- - European weblog on food, health and environment
News - Week 10 - 2009
Tiny tool to control growing blood
vessels opens new potential in tumor research
Researchers at Uppsala University have developed a new tool that makes it possible to
study the signals in the body that control the generation of blood vessels. The
researchers' findings, published in the new issue of Lab on a Chip, enable scientists to
determine what signals in the body attract or repel blood vessels, knowledge that is
extremely interesting in tumor research. The new invention is a tiny cell cultivation
chamber of silicon plastic in which researchers can cultivate blood-vessel-rich tissue and
simultaneously create targeted signals that instruct the vessels to go in a certain
direction. This is of great interest to the international research world. Angiogenesis is
the process in the body that forms new blood cells, a process that is vital for life but
can also be fatal in the worst case. Angiogenesis is desirable, for instance, in
connection with wound healing, when new tissue needs to be grown. Undesirable
angiogenesis, on the other hand, often occurs in connection with tumor growth. Through the
newly generated blood vessels in the vicinity of the tumor, tumor cells receive
nourishment and oxygen, which creates the conditions for tumor growth. One way to limit
tumor growth may therefore be to counteract the new formation of blood vessels in the
tumor, thereby cutting off the supply of nourishment and oxygen to the diseased area. The
scientists Irmeli Berkefors and Johan Kreuger's research is geared toward understanding
the signals that control both normal and pathological angiogenesis. To understand this, it
is important to construct experimental model systems in which they can study how
concentration gradients of various signal proteins affect the direction in which a vessel
grows. "Our new method enables us to recreate and study gradients that control how
blood vessels grow in the body. This is something of a research breakthrough. Now we can
systematically evaluate newly identified signals that we hope can ultimately be used to
control angiogenesis," says Johan Kreuger. The method can also be used to unearth new
knowledge regarding how tumor cells and nerve cells grow and move toward gradients of
signal proteins.
A deep-sea fish with a transparent
head and tubular eyes
Clinical trials' review finds only
exercise to prevent low-back problems
Low-back pain continues to impose a huge burden on industrialized societies, in terms of
symptoms, medical costs, productivity, and work absence. Annual costs related to back pain
in the United States alone may run as high as $100 billion per year. But a systematic
review of the literature for high-quality scientific trials published in the February
issue of The Spine Journal finds exercise in workplace and community settings effective in
preventing new episodes of low-back problems. "Strong and consistent evidence finds
many popular prevention methods to fail while exercise has a significant impact, both in
terms of preventing symptoms and reducing back pain-related work loss," said Dr.
Stanley J. Bigos, University of Washington professor emeritus of orthopaedic surgery and
environmental health. Bigos and his colleagues assessed methodological quality and
potential for bias of clinical trials in preventing episodes of back problems. The
researchers found 20 controlled trials to be high-quality according to Cochrane
Collaboration Back Review Group criteria. Seven of the eight high-quality trials promoting
various exercise programs were found effective, but other common and popular methods
failed including: reduced lifting programs, back or ergonomic educational interventions,
lumbar supports, shoe inserts and stress management. "Passive interventions such as
lumbar belts and shoe inserts do not appear to work," Bigos said. "And eight
trials found ergonomic interventions, of either reducing lifting, or back or ergonomic
training sessions to be ineffective in preventing back problems."
Young smokers increase risk for
multiple sclerosis
People who start smoking before age 17 may increase their risk for developing multiple
sclerosis (MS), according to a study released today that will be presented at the American
Academy of Neurology's 61st Annual Meeting in Seattle, April 25 to May 2, 2009. The study
involved 87 people with MS who were among more than 30,000 people in a larger study. The
people with MS were divided into three groups: non-smokers, early smokers (smokers who
began before age 17), and late smokers (those who started smoking at 17 or older), and
matched by age, gender, and race to 435 people without MS. Early smokers were 2.7 times
more likely to develop MS than nonsmokers. Late smokers did not have an increased risk for
the disease. More than 32 percent of the MS patients were early smokers, compared to 19
percent of the people without MS. "Studies show that environmental factors play a
prominent role in multiple sclerosis," said study author Joseph Finkelstein, MD, PhD,
of Johns Hopkins University School of Medicine, in Baltimore, MD, which conducted the
study in collaboration with Veterans Affairs MS Center for Excellence. "Early smoking
is an environmental factor that can be avoided."
Can Breastfeeding Reduce Multiple
Sclerosis Relapses?
Women who have multiple sclerosis may reduce their risk of relapses after pregnancy if
they breastfeed their babies, according to a study released today that will be presented
at the American Academy of Neurology’s 61st Annual Meeting in Seattle, April 25 to
May 2, 2009. For the study, researchers followed 32 pregnant women with MS and 29 pregnant
women without MS during each trimester and up to a year after they gave birth. The women
were interviewed about their breastfeeding and menstrual period history. A total of 52
percent of the women with MS did not breastfeed or began supplemental formula feedings
within two months of giving birth. Of those, 87 percent had a relapse after pregnancy
compared to 36 percent of women with MS who breastfed exclusively for at least two months
after pregnancy.
Study Indicates How We Maintain
Visual Details In Short Term Memory
Working memory (also known as short term memory) is our ability to keep a small amount of
information active in our mind. This is useful for information we need to know on-the-fly,
such as a phone number or the few items we need to pick up from the grocery store. We hang
on to the information for a brief period of time, just long enough to make a phone call or
get through the checkout line, and then we forget it forever. We receive much of our
information through our visual system, but it was unknown how much of this visual
information is actively involved in short term memory. Psychologists John T. Serences from
the University of California, San Diego, along with Edward F. Ester, Edward K. Vogel and
Edward Awh from the University of Oregon wanted to examine which neural systems enable the
maintenance of these visual details in short term memory. While undergoing functional
magnetic resonance imaging (fMRI) scans, volunteers were shown an image for one second and
were instructed to remember either the color or the orientation of the image. Following
the image, volunteers saw a blank screen for 10 seconds, then were shown another image and
had to indicate if it was the identical color or orientation (depending on which they were
told to remember) as the first image. The researchers analyzed brain activity during the
10 second delay (when short term memory is active) in the primary visual cortex, the main
region of the brain which handles visual information.
How We Think Before We Speak -
Making Sense of Sentences
We engage in numerous discussions throughout the day, about a variety of topics, from work
assignments to the Super Bowl to what we are having for dinner that evening. We
effortlessly move from conversation to conversation, probably not thinking twice about our
brain's ability to understand everything that is being said to us. How does the brain turn
seemingly random sounds and letters into sentences with clear meaning? In a new report in
Current Directions in Psychological Science, a journal of the Association for
Psychological Science, psychologist Jos J.A. Van Berkum from the Max Planck Institute in
The Netherlands describes recent experiments using brain waves to understand how we are
able to make sense of sentences. In these experiments, Van Berkum and his colleagues
examined Event Related Potentials (or ERPs) as people read or heard critical sentences as
part of a longer text, or placed in some other type of context. ERPs are changes in brain
activity that occur when we hear a certain stimulus, such as a tone or a word. Due to
their speed, ERPs are useful for detecting the incredibly fast processes involved in
understanding language. Analysis of the ERPs has consistently indicated just how quickly
the brain is able to relate unfolding sentences to earlier ones. For example, Van Berkum
and colleagues have shown that listeners only need a fraction of a second to determine
that a word is out of place, given what the wider story is about. As soon as listeners
hear an unexpected word, their brain generates a specific ERP, the N400 effect (so named
because it is a negative deflection peaking around 400 milliseconds). And even more
interesting, this ERP will usually occur before the word is even finished being spoken.
Shiitake mushrooms exceptional
source of vitamin D
Shiitake mushrooms can be an exceptional source of vitamin D, as noted in research
published in Paul Stamets’ book, Mycelium Running. Shiitake mushrooms grown and dried
indoors have only 110 IU of vitamin D per 100 grams. But when the same mushrooms were
dried in the sun, the vitamin D content rose to 21,400 IUs per 100 grams. even more
surprising, when the same mushrooms were dried with their gills facing up in the sun,
their content rose to 46,000 IU!
Get personal to improve heart
health
Scare tactics may not be necessary when trying to get patients at risk of heart disease to
change their diet or behaviour, a new study has found. Instead, doctors and nurses should
be aware of the stage of life their patients are at, and offer them very specific and
targeted advice. "The goal is to produce interventions which are sensitive to the
lives and social position of those who find themselves at 'high risk' of coronary heart
disease (CHD) in later-middle age, and which inspire change rather than inhibit it,"
say researchers, from Egenis, the ESRC Centre for Genomics in Society at the University of
Exeter. High-risk patients will often downgrade their risk in their own minds, yet could
still be receptive to the behavioural change which is the purpose of CHD screening,
explained Dr Hannah Farrimond, who studied the reaction of patients to being told they
were at high risk. Boosting patients' sense of vulnerability does not help, and may even
hinder, their efforts to change, the study found. "Once patients have got over the
shock of being at high risk of heart disease, they then tend to underplay their
risk," says Dr Farrimond. "They compare themselves favourably with, say, others
of the same age. In the past, researchers have thought we need to scare people into
feeling at risk to make them change. This study suggests that even those who downplayed
their risk still made changes, such as taking statins or exercising more. In other words,
we don't need to scare people to get results. Clinical staff need to find other ways of
encouraging patients to make the necessary lifestyle changes, such as offering
personalised advice."
