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| - - European weblog on food, health and environment |
The 21st century - time to wake
up….
Cancer to be the leading cause of death in
2010 through deadly cocktail of toxins ? We destroy our lungs with cigarettes, feed our
kids fast sugars. trans fats, salt, artificial flavors and colors, chemical sugars,
vaccines, etc. Then we wonder how it is that an increasing percentage of the population
develops chronic diseases such as asthma, allergies, diabetes, cancer, food intolerances,
skin problems and bowel problems. Mercury in fish and thermometers poses a problem for
most, but in tooth fillings or flu shots it doesn't seem to be a problem. Where's the
logic in that? We have the same ambivalence about antibiotics, the 'wonder drug' for
bacterial infections but also the great killer of your intestinal flora. Never mind that
friendly gut bacteria play a crucial role in maintaining long-term health. According to
ancient Chinese wisdom death resides in the bowels.
Read
full introduction article here
Ron Fonteine
News - Week 28 - 2009
Kidney Damage from Medical Imaging
Procedures Can Cause Long-Term Health Problems
Kidney injury that can arise after undergoing certain medical imaging procedures increases
a patient’s risk of having a stroke or heart attack over the next year or two,
according to a study appearing in an upcoming issue of the Clinical Journal of the
American Society Nephrology (CJASN). The findings indicate that seemingly minor and
reversible kidney damage from these common clinical procedures is a serious health threat.
Medical imaging often uses contrast agents, substances such as iodine and barium that
enhance the contrast of structures or fluids within the body. For example, contrast agents
may be used during cardiac angiography and computed tomography procedures to visualize
blood vessels and changes in tissues. Exposure to contrast agents can injure the kidneys,
but patients are often told that this is only a temporary side effect. Recent research has
suggested that such contrast-induced kidney damage may actually be more serious, although
no thorough studies have looked into the hypothesis.To investigate the issue, Richard
Solomon, MD (University of Vermont), and his colleagues studied 294 patients with kidney
disease who were exposed to contrast agents during cardiac angiography. Patients in the
CARE (Cardiac Angiography in REnally Impaired Patients) trial were randomly divided to
receive one of two contrast agents: iopamidol or iodixanol. After following patients for
at least one year, the researchers found that 92 (31%) of the patients experienced
negative health effects. Thirty-eight (13%) of the patients experienced a major event,
such as death, stroke, heart attack, or end-stage renal disease. Individuals who developed
contrast-induced kidney injuries had twice as many long-term negative health effects
compared with patients whose kidneys were not damaged. In the absence of contrast-induced
kidney injury, there was no difference in the incidence of long-term negative health
effects between patients taking iopamidol or iodixanol. However, the investigators found
that patients taking iopamidol had reduced incidences of both kidney damage and long-term
negative effects. These parallel decreased incidences support the theory that
contrast-induced kidney injury causes long-term negative effects. The CARE trial findings
should prompt investigators to design additional studies on the long-term negative health
effects of contrast-induced kidney damage.
Groin Injuries May be More Serious
than a Pulled Muscle
Some athletes are diagnosed with a pulled groin muscle when they actually might be
suffering from a much more serious hip injury. “Because the hip is located closely to
the groin area, many people mistake hip injuries for groin pulls and are
misdiagnosed,” said Dr. Kaare Kolstad, an orthopedic surgeon with The Methodist
Hospital in Houston. “This can lead to bigger problems down the road.” The groin
muscles consist of six muscles that cover the area from the inner pelvis to the inner part
of the femur (thigh bone). These muscles pull the leg together and also help with other
movements of the hip joint. This is why a hip injury is sometimes mistaken for a groin
pull, an injury to the inner thigh. “It can happen with any athlete, but we see a
misdiagnosis more with sports that require a lot of lateral movement like soccer, hockey
and baseball,” Kolstad said. “In fact, this is the same type of thing that put
New York Yankees third baseman Alex Rodriguez on the disabled list earlier this
year.”The two most common sports-related hip injuries are a labral tear, which can be
caused by sudden stops and turns on the field and cause pain in the groin area, and a
stress fracture, which are hairline cracks in the bone that can get worse over time. A hip
injury brought on by athletic activity will cause deep, persistent pain that can last for
weeks. The pain can get so bad that it can even hurt to sit down. Doctors can determine
from an X-ray or MRI if the problem is a groin pull or hip injury that would require
either physical therapy, cortisone injections or surgery. If hip surgery is necessary, a
minimally-invasive procedure is now available that will get athletes back on their feet in
four to six weeks as opposed to four to five months with open surgery.
Migraines More Prevalent in Women
Headaches are a widespread problem in the United States, affecting roughly 45 million
people. Migraine headaches affect millions of Americans each year they are the most common
type of headache that sends patients running to their doctor’s office. Migraines
occur when constricting blood vessels in the brain cause intense, recurring vascular
headaches. Like other forms of headaches, women suffer from migraines more frequently than
men. Approximately three out of four migraine sufferers are women. Researchers have often
cited hormones as a possible explanation. According to the U.S. Department of Health and
Human Services, more than half of migraines in women transpire right before, during or
after a woman has her menstrual period. And although some women experience migraines
throughout their cycle, menstrual-related migraines may explain one trigger of the
condition.Right before a woman’s cycle begins, the levels of estrogen and
progesterone drop sharply. This decrease in hormone levels may initiate migraine headaches
because estrogen has been shown to control brain chemicals that affect pain sensation in
women. “Like in all neurological diseases, a combination of genetics and environment
play a role,” says Richard Pearl, MD, a clinical neurologist in Suffolk County, N.Y.
“One environmental factor is estrogen but a genetic predisposition has been firmly
established.”
Experts - Big Tobacco Dead by 2047,
Possibly Sooner
President Barack Obama’s signature on a bill this week to grant the Food and Drug
Administration (FDA) regulatory authority over tobacco was historic, and represents a step
in the march to eliminate tobacco use in this country by 2047, two national tobacco
experts said today (June 25). The pair published “Stealing a March in the 21st
Century: Accelerating Progress in the 100-Year War Against Tobacco Addiction in the United
States” in the July issue of the American Journal of Public Health. Michael Fiore and
Timothy Baker, director and associate director of the University of Wisconsin-Madison
Center for Tobacco Research and Intervention (UW-CTRI), respectively, chart milestones in
beating tobacco addiction and map a battle plan to eradicate tobacco use in the next few
decades. The researchers analyzed data from the 1960s, when the first systemic tracking of
smoking rates began, until the present. “Numerous observers have claimed over time
that tobacco use has plateaued and progress against its use has stalled,” the authors
write. “However, the remarkable decline in rates of tobacco use since the 1960s
belies this claim and underscores the remarkable success of tobacco control efforts to
date.” Data from the Centers for Disease Control and Prevention show adults smoking
between 1965 and 2007 dropped by an average of one half of one percentage point per year,
from 42 percent to the current rate of about 20 percent rate. While this rate of decline
hasn’t occurred each year, the overall decrease has been quite steady.
Selenium Intake May Worsen Prostate
Cancer in Some
Higher selenium levels in the blood may worsen prostate cancer in some men who already
have the disease, according to a study by researchers at Dana-Farber Cancer Institute and
the University of California, San Francisco. A higher risk of more-aggressive prostate
cancer was seen in men with a certain genetic variant found in about 75 percent of the
prostate cancer patients in the study. In those subjects, having a high level of selenium
in the blood was associated with a two-fold greater risk of poorer outcomes than men with
the lowest amounts of selenium. By contrast, the 25 percent of men with a different
variant of the same gene and who had high selenium levels were at 40 percent lower risk of
aggressive disease. The variants are slightly different forms of a gene that instructs
cells to make manganese superoxide dismutase (SOD2), an enzyme that protects the body
against harmful oxygen compounds.The research findings suggest that “if you already
have prostate cancer, it may be a bad thing to take selenium,” says Philip Kantoff,
MD, director of Dana-Farber’s Lank Center for Genitourinary Oncology and senior
author of the study that is published by the Journal of Clinical Oncology on its website
now and later will be in a print journal. The lead author is June Chan, ScD, of the
University of California, San Francisco.The unexpected results are the first to raise
concern about this potentially harmful consequence of taking supplemental selenium.
Kantoff says, “These findings are interesting particularly in light of the recent
negative results from the SELECT prevention study, which asked if selenium could protect
against prostate cancer.”The new study reveals the strong interaction between
selenium and SOD2 to influence the biology of prostate cancer, a finding that these
investigators had shown in a previous study. The authors say the current research
demonstrated that variations in the make up of the SOD2 gene dramatically alter the
effects of selenium on the risk of aggressive prostate cancer.
Cells Use Same Machinery to Import
and Export Goods
In the bustling economy of the cell, little bubbles called vesicles serve as container
ships, ferrying cargo to and from the port - the cell membrane. Some of these vesicles,
called post-Golgi vesicles, export cargo made by the cell's protein factory. Scientists
have long believed that other, similar vesicles handle the reverse function, importing
life-supporting nutrients and proteins through an independent process. By using a finely
honed type of microscopy to more precisely examine these transactions, new research shows
the processes are not as independent as assumed: certain molecules handle cargo moving in
both directions. Like stevedores, they're involved in both loading and unloading the
cell's container ships. Jyoti Jaiswal, a research assistant professor, and Sanford Simon,
head of the Laboratory of Cellular Biophysics at Rockefeller University, examined the most
common form of cellular export process called constitutive exocytosis, a continual
ferrying of goods involved in the regular life and maintenance of all eukaryotic cells.
This sort of shipping was assumed to end with the vesicles fusing completely to the
membrane and delivering their whole load of proteins and lipids, in contrast to the more
discriminating process by which similar container ships import proteins from outside the
cell, called endocytosis. But, in a paper to be published June 26 in Cell, Jaiswal and
Simon show that some of the key molecules regulating endocytosis, such as clathrin,
dynamin and actin, are also at work in exocytosis.
Vitamin-A Derivative Provides Clues
to Better Breast Cancer Drugs
Retinoic acid, a derivative of vitamin A, could lead researchers to a new set of drug
targets for treating breast cancer, researchers from the University of Chicago report in
the June 25, 2009, issue of the journal Cell. The most common forms of breast cancer are
fueled by the female hormone estrogen. By comparing the effects of estrogen and retinoic
acid on the entire genome, the researchers found that they have a "yin-yang"
effect. They alter the expression of many of the same genes, with estrogen tipping the
scales towards cell proliferation and retinoic acid restoring the balance by inhibiting
cellular growth. This balanced control of gene expression regulates fundamental cellular
processes, say the authors. When it is dysregulated, it can lead to cancer.
"Understanding all the components of this process could be used against breast cancer
care in three ways," said study leader, Kevin White, PhD, professor of human genetics
and director of the Institute for Genomics and System Biology at the University of
Chicago. "It suggests new ways to think about preventing the disease in those at high
risk. It offers molecular tools that could provide a more precise diagnosis and predict
outcomes. It could also be used to enhance current therapies, making existing drugs, such
as tamoxifen, that selectively block estrogen's effects even more powerful, or even to
develop new anti-cancer drugs."
