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Week 40
Rare genetic disease successfully
reversed using stem cell transplantation
A recent study by Scripps Research Institute scientists offers good news for families of
children afflicted with the rare genetic disorder, cystinosis. In research that holds out
hope for one day developing a potential therapy to treat the fatal disorder, the study
shows that the genetic defect in mice can be corrected with stem cell transplantation.
"After meeting the children who suffer from this disease, like an 18-year-old who has
already had three kidney transplants, and the families who are desperately searching for
help, our team is committed to moving toward a cure for cystinosis, a lysosomal storage
disorder," says principal investigator Stephanie Cherqui, assistant professor in the
Department of Molecular and Experimental Medicine. "This study is an important step
toward that goal."In the study, which is published in the September 17, 2009 print
edition of the journal Blood, the Scripps Research team used bone marrow stem cell
transplantation to address symptoms of cystinosis in a mouse model. The procedure
virtually halted the cystine accumulation responsible for the disease and the cascade of
cell death that follows. Cystine is a byproduct of the break down of cellular components
the body no longer needs in the cell's "housekeeping" organelles, called
lysosomes. Normally, cystine is shunted out of cells, but in cystinosis a gene defect of
the lysosomal cystine transporter causes it to build up, forming crystals that are
especially damaging to the kidneys and eyes.
Solar Cycle Driven by More than
Sunspots; Sun Also Bombards Earth with High-Speed Streams of Wind
Challenging conventional wisdom, new research finds that the number of sunspots provides
an incomplete measure of changes in the Sun's impact on Earth over the course of the
11-year solar cycle. The study, led by scientists at the High Altitude Observatory of the
National Center for Atmospheric Research (NCAR) and the University of Michigan, finds that
Earth was bombarded last year with high levels of solar energy at a time when the Sun was
in an unusually quiet phase and sunspots had virtually disappeared. "The Sun
continues to surprise us," says NCAR scientist Sarah Gibson, the lead author.
"The solar wind can hit Earth like a fire hose even when there are virtually no
sunspots." The study, also written by scientists at NOAA and NASA, is being published
today in the Journal of Geophysical Research - Space Physics. It was funded by NASA and by
the National Science Foundation, NCAR's sponsor.
Rare cases of restored vision
reveal how the brain learns to see
By testing formerly blind patients within weeks of sight restoration, Sinha and his
colleagues found that subjects had very limited ability to distinguish an object from its
background, identify overlapping objects, or even piece together the different parts of an
object. The patients gradually improved over time, and the new study suggests that dynamic
information — that is, input from moving objects — is critical to the brain's
ability to learn to segregate objects from their backgrounds (a task known as visual
integration)
Killing Cancer Like a Vampire
Slayer
Like vampires, cancer tumors require an ample supply of blood to stay alive. Without fresh
blood for sustenance, cancer cells shrivel up like raisins and die. To that end, Dr. Ronit
Satchi-Fainaro of Tel Aviv University's Department of Physiology and Pharmacology, Sackler
School of Medicine, and her team of researchers have developed a new drug carrier to
deliver compounds straight to the tumor. Ferrying a variety of existing life-saving
therapies right to their target so they can work more effectively, this new invention may
alleviate particularly nasty forms of cancers like osteosarcomas and bone metastases. Dr.
Satchi-Fainaro believes that her technology can also combat resistance to anti-cancer
drugs like Taxol, keeping other normal healthy cells around the tumor safe. Dr.
Satchi-Fainaro, together with two of her doctoral students, Ehud Segal and Keren Miller,
has just published papers in the prestigious journals Angewandte Chemie and PLoS One on
their pre-clinical findings in cellular and animal models using this new discovery.
Chemobrain – the flip side of
surviving cancer
Study shows deterioration in brain function following breast cancer therapy has negative
effects on quality of life. One of the most problematic side effects of cancer treatment,
chemobrain – a range of symptoms including memory loss, inability to concentrate,
difficulty thinking and other subtle cognitive changes following chemotherapy –
seriously diminishes women’s quality of life and daily functioning. As a result, they
have to adopt a range of coping strategies to manage their restricted social and
professional lives. Breast cancer survivors tell their story in a descriptive study1 of
the effects that cognitive impairment has on women’s work, social networks and
dealings with the health care profession. Dr. Saskia Subramanian from the UCLA Center for
Culture and Health in the US and her colleagues have just published their work online in
Springer’s Journal of Cancer Survivorship. An increasing number of women survive
breast cancer, yet survival comes at a price. Mild cognitive impairment following
chemotherapy, known as “chemobrain” or “chemofog” is one of the most
commonly reported post-treatment symptoms by breast cancer survivors. Dr. Subramanian and
colleagues’ work shows that this deterioration in brain function has devastating
effects on breast cancer survivors’ quality of life. Through a combination of focus
groups and in-depth interviews among 74 women who had completed their course of cancer
treatment at least a year earlier, the researchers gathered data on patients’ medical
background, treatment experience, post-treatment symptoms, reactions from medical staff
and from family and friends, self-management, strength of social networks and their
perceptions of themselves. The women described a variety of cognitive changes which they
found both frustrating and upsetting. Some were less able to retain material or to digest
new information and recognized that they were not functioning as they once did. Others
faced reduced independence, becoming limited in their ability to manage certain
responsibilities or get around. These changes made women feel scared, dependent and
emotionally drained.
University of the Basque Country
researcher makes progress in optimising solid oxide fuel cells
While our standard of life increases, so does the worldwide energy demand. In this vein,
the application of technologies based on fuel cells is put forward as an alternative to
the massive consumption of fossil fuels. One of the fuel cells of greatest current
interest is the solid oxide one. The PhD thesis by researcher at the University of the
Basque Country (UPV/EHU), Ms Ana Martínez Amesti, focused on optimising solid oxide fuel
cells, one of the most promising technologies of the future for various applications
(residential, commercial, portable devices, electric power stations, and so on). The
author has entitled her thesis Solid oxide fuel cells. Studies on reactivity and
optimisation of cathode-electrolyte interlayer. Solid oxide fuel cells are the type of
cells most studied in recent years. They have basically two outstanding characteristics:
the electrodes and the electrolyte are solid and the versatility in the choice of fuels
and oxidants due to high operational temperatures. As regards problems arising with this
kind of cell, there are also two important ones: on the one hand, the difficulties in
manufacturing, given that the ceramic materials of which they are made require high
temperatures for their processing and, on the other, in some cases, the solid electrolyte
degrades easily at the cell’s working temperature, thus affecting its stability.
UCSF scientists illuminate how
microRNAs drive tumor progression
UCSF researchers have identified collections of tiny molecules known as microRNAs that
affect distinct processes critical for the progression of cancer. The findings, they say,
expand researchers’ understanding of the important regulatory function of microRNAs
in tumor biology and point to new directions for future study and potential treatments.
The researchers refer to these microRNA collections as signatures, and their study results
are reported in the September 15 issue of “Genes & Development.’’ The
study, available online at http://genesdev.cshlp.org/, was led by the laboratory of
Douglas Hanahan, PhD, an American Cancer Society Research Professor in the Department of
Biochemistry and Biophysics at UCSF. Approximately five percent of all known human genes
encode, or produce, microRNAs, yet scientists are only now – nearly a decade after
their discovery—beginning to unlock the mystery of their functions.
Researchers to probe whether Lyme
disease will follow spread of ticks across U.S.
