- - European weblog on food, health and environment
News - Week 5 - 2009
Scientists on track to develop
insulin chewing gum
Robert Doyle, a chemist at Syracuse University in New York state, has a potential
solution. Based on successful tests on on rats, Doyle suggests binding insulin molecules
to vitamin B12 so that it can hitch a ride on this protected supply chain.
Images that for the first time show bleeding inside the heart after people have suffered a
heart attack have been captured by scientists, in a new study published today in the
journal Radiology. The research shows that the amount of bleeding can indicate how damaged
a person's heart is after a heart attack. The researchers, from the MRC Clinical Sciences
Centre at Imperial College London, hope that this kind of imaging will be used alongside
other tests to create a fuller picture of a patient's condition and their chances of
recovery. The research was funded by the Medical Research Council, the British Heart
Foundation and the Department of Health, UK. People suffer heart attacks when an artery
that feeds blood to the heart becomes blocked, stopping the heart's blood supply and
depriving the heart muscle of oxygen. Currently, most people treated for a heart attack
are fitted with a metal tube called a stent to keep the blocked artery clear. Recent
research has shown that some people experience bleeding inside the heart muscle once blood
starts to pump into it again. However, the significance of this bleeding is currently not
understood. For the new small study, the researchers captured images of bleeding inside
the heart in 15 patients from Imperial College Healthcare NHS Trust who had recently
suffered a heart attack, using Magnetic Resonance Imaging (MRI). Analysis of the MRI scans
revealed that the amount of bleeding correlated with how much damage the heart muscle had
sustained.
Childhood obesity risk increased by
newly-discovered genetic mutations, says study
Three new genetic variations that increase the risk of obesity are revealed in a new
study, published today in the journal Nature Genetics. The authors suggest that if each
acted independently, these variants could be responsible for up to 50% of cases of severe
obesity. Together with existing research, the new findings should ultimately provide the
tools to predict which young children are at risk of becoming obese. Health professionals
could then intervene to help such children before they develop weight problems, say the
researchers from Imperial College London, the French National Research Institute CNRS and
other international institutions.
New step in DNA damage response in
neurons discovered
Researchers have identified a biochemical switch required for nerve cells to respond to
DNA damage. The finding, scheduled for advance online publication in Nature Cell Biology,
illuminates a connection between proteins involved in neurodegenerative disease and in
cells' response to DNA damage. Most children with the inherited disease ataxia
telangiectasia are wheelchair-bound by age 10 because of neurological problems. Patients
also have weakened immune systems and more frequent leukemias, and are more sensitive to
radiation. The underlying problem comes from mutations in the ATM (ataxia telangiectasia
mutated) gene, which encodes an enzyme that controls cells' response to and repair of DNA
damage. ATM can be turned on experimentally by treating cells with chemicals that damage
DNA. After other proteins in the cell detected broken DNA needing repair, scientists had
thought that the ATM protein could activate itself directly. Emory researchers have shown
that an additional step is necessary first. "In neurons that are not dividing
anymore, we now know that another regulator is involved: Cdk5," says Zixu Mao, MD,
PhD, associate professor of pharmacology and neurology at Emory University School of
Medicine. Working with postdoctoral fellows Bo Tian, PhD and Qian Yang, PhD, Mao found
that the Cdk5 protein must activate ATM before ATM can do its job in neurons. The results
support the idea that Cdk5 may be a potential drug target. Cdk5 contributes to normal
brain development, and aberrant Cdk5 activity is known to be involved in the death of
neurons in several neurodegenerative diseases, including Alzheimer's, Parkinson's and
amyotrophic lateral sclerosis.
Fruits and Vegetables in Cancer
Prevention and Treatment
Relatively recently, researchers have become keenly interested in exploring which food
compounds are beneficial in treating and preventing serious diseases such as cancer and
osteoporosis. Omer Kucuk, MD, is one of those researchers. Kucuk, a professor of
hematology and medical oncology at Emory Winship Cancer Institute, studies specific food
compounds and their effect on cancer prevention and treatment. Evidence indicates that
some food compounds, such as soy isoflavones and curcumin, can increase the effectiveness
of chemotherapy and radiation therapy. To listen to Kucuk’s own words about which
food compounds affect cancer prevention and treatment, access Emory's new Sound Science
podcast. Kucuk conducted the first clinical trials to show the benefits of soy and
lycopene supplements in prostate cancer treatment. “In our preclinical studies we
have observed that taking soy isoflavones during chemotherapy and radiation for advanced
prostate cancer can improve the efficacy of the treatments," says Kucuk. “The
compounds sensitize the cancer cells to chemotherapy and radiation while at the same time
they protect the normal tissues from side effects.” Most nutritional compounds used
for therapy or disease prevention can be taken as part of a routine diet and have little
if any side effects, Kucuk says. “People can get enough lycopene by eating tomato
paste and tomato sauce, which is very rich in lycopene. So, if people ate a couple of
ounces of tomato paste a day as part of a regular diet, they would eat enough to get all
the benefits,” he says. Kucuk and his colleagues are currently exploring how soy
isoflavones make chemotherapy and radiation more effective. “These are pleiotropic
agents. That means they affect multiple pathways in cancer cells as well as other
cells,” Kucuk says. “This is actually good, because a lot of the drugs that are
developed target one pathway, and they’re usually very toxic. But because nontoxic
nutritional compounds work with multiple pathways they have mild side effects making them
very attractive for treatment.”
Important advance in the treatment
of cancer and viral infections
Dr. André Veillette, a researcher at the Institut de recherches cliniques de Montréal
(IRCM), and his team led by postdoctoral fellow Dr. Mario-Ernesto Cruz-Munoz, will publish
in the upcoming issue of the prestigious journal Nature Immunology of Nature Publishing
Group. This discovery could have a significant impact on the treatment of cancers and
infectious diseases. Current treatments frequently achieve only limited results with these
types of diseases, which affect hundreds of thousands of Canadians. Dr. Veillette's team
identified one of the basic mechanisms controlling NK ("natural killer") cell
activity. Produced by the immune system, NK cells are responsible for recognizing and
killing cancer cells and cells infected by viruses, such as viruses causing hepatitis and
herpes. NK cell deficiency is associated with a higher incidence of cancers and serious
infections. "Our breakthrough, comments Dr. Veillette, demonstrates that a molecule
known as CRACC, which is present at the surface of NK cells, increases their killer
function." Using mice, the researchers have shown that CRACC greatly improves the
animals' ability to eliminate cancer cells such as melanoma (a skin cancer) and lymphoma
(a blood cancer). Mice lacking the CRACC gene, generated in Dr. Veillette's laboratory,
were found to be more susceptible to cancer persistence. Conversely, stimulation of CRACC
function was found to improve cancer cell elimination. Thus, stimulating CRACC could boost
NK cell activity, helping to fight cancers. In addition, it could improve the ability to
fight infections, which are also handled by NK cells. Increasing the activity of CRACC by
gene therapy or drugs could become an option in the future to stimulate the killer
function of NK cells, and to improve their capacity to destroy cancer and virus-infected
cells. These approaches could be used in combination with chemotherapy and radiotherapy to
increase the effectiveness of anti-cancer treatments. Teams of scientists around the world
have been trying for many years without success to develop methods to increase NK cell
activity. In this light, the discovery of Dr. Veillette's team opens new avenues for the
treatment of cancers and viral infections.
Study links water pollution with
declining male fertility
New research strengthens the link between water pollution and rising male fertility
problems. The study, by Brunel University, the Universities of Exeter and Reading and the
Centre for Ecology & Hydrology, shows for the first time how a group of
testosterone-blocking chemicals is finding its way into UK rivers, affecting wildlife and
potentially humans. The research was supported by the Natural Environment Research Council
and is now published in the journal Environmental Health Perspectives. The study
identified a new group of chemicals that act as ‘anti-androgens’. This means
that they inhibit the function of the male hormone, testosterone, reducing male fertility.
Some of these are contained in medicines, including cancer treatments, pharmaceutical
treatments, and pesticides used in agriculture. The research suggests that when they get
into the water system, these chemicals may play a pivotal role in causing feminising
effects in male fish.Earlier research by Brunel University and the University of Exeter
has shown how female sex hormones (estrogens), and chemicals that mimic estrogens, are
leading to ‘feminisation’ of male fish. Found in some industrial chemicals and
the contraceptive pill, they enter rivers via sewage treatment works. This causes
reproductive problems by reducing fish breeding capability and in some cases can lead to
male fish changing sex. Other studies have also suggested that there may be a link between
this phenomenon and the increase in human male fertility problems caused by testicular
dysgenesis syndrome. Until now, this link lacked credence because the list of suspects
causing effects in fish was limited to estrogenic chemicals whilst testicular dysgenesis
is known to be caused by exposure to a range of anti-androgens.
Electric fields, Power lines and
Radon gas dangers Documentary - 40:46
Power lines cancer danger Dispatches Documentary shown on British TV C4 about 1993.
Video 40 minuets uploded in wma format. Posted on July 2, 2006 by TruthSeeker Strongest
Evidence Yet Of Cancer Risk Near Power Lines By Jonathan Leake and Chris Dignan A British
scientist has produced the most powerful evidence yet of a link between cancer and
electricity power lines. His study confirms that people living near them are exposed to
radiation levels dozens of times greater than the legal limit.The research, to be released
this week, firmly links the power lines with childhood leukaemia and other forms of
cancer. The levels recorded in some areas were two times higher than the legal maximum
allowed for adult nuclear power workers — the group permitted maximum radiation
exposure.Its most serious implication is that more than 23,000 homes built under or near
power lines are unsafe, especially for children. The effect of the fields can extend more
than 100 yards either side of the lines.Professor Denis Henshaw, of Bristol
University’s human radiation effects group, showed three years ago that there was a
theoretical mechanism whereby power lines could increase human uptake of the radioactive
gases produced naturally in the soil and also of traffic pollutants. His latest study
quantifies this effect in the field and shows that power lines are indeed linked to
childhood leukaemia and other cancers.