Better diagnosis and treatment
lower aneurysm risk
Advances made in diagnosis and treatment over the last 30 years have reduced the risk of
patients dying from aneurysmal subarachnoid haemorrhage (the bursting of a blood vessel on
the surface of the brain), shows new Dutch research, published in The Lancet Neurology.The
study, an updated meta-analysis to assess changes in case fatality and morbidity and
differences based on age, sex and region, shows that 8 in 100 000 people suffer from
aneurysmal subarachnoid haemorrhage (SAH) each year. SAH is also responsible for 5 -10% of
incident stroke cases. The research also indicates that around a third of the patients die
within 24 hours. Over 25% of those who survive are left disabled. Thanks to improvements
in diagnosis like more advanced computed tomography (CT) and magnetic resonance imaging
(MRI) techniques for detection of aneurysms, dedicated stroke units and treatments like
endovascular coiling of burst aneurysms, physicians have been able to provide better
prognoses for patients who are treatable.
Researchers pinpoint a new enemy
for tumor-suppressor p53
Researchers at The University of Texas M. D. Anderson Cancer Center have identified a
protein that marks the tumor suppressor p53 for destruction, providing a potential new
avenue for restoring p53 in cancer cells. The new protein, called Trim24, feeds p53 to a
protein-shredding complex known as the proteasome by attaching targeting molecules called
ubiquitins to the tumor suppressor, the team reported this week in the Proceedings of the
National Academy of Sciences Online Early Edition. "Targeting Trim24 may offer a
therapeutic approach to restoring p53 and killing tumor cells," said senior author
Michelle Barton, Ph.D., professor in M. D. Anderson's Department of Biochemistry and
Molecular Biology. The discovery is based on an unusual approach to studying p53, which
normally forces potentially cancerous cells to kill themselves and is shut down or
depleted in most human cancers. Studies of the p53 protein and gene tend to focus on
cancer cell lines or tumors, where the dysfunction already is established, Barton said.
"We wanted to purify p53 from normal cells to better understand the mechanisms that
regulate it." The team developed a strain of mice with a biochemical tag attached to
every p53 protein expressed. After first assuring that the tagged p53 behaved like normal
p53, the team then used the tag, or hook, to extract the protein. "We could then
identify proteins that were attached to p53, interacting with it, through mass
spectrometry," Barton said.
M. D. Anderson Study Finds Even
Stronger Relationship Between High Body Mass Index, Pancreatic Cancer
In reviewing the weight history of pancreatic cancer patients across their life spans,
researchers at The University of Texas M. D. Anderson Cancer Center have determined that a
high body mass index in early adulthood may play a significant role in an individual
developing the disease at an earlier age. The study, published in the June 24 issue of the
Journal of the American Medical Association, also found that patients who are obese the
year before diagnosis have a poorer outcome than those who are not. While excess weight is
a known risk factor associated with pancreatic cancer, before now, few studies have looked
at patients' body mass index (BMI) throughout their lifetime rather than simply at
adulthood and/or year of disease diagnosis. "This is the first study to explore at
which ages excess body weight predisposes an individual to pancreatic cancer," said
Donghui Li, Ph.D., professor in M. D. Anderson's Department of Gastrointestinal Medical
Oncology and the study's corresponding author. "With our epidemiological research, we
aimed to demonstrate the relationship between BMI and risk of pancreatic cancer across a
patient's life span and determine if there was a time period that specifically predisposes
an individual to the disease, as well as the link between BMI and cancer occurrence and
overall survival of the disease." Pancreatic cancer is the fourth leading cause of
cancer death in men and women in this country. It is a highly lethal disease - according
to the American Cancer Society, more than 42,470 persons will be diagnosed and 35,240 will
likely die from the disease in 2009. The median survival for patients with the disease is
less than 10 months and the five-year survival rate is less than five percent. Obesity and
smoking are the major modifiable risk factors associated with the disease; it's estimated
that 25 percent of the pancreatic cancer cases are associated with the former and 27
percent with the latter, said Li. While the number of adults smoking is on the decline,
the number of adults dangerously overweight is on the rise. In the U.S., obesity in adults
has increased by 60 percent in the last 20 years, and is considered an epidemic by the
Centers for Disease Control. "With our study, we hoped to better understand the
cause-and-effect relationship between this modifiable risk factor that contributes to the
development of pancreatic cancer, in hopes that high-risk individuals can be identified
and preventive measures discovered for this lethal disease," said Li.
Eboek - The Milk Imperative
New discoveries are revealing that dairy
milk may be the biggest cause of illness in the world today. The Milk Imperative breaks
new ground by revealing exactly how dairy milk causes osteoporosis and prostate cancer,
backed up with the latest scientific studies. This book is sending shock waves through the
dairy industry, and whether or not you consume dairy milk The Milk Imperative will change
your life forever. Many non-dairy milk recipes also included. Here are some of the secrets
that milk suppliers don't tell you:
1. Low-fat milk is actually more fattening
than regular whole milk! This is so for several reasons. For example, enzymes in regular
milk get removed in low-fat milk: with no enzymes to 'eat up' the fat, more fat gets
stored as surplus body fat. The Milk Imperative explains exactly why low-fat milk is not
only more fattening, but much worse for health than regular milk.
2. Virtually all the latest research is
saying that dairy milk is the single biggest cause of prostate cancer in men. This is no
exaggeration. Here is an extract from one of the many similar studies quoted in The Milk
Imperative:
" A summary of studies of prostate
cancer shows a repeated association between consumption of dairy products and an elevated
risk of developing prostate cancer. For example, in one study consuming two glasses of
milk per day was associated with a 50% greater risk." Report from the 'Harvard School
Of Public Health Nutrition Roundtable', Section 3: 'Calcium: Too Much of a Good Thing?'
3. Dairy milk is bad for motherhood. Did
you know that dairy milk can harm a baby even before it is born? Milk contains a cocktail
of harmful hormones, allergens, antibiotics, bad fats, rancid cholesterol, toxins, cow
blood, bacteria, viruses, PCB's, dioxins, heavy metals, and more. Some of these harmful
substances get passed into the delicate body of the unborn child, and later cause
ill-health and impaired development as he/she grows up. For the mother, after giving birth
dairy milk creates hormonal changes that prevent her from losing weight and regaining a
slim figure.
We've all heard about lactose intolerance
and milk allergies, but this is just the tip of the iceberg: dairy milk causes more
disease than just about anything else by promoting harmful calcification. As fully
revealed in The Milk Imperative, new discoveries are revealing for the first time that
harmful calcification (and microcalfication) is at the root of most human illness, from
cancer to heart disease. Even more shocking is to discover that the calcium and phosphorus
in dairy milk play a major role in causing harmful calcification.
Price: US$ 17.50
Link
Cancer researchers link DICER1 gene
mutation to rare childhood cancer
Research published today in Science Express from the journal Science demonstrates the
first definitive link between mutations in the gene DICER1 and cancer. By studying the
patterns of DNA from 11 families with an unusual predisposition to the rare childhood lung
cancer pleuropulmonary blastoma (PPB) investigators found that children with the cancer
carried a mutation in one of their two DICER1 gene copies. DICER1 makes an important
protein that works to suppress other genes through intermediary molecules known as
microRNAs. Scientists have learned that microRNAs can fine-tune the expression of many
other genes, which is particularly important in normal human development. Recent research
has also focused on DICER1 as having a potential role in cancer because the micro-RNA
molecules it produces appear vastly different from normal when found in cancer cells; some
suggest that the pattern of microRNAs in cancers resembles an embryonic stage. "When
we realized that DICER1 was in the segment of chromosome that was shared among children
with PPB we were very excited," said D. Ashley Hill, MD, lead author and chief of
Pathology at Children's National Medical Center. "PPB is a tumor that appears to
arise out of a localized area of abnormal lung development. The implications of a defect
in a master controller gene for normal organ development would be significant." Hill
says not everyone who inherits a mutation develops PPB and children with PPB are typically
normal in every other way. The team theorizes that something else must happen to the
normal copy of DICER1 in lung cells for a tumor to develop. When the research team looked
at PPB tumors to see if there is any DICER1 protein being made from the remaining normal
copy of the gene, they were surprised by the results: "We expected to see that the
tumor cells had no DICER1 protein giving us a nice explanation for why the tumor cells had
gone haywire." But that wasn't the case.
New gene discovery links obesity to
the brain
A variation in a gene that is active in the central nervous system is associated with
increased risk for obesity, according to an international study in which Albert Einstein
College of Medicine of Yeshiva University played a major role. The research adds to
evidence that genes influence appetite and that the brain plays a key role in obesity.
Robert Kaplan, Ph.D., associate professor of epidemiology & population health, helped
direct the international study, which involved 34 research institutions and is published
online in PLoS Genetics. Dr. Kaplan and his U.S. and European colleagues found that people
who have inherited the gene variant NRXN3 have a 10-15 percent increased risk of being
obese compared with people who do not have the variant. The researchers examined data from
eight studies involving genes and body weight. These studies included more than 31,000
people of European origin, ages 45 to 76, representing a broad range of dietary habits and
health behaviors. After analyzing more than two million regions of the human genome, the
researchers found that the NRXN3 gene variant ? previously associated with alcohol
dependence, cocaine addiction, and illegal substance abuse ? also predicts the tendency to
become obese. Altogether, researchers found the gene variant in 20 percent of the people
studied. "We've known for a long time that obesity is an inherited trait, but
specific genes linked to it have been difficult to find," says Dr. Kaplan. "A
lot of factors ? the types and quantity of foods you eat, how much you exercise, and how
you metabolize foods, for example ? affect your body shape and size. So we are looking for
genes that may have a small role to play in a complex situation." NRXN3 is the third
obesity-associated gene to be identified. The fact that all three genes are highly active
in encoding brain proteins is significant, says Dr. Kaplan. "Considering how many
factors are involved in obesity, it is interesting that research is increasingly pointing
to the brain as being very important in its development," he said.
Tryptophan deficiency may underlie
quinine side effects
Researchers have found that the anti-malarial drug quinine can block a cell's ability to
take up the essential amino acid tryptophan, a discovery that may explain many of the
adverse side-effects associated with quinine. Once confirmed, these findings would suggest
that dietary tryptophan supplements could be a simple and inexpensive way to improve the
performance of this important drug. Quinine is a very commonly used anti-malarial drug,
yet to this day the principal mode of quinine action against the malaria parasite is still
largely unclear, as is the basis for adverse reactions like nausea, headaches, and blurred
vision. To address these gaps, Simon Avery and colleagues at the University of Nottingham
took advantage of yeast genetics, examining the effects of quinine on a collection of 6000
yeast mutants, each one lacking exactly one of the yeast's 6000 genes. While quite
different from humans, yeast is comparable on a cellular level and yeast is frequently,
and successfully, used as front-line agents in testing chemicals and small molecule drugs.
