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News - Week 1 - 2009
The Beautiful Truth - MSG
U. S. Senate Minority
Report: More Than 650 International Scientists Dissent Over Man-Made Global Warming Claims
Scientists Continue to Debunk “Consensus” in 2008
Over 650 dissenting scientists from
around the globe challenged man-made global warming claims made by the United Nations
Intergovernmental Panel on Climate Change (IPCC) and former Vice President Al Gore. This
new 231-page U.S. Senate Minority Report -- updated from 2007’s groundbreaking report
of over 400 scientists who voiced skepticism about the so-called global warming
“consensus” -- features the skeptical voices of over 650 prominent international
scientists, including many current and former UN IPCC scientists, who have now turned
against the UN IPCC. This updated report includes an additional 250 (and growing)
scientists and climate researchers since the initial release in December 2007. The over
650 dissenting scientists are more than 12 times the number of UN scientists (52) who
authored the media-hyped IPCC 2007 Summary for Policymakers.
The chorus of skeptical scientific voices grow louder in 2008 as a steady stream of
peerreviewed studies, analyses, real world data and inconvenient developments challenged
the UN’s and former Vice President Al Gore's claims that the "science is
settled" and there is a "consensus." On a range of issues, 2008 proved to
be challenging for the promoters of manmade climate fears. Promoters of anthropogenic
warming fears endured the following: Global temperatures failing to warm; Peer-reviewed
studies predicting a continued lack of warming; a failed attempt to revive the discredited
“Hockey Stick”; inconvenient developments and studies regarding rising CO2; the
Sun; Clouds; Antarctica; the Arctic; Greenland’s ice; Mount Kilimanjaro; Causes of
Hurricanes; Extreme Storms; Extinctions; Floods; Droughts; Ocean Acidification; Polar
Bears; Extreme weather deaths; Frogs; lack of atmospheric dust; Malaria; the failure of
oceans to warm and rise as predicted.
AngloINFO
AngloINFO is the world's top network
of websites for English-speakers living abroad. It operates in many regions of countries
around the world providing vital support and information to the local international
communities.
The brain acts as a computer to both store information and process that information. In a
computer, separate devices perform these roles; while a hard disk stores information, the
central processing unit (CPU) does the processing. But the brain is thought to perform
both these functions in the same cells – neurons – leading researchers to ask if
distinct molecules within the brain cells serve these different functions. In a discovery
that may one day lead to the ability to erase debilitating painful memories and addictions
from the brain, researchers at SUNY Downstate Medical Center have found that a molecule
known to preserve memories – PKMzeta – specifically stores complex, high-quality
memories that provide detailed information about an animal's location, fears, and actions,
but does not control the ability to process or express this information. This finding
suggests that PKMzeta erasure that is designed to target specific debilitating memories
could be effective against the offending memory while sparing the computational function
of brain.
UCSB scientists show how certain
vegetables combat cancer
Women should go for the broccoli when the relish tray comes around during holiday
celebrations this season. While it has been known for some time that eating cruciferous
vegetables, such as broccoli, cauliflower, and cabbage, can help prevent breast cancer,
the mechanism by which the active substances in these vegetables inhibit cell
proliferation was unknown — until now. Scientists in the UC Santa Barbara
laboratories of Leslie Wilson, professor of biochemistry and pharmacology, and Mary Ann
Jordan, adjunct professor in the Department of Molecular, Cellular, and Developmental
Biology, have shown how the healing power of these vegetables works at the cellular level.
Their research is published in this month's journal Carcinogenesis. "Breast cancer,
the second leading cause of cancer deaths in women, can be protected against by eating
cruciferous vegetables such as cabbage and near relatives of cabbage such as broccoli and
cauliflower," said first author Olga Azarenko, who is a graduate student at UCSB.
"These vegetables contain compounds called isothiocyanates which we believe to be
responsible for the cancer-preventive and anti-carcinogenic activities in these
vegetables. Broccoli and broccoli sprouts have the highest amount of the isothiocyanates.