Henshaw took 2,000 field measurements to support his research.A university insider
described the findings as dynamite. “The study has serious implications for the
electricity industry, which could face huge compensation claims and pressure to move its
pylons.”Children are especially vulnerable to radiation and pollution damage because
they have more growing and dividing cells than adults. Such cells are far more prone than
adult ones to become cancerous when exposed to hazardous substances.The research will be
published in the International Journal of Radiation Biology. Its editor, Professor Gordon
Steel, said it was a comprehensive study of how electric fields of the kind generated by
power lines and, to a lesser extent, domestic appliances, could increase the uptake of
radioactive gases and pollutants by humans. Details will be revealed at a press conference
at the Institute of Mechanical Engineers in London on Wednesday.The study, funded by the
Department of Health and the Medical Research Council, is backed by another carried out by
Sir Richard Doll, due for publication in The Lancet on Friday. Doll, who discovered the
link between tobacco and lung cancer, has collated details of every childhood leukaemia
case in the past four years to try to find common causes, including links with electric
fields.Childhood leukaemia has long been seen as a target for such studies since it occurs
in clusters, suggesting a common cause that is probably linked to local environmental
factors.
Clusters associated with power lines have been noted for years but the electricity
industry has insisted such associations were too weak to be significant.Three years ago
Henshaw discovered the complex interactions between the alternating electric fields
surrounding power lines and the radioactive breakdown products of naturally occurring
radon gas. His theory was dismissed by the electricity industry and, more importantly, the
government’s National Radiological Protection Board (NRPB).Henshaw is understood to
have shown that in some areas children living near power lines could receive doses of 95
millisieverts of radiation a year, compared with the maximum for homes of one
millisievert. Nuclear workers are allowed a maximum dose of 50, soon to be reduced to
20.Henshaw was unwilling to comment on the study before publication but said: “It is
clear that if there is radon gas or traffic fumes in the air near pylons, then people
living nearby will suffer increased exposure because of the electric field.”The
National Grid and electricity distribution companies could find themselves in a difficult
position. A spokesman said it was too early to comment.The findings will be welcomed by
victims and their families, some of whom have tried to sue for compensation. Ray and
Denise Studholme, of Bolton, launched the first legal case of its kind in Europe in 1994,
when they took Norweb, the electricity supplier, to court after their son Simon, 13, died
from leukaemia in 1992. They had to drop their action in 1997 after an American study, now
criticised as flawed, raised doubts over a link. This weekend Ray, 51, said he would
consider restarting legal action in the light of the new evidence.
Rethinking the genetic theory of
inheritance
Scientists at the Centre for Addiction and Mental Health (CAMH) have detected evidence
that DNA may not be the only carrier of heritable information; a secondary molecular
mechanism called epigenetics may also account for some inherited traits and diseases.
These findings challenge the fundamental principles of genetics and inheritance, and
potentially provide a new insight into the primary causes of human diseases. Your mother's
eyes, your father's height, your predisposition to disease-- these are traits inherited
from your parents. Traditionally, 'heritability' is estimated by comparing monozygotic
(genetically identical) twins to dizygotic (genetically different) twins. A trait or
disease is called heritable if monozygotic twins are more similar to each other than
dizygotic twins. In molecular terms, heritability has traditionally been attributed to
variations in the DNA sequence. CAMH's Dr. Art Petronis, head of the Krembil Family
Epigenetics Laboratory, and his team conducted a comprehensive epigenetic analysis of 100
sets of monozygotic and dizygotic twins in the first study of its kind. Said Dr. Petronis,
"We investigated molecules that attach to DNA and regulate various gene activities.
These DNA modifications are called epigenetic factors." The CAMH study showed that
epigenetic factors – acting independently from DNA – were more similar in
monozygotic twins than dizygotic twins. This finding suggests that there is a secondary
molecular mechanism of heredity. The epigenetic heritability may help explain currently
unclear issues in human disease, such as the presence of a disease in only one monozygotic
twin, the different susceptibility of males (e.g. to autism) and females (e.g. to lupus),
significant fluctuations in the course of a disease (e.g. bipolar disorder, inflammatory
bowel disease, multiple sclerosis), among numerous others. "Traditionally, it has
been assumed that only the DNA sequence can account for the capability of normal traits
and diseases to be inherited," says Dr. Petronis. "Over the last several
decades, there has been an enormous effort to identify specific DNA sequence changes
predisposing people to psychiatric, neurodegenerative, malignant, metabolic, and
autoimmune diseases, but with only moderate success. Our findings represent a new way to
look for the molecular cause of disease, and eventually may lead to improved diagnostics
and treatment."
Gene technology to fight lethal
hospital acquired infection
Scientists at The University of Nottingham are leading a major European study to unravel
the genetic code of one of the most lethal strains of hospital acquired infections. The 3
million euro, three-year study will use gene knock-out technology developed in Nottingham
to study the function of genes in a ‘super’ strain of the bacteria Clostridium
difficile to discover why it causes more severe disease, kills more people, is harder to
eradicate and more resistant to antibiotics. It is hoped that the HYPERDIFF study, which
involves partners from the UK, Slovenia, Italy, France, The Netherlands and Germany and is
funded with a grant from the European Community, will lead to better tests to diagnose
‘super’ strains of C.difficile, more effective treatments and, possibly, even a
vaccine to protect against the disease. Since the turn of the new millennium there has
been a dramatic increase in the incidence of C.difficile. Currently the most frequently
occurring healthcare associated infection, last year it killed more than seven times as
many people in the UK as MRSA. Reasons for this increase may include improvements in
reporting procedures, the increasing age of the population as the elderly are especially
vulnerable, lower standards of hygiene and overcrowding on hospital wards. However, a
further significant factor has been the arrival in Europe of so-called
‘hypervirulent’ strains such as ribotype 027, which are responsible for more
severe disease and are more difficult to treat.
Baby chicks on a conveyor belt, modern chicken production, from German documentary
Unser täglich Brot, Our Daily Bread.
Socially active and not easily
stressed? You may not develop dementia
A new study shows that people who are socially active and not easily stressed may be less
likely to develop dementia. The research is published in the January 20, 2009, print issue
of Neurology®, the medical journal of the American Academy of Neurology. The study
involves 506 older people who did not have dementia when first examined. The group was
given questionnaires about their personality traits and lifestyle. The personality
questions identified people with different degrees of neuroticism, a term meaning easily
distressed. The questions also measured extraversion, or openness to talking to people.
Those who were not easily distressed were calm and self-satisfied, whereas people who were
easily distressed were emotionally unstable, negative and nervous. Outgoing people scored
high on the extraversion scale and were socially active and optimistic compared to people
with low extraversion who were reserved and introspective. The lifestyle questionnaire
determined how often each person regularly participated in leisure or organizational
activities and the richness of their social network. Participants were followed for six
years. During that time, 144 developed dementia.
In the United States, there has been a recent dramatic rise in the number of children
classified as obese and diagnosed with obesity-related diseases, such as type 2 diabetes
and nonalcoholic fatty liver disease (NAFLD). One factor thought to contribute to this
rise is obesity of the mother during pregnancy. However, a team of researchers, at Oregon
Health and Science University, Beaverton, and the University of Colorado School of
Medicine, Aurora, have found the offspring of both lean and obese nonhuman primate mothers
chronically consuming a high-fat diet exhibited an increased risk of developing NAFLD.
Importantly, if mothers fed a high-fat diet were reverted to a low-fat diet during a
subsequent pregnancy, this second offspring exhibited fewer signs of NAFLD. The team, led
by Kevin Grove and Jacob Friedman, therefore suggests that a developing fetus is highly
susceptible to maternal consumption of excess fat, whether or not the mother is obese, and
that a healthy maternal diet is most important for the obesity-related health of a
developing fetus.
Less severe first heart attacks
linked to heart disease death reductions
The severity of first heart attacks has dropped significantly in the United States —
propelling a decline in coronary heart disease deaths, researchers reported in
Circulation: Journal of the American Heart Association. “This landmark study suggests
that better prevention and better management in the hospital have contributed to the
reduction in deaths,” said Merle Myerson, M.D., Ed.D., lead author of the study,
cardiologist and director of the Cardiovascular Disease Prevention Program at St.
Luke’s-Roosevelt Hospital of Columbia University in New York City. “Better
control of risk factors for heart disease, such as blood pressure and cholesterol as well
as improvements in hospital management may lessen the severity if somebody has a heart
attack,” Myerson said. “We also considered whether people had less severity
because they got to the hospital sooner, but that was not the case.” The study
extends previous findings from the Atherosclerosis Risk in Communities (ARIC), an ongoing
epidemiologic study that includes data from four areas — Forsythe County, N.C.,
including Winston-Salem; Washington County, Md., including Hagerstown; and the suburbs of
Minneapolis, Minn. and Jackson, Miss. Both whites and African-Americans were included in
the study.
Low-carbohydrate diet burns more
excess liver fat than low-calorie diet, UT Southwestern study finds
People on low-carbohydrate diets are more dependent on the oxidation of fat in the liver
for energy than those on a low-calorie diet, researchers at UT Southwestern Medical Center
have found in a small clinical study. The findings, published in the journal Hepatology,
could have implications for treating obesity and related diseases such as diabetes,
insulin resistance and nonalcoholic fatty liver disease, said Dr. Jeffrey Browning,
assistant professor in the UT Southwestern Advanced Imaging Research Center and of
internal medicine at the medical center. "Instead of looking at drugs to combat
obesity and the diseases that stem from it, maybe optimizing diet can not only manage and
treat these diseases, but also prevent them," said Dr. Browning, the study's lead
author. Although the study was not designed to determine which diet was more effective for
losing weight, the average weight loss for the low-calorie dieters was about 5 pounds
after two weeks, while the low-carbohydrate dieters lost about 9½ pounds on average.