Their screen revealed that strains unable to make tryptophan were extremely susceptible to
quinine poisoning, which led them to identify a tryptophan transporter as a key quinine
target (yeast that cannot make their own tryptophan have to rely exclusively on external
sources, and thus die if tryptophan transport is blocked). This discovery fits in well
with evidence that quinine reactions are more severe in malnourished individuals. Unlike
yeast, humans cannot make their own tryptophan and thus require dietary tryptophan, which
is abundant in meat but limited in yams, a staple food crop in the tropics where malaria
is prevalent. If quinine severely reduces tryptophan uptake, then it follows that people
with preexisting tryptophan deficiencies would be especially at risk to this drug. The
authors also note that tryptophan is important as a precursor for the brain chemical
serotonin, so the enhanced tryptophan deficiency induced by quinine could explain why many
of quinine's side effects are localized to the head region. They also note that
side-effects could be averted simply by taking dietary tryptophan supplements in
conjunction with quinine treatments, though it is not yet known if tryptophan may affect
quinine action against the malaria parasite.
Study shows 1 in 25 deaths
worldwide attributable to alcohol
Research from Canada's own Centre for Addiction and Mental Health (CAMH) featured in this
week's edition of the Lancet shows that worldwide, 1 in 25 deaths are directly
attributable to alcohol consumption. This rise since 2000 is mainly due to increases in
the number of women drinking. CAMH's Dr Jürgen Rehm and his colleagues found that
alcohol-attributable disorders are among the most disabling disease categories within the
global burden of disease, especially for men. And in contrast to other traditional risk
factors for disease, the burden attributable to alcohol lies more with younger people than
with the older population. Dr. Rehm still takes an optimistic 'glass half full' response
to this large and increasing alcohol-attributable burden. "Today, we know more than
ever about which strategies can effectively and cost-effectively control alcohol-related
harms," Dr. Rehm said today. "Provided that our public policy makers act on
these practical strategies expeditiously, we could see an enormous impact in reducing
damage." The study showed that Europe had a high proportion of deaths related to
alcohol, with 1 in 10 deaths directly attributable (up to 15% in the former Soviet Union).
Average alcohol consumption in Europe in the adult population is somewhat higher than in
North America: 13 standard drinks per person per week (1 standard drink = 13.6 grams of
pure ethanol and corresponds to a can of beer, one glass or wine and one shot of spirits)
compared to North America's 10 to 11 standard drinks. The recent Canadian consumption rate
is equivalent of almost 9 standard drinks per person per week age 15 plus, and has been
going up, as has high risk drinking. Globally, the average is around 7 standard drinks per
person per week (despite the fact that most of the adult population worldwide actually
abstains from drinking alcohol).
Safer stem cells for therapy
When stem cell researchers in Japan and the United States announced in 2007 that they had
developed long-sought methods to return fully developed adult human cells to an
embryonic-like state, the world of stem cell research was turned upside down. Media
reports and conservative politicians prematurely hailed the discovery as a way to end the
debate over the use of human embryonic stem cells. The discovery seemed to promise a way
to produce endless supplies of stem cells that could be used to understand and treat a
host of degenerative diseases including Alzheimer’s, Parkinson’s, diabetes,
heart disease, and ALS, or Lou Gehrig’s disease.
Gold treatment relieves pain
Many animals and people experience chronic joint pain. In dogs, a common source of joint
pain is hip dysplasia, a developmental defect of the hip joint. Implantation of gold into
the soft tissues around the hip joints of dogs with dysplasia can relieve pain and lessen
stiffness for several years. Joint pain in animals and man may be due to injury, wear or
deformity. Hip dysplasia of dogs is a congenital defect that makes itself known during the
growth phase, leading to varying degrees of pain and loss of function as the dogs age. Dog
owners will as a rule notice that their dogs are reluctant to jump, that they lag behind
on longer walks, or that they are stiff and sore when standing after resting. Some dogs
also become lame after longer walks. Early in the 1970's, an American veterinary surgeon
and acupuncturist described a form of pain relief in dogs that involved implanting small
grains of pure gold into acupuncture points round painful joints in dogs. The theory
behind the treatment was that the gold grains implanted into the acupuncture points would
provide chronic stimulation of the points.
New nanoparticles could
revolutionise therapeutic drug discovery
A revolutionary new protein stabilisation technique has been developed by scientists
funded by the Biotechnology and Biological Sciences Research Council (BBSRC) which could
lead to 30 per cent more proteins being available as potential targets for drug
development - opening up exciting possibilities in drug discovery. Understanding the
structure of proteins is a vital first step in developing new drugs, but to date, drug
development has been slowed because due to their instability, proteins are difficult to
work with in lab conditions. However, using nanoparticles, scientists from the
Universities of Birmingham and Warwick have found a way to preserve membrane proteins
intact, enabling detailed analysis of their structure and molecular functions. These new
findings, which have just been published online in the Journal of the American Chemical
Society, will give scientists access to previously ignored proteins deemed too unstable to
work with.
Artificial liver for drug tests
If you have hay fever, headaches or a cold, it’s only a short way to the nearest
chemist. The drugs, on the other hand, can take eight to ten years to develop. Until now
animal experiments have been an essential step, yet they continue to raise ethical issues.
“Our artificial organ systems are aimed at offering an alternative to animal
experiments,” says Professor Heike Mertsching of the Fraunhofer Institute for
Interfacial Engineering and Biotechnology IGB in Stuttgart. “Particularly as humans
and animals have different metabolisms. 30 per cent of all side effects come to light in
clinical trials.” The test system, which Professor Mertsching has developed jointly
with Dr. Johanna Schanz, should in future give pharmaceutical companies greater security
and shorten the path to new drugs. Both researchers received the “Human-centered
Technology” prize for their work.“The special feature, in our liver model for
example, is a functioning system of blood vessels,” says Dr. Schanz. “This
creates a natural environment for cells.” Traditional models do not have this, and
the cells become inactive. “We don’t build artificial blood vessels for this,
but use existing ones – from a piece of pig’s intestine.” All of the pig
cells are removed, but the blood vessels are preserved. Human cells are then seeded onto
this structure – hepatocytes, which, as in the body, are responsible for transforming
and breaking down drugs, and endothelial cells, which act as a barrier between blood and
tissue cells.
New MRI technique could mean fewer
breast biopsies in high-risk women
A University of Wisconsin-Madison biomedical engineer and colleagues have developed a
method that, applied in MRI scans of the breast, could spare some women with increased
breast cancer risk the pain and stress of having to endure a biopsy of a questionable lump
or lesion.The universal technology will give radiologists greater confidence in visually
classifying a lesion as malignant or benign. The American Cancer Society recommends that
women with certain breast cancer risk factors — including inherited genetic
mutations, family or personal history of breast cancer, or previous radiation therapy to
the chest — receive an annual MRI screening in addition to their yearly
mammogram.During a breast MRI, which lasts about a half hour, the technician injects a
contrast agent into a vein in the patient's arm. Over time, the contrast agent flows
throughout the body, including the breasts. Because they are growing quickly, cancerous
lesions often have immature vasculature, and the contrast agent flows in and
"leaks" out quickly. Conversely, benign lesions show more gradual in and out
flow. "The tricky ones are the ones that enhance quickly and then fall off more
slowly," says Wally Block, a UW-Madison associate professor of biomedical engineering
and medical physics. "Many of these lesions turn out to be difficult to classify and
lead to biopsy."Yet, it turns out that with the right kind of MRI scan, radiologists
can visually identify a cancerous lesion based on characteristics about its shape. For
example, breaks or interruptions in a lesion can indicate a benign fibroadenoma. Lumps
with smooth edges often are benign, while those with jagged edges can signal cancer. To
generate the kind of crisp, three-dimensional images necessary for such a diagnosis,
Block, UW-Madison radiology associate professor Fred Kelcz and graduate student Catherine
Moran are capitalizing on their unique MRI data-acquisition method. An MR image is made up
of thousands of smaller pieces of information. The conventional data-acquisition method
gathers that information slowly, and it's designed to be viewed from a single imaging
plane. "What people do now is they compromise," says Block. "They don't get
resolution in the other planes to make it a reasonable scan time. We found a way around
that."
Gene expression findings a step
toward better classification and treatment of juvenile arthritis
Scientists have discovered gene expression differences that could lead to better ways to
classify, predict outcome, and treat juvenile idiopathic arthritis (JIA). Eventually such
findings could enable doctors to target more aggressive treatment to children at risk of
more severe arthritis, while those likely to have milder disease could be spared the
stronger treatments that carry a greater risk of side effects. The researchers were
supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases
(NIAMS), a part of the National Institutes of Health. JIA is an inflammatory and sometimes
disabling joint disease that affects an estimated 294,000 children in the United States.
At present, making a diagnosis of JIA is imprecise and based largely on the presence of
joint inflammation persisting for at least six weeks, for which no other cause can be
determined, says Robert A. Colbert, M.D., Ph.D., chief of the NIAMS Pediatric
Translational Research Branch. Based on the number of joints involved and other clinical
features (fever and rash, for example), doctors classify patients into one of four or five
major subtypes of JIA, which helps them predict a patient's most likely outcome and guide
appropriate treatments. "But, recent research suggests there is more variability in
JIA than the four or five major subtypes we currently recognize," Dr. Colbert says.
In the first of two such NIAMS-supported studies to be published in the July issue of
Arthritis & Rheumatism, scientists led by Michael Barnes, Ph.D., of Cincinnati
Children's Hospital Medical Center used a large data set to compare a number of children
newly diagnosed with one of four major subtypes of JIA – persistent oligoarthritis
(affecting four or fewer joints), polyarthritis (affecting five or more joints), systemic
arthritis (with fever and rash and inflammation throughout the body) and
enthesitis-related arthritis (affecting the junctions between tendons and bones). Using
gene expression technology – a method by which scientists can determine the relative
levels of expression of thousands of different genes at the same time and compare a
pattern from one subject with another – the researchers looked for differences in the
children's blood samples that corresponded with the different forms of JIA. "We
analyzed gene expression patterns in blood cells and found that we could indeed
distinguish the major subtypes of JIA," says Dr. Colbert, who was a leader of this
research program at Cincinnati Children's Hospital Medical Center before coming to NIAMS.
"Many of the genes whose expression is altered function in the immune system. This
means that not only is there immune activation, but it differs depending on the subtype of
JIA that is present."
Mayo Clinic Proceedings reviews
deep brain stimulation to treat psychiatric diseases
Pioneering therapeutic trials to investigate the effectiveness of deep brain stimulation
(DBS) in hard-to-treat depression, obsessive-compulsive disorder (OCD) and Tourette's
syndrome are underway at multiple medical centers around the world, according to a review
in the June 2009 issue of Mayo Clinic Proceedings. "Deep brain stimulation has long
been seen as valuable for controlling movement disorders," according to the review,
written by Susannah Tye, Ph.D., Mark Frye, M.D., from the Mayo Clinic Department of
Psychiatry and Psychology, and Kendall Lee, M.D., Ph.D., Mayo Clinic Department of
Neurosurgery. "It now is being investigated for hard-to-treat psychiatric
disorders," according to the authors."Early results indicate the effect on
depression and obsessive compulsive disorder is beneficial, but the therapy needs further
study," Dr. Lee says. The potential for this breakthrough treatment is enormous in
reducing the toll of mental illness on patients, their families and society, according to
the review. Unlike electroshock therapy (ECT), which stimulates the entire brain, DBS
stimulates specific parts of the brain. DBS is thought to be functionally equivalent to
creating a lesion on the brain, but with the advantage of being adjustable and reversible.
