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News - Week 22 - 2009
Autism in the UK costs more than
$41 billion every year, shows new research
Research published this week in the Journal Autism, published by SAGE, estimate the annual
costs of autism spectrum disorder (ASD) to be more than £27 billion a year. The costs of
supporting children with ASDs were estimated to be £2.7 billion per year, £25 billion
each year for adults. The findings will be presented at the Autism & Employment
Workshop taking place today at Goldsmiths, University of London. With the National Audit
Office report on the provision of services for Autism imminent, participants at the
workshop will review current research, policy and services and discuss the challenges
facing people with ASDs finding work and in the workplace. The Economic impacts of autism
research, led by Professor Martin Knapp of the London School of Economics, provides the
most comprehensive analysis of the economic impacts of ASD in the UK to date. Speaking at
the Goldsmiths event, Knapp will reveal the significant costs to the public sector, in
particular the health system, social care agencies, education and housing budgets. He will
also outline the steep rise in costs for adults, calling for increased early intervention
for those with ASDs. Costs were based on estimates for 539,766 people with ASD in the UK:
432,750 adults (aged 18 and over) and 107,016 children and adolescents (aged 0-17). There
was no single, nationally representative data source in the UK looking at these costs, so
the researchers combined existing data estimating prevalence; intellectual disability;
place of residence; service use; lost productivity; and costs per individual. Average
annual costs were also aggregated to estimate the lifetime cost of someone with ASD,
calculated by combining costs for different age groups with life expectancy estimates.
The costs of supporting children with ASDs were estimated to be £2.7 billion per
year. For adults, these costs rise to £25 billion each year. Lifetime costs for someone
with autism were calculated as £0.8 million for someone with autism without intellectual
disability, and £1.2 million for someone with autism who was also intellectually disabled
(50 percent higher). Significant costs were attributed to public services. For children,
the highest costs were for special education, health and social care and respite care. 95
percent of the total national cost for children was accounted for by services funded by
the state, and 5 percent by family expenses. For adults, the largest cost elements were
staffed/supported accommodation, lost productivity because the individual with ASD was not
employed, and hospital services. For non-intellectually disabled adults, the largest
elements were lost productivity for the individual, hospital costs, and lost productivity
for parents. 59 percent of the total was attributable to publicly funded services, 36
percent to lost employment for the individual with ASD, and the remaining 5 percent to
family expenses. The researchers suggest that the high costs associated with supporting
adults with ASD warrant attention, supporting calls for wider provisions of early
interventions with children and young people with ASD, which have been shown to alter
patterns of behaviour. They also call on the government to review policy frameworks for
supporting those with ASDs, in particular reviewing support for independent living and for
increasing productivity. The researchers however caution that the effectiveness and
cost-effectiveness of intervention must be evaluated further. They add, "given the
autistic spectrum includes a number of disorders and a wide range of needs, symptoms and
characteristics, it is likely that a wide range of behavioural, educational and medical
interventions could be required in order to meet some or all individual needs."
They conclude, "the costs presented in this paper certainly do not provide an
economic case for early intervention, but they do emphasise the importance of addressing
just that question. If early intervention could successfully change some aspects of
behaviour that are cost-raising, both in childhood and subsequently, it may allow cost
savings to be made and quality of life improvements to be achieved."
Babies born to native high-altitude
mothers have decreased risk of low birth weight
Pregnant women who are indigenous to the
Andes Mountains deliver more blood and oxygen to their fetuses at high altitude than do
women of European descent. The study helps explain why babies of Andean descent born at
high altitude weigh more than European babies born at altitude. The research, published in
The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
found that at high altitude - the uterine artery of Andean women delivered more blood and
oxygen to the fetus compared to women of European descent, the babies of Andean women
weighed an average of nine ounces more at birth, the greater the mother’s Andean
heritage, the greater the uterine artery blood flow, the greater the oxygen delivery to
the fetus and the greater the baby’s birth weight These differences between the
Andean and European women and their babies did not exist at low altitude. The question of
why babies born at high altitude are smaller is not an academic one. Low birthweight is
associated with higher rates of illness and mortality. By understanding this physiology,
researchers hope to find out how to protect from reductions in fetal growth even in
low-oxygen environments.
The future of personalized cancer
treatment - An entirely new direction for RNAi delivery
In technology that promises to one day
allow drug delivery to be tailored to an individual patient and a particular cancer tumor,
researchers at the University of California, San Diego School of Medicine, have developed
an efficient system for delivering siRNA into primary cells. The work will be published in
the May 17 in the advance on-line edition of Nature Biotechnology. "RNAi has an
unbelievable potential to manage cancer and treat it," said Steven Dowdy, PhD, Howard
Hughes Medical Institute Investigator and professor of cellular and molecular medicine at
UC San Diego School of Medicine. "While there's still a long way to go, we have
successfully developed a technology that allows for siRNA drug delivery into the entire
population of cells, both primary and tumor-causing, without being toxic to the
cells." For many years, Dowdy has studied the cancer therapy potential of RNA
inhibition which can be used to silence genes through short interfering, double-stranded
RNA fragments called siRNAs. But delivery of siRNAs has proven difficult due to their size
and negative electrical charge – which prohibits them from readily entering cells. A
small section of protein called a peptide transduction domain (PTD) has the ability to
permeate cell membranes. Dowdy and colleagues saw the potential for PTDs as a delivery
mechanism for getting siRNAs into cancer cells. He and his team had previously generated
more than 50 "fusion proteins" using PTDs linked to tumor-suppressor proteins.
"Simply adding the siRNAs to a PTD didn't work, because siRNAs are highly negatively
charged, while PTDs are positively charged, which results in aggregation with no cellular
delivery," Dowdy explained. The team solved the problem by making a PTD fusion
protein with a double-stranded RNA-binding domain, termed PTD-DRBD, which masks the
siRNA's negative charge. This allows the resultant fusion protein to enter the cell and
deliver the siRNA into the cytoplasm where it specifically targets mRNAs from
cancer-promoting genes and silences them.
Study finds genetic links to age of
first menstrual period and menopause
Newly identified gene variants associated
with the age at which females experience their first menstrual period and the onset of
menopause may help shed light on the prevention of breast and endometrial cancer,
osteoporosis, and cardiovascular disease. In a new study, researchers from Harvard School
of Public Health (HSPH), Brigham and Women's Hospital (BWH), National Cancer Institute
(NCI), and the Broad Institute of Harvard and MIT report that they have identified 10
genetic variants in two chromosomal regions associated with age at menarche (the first
menstrual period), and 13 genetic variants in four chromosomal regions associated with age
at natural menopause. The paper, "Genome-wide association studies identify loci
associated with age at menarche and at natural menopause," will publish online in
Nature Genetics on May 17, 2009 (
http://www.nature.com/ng/journal/vaop/ncurrent/index.html ). Menarche and natural
menopause are two important physiological events in a woman's life. An early onset of
menarche and later menopause are well-established risk factors for the development of
breast cancer and endometrial cancer, the researchers explain. On the other hand, early
menopause increases risk of osteoporosis and cardiovascular disease.
Previous studies have suggested both menarche and menopause may be partially under genetic
control. To identify common genetic variants influencing these states, the researchers
analyzed more than 317,000 gene variants in a total of 17,438 women from the Nurses'
Health Study (NHS) and the Women's Genome Health Study (WGHS) based at BWH. "At these
newly identified loci, fine mapping or sequencing might lead to identification of the
causal variants, and thus expand our knowledge of the underlying physiology and biological
regulation of these traits," said lead author Chunyan He, who was a doctoral student
in the HSPH Department of Epidemiology while conducting the research. "Insights into
the genetic factors in?uencing the timing of menarche and natural menopause might shed
light on normal reproductive function and the prevention of the diseases associated with
these two traits."
Sodium channel blocker shows
promise as a potential treatment for cystic fibrosis
Cystic fibrosis patients may benefit from a
new therapy that increases airway hydration, preventing the buildup of mucous, which is a
key factor in the disease, according to researchers at Parion Sciences in Durham, N.C. The
research will be presented on Sunday, May 17, during the American Thoracic Society's 105th
International Conference in San Diego. "Our results suggest that we have identified a
new agent that acts directly on a specific pathway, which is involved in the development
of cystic fibrosis," said lead author Andrew Hirsh, Ph.D., senior director of drug
discovery and preclinical development for Parion Sciences.
In normal respiration, the moist surface of the airway allows individuals to effectively
clear mucous, keeping airways open and viable. But in individuals with cystic fibrosis,
the hydration level of the airway is altered and the airway mucous builds up, interfering
with normal respiration. One of the mechanisms causing airways to not clear mucous
correctly in these patients involves the body's natural homeostasis of sodium which, when
absorbed too quickly from the surface of the airway, causes moisture to become absorbed
too quickly. "Cystic fibrosis patients have a genetic ion transport defect, which
decreases the hydration level on the airway surface and therefore reduces the body's
ability to effectively clear mucous, which is a primary defense mechanism of the
respiratory system," Dr. Hirsh said. "Diminished mucous clearance leads to
chronic respiratory infection and impaired pulmonary function. Currently there are no
therapies available to specifically target this channel in patients with cystic
fibrosis." The aerosol-based therapy uses a specific epithelial sodium
channel-blocking agent called GS-9411, which prevents sodium from being absorbed across
the airway, allowing the surface to remain moist. The increase in moisture allows
individuals to more effectively clear the airway of mucous and infectious agents.
Sick of the same old thing? U of
Minnesota researcher finds satiation solution
Have you ever gotten sick of pizza, playing the same computer game, or had a song stuck in
your head for so long you never wanted to hear it again? If you have, you may suffer from
variety amnesia. In new research, Joseph Redden, professor of marketing at the University
of Minnesota's Carlson School of Management, may have found a cure for your satiation
blues. "People forget about the abundance of different experiences they have had and
tend to focus on the repetition," said Redden. "Simply thinking about the
variety of songs they have listened to or meals they have eaten will make people enjoy the
activity again." Satiation, the process of consuming products and experiences to the
point where they are less enjoyable, is a big problem for consumers and retailers. In the
past, time and variety have been seen as the only ways to cure satiation. In their new
article forthcoming in the Journal of Consumer Research, Redden and co-authors find that
just recalling variety may cure satiation faster. "Intuition says that if time passes
we will like something again: we call this 'spontaneous recovery,' " said Redden.
"This isn't the whole story. People don't fully recover on their own with the mere
passage of time. If I'm sick of chocolate, simply thinking about all the other desserts
I've had since the last time I had chocolate helps cure my satiation. Time doesn't seem to
do that very well." In one of the three studies conducted for this research, Redden
and his co-authors asked participants to listen to the chorus of a favorite song 20 times
in a row. Then they were asked to rate the clip. Not surprisingly, after 20 repetitions
their enjoyment of the song dropped a great deal. Three weeks later, the participants came
back and half were asked to recall any television shows they'd seen since the study, while
the other half listed all of the musicians they'd listened to since the first session. The
group that listed the TV shows was still just as satiated – they didn't like the
song. However, those recalling variety in the music category almost totally recovered.
"The participants' comments were the most revealing," said Redden. "Those
who recalled the TV shows were actually angry to have a song they like 'ruined,' but the
ones who recalled musicians enjoyed taking a study with music, etc. If something seems
like 'more of the same,' people are just less interested."
U of M researcher develops
brain-scanning process that could lead to major breakthroughs in epilepsy treatments
niversity of Minnesota McKnight professor Bin He has developed a new technique that has
led to preliminary successes in noninvasive imaging of seizure foci. He's technique
promises to play an important role in the treatment of epileptic seizures. He's research,
called Functional Neuroimaging, has completed its first round of testing in epilepsy data
collected at the Mayo Clinic. He's medical device images the brain while epilepsy patients
have a seizure and then allows surgeons to identify the network where the seizure is
caused. Approximately one-third of people who suffer from epileptic seizures cannot be
treated by medication, and this process could lead to further advancements in surgical
treatment.