Glucose, a form of sugar, and fat are both sources of energy that are metabolized in the
liver and used as energy in the body. Glucose can be formed from lactate, amino acids or
glycerol. In order to determine how diet affects glucose production and utilization in the
liver, the researchers randomly assigned 14 obese or overweight adults to either a
low-carbohydrate or low-calorie diet and monitored seven lean subjects on a regular diet.
After two weeks, researchers used advanced imaging techniques to analyze the different
methods, or biochemical pathways, the subjects used to make glucose."We saw a
dramatic change in where and how the liver was producing glucose, depending on diet,"
said Dr. Browning.
Mayo Clinic Researchers Find
Experimental Therapy Turns on Tumor Suppressor Gene in Cancer Cells
Researchers at Mayo Clinic have found that the experimental drug they are testing to treat
a deadly form of thyroid cancer turns on a powerful tumor suppressor capable of halting
cell growth. Few other cancer drugs have this property, they say. In the Feb. 15 issue of
Cancer Research (available online Jan. 20), they report that RS5444, being tested in a
Phase 1/2 clinical trial to treat anaplastic thyroid cancer, might be useful for treating
other cancers. The agent is also known as CS-7017. From previous research, the
investigators knew that RS5444 binds to a protein known as PPAR-gamma, a transcriptional
factor that increases the expression of many genes. They had found that human anaplastic
thyroid tumor cells treated with RS5444 expressed a protein known as p21, which inhibited
cell replication and tumor growth. But they did not understand how. They have now
discovered that the agent actually forces PPAR-gamma to turn on the RhoB tumor suppressor
gene, which in turn induces p21 expression. "This is very unusual," says the
study's lead investigator, John Copland, Ph.D., a cancer biologist at the Mayo Clinic
campus at Jacksonville. "Drugs typically target genes and proteins that are
over-expressed and turn them off. We found that RS5444 turns on a valuable tumor
suppressor gene. We rarely find a drug that can take a suppressed gene and cause it to be
re-expressed."
Motor skill learning may be
enhanced by mild brain stimulation
People who received a mild electrical current to a motor control area of the brain were
significantly better able to learn and perform a complex motor task than those in control
groups. The findings could hold promise for enhancing rehabilitation for people with
traumatic brain injury, stroke and other conditions. The study is presented in the January
20, 2009 early online edition of the Proceedings of the National Academy of Sciences, and
was conducted by researchers at the National Institutes of Health (NIH). The research team
from NIH's National Institute of Neurological Disorders and Stroke (NINDS) worked in
collaboration with investigators at Columbia University in New York City and Johns Hopkins
University in Baltimore. Motor skills, which are used for activities from typing and
driving, to sports, require practice and learning over a prolonged period of time. During
practice, the brain encodes information about how to perform the task, but even during
periods of rest, the brain is still at work strengthening the memory of doing the task.
This process is known as consolidation.
Study shows rise in antibiotic
resistant pediatric head and neck infections
A report by researchers in the Jan. 19, 2009 Archives of Otolaryngology-Head and Neck
Surgery shows that there was nationwide increase in the prevalence of pediatric
methicillin-resistant Staphylococcus aureus (MRSA) head and neck infections from January
2001 to December 2006. The increase in antibiotic-resistant infections has become a big
concern for researchers and clinicians over the years. MRSA was once a condition that was
only found in hospital settings; however, over the last decade MRSA outbreaks have
increasingly been found in patients without risk factors. In an attempt to identify trends
in the susceptibility of antibiotic-resistant infections, researchers from Emory
University School of Medicine and Children's Healthcare of Atlanta studied data on
pediatric patients from nationwide hospitals. "The growing concern about the recent
worldwide MRSA epidemic has fueled the curiosity of the scientific community to gain
insight into the clinical and epidemiologic manifestations of this microbe," says
Steven E. Sobol, MD, MSc, primary investigator of the study and director of Pediatric
Otolaryngology in the Department of Otolaryngology - Head and Neck Surgery at Emory.
"Previous studies have established that skin and soft tissue infections in some
communities are due to MRSA," he says. "However, it has been observed in several
institutions that there is a significant rise in pediatric head and neck infections as
well." The researchers reviewed a total of 21,009 pediatric head and neck S. aureus
infections from 300 hospitals nationwide that occurred between Jan. 1, 2001 and Dec. 31,
2006. Patients ranged in ages from birth to 18.
Food advertisements in your
magazine: How healthy are they?
Newcastle University researchers collected and compared data on the nutritional content of
the foods advertised in 30 most widely-read weekly magazines during November 2007. A
detailed nutritional analysis of the foods in the adverts found that the products
advertised were generally much higher in sugar and salt, and lower in fibre than the World
Health Organisation (WHO) recommendations. The study published online today in the
European Journal of Public Health shows that over a quarter of the food adverts (25.5%)
were for ready-meals, sauces and soups which tend to be high in salt and sugar. Almost one
quarter (23%) of the foods advertised were categorised as "containing fat or
sugar" including products such as ice-cream, chocolate bars, sweets and full sugar
soft drinks. Government guidelines recommend these should be eaten only
"sparingly". More of these adverts were found in magazines with a higher
proportion of women readers or readers of a lower social class. In contrast, very few of
the ads, only 1.8%, were for fruit and vegetables and these were mainly in high-end
magazines. "Health bodies and the government are trying to encourage all of us to eat
a healthier diet, yet we found that many of the magazines, especially those targeting
lower-income families are full of adverts promoting food that is largely unhealthy,"
says Dr Adams. "Families are facing so many social pressures that it's a constant
battle to stay on the right track when choosing and preparing meals and these adverts are
doing little to help."
Research exposes the risk to
infants from the chemicals used in liquid medicines
A team of medical scientists from the University of Leicester has published research which
looks into the harmful substances in liquid medicines that premature babies are being
exposed to. Research published today (Jan 20) ahead of print in the Fetal & Neonatal
Edition of Archives of Disease in Childhood documents the non-drug ingredients
(excipients) present in liquid medicines given to premature infants as part of their
medical care. The study led by Dr Hitesh Pandya, Senior Lecturer in Child Health in the
Department of Infection, Immunity and Inflammation at the University of Leicester and
Consultant Paediatrician at the University Hospitals of Leicester NHS Trust, revealed that
the chemicals added to medicines to improve their taste, absorption and to prolong their
shelf-life could be potentially harmful to very small babies. The chemicals generally used
are ethanol, sorbitol and Ponceaau 4R (a colouring agent). The study revealed that
premature babies are exposed to these potentially harmful excipients in amounts equivalent
to over three pints of beer per week.
Discovery could help scientists
stop the “death cascade” of neurons after a stroke
Distressed swimmers often panic, sapping the strength they need to keep their heads above
water until help arrives. When desperate for oxygen, neurons behave in a similar way. They
freak out, discharging energy until they drown in a sea of their own extruded salts. Every
year, millions of victims of stroke or brain trauma suffer permanent brain damage because
of this mad rush to oblivion that begins once a part of the brain is deprived of blood. It
is well known that a ubiquitous cell receptor drives these oxygen-starved neurons’
lemming-like behaviour. But this particular receptor, for the neurotransmitter glutamate,
is also responsible for the rapid transmission of information between neurons required for
all cognition, among other things. Shutting it off has serious consequences, like coma.
Now, a team of scientists at The Rockefeller University has identified a single subunit of
this receptor that drives neuronal death. This new discovery suggests that drugs targeting
a specific subunit of the complex glutamate receptor might be able to slow brain damage
without disrupting other crucial brain functions. “We have found that you can make
mice resistant to this kind of cell death by blocking one piece of the receptor without
the terrible side effects you get by blocking the whole thing,” says Sidney
Strickland, head of the Laboratory of Neurobiology and Genetics, who directed the
research. “Now we can start exploring potential drugs to do that in humans.” The
neuronal panic that occurs when a clot or other insult blocks the flow of blood to part of
the brain is called excitotoxic neurodegeneration. It results in the brain cells spitting
out glutamate, which then accumulates in the synapses between neurons and stimulates the
release of more glutamate. It’s a vicious cycle that kills the cells quickly and
continues until blood flow is restored. Doctors often treat stroke victims by
administering a heavy dose of a clot-buster called tissue plasminogen activator (tPA), a
protein that can stimulate the dissolution of clots. Ironically, however, the same drug
that does this crucial clot-busting also accelerates the panicky process that kills
neurons, research by Strickland and others has shown. Investigating exactly how tPA does
that is what led Strickland’s team to the recent discovery.
Immunotherapy alleviates hay fever
and asthma in children
The results confirmed the effect of the grass pollen tablets: hay fever symptoms were up
24% less pronounced in the group taking the active substance than in the placebo group.
Accordingly, the group needed 34% less medication. Asthma symptoms decreased by up to 64%.
The immunological blood tests confirmed the effect of the tablet. In general, the grass
pollen tablets were well tolerated, apart from frequent itchiness in the mouth as a
temporary side effect. "Just as with adults, this immunotherapy with the tablet being
placed under the tongue is also very promising in children", concludes Prof. Bufe.
Further studies will be necessary to see whether there are any long-term improvements in
the allergy. "For a long time now, standard hay fever treatment has consisted of
desensitization/immunotherapy with the allergens being injected under the skin. If it
transpires that the grass tablets have a similarly effective long-term impact, in future
it will be possible to replace the injection therapy with sublingual treatment, and now
also in children."
Off-Label Use of Prescription Drugs
in Childhood and Adolescence
The methodology enables characterization of off-label prescription and identification of
fields where further research is needed. With regard to the EU regulation on medicinal
products for pediatric use, this could assume increasing importance and contribute to the
development of appropriate and safe medicines for children.