"It is like implanting a pacemaker for the brain," says Dr. Lee. The patient is
awake during deep brain stimulation surgery while a neurosurgeon implants the electrodes.
Patients are able to give immediate feedback. Additionally, patients do not feel any pain
during the implantation procedure since the brain is without pain receptors. In the
developed world, major depression is second only to cardiovascular disease in premature
mortality and time lived with disability according to the review. In persons aged 15 to 44
years, depression is the most disabling medical illness in the United States. The
prevalence of major depression, known to be a chronic and relapsing illness, is
approximately 17 percent, affecting almost 1 in 5 persons.
First Single-incision Total
Colectomy Performed at Mayo Clinic
A 32-year-old woman from Maricopa, Ariz., who was at risk for colon cancer, is believed to
be the first patient in the U.S. to undergo single-incision total colectomy — an
operation in which in the entire colon is removed. Single-incision surgery is unique in
that a single, small, three-centimeter incision is made around the navel to allow
instruments to be placed within to extract the colon. In this case, it was the only
incision made for what was a complex surgery in which the right colon, transverse colon,
descending and sigmoid colon were removed, and the patient's small bowel was joined
directly to the rectum. In traditional laparoscopic colectomy, four or five small
incisions are required to perform the operation and remove the colon.
Second gene linked to familial
testicular cancer
Specific variations or mutations in a particular can gene raise a man's risk of familial,
or inherited, testicular germ-cell cancer, the most common form of this disease, according
to new research by scientists at the National Institutes of Health. This is only the
second gene to be identified that affects the risk of familial testicular cancer, and the
first gene in a key biochemical pathway. The study appears in the July 2009 Cancer
Research. Researchers have suspected for years that heredity plays a role in some patients
with testicular germ-cell cancer, although attempts to identify a single gene with very
strong effects have been unsuccessful thus far. Scientists currently believe that multiple
genes with weaker individual effects--but acting together--probably influence an
individual's risk of familial testicular cancer. Men with a family member who had a
testicular germ cell cancer are at three-to six-fold greater risk than other men of
developing testicular cancer. Although a family history of testicular cancer probably
accounts for less than five percent of all testicular cancers, the careful study of rare
familial cancer clusters has often led to important new understanding of the non-familial
versions of the same cancer. There will be an estimated 8,400 new cases of testicular
cancer diagnosed in 2009 with about 90 percent of them being germ-cell cancers, according
to the National Cancer Institute (NCI). "This study contributes to our understanding
of why testicular germ cell cancer appears to run in families," said Raynard Kington,
M.D., Acting NIH Director. "The findings may also lead to new ways to identify men at
high risk, as well as more effective ways to prevent and treat testicular germ cell
cancer." The key pathway in this disease is the cyclic AMP pathway, which regulates
how cells respond to such signals as hormones. Drugs that affect the cyclic AMP pathway
are widely available, and, in theory, could affect progression of testicular cancer. In
this study, Anelia Horvath, Ph.D., Eunice Kennedy Shriver National Institute of Child
Health and Human Development (NICHD), performed the laboratory research and Larissa Korde,
M.D., NCI, led the clinical cancer genetics study which identified the multiple-case
testicular cancer families used for the DNA analysis. The NICHD and NCI are parts of NIH.
The researchers found that seven different mutations in the gene in question, PDE11A,
created abnormal versions of the PDE11A enzyme that slowed down the enzyme's destruction
of cyclic AMP.
New, less invasive genetic test
greatly improves pregnancy rates in older women with poor prognosis
A new test examining chromosomes in human eggs a few hours after fertilisation can
identify those that are capable of forming a healthy baby, a researcher told the 25th
annual conference of the European Society of Human Reproduction and Embryology today
(Monday 29 June). Dr. Elpida Fragouli, from the Department of Obstetrics and Gynaecology,
University of Oxford, UK, and Reprogenetics UK, said that her team's work had already
enabled seven ongoing pregnancies in a group of older women with a history of multiple
failed IVF attempts. "Out of 35 patients who had embryo transfers after the test, we
achieved a pregnancy rate of 20%, which is exceptional considering the extremely poor
prognosis of the women involved." she said. "This represents a doubling of the
usual pregnancy rate for women who fall into this category, which is otherwise, at best,
under 10% and, at worst, zero. To date, we have two live births from this group, and all
the other women who became pregnant have maintained their pregnancies. The study is
continuing, and we believe that we will achieve more pregnancies with the help of this
technology in the future." The scientists used the Comparative Genomic Hybridisation
(CGH) technique to count the chromosomes in each egg. Unlike conventional screening
strategies, using the fluorescent in situ hybridisation (FISH) method, which allows less
than half of the chromosomes of an embryonic cell to be examined, CGH enables the
evaluation of the entire chromosome complement. CGH was used to examine the fertilised
eggs by looking at polar bodies, tiny cells that are a by-product of egg development. The
chromosomes of polar bodies provide an indication of whether the corresponding egg is
normal or abnormal; if the polar bodies have the wrong number of chromosomes, so does the
egg. Looking at polar bodies is a less invasive way of obtaining information about the
chromosome content of an egg and its resulting embryo than other alternatives, such as
day-three biopsy, which take place during conventional screening strategies involving the
use of the FISH technique. The removal of the polar bodies does not adversely affect the
subsequent development of the embryo. Additionally, the results obtained after CGH
analysis of polar bodies are not affected by the presence of chromosomal mosaicism (the
presence of two populations of cells with different genotypes) and therefore may be more
accurate than conventional methods based upon screening of cells removed from embryos.
New tool finds best heart disease
and stroke treatments for patients with diabetes
Researchers from North Carolina State University and Mayo Clinic have developed a computer
model that medical doctors can use to determine the best time to begin using statin
therapy in diabetes patients to help prevent heart disease and stroke. "The research
is significant because patients with diabetes are at high risk for cardiovascular disease
and statins are the single most commonly used treatment for patients at risk of heart
disease and/or stroke," says Dr. Brian Denton, "and this model can help
determine the best course of action for individual patients based on their risk of
developing cardiovascular disease." Denton is an assistant professor in NC State's
Edward P. Fitts Department of Industrial & Systems Engineering and lead author of the
study. Statins are a key component of current cardiovascular medical treatment guidelines,
Denton says. They lower cholesterol levels and may significantly reduce the risk of heart
attack and stroke, particularly in patients that are considered to be at high risk. The
researchers developed a new mathematical model that examines various possible treatment
policies to see how they influence short-term and long-term health outcomes for patients.
The model shows how people are affected by diabetes, and how their health changes over
time as the disease advances and patients age. The new model incorporates patient-specific
data. An established risk model calculates each patient's probability of heart attack and
stroke based on risk factors, such as their cholesterol, blood pressure, etc. This overall
risk "score" is used to weigh the medical advantages of beginning statin therapy
against the financial cost of the statins.
Risk of colon cancer
Scientists discover novel mechanism that increases the risk of common colorectal cancer.
Finnish Academy Professors Lauri Aaltonen and Jussi Taipale have identified and described
a mechanism whereby a single-base change in the human genome increases the risk of
colorectal cancer. The focus in this study was on a common single-base variant occurring
in chromosome 8, which in itself causes only a slightly increased risk of cancer. However,
the risk allele is carried by 75% of people of European origin and by almost 100% of
African populations. The high frequency of the gene variant makes it a very common cause
of cancer at the population level. At the individual level, however, the variant does not
cause significant disease predisposition because that can often be considerably reduced by
lifestyle changes. Colorectal cancer is the third most common cancer worldwide and a major
cause of cancer mortality. The variant that increases the risk of colorectal cancer was
found to be located in a regulatory region, where it changes the function of a key
regulatory element important for the development of colorectal cancer. The scientists
showed that the risk allele strengthens the binding of a regulatory factor in cancer
cells, which activates pathways that are central to the development of cancer. The impacts
of this altered genetic regulation on cell division are probably mediated via the MYC
cancer gene, which is one of the best known accelerator genes in cancer. Single-base
changes are the most common type of variation found in the human genome. Genome-wide
studies of interindividual differences in common variants can be studied using DNA chip
technology, which has greatly facilitated efforts to understand the genetic basis of
multifactorial diseases. To date, scientists have identified more than 400 variants in the
human genome that are associated with an increased risk of common diseases, such as
cancer, diabetes and cardiovascular diseases. The findings of this research lend support
to the theory that human disease susceptibility is explained in part by differences in
regulatory regions of the genome, and in gene expression. A closer understanding of the
biological mechanisms involved will help to clarify the aetiology of colorectal cancer and
pave the way to more effective cancer prevention. Apart from hereditary tumor
predisposition, another area of major strength for Finnish research is gene regulation. It
was hardly surprising therefore that Aaltonen's and Taipale's research teams found each
other so easily. The research project supervised by Aaltonen and Taipale involved
molecular biologists, medical doctors and data processing researchers from Finland and the
UK. For instance, the project made use of the EEL software developed by Professor Esko
Ukkonen and his team at the CoE for Algorithmic Data Analysis.
Debate on administration of
magnesium sulfate to pregnant women to prevent cerebral palsy in preterm infant
Cerebral palsy (CP) is the most prevalent chronic childhood motor disability with an
estimated lifetime cost of nearly $1 million per individual. There is evidence that
magnesium sulfate (MgSO4) can reduce the incidence of CP for very early preterm infants.
Many thousands of pregnant women and their fetuses are exposed to MgSO4 every year in the
United States for a variety of indications, and most obstetricians are comfortable with
its use. Yet, there is still some controversy over whether magnesium sulfate is truly
protective against CP. In three articles published in the June 2009 issue of the American
Journal of Obstetrics & Gynecology, the authors shed some light on the debate.
Investigators from the Perinatology Research Branch (Division of Intramural Research),
Eunice Kennedy Shriver National Institute of Child Health and Human Development, of the
NIH, Bethesda, and Detroit, and the Center for Molecular Medicine and Genetics, Wayne
State University, Detroit, conducted a systematic review and meta-analysis of six
randomized controlled trials involving 4796 women and 5357 infants. Writing in the
article, Dr. Roberto Romero and Dr. Agustin Conde-Agudelo concluded that "Antenatal
magnesium sulfate should be considered for use in women at high risk of delivery before 34
weeks of gestation, mainly in those with premature rupture of membranes, labor in active
phase, and planned delivery within 24 hours." They found persuasive evidence that
administration of magnesium sulfate significantly reduces the risk of cerebral palsy in
children at risk. Continuing the debate, in an article summarizing a roundtable discussion
at the 29th Annual Meeting of the Society for Maternal–Fetal Medicine, San Diego, CA,
January 30, 2009, two researchers from the Division of Maternal–Fetal Medicine,
Department of Obstetrics and Gynecology, Washington University–St. Louis,, and the
Division of Maternal–Fetal Medicine, Department of Obstetrics, Gynecology, and
Reproductive Sciences, University of California–San Francisco, enumerate the pros and
cons of magnesium sulfate use for CP prevention. In a spirited conversation, they each
talk about the available trials and observational studies and the strengths and weaknesses
of each. Participating in the roundtable, Alison G. Cahill, MD, MSCI, and Aaron B.