The Obama Deception (2009) ~
Trailer || High Quality
The Truth about MSG Monosodium
Glutamate
Second-hand smoke could cause
dementia
First large scale study demonstrates link between exposure to passive smoking and
cognitive problems. Researchers from the Peninsula Medical School, the University of
Cambridge and the University of Michigan have published the results of the first
large-scale study to indicate that second-hand smoke exposure could lead to dementia and
other neurological problems. The Peninsula Medical School is a joint entity of the
Universities of Exeter and Plymouth. The results are published by the BMJ online. Research
has already identified possible links between active smoking and cognitive impairment, and
previous findings have suggested exposure to second-hand smoke is linked to poor cognitive
performance in children and adolescents. However, this is the first study of its kind to
link second-hand smoke exposure to cognitive impairment in adult non-smokers. The research
team examined saliva samples from almost 5000 non-smoking adults over the age of 50, using
data from the 1998, 1999 and 2001 waves of the Health Survey and England. The participants
subsequently took part in the English Longitudinal Study of Ageing. The saliva samples
were tested for cotinine, a product of nicotine that remains in the saliva for about 25
hours after exposure to second-hand smoke. Those who took part in the study also provided
a detailed smoking history, and those who had never smoked, or who were previous smokers,
were assessed separately. Established neuropsychological tests were used to assess brain
function and cognitive impairment. These focused on memory function, numeracy and verbal
fluency. The test results were added together to provide a global score for cognitive
function. Those whose scores were in the lowest 10 per cent were identified as suffering
from cognitive impairment. The researchers believe that the link between second-hand smoke
and cognitive impairment could be explained by the fact that heart disease increases the
risk of developing dementia, and that exposure to second-hand smoke is known to cause
heart disease.
What is potentially pathogenic role
of anti-tTG IgA in the development of celiac disease?
The recent detection of antibodies in celiac patients specific for deamidated gliadin
peptides (DGP), the product of tTG binding to gliadin peptides, provides an opportunity to
address the correlation between the production of anti-tTG IgA and the antibodies against
DGP in celiac patients A research article to be published on February 21, 2009 in the
World Journal of Gastroenterology addresses this question. The study group is led by Dr.
Marietta, Rashtak, and Murray from the Mayo Clinic in Rochester, MN are of interest to the
Celiac Disease community, since the data demonstrate that the serum level of anti-tTG IgA
is significantly correlated with the serum level of anti-DGP of both the IgG and IgA
isotypes in untreated patients. In contrast, only a weak correlation exists between the
production of anti-tTG IgG and anti-DGP IgG/IgA. These data would indicate that the immune
response by T and B cells to deamidated gliadin is fundamentally different from the immune
response by T and B cells to tissue transglutaminase in celiac patients. These data would
also indicate, however, that the immune responses against deamidated gliadin and tTG are
significantly correlated with each other, and thereby provide support for the
hapten-carrier theory for the origin of anti-tTG IgA.
Calculating gene and protein
connections in a Parkinson's disease model
A novel approach to analyzing cellular data is yielding new understanding of Parkinson's
disease's destructive pathways. Whitehead Institute and Massachusetts Institute of
Technology (MIT) scientists have employed this new computational technique to analyze
alpha-synuclein, a mysterious protein that is associated with Parkinson's disease. Cells
are constantly adapting to various stimuli, including changes in their environment and
mutations, through an intricate web of molecular interactions. Knowledge of these changes
is crucial for developing new treatments for diseases. To decipher how a cell responds to
various stimuli, laboratories worldwide have been turning to new technologies that produce
vast amounts of data. Such data typically exists in two major forms: genetic screen data
(the results from deleting a gene from a cell's genome and seeing what observable traits
appear in the cell) and information on the cellular levels of messenger RNA (mRNA, which
is the template for proteins). Historically, these two types of data have largely been
analyzed independently of each other, revealing only glimpses of the cell's internal
workings. Each type of data is actually biased toward identifying different aspects of
cellular response, something that researchers had not realized until now. However, the new
algorithm, known as ResponseNet, exploits these biases and allows for combined analysis.
In this combined analysis, both data types are integrated with molecular interactions data
into a diagram that connects the experimentally identified proteins and genes. While this
typically results in an extraordinarily complicated diagram, sometimes jokingly referred
to as a "hairball", ResponseNet is designed to whittle the hairball down to the
most probable pathways connecting various genes and proteins.
New clues to healing arthritis
caused by traumatic injury
A strain of laboratory mice that has "superhealing" powers has been found to
resist inflammation after a knee injury, and also to avoid developing arthritis at the
injury site in the long term, according to researchers at Duke University Medical Center.
Their findings illuminate the mechanisms of post-traumatic arthritis and could point to
therapies for this condition, which commonly afflicts younger people who lose productivity
during their prime working years. "After a patient's traumatic injury, orthopaedic
surgeons realign the joint surface as anatomically as possible and then hope for the
best," said Steven A. Olson, MD, FACS, principal investigator of the post-traumatic
arthritis project and chief of the Duke orthopaedic trauma section. "They haven't
been thinking about why patients with injuries are subsequently getting arthritis. Our
research examines how we could possibly prevent arthritis development with growth factors
and anti-inflammatory therapies after a fracture, either before or at the time of the
surgery to fix it." Olson said 10 percent of all arthritis cases - about 4.6 million
- are post-traumatic arthritis patients, many of whom suffer for years and are too young
for joint replacement surgeries. The economic cost thus is about $12.8 billion annually
for this group, according to Arthritis Foundation statistics. The scientists examined the
differences in inflammatory response between two types of mice: one type known as
superhealers (or MRL/MpJ) versus a strain of control mice (C57BL/6). Previously,
scientists discovered that the superhealer mice had such regenerative powers that holes
made in their ears for lab identification purposes grew over completely with no sign of
scar tissue. Earlier work done at Duke showed no differences between healthy and fractured
limbs when the superhealers healed from a fracture of the knee joint.
Newly Discovered Gene Could Be a
Prime Target in the Most Lethal Brain Cancer
Scientists at Duke University Medical Center and Johns Hopkins University have discovered
mutations in two genes that could become therapeutic targets in malignant glioma, a
dangerous class of brain tumors. "The fact that the defective genes code for
metabolic enzymes found only in malignant glioma, and not in normal tissue, could make the
gene products therapeutic targets," says Hai Yan, MD, PhD, lead author, an assistant
professor in the Duke Department of Pathology. The findings are published in the Feb. 19
issue of the New England Journal of Medicine. These genetic flaws might also help
distinguish between primary and secondary glioblastoma multiforme (GBM), two subtypes of
especially deadly malignant gliomas, with survival of only months after their diagnosis.
Patients that have mutation of the genes, isocitrate dehydrogenase 1, gene 1 and 2 (IDH1
and IDH2), also had a longer survival time.
Duke Scientists Find Rare, Potent
Antibody to HIV-1
Scientists at Duke University Medical Center have for the first time isolated an important
antibody in human serum that could potentially play a key role in the design of an AIDS
vaccine. The research appears as a highlighted feature online in the Journal of Virology.
"The 2F5-like antibody is one of the gold standards for what an HIV vaccine needs to
induce, but no one had ever found it before circulating in the blood of infected
patients," says Georgia Tomaras, PhD, associate professor of surgery, immunology and
molecular genetics and microbiology in the Duke Human Vaccine Institute and the senior
author of the study. The 2F5 antibody is especially valuable because previous research has
shown it can successfully neutralize 80 percent of transmitted HIV viruses. Now that
researchers have found the antibody in circulating blood, Tomaras says they might be able
to find ways to duplicate or enhance it, thereby boosting the body's defense system.
Scientists mine drugs database for
new diabetes treatment
Scientists funded by the Biotechnology and Biological Sciences Research Council have
harnessed a new drug discovery tool to identify a new player in the body's insulin
secretion process. This finding could spark a completely new class of drugs to treat type
2 diabetes. In work published today (22 February) in Nature Chemical Biology researchers
at the University of Oxford explain how they have exploited new technology to create a
cheap and efficient method of drug discovery that will allow small academic labs to search
a large database of drugs to find treatments for diabetes and many other diseases. They
have used this new method to identify a small molecule which they are using to understand
how insulin is secreted in response to increases in blood sugar. Lead researcher Dr Grant
Churchill said: "A lot of diseases are caused by problems with important proteins
within cells. We need to find small molecules that change the function of these proteins
both to discover how they work and in addition because these small molecules may also work
as treatments for disease. The approach we have developed allows us to do this much more
quickly and cheaply than many of the current methods. Ultimately this will speed up the
process of getting better treatments into the clinic for patients." Starting with a
natural chemical and systematically modifying its chemical structure is a proven technique
and common drugs such as beta-blockers and anti-histamines were discovered this way.
However, these discoveries involved lengthy chemical syntheses starting with the natural
chemical (adrenalin and histamine respectively).
Patient knowledge of health
information influences cancer treatment
A new analysis finds that when colorectal cancer patients seek out health information from
the internet and news media, they are more likely to be aware of and receive the latest
treatments for their disease. Published in the April 1, 2009 issue of CANCER, a
peer-reviewed journal of the American Cancer Society, the study indicates that patients
can influence their own treatment, in some cases in inappropriate ways. In their review,
authors led by Stacy Gray, M.D. of the Dana-Farber Cancer Institute in Boston note that in
the last several decades, patients have become more involved in their health care as
patient autonomy has become increasingly important. That change has been accompanied by
unprecedented growth in the amount of health information available to patients. Studies
show nearly four out of ten of cancer patients seek cancer information on the internet.
But the authors say it is unclear how these phenomena influence a cancer patient's
treatment. Dr. Gray and colleagues from the NCI Center of Excellence in Cancer
Communication Research at the University of Pennsylvania Annenberg School designed a study
to examine the relationship between information-seeking among 633 colorectal cancer
patients chosen at random from the Pennsylvania Cancer Registry and the use of novel new
agents for the disease. The investigators focused on the use of the targeted therapies
bevacizumab (Avastin) and cetuximab (Erbitux) because of these drugs' clinical importance,
significant media coverage, and recent approval by the U.S. Food and Drug Administration.