Potentially debilitating Lyme disease doesn’t afflict people everywhere that the
ticks harboring it are found. At least not yet. A five-university consortium led by a
Michigan State University researcher wants to find out why. “These ticks are on the
move. As ticks expand into new areas, more people will likely become infected,” said
MSU fisheries and wildlife assistant professor Jean Tsao, who will lead the four-year,
$2.5 million study. “We have a really intriguing scientific puzzle to solve –
many factors change as we move from north to south, and we need to be smart with our study
design to unravel these,” she said. “Our study also has practical goals –
we aim to provide the health community and the public in the various states with some
reassurance, or warning, about what their future will hold for spread of Lyme disease.
Understanding the reasons why Lyme disease is such a problem in some areas will help us
manage the disease better, and lower the risk to human health.” In 30 years, the tiny
blacklegged tick has cut a huge swath through 10 northern states by carrying a bacterial
infection now annually afflicting more than 20,000 North Americans. Curiously, the same
parasite commonly known as the deer tick also is found in southern states, where Lyme
disease is comparatively rare. “Researchers do not know how climate, vertebrate
biodiversity, tick genetics or other factors affect the maintenance of the pathogen and
its relative abundance in an area,” Tsao said. “So as the ticks spread, will
tick populations in new areas be infected like northern populations or mainly clean of
infection like southern populations?”
Weill Cornell Researchers Discover
New Anti-Tuberculosis (TB) Compounds
Attempts to eradicate tuberculosis (TB) are stymied by the fact that the disease-causing
bacteria have a sophisticated mechanism for surviving dormant in infected cells. Now, a
team of scientists led by researchers from Weill Cornell Medical College has identified
compounds that inhibit that mechanism — without damaging human cells. The results,
described in the next issue of Nature and published online today, include structural
studies of how the inhibitor molecules interact with bacterial proteins, and could lead to
the design of new anti-TB drugs. "We believe these findings represent a new approach
for developing antibiotics in the fight against TB," says Dr. Carl Nathan, senior
author and chairman of the Department of Microbiology and Immunology, R.A. Rees Pritchett
Professor of Microbiology and director of the Abby and Howard P. Milstein Program in
Chemical Biology of Infectious Disease at Weill Cornell Medical College. "This is
important because we are running out of effective antibiotics that are currently
available. There are few drugs that successfully combat TB in its dormant stage, which
makes the bacterium so resilient in the body. More important, there are many antibiotics
that kill bacteria by blocking the synthesis of proteins, but there are none that kill
bacteria by interfering with protein breakdown, as we have found here." Mycobacterium
tuberculosis, the bacterium that causes TB, infects one person in three worldwide. Most
infected people remain symptom-free because the bacterium is kept in check within immune
system cells. These cells produce compounds such as nitric oxide, which scientists believe
damage or destroy the bacteria's proteins. If allowed to accumulate, the damaged proteins
would kill the bacteria.
Postmenopausal women benefit from
endurance training as much as younger women
In a paper appearing in the September issue of the journal Metabolism - Clinical and
Experimental, Brooks and Zarins report that participants increased their body's capacity
to consume and use oxygen - their VO2 max - by an average of 16 percent and dropped their
resting heart rates by an average of 4 beats per minute. Brooks said that after the age of
30, people lose the capacity to consume and use oxygen at about 1 percent per year.
"So, in effect, the women in our study had the cardiovascular and metabolic
capabilities of women 16 years younger," he said. By the end of the study, the
women's blood pressure during exercise had dropped by 8 millimeters of mercury, while
their heart rates were 19 beats per minute less when performing at the same intensity as
early in the study. In addition, the women decreased their carbohydrate burning during
exercise and increased their fat burning by about 10 percent. Women in the study
maintained their body weight as a way to balance energy input and expenditures.
Medications Effective in Reducing
Risks for Breast Cancer Can Also Cause Serious Side Effects
hree drugs that reduce a woman's chance of getting breast cancer also have been shown to
cause adverse effects, according to a new report from the Agency for Healthcare Research
and Quality (AHRQ), U.S. Department of Health & Human Services. The report is based on
a study led by Heidi D. Nelson, M.D., M.P.H., research professor in the Oregon
Evidence-Based Practice Center at Oregon Health & Science University and medical
director of the Women and Children's Program and Research Center at Providence Health
& Services. It is published online in the Sept. 15 issue of theAnnals of Internal
Medicine. The study is the first to make a direct, comprehensive comparison of drugs that
reduce the risk of breast cancer so that women and their health care providers can assess
their potential effectiveness and adverse effects. It compares the use of tamoxifen,
raloxifene and tibolone to reduce the risks of getting breast cancer in women without
pre-existing cancer. Tamoxifen, raloxifene and tibolone can be prescribed to women with a
family history of breast cancer or other risk factors, but prescribing practices vary
widely. According to the study, all three drugs significantly reduce invasive breast
cancer in midlife and older women, but benefits and adverse effects can vary depending on
the drug and the patient.
Antioxidant controls spinal cord
development
Researchers at the Johns Hopkins School of Medicine have discovered how one antioxidant
protein controls the activity of another protein, critical for the development of spinal
cord neurons. The research, publishing this week in Cell, describes a never-before known
mechanism of protein control. “This is the first time we’ve seen this type of
chemical reaction control neuronal differentiation,” says Shanthini Sockanathan,
Ph.D., an associate professor at the Johns Hopkins Solomon H. Snyder Department of
Neuroscience. “And it’s probably not specific for motor neurons that we study,
but also for development of a wide variety of neurons.” Previous research had shown
that the GDE2 protein can cause immature cells in the spinal cord to differentiate into
motor neurons, the nerve cells that connect to and control muscle contraction. Too little
GDE2 causes motor neurons to not develop, while too much GDE2 causes them to develop too
quickly, depleting progenitor pools. “We reasoned that there must be tight control of
GDE2 so we set out to look for the regulator by looking for other proteins that can bind
to GDE2,” says Sockanathan.
Weight Loss is Good for the Kidneys
Losing weight may preserve kidney function in obese people with kidney disease, according
to a study appearing in an upcoming issue of the Clinical Journal of the American Society
Nephrology (CJASN). The findings indicate that taking off the pounds could be an important
step kidney disease patients can take to protect their health. More than a third of US
adults are either obese or overweight. Weight loss can improve a number of health
problems; for example, it can improve control of diabetes, lower blood pressure and
cholesterol levels, and reduce the effects of heart disease. To see if losing weight might
also have beneficial effects on the kidneys, Sankar Navaneethan, MD, (Cleveland Clinic),
and his colleagues analyzed the studies that examined the effects of weight loss
interventions in obese kidney disease patients. The investigators searched the medical
literature and identified data from thirteen relevant studies that assessed the impact of
diet, exercise, and surgical procedures on kidney function.
Anemic Patients With MDS Gain
Long-Term Benefits From Erythropoietin and Myeloid Growth Factor Hormones
Myelodysplastic syndromes (MDS), a group of blood disorders that can lead to acute myeloid
leukemia (AML) in some patients, often cause severe anemia (when the body lacks a
sufficient number of functional red blood cells). While certain treatments can help manage
the symptoms of anemia, some studies have suggested that they may lead to complications. A
new study, however, demonstrates that MDS patients with anemia may benefit from treatment
with an erythropoietin (EPO)-based regimen plus supportive care without added
complications as compared with those receiving supportive care alone. The study will
appear in the September 17 issue of Blood, the official journal of the American Society of
Hematology. The phase III prospective, randomized trial, conducted by research teams of
the Eastern Cooperative Oncology Group, was designed to evaluate the efficacy and safety
of EPO with or without myeloid growth factor treatment (G-CSF, or granulocyte
colony-stimulating factor) and supportive care (SC) with red blood cell transfusions for
patients with early-stage MDS (n=53), in comparison to supportive care alone (n=57).