Penn Study Finds Reduction in
Antibody Gene Rearrangement in B Cells Related to Type 1 Diabetes, Lupus
More drafts usually mean a better product and so it also seems to go with the human immune
system. As B cells develop, genes rearrange to allow their antibodies to recognize
different foreign invaders or pathogens. But sometimes antibodies are created that
recognize and attack the body’s own cells. These self-reactive antibodies, like early
drafts of a manuscript, must be edited into safer versions. This process is called
receptor editing and is important for central or early B cell tolerance, which occurs
while B cells are still developing in the bone marrow. A research team led by Nina Luning
Prak, M.D., Ph.D, Assistant Professor in the Department of Pathology and Laboratory
Medicine at the University of Pennsylvania School of Medicine, has discovered that this
editing process may go awry in people with certain types of autoimmune diseases.
A new light on tumor immunotherapy
for gastric cancer
Dendritic cells (DCs) are professional antigen presenting cells (APCs) that both initiate
and modulate the immune response. DCs are cells in the pathway of antigen capture and
presentation to T cells, with the unique ability to directly prime naïve CD4+ and CD8+ T
cells. Gastric cancer is one of the most common cancers. Although gastric cancer therapy
has made great progress, it is still difficult to treat advanced gastric cancer, as it has
spread to the lymph glands and metastasized. Currently, tumor immunotherapy for gastric
cancer has potential. DCs are believed to be essential for stimulating tumor-specific
cytotoxic T lymphocyte (CTL) and inducing the protective and therapeutic anti-tumor
immunity. A research team led by Dr. Liang Wang from China investigated whether bone
marrow-derived DCs (BM-DCs) pulsed with tumor lysates induce immunity against gastric
cancer. Their results will be published on December 14, 2008 in the World Journal of
Gastroenterology.
A potential drug for
ischemia/reperfusion related liver injury
Hepatic injury caused by ischemia/reperfusion (I/R) has been proposed as a key clinical
problem associated with liver transplantation and major liver surgery. The production of
reactive oxygen species (ROS), including superoxide, hydrogen peroxide, and hydroxyl
radical, has been demonstrated in reperfusion injury. Resveratrol has been reported to
have several biologic effects such as a potent antioxidative effect via prevention of
lipid peroxidation. A research team led by Ercan Gedik from Turkey evaluated the possible
protective effect of resveratrol against I/R-induced hepatic injury, using biochemical and
histological parameters. This will be published on December 14, 2008 in the World Journal
of Gastroenterology.
The ability to regenerate after major tissue damage or surgical intervention is an
important property of the liver. Since liver resection is an established therapeutic
measure for severe liver diseases, it would be of importance to know which molecular
events underly the regenerative process and if they depend on the extent of resection, as
indicated in previous studies. The group led by Prof. Schlaak from the Department of
Gastroenterology and Hepatology of the University Hospital of Essen compared rats
undergoing 70% and 90% liver resection. Serum parameters, activation of transcription
factors, expression of cytokines known as imperative for the start of liver regeneration
and apoptosis in the regenerating liver tissue were analyzed. A broad spectrum of methods
came into use, including quantitative real time PCR on mRNA-isolates and TUNEL staining of
histological samples. This will be published on December 14, 2008 in the World Journal of
Gastroenterology. They found that apart from increased liver damage and reduced liver
function parameters found in serum samples, molecular events as cytokine expression,
especially IL-6 and TNF-alpha were strongly reduced after extensive resection. In addition
the activation of NF-kappa B was delayed by almost 24 h. Programmed cellular death, known
as apoptosis, was partially increased at 24 h and at 7 d postoperatively in the livers of
animals which underwent 90% resection in comparison to rats which only had 70% of their
liver resected.
Vitamin D deficiency associated
with greater rates of cesarean sections
Researchers from Boston University School of Medicine (BUSM) and Boston Medical Center
(BMC) found that pregnant women who are vitamin D deficient are also at an increased risk
for delivering a baby by caesarean section as compared to pregnant women who are not
vitamin D deficient. These findings currently appear on-line in the Journal of Clinical
Endocrinology & Metabolism. At the turn of the 20th century, women commonly died in
childbirth due to "rachitic pelvis" rickets of the pelvis. While rickets
virtually disappeared with the discovery of vitamin D, recent reports suggest that vitamin
D deficiency is widespread in industrialized nations. Over a two-year period, the
researchers analyzed the relationship between maternal serum 25-hydroxyvitamin D [25(OH)D]
and the prevalence of primary caesarean section. In total, 253 women were enrolled in this
study, of whom 43 (17 percent) had a caesarean section. The researchers found that 28
percent of women with serum 25(OH)D less than 37.5 nmol/L had a caesarean section,
compared to only 14 percent of women with 25(OH)D greater than 37.5 nmol/L. "In our
analysis, pregnant women who were vitamin D deficient at the time of delivery had almost
four times the odds of caesarean birth than women who were not deficient," said
senior author Michael Holick, MD, PhD, director of the General Clinical Research Center
and professor of medicine, physiology and biophysics at BUSM and Anne Merewood assistant
professor of pediatrics at BUSM and lead author of the study.