Dr. Gray and her team hypothesized that there would be a relationship between information
seeking and awareness of these targeted therapies among colorectal cancer patients. They
also hypothesized that patients who seek information may ask their physicians about these
targeted therapies and may be more likely to receive them than patients who do not seek
information. The researchers found that high levels of information seeking were strongly
associated with both awareness of and receiving treatment using targeted therapies.
Patients who sought information about treatments for colorectal cancer were 2.83 times
more likely to have heard about targeted therapies and 3.22 times more likely to have
received targeted therapies than people who did not seek information. These associations
were present for patients with advanced disease where use of targeted therapies is FDA
approved as well as for patients with early stages of the disease where their use is not
FDA approved.
Suppressing cancer with a master
control gene
Starting with the tiny fruit fly and then moving into mice and humans, researchers at VIB
and K. U. Leuven show that expression of the same gene suppresses cancer in all three
organisms. Reciprocally, switching off the gene – called Ato in flies and ATOH1 in
mammals – leads to cancer. The authors show there is a good chance that the gene can
be switched on again with a drug. They report their findings in two papers in the leading
online open access journal PLoS Biology. All of us begin our lives as a single cell (made
when an egg and sperm fuse) which repeatedly divides into the few billion cells that
constitute an adult human. During these divisions cells become increasingly differentiated
from each other, until in an adult almost all cells are highly specialized to perform a
specific function – skin cells, liver cells, eye lens cells, nerve cells, etc. Cancer
is a collection of cells without a function, which grow when normal genetic controls of
cell division are interrupted. Cancer cells are less differentiated than normal cells
– leading to the hypothesis that the final steps of differentiation prevent cells
from becoming cancerous. New work conducted by Wouter Bossuyt, Bassem Hassan, and
colleagues at VIB and K. U. Leuven has tested this theory. They demonstrate that in the
fruit fly, master control genes steering the specialization step inhibit tumor formation.
In collaboration with colleagues from the United States, they show that loss of one of
those genes, Atonal homolog 1 (ATOH1), causes colon cancer in mice. The gene regulates the
last step in the specialization to epithelial cells of the colon. Humans with colon cancer
frequently have an inactivated ATOH1 gene, the researchers show. The researchers could
reactivate the gene in human colon cancer cells grown in culture. This caused the tumor
cells to stop growing and commit suicide. This exciting, but preliminary, result suggests
that it may be possible to switch the gene back on in living patients to target their
cancers. Taking this work in the test tube and using it to develop a therapy is an
exciting but complicated challenge. Therefore, more work will be required to further
understand the role of ATOH1 in suppressing cancer formation.
Stephen Petranek: 10 ways the world
could end
Human stem cells provide a new
model for Lou Gehrig's disease
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a devastating
condition in which motor neuron degeneration causes progressive loss of movement and
muscle tone, leading to death. Overcoming the limited success of previous models, a report
published in Disease Models & Mechanisms (DMM), dmm.biologists.org describes how
neurons can be derived from human stem cells, and engineered to mimic inherited ALS.
Researchers at the University of California Los Angeles developed an optimized protocol to
generate motor neurons from human embryonic stem cells (ES cells), which express normal or
mutant forms of the SOD-1 gene, which is linked to inherited, familial ALS. Resulting
cells exhibit hallmark characteristics of motor nerve cells, and neurons expressing mutant
SOD-1 display abnormalities typical of ALS. Defects included shortened cell projections
and a reduced life span compared to cells containing the normal SOD-1 gene. This human
cell-derived model of ALS provides a new method of studying this disease and testing novel
therapeutics. This is especially helpful as only one drug is approved to help slow ALS
progression, and animal models currently used in drug development have had limited
success. Additionally, this research may aid other gene-linked neurodegenerative diseases,
as they too may benefit from studies in a human cell-derived model.
The brain’s reserve cells can
be activated after stroke
Scientists at the Swedish medical university Karolinska Institutet have found a way of
activating the neuronal reserves in the brains of mice by switching off the signal that
inhibits the formation of new nerve cells. The study is presented in the online edition of
the scientific journal Nature Neuroscience. "So far, this is just basic research of
no immediate practical significance, but the results are very exciting nonetheless,"
says Professor Jonas Frisén at the Department of Cell and Molecular Biology, who led the
study. New nerve cells are formed from stem cells in specific areas of the human brain.
This process increases after a stroke, something that might explain the recovery that is
often observed in patients, particularly in the first year following the onset of illness.
In the present study, the scientists have demonstrated how a type of cell that does not
give rise to new cells in the healthy brain is activated after a stroke in laboratory
animals.In addition to the stem cells that are normally active, there is therefore also a
kind of reserve stock of cells the can be activated when demand increases. The team have
identified the molecular mechanisms that control the activation of these cells, and shown
that it is possible to increase the formation of new nerve cells in healthy mice by
switching off the so-called Notch signalling pathway, which inhibits the creation of new
nerve cells.
Childhood trauma has life-long
effect on genes and the brain
McGill University and Douglas Institute scientists have discovered that childhood trauma
can actually alter your DNA and shape the way your genes work. This confirms in humans
earlier findings in rats, that maternal care plays a significant role in influencing the
genes that control our stress response. Using a sample of 36 brains; 12 suicide victims
who were abused; 12 suicide victims who were not abused and 12 controls, the researchers
discovered different epigenetic markings in the brains of the abused group. These markings
influence the hypothalamic-pituitary-adrenal (HPA) function, a stress-response which
increases the risk of suicide. This research builds upon findings published last May that
showed how child abuse can leave epigenetic marks on DNA. But, in this, the first study of
its kind, Moshe Szyf, a professor in the Department of Pharmacology and Therapeutics;
Gustavo Turecki, associate professor in the Department of Psychiatry who practices at the
Douglas Mental Health University Institute; Michael Meaney, a professor in the Departments
of Psychiatry and Neurology and Neurosurgery, who is also at the Douglas; and McGill
postdoctoral research fellow Patrick McGowan have built on their world-renowned
epigenetics work to uncover how parental care affects the DNA in the brains of a group of
Quebec male suicide victims who suffered abuse as children. The all-McGill study is set to
be published in the February 22, issue of the journal Nature Neuroscience.“We know
from clinical experience that a difficult childhood can have an impact on the course of a
person’s life”, said Dr. Turecki.
Physical fitness improves spatial
memory, increases size of brain structure
When it comes to the hippocampus, a brain structure vital to certain types of memory, size
matters. Numerous studies have shown that bigger is usually better. Now researchers have
found that elderly adults who are more physically fit tend to have bigger hippocampi and
better spatial memory than those who are less fit.The study, in the journal Hippocampus,
shows that hippocampus size in physically fit adults accounts for about 40 percent of
their advantage in spatial memory. The hippocampus, a curved structure deep inside the
medial temporal lobe of the brain, is essential to memory formation. Remove it – as
was done in the well-known case of surgical patient Henry Gustav Molaison – and a
person's ability to store most new experiences in memory is destroyed. The hippocampus
also is a key player in spatial navigation and other types of relational memory. Certain
activities are believed to modify hippocampus size in humans. For example, a study of
London taxi drivers found that the posterior portion of the hippocampus was larger in
experienced taxi drivers than in other subjects. And a study of German medical students
found that the same region of the hippocampus increased in size as they studied for their
final exams. Studies also have found that the hippocampus shrinks with age, a process that
coincides with small but significant cognitive declines. The rate at which this occurs,
however, differs among individuals. Earlier studies found that exercise increases
hippocampus size and spatial memory in rodents, but the new study is the first to
demonstrate that exercise can affect hippocampus size and memory in humans.
Concussions linked to suppressed
brain functioning years later
Word is spreading, on the sidelines, in the locker rooms, and in the media, that an
athlete whose bell has been rung – that is, suffered a concussion – may have
experienced an injury that could take a more serious toll later in life. Results of a new
study by researchers in the department of kinesiology and community health at the
University of Illinois support that speculation. The study is outlined in the current
online edition of the Journal of Neutrotrauma. “We were able to show that while our
group of club and intercollegiate athletes, who were on average 3 ½ years post-injury,
performed normally on standard tests a sports-medicine practitioner would use to diagnose
and evaluate someone for concussion, they had suppressed brain functioning,” said U.
of I. kinesiology professor Steven Broglio. “And that included a decrease in
attention allocation to things going on in their environment.” With respect to
existing information linking concussions – medically classified as mild traumatic
brain injuries – and the later onset of more serious health problems, Broglio said
“there’s a lot of information coming to light, but a lot of it’s been
anecdotal.” Much of the buzz, he added, is especially loud around Super Bowl time
each year. “There’s some data coming out of the NFL showing that retired
athletes who have had several concussions over their career have increased rates of
depression, mild cognitive impairment and early onset of Alzheimer’s disease.”
However, he said, “there’s been no link between young adults with concussions
and what we are seeing in the older, retired athletes. So we wanted to get a better idea
of what was happening at the brain level to try to figure out what these athletes were
reporting.”
Researchers Generate Functional
Neurons From Somatic Cells
In a new study, researchers were able to generate functionally mature motor neurons from
induced pluripotent stem (iPS) cells, which are engineered from adult somatic cells and
can differentiate into most other cell types. A potential new source of motor neurons that
does not require human eggs or embryos could be an enormous boon to research into
conditions such as amyotrophic lateral sclerosis (ALS) and spinal cord injury and could
open the door to eventual treatments. The study is published in Stem Cells. This study is
the first to use human iPS cells to generate electrically active motor neurons, a key
hallmark of functional maturation that is essential for any future application of iPS
cells. “To our knowledge, our results present the first demonstration of the
electrical activity of iPS-derived neurons and further suggest the feasibility of using
these cells to explore how changes in motor neuron activity contributes to the
degeneration of these cells underlying these disorders,” the authors state. Led by
William Lowry, and in collaboration with Bennett Novitch, Harley Kornblum, and Martina
Wiedau-Pazos of the University of California Los Angeles, researchers compared the ability
of different human cell lines to generate motor neuron progenitors and fully
differentiated motor neurons. “These findings support the possibility that
reprogrammed somatic cells might prove to be a viable alternative to embryo-derived cells
in regenerative medicine,” the authors note.