Studies at the University of Pennsylvania School of Medicine on brain electrical signaling
offer a fresh perspective on vertebrate evolution, provide additional evidence supporting
Darwinian views of evolution, and may also lead to more effective treatment of epileptic
seizures in infants. Researchers discovered how evolutionary changes produced a series of
improvements in molecules generating electrical signals in nerves between 550 and 400
million years ago. By making nervous systems faster and smarter, these innovations appear
to have contributed to the evolutionary success and diversity of vertebrate animals. In an
evolutionary comparison of nerve cell genes appearing in PLoS Genetics last month, Penn
scientists show that improvements in the molecules that govern rapid nerve impulses
occurred at major turning points in evolutionary history. By making nerve signals faster
and more controllable, these innovations appear to have contributed to the building of
smarter brains, and perhaps even to the success and diversity of vertebrates. In other
experiments presented at the Society for Neuroscience meeting in November and soon to
appear in the Annals of Neurology, the scientists found that the same electrical signaling
molecules appear to be an effective target for anti-seizure drugs for human newborns. The
electrical signaling molecules at the center of both studies are two related types of
nerve cell proteins called sodium and potassium channels. A decade ago, researchers found
that mutations in genes for these molecules were a cause of some forms of epilepsy in
newborn babies and infants. Sodium channels were already targets of anti-epileptic drugs.
The team led by Assistant Professor of Neurology Edward C. Cooper, MD, PhD, focused on the
potassium channels for therapeutic development.
Researchers led by Drs. Lillian Maggio-Price and Brian Iritani at The University of
Washington found that mice that lack the immune inhibitory molecule Smad3 are acutely
sensitive to both bacterially-induced inflammation and cancer. They report these findings
in the January 2009 issue of The American Journal of Pathology. Bacteria contribute to the
development of certain cancers, in some measure, by stimulating chronic inflammation.
Absence of a molecule that inhibits inflammation, Smad3, may therefore increase
susceptibility to colon cancer. To examine whether Smad3 signaling contributes to
development of colon cancer, Maggio-Price et al examined mice deficient in Smad3 that lack
of adaptive immune responses. They found that these mice are acutely sensitive to
bacterially-induced inflammation and cancer due to both deficient T regulatory cell
function and increased expression of proinflammatory cytokines. Through increased
expression of both pro-oncogenic and anti-apoptotic proteins, epithelial cells in colonic
tissues underwent both enhanced proliferation and survival. "That the inflammatory
response to microorganisms is a key event in these results reveals important
'tumor-suppressive' functions for Smad3 in T effector cells, T regulatory cells, and
intestinal epithelial cells, all of which may normally limit the development of colon
cancer in response to bacterial inflammation," explains the groups led by Dr.
Maggio-Price and Dr. Iritani.
Researchers describe protease
inhibitor that may aid in diabetic retinopathy treatment
Researchers from Joslin Diabetes Center, Boston, and ActiveSite Pharmaceuticals, Inc., San
Francisco, announced today that they have demonstrated that a specific inhibitor of the
protease plasma kallikrein, ASP-440, developed by ActiveSite Pharmaceuticals, may provide
a new therapeutic approach for treatment of diabetic retinopathy, the most common
eye-related complication of diabetes. The study, which was partly funded by the Juvenile
Diabetes Research Foundation (JDRF), is published in the February 2009 issue of the
journal Hypertension. In the published study, led by Edward P. Feener, Ph.D., an
Investigator in the Section on Vascular Cell Biology at the Joslin Diabetes Center and
Associate Professor of Medicine at Harvard Medical School, continuous systemic
administration of ASP-440 proved effective in decreasing hypertension-induced increased
retinal vascular permeability in rodents, by as much as 70%. Increased retinal vascular
permeability is a characteristic finding in diabetic retinopathy and a primary cause of
diabetic macular edema, a leading cause of visual impairment associated with diabetes.
Hypertension is a known risk factor for the development of retinopathy. ASP-440 was also
found to be effective in lowering the elevated blood pressure in these animals.
"These findings represent a pivotal step towards understanding the importance of
plasma kallikrein as a target in diabetic eye disease and how its inhibition may support
the development of a safe and effective therapy for diabetic retinopathy," said
Barbara Araneo, Director of Complications Research for the Juvenile Diabetes Research
Foundation. "While further studies are needed to determine the therapeutic potential
of ASP-440, the research underscores the relevance of the kallikrein system in diabetic
microvascular disease."
Research exposes the risk to
infants from the chemicals used in liquid medicines
A team of medical scientists from the University of Leicester has published research which
looks into the harmful substances in liquid medicines that premature babies are being
exposed to. Research published today (Jan 20) ahead of print in the Fetal & Neonatal
Edition of Archives of Disease in Childhood documents the non-drug ingredients
(excipients) present in liquid medicines given to premature infants as part of their
medical care. The study led by Dr Hitesh Pandya, Senior Lecturer in Child Health in the
Department of Infection, Immunity and Inflammation at the University of Leicester and
Consultant Paediatrician at the University Hospitals of Leicester NHS Trust, revealed that
the chemicals added to medicines to improve their taste, absorption and to prolong their
shelf-life could be potentially harmful to very small babies. The chemicals generally used
are ethanol, sorbitol and Ponceaau 4R (a colouring agent). The study revealed that
premature babies are exposed to these potentially harmful excipients in amounts equivalent
to over three pints of beer per week.
Binge drinking leads to a greater
risk of preterm birth
A new study from the Telethon Institute for Child Health Research has revealed the
consequences of heavy and binge drinking on pregnancy even after these drinking patterns
have stopped. The study, to be published in BJOG - An International Journal of Obstetrics
and Gynaecology, investigated the relationship between prenatal exposure to alcohol and
the effects on fetal growth and preterm birth.A random sample of 4,719 women who gave
birth in Western Australia between 1995 and 1997 took part in a survey. Data such as how
often participants drank alcohol, the amount of alcohol consumed in each occasion and the
types of alcoholic beverage consumed were collated. The researcher team from the Institute
with the National Perinatal Epidemiology Unit at the University of Oxford found that, on
average, levels of alcohol intake decreased from the pre-pregnancy period to the second
and third trimester. There was no difference in outcomes for women who drank low levels of
alcohol during their pregnancy and those that abstained. The incidence of preterm birth
was highest amongst women who binged (9.5%) or drank heavily, even if the mother stopped
drinking prior to the second trimester (13.6%), compared with less than 6% in women who
did not drink during pregnancy. There was a 2.3-fold increased odds of preterm birth in
women who drank heavily in early pregnancy but then stopped (CI 0.7, 7.7) after taking
into account maternal smoking, drug use, socioeconomic status and maternal health.
Researchers suggest that a possible reason why this occurs is because the cessation of
alcohol consumption before the second trimester may trigger a metabolic or inflammatory
response resulting in preterm birth. There was no evidence of an increased likelihood of
preterm birth at low levels of alcohol consumption.
Doctors are not doing enough to pick up on problems with excessive weight loss, says a
Saint Louis University physician who helped draft recent guidelines to diagnose the
condition called "cachexia" (kuh-kex-ee-uh). "In sick people, weight loss
is an important indicator of disease and potentially impending death," said John
Morley, M.D., an endocrinologist and director of the division of geriatric medicine at
Saint Louis University School of Medicine. "Cachexia is an extraordinary problem for
people who are having other health problems, yet this is something that many physicians
don't pay attention to." A group of physicians and scientists agreed on a definition
of cachexia, which was published in the December edition of the medical journal, Clinical
Nutrition. "The definition is important because it gives physicians the guidelines to
make a diagnosis and treat the condition," Morley said. "A definition of
cachexia also makes it easier for scientists to conduct research and potentially develop
new therapies for the problem." About half of hospitalized patients and between 10
and 15 percent of sick patients who see a doctor have cachexia. The condition accompanies
diseases such as cancer, congestive heart failure, HIV, diabetes, kidney failure and COPD
(chronic obstructive pulmonary disease).
Mice from a strain that ordinarily develops systemic lupus erythematosus (SLE), but bred
with a deficiency in receptor for the protein Interleukin 21, stayed healthy and exhibited
none of the symptoms of the disease, researchers at The Jackson Laboratory and National
Institutes of Health report. SLE is an autoimmune disease, with symptoms of varying
severity including include painful or swollen joints, unexplained fever and extreme
fatigue. An estimated 2 million Americans --nine out of 10 of them female -- live with
SLE. The primary job of the immune system is to identify and vanquish potentially
dangerous infectious pathogens. Autoimmune diseases develop when immune system instead
unleashes this potent defense system against the individual's own tissues, with
predictably severe consequences. Unlike other autoimmune diseases such as Type 1 diabetes,
in which the immune response is focused on certain tissues, SLE is a systemic disease in
which abnormal antibodies are produced that injure a variety of tissues and organs,
including the skin, heart, lungs and kidneys. The cause of SLE is not well understood, but
recent work by a Jackson Laboratory research team led by Professor Derry Roopenian is
shedding light on how the disease develops and offers hope for better therapies.
Magnesium sulphate protects babies
against cerebral palsy
Giving pregnant mothers magnesium sulphate when they are at risk of very preterm birth can
help protect their babies from cerebral palsy, according to an international review of
research involving the University of Adelaide, Australia. The findings of this review
– published today on the international research website The Cochrane Library –
could help decrease the incidence of this disabling condition, which affects one in 500
newborn babies overall and one in 10 very premature babies (less than 28 weeks gestation).
Magnesium sulphate therapy involves giving doses of magnesium sulphate to pregnant women
via injection. The potential for magnesium sulphate to decrease the risk of cerebral palsy
in babies was first proposed in the early 1990s. The new Cochrane review, which supports
this suggestion, was carried out by leading researchers from Australia (University of
Melbourne and University of Adelaide), France (University Hospital, Rouen) and the United
States (University of Alabama).The review involved data from 6145 babies included in five
trials of antenatal magnesium sulphate therapy.