Nutritious fast-food kids’
meals are scarce, researchers find
Only 3 percent of kids’ meals served at fast-food restaurants met federal dietary
guidelines in the first study to examine the nutrient quality of such meals in a major
U.S. metropolitan market. Michigan State University’s Sharon Hoerr, a food science
and human nutrition researcher with the Michigan Agricultural Experiment Station, teamed
up with economist Sharon O’Donnell and pediatrician Jason Mendoza from Baylor College
of Medicine in Houston to assess the nutritional status of kids’ meals in the Houston
market. The small percentage of meals that did meet dietary guidelines included fruit as a
side dish and milk, and nearly all were deli-sandwich meals. They also had about one-third
the fat, one-sixth the added sugars, twice the iron and three times the amount of vitamin
A and calcium as did meals not meeting the criteria.
Simple Model Predicts Those at Risk
for Chronic Kidney Disease
Traditionally, doctors have had no clear way to predict which of their patients might be
headed down the road to chronic kidney disease (CKD). Now, researchers at
NewYork-Presbyterian Hospital/Weill Cornell Medical Center and the University of North
Carolina at Chapel Hill have created a simple eight-point risk factor checklist to do just
that. As reported in a special double issue (Dec. 8 and 22) of the Archives of Internal
Medicine, the model accurately stratifies middle-aged and older patients at high risk for
newly diagnosed CKD, which involves a gradual, even fatal loss of kidney function over
time. According to the National Kidney Foundation, 26 million American adults have CKD and
millions of others are at increased risk. "These patients are often battling
concurrent conditions such as diabetes or heart disease, so anything we can do to predict
and then lower their risk for kidney disease will be invaluable," says study senior
author Dr. Phyllis A. August, the Ralph A. Baer Professor of Medical Research at Weill
Cornell Medical College, and an internist and nephrologist at NewYork-Presbyterian
Hospital/Weill Cornell Medical Center.
New evidence that people make
aspirin's active principle -- salicylic acid
Scientists in the United Kingdom are reporting new evidence that humans can make their own
salicylic acid (SA) — the material formed when aspirin breaks down in the body. SA,
which is responsible for aspirin's renowned effects in relieving pain and inflammation,
may be the first in a new class of bioregulators, according to a study scheduled for the
Dec. 24 issue of ACS' biweekly Journal of Agricultural and Food Chemistry. In the report,
Gwendoline Baxter, Ph.D. and colleagues discuss how their past research revealed that SA
exists in the blood of people who have not recently taken aspirin. Vegetarians had much
higher levels, almost matching those in patients taking low doses of aspirin. Based on
those findings, the researchers previously concluded that this endogenous SA came from the
diet, since SA is a natural substance found in fruits and vegetables.
Immune cells contribute to the
development of Parkinson's disease
Parkinson disease is a neurodegenerative disorder that impairs movement, balance, speech,
and other functions. It is characterized by the loss of nerves in the brain that produce a
substance known as dopamine. Although the loss of dopamine-containing nerves is
accompanied by accumulation of immune cells known as T cells, these accumulating T cells
were not thought to have a role in the development of disease. However, Stéphane Hunot,
Etienne C. Hirsch, and colleagues, at INSERM UMR 679, France, have now shown that CD4+ T
cells make a significant contribution to the development of disease in a mouse model of
Parkinson disease.
