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Week 37
Stop emitting CO2 or geoengineering
could be our only hope
The future of the Earth could rest on potentially dangerous and unproven geoengineering
technologies unless emissions of carbon dioxide can be greatly reduced, the latest Royal
Society report has found. The report (published today,1st September, by the Royal
Society(1), the UK’s national academy of science) found that unless future efforts to
reduce greenhouse gas emissions are much more successful than they have been so far,
additional action in the form of geoengineering will be necessary if we are to cool the
planet. Geoengineering technologies were found to be very likely to be technically
possible and some were considered to be potentially useful to augment the continuing
efforts to mitigate climate change by reducing emissions. However, the report identified
major uncertainties regarding their effectiveness, costs and environmental impacts.
Professor John Shepherd, who chaired the Royal Society’s geoengineering study(2),
said, “It is an unpalatable truth that unless we can succeed in greatly reducing CO2
emissions we are headed for a very uncomfortable and challenging climate future, and
geoengineering will be the only option left to limit further temperature increases. Our
research found that some geoengineering techniques could have serious unintended and
detrimental effects on many people and ecosystems - yet we are still failing to take the
only action that will prevent us from having to rely on them. Geoengineering and its
consequences are the price we may have to pay for failure to act on climate change.”
Is Tetris good for the brain?
Brain imaging shows playing Tetris leads to a thicker cortex and may also increase brain
efficiency, according to research published in the open access journal BMC Research Notes.
A research team based in New Mexico is one of the first to investigate the effects of
practice in the brain using two image techniques. Researchers from Mind Research Network
in Albuquerque used brain imaging and Tetris to investigate whether practice makes the
brain efficient because it increases gray matter. For 30 minutes a day over a three-month
period, 26 adolescent girls played Tetris, a computer game requiring a combination of
cognitive skills. The girls completed both structural and functional MRI scans before and
after the three-month practice period, as did girls in the control group who did not play
Tetris. A structural MRI was used to assess cortical thickness, and a functional MRI was
used to assess efficient activity. The girls who practiced showed greater brain
efficiency, consistent with earlier studies. Compared to controls, the girls that
practiced also had a thicker cortex, but not in the same brain areas where efficiency
occurred [see image: http://www.biomedcentral.com/graphics/email/images/tetris_brain.jpg].
The areas of the brain that showed relatively thicker cortex were the Brodmann Area (BA) 6
in the left frontal lobe and BA 22 and BA 38 in the left temporal lobe. Scientists believe
BA 6 plays a role in the planning of complex, coordinated movements. BA 22 and BA 38 are
believed to be the part of the brain active in multisensory integration—or our
brain’s coordination of visual, tactile, auditory, and internal physiological
information. Functional MRI (fMRI) showed greater efficiency after practice mostly in the
right frontal and parietal lobes including BAs 32, 6, 8, 9, 46 and BA 40. These areas are
associated with critical thinking, reasoning, and language and processing. “One of
the most surprising findings of brain research in the last five years was that juggling
practice increased gray matter in the motor areas of the brain,” said Dr. Rex Jung, a
co-investigator on the Tetris study and a clinical neuropsychologist. “We did our
Tetris study to see if mental practice increased cortical thickness, a sign of more gray
matter. If it did, it could be an explanation for why previous studies have shown that
mental practice increases brain efficiency. More gray matter in an area could mean that
the area would not need to work as hard during Tetris play.”
Hospital infections cost $1 billion
in lost bed days
Infections caught in hospital are costing the Australian healthcare system more than
850,000 lost bed days, according to a new study by Queensland University of Technology.
Associate Professor Nick Graves, from QUT's Institute of Health and Biomedical Innovation,
said there were 175,153 cases where patients had acquired an infection during their
hospital stay. "If rates were reduced by just one per cent, then 150,158 bed days
would be released for alternative uses, allowing an estimated 38,500 additional admissions
annually," he said. The results, which have been published in the Australian journal
Healthcare Infection, calculate the economic consequences of
healthcare-acquired-infections arising among admissions to Australian acute care
hospitals. Professor Graves said the research revealed there was an opportunity to improve
the efficiency of the Australian healthcare system. "Acute hospitals in Australia
cannot meet current demand," he said. "Waiting lists for elective surgery and
specialist outpatient appointments are lengthening in every state and territory."
Professor Graves said many infections were preventable and Australian infection control
practitioners could reduce rates if they had additional resources.
"Healthcare-acquired infection rates are about five per cent of all admissions at the
moment and with bed days valued at $1005 each, the total economic burden is close to $1
billion per annum," he said.