Caughey, MD, PhD, observe, "Despite well-designed and executed studies, the answer to
the question of whether evidence-based medicine supports the use of magnesium for
neuroprophylaxis in all preterm pregnancies remains unclear." Dwight J. Rouse, MD, of
the Center for Women's Reproductive Health, University of Alabama at Birmingham, offers
his clinical opinion on the use of MgSO4 to prevent cerebral palsy. He notes that
"three large, randomized placebo-controlled trials of antenatal magnesium sulfate
(MgSO4) for fetal neuroprotection have recently been conducted and reported. The results
of these trials provide strong support for the utilization of MgSO4 to lower the risk of
cerebral palsy among the survivors of early preterm birth. In the United States, the use
of MgSO4 for fetal neuroprotection has the potential to prevent 1000 cases of handicapping
cerebral palsy annually."
IU researchers find vibrator use to
be common, linked to sexual health
Two Indiana University studies conducted among nationally representative samples of adult
American men and women show that vibrator use during sexual interactions is common, with
use being reported by approximately 53 percent of women and 45 percent of men ages 18 to
60. Not only is vibrator use common, but the two studies also show that vibrator use is
associated with more positive sexual function and being more proactive in caring for one's
sexual health. The studies, led by researchers at the Center for Sexual Health Promotion
in IU's School of Health, Physical Education and Recreation, are the first to publish data
about vibrator use from nationally representative samples of the U.S. population. This
lack of data has existed despite a longstanding practice by many physicians and therapists
to recommend vibrator use to help treat sexual dysfunctions or to improve sexual
enjoyment. One study surveyed women. The other surveyed men. Both were published this week
by the "Journal of Sexual Medicine," a leading peer-reviewed journal in the area
of urology and sexual health. "The study about women's vibrator use affirms what many
doctors and therapists have known for decades -- that vibrator use is common, it's linked
to positive sexual function such as desire and ease of orgasm, and it's rarely associated
with any side effects," said Debby Herbenick, associate director of the Center for
Sexual Health Promotion. Michael Reece, director of the Center for Sexual Health
Promotion, said the studies are important for the contributions they make to an
understanding of the sexual behaviors and sexual health of adults in today's society.
"The study about male vibrator use is additionally important because it shows that
vibrator use is also common among men, something that has not been documented
before," Reece said. "Also, both studies help us to further understand the way
in which American consumers are turning to the marketplace for products that promote their
sexual health, and that has important economic implications."The studies are the
first to document insights into how and why people use vibrators, examine side effects and
to explore associations with sexual health behaviors, sexual enjoyment and quality of life
measures.
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.
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.”
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.
For Women With PCOS, Acupuncture
And Exercise May Bring Relief, Reduce Risks
Exercise and electro-acupuncture treatments can reduce sympathetic nerve activity in women
with polycystic ovarian syndrome (PCOS), according to a new study. The finding is
important because women with PCOS often have elevated sympathetic nerve activity, which
plays a role in hyperinsulinemia, insulin resistance, obesity and cardiovascular disease
The study also found that the electro-acupuncture treatments led to more regular menstrual
cycles, reduced testosterone levels and reduced waist circumference. Exercise had no
effect on the irregular or non-existent menstrual cycles that are common among women with
PCOS, nor did it reduce waist circumference. However, exercise did lead to reductions in
weight and body mass index. “The findings that low-frequency electro-acupuncture and
exercise decrease sympathetic nerve activity in women with PCOS indicates a possible
alternative non-pharmacologic approach to reduce cardiovascular risk in these
patients,” said one of the researchers, Dr. Elisabet Stener-Victorin of the
University of Gothenburg, Sweden. The findings regarding menstrual cycles and decrease in
testosterone levels in the low-frequency electro-acupuncture are also of interest,
according to the researcher. The study, “Low-frequency electro-acupuncture and
physical exercise decrease high muscle sympathetic nerve activity in polycystic ovary
syndrome” was conducted by Elisabet Stener-Victorin, Elizabeth Jedel, Per Olof Janson
and Vrsa Bergmann Sverrisdottir, all of the Sahlgrenska Academy, University of Gothenburg,
Sweden and the Karolinska Institute, Stockholm, Sweden. The study is in the online edition
of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology,
published by The American Physiological Society.
Intestinal cells surprisingly
active in pursuit of nutrition and defense
Every cell lining the small intestine bristles with thousands of tightly packed microvilli
that project into the gut lumen, forming a brush border that absorbs nutrients and
protects the body from intestinal bacteria. In the June 29, 2009 issue of the Journal of
Cell Biology (www.jcb.org), Matthew McConnell, Matthew Tyska, and colleagues now find that
microvilli extend their functional reach even further using a molecular motor to send
vesicles packed with gut enzymes out into the lumen to get a head start on breaking down
their substrates. Microvilli have traditionally been viewed as passive scaffolds that
increase the surface area of the gut wall. The apical plasma membrane tightly wraps around
each protrusive bundle of actin, providing more space for nutrient processing and
absorption. The motor protein myosin-1a (myo1a) maintains this structure by connecting the
plasma membrane to the actin filaments. In 2007, Tyska and colleagues found that myo1a
functions in isolated brush borders to actively move membrane along the length of the
microvilli, like a "membrane escalator." To their surprise, at the top of these
escalators—the tips of the microvilli—the membrane pinched off to form small
vesicles that were released into the surrounding medium. According to Tyska, when they
showed their data to gastroenterologists, they immediately asked "Why would brush
borders do that? They're wasting perfectly good apical membrane!" Tyska therefore
wanted to see if vesicle shedding was a bona fide physiological function for microvilli.
New control system of the body
discovered
It has been known for a long time that T cells can attack the body's own structures and,
if they infiltrate the CNS, cause diseases such as multiple sclerosis (MS). The T cells
damage the myelin sheath, the material that surrounds and protects the fibers of nerve
cells. This damage slows down or blocks messages between the brain and the body, leading
to various symptoms of MS such as impaired movements. The molecular analysis of damaged
tissue from patients with MS led the researchers to the B1-receptor. The data they
evaluated showed that two different pathways known to play a crucial role in the
cardiovascular area also seem to play an important role in the CNS: namely, the
renin-angiotensin-system, and the kallikrein-kinin-system, the latter of which the
researchers in Berlin put their focus on. The B1-receptor is part of the
kallikrein-kinin-system. Together with Professor Alexandre Prat from the Université de
Montréal, Montréal, Canada, and Professor Lawrence Steinman from Stanford University in
Stanford, California, USA, the researchers in Berlin detected the B1-receptor on T cells
of MS patients as well as on T cells of mice with encephalitis, an inflammation of the
brain. The disease got worse in those mice that lacked B1 on their T cells. Therefore,
using a certain substance (Sar-[D-Phe]desArg9-bradykinin), they activated the receptor in
mice which had B1 on their T cells. As a result, the entry of T cells into the CNS slowed
down and the clinical symptoms of the inflammation markedly decreased. "We have
discovered a control mechanism, which reduces inflammation caused by the immune
system" neurologist and MDC research group leader Professor Zipp explains. "It
remains to be seen if we succeed in developing a new therapy for chronic inflammation in
the CNS, such as MS, in the future."
Reading the brain without poking it
Experimental devices that read brain signals have helped paralyzed people use computers
and may let amputees control bionic limbs. But existing devices use tiny electrodes that
poke into the brain. Now, a University of Utah study shows that brain signals controlling
arm movements can be detected accurately using new microelectrodes that sit on the brain
but don't penetrate it. "The unique thing about this technology is that it provides
lots of information out of the brain without having to put the electrodes into the
brain," says Bradley Greger, an assistant professor of bioengineering and coauthor of
the study. "That lets neurosurgeons put this device under the skull but over brain
areas where it would be risky to place penetrating electrodes: areas that control speech,
memory and other cognitive functions." For example, the new array of microelectrodes
someday might be placed over the brain's speech center in patients who cannot communicate
because they are paralyzed by spinal injury, stroke, Lou Gehrig's disease or other
disorders, he adds. The electrodes would send speech signals to a computer that would
covert the thoughts to audible words.For people who have lost a limb or are paralyzed,
"this device should allow a high level of control over a prosthetic limb or computer
interface," Greger says. "It will enable amputees or people with severe
paralysis to interact with their environment using a prosthetic arm or a computer
interface that decodes signals from the brain." The study is scheduled for online
publication July 1 in the journal Neurosurgical Focus.
Singapore nanotechnology combats
fatal brain infections
Doctors may get a new arsenal for meningitis treatment and the war on drug-resistant
bacteria and fungal infections with novel peptide nanoparticles developed by scientists at
the Institute of Bioengineering and Nanotechnology (IBN) of Singapore and reported in
Nature Nanotechnology.The stable bioengineered nanoparticles devised at IBN effectively
seek out and destroy bacteria and fungal cells that could cause fatal infections and are
highly therapeutic. Major brain infections such as meningitis and encephalitis are a
leading cause of death, hearing loss, learning disability and brain damage in patients.
IBN's peptide nanoparticles, on the other hand, contain a membrane-penetrating component
that enables them to pass through the blood brain barrier to the infected areas of the
brain that require treatment. The ability of IBN's peptide nanoparticles to traverse the
blood brain barrier offers a superior alternative to existing treatments for brain
infections. The brain membrane is impenetrable to most conventional antibiotics because
the molecular structure of most drugs is too big to enter the membrane. "Our
treatment damages the structure of the pathogen and literally breaks it apart," said
Yiyan Yang, Ph.D., group leader at IBN, one of the research institutes sponsored by
Singapore's A*STAR (Agency for Science, Technology and Research). "Our oligopeptide
has a unique chemical structure that forms nanoparticles with membranepenetrating
components on their surface," Dr. Yang added. "These nanoparticles can easily
enter bacteria, yeast or fungal cells and destabilize them to cause cell death. For
example, the nanoparticles cause damage to bacteria cell walls and prevent further
bacterial growth." The IBN research team has demonstrated that these engineered
peptide nanoparticles have high antimicrobial activity and are highly effective in killing
microbes. Additionally, the peptide nanoparticles are more powerful in inhibiting the
growth of fungal infections than conventionally available anti-fungal drugs such as
fluconazole and amphotericin B.
New trigger for chronic
inflammation in rheumatoid arthritis discovered
A signal molecule made by the human body that triggers the immune system into action may
be important in rheumatoid arthritis, according to new research published today in Nature
Medicine. The authors of the study, from Imperial College London, say that if scientists
could block this signal, it may be possible to develop more effective arthritis
treatments. Rheumatoid arthritis is the most common autoimmune disease, affecting around 1
in 100 people. It causes painful and persistent swelling in the joints that can result in
damage to the bone and cartilage. Around half of all patients do not respond to one or
more of the treatments currently available, and even these can become less successful over
time. The researchers behind the new study say stopping the disease closer to the root of
the problem could be the best way to treat it, and their results suggest a new target for
therapies. When a microbe infects the body, the body responds by turning on a molecular
switch to set the immune system into action and protect the body from disease. Today's
findings show that a signal molecule called tenascin-C can trigger the same molecular
switch and also activate the immune system. High levels of tenascin-C present in joints
therefore may cause the activated immune system to attack the joint leading to the
persistent inflammation of rheumatoid arthritis. The molecular switch is called TLR4, and
is found on the surface of immune cells. Previous research has shown that mice without
TLR4 do not show chronic joint inflammation. The researchers hope scientists can develop
new treatments that target the interaction between tenascin-C and TLR4, which may help to
combat rheumatoid arthritis.Dr Kim Midwood, lead author of the study from the Kennedy
Institute of Rheumatology at Imperial College London, said: "Rheumatoid arthritis is
a debilitating and painful disease and, unfortunately, there is no cure. Furthermore,
current treatments are not effective for many patients." "We have uncovered one
way that the immune system may be triggered to attack the joints in patients with
rheumatoid arthritis. We hope our new findings can be used to develop new therapies that
interfere with tenascin-C activation of the immune system and that these will reduce the
painful inflammation that is a hallmark of this condition," added Dr Midwood.