Potential autoimmunity-inducing
cells found in healthy adults
It's not just patients with autoimmune diseases like lupus and rheumatoid arthritis (RA)
that have self-attacking immune cells—healthy people have them too, according to a
new report in the Journal of Experimental Medicine. In healthy adults, however, these
cells are maintained in an 'off' state, perhaps explaining their innocuous nature. Whether
these cells are the true predecessors of the self-attacking cells prevalent in lupus and
RA and, if so, what prevents them from causing disease in everyone is not yet known. The
new study will appear online on December 22nd. As antibody-producing B cells develop in
the bone marrow, the body tests them to determine whether their antigen receptors are apt
to confuse self tissues for intruders. If so, their receptors are either rearranged to
make new, non-autoreactive versions—a process called 'receptor editing'—or the
cells are killed off while still in the bone marrow. Yet a minority manages to escape,
slipping into the body as mature B cells with a propensity for self-attack.
Tobacco firm used extensive
strategy to undermine secondhand smoke policy in China
British American Tobacco (BAT), one of the world's largest transnational tobacco companies
(TTCs), carried out an extensive, multi-pronged strategy to undermine the health policy
agenda on secondhand smoke (SHS) in China, finds a new study published in PLoS Medicine.
In 2007, the Chinese Ministry of Health estimated that 540 million Chinese were exposed to
SHS, resulting in over 100,000 deaths annually. The only effective way to reduce tobacco
smoke exposure indoors is to implement 100% smoke-free environments (alternatives such as
ventilation, filtration, and the provision of segregated areas for smokers and nonsmokers
are insufficient). Smoke-free policies are proven to decrease overall cigarette
consumption, to encourage smokers to quit, and to protect the health of nonsmokers.
Monique Muggli (Mayo Clinic, Rochester, USA) and colleagues analyzed internal corporate
documents produced by BAT, the predominant TTC in China, in response to litigation against
major cigarette manufacturers. The documents are stored in depositories in Minnesota, USA
and Guildford, UK. Among these documents, they found evidence that BAT had attempted to
divert attention away from SHS issues toward liver disease prevention by funding the
Beijing Liver Foundation (BLF) from its inception in 1997 until at least 2002 (the most
recent year that BAT's corporate records are available for public review).
Tobacco company scientist gained
access to WHO collaborating center
A new study of previously confidential tobacco industry documents shows that a Philip
Morris scientist established close connections with a WHO Collaborating Centre in Thailand
called the Chulabhorn Research Institute (CRI). The study is published in this week's PLoS
Medicine. The CRI is an internationally renowned teaching institution for a variety of
scientific disciplines, including environmental toxicology (the study of how chemicals in
the environment, such as tobacco smoke, can affect human health). The institute is
designated a WHO Collaborating Centre, carrying out activities in support of the WHO's
public health programs.Ross MacKenzie (School of Public Health, University of Sydney,
Australia) and Jeff Collin (Centre for International Public Health Policy, University of
Edinburgh, Scotland) analyzed tobacco company documents that were made publicly available
online following litigation in the United States. Philip Morris documents revealed that
ostensibly independent overseas scientists, now identified as industry consultants, were
able to gain access to the Thai scientific community. Most significantly, a Philip Morris
scientist called Roger Walk established close connections with the CRI.
Newly identified gene powerful
predictor of colon cancer metastasis
Cancer Researchers at the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch
and the Charité – Universitäts Medizin Berlin (Germany) have identified a gene
which enables them to predict for the first time with high probability if colon cancer is
going to metastasize. Assistant Professor Dr. Ulrike Stein, Professor Peter M. Schlag, and
Professor Walter Birchmeier were able to demonstrate that the gene MACC1
(Metastasis-Associated in Colon Cancer 1) not only promotes tumor growth but also the
development of metastasis.When MACC1 gene activity is low, the life expectancy of patients
with colon cancer is longer in comparison to patients with high MACC1 levels. (Nature
Medicine, doi 10.1038/nm.1889)*.According to the National Institutes of Health in
Bethesda, Maryland, USA, more than 108,000 people developed colon cancer in the US in
2008. Despite surgery, chemo- and radiotherapy, only 50 percent of patients can be cured
because 20 percent of the patients have already developed metastasis by the time their
colon cancer is diagnosed. In addition, one-third of patients whose treatment of the
original colon cancer was successful will, nevertheless, go on to develop metastasis.