Cocaine - Perceived as a reward by
the brain?
Cocaine is one of the oldest drugs known to humans, and its abuse has become widespread
since the end of the 19th century. At the same time, we know rather little about its
effects on the human brain or the mechanisms that lead to cocaine addiction. The latest
article by Dr. Marco Leyton, of the Montreal Neurological Institute (MNI), McGill
University and the McGill University Health Centre, which was published in the journal
Biological Psychiatry on May 15, 2009, not only demonstrates a link between cocaine and
the reward circuits in the brain but also associates the susceptibility to addiction with
these mechanisms. The results of this study show that sniffing cocaine triggers high
levels of dopamine secretion in a central region of the brain called the striatum.
Dopamine is known to play a critical role in the brain's response to reward as well as in
its response to addictive drugs. This study was carried out in ten non-addicted users of
cocaine, all of whom sniffed cocaine on one test day and placebo powder on another.
Participants underwent blood tests before and after taking the drug, and dopamine release
in the brain was measured using PET scans. "The ability of cocaine to activate
dopamine release varies markedly from person to person. Our study suggests that this is
related to how much of the drug the person consumed in the past," explained Dr.
Leyton. The more cocaine someone has used in his or her lifetime, the more the brain will
secrete dopamine during subsequent cocaine use. "It's possible therefore that the
intensity of the reward-circuit response is related to increased susceptibility to
addiction," stated Dr. Leyton. Although the relationship between the intensity of
dopamine secretion and the frequency of drug use has been demonstrated, researchers still
do not fully understand its mechanism of action. Is it the repeated stimulation of the
reward circuit that leads to addiction, or is it an inherent sensitivity to addiction that
leads to the increased secretion of dopamine? This question is not easy to answer,
especially since other factors come into play, such as other aspects of the subject's
personal history. Whatever the answer, the relationship between dopamine and cocaine means
that this hormone could be a potential target for treatment against addiction. More
research is required before treatments are available, but this study opens a new door in
this direction.
Proteomics - Finding the key
ingredients of disease
International collaboration between McGill, the McGill University Health Centre and HUPO
cooks up the right recipe. The winner of the chilli cook-off, usually has a key secret
ingredient, which is hard to identify. Similarly, many diseases have crucial proteins,
which change the dynamics of cells from benign to deadly. New findings from an
international collaboration, involving McGill University, the Research Institute of the
McGill University Health Centre (MUHC) and the Human Proteome Organisation (HUPO) just
made identifying these changes one step easier. Their findings published in Nature
Methods, show how to improve protein analysis to tease out relevant potential
disease-causing molecules. "Proteomics is the field that singles out the few
significant proteins from the hundreds that may be present in a diagnostic sample,"
says co-author and recent new recruit of the Research Institute of the MUHC and of McGill
Unversity, Dr. Tommy Nilsson. "It is important to associate the correct proteins with
the correct condition. This process is incredibly complex. The aim of our study was to
benchmark current analysis techniques worldwide and to identify potential
bottlenecks." Twenty-seven labs worldwide were sent a standard sample of proteins to
analyse using their usual techniques. Only seven of the 27 participating labs were
accurate in detecting all the proteins and in the more challenging part of the study, only
one lab succeeded. However, further analysis of their raw data, showed that all the
proteins had been initially detected by all the labs involved but they had been rejected
in later analyses. "Our centralized analysis showed us the problems encountered while
conducting this type of testing," says Dr. John Bergeron, senior author from McGill
University and HUPO. "We found that a major contributing factor to erroneous
reporting is at the database level. We expect once databases and search engines improve,
the accuracy of reporting will as well."
Genetic factors may predict
depression in heart disease patients
Individuals with heart disease are twice as likely to suffer from depression as the
general population, an association the medical community has largely been unable to
explain. Now, a new study by researchers at The Miriam Hospital, in conjunction with The
Montréal Heart Institute, University of Montréal and McGill University, reveals there
may be genetic variations that contribute to depression in heart disease patients.
According to the study, published in the April issue of the American Journal of Medical
Genetics Part B: Neuropsychiatric Genetics, the genes are related to the vascular system,
suggesting that vascular health – which includes the body's network of blood vessels,
arteries and veins – may be a predictor of depression in individuals with heart
disease. This is the first large-scale genetic study of depressive symptoms in cardiac
patients. "Depression can significantly impact quality of life for heart disease
patients and can increase the risk for additional cardiac events or even death," said
lead author Jeanne M. McCaffery, PhD, of The Miriam Hospital's Weight Control and Diabetes
Research Center. "Although it's too early to begin to speculate about the possible
clinical implications of these findings, it's intriguing to think that there may be a
genetic explanation as to why people with heart disease are more susceptible to
depression." Researchers say several mechanisms have been suggested to account for
the greater prevalence of depression among cardiac patients, including the stress of a
poor prognosis and systemic inflammation, although little attention has been paid to date
about the possibility of a genetic cause. According to previous studies, approximately 15
to 20 percent of heart disease patients experience depression, with the highest rates seen
among those who recently experienced a cardiac event. In contrast, depression affects
about seven percent of the general population in the United States. The current study
focused on 977 patients with cardiovascular disease who had either a 50 percent or higher
blockage in at least one major coronary artery or a documented heart attack. Of these
patients, 21 percent were female and the average age was 59 years. Symptoms of depression
were measured using a standardized self-reported questionnaire recommended by the National
Heart, Lung and Blood Institute (NHLBI).
Breakthrough in radiotherapy
promises targeted cancer treatment
Current radiation therapy treatment damages a patient’s healthy tissue as well as
eradicating the tumour it is intended to destroy, making the treatment especially invasive
and often causing nasty side effects. A new development in radiotherapy will enable a far
more precise and accurate treatment for cancerous tumours by using real-time images to
guide the radiation beam. Real-time image-guided radiotherapy, combining radiation
treatment with non-invasive MR imaging, would be far less harmful for patients as it would
leave less healthy tissue damaged and give radiation oncologists the possibility of
instantly modifying the treatment dose as tumours change in size and shift. Published in
issue 12 of IOP Publishing’s Physics in Medicine & Biology the findings of a
research group from the University Medical Centre Utrecht in the Netherlands are set to
“open the door to start testing MRI-guided radiation therapy in the clinic”.
'Singing brains' offers epilepsy
and schizophrenia clues
Studying the way a person's brain 'sings' could improve our understanding of conditions
such as epilepsy and schizophrenia and help develop better treatments, scientists at
Cardiff University have discovered. Research by a team working in Cardiff University's
Brain Research Imaging Centre (CUBRIC) has discovered that a person's brain produces a
unique electrical oscillation at a particular frequency when a person looks at a visual
pattern. Importantly, the team found that the frequency of this oscillation appears to be
determined by the concentration of a neurotransmitter chemical, GABA, in the visual cortex
of each person's brain. The more GABA was present, the higher the frequency or
"note" of the oscillation. GABA is a key inhibitory neurotransmitter and is
essential for the normal operation of the brain. The research was primarily carried out by
Dr Suresh Muthukumaraswamy and Dr Richard Edden and has just been published in the
Proceedings of the National Academy of Sciences, USA. Professor Krish Singh of Cardiff
University's School of Psychology, who led the research, said: "Using sophisticated
MEG and MRI brain imaging equipment, we've found that when a person looks at a visual
pattern their brain produces an electrical signal, known as a gamma oscillation, at a set
frequency. "In effect, each person's brain 'sings' at a different note in the range
40-70 Hz. This is similar to the notes in the lowest octaves of a standard piano keyboard
or the lower notes on a bass guitar. Importantly, we also found that this frequency
appears to be controlled by how much of an essential neurotransmitter, GABA, is present in
a person's visual cortex." The researchers believe that their findings will have
important implications for future clinical studies, especially in terms of increasing our
understanding of conditions such as epilepsy and schizophrenia, where it is known that
there may be a problem with GABA. Professor Singh added "As a result of our research,
we are already looking to share this work with our medical colleagues. In particular, we
hope that the study of gamma oscillation frequency will provide a new window into the
action of neurotransmitters such as GABA and how their function is compromised in diseases
such as epilepsy and schizophrenia." "We also believe that our findings could
have important implications for the development, production and effectiveness of drugs to
treat these and other neurological conditions."
Salmonella's sweet tooth predicts
its downfall
For the first time UK scientists have shown what the food poisoning bug Salmonella feeds
on to survive as it causes infection: glucose. Their discovery of Salmonella's weakness
for sugar could provide a new way to vaccinate against it. The discovery could also lead
to vaccine strains to protect against other disease-causing bacteria, including superbugs.
"This is the first time that anyone has identified the nutrients that sustain
Salmonella while it is infecting a host's body," says Dr Arthur Thompson from the
Institute of Food Research. The nutrition of bacteria during infection is an emerging
science. This is one of the first major breakthroughs, achieved in collaboration with Dr.
Gary Rowley at the University of East Anglia. Salmonella food poisoning causes infection
in around 20 million people worldwide each year and is responsible for about 200,000 human
deaths. It also infects farm animals and attaches to salad vegetables. During infection,
Salmonella bacteria are engulfed by immune cells designed to kill them. But instead the
bacteria multiply. Salmonella must acquire nutrients to replicate. The scientists focused
on glycolysis, the process by which sugars are broken down to create chemical energy. They
constructed Salmonella mutants unable to transport glucose into the immune cells they
occupy and unable to use glucose as food. These mutant strains lost their ability to
replicate within immune cells, rendering them harmless"Our experiments showed that
glucose is the major sugar used by Salmonella during infection," said Dr Thompson.
Research points to a new way to
protect kidneys threatened by insufficient blood or toxins
Better treatments for acute renal failure may be possible by blocking the mitochondrial
fragmentation that occurs when kidneys don't get enough blood or are exposed to toxins,
researchers at the Medical College of Georgia report in the may issue of The Journal of
Clinical Investigation. Stress on kidney cells caused by vascular obstruction, trauma,
chemotherapy, even antibiotics cause mitochondria - the cell’s powerhouse - to
“go to pieces,” says Dr. Zheng Dong, cell biologist in the MCG Schools of
Medicine and Graduate Studies and at the Charlie Norwood Veterans Affairs Medical Center.
Fragmentation sets in motion a chain of events that prompts kidney cells to commit suicide
and leads to acute renal failure. "When mitochondrial fragmentation is blocked, it
can save the cells and the kidneys," he says.
Protein that suppresses androgen
receptors could improve prostate cancer diagnosis, treatment
A protein that helps regulate expression of androgen receptors could prove a new focal
point for staging and treating testosterone-fueled prostate cancer, Medical College of
Georgia researchers say. Levels of the protein, ?arrestin2, are lower in some prostate
cancer cells than in normal prostate cells while expression of testosterone-fed androgen
receptors is higher, they report in Proceedings of the National Academy of Sciences Online
Early Edition this week. "An increase in the number of androgen receptors is believed
responsible for prostate cancer progression in men with advanced disease," says the
study's corresponding author, Dr. Yehia Daaka, Distinguished Chair in Oncologic Pathology
in the MCG School of Medicine.
ISU researcher identifies genetic
pathway responsible for much of plant growth
Researchers at Iowa State University have discovered a previously unknown pathway in plant
cells that regulates plant growth. Yanhai Yin, an assistant professor in genetics,
development and cell biology, examined signaling mechanisms of a plant hormone called
brassinosteroids. The hormone controls the growth of cells. The brassinosteroids (BRs)
have a major impact on how large the plant grows, says Yin. "Previously, we knew that
steroids promote growth," said Yin. "In model plants like Arabidopsis (a
relative of mustard) and crops such as corn and rice, if you have more steroids, you have
more growth, and if you have less steroids, you have less growth and the plant is
smaller." Now Yin knows that the HERK1 (named for Hercules -- the Greek and Roman god
who possessed superhuman strength) pathway, induced by BRs, is controlling much of that
growth.