Penn State College of Medicine
research isolates liver cancer stem cells prior to tumor formation
– Penn State College of Medicine researchers, in collaboration with colleagues at the
University of Southern California, have taken an important step in understanding the role
of stem cells in development of liver cancer. Using a unique approach that involves study
of individual cells, the team, led by C. Bart Rountree, M.D., has demonstrated for the
first time a population of cancer stem cells in the liver prior to tumor formation. The
research, published in the journal Stem Cells, shows a potential link between liver stem
cells and liver cancer. Using a liver-specific PTEN (phosphatase and tensin homolog
deleted on chromosome 10) mouse model allowed Rountree and his colleagues to study the
microenvironment of the liver without affecting the rest of the mouse. "The PTEN
knock-out mouse is one model of chronic liver injury that ultimately leads to liver
cancer. During chronic injury, liver stem cells proliferate, and at times of healthy
liver, the liver stem cells are very rare," Rountree said. "We were initially
looking for what is driving liver stem cell proliferation during chronic liver injury.
"We started investigating liver stem cells in many different liver injury models with
the idea we may be able to help people with liver disease, but we discovered that some
cells we isolated were malignant," Rountree said. "It was quite a surprise for
us because there were not any tumors in the mice when we isolated the cells." The
liver is the only organ in the body that is able to fully regenerate itself. The cells of
the liver, including hepatocytes and cholangiocytes, can divide and repopulate themselves.
With chronic liver injury, including by a virus or alcoholism, the hepatocytes lose the
ability to make more of themselves. In that setting, liver stem cells proliferate and can
make either of the cell types. However, patients with chronic injury also develop liver
cancer, opening the possibility that the stem cells are involved in tumor formation.
"There's been a groundswell of interest in understanding the role of specific stem
cells in the development of liver cancer," Rountree said. "There is a cancer
stem cell lurking out there that may be very bad. It has stem cell properties and is
malignant, resistant to chemotherapy. These properties make it harder to treat these
cancers.
A Chip for the Eye - Artificial
Vision Enhancers Being Put to the Test
Visually impaired or blind patients with degenerative retina conditions would be very
happy if they were able to regain mobility, find their way around, be able to lead an
independent life and to recognize faces and read again. These wishes were documented by a
survey conducted by a research team ten years ago to find out what patients’
expectations of electronic retina prostheses (retina implants) were. Today these wishes
look set to become reality, as the presentations to be given at the international
symposium “Artificial Vision” on 19 September 2009 at the Wissenschaftszentrum
Bonn demonstrate. The symposium is being staged by the Retina Implant Foundation and the
Pro Retina Stiftung zur Verhütung von Blindheit (Pro Retina Foundation for the Prevention
of Blindness), a foundation of the patients’ organization Pro Retina Deutschland e.V.
Scientists have been working on developing retina prostheses for more than twenty years
now. Research has been conducted particularly intensively in Germany, where scientists and
patients have worked in tandem and have succeeded in obtaining government funding.
“Back then we didn’t want high-tech just for space and defence programs but
finally high-tech for people as well,” Professor Rolf Eckmiller, a neuro-informatics
specialist at the University of Bonn and a pioneer in the field, recalls. This investment
is now bearing fruit. The German research consortiums lead the field in this area of
research. Three of the four research teams presenting their findings in Bonn are from
Germany.
New Dangers of “Clubbing
Drugs” on the Web
Two University of Hertfordshire academics will release new evidence about the dangers of
‘Spice’ drugs today at the first International Psychonaut Web Mapping Conference
in Ancona, Italy. Professor Fabrizio Schifano and Dr Ornella Corazza from the
University’s School of Pharmacy will describe the pharmacological aspects of novel
drugs of abuse and provide an overview of ‘Spice’ drugs at the conference which
taks place as a result of a two-year European Commission-funded study to implement a
regular monitoring of the World Wide Web in respect to novel recreational drugs.
‘Spice’ is a brand name for a herbal mix widely sold as an ‘incense’
or legal substitute for cannabis. It comes under a variety of names according to its
‘flavours’, such as ‘Spice Diamond’, ‘Spice Gold’,
‘Spice Silver’, 2Spicy’, ‘Spice of Life’, etc, which according to
users, are meant to produce subtly different effects. According to initial results of the
Psychonaut Web Mapping study on Spice carried out by Dr Corazza, the drug is accessible to
children and young people, as there are no or very limited controls on any of the websites
selling the drug.
Seasonal influenza - not enough
healthcare workers have themselves vaccinated
Less than one third of healthcare workers have themselves vaccinated against classic
influenza. This reluctance is astounding, firstly because vaccination against influenza
viruses is considered safe and effective and secondly because it has been proved to
prevent nosocomial transmission of disease to patients—provided at least 50% of
employees have been vaccinated. In the new issue of Deutsches Ärzteblatt International
(Dtsch Arztebl Int 2009; 106(36): 567-72), Sabine Wicker of Johann Wolfgang Goethe
University Hospital, Frankfurt and her co-authors reveal why vaccination rates have stayed
so low and how they can be improved. The attitudes of healthcare personnel to influenza
vaccination were investigated by means of several anonymous questionnaires. Those who
opted for vaccination did so principally to protect themselves and their family, friends,
and colleagues. Concern for patients was relegated to third place. The most frequent
reasons given for refusing vaccination were low estimation of the risk of infection, fear
of adverse effects, and scepticism whether the vaccine offered adequate protection. In the
influenza season 2008/2009, the vaccination rate at Frankfurt University Hospital was
greatly improved by making it mandatory for all unvaccinated employees to wear a
protective mask in order to break chains of infection in the hospital. Within 10 days the
vaccination coverage rose from 33% to 57.7%. The authors conclude that satisfactory
vaccination rates obviously cannot be achieved by means of voluntary, free-of-charge
vaccination programs and information campaigns. They recommend, therefore, that hospital
authorities consider compulsory vaccination for employees who care for immune-compromised
patients.
Insufficient levels of vitamin D
puts elderly at increased risk of dying from heart disease
A new study by researchers at the University of Colorado Denver and Massachusetts General
Hospital (MGH) shows vitamin D plays a vital role in reducing the risk of death associated
with older age. The research, just published in the Journal of the American Geriatrics
Society, evaluated the association between vitamin D levels in the blood and the death
rates of those 65 and older. The study found that older adults with insufficient levels of
vitamin D die from heart disease at greater rates that those with adequate levels of the
vitamin. "It's likely that more than one-third of older adults now have vitamin D
levels associated with higher risks of death and few have levels associated with optimum
survival," said Adit Ginde, MD, MPH, an assistant professor at the University of
Colorado Denver School of Medicine's Division of Emergency Medicine and lead author on the
study. "Given the aging population and the simplicity of increasing a person's level
of vitamin D, a small improvement in death rates could have a substantial impact on public
health." Older adults are at high risk for vitamin D deficiency because their skin
has less exposure to the sun due to more limited outdoor activities as well as reduced
ability to make vitamin D. The study analyzed data from the Third National Health and
Nutrition Examination Survey conducted by the National Center for Health Statistics. The
research team analyzed vitamin D in blood samples of more than 3,400 participants that
were selected to be representative of the 24 million older adults in the United States.
Compared to those with optimal vitamin D status, those with low vitamin D levels were 3
times more likely to die from heart disease and 2.5 times more likely to die from any
cause. Dr. Ginde says the findings suggest that current daily recommendations of vitamin D
may not be enough for older adults to maintain optimal health. The research team has
applied for research funding from the National Institutes of Health to perform a large,
population-based clinical trial of vitamin D supplementation in older adults to see if it
can improve survival and reduce the incidence of heart disease. "Confirmation of
these results in large randomized trials is critically important for advancing public
health," says Carlos Camargo, MD, DrPH, of the MGH Department of Emergency Medicine,
the senior author of the study and an associate professor of medicine at Harvard Medical
School.