Clinical trials - Unfavorable
results often go unpublished
Trials showing a positive treatment effect, or those with important or striking findings,
were much more likely to be published in scientific journals than those with negative
findings, a new review from The Cochrane Library has found."This publication bias has
important implications for healthcare. Unless both positive and negative findings from
clinical trials are made available, it is impossible to make a fair assessment of a drug's
safety and efficacy," says lead researcher, Sally Hopewell of the UK Cochrane Centre
in Oxford, UK.The international team of researchers carried out a systematic review of all
the existing research in this area. In addition to showing that negative results were
published less often, they found that if these results were eventually published, they
would take between one and four more years to appear in journals than studies showing
positive results.Results from one of the five studies in the review indicated that
investigators and not editors might be to blame. The reasons most commonly given for not
publishing were that investigators thought their findings were not interesting enough or
did not have time. "The registration of all clinical trial protocols before they
start should make it easier to identify where we are missing results," says Kay
Dickersin from Johns Hopkins University in Baltimore, USA, another of the researchers on
this project.
A cure for debilitating genetic diseases such as Huntington's disease, Friedreich's ataxia
and Fragile X syndrome is a step closer to reality, thanks to a recent scientific
breakthrough. The finding, which was published in Science on January 15, is the result of
a collaboration between a team led by Dr Sureshkumar Balasubramanian at The University of
Queensland's School of Biological Sciences and Professor Dr Detlef Weigel at the Max
Planck Institute for Developmental Biology in Germany. It identifies an expansion of a
repeat pattern in the DNA of the plant Arabidopsis thaliana that has striking parallels to
the DNA repeat patterns observed in humans suffering from neuronal disorders such as
Huntington's disease and Fredereich's ataxia. Lead researcher from UQ, Dr Balasubramanian,
said being able to use the plant as a model would pave the way toward better understanding
of how these patterns change over multiple generations. "It opens up a whole new
array of possibilities for future research, some of which could have potential
implications for humans," Dr Balasubramanian said.
“Warrior Gene” Predicts
Aggressive Behavior After Provocation
Individuals with the so-called “warrior gene” display higher levels of
aggression in response to provocation, according to new research co-authored by Rose
McDermott, professor of political science at Brown University. In the experiment, which is
the first to examine a behavioral measure of aggression in response to provocation,
subjects were asked to cause physical pain to an opponent they believed had taken money
from them by administering varying amounts of hot sauce. The findings are published in the
Proceedings of the National Academy of Sciences. In addition to McDermott, the research
team included Dustin Tingley of Princeton University, Jonathan Cowden of the University of
California–Santa Barbara, Giovanni Frazetto from the London School of Economics, and
Dominic Johnson from the University of Edinburgh. Their experiment synthesized work in
psychology and behavioral economics. Monoamine oxidase A is an enzyme that breaks down
important neurotransmitters in the brain, including dopamine, norepinephrine, and
serotonin. The enzyme is regulated by monoamine oxidase A gene (MAOA). Humans have various
forms of the gene, resulting in different levels of enzymatic activity. People with the
low-activity form (MAOA-L) produce less of the enzyme, while the high-activity form
(MAOA-H) produces more of the enzyme. Several studies have found a correlation between the
low-activity form of MAOA and aggression in observational and survey-based studies. Only
about a third of people in Western populations have the low-activity form of MAOA. By
comparison, low-activity MAOA has been reported to be much more frequent (approaching
two-thirds of people) in some populations that had a history of warfare. This led to a
controversy over MAOA being dubbed the “warrior gene.”
Researchers discover 3 genes that
increase risk of severe obesity in kids and adults
European and Canadian researchers have, for the first time, drawn a map of genetic risk
factors that can lead to two forms of severe obesity: early-onset obesity in children, and
morbid obesity in adults. A genetic study of 1,380 Europeans with early-onset and morbid
adult obesity was led by French researchers Dr. David Meyre, of the Institut national de
la santé et de la recherche médicale (Inserm), and Dr. Philippe Froguel, director of the
Centre National de la Recherche Scientifique (CNRS). Dr. Rob Sladek, Dr. Constantin
Polychronakos and Dr. Alexandre Montpetit, of McGill University and the McGill University
and Génome Québec Innovation Centre, made key contributions to the discovery, along with
researchers from France, Britain, Finland, Switzerland and Germany. The results were
published Jan. 19 in the journal Nature Genetics. Finding the genetic cause of a medical
problem can often lead researchers along the right path toward an eventual treatment or
cure or to help identify people who might be at risk. "The idea was not just to look
at run-of-the-mill obesity, but look for genetic factors that may affect people who have
more severe problems with their weight," said Dr. Sladek, an assistant professor in
the Department of Human Genetics and Endocrinology. "This includes children who
become obese at a young age, before the age of six. We also studied the genomes of adults
who had a familial history of severe obesity, with a body-mass index greater than
40." People are generally defined as "overweight" if they have a body-mass
index greater than 25. "The family approach being undertaken by our collaboration
with our colleagues in France is going to become important for future large-scale genetic
studies," Sladek continued. "Our suspicion is that a lot of the genetic changes
that make people obese will turn out to be variants that run in families or in segments of
the population, rather than things that are very common across the population. In terms of
diabetes, we think that perhaps 90 per cent of the genetic risk could come from these
familial or even personal genetic variants."
An enzyme that lives in MRSA and helps the dangerous bacterium to grow and spread
infection through the human body has been visualised for the first time, according to a
study out today in Proceedings of the National Academy of Sciences (PNAS). Now, armed with
detailed information about the structure of this enzyme, researchers hope to design new
drugs that will seek it out and disable it, providing a new way of combating MRSA and
other bacterial infections. The enzyme, a 'worker-protein' called LtaS, produces an
important component of the protective outer-layer that surrounds all Staphylococcus aureus
cells as well as many other bacteria that cause disease. Staphylococcus aureus is a type
of bacterium that causes a variety of infections in the human body, including skin
infections and abscesses, sometimes leading to blood poisoning and life-threatening lung
or brain infections. MRSA is a particular strain of Staphylococcus aureus, which has
evolved to be resistant to the antibiotic methicillin and a large number of other
antibiotics, and can be life threatening. To counter this drug resistance and ensure that
it is possible to treat MRSA infection in the future, new antibiotics are needed that work
differently, for example by attacking parts of the pathogen that are not targeted by
current drugs. The team from Imperial College London behind today's study, funded by the
Medical Research Council, thinks that LtaS might be a good candidate target for a new
antibiotic to which MRSA will not be resistant. This is because its job is to build a
polymer called lipoteichoic acid (LTA), which is an important structure found on the
surface of Staphylococcus aureus cells.
Unexpected finding opens up new way
to stop autoimmune diseases and transplant rejection
After several years of battling recurring infections, the last thing a patient and her
doctors ever expected was that the cause of her problems might actually help millions live
longer, more active lives. Now, researchers have high hopes because Edward Goetzl and his
colleagues from the University of California and The Ohio State University discovered that
the patient made a unique antibody to her own T cells, the cells that mediate much of
autoimmunity. Acting on the surface of T cells via a novel mechanism, the antibody reduced
the number of T cells in her blood stream: a result that usually requires a host of
"immunosuppressive" and possibly toxic drugs. Their research discovery,
published online in The FASEB Journal, may lead to entirely new therapies for a wide range
of autoimmune disorders, such as colitis, lupus, rheumatoid arthritis, inflammatory bowel
disease, and multiple sclerosis, as well as new ways to prevent transplant
rejection."The possibility that these antibodies can be used to treat diverse
autoimmune diseases with minimal risk of infections represents a new horizon for reversing
these disabling and often fatal conditions," said Edward Goetzl, a senior researcher
involved in the study.
New study provides further evidence
that apple juice can delay onset of Alzheimer's disease
A growing body of evidence demonstrates that we can take steps to delay age-related
cognitive decline, including in some cases that which accompanies Alzheimer's disease,
according to a study published in the January 2009 issue of the Journal of Alzheimer's
Disease. Thomas B. Shea, PhD, of the Center for Cellular Neurobiology; Neurodegeneration
Research University of Massachusetts, Lowell and his research team have carried out a
number of laboratory studies demonstrating that drinking apple juice helped mice perform
better than normal in maze trials, and prevented the decline in performance that was
otherwise observed as these mice aged. In the most recent study Shea and his team
demonstrated that mice receiving the human equivalent of 2 glasses of apple juice per day
for 1 month produced less of a small protein fragment, called "beta-amyloid"
that is responsible for forming the "senile plaques" that are commonly found in
brains of individuals suffering from Alzheimer's disease.
'Sunshine vitamin' link to
cognitive problems in older people
Researchers from the Peninsula Medical School, the University of Cambridge and the
University of Michigan, have for the first time identified a relationship between Vitamin
D, the "sunshine vitamin", and cognitive impairment in a large-scale study of
older people. The importance of these findings lies in the connection between cognitive
function and dementia: people who have impaired cognitive function are more likely to
develop dementia. The paper will appear in a forthcoming issue of the Journal of Geriatric
Psychology and Neurology. The study was based on data on almost 2000 adults aged 65 and
over who participated in the Health Survey for England in 2000 and whose levels of
cognitive function were assessed. The study found that as levels of Vitamin D went down,
levels of cognitive impairment went up. Compared to those with optimum levels of Vitamin
D, those with the lowest levels were more than twice as likely to be cognitively impaired.
Vitamin D is important in maintaining bone health, in the absorption of calcium and
phosphorus, and in helping our immune system. In humans, Vitamin D comes from three main
sources – exposure to sunlight, foods such as oily fish, and foods that are fortified
with vitamin D (such as milk, cereals, and soya drinks). One problem faced by older people
is that the capacity of the skin to absorb Vitamin D from sunlight decreases as the body
ages, so they are more reliant on obtaining Vitamin D from other sources. According to the
Alzheimer's Society, dementia affects 700,000 people in the UK and it is predicted that
this figure will rise to over 1 million by 2025. Two-thirds of sufferers are women, and
60,000 deaths a year are attributable to the condition. It is believed that the financial
cost of dementia to the UK is over £17 billion a year.