ESC reaffirms advice on
cardiovascular risks associated with long-haul flights
Following a review by The Lancet of the medical issues associated with commercial air
travel, the European Society of Cardiology has reaffirmed its advice about the risks of
venous thromboembolism (VTE), whose risk, according to The Lancet, is increased “up
to four-fold” by long-haul flight. Dr Steen Kristensen, Vice-president of the ESC,
says: “Long distance flying is associated with an increase in deep venous thrombosis,
which in some cases may lead to clotting of the lungs. People who are immobile, pregnant,
taking contraceptive pills or have had venous thrombosis in the past are particularly at
risk. To minimise the risk it is important to drink plenty of non-alcoholic fluid and to
walk (exercise) before and during the flight. The use of compression stockings is for some
travelers an important way of preventing deep venous thrombosis.” Studies cited by
The Lancet suggest that the risk of VTE increases when flight duration exceeds four hours.
This raised risk is related to immobility, dehydration, and reduced oxygen in the cabin,
as well as to individual risk factors such as obesity, recent surgery and predispositions
to thrombosis (thrombophilias). On the subject of risk Professor Kurt Huber, ESC
spokesperson on Thrombosis, writes: “Prone to thromboembolic risk are those with a
history of venous thrombosis or pulmonary embolism, but also those with a history of
atherothrombotic diseases (for example, myocardial infarction or stroke) and those with
heart failure, atrial fibrillation, and physical immobilisation.” Professor Huber
adds that even healthy people may develop thrombotic problems on a long-distance flight,
notably pregnant women, women taking oral contraceptives (especially if they smoke) and
the elderly. Those with concerns, he adds, should ask their doctor about their individual
risk and the applicability of preventive measures, including medication.
Raw for 30 Days new trailer
Children with hypertension have
trouble with thinking, memory
Children with high blood pressure are not as good at complicated, goal-directed tasks,
have more working memory problems and are not as adept at planning as their peers without
hypertension, according to recent research. If they are both hypertensive and obese, they
are also more likely to have anxiety and depression. Considering the demands on a child's
brain – both in continued development and in education – and the fact that up to
10 percent of the increasing population of obese children have hypertension, these novel
findings could give physicians and parents more impetus to diagnose and treat high blood
pressure in children. "These results were very surprising to me, despite similar
findings in adults," said Marc Lande, M.D., a pediatric nephrologist at the
University of Rochester Medical Center and author of the paper published in the Journal of
Pediatrics this month. "Adults with hypertension often have other problems that might
affect cognition such as chronic disease, smoking or alcohol use. However, children with
hypertension usually do not have these comorbidities." In adults, high blood pressure
can lead to stroke, heart disease, heart attack, heart failure and kidney failure. Lande
postulates that the cognitive changes demonstrated in this study may represent very early
manifestations of hypertensive damage to the brain, which may long precede more overt
damage such as stroke. In addition, more than half the children with both hypertension and
obesity demonstrated clinically significant anxiety and depression. Lande said he was
initially looking at anxiety and depression only to rule out its interplay with executive
function, which is a collection of cognitive abilities that help plan for and respond to
complex situations; he did not expect to tease out this new finding.
Plasminogen activator inhibitor
type-1 -- a potential link between heart failure and diabetes
Researchers at the University of Vermont Cardiovascular Research Institute, Colchester,
Vermont have found that increased expression in the heart of plasminogen activator
inhibitor type-1 (PAI-1) is profibrotic. The results, which appear in the March 2009 issue
of Experimental Biology and Medicine, implicate PAI-1 overexpression, known to accompany
insulin resistance and type 2 diabetes, as a factor contributing to the high incidence of
heart failure after myocardial infarction in people with diabetes. The research team, Dr.
A.K.M. Tarikuz Zaman, a research associate, Mr. Christopher J. French, medical and
graduate student, Dr. David J. Schneider, Professor of Medicine and Director of the
Cardiology and Vascular Biology Units, and Dr. Burton E. Sobel, Professor of Medicine and
Director of the Cardiovascular Research Institute, performed studies in 10 week old mice
subjected to coronary occlusion. Controls and PAI-1 overexpressing mice congenic on a
C57BL6 background had comparable PAI-1 content in left ventricular myocardium despite a
marked elevation of PAI-1 in plasma in the latter. 6 weeks after coronary occlusion the
PAI-1 overexpressing mice exhibited a 2-fold increase in left ventricular (LV) PAI-1
content. Histochemical analysis demonstrated 33% more LV fibrosis as well. The increased
fibrosis associated with increased PAI-1 was accompanied by functional derangements
including diminished LV wall thickness in both diastole and systole, increased end
systolic LV dimensions, depressed fractional shortening, a greater impairment of LV
segmental function, and greater transmitral E-wave amplitude.
Transcendental Meditation buffers
students against college stress
Transcendental Meditation may be an effective non-medicinal tool for students to buffer
themselves against the intense stresses of college life, according to a new study to be
published in the February 24 issue of the peer-reviewed International Journal of
Psychophysiology. "Effects of Transcendental Meditation practice on brain functioning
and stress reactivity in college students" is the first random assignment study of
the effects of meditation practice on brain and physiological functioning in college
students. The study was a collaboration between the American University Department of
Psychology in Washington, D.C., and the Center for Brain, Consciousness, and Cognition at
Maharishi University of Management in Fairfield, Iowa. The study investigated the effects
of 10-weeks of Transcendental Meditation (TM) practice on "Brain Integration
Scale" scores (broadband frontal coherence, power ratios, and preparatory brain
responses), electrodermal habituation to a stressful stimulus, and sleepiness in 50
students from American University and other Washington, D.C., area universities.
Mechanisms that prevent Alzheimer's
Disease
In a project involving the collaboration of several institutes, research scientists of the
Johannes Gutenberg University Mainz have succeeded in gaining further insight in the
functioning of endogenous mechanisms that protect against the development of Alzheimer's
disease. It was found that the activity of the enzyme ?-secretase is mainly responsible
for the protective effect. "In the past, we postulated that the enzyme ?-secretase
was involved in preventing the formation of cerebral plaques characteristic of Alzheimer's
disease and also enhanced cerebral functions, such as learning and memory," explained
Professor Falk Fahrenholz of the Institute of Biochemistry. His research group has been
working in cooperation with the Clinic of Psychiatry and Psychotherapy of the university's
Faculty of Medicine and the Central Animal Laboratory Facility (ZVTE) to discover the
mechanism for the beneficial effects of ?-secretase. The Journal of Alzheimer's Disease
(JAD) presents the results of this project in its February 2009 issue. ?-secretase is an
endogenous enzyme that is present in the nerve cells of the brain, where it is responsible
for the cleavage of an A? into A? domain. The result is a soluble protein fragment that
promotes the growth of nerve cells and thus prevents the development of cerebral
deterioration caused by A?. However, if the enzyme ?-secretase is active, a chain reaction
is initiated that subsequently results in the development A? initializing the cascade of
Alzheimer's disease through formation of A?. "You could say that ?-secretase is the
good enzyme, and ?-secretase the bad en-zyme," Fahrenholz commented. "We now
want to find out how to activate this 'good' enzyme or increase its concentrations in the
brain as a way of combating this disease."
Case Western Reserve researchers
develop 'wireless' activation of brain circuits
Traditionally, stimulating nerves or brain tissue involves cumbersome wiring and a sharp
metal electrode. But a team of researchers at Case Western Reserve University is going
"wireless." And it's a unique collaboration between chemists and neuroscientists
that led to the discovery of a remarkable new way to use light to activate brain circuits
with nanoparticles. Ben Strowbridge, an associate professor in the neurosciences
department in the Case Western Reserve School of Medicine and Clemens Burda, an associate
professor in chemistry, say it's rare in science that people from very different fields
get together and do something that is both useful and that no one had thought of before.
But that is exactly what they've done. By using semiconductor nanoparticles as tiny solar
cells, the scientists can excite neurons in single cells or groups of cells with infrared
light. This eliminates the need for the complex wiring by embedding the light-activated
nanoparticles directly into the tissue. This method allows for a more controlled reaction
and closely replicates the sophisticated focal patterns created by natural stimuli. The
electrodes used in previous nerve stimulations don't accurately recreate spatial patterns
created by the stimuli and also have potential damaging side effects.
Our hair bleaches itself as we grow
older
Wash away your gray? Maybe. A team of European scientists have finally solved a mystery
that has perplexed humans throughout the ages - why we turn gray. Despite the notion that
gray hair is a sign of wisdom, these researchers show in a research report published
online in The FASEB Journal that wisdom has nothing to do with it. Going gray is caused by
a massive build up of hydrogen peroxide due to wear and tear of our hair follicles. The
peroxide winds up blocking the normal synthesis of melanin, our hair's natural
pigment."Not only blondes change their hair color with hydrogen peroxide," said
Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal. "All of our hair cells
make a tiny bit of hydrogen peroxide, but as we get older, this little bit becomes a lot.
We bleach our hair pigment from within, and our hair turns gray and then white. This
research, however, is an important first step to get at the root of the problem, so to
speak."The researchers made this discovery by examining cell cultures of human hair
follicles. They found that the build up of hydrogen peroxide was caused by a reduction of
an enzyme that breaks up hydrogen peroxide into water and oxygen (catalase). They also
discovered that hair follicles could not repair the damage caused by the hydrogen peroxide
because of low levels of enzymes that normally serve this function (MSR A and B). Further
complicating matters, the high levels of hydrogen peroxide and low levels of MSR A and B,
disrupt the formation of an enzyme (tyrosinase) that leads to the production of melanin in
hair follicles. Melanin is the pigment responsible for hair color, skin color, and eye
color. The researchers speculate that a similar breakdown in the skin could be the root
cause of vitiligo."As any blue-haired lady will attest, sometimes hair dyes don't
quite work as anticipated," Weissmann added. "This study is a prime example of
how basic research in biology can benefit us in ways never imagined."