Schizophrenia does not increase
risk of violent crime
A new study from the Swedish medical university Karolinska Institutet and the University
of Oxford finds that the severe mental disorder schizophrenia only marginally increases
the risk of committing violent crime. Rather, the overrepresentation of individuals with
schizophrenia in violent crime is almost entirely attributable to concurrent substance
abuse.In the debate surrounding violent crimes referred to as "acts of madness"
or the like, it is often assumed that the violence is a direct result of the perpetrator's
mental illness. Previous research suggests that people with schizophrenia, a major
psychotic disorder, are at higher risk for violent behaviour. However, there has been some
uncertainty as to the magnitude of this risk increase and if it can really be attributed
to the violence itself or to other factors. The new study, presented in the May 20 issue
of the scientific journal JAMA, is the largest in this field to date. In it, researchers
compared the rate of violent crime in over 8,000 people diagnosed with schizophrenia
between 1973 and 2006, and a control group of 80,000 people from the general population of
Sweden. Twenty-eight per cent of those with schizophrenia and co-occurring substance abuse
were convicted of violent crime, compared to eight per cent of those with schizophrenia
and no substance abuse, and five per cent of the general population.
Automated analysis of MR images may
identify early Alzheimer’s disease
Analyzing MRI studies of the brain with software developed at the Martinos Center for
Biomedical Imaging at Massachusetts General Hospital (MGH) may allow diagnosis of
Alzheimer's disease and of mild cognitive impairment, a lesser form of dementia that
precedes the development of Alzheimer's by several years. In their report that will appear
in the journal Brain and has been released online, the MGH/Martinos team show how their
software program can accurately differentiate patients with mild cognitive impairment or
Alzheimer's disease from normal elderly individuals based on anatomic differences in brain
structures known to be affected by the disease. "Traditionally Alzheimer's has been
diagnosed based on a combination of factors – such as a neurologic exam, detailed
medical history and written tests of cognitive functioning – with neuroimaging used
primarily to rule out other diseases such as stroke or a brain tumor," says Rahul
Desikan MD, PhD, of the Martinos Center and Boston University School of Medicine, lead
author of the Brain paper. "Our findings show the feasibility and importance of using
automated, MRI-based neuroanatomic measures as a diagnostic marker for Alzheimer's
disease." The researchers note that mild cognitive impairment occurs in about 20
percent of elderly individuals – as many as 40 percent of those over 85 – 80
percent of whom develop Alzheimer's within five or six years. Since drugs that may slow
the progression of Alzheimer's are in development, the ability to treat patients in the
earliest stages of the disease may significantly delay progression to dementia. To
investigate whether MR imaging can produce diagnostic markers for mild cognitive
impairment and Alzheimer's disease, the research team used FreeSurfer – an openly
available imaging software package developed at the Martinos Center and the University of
California at San Diego – to examine a number of neuroanatomic regions across a range
of normal individuals and patients with mild cognitive impairment and Alzheimer's disease.
BPA, chemical used to make
plastics, found to leach from polycarbonate drinking bottles into humans
A new study from Harvard School of Public Health (HSPH) researchers found that
participants who drank for a week from polycarbonate bottles, the popular, hard-plastic
drinking bottles and baby bottles, showed a two-thirds increase in their urine of the
chemical bisphenol A (BPA). Exposure to BPA, used in the manufacture of polycarbonate and
other plastics, has been shown to interfere with reproductive development in animals and
has been linked with cardiovascular disease and diabetes in humans. The study is the first
to show that drinking from polycarbonate bottles increased the level of urinary BPA, and
thus suggests that drinking containers made with BPA release the chemical into the liquid
that people drink in sufficient amounts to increase the level of BPA excreted in human
urine. In addition to polycarbonate bottles, which are refillable and a popular container
among students, campers and others and are also used as baby bottles, BPA is also found in
dentistry composites and sealants and in the lining of aluminum food and beverage cans.
(In bottles, polycarbonate can be identified by the recycling number 7.) Numerous studies
have shown that it acts as an endocrine-disruptor in animals, including early onset of
sexual maturation, altered development and tissue organization of the mammary gland and
decreased sperm production in offspring. It may be most harmful in the stages of early
development. "We found that drinking cold liquids from polycarbonate bottles for just
one week increased urinary BPA levels by more than two-thirds. If you heat those bottles,
as is the case with baby bottles, we would expect the levels to be considerably higher.
This would be of concern since infants may be particularly susceptible to BPA's
endocrine-disrupting potential," said Karin B. Michels, associate professor of
epidemiology at HSPH and Harvard Medical School and senior author of the study. The
researchers, led by first author Jenny Carwile, a doctoral student in the department of
epidemiology at HSPH, and Michels, recruited Harvard College students for the study in
April 2008. The 77 participants began the study with a seven-day "washout" phase
in which they drank all cold beverages from stainless steel bottles in order to minimize
BPA exposure. Participants provided urine samples during the washout period. They were
then given two polycarbonate bottles and asked to drink all cold beverages from the
bottles during the next week; urine samples were also provided during that time.The
results showed that the participants' urinary BPA concentrations increased 69% after
drinking from the polycarbonate bottles. (The study authors noted that BPA concentrations
in the college population were similar to those reported for the U.S. general population.)
Previous studies had found that BPA could leach from polycarbonate bottles into their
contents; this study is the first to show a corresponding increase in urinary BPA
concentrations in humans.
Gene Therapy Could Expand Stem
Cells' Promise
Once placed into a patient's body, stem cells intended to treat or cure a disease could
end up wreaking havoc simply because they are no longer under the control of the
clinician. But gene therapy has the potential to solve this problem, according to a
perspective article from physician-scientists at NewYork-Presbyterian Hospital/Weill
Cornell Medical Center published in a recent issue of the journal Cell Stem Cell. The
paper details strategies for genetically modifying stem cells prior to transplantation in
order to ensure their safety. "Stem cell therapy offers enormous potential to treat
and even cure serious diseases. But wayward stem cells can turn into a runaway train
without a conductor. This is an issue that can be dealt with and we have the technology to
do that in the form of gene therapy," says senior author Dr. Ronald G. Crystal, chief
of the Division of Pulmonary and Critical Care Medicine at NewYork-Presbyterian
Hospital/Weill Cornell Medical Center, and the Bruce Webster Professor of Internal
Medicine and Professor of Genetic Medicine at Weill Cornell Medical College. Stem cells
have the capacity to differentiate into any of the different tissues making up the human
body, thus holding the promise of treating or curing diseases such as multiple sclerosis
or spinal-cord injury by replacing diseased cells with healthy cells. But unlike other
therapies such as chemotherapy, antibiotics or aspirin, stem cells have no expiration
date, and that poses a real problem. "Almost all therapeutics we use have a half
life. They only last a certain amount of time," Dr. Crystal says. "Stem cells
are the opposite. Once the future stem cell therapist does the therapy, stem cells have
the innate potential to produce more cells."
Genetic testing for breast or
ovarian cancer risk may be greatly underutilized
Although a test for gene mutations known to significantly increase the risk of hereditary
breast or ovarian cancer has been available for more than a decade, a new study finds that
few women with family histories of these cancers are even discussing genetic testing with
their physicians or other health care providers. In a report in the Journal of General
Internal Medicine, which has been released online, investigators from the Massachusetts
General Hospital (MGH) Institute of Health Policy and Dana-Farber Cancer Institute note
that their findings illustrate the challenges of bringing genetic information into
real-world clinical practice. "Testing for BRCA1 and 2 mutations has been around a
long time and should be a good indicator of whether genetic testing is making its way into
regular medical practice," says Douglas Levy, PhD, of the MGH Institute for Health
Policy, the study's lead author. "When a well-established genetic test is not being
incorporated into clinical practice when appropriate, we are a long way from meeting the
promise of personalized, genetically-tailored medical care." Most women's lifetime
risk of breast cancer is about 13 percent, and the risk for ovarian cancer is less than 2
percent. But women with mutations in the BRCA1 or BRCA2 genes may be 3 to 7 times more
likely to develop breast cancer and 9 to 30 times more likely to develop ovarian cancer
than women with unaltered forms of the genes. Several organizations have issued clinical
guidelines designating who should be screened for BRCA1/2 mutations, and while there have
been discrepancies among the guidelines, all of them include a history of breast or
ovarian cancer in close relatives among the criteria indicating elevated risk. The authors
note that most U.S. health insurers cover at least part of the cost of BRCA1/2 testing for
at-risk women. The current study analyzed data from the 2000 and 2005 National Health
Interview Surveys, both of which included supplementary questions assessing cancer
control. More than 35,000 women participating in those surveys did not have a personal
history of breast or ovarian cancer, and around 1 percent of them were determined to be at
high risk because a mother, sister or daughter had such a tumor. Among these high-risk
women, about half were aware that genetic testing was available, but only 10 percent had
discussed it with a physician, less than 5 percent had been advised to have the test, and
only 2 percent had done so.
Lower legal drinking age increases
poor birth outcomes
mid renewed calls to consider reducing the legal drinking age, a new University of Georgia
study finds that lower drinking ages increase unplanned pregnancies and pre-term births
among young people. “Our findings suggest that a lower drinking age increases risky
sexual behavior among young people, and that leads to more unplanned pregnancies that
result in premature birth and low birth weight,” said study author Angela Fertig,
assistant professor in the UGA College of Public Health. “The take-home message is
that when it’s easier for young people to get alcohol, birth outcomes are
worse.” Fertig, who is also a public service assistant in the university’s Carl
Vinson Institute of Government, co-authored the study with Tara Watson, assistant
professor of economics at Williams College in Massachusetts. Their results appear in the
May issue of the Journal of Health Economics. The team examined birth records and survey
data on alcohol use for the years 1978 to 1988, a period when state minimum drinking age
laws were in flux. Fertig said the consensus among researchers is that a higher minimum
drinking age reduces fatal car crashes and alcohol consumption among young adults, but
there is little data on how drinking age laws influence infant health.
LSUHSC research describes function
of key protein in cancer spread
Research led by David Worthylake, PhD, Assistant Professor of Biochemistry and Molecular
Biology at LSU Health Sciences Center New Orleans, may help lay the groundwork for the
development of a compound to prevent the spread of cancer. The research will be published
in the May 29, 2009 issue of the Journal of Biological Chemistry. During the transition
from a localized tumor to metastatic disease, cancer cells acquire the ability to detach
from their neighboring cells and move to and invade tissue at distant points in the body.
"Because tumor metastasis leads to a poor prognosis and tremendously complicates
treatment, it is of utmost importance that we understand, at a molecular level, the
processes that regulate cell adhesion, migration and invasion," notes Dr. Worthylake.
He and his colleagues studied a protein in cells that is involved in regulating cell
structure, cell-to-cell contact, and cell movement. When too much of this protein, called
IQGAP1, is produced, it can weaken cell-to-cell contacts and promote cell migration and
invasion – processes that occur during tumor metastasis. The research team focused on
the area of IQGAP1 that interacts with two smaller proteins Cdc42 and Rac which, when
activated, contribute to cell destabilization, cell movement, and invasion. This region on
IQGAP1 is related to proteins that accelerate deactivation of another small protein
similar to Cdc42 and Rac. However, IQGAP1 does not deactivate Cdc42 and Rac – in
fact, IQGAP1 prolongs their activated states. The researchers determined the atomic
structure of this region of IQGAP1 and furthermore, built a model of their IQGAP1
structure bound to the previously determined structure of Cdc42 in order to understand why
IQGAP1 does not deactivate Cdc42. The model provides detailed information about the
(likely) specific contacts made between IQGAP1 and Cdc42. The model also shows that IQGAP1
is missing a key component required to rapidly deactivate Cdc42, and that binding to
IQGAP1 likely disturbs the positions of components of Cdc42 that are required for even
normal rates of deactivation, explaining how IQGAP1 prolongs the activated state of Cdc42.