Two cardiovascular proteins pose a
double whammy in Alzheimer's
Researchers have found that two proteins which work in tandem in the brain's blood vessels
present a double whammy in Alzheimer's disease. Not only do the proteins lessen blood flow
in the brain, but they also reduce the rate at which the brain is able to remove amyloid
beta, the protein that builds up in toxic quantities in the brains of patients with the
disease. The work, described in a paper published online Dec. 21 in the journal Nature
Cell Biology, provides hard evidence directly linking two processes thought to be at play
in Alzheimer's disease: reduction in blood flow and the buildup of toxic amyloid beta. The
research makes the interaction between the two proteins a seductive target for researchers
seeking to address both issues. Scientists were surprised at the finding, which puts two
proteins known for their role in the cardiovascular system front and center in the
development of Alzheimer's disease. "This is quite unexpected," said Berislav
Zlokovic, M.D., Ph.D., a neuroscientist and a senior author of the study. "On the
other hand, both of these processes are mediated by the smooth muscle cells along blood
vessel walls, and we know that those are seriously compromised in patients with
Alzheimer's disease, so perhaps we shouldn't be completely surprised." The new
findings are the result of a seven-year collaboration between two laboratories. Zlokovic
heads the Center for Neurodegenerative and Vascular Brain Disorders, looking at molecular
roots of diseases like Alzheimer's. Several years ago, after he found that several genes
well known to cardiovascular researchers seemed to be especially affected in Alzheimer's
patients, he turned to Joseph Miano, Ph.D. to help analyze the findings. Miano is interim
director of Aab Cardiovascular Research Institute and associate professor of Medicine, and
he is senior co-author of the new study.
Th1 inflammatory diseases are characterized by the generation of Interferon-gamma and with
it, 1,25-dihydroxyvitamin-D in response to intracellular bacteria. We are researching
which diseases show scientific evidence that they are due to a Th1 immune system
inflammatory response. There are hundreds of so-called 'autoimmune' diseases. Autoimmune
is a misnomer since the body's immune system is not attacking itself. We use this term
only because it is familiar and easily recognizable not because it is accurate. Many
common diseases like atherosclerosis are being recognised as having an inflammatory
component. We can make an educated guess about which diseases would be more difficult to
treat with the MP because the symptom exacerbation might be difficult to manage.
The Marshall Protocol is a curative treatment for diseases having a TH1 type immune
response. Patients having been diagnosed with one or more of a wide range of diseases have
been successfully treated using this protocol. It works by enabling the immune system to
destroy the intracellular bacteria that are thought to be the root cause of the illness.
CureMyTh1.org is moderated by folks with Th1 inflammatory disease who are being treated
with the Marshall Protocol (MP). They do not have medical expertise but are knowledgeable
about the disease process and the MP. They are eager to answer your basic questions so you
can decide if you would like to participate in the clinical study of the Marshall
Protocol.
Professor Trevor G. Marshall began studying chronic disease at the University of Western
Australia in 1978, with a focus on diabetes, infertility, and sarcoidosis. At the turn of
the 21st Century, he identified the pathogenesis of the Th1 immune system response —
an antibiotic-resistant, intra-phagocytic, metagenomic microbiota, consisting primarily of
pleomorphic, cell-wall-deficient (CWD) bacteria [1]. Tools of modern molecular genomics
enabled Dr. Marshall to develop an antibacterial protocol which stimulates innate immunity
at the same time as it weakens this metagenomic microbiota. The Phase II clinical trial
conducted by the Autoimmunity Research Foundation has demonstrated applicability of this
antibacterial therapy to a wide range of chronic Th1 immune illnesses [2]. This confirms
Dr. Marshall’s prediction that most chronic disease springs from genomic variations
of the same fundamental mix of relatively common pathogens.
The Marshalls’ paper "Antibiotics in Sarcoidosis" [1] states that there are
many different species of Cell Wall Deficient (CWD) bacteria which can contribute to Th1
inflammation. It has become clear that low dose, pulsed Minocycline (Mino) used in Phase
One of the MP, while very effective, does not eliminate all the species of
intra-phagocytic bacteria needed to effect a cure. After exhaustive research, the
Marshalls have identified several other antibiotics which work by exerting a complimentary
blockade of bacterial-protein synthesis. When these antibiotics are taken along with Mino
(at low-dose, pulsed intervals), they are far more effective than if they were taken
alone. Benicar, taken 40mg every six hours both provides an inflammatory blockade and
re-activates the VDR Nuclear Receptor.