New technique for cancer screening
Current research suggests that a new technique to determine tumor methylation status can
be used in archived tissue samples. The related report by Balic et al, "High quality
assessment of DNA methylation in archival tissues from colorectal cancer patients using
quantitative high-resolution melting analysis," appears in the March 2009 issue of
The Journal of Molecular Diagnostics.DNA in tumors is often altered compared with DNA in
normal tissues. One common DNA alteration in cancerous tissue is hypermethylation, which
results in loss of gene expression. The difference in methylation between normal and
cancerous tissues can be used as a biomarker for early cancer diagnosis, risk assessment,
and response to therapy. Archival tissues, or tissues that are formalin-fixed and
paraffin-embedded for long-term storage, are difficult to screen for cancer biomarkers due
to the low quality of their DNA. It is therefore important to develop new techniques to
screen for DNA methylation that can be used in archival tissues. Balic and colleagues
examined the ability of high-resolution melting analysis (HRM) to detect methylation on
archival tissues from colorectal cancer patients. They found that HRM provided similar
results between archival and fresh tissues. In addition, they validated the results using
the widely used MethyLight assay.
Lowering Your Cholesterol May
Decrease Your Risk of Cancer
Current research suggests that lowering cholesterol may block the growth of prostate
tumors. The related report by Solomon et al, “Ezetimibe Is an Inhibitor of Tumor
Angiogenesis,” appears in the March 2009 issue of The American Journal of Pathology.
High cholesterol not only leads to atherosclerosis and heart disease, but may also
contribute to cancer growth and progression. Prostate cancer is the most common non-skin
cancer in the United States, affecting approximately 1 in 6 men. Prostate tumors
accumulate high levels of cholesterol, and tumor incidence correlates with eating a high
fat/high cholesterol diet “Western” diet. In addition, prostate tumor
progression has been linked to serum cholesterol levels. To examine the role of high
cholesterol in prostate cancer, Dr. Keith Solomon and colleagues fed mice a high fat/high
cholesterol “Western” diet. They found that high cholesterol levels promoted
tumor growth and that Ezetimibe (Zetia™), which blocks the absorption of cholesterol
from the intestine, could prevent this increased tumor growth. Ezetimibe also blocked a
cholesterol-mediated increase in angiogenesis, the growth of new blood vessels required
for tumor progression. These data suggest that reducing cholesterol levels may inhibit
prostate cancer growth specifically by inhibiting tumor angiogenesis.
What Should Be Done To Tackle
Ghostwriting in the Medical Literature?
Ghostwriting occurs when someone makes substantial contributions to a manuscript without
attribution or disclosure. It is considered bad publication practice in the medical
sciences, and some argue it is scientific misconduct. At its extreme, medical ghostwriting
involves pharmaceutical companies hiring professional writers to produce papers promoting
their products but hiding those contributions and instead naming academic physicians or
scientists as the authors. To improve transparency, many editors' associations and
journals allow professional medical writers to contribute to the writing of papers without
being listed as authors provided their role is acknowledged. This debate examines how best
to tackle ghostwriting in the medical literature from the perspectives of a researcher, an
editor, and the professional medical writer.
Stunning finding - Compounds
protect against cerebral palsy
Two compounds developed by Northwestern University chemists have been shown to be
effective in pre-clinical trials in protecting against cerebral palsy, a condition caused
by neurodegeneration that affects body movement and muscle coordination. "The results
were just stunning, absolutely amazing," said Richard B. Silverman, John Evans
Professor of Chemistry in the Weinberg College of Arts and Sciences at Northwestern, who
led the drug development effort. "There was a remarkable difference between animals
treated with a small dose of one of our compounds and those that were not." The
findings, which are published online by the journal Annals of Neurology, suggest that a
preventive strategy for cerebral palsy may be feasible for humans in the future. (The
paper also will appear in the journal's February issue, in print the week of March 2.)
None of the fetuses born to animals treated with the two compounds died; more than half of
those born to untreated animals died. Eighty-three percent of animals treated with one of
the compounds were born normal, with no cerebral palsy characteristics. Sixty-nine percent
of animals treated with the other compound were born normal. There was no sign of toxicity
in the treated animals, and their blood pressure was normal. Cerebral palsy is caused by
an injury to the brain before, during or shortly after birth, although it typically is not
diagnosed until after the age of one. Approximately 750,000 children and adults in the
United States have a form of cerebral palsy, with the majority having been born with the
condition. The new compounds Silverman and his team developed inhibit an enzyme found in
brain cells that produces nitric oxide, thus lowering nitric oxide levels. At normal
levels, nitric oxide acts as a neurotransmitter and is important to neuronal functioning,
but at high levels it has been shown to damage brain tissue. An overabundance of nitric
oxide is believed to play a role in cerebral palsy. After a lengthy drug development
process, Silverman went to his collaborator Sidhartha Tan, M.D., a neonatologist from
NorthShore University HealthSystem, to test the two best compounds on Tan's cerebral palsy
animal model. A diminished supply of oxygen (hypoxia) from mother to fetus causes an
increase in nitric oxide levels in the brain, which leads to brain damage and newborns
with cerebral palsy characteristics. Silverman and Tan wanted to see if they could prevent
brain damage in the fetuses by administering one of the compounds to the mother before the
hypoxic event. They expected some degree of success but were surprised by how effective
the treatment was. The researchers attribute the protection from cerebral palsy to the
decrease in the brain enzyme and the nitric oxide that is produced. "We still have to
bring the phenomenon to humans, which would be very exciting," said Tan, who has been
investigating the impact of nitric oxide on neuronal damage. "There is such a dire
need. If we could safely give the drug early to mothers in at-risk situations, we could
prevent the fetal brain injury that results in cerebral palsy."
An angry heart can lead to sudden
death, Yale researchers find
Before flying off the handle the next time someone cuts you off in traffic, consider the
latest research from Yale School of Medicine researchers that links changes brought on by
anger or other strong emotions to future arrhythmias and sudden cardiac arrests, which are
blamed for 400,000 deaths annually. The study—led by Rachel Lampert, M.D., associate
professor of medicine at Yale School of Medicine, and published in the Journal of the
American College of Cardiology—deepens our understanding of how anger and other types
of mental stress can trigger potentially lethal ventricular arrhythmias. Lampert and her
team studied 62 patients with implantable cardioverter-defibrillators (ICDs) and enlarged
hearts. They were monitored three months after the ICD was implanted and then given a
mental stress test requiring them to recall a stressful situation that angered them.
Lampert and her team sought to discover whether T-wave alternans (TWA), which monitor
electrical instability in the heart induced by anger, would predict future ventricular
arrhythmias. The team found that those in the group with more anger-induced electrical
instability were more likely to experience arrhythmias one year after the study than those
in the control group. "Further studies are needed to determine whether there is a
role for therapies which may reduce anger and the body's response to stress, thereby
preventing arrhythmias in those at risk," said Lampert. Lampert's work builds on past
research linking strong emotion to sudden cardiac death. It has been found that
devastating disasters, such as earthquakes, are linked to sudden death.
Treating drug-addicted doctors is
good medicine
Doctors who become addicted to alcohol and other drugs can be treated successfully and
returned to medical practice with the help of special programs that couple referral to
treatment and monitoring with rapid responses to noncompliance, University of Florida
researchers report. The study is the first national-level analysis of such Physician
Health Programs, and confirms they are effective alternatives to simply punishing
drug-addicted doctors. The findings are published in the March issue of the Journal of
Substance Abuse Treatment. More than three-quarters of doctors enrolled in state programs
stayed drug-free over a five-year monitoring period. The results were the same regardless
of whether the doctor's drug of choice was alcohol, crack cocaine, prescription drugs or
other substances. "Treatment works," said Dr. Mark Gold, psychiatry chairman at
the UF College of Medicine and the McKnight Brain Institute. "It has been shown now
to be safe and effective and cost-effective." But it's not just for doctors, said
Gold, who with UF colleagues pioneered evaluation and treatment for drug-addicted doctors.
"It should be a model for treatment of anyone with these diagnoses." In general,
rates of illicit drug use are lower among physicians than the general public, but rates of
prescription misuse are five times higher among physicians, according to a 2008 review
Gold co-authored in the Harvard Review of Psychiatry. Gold and others conclude that drug
problems in doctors are related to medical specialties that put them in regular contact
with drugs of addiction, ease of access to drugs, stress and lack of early detection.
Addiction also appears linked to physician-suicide.
Researchers Uncover 'Obesity Gene'
Involved In Weight Gain Response to High-Fat Diet
Scientists have determined that a specific gene plays a role in the weight-gain response
to a high-fat diet. The finding in an animal study suggests that blocking this gene could
one day be a therapeutic strategy to reduce diet-related obesity and associated disorders,
such as diabetes and liver damage, in humans.The researchers found that a diet rich in fat
induced production of this gene, called protein kinase C beta (PKC beta), in the fat cells
of mice. These mice rapidly gained weight while eating a high-fat diet for 12 weeks.
The ultimate in 'green' energy -
plants inspire new generation ofsolar cells
The ability of plants to turn sunlight into energy through photosynthesis has been
successfully mimicked by scientists at the University of Southampton to produce a new
generation of solar cells. The Southampton team led by Professor Pavlos Lagoudakis of the
University's School of Physics and Astronomy, has developed a new range of photovoltaic
devices that use a process found in vegetative methods of light harvesting, to deliver
unprecedented amounts of electrical current from light. In photosynthesis each molecule
has evolved to deliver a function that complements the perpetual cycle of light to energy
conversion. With the advent of nanoscience, scientists are now able to build devices of
multiple nanoscale components, each one designed to deliver a specific functionality.