Racial Disparities in Diabetes
Prevalence Linked to Living Conditions
The higher incidence of diabetes among African Americans when compared to whites may have
more to do with living conditions than genetics, according to a study led by researchers
at the Johns Hopkins Bloomberg School of Public Health. The study, available online in
advance of publication in the October 2009 edition of the Journal of General Internal
Medicine, found that when African Americans and whites live in similar environments and
have similar incomes, their diabetes rates are similar, which contrasts with the fact that
nationally diabetes is more prevalent among African Americans than whites. Researchers
from the Hopkins Center for Health Disparities Solutions and Case Western Reserve
University School of Medicine compared data from the 2003 National Health Interview Survey
(NHIS) with the Exploring Health Disparities in Integrated Communities Southwest Baltimore
(EHDIC-SWB) Study. The Baltimore study was conducted in a racially integrated urban
community without race differences in socioeconomic status. In recent decades the United
States has seen a sharp increase in diabetes prevalence, with African Americans having a
considerably higher occurrence of type 2 diabetes and other related complications compared
to whites. “While we often hear media reports of genes that account for race
differences in health outcomes, genes are but one of many factors that lead to the major
health conditions that account for most deaths in the United States,” said Thomas
LaVeist, PhD, director of the Hopkins Center for Health Disparities Solutions and lead
author of the study.
Nanoresearchers challenge dogma in
protein transportation in cells
New data on signalling proteins, called G proteins, may prove important in fighting
diseases such as cardiovascular, neurodegenerative disorders, and cancer. For many decades
scientists have puzzled on "How signalling proteins transport and organize in
specific areas of the cell?" Researchers from Nano-Science Center and Department of
Neuroscience and Pharmacology provide yet unrecognized clues to solve this mystery. - We
now begin to understand how signalling proteins recognize and transport to certain areas
of the cell and get a more clear insight on the mechanism of major cellular processes such
as cell signalling and growth. This valuable knowledge could be used in the future to
understand and cure disease such as depression and Alzheimer's explains Associate
Professor Dimitrios Stamou, Nano-Science Center and Department of Neuroscience and
Pharmacology, who led the work.Cells depend critically on their ability to selectively,
transport and isolate proteins in specific areas. Earlier ideas that proposed proteins to
move around in the cell by recognizing nanoscale patches in their surrounding membrane,
also called lipid rafts, are currently under intense debate. However researchers from
Nano-Science Center found a new unsuspected mechanism based on the shape of the membrane
and just had their results published in the prominent scientific journal Nature Chemical
Biology.
Allergies among youth on the rise
Asthma, nasal symptoms and eczema is a major public health problem in Sweden, not least
among young people. Half of all teenagers are affected in Västra Götaland County in West
Sweden. This is shown in a study conducted in 2008 by the Sahlgrenska Academy at the
University of Gothenburg, on the request of the Public Health Committee, Region Västra
Götaland. The study also shows that the prevalence of allergies among young people has
increased by ten percentage points since the year 2000. The study includes all residents
of Västra Götaland County (pop. 1.5 million) born in 1992, and is a follow-up to a
similar study conducted in 2000. The results show that 49 percent of the teenagers suffer
from physician-diagnosed asthma, nasal symptoms or atopic eczema. The most common problem
is nasal symptoms, followed by asthma and atopic eczema, and allergies are more common
among girls than boys.
Large fat cells may increase risk
of type 2 diabetes in women
Middle-aged women with large abdominal fat cells have a higher risk of developing type 2
diabetes later in life compared to women with smaller fat cells. Waist circumference
divided by body height can also be used to determine which women are at risk. This is
shown in a new study from the Sahlgrenska Academy at the University of Gothenburg, Sweden.
The study, which will be published in the next issue of the scientific journal FASEB
Journal, is based on the extensive population study of women in Gothenburg
Kvinnoundersökningen i Göteborg. 'The results indicate that large fat cells contribute
to the development of type 2 diabetes, and we will now begin investigating the mechanisms
behind this finding. Increased knowledge about large fat cells and their effects may lead
to new preventive and therapeutic alternativs, says Malin Lönn, associate professor in
experimental medicine at the Sahlgrenska Academy.
Short-term stress enhances
anti-tumor activity in mice, Stanford study shows
Public speaking, anyone? Or maybe a big job interview? Dry your palms and take a deep,
calming breath; there may be a silver lining. Researchers at the Stanford University
School of Medicine have shown that, at least in laboratory mice, bouts of relatively
short-term stress can boost the immune system and protect against one type of cancer.
Furthermore, the beneficial effects of this occasional angst seem to last for weeks after
the stressful situation has ended. The finding is surprising because chronic stress has
the opposite effect -- taxing the immune system and increasing susceptibility to disease.
"This is the first evidence that this type of short-lived stress may enhance
anti-tumor activity," said Firdaus Dhabhar, PhD, associate professor of psychiatry
and behavioral sciences and a member of Stanford's Cancer Center, and Institute for
Immunity, Transplantation and Infection. "This is a promising new way of thinking
that calls for more research. We hope that it will eventually lead to applications that
help us to care for those who are ill, by maximally harnessing the body's natural defenses
while also using other medical treatments." The study will be published in a future
print issue of the journal Brain, Behavior, and Immunity, and a review copy of the article
is now available on the journal's Web site.
University of Iowa scientists use
blood-brain barrier as therapy delivery system
The blood brain barrier is generally considered an obstacle to delivering therapies from
the bloodstream to the brain. However, University of Iowa researchers have discovered a
way to turn the blood vessels surrounding brain cells into a production and delivery
system for getting therapeutic molecules directly into brain cells. Working with animal
models of a group of fatal neurological disorders called lysosomal storage diseases, the
UI team found that these diseases cause unique and disease-specific alterations to the
blood vessels of the blood brain barrier. The scientists used these distinct alterations
to target the brain with gene therapy, which reversed the neurological damage caused by
the diseases. The findings, which were published Sept. 13 in Nature Medicine's Advance
Online Publication (AOP), could lead to a new non-invasive approach for treating
neurological damage caused by lysosomal storage diseases. "This is the first time an
enzyme delivered through the bloodstream has corrected deficiencies in the brain,"
said lead investigator Beverly Davidson, Ph.D., UI professor of internal medicine,
neurology, and molecular physiology and biophysics. "This provides a real opportunity
to deliver enzyme therapy without surgically entering the brain to treat lysosomal storage
diseases. "In addition, we have discovered that these neurological diseases affect
not just the brain cells that we often focus on, but also the blood vessels throughout the
brain. We have taken advantage of that finding to delivery gene therapy, but we also can
use this knowledge to better understand how the diseases impact other cell types such as
neurons," she added. Lysosomal storage diseases are individually quite rare, but as a
group they affect approximately 1 in 8,000 live births. The diseases are caused by
deficiencies in enzymes that break down larger molecules. Without these enzymes, the large
molecules accumulate inside cells and cause cell damage and destruction.