I know what you're thinking -- "But Asian folks have been eating soy forever!"
Not true, in a couple of ways. First of all, soy has only been part of the Asian diet for
several hundred years, a far shorter time than most grains and beans -- and all grains and
beans have to be considered newcomers to the human diet. Secondly, Glycine soja, the
soybean originally cultivated by Asian folks, is a different species than the highly
hybridized Glycine max, the soybean now in use. Among other things, Glycine max has been
bred for higher protein concentration -- which sounds good, but if soy protein is a
problem, then higher levels of it are a worse problem. Breeding is also suspected to have
increased the levels of isoflavones, which the soy plant apparently produces as a
protection against pests.
How chromosomes meet in the dark --
Switch that turns on X chromosome matchmaking
A research group lead by scientists at the University of Warwick has discovered the
trigger that pulls together X chromosomes in female cells at a crucial stage of embryo
development. Their discovery could also provide new insights into how other similar
chromosomes spontaneously recognize each other and are bound together at key parts of
analogous cell processes. This is an important mechanism as the binding togetgher of too
many of too few of a particular chromosome can cause a number of medical conditions such
as Down's Syndrome or Turner's Syndrome. In our cells most genes are expressed from both
types of each chromosome linked gene, but the most notable exception to this rule are
X-linked genes in female mammals. During embryo development, in a step necessary to
survival, one of the X chromosomes is silenced in each female cell to ensure that the
levels of X-derived products are equalized in XX females and XY males, via a process known
as X-Chromosome Inactivation (XCI). Recent discoveries have revealed that for that stage
in the process to happen the X chromosomes have to quickly pair off (or colocalize) in a
way that allows each part of those pairs of X chromosomes to be very close together and be
aligned in a particular way. Failure to achieve this close physical colocalization of the
two X chromosomes will lead to XCI failure and cell death.
Apolipoprotein(a) - A natural
regulator of inflammation
In a study to be published in the January 09 issue of Experimental Biology and Medicine,
Hoover-Plow and co-workers in seeking to define a role of apo(a) in leukocyte recruitment
have identified a novel activity of apo(a) apolipoprotein that may function as a natural
and cell specific suppressor of the inflammatory response in vivo. In addition, a
mechanism for this novel function of apo(a) was also identified: its selective regulation
of cytokine production. These effects of apo(a) are independent of its molecular mimicry
of Plg. Lipoprotein(a) (Lp(a)) is similar to low density lipoprotein (LDL), but contains
an additional apolipoprotein, apo(a). Numerous clinical studies conducted over the past 40
years have identified Lp(a) as a risk factor independent from LDL for a variety of
cardiovascular pathologies. Much of the focus of apo(a) pathogenic activities has centered
on its strong resemblance to plasminogen, the zymogen for plasmin, the primary enzyme for
blood clot degradation. In addition to its important role in clot lysis, plasmin is
required for leukocyte recruitment in inflammation. While several in vitro studies have
demonstrated the interference of apo(a) in plasminogen leukocyte recruitment, evidence for
this in vivo has been lacking.
Rice psychologist identifies area
of brain key to choosing words
New research by a Rice University psychologist clearly identifies the parts of the brain
involved in the process of choosing appropriate words during speech. The study, published
in the current issue of the Proceedings of the National Academy of Sciences, could help
researchers better understand the speech problems that stroke patients experience. When
speaking, a person must select one word from a competing set of words. For example, if the
speaker wants to mention a specific animal, he has to single out "dog" from
"cat," "horse" and other possibilities. If he wants to describe
someone's temperament, he has to choose whether "happy," "sad,"
"ecstatic" or some other adjective is more appropriate.
Brain starvation as we age appears
to trigger Alzheimer's
A slow, chronic starvation of the brain as we age appears to be one of the major triggers
of a biochemical process that causes some forms of Alzheimer's disease. A new study from
Northwestern University's Feinberg School of Medicine has found when the brain doesn't get
enough sugar glucose -- as might occur when cardiovascular disease restricts blood flow in
arteries to the brain -- a process is launched that ultimately produces the sticky clumps
of protein that appear to be a cause of Alzheimer's. Robert Vassar, lead author,
discovered a key brain protein is altered when the brain has a deficient supply of energy.
