel, closed-chest,
ultrasound-guided injection technique developed by Yeghiazarians and his colleagues, the
team administered three different groups with bone marrow cells, bone marrow cell extract,
or saline (for the control group). The injections were administered at day three after
heart attack – a timeframe somewhat similar to human biology on days six-to-seven
after heart attack. The team found at day 28 that both the bone marrow cell group and the
extract group had significantly smaller heart damage than the control group.
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