Experimental drug lets B cells live
and lymphoma cells die
An investigative drug deprived non-Hodgkin lymphoma cells of their ability to survive too
long and multiply too fast, according to an early study published recently in the journal
Experimental Hematology. To function normally, the cells that make up bodily tissues must
"decide" when to divide and multiply (proliferate) and when to die. Cell death
restricts the human cell population as a counterbalance to growth, and billions of cells
must die each year just to hold the number constant. Cell growth and death are carefully
regulated by signaling networks, which either encourage or discourage survival. When this
counterpoise mistakenly shifts too far in favor of growth, tumors result. One such network
revolves around neurotropins, which "tell" nerve cells not to die, and to keep
multiplying, as part of normal function. The same neurotrophic signals are known to cause
cancers of the central nervous system when unbalanced by carcinogens. The current study
found that neurotrophins also cause key immune cells to resist cell death and proliferate
as part of the most deadly of lymphomas, and that an experimental compound, the fungal
chemical called K252a, restored their ability to die. Non-Hodgkin Lymphoma (NHL) is the
umbrella for more than 30 cancer types that develop in an important type of white blood
cell, the lymphocyte. Lymphocytes include B cells, workhorses of the immune system that
attach to invaders (e.g. bacteria, viruses) and produce an army of antibodies designed to
attack the specific pathogen at hand. In NHL, B cells in the lymphatic system grow
abnormally, and most patients are diagnosed too late to benefit from conventional
chemotherapy. "New approaches to the treatment of non-Hodgkin Lymphoma are urgently
needed, and the results of this study outline one with unusual promise," said Sanjay
Maggirwar, Ph.D., associate professor in the Department of Microbiology & Immunology
at the University of Rochester Medical Center, and corresponding author of the study.
"We believe we have found a subtle, precise mechanism that shortens the lifespan of
many kinds of cancer cells while enabling normal B cells to live on."
MDC researchers discover molecule
responsible for axonal branching
The human brain consists of about 100 billion (1011) neurons, which altogether form about
100 trillion (1014) synaptic connections with each other. A crucial mechanism for the
generation of this complex wiring pattern is the formation of neuronal branches. The
neurobiologists Dr. Hannes Schmidt and Professor Fritz G. Rathjen at the Max Delbrück
Center for Molecular Medicine (MDC) Berlin-Buch, Germany, have now discovered a molecule
that regulates this vital process. At the same time they have succeeded in elucidating the
signaling cascade induced by this molecule (PNAS, Early Edition, 2009, doi:10.1073)*.
Through the ramification of its fiber-like axon, a single neuron can send branches and
thus transmit information into several target areas at the same time. In principle,
neurobiologists distinguish between two kinds of axonal branching: branching of the growth
cone at the tip of an axon and the sprouting of collaterals (interstitial branching) from
the axon shaft. Both forms of axonal branching can be observed in sensory neurons, which
transmit the sensation of touch, pain and temperature, among others. When the axons of
these neurons reach the spinal cord, their growth cones first split (bifurcate) and
consequently the axons divide into two branches growing in opposite directions. Later new
branches sprout from the shaft of these daughter axons which penetrate the gray matter of
the spinal cord. Through investigations on sensory neurons, Dr. Hannes Schmidt and his
colleagues were able to identify a protein which triggers the splitting of the growth cone
of the sensory axons: the peptide CNP (the abbreviation stands for C-type natriuretic
peptide). In transgenic mice the scientists were able to show that CNP is formed in the
spinal cord precisely when sensory neurons grow into it. In the absence of CNP bifurcation
can no longer occur which results in reduced neuronal connectivity in the spinal cord.
Treating depression in pregnancy
A new report from the American Psychiatric Association (APA) and the American College of
Obstetricians and Gynecologists, which is published by Elsevier in the September-October
2009 issue of General Hospital Psychiatry
(http://journals.elsevierhealth.com/periodicals/ghp/home), explores the management of
pregnancy and depression. Depression is not uncommon in pregnant women. Between 14 and 23%
of pregnant women will experience a depressive disorder while pregnant. In 2003,
approximately 13% of pregnant women took an anti-depressant at some point during their
pregnancy. This rate has doubled since 1999. Many women go untreated due to concerns
regarding the safety of treating pregnant women. "The management of depression during
pregnancy: a report from the American Psychiatric Association and the American College of
Obstetricians and Gynecologists" describes results from an unusual collaboration of
authors from the American Psychiatric Association and American College of Obstetricians
and Gynecologists, as well as a consulting developmental pediatrician. These authors
reviewed the world's English-language literature and reported results describing the
association of depressive symptoms and anti-depressant treatment on fetal and neonatal
outcomes. Both depressive symptoms and anti-depressant exposure were found to be
associated with fetal growth changes and shorter gestations. Short-term neonatal
irritability and neurobehavioral changes were also linked with both maternal depression
and anti-depressant treatment. Some, but not all, studies reported low rates of fetal
malformations with first trimester exposure, but there was no specific pattern of defects
for individual medications or class of agents.
Ben-Gurion University Alzheimer's
researcher demonstrates specific immune response to vaccine
A researcher who is working on a vaccine for Alzheimer's disease (AD) has demonstrated
that it is possible to test and measure specific immune responses in mice carrying human
genes and to anticipate the immune response in Alzheimer's patients. This continuing
research at Ben-Gurion University of the Negev could one day lead to specific Alzheimer's
vaccines that reduce plaque, neuronal damage and inflammation associated with the disease.
Amyloid beta-peptide accumulates in the brain of AD patients where it appears to promote
neuronal damage. In the new article published in the Journal of Immunology, BGU researcher
Dr. Alon Monsonego determined that introducing A-beta into the brain triggers a natural
immune response which can be detected in humans. Importantly, the research team showed
that the specificity and magnitude of this body response to A-beta depends on certain key
genes of the immune system, which are highly polymorphic in the population (this means
that except for identical twins, almost each of us has a different combination of genes
termed "HLA alleles"). Furthermore, this research took an unusual approach
combining humans and humanized mouse models. "We began with characterizing the genes
in humans in a collaboration with the laboratories of Dr. Weiner and Dr. Selkoe at
Harvard, then did the same study in mice using a mouse model of multiple sclerosis witht
the laboratory of Dr. Altmann- Imperial College School of Medicine, UK," Monsonego
explains. "We then generated a humanized mouse model of AD, with a specific gene that
was present in approximately 30 percent of our study group (HLA DR15 allele). Conceivably,
those people that have this gene could receive the same vaccine which will teach a
person's immune system to better fight the disease." Monsonego continues, "As in
other mouse models of the disease, we show that with aging A-beta aggregates accumulate in
brain areas of cognitive functions and stimulate an inflammatory reaction in the brain.
However, stimulating an immune response to A-beta in these humanized mice not only
resulted in a highly efficient clearance of A-beta (plaque) from the brain, but also in a
markedly reduced inflammatory reaction. Furthermore, we were able to predict that the
characteristics of immune response in mice were the same as in the humans. "This
study thus provides the basis for developing an individual-based (personalized medicine)
immunotherapeutic approach to Alzheimer's disease since different populations will respond
differently to a vaccine based on their genetic background," Monsonego explains.
"Now that we've proven we can anticipate the specific responses for several abundant
genes in the population, further study is needed to ensure safety and efficacy in our
humanized mouse model of AD."
Vijf Harvard onderzoekers
accepteren de vitamine D theorie mbt autisme
Last month, Dr. Dennis Kinney and four of
his colleagues at Harvard University accepted the Vitamin D theory of autism and then
expanded it by adding five usual suspects. While I was thrilled to see the Vitamin D
theory accepted, appreciate them crediting the theory to me, and loved seeing their paper
in the same journal that published the original theory, Medical Hypotheses, their five
additions are all toxins, the usual suspects. The authors imply these toxins are delivered
to our genome by air or water pollution, such as mercury contaminated seafood, where these
toxins selectively damage the genome of those silly enough to be Vitamin D deficient.