Inflammation worsens danger due to
atherosclerosis
Current research suggests that inflammation increases the risk of plaque rupture in
atherosclerosis. The related report by Ovchinnikova et al, "T cell activation leads
to reduced collagen maturation in atherosclerotic plaques of ApoE-deficient- mice,"
appears in the February 2009 issue of The American Journal of Pathology. Atherosclerosis
is a disease of arterial blood vessels where fats, cholesterol, blood cells, and fibers
form hardened plaques on the artery wall. These plaques restrict blood flow to tissues
such as the heart and brain by narrowing the artery. Atherosclerosis can be caused by high
blood pressure, high fat and high cholesterol diets, smoking, and diabetes. People with
atherosclerotic plaques often show no symptoms for decades. Atherosclerotic plaques
consist of lipid cores covered by collagen fiber caps. These plaques can suddenly rupture,
resulting in blood clots that completely block blood flow and lead to heart attack or
stroke in otherwise healthy individuals. One potential cause of plaque rupture is the
thinning of the collagen fiber cap covering the plaque. Inflammatory cells are often
observed at the site of plaque rupture. Researchers led by Dr. Göran K Hansson at the
Karolinska Institute explored the role of inflammatory cells in atherosclerotic plaque
rupture using an animal model of atherosclerosis with hyper-activated immune cells. They
found that inflammation leads to a reduction of mature collagen in atherosclerotic
plaques, leading to thinner caps that are more likely to rupture. They then identified a
collagen-maturing enzyme, lysyl-oxidase (LOX), which represents a novel target in
inflammation-induced plaque rupture.
Jefferson scientists discover a key
protein regulator of inflammation and cell death
Reporting in the journal Nature, researchers led by Emad Alnemri, Ph.D., professor of
Biochemistry and Molecular Biology in the Kimmel Cancer Center at Jefferson, discovered a
key protein component involved in inflammation. The protein, AIM2 (absent in melanoma 2),
is involved in the detection and reaction to dangerous cytoplasmic DNA that is produced by
infection with viral or microbial pathogens, or by tissue damage. AIM2 also appears to be
a tumor suppressor, and its inactivation may play a role in the development of cancer,
according to Dr. Alnemri. AIM2 belongs to a class of proteins called inflammasomes, which
are multi-protein complexes that play major roles as guardians against both viral and
bacterial infections. Inflammasomes also detect dangerous self-molecules associated with
tissue damage. According to Dr. Alnemri, when cells are infected with pathogens, AIM2
senses the presence of the pathogen's DNA in the cytoplasm. It then binds to the foreign
DNA and causes a rapid inflammatory reaction that sends a danger signal alerting the body
to the invading pathogen. When AIM2 binds to the foreign DNA, it recruits a cytoplasmic
protein called ASC. ASC and AIM2 then work together to activate caspase-1, a cysteine
protease involved in the production of interleukin1beta and other inflammatory cytokines
that cause inflammation.
Altered brain activity in
schizophrenia may cause exaggerated focus on self
Schizophrenia may blur the boundary between internal and external realities by
overactivating a brain system that is involved in self-reflection, and thus causing an
exaggerated focus on self, a new MIT and Harvard brain imaging study has found. The
traditional view of schizophrenia is that the disturbed thoughts, perceptions and emotions
that characterize the disease are caused by disconnections among the brain regions that
control these different functions. But this study, appearing Jan. 19 in the advance online
issue of the Proceedings of the National Academy of Sciences, found that schizophrenia
also involves an excess of connectivity between the so-called default brain regions, which
are involved in self-reflection and become active when we are thinking about nothing in
particular, or thinking about ourselves. "People normally suppress this default
system when they perform challenging tasks, but we found that patients with schizophrenia
don't do this," said John D. Gabrieli, a professor in the McGovern Institute for
Brain Research at MIT and one of the study's 13 authors. "We think this could help to
explain the cognitive and psychological symptoms of schizophrenia." Gabrieli added
that he hopes the research might lead to ways of predicting or monitoring individual
patients' response to treatments for this mental illness, which occurs in about 1 percent
of the population. Schizophrenia has a strong genetic component, and first-degree
relatives of patients (who share half their genes) are 10 times more likely to develop the
disease than the general population. The identities of these genes and how they affect the
brain are largely unknown. The researchers thus studied three carefully matched groups of
13 subjects each: schizophrenia patients, nonpsychotic first-degree relatives of patients
and healthy controls. They selected patients who were recently diagnosed, so that
differences in prior treatment or psychotic episodes would not bias the results.
Researchers long ago established a link between inflammation, cancer and the compound
nitric oxide, which may be produced when the immune system responds to bacterial
infections, including those of the colon. However, the exact nature of the relationship
was unknown -- until now. Scientists from MIT's Division of Comparative Medicine and
Department of Biological Engineering have found that nitric oxide produced by inflammatory
cells during bacterial infection can cause colon cells to become cancerous. The finding
suggests that blocking the compound may help prevent or treat colon cancer, the third most
common form of cancer in the United States. The researchers, led by James Fox, director of
the Division of Comparative Medicine (DCM), report their findings in the Jan. 19 online
edition of the Proceedings of the National Academy of Sciences. Many years ago it was
discovered that gastrointestinal infection by H. pylori is often linked to cancer in
humans; a related bacteria called H. hepaticus has similar effects in mice. Nitric oxide
is produced during the inflammatory response to such bacterial infection, but it has been
unclear whether it was damaging cells or protecting them. By studying mice, the MIT team
found that nitric oxide produced by different types of cells has different effects.
Researchers genetically link Lou
Gehrig's disease in humans to dog disease
An incurable, paralyzing disease in humans is now genetically linked to a similar disease
in dogs. Researchers from the University of Missouri and the Broad Institute have found
that the genetic mutation responsible for degenerative myelopathy (DM) in dogs is the same
mutation that causes amyotrophic lateral sclerosis (ALS), the human disease also known as
Lou Gehrig's Disease. As a result of the discovery, which will be published in the
Proceedings of the National Academy of Sciences this week, researchers can now use dogs
with DM as animal models to help identify therapeutic interventions for curing the human
disease, ALS. "We uncovered the genetic mutation of degenerative myelopathy, which
has been unknown for 30 years, and linked it to ALS, a human disease that has no
cure," said Joan Coates, a veterinary neurologist and associate professor of
veterinary medicine and surgery in the MU College of Veterinary Medicine. "Dogs with
DM are likely to provide scientists with a more reliable animal model for ALS. Also, this
discovery will pave the way for DNA tests that will aid dog breeders in avoiding DM in the
future." Previously, ALS research has relied heavily on transgenic rodents that
expressed the mutant human gene SOD1, which causes ALS. Researchers found that dogs with
DM also had mutations in their SOD1 gene. Many rodent models possess very high levels of
the SOD1 protein that can produce pathologic processes distinct from those occurring in
ALS patients. Since the SOD1 mutation is spontaneous in dogs, the clinical spectrum in
dogs may represent more accurately that of human ALS. "Compared with the rodent
models for ALS, dogs with DM are more similar to people in size, structure and complexity
of their nervous systems, and duration of the disease," said Gary Johnson, associate
professor of veterinary pathobiology in the MU College of Veterinary Medicine. "The
results from clinical trials conducted with DM-affected dogs may better predict the
efficacies of therapeutic interventions for treating ALS in humans."
UC Davis study links smoking with
most male cancer deaths
he association between tobacco smoke and cancer deaths — beyond lung cancer deaths
— has been strengthened by a recent study from a UC Davis researcher, suggesting that
increased tobacco control efforts could save more lives than previously estimated. The
epidemiological analysis, published online in BMC Cancer, linked smoking to more than 70
percent of the cancer death burden among Massachusetts men in 2003. This percentage is
much higher than the previous estimate of 34 percent in 2001. "This study provides
support for the growing understanding among researchers that smoking is a cause of many
more cancer deaths besides lung cancer," said lead author Bruce Leistikow, a UC Davis
associate adjunct professor of public health sciences. "The full impacts of tobacco
smoke, including secondhand smoke, have been overlooked in the rush to examine such
potential cancer factors as diet and environmental contaminants. As it turns out, much of
the answer was probably smoking all along." Leistikow used National Center for Health
Statistics data to compare death rates from lung cancer to death rates from all other
cancers among Massachusetts males. The assessment revealed that the two rates changed in
tandem year-by-year from 1979 to 2003, with the strongest association among males aged
30-to-74 years. Smoking is a known cause of most lung cancers, and the study authors
concluded that the very close relationship over twenty-five years between lung and other
cancer death rates suggests a single cause for both: tobacco smoke. Leistikow, whose
research is dedicated to uncovering the causes of premature mortality, said, "The
fact that lung and non-lung cancer death rates are almost perfectly associated means that
smokers and nonsmokers alike should do what they can to avoid tobacco smoke. It also
suggests that increased attention should be paid to smoking prevention in health care
reforms and health promotion campaigns."
What we learn about autism from
studying fragile X syndrome
Individuals with autism and fragile X syndrome share many symptoms, and there may be
common neurobiological abnormalities underlying these symptoms. David Hessl, an associate
professor in the Department of Psychiatry and Behavioral Sciences and a researcher at the
M.I.N.D. Institute, will share recent findings from his laboratory and others focusing on
this topic in the Jan. 22 Minds Behind the M.I.N.D. lecture.
Americans owe 5 months of their
lives to cleaner air
A new study by researchers at Brigham Young University and Harvard School of Public Health
shows that average life expectancy in 51 U.S. cities increased nearly three years over
recent decades, and approximately five months of that increase came thanks to cleaner air.