A potent and selective anti-tumor
agent on human gastric cancer
A research article to be published on June 21, 2009 in the World Journal of
Gastroenterology addresses this question. The research team led by Professor Yan Li from
Shengjing Hospital of China Medical University studied the growth inhibitory effects of
Alisol B acetat and determined its mechanism of antitumor activity in human gastric cancer
cell line SGC7901. Professor Li and his colleagues found that Alisol B acetat could
inhibit the proliferation of SGC7901 cell in a time and dose dependent manner. Among the
various phases of cell cycle, the percentage of cells in S phase was significantly
decreased, while the percentage of cells in G1 phase was increased. Flow cytometry assay
also showed Alisol B acetate had positive effect on apoptosis. Typical apoptotic
morphology such as condensation and fragmentation of nuclei and formation of apoptotic
bodies could be observed through electron microscope and phase-contrast microscope.
Further investigating the molecular mechanism behind Alisol B acetat -induced apoptosis,
cells treated with Alisol B acetat underwent a rapid loss of mitochondrial transmembrane
potential, activition of caspase-3, -9, upregulation of Apaf-1 and Bax, and inhibition of
the PI3K/Akt in a time-dependent manner. The researches domenstrated for the first time
that Alisol B acetate induced human gastric cancer apoptosis through regulation of
mitochondrial and PI3K/AKT signaling pathways Their research results indicate that Alisol
B acetate might be used to treat gastric cancer , one of the most common cancers
worldwide. By knowing the mechanism of action of Alisol B acetate, it may provide a new
therapeutic option, as a potential anticancer agent, in the treatment of gastric cancer.
Study could help target new
pancreatitis treatments
Pancreatitis is often a fatal condition, in which the pancreas digests itself and
surrounding tissue. Scientists have previously found that alcohol can trigger the
condition by combining with fatty acids in the pancreas, which leads to an excessive
release of stored calcium ions. Once calcium ions enter cell fluid in the pancreas it
activates digestive enzymes and damages the cells. The team, in collaboration with the
RIKEN Brain Science Institute in Japan, have now identified channels within special stores
that allow calcium to enter the fluid inside pancreatic cells. They have also found that
toxic calcium release can be significantly reduced if the gene responsible for the
production of these channels is ‘deleted’ (or knocked-out). Professor Ole
Petersen, from the University’s School of Biomedical Sciences, explains: “The
pancreas releases enzymes into the gut, where they become activated and digest our food.
When these digestive enzymes are activated inside the cells, however, they start to digest
the pancreas itself, causing serious damage and often death. Alcohol is widely recognised
as one of the triggers for this process, but the reasons behind it have been unclear.
New, less invasive genetic test
greatly improves pregnancy rates in older women with poor prognosis
A new test examining chromosomes in human eggs a few hours after fertilisation can
identify those that are capable of forming a healthy baby, a researcher told the 25th
annual conference of the European Society of Human Reproduction and Embryology today
(Monday 29 June). Dr. Elpida Fragouli, from the Department of Obstetrics and Gynaecology,
University of Oxford, UK, and Reprogenetics UK, said that her team’s work had already
enabled seven ongoing pregnancies in a group of older women with a history of multiple
failed IVF attempts. “Out of 35 patients who had embryo transfers after the test, we
achieved a pregnancy rate of 20%, which is exceptional considering the extremely poor
prognosis of the women involved.” she said. “This represents a doubling of the
usual pregnancy rate for women who fall into this category, which is otherwise, at best,
under 10% and, at worst, zero. To date, we have two live births from this group, and all
the other women who became pregnant have maintained their pregnancies. The study is
continuing, and we believe that we will achieve more pregnancies with the help of this
technology in the future.” The scientists used the Comparative Genomic Hybridisation
(CGH) technique to count the chromosomes in each egg. Unlike conventional screening
strategies, using the fluorescent in situ hybridisation (FISH) method, which allows less
than half of the chromosomes of an embryonic cell to be examined, CGH enables the
evaluation of the entire chromosome complement. CGH was used to examine the fertilised
eggs by looking at polar bodies, tiny cells that are a by-product of egg development. The
chromosomes of polar bodies provide an indication of whether the corresponding egg is
normal or abnormal; if the polar bodies have the wrong number of chromosomes, so does the
egg.
High levels of cycling training
damage sperm – what can be done to protect triathletes from infertility?
The high-intensity training undertaken by triathletes has a significant impact on the
quality of their sperm, the 25th annual conference of the European Society of Human
Reproduction and Embryology heard today (Monday 29 June). Professor Diana Vaamonde, from
the University of Cordoba Medical School, Cordoba, Spain, said that the triathletes who
did the most cycling training had the worst sperm morphology. Professor Vaamonde’s
team has previously shown that both high exercise intensity and high exercise volume may
be detrimental to sperm quality. They decided to take a more profound look at the
sportsmen who seemed to show the greatest alteration – the triathletes – and
assess the correlation between the volume of training in each activity and sperm quality.
Of the three modalities, only cycling, the activity for which triathletes undertake the
most training, showed a clear correlation with sperm quality. The more cycling training
the sportsmen undertook, both in time and kilometres, the worse their sperm quality
became.
Dutch researchers find first
evidence that female human embryos adjust the balance of X
Dutch researchers have found the first evidence that a process of inactivating the X
chromosome during embryo development and implantation, which was known to occur in mice
but unknown in humans, does, in fact, take place in human female embryos prior to
implantation in the womb. Ms Ilse van den Berg told the 25th annual meeting of the
European Society of Human Reproduction and Embryology in Amsterdam today (Monday) that her
findings may have implications for the laboratory cultures that embryos are grown in
before transfer to a woman’s womb during fertility treatment, as well as for embryo
stem cell research. Males and females have two sex chromosomes: X and Y. While females
have two X chromosomes and no Y chromosome, males have one of each. As the X chromosome is
much larger then the Y chromosome, males and females also differ in their numbers of genes
and gene expression. To equalise this difference in gene expression, females need to
silence one X chromosome in every cell – a process known as X chromosome inactivation
(or XCI).
C-section births cause genetic
changes that may increase odds for developing diseases in later life
Swedish researchers have discovered that babies born by Caesarean section experience
changes to the DNA pool in their white blood cells, which could be connected to altered
stress levels during this method of delivery, according to the July issue of Acta
Paediatrica. It is thought that these genetic changes, which differ from normal vaginal
deliveries, could explain why people delivered by C-section are more susceptible to
immunological diseases such as diabetes and asthma in later life, when those genetic
changes combine with environmental triggers. Blood was sampled from the umbilical cords of
37 newborn infants just after delivery and then three to five days after the birth. It was
analysed to see the degree of DNA-methylation in the white blood cells - a vital part of
the immune system. This showed that the 16 babies born by C-section exhibited higher
DNA-methylation rates immediately after delivery than the 21 born by vaginal delivery.
Three to five days after birth, DNA-methylation levels had dropped in infants delivered by
C-section so that there were no longer significant differences between the two groups.
“Delivery by C-section has been associated with increased allergy, diabetes and
leukaemia risks” says Professor Mikael Norman, who specialises in paediatrics at the
Karolinska Institutet in Stockholm, Sweden. “Although the underlying cause is
unknown, our theory is that altered birth conditions could cause a genetic imprint in the
immune cells that could play a role later in life.
Fish intake of Swedish male
adolescents is a predictor of cognitive performance
Frequent fish intake at age 15 was associated with significantly higher cognitive
performance 3 years later.
Agrichemicals in surface water and
birth defects in the United States
Elevated concentrations of agrichemicals in surface water in April–July coincided
with higher risk of birth defects in live births with LMPs April–July. While a causal
link between agrichemicals and birth defectscannot be proven from this study an
association might provide clues to common factors shared by both variables.
Reported symptoms of food
hypersensitivity and sensitization to common foods in 4-year-old children
FHS was reported in 11% of the children (n = 397). Eczema was the most commonly reported
symptom and the only symptom in half of these children. Food-related reactions from the
airways, facial oedema or urticaria were reported in 198 children, and the majority of
these children (75%) reported multiple symptoms. Furthermore, a combination of airway
symptoms, facial oedema or urticaria together with sensitization to food suggested a more
severe form of FHS. This was found in 1.6% of all children. Symptoms caused by peanut were
closely associated with sensitization to peanut (p < 0.001). Food hypersensitivity in
4-year-old children with any of asthma, rhino-conjunctivitis, facial oedema or urticaria
in combination is in most cases associated to sensitization to food. This phenotype of FHS
is likely to represent a more severe form of food hypersensitivity.
Could Estrogen Improve Outcomes
After Traumatic Brain Injury, Shock?
UT Southwestern Medical Center researchers are conducting two pilot clinical trials to
determine whether a single, early dose of estrogen can improve survival and neurological
outcomes after severe traumatic brain injury or traumatic hemorrhagic shock. In these
double-blind studies, male patients transported to Parkland Memorial Hospital following
severe traumatic brain injury or severe blood loss associated with a traumatic injury will
be assigned randomly to receive either Premarin (estrogen) or a placebo intravenously
after arriving in the emergency department. Estrogen or a placebo will be administered as
a single-dose within two hours of injury. The researchers will measure biomarkers of
injury and repair in different body fluids during the first few days after injury, and
also will evaluate survival and neurological outcomes. Despite advances in surgical
interventions and intensive care management, about 35 percent of patients with severe
traumatic brain injury and hemorrhagic shock die. Many survivors do not fully recover and
are left with permanent disability.“Following traumatic brain injury or hemorrhagic
shock, secondary injury, such as inflammation, begins rapidly and greatly worsens the
initial injury,” said Dr. Jane Wigginton, assistant professor of emergency medicine
at UT Southwestern and the trials’ principal investigator. “Hundreds of animal
studies have shown that estrogen significantly reduces secondary injury. Those studies
give us hope that this new therapy offers considerable promise and minimal risk following
one dose in patients with life-threatening traumatic injuries.”
Site for Alcohol’s Action in
the Brain Discovered
Alcohol's inebriating effects are familiar to everyone. But the molecular details of
alcohol's impact on brain activity remain a mystery. A new study by researchers at the
Salk Institute for Biological Studies brings us closer to understanding how alcohol alters
the way brain cells work.