Professor Lagoudakis comments "We looked at the ways that energy is funnelled in
nature and through reverse engineering, using multiple nanoscale components, we designed
and fabricated a hybrid photovoltaic device that can absorb light and efficiently convert
it to electric current.
Study shows maritime shipping makes
hefty contribution to air pollution
Commercial ships emit almost half as much particulate pollutants into the air globally as
the total amount released by the world's cars, according to a new study led by the
National Oceanic and Atmospheric Administration and the University of Colorado at Boulder.
The study is the first to provide a global estimate of maritime shipping's total
contribution to air particle pollution based on direct emission measurements. The authors
estimate ships emit about 1,100 tons of particle pollution globally each year. Ship
pollutants affect both global climate and the health of people living along coastlines,
according to the study authors. The findings appear online the week of Feb. 23 in the
Journal of Geophysical Research. "Since more than 70 percent of shipping traffic
takes place within 250 miles of the coastline, this is a significant health concern for
coastal communities," said lead study author Daniel Lack, a researcher with the
NOAA-supported CU Cooperative Institute for Research in Environmental Sciences based at
NOAA's Earth System Research Laboratory in Boulder. Earlier research by one of the study's
co-authors, James Corbett of the University of Delaware, linked particle pollution to
premature deaths among coastal populations. Commercial ships emit both particle pollution
and carbon dioxide, but they have opposite effects on the climate, said the researchers.
The particles have a global cooling effect that is at least five times greater than the
global warming effect from the ships' CO2 emissions. The particles affect both climate and
health, said the researchers. CO2 from ships makes up roughly 3 percent of all
human-emitted CO2 and almost 30 percent of smog-forming nitrogen oxide gases. During
summer 2006, Lack and colleagues aboard the NOAA ship Ronald H. Brown analyzed the exhaust
from over 200 commercial vessels, including cargo ships, tankers and cruise ships in the
Gulf of Mexico, Galveston Bay and the Houston Ship Channel. The researchers also examined
the chemistry of particles in ship exhaust to understand what makes ships such hefty
polluters. Ships emit sulfates, the same particles associated with diesel-engine cars and
trucks and which have resulted in tighter regulations regarding on-road vehicle fuel
standards, according to the research team. Sulfate emissions from ships vary with the
concentration of sulfur in ship fuel, the authors found.
Liver Transplant Recipients with
Hepatitis B May Need Lifelong Antiviral Treatment
Patients who undergo liver transplantation for hepatitis B-related liver damage should
receive lifelong antiviral treatment to keep the disease from coming back. A new study
shows that they lack cellular immunity against the disease, making recurrence likely if
antiviral treatment is withdrawn. These findings are in the March issue of Liver
Transplantation, a journal published by John Wiley & Sons.
Muscling in on type 2 diabetes
Research by kinesiology investigator Dustin Hittel, PhD, has proven that muscle in
extremely obese individuals produces large amounts of a protein called myostatin, which
normally inhibits muscle growth—suggesting that for Type 2 diabetics, and the very
obese, the task of getting healthy may be more difficult than initially thought. It has
been known for some years that naturally occurring mutations in the gene which controls
myostatin results in double—muscling in cattle, dogs and even humans. Many in the
body building community believe that blocking myostatin is a shortcut to the Arnold
Schwarzenegger body. The flipside is that producing too much myostatin has been linked
with muscle wasting conditions such as HIV-AIDS, starvation and now, Type 2 diabetes.
Hittel believes this may be due to a pre-diabetic condition known as insulin resistance
that "tricks" the muscles into thinking the body is starving despite the fact
that blood sugar levels are skyrocketing. "When that happens, the body reverses
muscle production using myostatin," says Hittel. "This is particularly worrisome
because losing muscle mass further erodes your ability to control your blood sugar with
exercise." One of the tell-tale signs of the transition between insulin resistance
and full-blown Type 2 diabetes is a loss of muscle mass. "Losing muscle mass makes
sense from an evolutionary perspective since having large muscles during famine puts you
at a serious risk for starvation," explains Hittel. "Unfortunately, this
survival mechanism has left us ill-equipped to deal with a Western lifestyle—lots of
calories, little exercise—and it has laid the groundwork for the current epidemic of
Type 2 diabetes." "The goal of my research is to understand how obesity, diet
and exercise influence our metabolism and interact with our genome. This research sheds
some light on an important part of the puzzle."
Proepithelin encourages cell growth
and migration in prostate cancer
Researchers from Thomas Jefferson University have identified a protein that appears to
play a significant role in the growth and migration of prostate cancer cells, especially
androgen-independent prostate cancer cells. The study was published in the American
Journal of Pathology. They also found that prostate cancer cells express more of the
protein when compared to normal prostate cells, according to Andrea Morrione, Ph.D., an
associate professor and director of Urology Research for the Kimmel Cancer Center at
Jefferson. Dr. Morrione conducted the study with Leonard Gomella, M.D., chairman of the
department of Urology, Raffaele Baffa, M.D., an associate professor in the department of
Urology, and Renato V. Iozzo, M.D., Ph.D., professor in the department of Pathology,
Anatomy and Cell Biology. Proepithelin is a growth factor that promotes cell cycle
progression and cell growth in many cellular systems. According to Dr. Morrione, the
overexpression of proepithelin by prostate cancer cells may prove to be a useful clinical
marker to diagnose prostate cancer. The presence of proepithelin also encourages cell
migration, which is necessary for tumor metastasis. Thus, it may serve as a marker for
metastasis. Proepithelin has previously been shown to play a role in the formation of
bladder cancer, and its overexpression is related to an aggressive form of breast cancer
according to Dr. Morrione. It also has been shown to play a role in many other cancers,
including glioblastomas, multiple myeloma, renal cell carcinoma, gastric cancer and
ovarian cancer."There are two possible implications of our findings," Dr.
Morrione said. "First, proepithelin could be a therapeutic target since it is
overexpressed in prostate cancers. Second, the overexpression of proepithelin could serve
as a biomarker and be a diagnostic tool for prostate cancer."
New findings measure precise impact
of fat on cancer spread
Researchers at Purdue University have precisely measured the impact of a high-fat diet on
the spread of cancer, finding that excessive dietary fat caused a 300 percent increase in
metastasizing tumor cells in laboratory animals.The researchers used an imaging technique
to document how increasing fat content causes cancer cells to undergo changes essential to
metastasis. Then they used another technique to count the number of cancer cells in the
bloodstream of mice fed a high-fat diet compared to animals fed a lean diet. The findings
suggest that the combined tools represent a possible new diagnostic technique to determine
whether a patient's cancer is spreading, said Ji-Xin Cheng, an assistant professor in
Purdue's Weldon School of Biomedical Engineering and Department of Chemistry.
Ethnic Differences Found for Fatty
Liver Disease and Insulin Resistance
A new study suggests that the metabolic response to obesity and insulin resistance,
particularly as it pertains to the liver, differs among ethnic groups in the U.S.
African-Americans are more resistant to the buildup of fat in the abdominal adipose tissue
and liver, and to high triglyceride levels associated with insulin resistance. These
findings are in the March issue of Hepatology, a journal published by John Wiley &
Sons on behalf of the American Association for the Study of Liver Diseases (AASLD).
Liver Tumors Associated with
Metabolic Syndrome Differ from Other Tumors
Liver cancer in patients whose only risk factor is metabolic syndrome has distinct forms
and structures compared to other liver tumors. These findings are in the March issue of
Hepatology, a journal published by John Wiley & Sons on behalf of the American
Association for the Study of Liver Diseases (AASLD). Cancer of the liver, also known as
hepatocellular carcinoma, is the fifth most common type of cancer in the world. It is
increasing in incidence, largely due to the spread of hepatitis C. Its growing prevalence
may also be related to the rise of obesity and type-2 diabetes, which are associated with
non-alcoholic fatty liver disease (NAFLD). However, liver cancers associated with NAFLD
have been poorly described.
Genetic evidences for future dental
treatments - forming enamel
A team of researchers lead by Professor Dr Thimios Mitsiadis at the University of Zurich,
Switzerland, has identified a gene responsible for the formation of enamel, which is the
key component of the teeth. The experiments were accomplished in mice carrying a deletion
of the transcription factor Tbx1, a gene that plays a principal role in several human
malformations (heart, thymus, parathyroid, face, and teeth) associated to the DiGeorge
syndrome. «Subjects afflicted by DiGeorge syndrome exhibit teeth with enamel defects. We
have demonstrated that a direct link between impaired Tbx1 function and enamel defects
exists. Enamel forms via the mineralization of specific enamel proteins that are secreted
by dental epithelial cells called ameloblasts. Our results clearly show that teeth of Tbx1
null mice lacked enamel and ameloblasts» explains Prof Mitsiadis. These findings, just
published in Development Biology, represent a major contribution to the understanding of
the production of enamel, the «hardest organic tissue» found in nature.
Frequency of T-cells Determines
Severity of Asthma
According to a new study, the frequency of regulatory T-cells (Treg) correlates to the
severity of inflammation in allergic asthma, suggesting that Treg may play an important
role in asthma pathogenesis. A study in Respirology, published by Wiley-Blackwell, used
mouse models and peripheral blood mononuclear cells from subjects with allergic asthma to
assess the association of the Treg cells with asthma phenotypes. Researchers found that
the frequency of Treg cells in the peripheral blood of allergic asthmatics were lower when
compared to healthy subjects. Lung Treg were also found to be associated with the severity
of eosinophillic airway inflammation in the mice. "The correlation of Treg with
asthma pathogenesis indicates that it is important to evaluate Tregs in allergic asthmatic
patients - especially in relation to clinical severity and the degree of airway
inflammation", said author Professor Hiromasa Inoue from the Research Institute for
Diseases of the Chest, Graduate School of Medical Science, Kyushu University.