"Such a significant increase in life expectancy attributable to reducing air
pollution is remarkable," said C. Arden Pope III, a BYU epidemiologist and lead
author on the study in the Jan. 22 issue of the New England Journal of Medicine. "We
find that we're getting a substantial return on our investments in improving our air
quality. Not only are we getting cleaner air that improves our environment, but it is
improving our public health." The research matched two sets of data from 51 cities
across the nation: changes in air pollution between about 1980 and about 2000; and
residents' life expectancies during those years. The scientists applied advanced
statistical models to account for other factors that could affect average life spans, such
as changes in population, income, education, migration, demographics and cigarette
smoking. In cities that had previously been the most polluted and cleaned up the most, the
cleaner air added approximately 10 months to the average resident's life. On average,
Americans were living 2.72 years longer at the end of the two-decade study period; up to
five months, or 15 percent, of that increase came because of reduced air pollution. Other
studies show that these gains are likely coming from reductions in the cardiovascular and
cardiopulmonary disease that typically accompany air pollution. "There is an
important positive message here that the efforts to reduce particulate air pollution
concentrations in the United States over the past 20 years have led to substantial and
measurable improvements in life expectancy," said study co-author Douglas Dockery,
chair of the Department of Environmental Health at Harvard School of Public Health.
A researcher from Boston University School of Medicine (BUSM) has determined that a
9-month old infant who was admitted to a local Boston hospital with seizures and a bulging
soft spot was actually suffering from rickets caused by vitamin D deficiency. This case
study describing the findings appear in the January 22nd issue of the New England Journal
of Medicine. A 9-month-old breast-fed male infant presented at a local hospital with a
seizure after a few days of nasal congestion, diarrhea, and possible fever. Examination
showed a bulging soft spot and a prominent forehead. Laboratory studies determined
hypocalcemia, hypophosphatemia, and elevated alkaline phosphatase. "In arriving at a
diagnosis, we needed to consider the causes of seizures and the consequences of breast
feeding without vitamin supplementation," said article author Michael Holick, MD,
PhD, director of the General Clinical Research Center and professor of medicine,
physiology and biophysics at BUSM and senior author of this case study. According to
Holick, who is an internationally recognized expert in vitamin D and skin research, this
child had marked hypocalcemia, which could have caused his seizure. "Hypocalcemia has
numerous causes and although rickets is a rare cause for this condition, it did merit
consideration," he added. Holick also pointed out that the child had received breast
milk exclusively as his major nutrition for almost 9 months, which could result in several
nutritional deficiencies, including iron and the fat soluble vitamins A, D, and K. Vitamin
D deficiency as well as rickets have become resurgent in this country in recent years,
particularly in infants who are solely breast fed. "In addition, the mother was of
African descent, and her dark skin puts her at risk for vitamin D deficiency, thus
increasing the breast-fed child's risk of vitamin D deficiency," said Holick. There
is essentially no vitamin D in human breast milk, on average about 25 IU per liter,
meaning this child's mother would have needed to ingest at least 2,000 to 4,000 IU of
vitamin D per day in order to transfer enough of the vitamin in her milk to satisfy the
infant's requirement," added Holick.
Measles Virus May Be Effective
Prostate Cancer Treatment
A new study appearing in The Prostate has found that certain measles virus vaccine strain
derivatives, including a strain known as MV-CEA, may prove to be an effective treatment
for patients with advanced prostate cancer. The findings show that this type of treatment,
called virotherapy, can effectively infect, replicate in and kill prostate cancer cells.
Prostate cancer is a leading cause death among males in the western world. It is currently
the second most common cause of cancer-related deaths among American men with 186,320 new
cases and 28,660 deaths expected to be recorded in 2008. A sizeable proportion of these
patients ultimately relapse, with a 5-year failure rate for treatment ranging from 14 to
34 percent. No curative therapy is currently available for locally advanced or metastatic
prostate cancer. The median survival time of MV-CEA-treated mice in the study almost
doubled compared to the controls, and complete tumor regression was observed in one-fifth
of treated animals. “Based on our preclinical results as well as the safety of
measles derivatives in clinical trials against other tumor types, these viral strains
could represent excellent candidates for clinical testing against advanced prostate
cancer, including androgen resistant tumors,” says Evanthia Galanis, M.D., of the
Mayo Clinic, senior author of the study. The study was supported by the Mayo Clinic
Specialized Program of Research Excellence (SPORE) in prostate cancer. These oncolytic
strains of measles virus, represent a novel class of therapeutic agents against cancer
that demonstrates no cross-resistance with existing treatment approaches, and can
therefore be combined with conventional treatment methods. Because primary tumor sites are
easily accessible in prostate cancer, locally recurrent disease represents a promising
target for virotherapy approaches. The virotherapy agent can easily be applied directly to
the prostate tumor via ultrasound-guided needle injections and close monitoring of therapy
can be achieved by non-invasive techniques including ultrasound and MRI.
A study from the University of Bath has found that smokers are twice as likely to kick the
habit if they use a support group rather than trying to give up alone. Researchers from
the UK Centre for Tobacco Control Studies led by Dr Linda Bauld at Bath, along with
colleagues from the University of Glasgow, have published research in the February issue
of Addiction journal comparing the success and cost-effectiveness of two types of stop
smoking support services offered by the NHS. These are community-based group stop smoking
support and one-to-one support provided in a pharmacy setting. The study, funded by the
Glasgow Centre for Population Health, NHS Greater Glasgow and Clyde and Health Scotland,
found that more than a third of smokers using support groups quit smoking after four
weeks; almost double the proportion of those using a pharmacy-based support scheme to help
them quit.
The scientists performed a 10-year follow-up study with healthy participants (206) aged
15-80 years at baseline in 1994, who participated in a nutrition survey in Valencia,
Spain. Data on diet, lifestyle factors, and body weight were obtained in 1994 and 2004
using a food frequency questionnaire (FFQ) and direct measurements. The average WG over
the study period was 3.41 kg. The data analysis of this study was limited by the number of
participants. The researchers did not perform separate analyses for men and women and
groups for statistical reasons (lack of sufficient statistical power). Concerning gender
differences there are some studies which have demonstrated different associations between
food group intake and weight changes among men and women. In conclusion, the researchers
found that increased fruit and vegetable intake was associated with significantly lower
risk of a medium WG (3,41 kg) over 10 years among adults of a Spanish Mediterranean
population. Dietary strategies to increase fruit and vegetable intake to prevent and
control overweight and obesity should be promoted more vigorously. The researchers
concluded that dietary patterns associated with a high intake of fruits and vegetables in
Mediterranean populations may reduce long-term risk of subsequent WG and obesity among
adults.
Sleep disordered breathing and
obesity: Independent effects, causes
In a study that addressed the issue of insulin sensitivity with respect to sleep
disordered breathing (SDB), Naresh Punjabi, M.D., Ph.D. sought to examine the relationship
between SDB and insulin resistance using the best tools at his disposal to do so. The
results definitively link SDB to pre-diabetic changes in insulin production and glucose
metabolism. It was published in the first issue for February of the American Journal of
Respiratory and Critical Care Medicine, published by the American Thoracic Society.
"In the past researchers have used body mass index, or BMI, as a proxy measure for
body fat, but we know this to be a variable and crude tool to assess the true percentage
of body fat," said Dr. Punjabi. "In addition, previous studies have used
surrogate measurements to assess the body's response to insulin without investigating the
interaction that occurs between reduced insulin sensitivity and increased insulin
production in the body." To address the shortcomings of previous studies, Dr. Punjabi
and colleagues used two tools in their investigation into the link between SDB and insulin
resistance: dual-energy x-ray absorptiometry (DEXA), a highly precise technique for
assessing body fat, and frequently sampled intravenous glucose tolerance test (FSIVGTT),
which provides a detailed picture of the subject's insulin sensitivity over time, rather
than a simple snapshot at a specific moment. They recruited 118 subjects, 39 who had no
SDB, and 79 who were newly diagnosed with SDB but who had not been treated. Each subject
underwent a sleep study to assess their level of SDB, and then underwent a FSIVGGT to
determine their glucose metabolism and insulin sensitivity/production the following day.
"Our major finding was that, as we suspected, SDB was strongly associated with a
decrease in the three major metabolic pathways that the body uses to metabolize
glucose— insulin sensitivity, glucose effectiveness, and pancreatic cell
function— independent of adiposity," said Dr. Punjabi. "What our research
tells us is that SDB is characterized by multiple physiological deficits that increase the
predisposition for type 2 diabetes mellitus."
If you are a mouse on the chubby side, then eating less may help you live longer. For lean
mice – and possibly for lean humans, the authors of a new study predict – the
anti-aging strategy known as caloric restriction may be a pointless, frustrating and even
dangerous exercise. "Today there are a lot of very healthy people who look like
skeletons because they bought into this," said Raj Sohal, professor at the University
of Southern California's School of Pharmacy. He and Michael Forster, of the University of
North Texas Health Science Center, compared the life span and caloric intake of two
genetically engineered strains of mice. The "fat" strain, known as C57BL/6,
roughly doubles in weight over its adult life. That strain benefited from caloric
restriction, Sohal said. The "lean" strain, DBA/2, does not become obese.
Caloric restriction did not extend the life of these mice, confirming previous work by
Forster and Sohal. The results appeared online Jan. 13 in advance of print publication in
the Journal of Nutrition. "Our study questions the paradigm that caloric restriction
is universally beneficial," Sohal said. "Contrary to what is widely believed,
caloric restriction does not extend (the) life span of all strains of mice." By
measuring the animals' metabolic rate, Sohal and his colleagues came to a deceptively
simple conclusion: Caloric restriction is only useful when, as in the case of the obese
mice, an animal eats more than it can burn off.
UCSF finds potential new antibody
treatment for autoimmune diseases
Scientists at UCSF have discovered an abnormality in a patient’s immune system that
may lead to safer therapies for autoimmune diseases such as rheumatoid arthritis and
colitis, as well as potential new ways to treat transplant rejection. The research
identified antibodies from a woman’s immune system that prevent infection-fighting T
cells from moving through her blood stream and entering her body’s organs to attack
invaders such as bacteria or viruses. Findings appear in the current online edition of
“The FASEB Journal,” the official journal of the Federation of American
Societies for Experimental Biology. Based on studies in which the woman’s antibodies
were transferred into mice, researchers hope these antibodies can be used to treat
patients with autoimmunity or transplant recipients whose immune systems attack a
transplanted organ or tissue. Autoimmunity occurs when the body perceives its own cells or
tissue as foreign organisms and creates an immune response to itself. Autoimmune diseases
affect approximately five to eight percent of Americans and their prevalence is
increasing, according to the National Institute of Allergy and Infectious Diseases. The
majority of people with autoimmune diseases are women.