The altered protein, called elF2alpha, increases the production of an enzyme that, in
turn, flips a switch to produce the sticky protein clumps. Vassar worked with human and
mice brains in his research.
Researchers have discovered two enzymes that, when combined, could be involved in the
earliest stages of cancer. Manipulating these enzymes genetically might lead to targeted
therapies aimed at slowing or preventing the onset of tumors. "We could conceivably
reactivate a completely normal gene in a tumor cell – a gene that could prevent the
growth of a tumor if reactivated," says David Jones, Ph.D., professor of oncological
sciences at the University of Utah and senior director of early translational research at
the university's Huntsman Cancer Institute (HCI). "We believe this could be one of
the earliest processes to go wrong in cancer," he adds. "By manipulating these
enzymes, we could possibly prevent or slow the onset of tumors." The enzymes appear
to control an "on–and-off switch" for critical genes that could trigger
cancer or numerous other diseases and birth defects. The research is published in the
December 26 issue of Cell. Using zebrafish that share similar genetics to humans, the HCI
scientists identified a previously unknown enzyme process that controls the levels of DNA
methylation on genes. "Methylation is a cellular process that is required for healthy
cell growth and development, but it can go awry in cancer and diseased cells," says
Brad Cairns, Ph.D., HCI investigator and professor of oncological sciences at the
University of Utah. "You can think of DNA methylation as an on-and-off switch.
Methylation silences or 'shuts off' genes that need to be turned off or are not
functioning as they should, whereas the reverse process called demethylation 'turns on'
healthy genes and genes needed at critical times in development," he says.
Our unconscious brain makes the
best decisions possible
Researchers at the University of Rochester have shown that the human brain—once
thought to be a seriously flawed decision maker—is actually hard-wired to allow us to
make the best decisions possible with the information we are given. The findings are
published in today's issue of the journal Neuron. Neuroscientists Daniel Kahneman and Amos
Tversky received a 2002 Nobel Prize for their 1979 research that argued humans rarely make
rational decisions. Since then, this has become conventional wisdom among cognition
researchers contrary to Kahnneman and Tversky's research, Alex Pouget, associate professor
of brain and cognitive sciences at the University of Rochester, has shown that people do
indeed make optimal decisions—but only when their unconscious brain makes the choice.
"A lot of the early work in this field was on conscious decision making, but most of
the decisions you make aren't based on conscious reasoning," says Pouget. "You
don't consciously decide to stop at a red light or steer around an obstacle in the road.
Once we started looking at the decisions our brains make without our knowledge, we found
that they almost always reach the right decision, given the information they had to work
with."
Modified Gene Targets Cancer Cells
a Thousand Times More Often Than Healthy Cells
Researchers at the University of Rochester have designed a gene that produces a thousand
times more protein in cancer cells than in healthy cells. The findings may help address
the prime challenge in anti-cancer therapy - improving treatments' ability to specifically
and effectively target cancer cells. Using this new approach, scientists should be able to
insert "self-destruct" codes into the modified gene, forcing cancer cells to
kill themselves while healthy cells remain largely unaffected. Though trials will be
necessary to determine if the difference is enough to destroy tumors without harming
healthy tissue, the initial findings, published in today's early edition of Proceedings of
the National Academy of Sciences, are promising, say the authors.
Sleep disorders - a warning sign
for neurodegenerative disease?
According to the latest study by Dr. Ronald Postuma from the Research Institute of the
MUHC and Dr. Jacques Montplaisir from the Université de Montréal and the Hôpital du
Sacré-Cœur de Montréal, 52.4 per cent of patients with REM sleep behaviour disorder
develop a neurodegenerative disease within 12 years following their initial diagnosis.
These results will be published on December 24, 2008 in the journal Neurology, the
official publication of the American Academy of Neurology.