Regulating the sugar factory in
diabetes
Scientists in Sydney and Boston believe they may have identified a gene that controls
abnormal production of sugar in the liver, a very troublesome problem for people with
diabetes. The liver is the sugar factory for the body - when blood sugar (glucose) levels
fall, the liver makes and releases more. In people with diabetes, especially Type 2
diabetes, the liver doesn't stop making sugar when it should, so blood sugar levels can
rise overnight while they sleep even though they haven't eaten. Dr Jenny Gunton, diabetes
specialist and endocrinologist from Sydney's Garvan Institute of Medical Research, in
collaboration with Dr Xiao Hui Wang and Professor Ronald Kahn from Harvard Medical School
and Joslin Diabetes Centre in Boston, have published their findings in the journal Cell
Metabolism, now online. "A lot of my patients will complain that they go to bed with
a blood sugar of 5 and wake up with a blood sugar of 12," said Dr Gunton. "It
upsets people when their blood sugar behaves as if they're getting up in the night and
having a really big snack. I have to tell them it's just one of those unfair things about
having diabetes." People with Type 2 diabetes do not produce enough insulin in the
pancreas after a meal. At the same time, they are less able to use that insulin to move
glucose into fat and muscle cells, a condition known as 'insulin resistance'. With her
colleagues in Boston, Gunton has been studying a transcription factor, or kind of 'master
regulator', called ARNT, which controls expression of other genes involved in processes
like glucose breakdown and insulin production. In an earlier study, the group showed that
there is 90% less ARNT in insulin-producing cells of people with Type 2 diabetes. The
current study looks at how ARNT might be affecting the liver, and its results confirmed Dr
Gunton's suspicions. "We've shown that there's likely to be decreased ARNT in the
liver of people with Type 2 diabetes compared to people without Type 2 diabetes," she
said.
New direction needed for obesity
research, Deakin health expert claims
Most of the current obesity research is not proving helpful in finding solutions to the
growing international epidemic, according to a Deakin University public health expert.
Professor Boyd Swinburn believes that research funding would be better directed at testing
possible solutions rather than continuing to unpick what is causing the rise in obesity.
"It seems counter intuitive, but knowing the causes or mechanisms for weight gain
does not always help with identifying the solutions," he said. "For an
individual person, we know the causes of weight gain over time include the obesogenic
environment, genetic predisposition, and increasing age – none of which can be
influenced by the health professional trying to help the person lose weight. At a
population level, the commercial drivers which promote our overconsumption of food are
unlikely to be reversed by the private sector because there is no commercial gain for the
food industry to promote eating fewer calories. "The twin bottom line is that we need
to re-orient our research towards testing potential solutions rather than just better
identifying the problem. The most promising approaches for individuals and populations
will involve identifying the right set of 'rules' or policies which lead to sustainable
environmental and behavioural changes." Professor Swinburn says that identifying
solutions needs specific solutions-oriented research and unfortunately most of the current
research into obesity is problem-oriented. "Interestingly, the solutions that are the
most likely to work seem to be 'rule-based' solutions," Professor Swinburn explained.
Ultrasound more cost efficient than
other medical imaging choices
In comparing ultrasound with other medical imaging methods such as MRI and CT scans, a
literature review of published studies in the May/June issue of Journal of Diagnostic
Medical Sonography (JDMS) describes the use of ultrasound to provide an accurate diagnosis
more cost effectively than the alternatives. Since its first uses in the 1950s, ultrasound
has been utilized mostly in hospital settings. But with the development of less costly,
portable equipment, its use has expanded to doctor's offices, trauma settings, and even to
outer space. The article compares the use of ultrasound to magnetic resonance (MR)
imaging, computed tomography (CT), contrast angiography (CA), and single-photon emission
computed tomography (SPECT). Ultrasound provides the ability to rapidly evaluate and
diagnose abnormalities throughout the spectrum of clinical medicine," write the
authors S. Michelle Bierig, MPH, RDCS, RDMS, FASE, FSDMS and Anne Jones, RN, BSN, RVT,
RDMS, FSVU. "Its accuracy and cost-effectiveness in a variety of applications has led
to its widespread adoption and use. The utilization of ultrasound compared to the use of
alternative imaging methods leads to increased cost efficiency in the diagnosis and
management of patients.""
Protein from Algae Shows Promise
for Stopping SARS
A protein from algae may have what it takes to stop Severe Acute Respiratory Syndrome
(SARS) infections, according to new research. A recent study has found that mice treated
with the protein, Griffithsin (GRFT), had a 100 percent survival rate after exposure to
the SARS coronavirus (SARS-CoV), as compared to a 30 percent survival for untreated mice.
Team Tracks Nanotube Cancer Killers
in Live Tissue
Nanotechnology scientists at two Arkansas research institutions have developed a method of
detecting, tracking, and killing cancer cells in real time with carbon nanotubes. The
discovery opens the prospect of a new, major front in the fight to eradicate cancer with
promise for a new generation of cancer treatment beyond surgery, radiation, and
chemotherapy. Dr. Alex Biris, University of Arkansas at Little Rock (UALR) chief scientist
at the Nanotechnology Center and assistant professor of applied science in University's
Donaghey College of Engineering and Information Technology, and Dr. Vladimir P. Zharov,
professor and director of the Phillips Classic Laser and Nanomedicine Laboratories in the
University of Arkansas for Medical Sciences (UAMS) Winthrop P. Rockefeller Cancer
Institute, published their findings in the latest issue of the Journal of Biomedical
Optics. “Until now, nobody has been able to fully understand and study in vivo and in
real time how these nanoparticles travel through a living system,” Biris said.
“By using Raman spectroscopy, we showed that it is possible not only to monitor and
detect nanomaterials moving through the circulation, but also to detect single cancer
cells tagged with carbon nanotubes. In this way, we can measure their clearance rate and
their biodistribution kinetics through the lymph and blood systems.”Zharov emphasized
that in vivo Raman flow cytometry is promising for the detection and identification of a
broad spectrum of various nanoparticles with strong Raman scattering properties, such as
cells, bacteria, and even viruses.
Identifying Pathways in the Brain
to Understand the Underlying Molecular Mechanism of Huntington's Disease
Florida Atlantic University researcher Dr. Jianning Wei, assistant professor of biomedical
sciences in the Charles E. Schmidt College of Biomedical Science at FAU, has received a
grant from the National Institutes of Health (NIH) to further her research into the
molecular mechanisms of Huntington’s disease (HD). Named after American physician
George Huntington, HD is a highly complex genetic, neurological disorder that causes
certain nerve cells in the brain to waste away. The disease, characterized by a selective
loss of neurons in the brain, affects the basal ganglia, which controls motor control,
cognition, learning and emotions. It also affects the outer surface of the brain, or the
cortex which controls thought, perception, and memory. Wei and her colleagues are working
to identify the pathways in the brain that are altered in response to mutant proteins, as
well as to understand the cellular processes impacted by the disease in order to
facilitate the development of effective pharmacological interventions. HD is a fatal,
inherited disease caused by abnormal repeats of a small segment in an individual's DNA, or
genetic code. The production of malfunctioning proteins in the body are results of these
mutations, and the more it is repeated, the worse the disease. A person who has the
disease carries one normal copy of the gene and one mutated copy in his or her cells.
These abnormal repeats also are involved in several other neurodegenerative diseases.
Although the mutated forms of these genes are known for their devastating effects, their
normal forms are critical for nerve function, embryonic development and other bodily
processes. “The underlying molecular mechanism of HD remains elusive,” said Wei.
“We hope that the information we obtain from our studies will improve the current
understanding of the molecular pathways that are altered in response to mutant huntingtin
or mHtt.” Wei’s findings may also represent a universal mechanism in the
pathogenesis of neurodegenerative diseases that are involved with protein misfolding and
aggregation (a phenomenon that occurs in many highly debilitating disorders including
neurodegenerative diseases). Preliminary data from their findings using an in vitro cell
model of HD suggest that there is a novel mechanism for mHtt induced cell death, or
apoptosis. Apoptosis has been proposed as one of the mechanisms leading to neuronal death
in HD. With this NIH grant, Wei and her colleagues will be testing their hypothesis in a
mouse model of HD. Although recent studies provide important clues, precisely how mHtt
triggers apoptosis still remains unclear.
Life in the universe? Almost
certainly
We are likely not alone in the universe, though it may feel like it, since life on other
planets is probably dominated by microbes or other nonspeaking creatures, according to
scientists who gave their take on extraterrestrial life at Harvard last week.
Healing powers of infra-red
Researchers at The Vision Centre have discovered compelling evidence that infra?red light
can reduce the severe damage caused to eyesight by exposure to bright light. Their world
first finding opens the possibility for one day successfully and painlessly treating some
forms of vision loss caused by overexposure to sunlight or artificial light. “It has
been known for some time that infra?red light, at certain wavelengths, can promote healing
of various body cells. We decided to carry out a series of experiments to see if it could
restore or prevent damage to vision cells that have been exposed to very bright
light,” says Dr Krisztina Valter of The Vision Centre (ARC Centre of Excellence in
Vision Science)and The Australian National University.
Saffron - the secret of good sight
The herb saffron may hold one of the keys to preventing the loss of sight in old age
– and may even help to improve vision in people suffering certain blinding eye
diseases. Research by Professor Silvia Bisti of the ARC Centre of Excellence in Vision
Science (The Vision Centre) and University of L’Aquila, Italy, has established that
saffron has remarkable effects on the genes which regulate the performance of the
eye’s key vision cells. Her research has shown that the high?priced golden culinary
herb made from crocus flowers not only protects the vision cells (photoreceptors) from
damage, it may also acts to slow and possibly even reverse the course of blinding diseases
such as age?related macular degeneration (AMD) and retinitis pigmentosa.A clinical trial
with patients suffering AMD in Rome has found early indications that treatment with a
dietary supplement of saffron may cause damaged eye cells to recover. “Saffron is not
simply an anti?oxidant. It seems to possess a number of other properties which are
protective to vision,” Prof Bisti, who is currently visiting colleagues in The Vision
Centre in Australia, says.“For example it appears to affect genes which regulate the
fatty acid content of the cell membrane, and this makes the vision cells tougher and more
resilient. “Secondly we have shown in animal models that a saffron diet will protect
the eye from the damaging effects of bright light – something we all suffer whenever
we go out in the sun.”Prof. Bisti says a third line of research has found that
saffron is active in affecting genetic diseases of the eye, such as retinitis pigmentosa,
which can cause life?long blindness in young people. Animal research here too offers the
prospect of slowing down the progression of sight loss.
Vitamin D may lessen age-related
cognitive decline
Eating fish – long considered ‘brain food’ – may really be good for
the old grey matter, as is a healthy dose of sunshine, new research suggests. University
of Manchester scientists, in collaboration with colleagues from other European centres,
have shown that higher levels of vitamin D – primarily synthesised in the skin
following sun exposure but also found in certain foods such as oily fish – are
associated with improved cognitive function in middle-aged and older men. The study,
published in the Journal of Neurology, Neurosurgery and Psychiatry, compared the cognitive
performance of more than 3,000 men aged 40 to 79 years at eight test centres across
Europe. The researchers found that men with higher levels of vitamin D performed
consistently better in a simple and sensitive neuropsychological test that assesses an
individual’s attention and speed of information processing. “Previous studies
exploring the relationship between vitamin D and cognitive performance in adults have
produced inconsistent findings but we observed a significant, independent association
between a slower information processing speed and lower levels of vitamin D,” said
lead author Dr David Lee, in Manchester’s School of Translational Medicine. “The
main strengths of our study are that it is based on a large population sample and took
into account potential interfering factors, such as depression, season and levels of
physical activity. “Interestingly, the association between increased vitamin D and
faster information processing was more significant in men aged over 60 years, although the
biological reasons for this remain unclear.” “The positive effects vitamin D
appears to have on the brain need to be explored further but certainly raise questions
about its potential benefit for minimising ageing-related declines in cognitive
performance.”