Many of the 40 million American adults who suffer from anxiety disorders also have
problems with balance. As increasing numbers of children are diagnosed with anxiety, Tel
Aviv University researchers have discovered that the link between balance and anxiety can
be assessed at an early age and that something can be done about it before it becomes a
problem.
Nicotine activates more than just
the brain's pleasure pathways
Duke University Medical System researchers have discovered there are differing taste
pathways for nicotine, which could provide a new approach for future smoking-cessation
products. "We learned some of nicotine's secrets," said Albino Oliveira-Maia,
M.D., Ph.D., a postdoctoral fellow of the Duke Department of Neurobiology. "This is
the first study to explore both the peripheral taste pathways activated by nicotine, and
how these pathways are integrated in sensory areas of the brain." The peripheral
nervous system refers to nerves that are outside of the brain and spinal cord. Using
genetic engineering and measurements of nervous system activity in mice, the researchers
found that nicotine sends signals directly to the brain's sensory systems by several
pathways, similar to the way taste is perceived. These findings complement what is known
about the effects of nicotine in the dopamine pathway. This is the classic pleasure
pathway in the brain, much studied by addiction experts. "Our study in no way
contradicts prior findings about nicotine and dopamine," Oliveira-Maia said.
"Our findings add to what is known and suggest new approaches for further
study." The findings appeared in the PNAS Early Edition slated for January 19.
"One reason that our findings are interesting is because they relate to previous work
that looked at humans with lesions in the insula region of the brain – they had an
easier time giving up cigarettes than most people," Oliveira-Maia said. "We
found that a part of the insula, the gustatory cortex, has robust responses to nicotine
and a capacity to integrate diverse peripheral information to create a unique sensory
representation for nicotine." One taste pathway the Duke researchers uncovered
involves nicotinic acetylcholine receptors (nAChR), which scientists previously proposed
were taste receptors for nicotine. The researchers found a previously unknown link between
these receptors and activity in the taste region of the insula.
Research elucidates way lungs fight
bacteria and prevent infection
Actor and pancreatic cancer patient Patrick Swayze's recent hospitalization with pneumonia
as a result of his compromised immune system underscores the sensitivity of the lungs:
many patients die from lung complications of a disease, rather than the disease itself.
Lungs are delicate and exposed to the environment, almost like an open wound.
Consequently, the body has developed an elaborate immuno-defense system to combat inhaled
pathogens and bacteria – in a healthy individual, this system effectively blocks
hundreds of potentially sickening assaults daily. It works like this - airway epithelial
cells initiate an immune response to inhaled bacteria by signaling for white blood cells
to move from the bloodstream into the lungs and airway to fight potential infection. For
the first time, researchers at Columbia University Medical Center have demonstrated that
this signaling cascade includes the activation of epithelial proteases, a type of enzyme
capable of opening the junctions between the cells in the airway mucosa, to enable the
white blood cells to get through to the site of the infection. The opening of these
junctions is initiated by a change in calcium levels. The work by Drs. Jarin Chun and
Alice Prince in the Departments of Pharmacology and Pediatrics at Columbia's College of
Physicians and Surgeons was published Jan. 22, 2009 in the journal Cell Host &
Microbe. Getting white blood cells to the site of an infection, however, is often a
double-edged sword. On the one hand, having as many white blood cells as possible at the
site of an infection is beneficial, but on the other hand too many white blood cells can
lead to excessive inflammation, interfering with breathing and damaging the airways.
Video games linked to poor
relationships with friends, family
A new study connects young adults' use of video games to poorer relationships with friends
and family – and the student co-author expresses disappointment at his own findings.
Brigham Young University undergrad Alex Jensen and his faculty mentor, Laura Walker,
publish their results Jan. 23 in the Journal of Youth and Adolescence. The research is
based on information collected from 813 college students around the country. As the amount
of time playing video games went up, the quality of relationships with peers and parents
went down. "It may be that young adults remove themselves from important social
settings to play video games, or that people who already struggle with relationships are
trying to find other ways to spend their time," Walker said. "My guess is that
it's some of both and becomes circular." For the record, Walker did not stand in the
way of her family's wish for a Nintendo Wii. Jensen had hoped to find some positive
results as justification for playing Madden NFL. Study participants reported how often
they play video games. They also answered a battery of questions measuring relationship
quality, including how much time, trust, support and affection they share with friends and
parents. But the researchers say video games do not themselves mean "game over"
for a relationship because the connection they found is modest. "Relationship quality
is one of a cluster of things that we found to be modestly associated with video
games," Walker said. "The most striking part is that everything we found
clustered around video game use is negative."
The first study documenting methicillin-resistant Staphylococcus aureus (MRSA) in swine
and swine workers in the United States has been published by University of Iowa
researchers.The investigators found a strain of MRSA, known as ST398, in a swine
production system in the Midwest, according to the paper published online Jan. 23 by the
science journal PLoS One. "Our results show that colonization of swine by MRSA was
very common in one of two corporate swine production systems we studied," said Tara
Smith, Ph.D., associate professor of epidemiology in the University of Iowa College of
Public Health and lead author of the study. "Because ST398 was found in both animals
and humans, it suggests transmission between the two. "Our findings also suggest that
once MRSA is introduced, it may spread broadly among both swine and their caretakers.
Agricultural animals could become an important reservoir for this bacterium," Smith
added. Staphylococcus aureus, often called "staph," are bacteria commonly
carried on the skin or in the nose of healthy people. MRSA is a type of staph that is
resistant to the broad-spectrum antibiotics commonly used to treat it. A recent study
estimated that MRSA caused 94,000 infections and more than 18,000 deaths in the United
States in 2005. MRSA has been found in a variety of animals, including horses, cattle,
dogs, cats and swine. Previous studies have shown that many swine and swine farmers in
Canada and the Netherlands are colonized with MRSA. However, the University of Iowa study
was the first to investigate carriage of MRSA among swine and swine farmers in the United
States. For the study, investigators analyzed nasal swabs of 299 swine and 20 swine
workers from two different production systems in Iowa and Illinois. At Production System
A, the overall prevalence of MRSA was 70 percent in swine and 64 percent in workers. At
Production System B, all swine and human samples were negative for MRSA. The researchers
could not determine why System A had a high prevalence rate of MRSA among its swine and
swine handlers, but listed several differences compared to System B. First, the systems
raised different breeds of swine. Second, System A was an older, more established
operation that had approximately twice the number of animals as System B. Third, both
systems imported sows from different sources, raising the possibility that ST398 may have
been introduced via live swine or pork products.
Implants mimic infection to rally
immune system against tumors
Bioengineers at Harvard University have shown that small plastic disks impregnated with
tumor-specific antigens and implanted under the skin can reprogram the mammalian immune
system to attack tumors. The research -- which ridded 90 percent of mice of an aggressive
form of melanoma that would usually kill the rodents within 25 days -- represents the most
effective demonstration to date of a cancer vaccine. Harvard's David J. Mooney and
colleagues describe the research in the current issue of the journal Nature Materials.
"Our immune systems work by recognizing and attacking foreign invaders, allowing most
cancer cells -- which originate inside the body -- to escape detection," says Mooney,
Gordon McKay Professor of Bioengineering in Harvard's School of Engineering and Applied
Sciences. "This technique, which redirects the immune system from inside the body,
appears to be easier and more effective than other approaches to cancer vaccination."
Most previous work on cancer vaccines has focused on removing immune cells from the body
and reprogramming them to attack malignant tissues. The altered cells are then reinjected
back into the body. While Mooney says ample theoretical work suggests this approach should
work, in experiments more than 90 percent of the reinjected cells have died before having
any effect. The implants developed by Mooney and colleagues are slender disks measuring
8.5 millimeters across. Made of an FDA-approved biodegradable polymer, they can be
inserted subcutaneously, much like the implantable contraceptives that can be placed in a
woman's arm. The disks are 90 percent air, making them highly permeable to immune cells.
They release cytokines, powerful attractants of immune-system messengers called dendritic
cells.
Harvard Medical School researchers have succeeded in developing a topical treatment that,
in mice, wipes out herpes virus, one of the most intractable sexually transmitted human
diseases. Judy Lieberman, professor of pediatrics and a senior investigator at the Immune
Disease Institute, has overseen the development of the treatment that uses RNA
interference, or RNAi, to disable key genes necessary for herpes virus transmission. That
cripples the virus in a molecular two-punch knockout, simultaneously disabling its ability
to replicate, as well as the host cell's ability to take up the virus. What's more, the
treatment is just as effective when applied anywhere from one week prior to a few hours
after exposure to the virus. In that sense, the basic biology of this prophylactic enables
a real-world utility.
Researchers find new molecule to
block ‘Hedgehog’ signaling in cancer, development
Researchers have achieved a feat drug developers had thought difficult, if not impossible,
discovering a compound that blocks the functioning of a key developmental protein by
binding to an “undruggable” target — an advance that may provide a new
avenue to fight skin, pancreatic, prostate, and other cancers. A team led by Stuart
Schreiber, the Morris Loeb Professor of Chemistry in Harvard’s Faculty of Arts and
Sciences and director of the Broad Institute of Harvard and MIT’s Chemical Biology
Program, discovered a small molecule they dubbed “robotnikinin” that binds
directly to a protein called Sonic Hedgehog. The protein was shown in 1978 to control the
early development of fruit flies, whose bodies developed spiny protrusions when the
protein was blocked. It is now known that Sonic Hedgehog plays an important developmental
role in mammals, including humans, regulating limb and brain development in the embryo and
controlling the division both of adult stem cells and several types of cancer cell.