Naturally produced estrogen may
protect women from Parkinson's disease
Women who have more years of fertility (the time from first menstruation to menopause)
have a lower risk of developing Parkinson’s disease than women with fewer years,
according to a large, new study by researchers at Albert Einstein College of Medicine of
Yeshiva University. “These findings, involving nearly 74,000 women, suggest that
longer exposure to the body’s own, or endogenous, hormones, including estrogen, may
help protect the brain cells that are affected by Parkinson’s disease,” says
lead author Rachel Saunders-Pullman, M.D., M.P.H., M.S., assistant professor of neurology
at Einstein and attending physician in neurology at Beth Israel Medical Center, an
affiliate of Einstein’s in Manhattan. An abstract of the study was released today by
the American Academy of Neurology (AAN). Further study details will be presented at
AAN’s 61st Annual Meeting in Seattle, April 25 - May 2, 2009. After Alzheimer’s
disease, Parkinson’s disease is the most common neurodegenerative disease. About 1.5
million Americans currently have Parkinson’s, characterized by symptoms that can
include tremor (shaking), slowness of movement, rigidity (stiffness), and difficulty with
balance. The condition typically develops after the age of 60, although 15 percent of
those diagnosed are under 50. There is no cure for Parkinson’s, although medications
or surgery can ease symptoms of the disease. Parkinson’s disease is almost twice as
common in men as in women, and researchers have long hypothesized that sex hormones might
play a role in the disease. In the current study, researchers analyzed the records of the
Women’s Health Initiative (WHI) Observational Study and focused on those women who
developed Parkinson’s disease. The study involved about 73,973 women who underwent
natural menopause. The study found that women who had a fertile lifespan of more than 39
years had about a 25 percent lower risk of developing Parkinson’s compared with women
who had a fertile lifespan shorter than 33 years. In addition, the data showed that women
who had four or more pregnancies were about 20 percent more likely to develop
Parkinson’s disease than were women who had three or fewer pregnancies. “One
explanation for this finding is that the post-partum period, which is typically one with
lower levels of estrogen, subtracts from a woman’s total fertile lifespan,” says
co-author Sylvia Wassertheil-Smoller, Ph.D., professor of epidemiology and population
health and the principal investigator of the WHI study at Einstein.
Compounds Protect Against Cerebral
Palsy
The new compounds Silverman and his team developed inhibit an enzyme found in brain cells
that produces nitric oxide, thus lowering nitric oxide levels. At normal levels, nitric
oxide acts as a neurotransmitter and is important to neuronal functioning, but at high
levels it has been shown to damage brain tissue. An overabundance of nitric oxide is
believed to play a role in cerebral palsy.
Scientists unlock the secrets of C.
difficile's protective shell, paving the way for new superbug drugs and vaccines
The detailed structure of a protective 'jacket' that surrounds cells of the Clostridium
difficile superbug, and which helps the dangerous pathogen stick to human host cells and
tissues, is revealed in part in the 1 March issue of Molecular Microbiology. Scientists
hope that unravelling the secrets of this protective layer's molecular structure might
reveal possible targets for new drugs to treat C. difficile infections. C. difficile cell.
The S-layer is believed to help C. difficile cells colonise the human gut, where they
release sickness-causing toxins.
Newly discovered gene plays vital
role in cancer
Gene p53 protects against cancer and is usually described as the most important gene in
cancer research. However, scientists at Karolinska Institutet have now shown that a
previously unknown gene, Wrap53, controls the activity of p53. As the regulation mechanism
is relatively unexplored, the study opens up new routes to solving the mystery of
cancer.The p53 gene makes sure that cells with damaged DNA either repair themselves or
commit suicide. If p53 itself is damaged, which is the case in roughly half of all cancer
tumours, cells that are on their way to becoming cancerous are allowed to survive. Much
cancer research revolves around the cell processes that p53 induces.A group of researchers
at Karolinska Institutet have now identified a new gene, called Wrap53, that regulates the
activity of p53. The study, which is published in the journal Molecular Cell, demonstrates
that Wrap53 gives rise to a molecule, called antisense RNA, the presence of which is
necessary for the production of sufficient quantities of p53 protein in the event of DNA
damage.According to Marianne Farnebo, one of the scientists involved in the study, the
results indicate that damage to Wrap53 can indirectly cause cancer. Wrap53 is therefore a
new potential target for future cancer therapies.
Prehistoric global cooling caused
by CO2, research finds
Ice in Antarctica suddenly appeared — in geologic terms — about 35 million years
ago. For the previous 100 million years the continent had been essentially ice-free. The
question for science has been, why? What triggered glaciers to form at the South Pole?
Matthew Huber, assistant professor of earth and atmospheric sciences at Purdue University,
says no evidence of global cooling during the period had been found. "Previous
evidence points paradoxically to a stable climate at the same time this event, one of the
biggest climate events in Earth's history, was happening," Huber says. However, in a
paper published this week in the journal Science, a team of researchers found evidence of
widespread cooling. Additional computer modeling of the cooling suggests that the cooling
was caused by a reduction of greenhouse gases in the atmosphere.
Researchers identify ALS gene
mutation
Research that has discovered a new gene whose mutations cause 5 percent of inherited cases
of ALS (amyotrophic lateral sclerosis) is part of a national study led by the Northwestern
University Feinberg School of Medicine. The study reported in Science today (Feb. 27)
points to a common cellular deficiency in the fatal neurological disorder, said Teepu
Siddique, M.D., Les Turner ALS Foundation/Herbert C. Wenske Foundation Professor in the
Davee Department of Neurology and Clinical Neurosciences and Department of Cell and
Molecular Biology and Director of the Division of Neuromuscular Medicine at the Feinberg
School. The new research is part of a national collaboration directed by Siddique, the
principal investigator for the "Genetics of ALS" project funded at Feinberg by
the National Institutes of Health. Earlier research by Siddique and colleagues extended
the genetic knowledge of familial (inherited) ALS by identifying the first and second ALS
genes (the SOD1 gene in 1993 and the ALSIN gene in 2001), in addition to identifying loci
on chromosomes 9, 15, 16, and X. The study published today discovered aFUS/TLS gene
mutations in ALS families collected through efforts of the NIH-funded multi-center project
and included among others a large Italian family previously studied by Siddique and
Cortelli.
U of I study shows benefits of
hormone found in fat tissue
It's called the obesity paradox. Although obese people are more apt to suffer from
inflammatory diseases, such as diabetes, heart disease, and stroke, they are also more
likely to survive a major attack caused by one of those conditions. University of Illinois
scientists Gregory Freund and Christina Sherry shed light on the reasons for this
phenomenon in a study in this month's issue of Endocrinology. "Fat is a very complex
and active tissue—it has important functions beyond providing energy and insulating
us from the cold," said Freund, a professor in the U of I College of Medicine's
Department of Pathology and a faculty member in the U of I Division of Nutritional
Sciences. "We now know that leptin, a hormone secreted by fat tissue, plays a key
role in regulating the immune system. When we exposed mice to hypoxia (simulating an
event, such as a heart attack, in which a part of the body is deprived of oxygen), leptin
triggered the immune system to increase production of an anti-inflammatory molecule,
interleukin-1 receptor antagonist (IL-1RA)," he said. "And, when we gave
non-obese mice leptin injections, they recovered three times faster. Leptin did not hasten
recovery though in IL-1RA knockout mice," Sherry said. That earlier work was
published in a recent issue of Brain, Behavior, and Immunity.
A worm-and-mouse tale - B cells
deserve more respect
By studying how mice fight off infection by intestinal worms – a condition that
affects more than 1 billion people worldwide – scientists have discovered that the
immune system is more versatile than has long been thought. The work with worms is opening
a new avenue of exploration in the search for treatments against autoimmune diseases like
diabetes and asthma, where the body mistakenly attacks its own tissues. The findings,
reported by scientists who performed the work at the Trudeau Institute in Saranac Lake,
N.Y., and who are now at the University of Rochester Medical Center, appear in the March
issue of the journal Immunity. The article was published online Feb. 26.The research
focuses mainly on B cells, one of many types of immune cells that the body maintains to
fight off invaders like bacteria, viruses, and parasites. Besides B cells, there are T
cells, macrophages, neutrophils, monocytes, mast cells and others, all working in concert
to keep an organism healthy. The cells cruise our bodies, looking to eliminate infectious
threats before they become a serious risk to our health. For many years, scientists
believed that the major job of B cells was to identify foreign invaders and tag them with
antibodies, marking the microbe for destruction by the immune system. But scientists are
discovering that B cells do much more, resulting in new information about our immune
system that could be useful for developing more effective vaccines and better treatments
for many types of disease. In the past few years, Frances Lund, Ph.D., professor of
Medicine in the Division of Allergy/Immunology and Rheumatology at the University of
Rochester Medical Center, has found an array of unexpected functions for B cells. In the
laboratory, she has found that B cells produce chemical signaling molecules known as
cytokines that spur other immune cells in the body to action. Her team has also shown that
B cells are crucial for presenting to T cells snippets of proteins from invaders, so that
the T cells can recognize the invader, a crucial step that allows T cells to mature into
useful cells which can then fight an infection efficiently.