My problem with the paper is the same problem I have with any of the air and water
pollution autism theories, why now? Certainly, if a toxin was causing autism, evidence
exists that exposure to that toxin has increased part and parcel with the epidemic of
autism. For awhile, that was one of the strongest arguments for the mercury in
vaccines theory; administration of more and more mercury-containing vaccines paralleled
the increase in autism. The problem with the vaccine theory is that when they took the
mercury out of vaccines, the incidence of autism went up, not down. What about air and
water pollution? Any self-respecting environmentalist will tell you pollution in the USA
is at record levels today; that is, American air and water has never been dirtier.
However, I am older than sixty, so that nonsense won’t work on me. I remember acid
lakes, burning eyes and blazing rivers. As a child, I remember thinking God wanted me to
see the air I breathed. That is, I remember the USA before the clean air and clean water
acts of the 1960s. If air and water pollution caused the autism epidemic, then that
epidemic began in the late 1940s, climbed dramatically in the 1950s, peaked in the 1960s
and then decreased in the late 1970s. Just did not happen.
One could accurately say that cleaner American air and water is associated with increasing
rates of autism, but with a significant lag time. Perhaps air pollution from Eastern
Europe, India and China, which has been increasing in the last 20 years, has engendered
the current crop of autism, the “foreigners did it” theory of autism. However,
why would foreign coal-burning air pollution of today do what good old American
coal-burning air pollution of the 50s and 60s could not? Take mercury in seafood,
terrible right? As mercury is one of the autism-causing toxins he listed, I assume Dr.
Kinney predicts mercury-containing seafood consumption during pregnancy would increase
risk of autism. However, I predict the opposite, that is, consumption of
mercury-containing seafood during pregnancy would improve the offspring’s mentation,
the benefits of Vitamin D in fish overwhelming any detriments of mercury. Consistent with
that prediction, the three largest studies found higher maternal consumption of
mercury-containing fish was associated with better, not worse, infant cognition with the
greatest benefit for infants whose mothers consumed the most mercury-containing fish. Do
not misunderstand me; the three studies below show mercury is bad, Vitamin D-rich fish and
mercury is better, and Vitamin D-rich fish without mercury is the best.
Oken E, et al. Maternal fish consumption, hair mercury, and infant cognition in a U.S.
Cohort. Environ Health Perspect. 2005 Oct;113(10):1376-80. [Link]
If you think the beneficial effect was from
omega-3 fats, you’d be wrong. In another Harvard study, the benefits for the child of
mother’s fish consumption again overwhelmed the harm from mercury. Omega-3 fats
consumption could not explain the beneficial effects of mercury-containing seafood, that
is, neither total maternal intake of omega-3, nor omega-3 content of mother’s red
blood cells, was associated with the child’s cognition.
Oken E, et al. Maternal fish intake during pregnancy, blood mercury levels, and child
cognition at age 3 years in a US cohort. Am J Epidemiol. 2008 May 15;167(10):1171-81. [Link
]
In yet a third study, NIH researchers found
benefits for mothers who ate mercury-containing seafood during pregnancy. Benefits of fish
consumption again overwhelmed the harm of toxins in fish. More importantly, low maternal
seafood consumption (and thus low seafood mercury consumption) resulted in children with
lower verbal IQs and suboptimal outcomes for pro-social behaviors, fine motor,
communication, and social development, that is, autistic symptoms.
Hibbeln JR, Maternal seafood consumption in pregnancy and neurodevelopmental outcomes in
childhood (ALSPAC study): an observational cohort study. Lancet. 2007 Feb
17;369(9561):578-85. [ Link
]
So I heartily recommend seafood to
expectant mothers and give my highest endorsement to vitamin D-rich, mercury-poor fish
like small salmon. (By the way, the omega-3 literature is hopelessly confounded by Vitamin
D.) However, the essence of Dr. Kinney and colleagues’ addition to the Vitamin D
theory is that at least some of the autism generating toxic genetic damage is done to the
father’s sperm, not the mother’s egg.
That is, toxins ingested by Vitamin D deficient men causes oxidative damage leading to
genetic mutations in sperm. The authors’ suggestion is to give Vitamin D to men,
before they go around impregnating women, to prevent genetic damage by toxins and thus
prevent autism. While I certainly agree men should take Vitamin D before they impregnate
anyone (and I suspect they will be more successful in their mission if they do), I doubt
healthy men will take Vitamin D any time soon.
Even if the new Food and Nutrition Board recommends 5,000 IU/day for healthy adults –
and they won’t – healthy men will ignore any new FNB recommendation because most
men will not take supplements, unless they think it prevents hair loss, increases sexual
abilities or improves athletic performance (Vitamin D has no effect on the first two but
certainly improves the third).
However, unlike men, pregnant women will take a supplement, and almost always do so, a
prenatal vitamin. Currently, that prenatal contains a meaningless 10 micrograms of Vitamin
D (400 IU). Say it contained a physiological amount, say 125 micrograms (5,000 IU). If it
did, I predict the incidence of congenital autism (obvious in the first few months of
life) would dramatically reduce almost immediately and the overall incidence would begin
decreasing in several years. However, it would not affect the autism caused by the severe
childhood Vitamin D deficiency that occurs when toddlers are weaned from Vitamin D rich
formula to my favorite toxin, natural organic fruit juice.
All in all, I liked Dr. Kinney and colleagues’ paper; I hope Dr. Kinney can wake
someone up at Autism Speaks, which funds Dr. Kinney. (If Autism Speaks doesn’t hurry
and help fund the Vitamin D Council, they won’t be able to get any credit at all for
helping discover the cause of autism.) The authors also listed evidence that strengthens
the Vitamin D theory of autism, evidence I discussed in the original paper. [ Link
]
That evidence is: 1) autism is more common
in cloudy and rainy areas; 2) dark-skinned immigrants have much higher rates of autism; 3)
there are more cases in the northern US than in the South, and 4) autism is more common in
urban than rural areas, just like rickets. The authors forgot to add a fifth fact, the NIH
found widespread bony abnormalities in autistic kids, abnormalities that look like the
effects of chronic low-grade rickets to me.
Also, if Dr. Kinney and colleagues are correct in their revision of my theory, then
Vitamin D should not have a treatment effect in children with autism, unless Vitamin D can
repair
genetic defects. I predict the opposite: Vitamin D will be found to have a treatment
effect in autism, as Vitamin D acts quickly to prevent further oxidative brain damage and
increases brain glutathione, which promptly dispatches the usual suspects.
John Cannell, MD
The Vitamin D Council
National autism research led by
Leicester specialist
The first ever major study into adults living with autism was published today (Tuesday
22nd September) by the NHS Information Centre. The report, entitled 'Autism Spectrum
Disorders in adults living in households throughout England 2007' was written by Professor
Terry Brugha, a Consultant Psychiatrist with Leicestershire Partnership NHS Trust and
Professor of Psychiatry at the University of Leicester with a team of UK researchers This
ground-breaking study shows for the first time an estimate of how many adults are living
with autism spectrum disorders (ASDs) in England. The study into the prevalence of autism
spectrum disorders among adults shows that one in every hundred adults living in
households has the condition – broadly the same rate as that cited for children.While
studies have been carried out into the prevalence of autism spectrum disorders among
children, the report is the first attempt to find and count adults and older people in the
community with an autism spectrum disorder, including Asperger syndrome. Professor Brugha,
a specialist in the assessment of adults who may have ASDs including Aspergers syndrome,
runs an NHS diagnostic clinic at the Brandon Mental Health Unit. He worked collaboratively
with a team of academics and researchers, including his colleagues from the University of
Leicester to develop a research programme and survey tool. The team surveyed thousands of
people across England to determine how many adults in the general population are likely to
be affected by ASD's. Months of analysis, much of which was undertaken at the University
of Leicester, and hundreds of face to face interviews and diagnostic assessments have for
first time ever, captured the typical characteristics of someone with an ASD, including
gender, age range, employment status, type of housing and use of health services.