Treating gum disease linked to
lower medical costs for patients with diabetes
A new report suggests that treating gum disease in patients who have diabetes with
procedures such as cleanings and periodontal scaling is linked to 10 to 12 percent lower
medical costs per month. The findings are encouraging but the study was not designed to
firmly establish cause and effect, said George Taylor, University of Michigan associate
professor of dentistry, who also has an appointment in epidemiology in the U-M School of
Public Health. Taylor led the research project to investigate whether routine,
non-surgical treatment for gum disease is linked to lower medical care costs for people
with diabetes. In periodontal disease, the body reacts to the bacteria causing the gum
infection by producing proteins or chemicals called inflammatory mediators. Ulcers and
open sores in the gums become passageways for these proteins and for the bacteria
themselves to enter the body's blood circulation. These inflammatory mediators, as well as
some parts of the bacteria, prevent the body from effectively removing glucose, or sugar,
from the blood. The higher level of blood sugar is known as poor diabetes control. Poor
diabetes control leads to serious diabetes complications such as vision disorders,
cardiovascular and kidney disease and amputations, among others.
Biomedical researchers create
artificial human bone marrow in a test tube
Artificial bone marrow that can continuously make red and white blood cells has been
created in a University of Michigan lab. This development could lead to simpler
pharmaceutical drug testing, closer study of immune system defects and a continuous supply
of blood for transfusions.
UC Davis discovery offers hope for
treating kidney cancer
Kidney cancer is typically without symptoms until it has spread to other organs, when it
is also the most difficult to treat. Newer chemotherapies show great promise for extending
survival during later disease stages, but they can also be highly toxic. In one of the
first discoveries of its kind, UC Davis Cancer Center researchers have identified ways to
block a cancer gene's own repair mechanism and, in so doing, help make chemotherapy for
kidney cancer more effective and better tolerated. The outcome is published in the current
issue of Cancer Biology and Therapy. "Cancer cells are notorious in their ability to
rapidly create copies of themselves. While the latest medications slow down that process,
they do not tend to be curative and have many side effects," said Robert Weiss, a UC
Davis professor of nephrology and chief of nephrology at the Sacramento VA Medical Center.
"We wanted to find ways to help make chemotherapeutics as effective as possible at
the lowest doses possible." Newer medications work by destabilizing cancer cells at
the DNA level, which reduces their ability to replicate. Knowing that the p21 gene has an
important role in restoring cancer cell DNA and potentially circumventing the benefits of
those treatments, Weiss sought to identify compounds that could interrupt this pathway.
UC Davis researchers find molecule
that targets brain tumors
UC Davis Cancer Center researchers report today the discovery of a molecule that targets
glioblastoma, a highly deadly form of cancer. The finding, which is published in the
January 2009 issue of the European Journal of Nuclear Medicine and Molecular Imaging,
provides hope for effectively treating an incurable cancer. Glioblastoma is the most
common and aggressive type of primary brain tumor in adults. It is marked by tumors with
irregular shapes and poorly defined borders that rapidly invade neighboring tissues,
making them difficult to remove surgically. "These brain tumors are currently treated
with surgery to remove as much of the tumor as possible followed by radiation to kill
cancer cells left behind and systemic chemotherapy to prevent spread to nearby
tissues," said Kit Lam, senior author of the study and UC Davis chief of hematology
and oncology. "It is unfortunate that this approach does not extend survival
significantly. Most patients survive less than one year."
Another reason to avoid high-fat
diet – it can disrupt our biological clock
Indulgence in a high-fat diet can not only lead to overweight because of excessive calorie
intake, but also can affect the balance of circadian rhythms – everyone’s
24-hour biological clock, Hebrew University of Jerusalem researchers have shown. The
biological clock regulates the expression and/or activity of enzymes and hormones involved
in metabolism, and disturbance of the clock can lead to such phenomena as hormone
imbalance, obesity, psychological and sleep disorders and cancer. While light is the
strongest factor affecting the circadian clock, Dr. Oren Froy and his colleagues of the
Institute of Biochemistry, Food Science and Nutrition at the Hebrew University’s
Robert H. Smith Faculty of Agriculture, Food and Environment in Rehovot, have demonstrated
in their experiments with laboratory mice that there is a cause-and-effect relation
between diet and biological clock imbalance. To examine this thesis, Froy and his
colleagues, Ph.D. student Maayan Barnea and Zecharia Madar, the Karl Bach Professor of
Agricultural Biochemistry, tested whether the clock controls the adiponectin signaling
pathway in the liver and, if so, how fasting and a high-fat diet affect this control.
Adiponectin is secreted from differentiated adipocytes (fat tissue) and is involved in
glucose and lipid metabolism. It increases fatty acid oxidation and promotes insulin
sensitivity, two highly important factors in maintaining proper metabolism.