European researchers look for new
ways to fight multi-drug-resistant bacterial infections
The Institute of Biotechnology and Biomedicine (IBB) belonging to Universitat Autònoma de
Barcelona (UAB) is directing the AntiPathoGN European research project aimed at looking
for new drug targets in pathogenic bacteria resistant to multiple antibiotics. To do so a
consortium was created by six institutions and firms in Spain, three in Germany, one in
France and one in Bulgaria. The project, which will cost approximately 7.7 million euros,
will be carried out during four years. The European Union has subsidised the project with
six million euros. In the past decade bacterial resistance to antibiotics has risen
significantly whereas in some cases the rise has been dramatic such as in hospital areas.
It has reached such a stage that the World Health Organization considers these
multi-drug-resistant microorganisms the cause of emerging infectious diseases. Currently a
large amount of antibiotics available are not apt for the treatment of resistant pathogens
belonging to an important group called gram-negative bacteria. On occasions, the choice
narrows down to one drug such as the "last-resort" antibiotic colistin to treat
infections caused by the bacteria Pseudomonas aeruginosa or Acinetobacter baumannii. At
the same time, the lack of economic benefits has reduced the amount of research
pharmaceutical companies dedicate to creating new antibiotics.
Evidence that cognitive therapy is
of no value in schizophrenia
Research co-led by an academic at the University of Hertfordshire, concludes that
Cognitive Behavioural Therapy (CBT) is of no value in schizophrenia and has limited effect
on depression. Professor Keith Laws, at the University's School of Psychology, is one of
the lead authors on a paper entitled: Cognitive behavioural therapy for major psychiatric
disorder: does it really work? A meta-analytical review of well-controlled trials, which
has just been published online in the journal Psychological Medicine. The paper reviews
the use of CBT in schizophrenia, bipolar disorder and major depression. The results of the
review suggest that not only is CBT ineffective in treating schizophrenia and in
preventing relapse, it is also ineffective in preventing relapses in bipolar disorder. The
review also suggests that CBT has only a weak effect in treating depression, but it has a
greater effect in preventing relapses in this disorder.
Insulin analogue glargine possibly
increases cancer risk
The risk of cancer possibly increases if patients with diabetes use the long-acting
insulin analogue glargine instead of human insulin. The Institute for Quality and
Efficiency in Health Care (IQWiG), in collaboration with the "Wissenschaftliches
Institut der AOK" (WIdO), the research institute of the German Local Health Care
Fund, analysed the data of almost 130,000 patients with diabetes in Germany who had been
treated with either human insulin or the insulin analogues lispro (trade name: Humalog),
aspart (Novorapid) or glargine (Lantus) between January 2001 and June 2005. The analysis
has now been published together with further studies in the scientific journal
Diabetologia, the official organ of the European Association for the Study of Diabetes
(EASD). The disturbing result is that malignancies were found more frequently in patients
treated with glargine than in those prescribed a comparable dose of human insulin.
"Our analysis does not provide absolute proof that glargine promotes cancer,"
says Peter T. Sawicki, IQWiG's Director and co-author of the study. "Our study does,
however, arouse an urgent suspicion which should have consequences for the treatment of
patients."No difference was found between the short-acting insulin analogues, lispro
and aspart, and human insulin. Insulin analogues are synthetic molecules that do not occur
naturally, whereas human insulin matches the insulin that the human body manufactures
itself. Is glargine the cause? IQWiG emphasises that the link found between prescribing
glargine and an increased cancer risk is a statistical association. Thus, it is possible
that other factors as yet unknown are the cause of the increased risk, rather than
glargine. However, it is disturbing that of three further studies published in the same
edition of Diabetologia, two also describe an increase in cancer risk associated with
glargine. Glargine has been approved in Germany since 2000. Since then, several laboratory
trials have been published which indicate that, under certain conditions, insulin
analogues can stimulate the growth of cancer cell lines more strongly than human insulin.
"These indications are discussed in the scientific world but have never been
dispelled by proper studies," says Sawicki. According to IQWiG, the overall
indications of a risk from glargine have now intensified to such an extent that the burden
of proof has been reversed for precautionary reasons: as long as reliable studies do not
prove the safety of glargine compared to human insulin, the drug should only be used if
there are particularly important reasons for doing so.
DOD, VA Should Take Stronger Steps
To Combat Tobacco Use in Military, Veteran Populations
Because tobacco use impairs military readiness, harms the health of soldiers and veterans,
and imposes a substantial financial burden on the departments of Defense and Veterans
Affairs, these agencies should implement a comprehensive strategy to achieve the Defense
Department's stated goal of a tobacco-free military, says a new report from the Institute
of Medicine. DOD should gradually phase in a ban on tobacco use in the military, starting
at military academies and officer training programs and among new recruits, the report
says. DOD should also stop selling tobacco products in Army and Air Force commissaries --
Navy and Marine Corps commissaries already do not sell them -- and should stop selling
them at a discount in military exchanges and other stores. In addition, Congress should
allow VA to establish tobacco-free medical centers. The report was requested by DOD and
VA, who asked the Institute of Medicine to identify policies and practices that could
lower rates of smoking and help soldiers and veterans quit. Tobacco use reduces soldiers'
physical fitness and endurance and is linked to higher rates of absenteeism and lost
productivity, the report says. In 2005, 32 percent of active-duty personnel and 22 percent
of veterans were smokers; rates among active-duty personnel have recently increased,
possibly because of growing tobacco use by deployed troops. "We found that the
adverse effects of tobacco use on military readiness, the health of both smokers and
nonsmokers, and the financial cost of the medical care of smoking-related illness in
military and veteran populations are a sound basis for moving systematically toward a
tobacco-free military," said Stuart Bondurant, professor of medicine and dean
emeritus of the School of Medicine at the University of North Carolina, Chapel Hill, and
chair of the committee that wrote the report. "The state of the art in tobacco
control is such that with well-managed programs, DOD and VA could eventually be tobacco
free with minimal disruption, and with substantial benefit to military personnel and
veterans." DOD and VA should ensure that all personnel have quick and easy access to
comprehensive, evidence-based tobacco-cessation services, the report says. All DOD and VA
health care providers should be able to provide brief counseling and nicotine-replacement
therapy to patients. In addition, the committee recommended that VA and DOD develop
toll-free "quitlines" to provide military personnel and veterans with counseling
on quitting tobacco. Quitline counselors should be trained to deal with issues related to
these populations, such as post-traumatic stress disorder.
Enzyme fights mutated protein in
inherited Parkinson's disease
An enzyme that naturally occurs in the brain helps destroy the mutated protein that is the
most common cause of inherited Parkinson’s disease, researchers at UT Southwestern
Medical Center have found. Their study, using human cells, provides a focus for further
research into halting the action of the mutated protein. One of the most famous carriers
of the mutation is Google co-founder Sergey Brin, who wrote about it on his blog in 2008.
“There are currently enormous efforts to identify potential therapies based on
inhibiting this mutated protein,” said Dr. Matthew Goldberg, assistant professor of
neurology and psychiatry and senior author of the paper, which appears online in the
journal Public Library of Science. “Our paper is a major advance because we identify
a protein that binds to the mutated protein and promotes its breakdown,” he said.
More gene mutations linked to
autism risk
More pieces in the complex autism inheritance puzzle are emerging in the latest study from
a research team including geneticists from The Children's Hospital of Philadelphia, the
University of Pennsylvania School of Medicine and several collaborating institutions. This
study identified 27 different genetic regions where rare copy number variations –
missing or extra copies of DNA segments – were found in the genes of children with
autism spectrum disorders (ASDs), but not in the healthy controls. The complex combination
of multiple genetic duplications and deletions is thought to interfere with gene function,
which can disrupt the production of proteins necessary for normal neurological
development. "We focused on changes in the exons of DNA—protein-coding areas in
which deletions or duplications are more likely to directly disrupt biological
functions," said study leader Hakon Hakonarson, M.D., Ph.D., director of the Center
for Applied Genomics at The Children's Hospital of Philadelphia and associate professor of
Pediatrics at the University of Pennsylvania School of Medicine. "We identified
additional autism susceptibility genes, many of which, as we previously found, belong to
the neuronal cell adhesion molecule family involved in the development of brain circuitry
in early childhood." He added that the team discovered many "private" gene
mutations, those found only in one or a few individuals or families—an indication of
genetic complexity, in which many different gene changes may contribute to an autism
spectrum disorder. "We are finding that both inherited and new, or de novo, genetic
mutations are scattered throughout the genome and we suspect that different combinations
of these variations contribute to autism susceptibility," said Maja Bucan, Ph.D.,
professor of Genetics at the University of Pennsylvania School of Medicine and Chair of
the Steering committee for Autism Speaks' Autism Genetic Resource Exchange (AGRE).
"We are grateful to families of children with autism spectrum disorders for their
willingness to participate in genetic studies because family-based studies have many
advantages. We have learned a lot both from genetic analyses of children with autism as
well as analyses of their patents and their unaffected siblings."
Public contracts: the Commission
decides to take Greece to the European Court
The European Commission has decided to
bring Greece before the European Court of Justice on the basis of Article 228 of the EC
Treaty. The Hellenic Republic has failed to take steps to comply with the Court's judgment
of 18 December 2007 in Case C-481/06 on the conformity of Greek legislation, which
allows a negotiated procedure to be used without a prior call for tenders for public
contracts for the supply of certain types of medical equipment.Article 228 provides that
in bringing the case before the Court of Justice the Commission must specify the amount of
the lump sum or penalty payment to be paid by the Member State concerned which it
considers appropriate in the circumstances. According to the same article, if the Court of
Justice finds that the Member State concerned has not complied with its judgment it may
impose a lump sum or penalty on it. The latest information on infringement proceedings
against the Member States is available on the following site:
http://ec.europa.eu/community_law/index_en.htm
Environment: Spain risking fines
over failures to comply with nature conservation laws
The European Commission is warning Spain
about two breaches of environmental legislation. The first case, which could result in
Court action, concerns a failure to assess the environmental impact of open-cast mining in
a Natura 2000 conservation area in Castille-León, which is home to a number of threatened
species such as brown bears and capercaillie, both of which are protected under European
law. The second case concerns a failure to designate and protect a number of natural areas
in the Canary Islands, one of the biodiversity hotspots of the EU, home to numerous
endemic species found nowhere else in the world. EU Environment Commissioner Stavros Dimas
said: "Our economies and our lifestyles depend on a healthy environment. Natura 2000
– Europe's network of protected areas – is vital for the environmental integrity
of our continent, and that integrity must be protected whenever it is at risk. Engineering
or construction projects are not per se forbidden in Natura 2000 sites, but assurance has
to be provided that they do not negatively affect the integrity of these important areas.
I therefore call on Spain to make good these shortcomings as soon as possible." Spain
is being referred to the Court of Justice for a failure to properly assess the impact of a
number of on-going and authorized open cast mines in Castille-Le ón. The coal mines in
question are located inside a Natura 2000 site in Laciana valley, near Villablino, Leon,
which is home to several critically endangered species including brown bear ( Ursus
arctos) and capercaillie ( Tetrao urogallus). Under Community law, adverse effects on
priority species under the Habitats Directive and endangered bird species protected under
the Birds Directive must be properly assessed before any work can commence. As the
Commission is not satisfied by the quality of the environmental assessments that have been
carried out to date, or by Spain's subsequent justifications, the country is being
referred to the Court of Justice. The Commission is also sending Spain a second written
warning about 174 protected sites in the Canary Islands that have not yet been afforded
adequate protection. Under Spanish law, the sites in question, which are parts of the
Natura 2000 network, needed to be classified as Special Areas of Conservation by December
2007. Spain claims that such processes are under way, but the Commission maintains that no
final date has yet been guaranteed for the designation, and that the appropriate
conservation measures are not yet in place.