Daytime sleepiness provides red
flag for cardiovascular disease
Clinicians should be alert to patients reporting "excessive" day time sleepiness
(EDS), says the European Society of Cardiology, after a French study found healthy elderly
people who regularly report feeling sleepy during the day have a significantly higher risk
of dying from cardiovascular disease. The Three City study, published in Stroke, by the
American Heart Association (Thursday, February 26), found that elderly people who reported
excessive day time sleepiness have a 49 % relative risk increase of cardiovascular death
(from cerebrovascular disease, myocardial infarction and heart failure) , compared to
those who do not report sleepiness."Based on this study asking patients the simple
question of whether they feel sleepy during the day, is a useful way of identifying a
subgroup of elderly patients at higher risk of cardiovascular disease who require a more
thorough follow up," said Professor Guy DeBacker, from the Division of Cardiology at
the University of Gent, Belgium, and former chair of the European Society of Cardiology
Joint Prevention Committee.Professor Torben Jorgensen, from the Research Centre for
Prevention and Health, Glostrup, Denmark, commented: "The study offers the
opportunity to practice prevention by investigating the underlying causes of patient's
sleep problems, and then introducing lifestyle changes with the intention of preventing
later cardiovascular complications." The Three City study represents the largest yet
investigation exploring the prospective association between EDS and mortality in the
community dwelling elderly, and the only study yet to have been conducted in Europe –
all the other studies were undertaken in North America. Criticisms of the study include a
low responder rate (37%) that could introduce an element of bias, and the fact that it
lacked objective measures of day time sleepiness (such as polysomnography readings),
instead using self reported patient responses.
Muscular dystrophy, which affects approximately 250,000 people in the United States,
occurs when damaged muscle tissue is replaced with fibrous, bony or fatty tissue and loses
function. While scientists have identified one protein, dystrophin, as an important piece
to curing the disease, another part of the mystery has eluded scientists for the past 14
years. Now, one University of Missouri scientist and his team have identified the location
of the genetic material responsible for a molecular compound that is vital to curing the
disease. Duchenne muscular dystrophy (DMD), predominantly affecting males, is the most
common type of muscular dystrophy. Patients with Duchenne muscular dystrophy have a gene
mutation that disrupts the production of dystrophin. Absence of dystrophin starts a chain
reaction that eventually leads to muscle cell degeneration and death. A previous study by
Dongsheng Duan, associate professor of molecular microbiology and immunology, discovered a
potential delivery method to replace the mutated genes with healthy genes. Following the
replacement of these genes, Duan observed that dystrophin production was restarted in
animals with muscular dystrophy. However, while dystrophin is vital for muscle
development, the protein also needs several "helpers" to maintain the muscle
tissue. One of these "helper" molecular compounds is nNOS, which produces nitric
oxide. This is important for muscles that are in use during high intensity movements, such
as exercise. "When you exercise, not only does the muscle contract, but the blood
vessels are constricted," Duan said. "nNOS is important because it produces
nitric oxide that relaxes the blood vessels, helping to maintain the muscle with a healthy
blood supply. If no blood reaches the muscle cells, they will eventually die. In DMD
patients, this means the disease will progress as the muscle cells are replaced by the
fibrous, bony or fatty tissue."
How yeast is helping us to
understand Parkinson's Disease
Teams of scientists from Australia and the United States have used yeast and mammalian
cells to discover a connection between genetic and environmental causes of Parkinson's
disease. Yeasts are single cell organisms, used widely in biological research because
their structure resembles that of cells found in animals and humans. Yeasts share many
genes, or their functional equivalents, with humans and offer the ability to screen or
test thousands of genes and analysing their effects. Two genes (alpha-synuclein and PARK9)
had separately been associated with forms of Parkinson's disease, while manganese
poisoning can cause PD-like symptoms in miners and welders exposed to high manganese
levels. Findings connecting alpha-synuclein, PARK9 and sensitivity to manganese, made
possible by yeast research, have been published online in the February issue of the
prestigious international journal, Nature Genetics. "This is the first time that
we've been able to connect three pieces of the Parkinson's disease jigsaw puzzle and it
tells us we're on the right track to understanding what goes wrong in this disease"
said Dr Antony Cooper from Sydney's Garvan Institute of Medical Research and head of the
project group in Australia. Parkinson's disease involves the degeneration of neurons that
produce the neurotransmitter dopamine. Autopsies show an abundance of the small protein
alpha-synuclein in affected regions of the brain, so scientists have known for some time
that over-expression of the protein is toxic. When a European group discovered PARK9's
involvement in an inherited form of Parkinson's disease they examined some of the
surviving neurons from patients who had 'sporadic' Parkinson's, as opposed to inherited
forms of the disease, and found they contained ten times the levels of PARK9 when compared
with similar parts of the brain in patients without the disease. "Its possible that
the surviving neurons remained functional, unlike the degenerated neurons surrounding
them, because high levels of PARK9 protected them in some way," said Cooper.
"Little was known of PARK9's function but as yeast contains an equivalent gene, we
were able to analyse its function."
Health campaigns that promote
exercise may cause people to eat more
New research from the University of Illinois suggests that weight-loss campaigns that
promote exercise may actually cause people to eat more. People who viewed posters
suggesting that they "join a gym" or "take a walk" ate more food after
looking at the posters than people who saw similarly designed posters prompting them to
"make friends" or "be in a group," the researchers found. Subliminal
words about being active had a similar effect on study participants, said psychology
professor Dolores Albarracín, who led the research. "Viewers of the exercise
messages ate significantly more (than their peers, who viewed other types of
messages)," she said. "They ate one-third more when exposed to the exercise
ads." Those exposed to subliminal words about activity during a computer task ate
about 20 percent more than those exposed to neutral words, she said. The study, which
appears in the journal Obesity, builds on previous research by Albarracín that suggests
that general messages to be active can prompt people to behave in a variety of ways, some
of which may have negative consequences.
Discovery provides hope for
sufferers of disfiguring bone disease
Researchers at the University of East Anglia (UEA) have made a major genetic discovery
that could lead to the effective treatment for sufferers of craniosynostosis - a severe
childhood bone disease. Craniosynostosis develops in the womb and affects one in every
2500 live births. Bones in the skulls and face of sufferers fuse together prematurely
causing a range of distressing developmental problems. Some of the affected children also
suffer from defects in the limbs, brain, kidneys and lungs. Depending on the severity of
their disease and its underlying cause, children suffering with craniosynostosis survive
from as little as a few days to as long as early adulthood.
Cologne Scientists find Relevance
of genetic Elicitor for Obesity
Obesity has become an epidemic in many parts of the western hemisphere; over 30 % of the
population of Germany are overweight. Scientists from the University of Cologne, in
cooperation with scientists from the University of Düsseldorf, have been able to verify
the relevance of a certain gene with regard to obesity for the first time. The results of
this work have been published in the international journal of science, Nature. In 2006,
scientists discovered increased amounts of variations of the FTO genes were in overweight
people. However, the relevance of this gene and its regular function remained unclear for
a long time. The team working for Prof. Dr. Jens Brüning, coordinator of the Cluster of
Excellence "Cellular Stress Responses in Aging-Associated Diseases", CECAD
Cologne, and Prof. Dr. Ulrich Rüther, University of Düsseldorf, have now been able to
show that mice which do not have FTO gene, do not become overweight and burn more energy.
These findings verify the importance of the FTO gene for the regulation of body weight.
The results of this research will become very important for the development of new ways of
treating obesity
Transport Protein for Vitamin B12
has been identified
Professor Dr. Peter Nürnberg of the Cologne Center for Genomics (CCG) at the University
Cologne and a team of international researchers have been successful in identifying the
cause of the rare genetic disease CblF. The cause of this disease is a vitamin B12
deficiency (cobalamin-deficiency) caused by a genetic disorder. Vitamin B12 is important
for cell division and haematopoiesis as well as for a functional nervous system. The body
is not able to produce this vitamin itself and therefore takes it from meat and dairy
products. What scientist have always known is that the vitamin is absorbed by small
organelles called lysosomes on its way into the cell where it is then used. However, the
manner in which these organelles entered the cells has now been discovered. Working with
Dr. Frank Rutsch from the paediatric clinic of the University Hospital of Münster, Prof.
Dr. Peter Nürnberg established an international research team comprising paediatricians,
geneticists and biologists from Germany France Canada and Switzerland. These scientists
examined 12 patients suffering from the rare genetic disorder CblF and were able to
identify an infinitesimal segment in the genetic information which was identical in almost
all of the patients and which featured a defect in a certain gene. From this the team
concluded that these patients, although from different countries, were in fact distantly
related and shared a common ancestor going back eight or max. nine generations, who passed
down the defective genetic information to them. People with one defective chromosome are
completely healthy: it is only when two carriers of this defective chromosome have
children that the disease occurs in the children of the carriers.
Expression of the Multiple
Sclerosis-Associated MHC Class II Allele HLA-DRB1*1501 Is Regulated by Vitamin D
Multiple Sclerosis (MS) is a complex neurological disease with a strong genetic component.
The Major Histocompatibility Complex (MHC) on chromosome 6 exerts the strongest genetic
effect on disease risk. A region at or near the HLA-DRB1 locus in the MHC influences the
risk of MS. HLA-DRB1 has over 400 different alleles. The dominant haplotype of Northern
Europe, marked by the presence of DRB1*1501, increases risk of MS by 3-fold. The
environment also plays a key role in MS. The most striking illustration of this is the
geographical distribution of the disease in populations matched for ethnicity. This has
led to the proposal that sunshine, and in particular, vitamin D, is an environmental
factor influencing the risk of MS. Circumstantial evidence supporting this comes from
studies showing the involvement of vitamin D in immune and nervous system function. The
current investigation sought to uncover any relationship between vitamin D and HLA-DRB1.
It was found that vitamin D specifically interacts with HLA-DRB1*1501 to influence its
expression. This study therefore provides more direct support for the already strong
epidemiological evidence implicating sunlight and vitamin D in the determination of MS
risk, and implies that vitamin D supplementation at critical time periods may be key to
disease prevention.
Vaccine Roll-Out Is Wrong Without
Honest Advice
Widespread use of the Gardasil vaccine should not be encouraged unless young women and
parents are given honest advice, including information that Gardisil is being linked to
serious negative reactions amongst teenagers in the U.S.
High triglycerides? It may be the
high fructose corn syrup
In contrast to ordinary sugar, HFCS can not be broken down by the muscles; it can not be
used as fuel for exercise. Instead, it goes directly to the liver and causes an increase
in the production of triglycerides.