New discovery reveals fate of
nanoparticles in human cells
Scientists funded by the Biotechnology and Biological Sciences Research Council (BBSRC)
have uncovered what happens to biomimetic nanoparticles when they enter human cells. They
found that the important proteins that make up the outer layer of these nanoparticles are
degraded by an enzyme called cathepsin L. Scientists now have to take this phenomenon into
account and overcome this process to ensure the exciting field of nanomedicine can
progress. The research is published today (22 September) in ACS Nano. Dr Raphaël Lévy, a
BBSRC David Phillips Fellow at the University of Liverpool and lead researcher on the
project said: “We’ve known for some time that nanoparticles are taken into cells
and there have been experiments done to establish their final destinations, but we
didn’t know until now what state they are in by the time they get there.” In
most biological applications, nanoparticles are coated with a layer of molecules, often
proteins, which determine the use of nanoparticles when they enter cells. The researchers
have confirmed, in a wide range of cells, that nanoparticles are taken into a region
called the endosome, where this essential coating is degraded by cathepsin L. Dr Violaine
Sée, also a BBSRC David Phillips Fellow at the University of Liverpool, and joint
corresponding author, added: “One of the promising applications of nanoparticles in
medicine is to use them as a method to deliver therapeutic protein molecules inside cells.
For these biological therapies to be effective the proteins have to be maintained with
high integrity and unfortunately we have seen this compromised by the degrading action of
cathepsin L.”
New multi-use device can shed light
on oxygen intake
A fiber-optic sensor created by a team of Purdue University researchers that is capable of
measuring oxygen intake rates could have broad applications ranging from plant root
development to assessing the effectiveness of chemotherapy drugs. The self-referencing
optrode, developed in the lab of Marshall Porterfield, an associate professor of
agricultural and biological engineering, is non-invasive, can deliver real-time data,
holds a calibration for the sensor's lifetime and doesn't consume oxygen like traditional
sensors that can compete with the sample being measured. A paper on the device was
released on the early online version of the journal The Analyst this week.
To regenerate muscle, cellular
garbage men must become builders
For scientists at the European Molecular Biology Laboratory (EMBL) in Monterotondo, Italy,
what seemed like a disappointing result turned out to be an important discovery. Their
findings, published online this week in the journal Proceedings of the National Academy of
Sciences (PNAS), provide conclusive proof that, when a muscle is injured, white blood
cells called macrophages play a crucial role in its regeneration. The scientists also
uncovered the genetic switch that controls this process, a finding that opens the door for
new therapeutic approaches not only to sports injuries but also to diseases such as
Duchenne muscular dystrophy. Normally, macrophages – the white blood cells known for
engulfing and eliminating bacteria and other infectious agents – are drawn to areas
of injury. Once there, they act as garbage men, eliminating the dead cells and releasing
pro-inflammatory factors, fending off infection. After clearing up the debris, macrophages
stop releasing those pro-inflammatory factors, and start making anti-inflammatory factors
that promote repair in the damaged area. This shift from clearing debris to promoting
building is known as macrophage polarization, and Claus Nerlov, Nadia Rosenthal and
colleagues proved that it is essential for muscles to regenerate properly.
A consistent decline in heart
attack rates following the implementation of smoking bans
Strongly enforced legislation to restrict smoking produces rapid and substantial
reductions in community rates of heart attack, according to a meta-analysis published
today in Circulation, the journal of the American Heart Association.(1) The analysis
pooled 13 studies from regions in North America, Italy, Scotland and Ireland and, despite
their geographical range, found a consistent reduced risk of hospitalisation for heart
attack (acute myocardial infarction, AMI) of 17% (ie, a relative risk for AMI of 0.83) at
12 months following implementation of the law. The investigators added that this benefit
"grows with time", reaching a gain of "about 36%" in three years. The
study was designed to determine the "consistent" effect of smoking bans on AMI
rates in communities, and was therefore concerned with both the direct and second-hand
effects of smoking. Several studies have shown that the effects of second-hand smoke on
many biological mediators associated with AMI risk occur rapidly and are nearly as large
as those from direct smoking. For example, a study reported last year showed that passive
exposure to second-hand smoke in as short a time as 24 hours led to "sustained
vascular injury" characterised by reduced endothelial function and activity of
endothelial progenitor cells.(2) According to the American Heart Association's Heart
Disease and Stroke Statistics 2009 Update, non-smokers exposed to second-hand smoke at
home or at work have a 25-30% increased risk of developing heart disease. Since the first
smoking bans were introduced (the first in Europe was in 2004 in Ireland) there have been
many reports showing a decline in hospital admissions for AMI following implementation.
Indeed, such laws are the best current examples of a clear association between prevention
policies and cardiovascular disease. In Europe reduced AMI rates following smoking bans
have been reported from France (15% decrease), Italy (11.2%), and Ireland (11%).
Cancer Predisposition From Gene
Variant Shows Strong Gender Bias
Cancer predisposition resulting from the presence of a specific gene variant shows a
strong gender bias, researchers at the University of Cincinnati (UC) have demonstrated. In
addition, the research indicates that the risk for development of cancer in individuals
harboring the gene variant can be further increased as a result of environmental exposure.
Peter Stambrook, PhD, a professor in the department of molecular genetics, biochemistry
and microbiology, and colleagues report their findings this week in Proceedings of the
National Academy of Sciences (PNAS). Co-authors include researchers from Wright State
University and the Laboratory for Health Protection Research, National Institute of Public
Health and the Environment, the Netherlands. Stambrook says the gene CHEK2 is part of a
DNA damage response pathway that can have an impact on whether or not cancers develop. A
CHEK2 variant, CHEK2*1100delC, is associated with increased risk of cancer.
New chemically-activated antigen
could expedite development of HIV vaccine
Scientists working to develop a vaccine for the human immunodeficiency virus (HIV) report
they have created the first antigen that induces protective antibodies capable of blocking
infection of human cells by genetically-diverse strains of HIV. The new antigen differs
from previously-tested vaccines by virtue of its chemically-activated property that
enables close sharing of electrons and produces strong covalent bonding. Researchers used
a mouse model to generate the antibodies. The report by researchers at The University of
Texas Health Science Center at Houston is online and will appear in a print issue of the
Journal of Biological Chemistry in November."The complexity of HIV has for long
thwarted development of an effective HIV vaccine. Our findings open a new path toward an
effective preventative and therapeutic vaccine," said Sudhir Paul, Ph.D., the study's
senior author and a professor in the Department of Pathology and Laboratory Medicine at
The University of Texas Medical School at Houston. "The new antigen is a prototype
vaccine. This prototype successfully eliminates nature's restrictions on the production of
broadly-neutralizing antibodies to HIV by the immune system." Thirty-three million
people were living with HIV at the end of 2007, according to the World Health
Organization. That same year, nearly 3 million people became newly infected, and 2 million
died of acquired immunodeficiency syndrome or AIDS, which occurs at the most advanced
stages of HIV infection. Vaccines work by introducing an antigen into the body, which
spurs the immune system to produce antibodies that guard against infection.
Previously-tested HIV vaccine candidates stimulated vigorous production of antibodies to
the mutable segments of the virus envelope. But, these vaccine candidates did not
stimulate the production of antibodies to the regions essential for virus attachment to
host T cells, the process that initiates infection.