Study Offers Insight Insights About
How Industry Funding Compromises Integrity in Academic Research
A new study from the University of Virginia Health System has found that academic
researchers who are highly reliant on industry support are most likely to have experienced
questionable pressure from sponsors and to have first-hand knowledge of integrity breeches
within their work environment. Those breeches not only compromise the well-being of
medical research participants but also impact research initiatives, publication of
results, interpretation of research data and scientific advancement. Funded by the
National Institutes of Health, through the Office of Research Integrity, the UVA study was
published in the March 2009 issue of Accountability in Research and marks the first
attempt to acquire updated empirical data about financial arrangements and conflicts of
interest between industry and investigators at academic research institutions. The study
was conducted via a survey mailed to 1,548 clinical and nonclinical researchers at the 33
U.S. universities that receive the most research funding. To encourage candor and protect
anonymity, the survey did not ask respondents to report their own behavior. Rather, it
asked about their first-hand knowledge of questionable research integrity practices in
their institutions and departments.
Researchers Uncover Mechanism That
Allows Influenza Virus To Evade The Body’s Immune Response
Researchers at the University of Southern California (USC) have identified a critical
molecular mechanism that allows the influenza virus to evade the body’s immune
response system. The study will be published in the May 21 issue of the journal Cell Host
& Microbe. “We have found a mechanism that the influenza virus uses to inhibit
the body’s immune response that emphasizes the vital role of a certain protein in
defending against viruses,”,” says Jae Jung, Ph.D., professor and chair of the
Department of Molecular Microbiology and Immunology at the Keck School of Medicine of USC,
and the principal investigator of the study. “Along with our previous studies (Nature
2007 and PNAS 2008), this finding could provide researchers with the information needed to
create a new drug to enhance immunity and block influenza virus infection and
replication.”Several specific intracellular receptors are responsible for detecting
the virus and activating the body’s defensive mechanisms. When a virus’ RNA
enters the intracellular fluid, a receptor known as retinoic-acid-inducible gene I (RIG-I)
detects it and triggers a response that limits virus replication and calls the body’s
defenses into action. RIG-I acts as the sensor and security force against attacks, Jung
explains. Then, a protein known as TRIM25 helps RIG-I transmit an alarm signal, which
ultimately floods the cell and surrounding tissue with antiviral interferons. The
influenza virus is highly infectious and poses a serious and sometimes deadly health risk
because of its ability to mutate into new strains and spread quickly during seasonal
epidemics, as seen in the recent outbreak of the H1N1 swine flu virus, Jung says.
Researchers have long been working to understand how respiratory influenza is able to slip
past the body’s innate immune responses. They have found that the influenza A virus
has evolved by incorporating Non-structural protein 1 (NS1) into its genome to escape the
RIG-I alarm system. This process is one reason why the virus kills an average of 36,000
people every year. In fact, the 1918 “Spanish flu” pandemic influenza virus,
which killed over 40 million people worldwide, muted the RIG-I response and interferon
activity much more efficiently than contemporary flu viruses, Jung notes.
Radical blow for snotty arteries
Controlling the green stuff in snot could help treat heart disease, reveals Professor
Michael Davies from the Faculty of Medicine and the Heart Research Institute. In an
exciting discovery, researchers from The University of Sydney, the Free Radical Centre at
the Heart Research Institute (HRI), and the Queensland University of Technology have found
agents that could stop the progression of heart disease by preventing damage by an enzyme
also found in snot."It might sound disgusting, but the same goop that makes snot
green gets dumped in our arteries during heart disease", Professor Davies. Snot
appears green due to the presence of the enzyme, myeloperoxidase.
New Data Show Drinking While
Pregnant Still a Problem
The number of women who drink alcohol while pregnant is not decreasing, according to a 15
year-study by the Centers for Disease Control and Prevention. Approximately 1 in 8 women
drank any amount of alcohol while pregnant, the study says. The drinking patterns
persisted despite repeated warnings from surgeons general about the dangers of drinking
alcohol while pregnant. The surgeons general have told pregnant women, and women who may
become pregnant to abstain from alcohol consumption in order to eliminate the chance of
giving birth to a baby with alcohol related birth defects.The CDC analysis, as well as a
study also published today by the U.S. Substance Abuse and Mental Health Services
Administration shows that far too many women use substances (especially alcohol) during
their pregnancies. The CDC study, “Alcohol Use Among Women of Childbearing Age,
United States, 1991-2005,” is in the CDC?s Morbidity and Mortality Weekly Report.The
CDC study also found that 1 of every 50 pregnant women engaged in binge drinking each year
during the 15 years. “Exposure to alcohol can cause lifelong physical and mental
disabilities that are preventable by avoiding alcoholic drinks while pregnant,” said
Edwin Trevathan, director of the CDC?s National Center on Birth Defects and Developmental
Disabilities. “All women should know that there is no known safe amount of alcohol to
drink or safe time to drink it during pregnancy. We encourage all women to pay attention
to the surgeon general warnings.”The study found that pregnant women most likely to
report any alcohol use were 35-44 years of age (17.7 percent), college graduates (14.4
percent), employed (13.7 percent), and unmarried (13.4 percent). Pregnant women who binge
drink were more likely to be employed and unmarried than were pregnant women who did not
binge drink. This study did not examine the reasons why women are still drinking while
pregnant.
Old Stain in a New Combination
Methylene blue can curb the spread of malaria parasites when administered together with
new malaria medication / Heidelberg researchers publish in PLoS One. New combinations of
agents based on the oldest synthetic malaria drug, the methylene blue stain, can curb the
spread of malaria parasites and make a significant contribution to the long-term
eradication called for by the international “Roll Back Malaria Initiative.” In a
study on 160 children with malaria in Burkina Faso, specialists in tropical medicine from
the Heidelberg University Hospital have shown that in combination with newer malaria
drugs, methylene blue prevents the malaria pathogen in infected persons from being
re-ingested by mosquitoes and then transmitted to others and is thus twice as effective as
the standard therapy. The results of the study were published in May 2009 in the online
journal PLoS One. Malaria is still one of the deadliest tropical diseases. Every year, 300
million people are infected with malaria and more than one million of them die or suffer
severe brain damage. Children under five years are particularly susceptible.
Protein identified as critical to
insulating the body's wiring could also become treatment target
A new protein identified as critical to insulating the wiring that connects the brain and
body could one day be a treatment target for divergent diseases, from rare ones that lower
the pain threshold to cancer, Medical College of Georgia researchers say. They report this
week in Proceedings of the National Academy of Sciences Online Early Edition that in the
peripheral nervous system that controls arms and legs, the protein erbin regulates the
protein neuregulin 1, stabilizing and interacting with the ErbB2 receptor on Schwann cells
so they can make myelin, which insulates the wiring. Their studies in mice have shown that
when erbin is missing or mutated, the insulation is inadequate, slowing communication.
"Erbin is like a tuner to make signaling stronger or weaker," says Dr. Lin Mei,
the study's corresponding author and director of MCG's Institute of Molecular Medicine and
Genetics. Without erbin, the myelin production system falls apart. Eventually raw,
over-exposed nerves can die.
Mutant genes in high-risk childhood
leukemias identified
A research team has pinpointed a new class of gene mutations, which identify cases of
childhood acute lymphoblastic leukemia (ALL) that have a high risk of relapse and death.
The finding suggests specific drugs that could treat this high-risk leukemia subtype in
children, particularly because such drugs are already in clinical trials for similar blood
diseases in adults. While the cure rate in pediatric ALL has reached about 85 percent, the
remaining high-risk cases have proven especially intractable because they arise from
different, unidentified genetic mutations. Discovery of the mutations was led by
scientists from St. Jude Children's Research Hospital, the Children's Oncology Group
(COG), the University of New Mexico Cancer Research and Treatment Center, Albuquerque,
N.M., and the National Cancer Institute (NCI), part of the National Institutes of Health
(NIH). This research was done as part of the NCI Therapeutically Applicable Research to
Generate Effective Treatments (TARGET) initiative, which seeks to utilize the study of
genomics to identify therapeutic targets in order to develop more effective treatments for
childhood cancers. The article appears online May 18 in the early edition of the
Proceedings of the National Academy of Sciences. "We have made such great progress in
curing children with ALL that the main challenge is now the remaining high-risk
patients," said St. Jude Scientific Director, James Downing, M.D., a co-senior author
of the study. "We still do not know how to accurately identify these patients and
effectively treat them to provide the highest chance for a cure. The problem is that this
high-risk group is likely a heterogeneous mixture of biologic subtypes." The new
study builds on the researchers' previous genetic analysis of the leukemic cells from
pediatric ALL patients.
Strong immune response to new siRNA
drugs in development may cause toxic side effects
Small synthetic fragments of genetic material called small interfering RNA (siRNA) can
block production of abnormal proteins; however, these exciting new drug candidates can
also induce a strong immune response, causing toxic side effects. Understanding how siRNA
stimulates this undesirable immune activity, how to test for it, and how to design siRNA
drugs to avoid it are critical topics explored in a timely review article published online
ahead of print in Oligonucleotides, a peer-reviewed journal published by Mary Ann Liebert,
Inc. (www.liebertpub.com) The article is available free online at www.liebertpub.com/oli
siRNAs are duplex structures comprised of short oligonucleotide sequences. The discovery
that naturally occurring and synthetic siRNAs can effectively prevent expression of a
disease gene sparked intense interest in developing siRNAs as drugs. However, depending on
the structure and sequence of a siRNA and how it is delivered, it may induce a potent
innate immune response in humans, stimulating the release of inflammatory chemicals such
as cytokines and interferons. Exploring the possibility of designing synthetic siRNAs and
developing novel delivery methods that would exploit the drug-like capabilities of siRNA
while preventing toxic side effects, researchers are working to understand the mechanism
by which siRNA stimulates the immune system. In the article entitled, "siRNA and
Innate Immunity," Marjorie Robbins, Adam Judge, and Ian MacLachlan, from Tekmira
Pharmaceuticals (Burnaby, British Columbia, Canada), describe the different possible
mechanisms for siRNA-mediated immune activation in various cell types, present preferable
siRNA sequences and strategies for chemically modifying the siRNA to minimize its
immunostimulatory effects, and suggest experimental methods for studying the safety of
siRNA therapeutics.
Action of ghrelin hormone increases
appetite and favors accumulation of abdominal fat
The ghrelin hormone not only stimulates the brain giving rise to an increase in appetite,
but also favours the accumulation of lipids in visceral fatty tissue, located in the
abdominal zone and considered to be the most harmful. This is the conclusion of research
undertaken at Metabolic Research Laboratory of the University Hospital of Navarra,
published recently in the International Journal of Obesity. Ghrelin is a hormone produced
in the stomach and the function of which is to tell the brain that the body has to be fed.
Thus, the level of this secretion increases before eating and decreases after. It is known
to be important in the development of obesity, given that, on stimulating the appetite, it
favours an increase in body weight, explained Ms Amaia Rodríguez Murueta-Goyena, doctor
in biology and main researcher of the study. However, researchers at the University
Hospital of Navarra have discovered that, besides stimulating the hypothalamus to generate
appetite, ghrelin also acts on the tabula rasa cortex. They observed how this hormone
favoured the accumulation of lipids in visceral fatty tissue. In concrete, it causes the
over-expression of the fatty genes that take part in the retention of lipids, explained Ms
Rodríguez. It is precisely this accumulated fat in the region of the abdomen that is
deemed to be most harmful, as it is accompanied by comorbilities, visceral obesity being
related to higher blood pressure or type 2 diabetes. Moreover, being located in the
abdominal zone and in direct contact with the liver, this type of fatty tissue favours the
formation of liver fat and increases the risk of developing resistance to insulin.
Normally, on being associated with hypertension, high levels of triglycerides, resistance
to insulin and hypercholesterolemia, visceral fat favours the metabolic syndrome, the
researcher pointed out. Ghrelin can show itself in acylated or deacylated form, the
difference being in the octanoic acid present in the composition of the former, according
to Ms Rodriguez. Previously it was thought that only the acylated form was active in the
process of weight increase, but many studies point to both hormones being biologically
functional.