The case was opened in February together
with a similar infringement case against Portugal for the Azores and Madeira, where swift
progress has been made. The Canary Islands are home to a large variety of endemic flora
and fauna that are found nowhere else in the world. The islands contain unique ecosystems
particular to these volcanic regions, and many of them – including coastal lagoons
and laurel forests – are under threat. Despite representing only 0.3% of the EU
territory, the region hosts almost 20% of its most important habitat types and 28% of its
protected plants, many of them endemic to the islands Europe's nature is protected by two
key pieces of legislation, the Birds Directive and the Habitats Directive. Under the Birds
Directive, Member States are obliged to designate suitable sites as Special Protection
Areas (SPAs) for the conservation of wild birds. The designation of SPAs must be based on
objective, verifiable scientific criteria. Under the Habitats Directive, Member States
draw up a list of Sites of Community Importance (SCIs) on their territory that can make a
significant contribution to preserving Europe's habitat types. Member States then have six
years to bring in domestic legislation turning the SCIs into strictly protected Special
Areas of Conservation (SAC). Taken together, SCIs, SPAs and SACs form the Natura 2000
network of protected areas, which is the EU's most important instrument for conserving
natural habitats and the animal and plant species they contain.
Article 226 of the Treaty gives the
Commission powers to take legal action against a Member State that is not respecting its
obligations. If the Commission considers that there may be an infringement of EU law that
warrants the opening of an infringement procedure, it addresses a "Letter of Formal
Notice" (first written warning) to the Member State concerned, requesting it to
submit its observations within a specified period, usually within two months. In the light
of the reply or absence of a reply from the Member State concerned, the Commission may
decide to address a "Reasoned Opinion" (final written warning) to the Member
State. This clearly and definitively sets out the reasons why it considers there to have
been an infringement of EU law and calls upon the Member State to comply within a
specified period, normally two months. If the Member State fails to comply with the
Reasoned Opinion, the Commission may decide to bring the case before the European Court of
Justice. Where the Court of Justice finds that the Treaty has been infringed, the
offending Member State is required to take the measures necessary to conform. Article 228
of the Treaty gives the Commission power to act against a Member State that does not
comply with a previous judgement of the European Court of Justice. The article also allows
the Commission to ask the Court to impose a financial penalty on the Member State
concerned.
State aid: Commission refers Italy
to Court for failure to respect Court ruling to recover illegal aid
The European Commission has decided to
refer Italy to the European Court of Justice (ECJ) for failure to implement a 2004 ruling
by the Court of Justice (case C-99/02) confirming a Commission decision of 1999 finding
that Italy had granted illegal and incompatible aid and ordering its recovery. The illegal
aid in question took the form of exemptions from social security contributions in cases where companies could not prove that new jobs had been created or prove that
the workers hired had special difficulties entering or re-entering the employment market.
Although over five years have elapsed since this judgement, Italy has still only recovered
a small part of the overall aid amount estimated at about 281 million euros. The
Commission therefore now requests the ECJ to impose fines on Italy under Article 228 of
the EC Treaty. Competition Commissioner Neelie Kroes commented: "The Commission will
take all necessary legal steps to ensure that Member States comply with their obligations
to recover illegal and incompatible state aid." On 1st April 2004 (case C-99/02), the
ECJ held that Italy had failed to meet the recovery obligations imposed in the Commission
Decision of 11 May 1999 (see IP/99/321
). The decision concerned aid measures aimed at promoting employment. The
Commission had found part of the aid incompatible with the Single Market because it was
not suitable to attain the declared objective of creating jobs and had therefore to b e
recovered from the beneficiaries. To date, Italy has still not informed the Commission
that the recovery has been completed. Based on the most recent calculations presented by
Italy, less than 20% of the total aid amount estimated at about 281 million euros has been
recovered more than ten years after the Commission's original recovery decision and more
than five years after the previous ECJ judgement. The Commission has therefore decided to
request the ECJ to impose fines in the form of a daily penalty payment, to be calculated
from the date of the ECJ judgement to be delivered and lasting until Italy manages to
complete the recovery, and of a lump sum payment covering the period since the Court's
previous judgement in 2004. In calculating the fines the Commission will apply its 2005
Communication on the application of Article 228. The proposal will thus take into
consideration the seriousness of the infringement, the very significant period which has
already elapsed since the previous Court judgement and the situation of the Member State.
Greece: Commission pursues legal
action over lack of measures to protect important wetland
The European Commission is launching legal
proceedings against Greece for failing to put in place adequate measures to protect one of
Europe's most important wetlands. The case relates to the pollution and degradation of Lake Koroneia in the region of Thessaloniki. Greece is being sent a first
written warning for failing to implement the legal protection and conservation framework
necessary for the site. The European Commission is sending Greece a first written
warning over inadequate protection and conservation measures for Lake Koroneia, an
internationally important wetland. Following infringement proceedings in 2002 relating to
the pollution and degradation of the lake, the Greek authorities committed to put in place
a specific legal framework and address illegal activities on the site. The Greek
authorities established the legal framework and adopted a management and restoration plan
to rehabilitate the wetland, with many of the actions to be co-financed by the Commission.
However, progress to implement the protection measures has been slow. The Commission
considers that Greece has not taken adequate action to prevent the degradation of the lake
and disturbance of fauna and flora. The Commission has therefore decided to open a new
infringement case and send a first written warning to Greece. Lake Koroneia is affected by
heavy water abstraction for irrigation purposes, which has drastically reduced the water
level of the lake. It is also seriously polluted by discharges of nutrients, heavy metals
and other pollutants from industries and towns in the surrounding area.
These nutrients promote excessive growth of
algae that chokes off other life, a process known as
eutrophication. The lake is a Natura 2000 site protected under the EU Birds and Habitats Directives. It hosts numerous threatened, endemic or rare habitats, species and
birds and is listed under the Ramsar Convention, an international treaty for the
conservation and sustainable use of natural wetlands. In addition, Greece has an
obligation under the Directive on the discharge of dangerous substances into the aquatic environment , and the Urban Wastewater Treatment Directive which requires Member States to conduct strict treatment of wastewater intended
to be released into sensitive areas. Article 226 of the Treaty gives the Commission powers
to take legal action against a Member State that is not respecting its obligations. If the
Commission considers that there may be an infringement of EU law that warrants the opening
of an infringement procedure, it addresses a "Letter of Formal Notice" (first
written warning) to the Member State concerned, requesting it to submit its observations
by a specified date, usually within two months.
In the light of the reply or absence of a
reply from the Member State concerned, the Commission may decide to address a
"Reasoned Opinion" (second and final written warning) to the Member State. This
clearly and definitively sets out the reasons why it considers there to have been an
infringement of EU law and calls upon the Member State to comply within a specified
period, normally two months. If the Member State fails to comply with the Reasoned
Opinion, the Commission may decide to bring the case before the European Court of Justice.
Where the Court of Justice finds that the Treaty has been infringed, the offending Member
State is required to take the measures necessary to conform. Article 228 of the Treaty
gives the Commission power to act against a Member State that does not comply with a
previous judgement of the European Court of Justice. The article also allows the
Commission to ask the Court to impose a financial penalty on the Member State concerned.
Direct taxation: The European
Commission requests Belgium to end discriminatory taxation of interest paid by foreign
banks to individuals
The European Commission has sent Belgium a
formal request to amend its legislation which leads to different taxation of interest
depending on where the bank paying such interest is established. According to the Belgian
legislation, interest paid by Belgian banks to individuals is exempted from tax up to the
amount of € 1660 whereas interest paid by foreign banks cannot benefit from the same
exemption. The Commission's request takes the form of a ‘reasoned opinion’
(second step of the infringement procedure of Article 226 of the EC Treaty). If Belgium
does not reply satisfactorily to the reasoned opinion within two months the Commission may
refer the matter to the European Court of Justice. Belgium offers an exemption from income
tax which is only applicable to interest paid by banks established in Belgium. Belgian
residents are, as a consequence, dissuaded from opening or maintaining savings accounts
with banks which are not established in Belgium. The exemption is an incentive for these
residents to open and maintain a savings account in Belgium and/or to repatriate their
savings to Belgium. Moreover, it is also an incentive for those who already have one or
several savings accounts with Belgian banks, to remain clients and not transfer their
accounts to a bank which is not established in Belgium. The difference in treatment
between interest paid by Belgian banks and interest paid by foreign banks amounts to an
obstacle to the free movement of capital within the meaning of Article 56 EC, and to the
freedom to provide services within the meaning of Article Articles 49 EC. In the
Commission's view the difference in treatment constitutes an arbitrary discrimination
which cannot be justified.
VAT: The European Commission
requests Portugal to modify its flat-rate scheme applied to farmers
The European Commission has formally
requested Portugal to change its law since it is of the opinion that Portugal does not
apply a flat rate scheme for farmers consistent with the objectives of the scheme which is
laid down in the VAT Directive. As a result farmers opting for the flat rate scheme may
face financial disadvantages. The request takes the form of a reasoned opinion (second
step of the infringement procedure provided for in article 226 of the EC Treaty). If the
relevant national legislation is not amended in order to comply with the respective
reasoned opinion, the Commission may decide to refer the matter to the European Court of
Justice. Where the application to farmers of the normal VAT arrangements is likely to give
rise to difficulties, Member States may apply a flat-rate scheme designed to offset the
VAT charged on purchases of goods and services made by the flat-rate farmers. When a
farmer opts for this flat rate scheme, he is no longer covered by the normal VAT rules: he
may not deduct the VAT paid on his inputs and he is released from his obligations relating
to payment of tax, invoicing, declaration and accounting. In order to compensate him for
the VAT paid on inputs which he cannot deduct, a flat-rate compensation (calculated by
each Member States on the basis of macro-economic statistics) will be paid to him. Instead
of introducing a flat rate scheme for farmers in line with the provisions of the VAT
Directive, Portugal has introduced an optional exemption for agricultural activities,
exempting VAT on supplies provided by the farmer, unless he opts to apply the normal VAT
arrangements. In addition, the flat-rate compensation percentage is fixed at a zero rate:
farmers are not compensated for the VAT paid on their inputs while they have to pay VAT on
agricultural inputs of 5-12%. Given that too much VAT is levied from the sector, Portugal
makes a substantial negative compensation in its own resources to compensate for this
factor. The Commission takes the view that the flat rate scheme applied to farmers in
Portugal clearly conflicts with the purpose of the scheme and is not in line with the VAT
Directive. The zero compensation may no more be applied. It is indeed a fact that at the
time of Portugal's accession to the Community, when the scheme was first adopted, many of
the products used for agricultural production were subject to a rate of zero per cent,
which would have accounted for the setting of a compensation percentage at 0%. However,
the conditions have since changed and now it seems that a number of agricultural inputs
are taxed at a rate of 5% in Portugal, while agricultural machinery and agricultural fuel
are even subject to a rate of 12%.
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