Study looks at using the immune
system to reduce prostate cancer risk
Immune therapies have been explored as a way to treat cancer after it develops. But a new
study from the University of Michigan Comprehensive Cancer Center suggests that genetic
risk of prostate cancer can be reduced by rescuing critical immune system cells. The study
was done in mice and would need further validation and extensive testing in the lab before
being available for humans. But the results are promising for people with a strong family
history of cancer or known cancer genes.
Discovery could improve hepatitis C
treatment
Walter and Eliza Hall Institute researchers are part of an international team that has
discovered a genetic variation that could identify those people infected with hepatitis C
who are most likely to benefit from current treatments. Dr Melanie Bahlo and Dr Max
Moldovan from the institute’s Bioinformatics division worked with researchers from
the University of Sydney and elsewhere to analyse the genomes of more than 800 people,
including more than 300 Australians, who were receiving treatment for chronic hepatitis C
infection. Their genome-wide association study of people receiving hepatitis C treatment
revealed that genetic variants near the interferon gene IL28B were associated with
people’s response to treatment. Three per cent of the world’s people are
infected with hepatitis C and few are able to clear the virus without treatment. The
standard treatment is a combination of pegylated interferon-alpha and ribavirin
(PEG-IFN-alpha/RBV). However this treatment is expensive ($20,000 per person in
Australia), can have serious adverse effects and is unsuccessful in 50-60 per cent of
cases.
UAB Research Finds Childbearing
Increases Chance of Developing the Metabolic Syndrome
Childbearing is associated directly with future development of the metabolic syndrome -
abdominal obesity, high triglycerides, insulin resistance and other cardiovascular disease
risk factors - and for women who have had gestational diabetes, the risk is more than
twice greater, according to a study co-authored by University of Alabama at Birmingham
(UAB) researchers published in the American Journal of Obstetrics and Gynecology. UAB
Professor of Preventive Medicine Cora E. Lewis, M.D., M.S.P.H., and colleagues used data
collected in the CARDIA (Coronary Artery Risk Development in Young Adults) study to
determine the correlation between a higher incidence of the metabolic syndrome among women
ages 18-30 at the start of the study who bore at least one child during the 20-year period
following. "Pregnancy can have lasting, adverse physiological effects and may result
in behavioral changes," Lewis said. "Some previous studies have shown an
association between childbearing and the metabolic syndrome, and some have shown that a
history of gestational diabetes is a strong predictor of Type 2 diabetes. "However,
these studies lacked the preconception measurements to establish a baseline with which to
measure the changes brought on by pregnancy," she said. "Many have not had
control groups of women who had not had pregnancies, and thus they have rarely provided
conclusive evidence linking pregnancy-related risk factor changes to disease onset. CARDIA
began following participants ages 18-30 years in 1985-1986 and continues today, and we had
the necessary information to track women both before and after pregnancy and to compare
women with pregnancies to those without."
Women with Atrial Fibrillation Are
at Significantly Higher Risk of Stroke and Death Compared to Men and Receive Less
Attention
Even though the incidence of atrial fibrillation is higher in men than women, a review of
past studies and medical literature completed by cardiac experts at Rush University
Medical Center shows that women are more likely than men to experience symptomatic
attacks, a higher frequency of recurrences, and significantly higher heart rates during
atrial fibrillation, which increases the risk of stroke. Findings from the review of past
studies will be published in the September issue of Gender Medicine. Atrial fibrillation
is a cardiovascular disorder affecting 2.2 million people in the United States. During
atrial fibrillation, the heart's atria, which are two small upper chambers, quiver instead
of beating effectively. Blood isn't pumped completely out of the atria, so it may pool and
clot. If a piece of a blood clot in the atria leaves the heart and becomes lodged in an
artery in the brain, a stroke results. In recent years, women have surpassed men in both
prevalence and mortality due to cardiovascular disease.
Study reveals 2/3 of prostate
cancer patients do not need treatment
In the largest study of its kind, the international team of pathologists studied an
initial 4,000 prostate cancer patients over a period of 15 years to further understanding
into the natural progression of the disease and how it should be managed. The research,
published in the British Journal of Cancer, could be used to develop a blood test to
distinguish between aggressive and non-aggressive forms of prostate cancer. Globally,
prostate cancer is the fifth most common malignancy and accounts for 13% of male deaths in
the UK. Studies have shown that men with non-aggressive prostate cancer can live with the
disease untreated for many years, but aggressive cancer requires immediate treatment.
Pathologists found that the presence of a protein, called Hsp-27, in cancer cells was an
indicator that the disease will progress and require treatment. The study showed, however,
that in more than 60% of cases the protein was not expressed and the cancer could be
managed by careful monitoring, rather than with active invention methods, such as drug
treatment or surgery. The protein normally has a positive function in the body, helping
healthy cells survive when they are placed under 'stressful' conditions, such as disease
or injury. If the protein is expressed in cancer, however, it can prevent the diseased
cells from dying, allowing the cancer to progress. The team, supported by Cancer Research
UK (CRUK) and in collaboration with scientists in London and New York, found that the
protein can be used to predict how the disease will behave and could help doctors advise
patients on how the disease could affect their daily lives. Professor Chris Foster, Head
of the University's Division of Pathology, explains: "Cancer of any kind is a very
distressing disease and has the ability to impact on every aspect of a person's life.
Chemotherapy and surgery can also have a significant effect on health and wellbeing and
that is why it is important that we first understand the biological nature of the disease
and how it will behave in each individual patient, before determining if and when a person
needs a particular type of treatment.
Trial of new treatment for advanced
melanoma shows rapid shrinking of tumors
Researchers have made significant advances in the treatment of metastatic malignant
melanoma – one of the most difficult cancers to treat successfully once it has
started to spread – according to a study to be presented at Europe's largest cancer
congress, ECCO 15 – ESMO 34 [1], in Berlin on Thursday. In the phase I extension
study, researchers have seen rapid and dramatic shrinking of metastatic tumours in
patients treated with a new compound that blocks the activity of the cancer-causing
mutation of the BRAF gene, which is implicated in about 50% melanomas and 5% of colorectal
cancers. In new results from 31 melanoma patients with the BRAF mutation who were treated
with 960mg of PLX4032 twice a day, 64% (14) of the 22 patients who could be evaluated so
far met the official criteria for partial response (this involves the diameter of tumours
shrinking by at least 30% for at least a month). A further six of the 22 patients also
showed a response, but, at the time of the congress presentation, it was too early to say
whether the tumours would shrink far enough to meet these criteria. Dr Paul Chapman, an
attending physician on the Melanoma/Sarcoma service at Memorial Sloan-Kettering Cancer
Center (New York, USA) and who was one of the leaders of the trial, told a news briefing:
"We are very excited about these results. Of the 22 patients we have been able to
evaluate so far, 20 have had some objective tumour shrinkage. This is impressive as they
all had metastatic disease and most of them had failed several prior therapies. A lot of
these patients were pretty sick but many of them had a significant and rapid improvement
in the way they function. We've had patients come off oxygen and we've got several
patients who have been able to come off narcotic pain medication soon after starting
treatment." The trial is investigating PLX4032 in patients with the BRAF mutation,
and results from the first 55 patients were reported at a cancer meeting earlier this year
(ASCO 2009). These data had been aimed at finding the best dose of PLX4032 to give to
patients. However, the phase I extension data reported at ECCO 15 – ESMO 34 focuses
on a subsequent group of an additional 31 patients who were all treated at the maximum
tolerated dose of the drug (a 960 mg pill twice a day). All the patients had the BRAF
mutation.
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