New strategies for cell therapy to
regenerate damaged heart
Research undertaken at the Center for Applied Medical Research (CIMA) and the University
Hospital of Navarra has shown that, in animal models, stem cells derived from bone marrow
and adipose tissue enhance heart function after a cardiac attack. In concrete, bone marrow
cells act on the damaged tissue, while fatty cells have the ability to transform
themselves into both blood vessels and cardiac cells. The results obtained with rats are
maintained over a long time period, explained biochemist Mr Manuel Mazo, principal
researcher. When a person suffers a heart attack, the artery feeding the heart is
obstructed The affected tissue dies and the scar tissue left des not contract. It is a
serious problem as cardiac muscle does not regenerate, with grave consequences for the
functional capacity of the heart, a situation which can trigger heart failure, explained
the scientist.
Geothermal energy - Instant Steam
gets into hot water
Geothermal energy -- thermal energy stored in the Earth’s crust – currently
supplies less than 1% of the world's energy. But with the advent of new technologies, such
as engineered geothermal systems (EGS) -- which can extract enough heat from lower grade
geothermal resources to generate electricity – geothermal energy could potentially be
used to produce enough electricity to meet a large portion of the world's energy demands.
A memorandum of understanding (MOU) signed between Oxford Catalysts and Potter Drilling to
explore the application of Oxford Catalysts' Instant Steam technology to Potter Drilling's
hydrothermal spallation drilling technology could bring the dream of widespread geothermal
electricity generation much closer. Geothermal wells can be slow and expensive to drill
using conventional rotary drilling methods. This is because the wells are often sunk deep
into hard crystalline rocks which are difficult and slow to penetrate and which quickly
wear down the drill bits. The slow penetration rates combined with the need for frequent
trips out of the hole to change bits adds greatly to the cost of the wells. Potter
Drilling's spallation technology overcomes these problems by using superheated fluid to
drill through the rocks, rather than relying on the abrasive cutting power of a rotating
drill bit. Under the terms of the MOU the two companies will be carrying out trials to
explore the application of Oxford Catalysts' Instant Steam technology to generate the
necessary heat for use in Potter Drilling's spallation drilling tool. In these tests the
Instant Steam catalyst will be contained in the drill head, which is attached to a
flexible coiled pipe that can be pulled out of the well quickly when required.
Researchers discover why eczema
often leads to asthma
Many young children who get a severe skin rash develop asthma months or years later.
Doctors call the progression from eczema, or atopic dermatitis, to breathing problems the
atopic march. Now scientists at Washington University School of Medicine in St. Louis have
uncovered what might be the key to atopic march. They've shown that a substance secreted
by damaged skin circulates through the body and triggers asthmatic symptoms in
allergen-exposed laboratory mice. The findings, published May 19, 2009, in Public Library
of Science Biology, suggest that early treatment of skin rash and inhibition of the
trigger substance might block asthma development in young patients with eczema. Fifty
percent to 70 percent of children with severe atopic dermatitis go on to develop asthma,
studies show. By comparison, the rate of asthma incidence among the general population is
only about 9 percent in children and 7 percent in adults. Seventeen percent of U.S.
children suffer from atopic dermatitis, although not all cases are considered severe.
"Over the years, the clinical community has struggled to explain atopic march,"
says study author Raphael Kopan, Ph.D., professor of developmental biology and of
dermatology. "So when we found that the skin of mice with an eczema-like condition
produced a substance previously implicated in asthma, we decided to investigate further.
We found that the mice also suffered from asthma-like responses to inhaled allergens,
implicating the substance, called TSLP, as the link between eczema and asthma."
Doctors and scientists had come up with theories to explain why a skin rash is sometimes
associated with asthma. Do some people have an immune system disorder that causes an
overreaction to allergens that contact the skin and lung airways? Or is it the opposite
— do they have defective skin and airways that trigger an excessive immune response?
Kopan's findings suggest the problem starts with damaged or defective skin. The
researchers found that cells in damaged skin can secrete TSLP (thymic stromal
lymphopoietin), a compound capable of eliciting a powerful immune response. And because
the skin is so effective in secreting TSLP into the blood system, the substance travels
throughout the body. When it reaches the lungs, it triggers the hypersensitivity
characteristic of asthma. Led by doctoral student Shadmehr (Shawn) Demehri, the
researchers studied mice that had been engineered with a genetic defect in patches of
their skin. In the affected areas, the typically ordered layers of skin cells were
disrupted, creating a condition similar to eczema. These patches were thickened and
inflamed. The defective skin secreted TSLP as part of an alarm system alerting the body
that its protective barrier function has failed — the substance activates an immune
response that fights invaders.Operating on the assumption that other barrier organs such
as the lung will understand this alarm, the researchers tested what happened when the mice
with skin defects inhaled an allergen. They found that their lungs reacted strongly —
their breathing became labored and their lung tissue took on the traits that mark asthma
in humans: mucous secretion, airway muscle contraction, invasion by white blood cells and
conversion of lung cells from one type to another. Additional experiments showed that mice
that had normal skin but were engineered to overproduce TSLP also developed the
asthma-like symptoms. "We are excited because we've narrowed down the problem of
atopic march to one molecule," Kopan says. "We've shown that skin can act as a
signaling organ and drive allergic inflammation in the lung by releasing TSLP. Now it will
be important to address how to prevent defective skin from producing TSLP. If that can be
done, the link between eczema and asthma could be broken."
Turmeric extract suppresses fat
tissue growth in rodent models
Curcumin, the major polyphenol found in turmeric, appears to reduce weight gain in mice
and suppress the growth of fat tissue in mice and cell models. Researchers at the Jean
Mayer USDA Human Nutrition Research Center on Aging at Tufts University (USDA HNRCA)
studied mice fed high fat diets supplemented with curcumin and cell cultures incubated
with curcumin. "Weight gain is the result of the growth and expansion of fat tissue,
which cannot happen unless new blood vessels form, a process known as angiogenesis."
said senior author Mohsen Meydani, DVM, PhD, director of the Vascular Biology Laboratory
at the USDA HNRCA. "Based on our data, curcumin appears to suppress angiogenic
activity in the fat tissue of mice fed high fat diets." Meydani continued, "It
is important to note, we don't know whether these results can be replicated in humans
because, to our knowledge, no studies have been done." Turmeric is known for
providing flavor to curry. One of its components is curcumin, a type of phytochemical
known as a polyphenol. Research findings suggest that phytochemicals, which are the
chemicals found in plants, appear to help prevent disease. As the bioactive component of
turmeric, curcumin is readily absorbed for use by the body. Meydani and colleagues studied
mice fed high fat diets for 12 weeks. The high fat diet of one group was supplemented with
500 mg of curcumin/ kg diet; the other group consumed no curcumin. Both groups ate the
same amount of food, indicating curcumin did not affect appetite, but mice fed the
curcumin supplemented diet did not gain as much weight as mice that were not fed curcumin.
"Curcumin appeared to be responsible for total lower body fat in the group that
received supplementation," said Meydani, who is also a professor at the Friedman
School of Nutrition Science and Policy at Tufts. "In those mice, we observed a
suppression of microvessel density in fat tissue, a sign of less blood vessel growth and
thus less expansion of fat. We also found lower blood cholesterol levels and fat in the
liver of those mice. In general, angiogenesis and an accumulation of lipids in fat cells
contribute to fat tissue growth." Writing in the May 2009 issue of the Journal of
Nutrition, the authors note similar results in cell cultures. Additionally, curcumin
appeared to interfere with expression of two genes, which contributed to angiogenesis
progression in both cell and rodent models. "Again, based on this data, we have no
way of telling whether curcumin could prevent fat tissue growth in humans." Meydani
said. "The mechanism or mechanisms by which curcumin appears to affect fat tissue
must be investigated in a randomized, clinical trial involving humans."
Excessive cola consumption can lead
to super-sized muscle problems warn doctors
Doctors have issued a warning about excessive cola consumption after noticing an increase
in the number of patients suffering from muscle problems, according to the June issue of
IJCP, the International Journal of Clinical Practice. "We are consuming more soft
drinks than ever before and a number of health issues have already been identified
including tooth problems, bone demineralisation and the development of metabolic syndrome
and diabetes" says Dr Moses Elisaf from the Department of Internal Medicine at the
University of Ioannina, Greece. "Evidence is increasing to suggest that excessive
cola consumption can also lead to hypokalaemia, in which the blood potassium levels fall,
causing an adverse effect on vital muscle functions." A research review carried out
by Dr Elisaf and his colleagues has shown that symptoms can range from mild weakness to
profound paralysis. Luckily all the patients studied made a rapid and full recovery after
they stopped drinking cola and took oral or intravenous potassium. The case studies looked
at patients whose consumption ranged from two to nine litres of cola a day. They included
two pregnant women who were admitted with low potassium levels. The first, a 21 year-old
woman, was consuming up to three litres of cola a day and complained of fatigue, appetite
loss and persistent vomiting. An electrocardiagram also revealed she had a heart blockage,
while blood tests showed she had low potassium levels. The second also had low potassium
levels and was suffering from increasing muscular weakness. It turned out she had been
drinking up to seven litres of cola a day for the last 10 months. In a commentary on the
paper, Dr Clifford Packer from the Louis Stokes Cleveland VA Medical Centre in Ohio
relates the strange case of the ostrich farmer who returned from the Australian outback
with muscle weakness. He had been drinking four litres of cola a day for the last three
years and drank up to 10 litres a day when he was in the outback, causing a rapid
reduction in his potassium levels. He also relates a puzzling case he saw in his own
clinical practice, which was solved when the patient turned up at his office with a
two-litre bottle of cola in the basket of his electric scooter. It turned out he routinely
drank up to four litres a day. He refused to stop drinking cola, but halved his
consumption and the muscle weakness he had been complaining of improved.
Of body and mind, and deep
meditation
Chinese researchers have unlocked the mechanism of an emerging mind-body technique that
produces measurable changes in attention and stress reduction in just five days of
practice. The practice -- integrative body-mind training (IBMT) -- was adapted from
traditional Chinese medicine in the 1990s in China, where it is practiced by thousands of
people. It is now being taught to undergraduates involved in research on the method at the
University of Oregon. In October 2007, researchers led by visiting UO professor Yi-Yuan
Tang and UO psychologist Michael Posner documented in the Proceeding of the National
Academy of Sciences that doing IBMT prior to a mental math test led to low levels of the
stress hormone cortisol among Chinese students. The experimental group also showed lower
levels of anxiety, depression, anger and fatigue than students in a relaxation control
group. "The previous paper indicated that IBMT subjects showed a reduced response to
stress." Tang said. "Why after five days did it work so fast?" The new
findings, he said, point to how IBMT alters blood flow and electrical activity in the
brain, breathing quality and even skin conductance, allowing for "a state of ah, much
like in the morning opening your eyes, looking outside the grass and sunshine, you feel
relaxed, calm and refresh without any stress, this is the meditation state." This
week, in a paper appearing online ahead of regular publication in PNAS, Tang and 13
Chinese colleagues define brain and physiological changes triggered by IBMT. Data were
drawn from several technologies in two experiments involving 86 undergraduate students at
Dalian University of Technology, where Tang is a professor. The data were analyzed and
prepared for publication at the UO with help from Posner and psychology professor Mary K.
Rothbart, who are not co-authors on the paper. "We were able to show that the
training improved the connection between a central nervous system structure, the anterior
cingulate, and the parasympathetic part of the autonomic nervous system to help put a
person into a more bodily state," Posner said. "The results seem to show
integration -- a connectivity of brain and body."
New tool helps researchers identify
DNA patterns of cancer, genetic disorders
A new tool will help researchers identify the minute changes in DNA patterns that lead to
cancer, Huntington's disease and a host of other genetic disorders. The tool was developed
at North Carolina State University and translates DNA sequences into graphic images, which
allows researchers to distinguish genetic patterns more quickly and efficiently than was
historically possible using computers. David Cox, a Ph.D. student in computer science at
NC State, devised the "symbolic scatter plot" tool to provide a visual
representation of a DNA sequence. Cox explains, "The human visual system is more
adept at identifying patterns, and differentiating between patterns, than existing
computer programs such as those that try to identify repetitions of DNA sequences."
In other words, the naked eye sees patterns better than computers can. Identifying
patterns in a sequence of DNA is important because it can help researchers identify the
minute genetic variations between subjects that suffer from a disease, such as cancer, and
subjects that do not. "Improved identification of relevant DNA sequences will
hopefully expedite the development of successful treatment for a range of diseases,"
Cox says, "by allowing researchers to focus on the components of DNA that are related
to the disease and improving our understanding of the genetic mechanisms of these
diseases. For example, what turns specific genes on and off?"
Dental researchers ID new target in
fight against osteoporosis, periodontitis
Osteoporosis and periodontitis are common diseases whose sufferers must cope with
weakness, injury and reduced function as they lose bone more quickly than it is formed.
While the mechanism of bone destruction in these diseases is understood, scientists have
had less information about how bone formation is impaired. Now, researchers at the UCLA
School of Dentistry, working with scientists at the University of Michigan and the
University of California, San Diego, have identified a potential new focus of treatments
for osteoporosis, periodontitis and similar diseases. In a paper published May 17 in the
online edition of the journal Nature Medicine, Cun-Yu Wang, who holds UCLA's No-Hee Park
Endowed Chair in the dental school's division of oral biology and medicine, and colleagues
suggest that inhibiting nuclear factor-kB (NF-kB), a master protein that controls genes
associated with inflammation and immunity, can prevent disabling bone loss by maintaining
bone formation. The findings could offer new hope to millions who struggle with
osteoporosis and periodontitis each year. The National Institutes of Health estimates that
in the United States alone, more than 10 million people have osteoporosis, and many more
have low bone mass, putting them at risk for the disease, as well as for broken bones.
According to the American Academy of Periodontology, mild to moderate periodontitis
affects a majority of adults, with between 5 and 20 percent of the population suffering
from a more severe stage of the disease. The NF-kB protein, a culprit in inflammatory and
immune disorders, plays a major role in both osteoporosis and periodontitis, disrupting
the healthy balance of bone destruction and formation. It is this balance that Wang and
his fellow scientists seek to restore, and perhaps even improve upon, by finding new ways
to promote net bone accumulation.
Popular cancer drug linked to often
fatal brain virus
The 57-year-old lawyer in New York had handily completed the New York Times' Saturday
crossword puzzle – the hardest of the week – for years. But one Saturday
morning, suddenly he couldn't retrieve the words to fill in the squares. In Chicago, an
83-year-old woman began parroting the same phrases over and over. When her doctor asked
her how she was, she replied, "I am fine. I am fine. I am fine." The symptoms of
the New York lawyer and the Chicago woman could have been mistaken for early dementia. But
an MRI brain scan and biopsy revealed something surprising. It looked like their brains
had been eaten away. A brain biopsy and a spinal tap confirmed the diagnosis of a swiftly
moving and often fatal viral brain infection called progressive multifocal
leukoencephalitis (PML) that attacks the brain's white matter. Both had lymphoma and had
been taking the popular cancer drug rituximab (brand name Rituxan) before they developed
the brain infection. The two patients are part of a new study from the Northwestern
University Feinberg School of Medicine RADAR project, led by Charles Bennett, M.D., that
links rituximab to PML. Rituximab is the most important and widely used cancer drug for
lymphoma. It is also approved for treatment of rheumatoid arthritis and is widely used
off-label to treat multiple sclerosis, lupus erythematosus and autoimmune anemias. Bennett
reports on 57 cases from 1997 to 2008 in which patients with anemia, rheumatoid arthritis
or lymphoma developed the fatal brain disease after taking rituximab. They died an average
of two months after being diagnosed. The study was published in the May 14 issue of the
journal Blood. "Rituximab is one of the most prominent drugs in a new class called
monoclonal antibodies. It's now the third monoclonal antibody that is associated with
PML," said Bennett, the A.C. Buehler Professor in Economics and Aging at
Northwestern's Feinberg School and a hematologist and oncologist at the Jesse Brown VA
Medical Center in Chicago. One of the other two drugs, Raptiva, was taken off the market
in April of this year because of the PML risk. The other drug, Tysabri, was removed from
the market for 1½ years because of similar concerns. Bennett said the brain infection is
often overlooked and undiagnosed because it is so subtle at first. "People may think
it's early Alzheimer's disease or depression," he said. "Many of these patients
have cancer and when they die, people assume it's the cancer that killed them." It is
not yet known how rituximab is connected to the brain virus and who may be at risk.
Bennett notes that the best information on the frequency of PML is among patients with
lupus with an estimated rate of 1 in 4,000 patients developing PML. Monoclonal antibodies
target one particular protein found on the surface of cells. In lymphoma, rituximab
targets a protein called CD20 on the outside of B-cell lymphomas. The antibody binds to
the protein, leading to the destruction of the cancerous cell.
Special protein helps maintain an
efficient brain
The instruction manual for maintaining an efficient brain may soon include a section on
synaptotagmin-IV (Syt-IV), a protein known to influence learning and memory, thanks to a
study by University of Wisconsin-Madison researchers. The study showed that Syt-IV keeps
the strength of synapses — connections between nerve cells where communication occurs
— within a useful range of neither too strong nor too weak. Synapses' ability to
adjust over time by becoming bigger and stronger or smaller and weaker — their
plasticity — is at the heart of remembering, forgetting and learning. A delicate
balance is required for this optimal brain plasticity. The study appears in Nature
Neuroscience's advanced online publication on May 17. The findings may be useful in the
future for treating neurodegenerative disorders such as Alzheimer's disease and
Parkinson's disease as well as epileptic seizures. Early stages of these disorders may
stem from synaptic deficits. "If a drug or genetic treatment could be designed to
control Syt-IV expression and modify its effect on other key players involved in synaptic
function, synapses might work better," says senior author Edwin R. Chapman, a Howard
Hughes Medical Institute professor at the UW-Madison School of Medicine and Public Health
(SMPH). Camin Dean, a postdoctoral fellow in Chapman's physiology department laboratory at
the SMPH, did most of the work on the study. The scientists have been studying
synaptotagmins for several years, making great strides in understanding their role in
releasing neurotransmitters and neuropeptides at both the sending and receiving sides of
the synapse. The team is particularly interested in the way neurotransmitter-filled sacs,
or vesicles, work at the nerve terminals.
Lettuce gets a healthy suntan
alad dressing aside, a pile of spinach has more nutritional value than a wedge of iceberg
lettuce. That's because darker colors in leafy vegetables are often signs of antioxidants
that are thought to have a variety of health benefits. Now a team of plant physiologists
has developed a way to make lettuce darker and redder—and therefore
healthier—using ultraviolet light-emitting diodes (LEDs). Steven Britz of the U.S.
Department of Agriculture in Beltsville, Md., and colleagues will present the research at
the 2009 Conference on Lasers and Electro Optics/International Quantum Electronics
Conference (CLEO/IQEC), which takes place May 31 to June 5 at the Baltimore Convention
Center. The dark red tinges on a leaf of red leaf lettuce are the plant kingdom's
equivalent of suntan lotion. When bombarded with ultraviolet rays from the sun, the
lettuce leaf creates UV-absorbing polyphenolic compounds in its outer layer of cells. Some
of these compounds are red and belong to the same family that gives color to berries and
apple skin. They help block ultraviolet radiation, which can mutate plant DNA and damage
the photosynthesis that allows a plant to make its food. Polyphenolic compounds,which
include flavonoids like quercetin and cyanidin, are also powerful antioxidants. Diets rich
in antioxidants are thought to provide a variety of health benefits to human beings, from
improving brain function to slowing the wear and tear of aging. To create red leaf lettuce
plants enriched with these compounds, Britz purchased low-power LEDs that shine with UVB
light, a component of natural sunlight. In small quantities, this ultraviolet light allows
humans to produce vitamin D, which has been cited for its health benefits. Britz exposed
the plants to levels of UVB light comparable to those that a beach goer would feel on a
sunny day, approximately 10 milliwatts per square meter. After 43 hours of exposure to UVB
light, the growing lettuce plants were noticeably redder than other plants that only saw
white light. Though the team has yet to quantify this effect, it appears to increase as
the intensity of the light increases. The effect also seems to be particularly sensitive
to the wavelength used – peaking at 282 and 296 nanometers, and absent for longer
wavelength UV. "We've been pleasantly surprised to see how effective the LEDs are,
and are now testing how much exposure is required, and whether the light should be pulsed
or continuous," says Britz. To cut transportation costs and feed the market in the
wintertime, more produce is grown in greenhouses. Crops grown in the winter in northern
climes receive very little UVB to begin with, and plants in greenhouses are further
shielded from UVB by the glass walls. Ultraviolet LEDs could provide a way to replace and
enhance this part of the electromagnetic spectrum to produce darker, more colorful
lettuces. Britz also discussed the potential for using UV LEDs to preserve nutrients in
vegetables that have already been harvested. Previous experiments have shown that the peel
of a picked apple stays redder for a longer period of time when exposed to ultraviolet
light. UVB LEDs are a promising technology for irradiating vegetables stored at low
temperatures to maintain or even boost the amount of phytonutrients they contain.
Triglycerides implicated in
diabetes nerve loss
common blood test for triglycerides – a well-known cardiovascular disease risk factor
– may also for the first time allow doctors to predict which patients with diabetes
are more likely to develop the serious, common complication of neuropathy. In a study now
online in the journal Diabetes, University of Michigan and Wayne State University
researchers analyzed data from 427 diabetes patients with neuropathy, a condition in which
nerves are damaged or lost with resulting numbness, tingling and pain, often in the hands,
arms, legs and feet. The data revealed that if a patient had elevated triglycerides, he or
she was significantly more likely to experience worsening neuropathy over a period of one
year. Other factors, such as higher levels of other fats in the blood or of blood glucose,
did not turn out to be significant. The study will appear in print in the journal's July
issue. "In our study, elevated serum triglycerides were the most accurate at
predicting nerve fiber loss, compared to all other measures," says Kelli A. Sullivan,
Ph.D., co-first author of the study and an assistant research professor in neurology at
the U-M Medical School. "These results set the stage for clinicians to be able to
address lowering lipid counts with their diabetes patients with neuropathy as vigilantly
as they pursue glucose control," says Eva L. Feldman, M.D., Ph.D., senior author of
the study and the Russell N. DeJong Professor of Neurology at the U-M Medical School. With
a readily available predictor for nerve damage – triglycerides are measured as part
of routine blood testing – doctors and patients can take pro-active steps when
interventions can do some good, says Feldman. "Aggressive treatment can be very
beneficial to patients in terms of their neuropathy," says Feldman, who is also
director of the A. Alfred Taubman Medical Research Institute and director of the Juvenile
Diabetes Research Foundation Center at U-M for the study of complications in diabetes.
People can reduce blood triglyceride levels with the same measures that reduce cholesterol
levels: by avoiding harmful fats in the diet and exercising regularly.
Heart disease patients carrying
extra pounds do better, live longer
Being overweight or obese is a leading contributor to cardiovascular disease (CVD) and
associated risk factors; however, in patients with established CVD, obesity appears to
play a protective role. In fact, data suggest obese patients with heart disease do better
and tend to live longer than leaner patients with the same severity of disease, according
to a review article published in the May 26, 2009, issue of the Journal of the American
College of Cardiology. "Obese patients with heart disease respond well to treatment
and have paradoxically better outcomes and survival than thinner patients," said Carl
Lavie, M.D., F.A.C.C., medical director of Cardiac Rehabilitation and Prevention, Ochsner
Medical Center, New Orleans, LA and lead author of the article. "Although these
patients have a more favorable short- and long-term prognosis, we don't yet understand the
mechanisms for why this might be the case." The obesity paradox in patients with CVD,
which was first noticed earlier this decade, is complex. It is likely due to a combination
of obesity's impact on fat cells and other metabolic processes (e.g., insulin resistance,
glucose metabolism, metabolic syndrome), as well as other consequences of being obese. Dr.
Lavie speculates that excess weight may be somewhat protective because these patients have
more reserves to fight disease than thinner patients. Another explanation might be that
obese patients present with problems earlier due to physical deconditioning (being out of
shape) and other non-cardiovascular symptoms and, therefore, have the opportunity to be
diagnosed with milder disease. Although obese patients appear to experience fewer
cardiovascular events and have better survival rates, Dr. Lavie is quick to caution that
patients with heart disease shouldn't incorrectly assume that gaining weight is the
answer. "Obesity is often what's causing high blood pressure, blockages in arteries,
and increased risk of sudden death in the first place. Such excess weight has adverse
effects on all of the major cardiovascular risk factors and has increased the prevalence
of heart disease," he said. "Taken together, most studies are supportive of
purposeful weight loss for preventing and treating cardiovascular disease."
Health-promoting behaviors to stay active and lose weight can also confer benefits beyond
initial heart disease. For example, patients who are overweight or obese are at heightened
risk of diabetes, which can further complicate treatment and outcomes. Patients who make
sustained lifestyle changes, including regular exercise and some weight reduction through
a reduction in calories, cut their risk of developing diabetes by roughly 60 percent.
Environmental Exposures May Damage
DNA in as Few as Three Days
Exposure to particulate matter has been
recognized as a contributing factor to lung cancer development for some time, but a new
study indicates inhalation of certain particulates can actually cause some genes to become
reprogrammed, affecting both the development and the outcome of cancers and other
diseases. The research will be presented on Sunday, May 17, at the 105th International
Conference of the American Thoracic Society in San Diego. “Recently, changes in gene
programming due to a chemical transformation called methylation have been found in the
blood and tissues of lung cancer patients,” said investigator Andrea Baccarelli,
M.D., Ph.D., assistant professor of applied biotechnology at the University of Milan.
“We aimed at investigating whether exposure to particulate matter induced changes in
DNA methylation in blood from healthy subjects who were exposed to high levels of
particulate matter in a foundry facility.” Researchers enrolled 63 healthy subjects
who worked in a foundry near Milan, Italy. Blood DNA samples were collected on the morning
of the first day of the work week, and again after three days of work. Comparing these
samples revealed that significant changes had occurred in four genes associated with tumor
suppression. “The changes were detectable after only three days of exposure to
particulate matter, indicating that environmental factors need little time to cause gene
reprogramming which is potentially associated
with disease outcomes,” Dr. Baccarelli said. “As several of the effects of
particulate matter in foundries are similar to those found after exposure to ambient air
pollution, our results open new hypotheses about how air pollutants modify human
health,” he added. “The changes in DNA methylation we observed are reversible
and some of them are currently being used as targets of cancer drugs.” Dr. Baccarelli
said the study results indicate that early interventions might be designed which would
reverse gene programming to normal levels, reducing the health risks of exposure. “We
need to evaluate how the changes in gene reprogramming we observed are related to cancer
risk,” he said. “Down the road, it will be particularly important not only to
show that these changes are associated with increased risk of cancer or other
environmentally-induced diseases, but that, if we were able to prevent or revert them,
these risks could be eliminated.”
Sleep may be factor in weight
control
Could sleep be a critical component to
maintaining a healthy body weight? According to new research to be presented on Sunday,
May 17, at the American Thoracic Society's 105th International Conference in San Diego,
body mass index (BMI) is linked to length and quality of sleep in a surprisingly
consistent fashion. As part of the Integrative Cardiac Health Project at Walter Reed Army
Medical Center, researchers analyzed the sleep, activity and energy expenditures of 14
nurses who had volunteered for a heart-health program at the Walter Reed, where the nurses
were employed. The program included nutritional counseling, exercise training, stress
management and sleep improvement. Each participant wore an actigraphy armband that
measured total activity, body temperature, body position and other indices of activity and
rest. "When we analyzed our data by splitting our subjects into 'short sleepers' and
'long sleepers,' we found that short sleepers tended to have a higher BMI, 28.3 kg/m2,
compared to long sleepers, who had an average BMI of 24.5. Short sleepers also had lower
sleep efficiency, experienced as greater difficulty getting to sleep and staying
asleep," said lead investigator Arn Eliasson, M.D. Surprisingly, overweight
individuals tended to be more active than their normal weight counterparts, taking
significantly more steps than normal weight individuals: 14,000 compared to 11,300, a
nearly 25 percent difference, and expending nearly 1,000 more calories a day—3,064
versus 2,080.
New tool isolates RNA within
specific cells
A team of University of Oregon biologists,
using fruit flies, has created a way to isolate RNA from specific cells, opening a new
window on how gene expression drives normal development and disease-causing breakdowns.
While DNA (deoxyribonucleic acid) provides an identical genetic blueprint in every cell,
RNA (ribonucleic acid) decodes genetic instructions that turn protein molecules on and off
in different cell types.
The new tagging method, tested in a variety of subsets of Drosophila brain cells, is
described in a paper put on line ahead of regular publication by the journal Nature
Methods. Instead of scientists needing to physically separate cell types, they now can
inject a chemically modified gene from the one-celled organism Toxoplasma gondii and
activate it in only one cell type within a tissue. Only newly generated RNA in this cell
type is then tagged and isolated. "By analyzing RNA from different cell types, we can
begin to understand how cellular differences are generated," said lead author Michael
R. Miller, a National Science Foundation-funded doctoral student in the lab of Chris Doe,
a UO biologist and Howard Hughes Medical Institute (HHMI) investigator. "Our new
TU-tagging method should be useful for isolating cell-type specific RNA from other
organisms, including mammals, and should be useful in broad areas of research including
studies of development, neurobiology and disease." The new non-toxic, non-invasive
method makes it possible to "listen in" to the messages -- in fact, messenger
RNA -- that the nucleus is sending each cell, without perturbing the cell, Doe said.
"It is much like eavesdropping on a phone conversation, rather than pulling the
person out of the house for questioning. The cell has no idea that its RNAs are being
'tagged' for isolation and study. That's good, because we get a more accurate idea of what
the cell is saying."
Genes that influence start of
menstruation identified for first time
Researchers from the Peninsula Medical
School, along with collaborators from research institutions across Europe and the United
States, have for the first time identified two genes that are involved in determining when
girls begin menstruation. The work will be published in Nature Genetics this weekend. The
findings of the study could have ramifications for normal human growth and weight too,
because early-age menstruation is also associated with shorter stature and increased body
weight. In general, girls who achieve menstruation earlier in life tend to have greater
body mass index (BMI) and a higher ratio of fat compared to those who begin menstruation
later. The study carried out an analysis of 17,510 women across eight different
international population-based sources. This number included women of European descent who
reported the age at which they reached menstruation of between nine and 17 years. The two
genes identified were on chromosomes nine and six. One in 20 females carry two copies of
each of the gene variations which result in menstruation starting earlier, and they will
start menstruating approximately four and half months earlier than those with no copies of
the gene variants.
DNA-Prokids - genetic
identification against traffic in human beings
DNA-Prokids, an international project on
human trafficking prevention and fight using genetic identification of victims and their
relatives, was officially presented today, at the University of Granada (UGR)
headquarters, in Spain. Traffic in human beings is one of the most frequent and profitable
crimes at the beginning of the 21st century. According to data from the United Nations
Office on Drugs and Crime (UNODC), approximately two million people are victims of human
trafficking across the world. UN Secretary-General, Ban Ki-Moon, stated recently that
“trafficking in weapons, drugs and blood diamonds has long been on the UN
agenda” and that now is the time to “add people to that list”. Upon
suggestion of the UGR Genetic Identification Laboratory, an international project for
genetic identification of missing children and their families was set up in 2004. The goal
was to not limit the scope of research to domestic crimes, but to spread results worldwide
with the aim of boosting the international fight against human trafficking. That was the
start of DNA-Prokids, an initiative which has been praised by authorities and experts in
genetic identification all over the world, and whose piloting experiences in countries
such as Guatemala, Mexico, Philippines and Indonesia are being extremely successful.
Two-thirds of adult population in
Spain eats no fruit at weekends
An international group of researchers has
studied the link between meal times and the choice of foods eaten by Spaniards aged
between 25 and 49. The study, which has been published in the latest issue of the journal
Appetite, analyses the cases of specific foodstuffs, in particular fruit. The results show
that 66% of adults living in Spain eat fruit with their main meals, particularly from
Monday to Friday.
The study, carried out on-line using a sample of 831 people living in Spain aged between
25 and 49, recorded their food intake during the day and related this to the social
context of these kinds of foods. The results show that we eat certain foods in preference
to others depending upon the time of the meal. When it comes to fruit, the study shows
that 66% of adults eat it with their main meals, although it is not a major component of
these meals. According to the study's authors, most fruit is consumed during the day
around 3pm and after 7pm. In addition, the data show that fruit is a "Monday to
Friday" food, as it is eaten less frequently at the weekend. The researchers have
also discovered links between some kinds of food and certain contexts. For example, there
is a relationship between the ‘sandwich' and ‘sweets and chocolates' categories
and working at a computer.
Air-fuelled battery could last up
to 10 times longer
Ground-breaking technology has huge
potential for electric cars and renewables. A new type of air-fuelled battery could give
up to ten times the energy storage of designs currently available. This step-change in
capacity could pave the way for a new generation of electric cars, mobile phones and
laptops. The research work, funded by the Engineering and Physical Sciences Research
Council (EPSRC), is being led by researchers at the University of St Andrews with partners
at Strathclyde and Newcastle. The new design has the potential to improve the performance
of portable electronic products and give a major boost to the renewable energy industry.
The batteries will enable a constant electrical output from sources such as wind or solar,
which stop generating when the weather changes or night falls. Improved capacity is thanks
to the addition of a component that uses oxygen drawn from the air during discharge,
replacing one chemical constituent used in rechargeable batteries today. Not having to
carry the chemicals around in the battery offers more energy for the same size battery.
Reducing the size and weight of batteries with the necessary charge capacity has been a
long-running battle for developers of electric cars. The STAIR (St Andrews Air) cell
should be cheaper than today’s rechargeables too. The new component is made of porous
carbon, which is far less expensive than the lithium cobalt oxide it replaces. This
four-year research project, which reaches its halfway mark in July, builds on the
discovery at the university that the carbon component’s interaction with air can be
repeated, creating a cycle of charge and discharge. Subsequent work has more than tripled
the capacity to store charge in the STAIR cell.
University of the Basque Country
researcher develops nanoparticles to be used in genic therapy
Genic therapy can be used both with rare
diseases, such as cystic fibrosis and disorders of the retina, as well as with more common
illnesses, such as AIDS, cancer and neurodegenerative diseases (for example,
Parkinson’s or Alzheimer’s). The author of the PhD is Ms Ana del Pozo Rodríguez
(Vitoria, 1980), a pharmacy graduate, who defended her thesis entitled, Development of
solid lipid nanoparticles as systems for and administration in genic therapy. The
directors of the PhD were Ms Alicia Rodríguez Gascón and Ms María Ángeles Solinís
Aspiazu from the Department of Pharmacy and Food Sciences at the Pharmacy Faculty of the
University of the Basque Country (UPV/EHU). In undertaking the research, the author of the
thesis worked with the Ernest Giralt team at the Institut de Reserca Biomèdica in
Barcelona (IRB Barcelona). Ms del Pozo Rodríguez is currently working as a researcher for
CIBER-BNN at the Pharmacy and Pharmaceutical Technological Laboratory at the Pharmacy
Faculty of the UPV/EHU.
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