Humans causing erosion comparable
to world’s largest rivers and glaciers
A new study finds that large-scale farming projects can erode the Earth's surface at rates
comparable to those of the world's largest rivers and glaciers. Published online in the
journal Nature Geoscience, the research offers stark evidence of how humans are reshaping
the planet. It also finds that - contrary to previous scholarship - rivers are as powerful
as glaciers at eroding landscapes. "Our initial goal was to investigate the
scientific claim that rivers are less erosive than glaciers," says Michele Koppes, a
professor of geography at the University of British Columbia (UBC) and lead author of the
study. "But while exploring that, we found that many of the areas currently
experiencing the highest rates of erosion are being caused by climate change and human
activity such as modern agriculture," says Koppes, who conducted the study with David
Montgomery of the University of Washington. In some cases, the researchers found
large-scale farming eroded lowland agricultural fields at rates comparable to glaciers and
rivers in the most tectonically active mountain belts. "This study shows that humans
are playing a significant role in speeding erosion in low lying areas," says Koppes.
"These low-altitude areas do not have the same rate of tectonic uplift, so the land
is being denuded at an unsustainable rate."
Exercise Minimizes Weight Regain By
Reducing Appetite, Burning Fat, And Lowering ‘Defended’ Body Weight
Exercise helps prevent weight regain after dieting by reducing appetite and by burning fat
before burning carbohydrates, according to a new study with rats. Burning fat first and
storing carbohydrates for use later in the day slows weight regain and may minimize
overeating by signaling a feeling of fullness to the brain. The University of Colorado
Denver study also found that exercise prevents the increase in the number of fat cells
that occurs during weight regain, challenging the conventional wisdom that the number of
fat cells is set and cannot be altered by dietary or lifestyle changes. These coordinated
physiological changes in the brain and the body lower the ‘defended’ weight,
that is, the weight that our physiology drives us to achieve, and suggest that the effects
of exercise on these physiological processes may make it easier to stay on a diet. The
study is “Regular exercise attenuates the metabolic drive to regain weight after long
term weight loss.” Paul S. MacLean, Janine A. Higgins, Holly R. Wyatt, Edward L.
Melanson, Ginger C. Johnson, Matthew R. Jackman, Erin D. Giles, Ian E. Brown and James O.
Hill, all of the University of Colorado Denver, conducted the study. The American
Physiological Society published the research in the American Journal of Physiology –
Regulatory, Integrative and Comparative Physiology.
Computational Process Zeroes in on
Top Genetic Cancer Suspects
Johns Hopkins engineers have devised innovative computer software that can sift through
hundreds of genetic mutations and highlight the DNA changes that are most likely to
promote cancer. The goal is to provide critical help to researchers who are poring over
numerous newly discovered gene mutations, many of which are harmless or have no connection
to cancer. According to its inventors, the new software will enable these scientists to
focus more of their attention on the mutations most likely to trigger tumors.
UB education expert urges schools
to help their students feel more involved
New research from a University at Buffalo expert on classroom education has identified six
factors that affect whether elementary, middle and high school students will engage in the
activities of their schools or feel alienated. Students who feel "disengaged"
from school are at greater risk for dropping out, avoiding challenging courses, scoring
low on standardized achievement tests and achieving less as adults, according to
researcher Jeremy D. Finn, professor of counseling, school and educational psychology in
the UB Graduate School of Education. "Disengagement is the failure to develop a sense
of school membership, failure to participate actively in class and school activities, or
failure to become cognitively involved in learning," says Finn. "Different
degrees of disengagement may be exhibited by students at all stages of schooling. The
extreme of disengagement is leaving school without graduating, thus severing connections
with school, teachers and activities that support learning."
Getting better visualization of
joint cartilage through cationic CT contrast agents
In its quest to find new strategies to treat osteoarthritis and other diseases, a Boston
University-led research team has reported finding a new computer tomography contrast agent
for visualizing the special distributions of glycosaminoglycans (GAGs) – the anionic
sugars that account for the strength of joint cartilage. Assessing the local variations in
GAGs are of significant interest for the study of cartilage biology and for the diagnosis
of cartilage disease like osteoarthritis, which afflicts more than 27 million in people in
the United States In their research paper, "Effect of Contrast Agent Change on
Visualization of Articular Cartilage Using Computer Tomography: Exploiting Electrostatic
Interactions for Improved Sensitivity," just published on line in the Journal of the
American Chemical Society, they describe new contrast agents that selectively bind to the
GAGs in articular cartilage. Articular or joint cartilage is the smooth hydrated tissue in
the ends of bones in load-bearing joints, such as knees, hips and shoulders. The loss of
GAGs from these joints is the hallmark of osteoarthritis, a degenerative joint disease in
which wear or trauma results in damage to the cartilage surface. To better see the
differentiation between healthy and unhealthy cartilage, contrast agents provide the
visual tool to assess GAG content. However, the current contrast agents used with computer
tomography or magnetic resonance imaging (MRI) rely on limited diffusion of the anionic or
negative ion-charged contrast agents into the target tissue, the study noted. So
researchers hypothesized that cationic contrast agents would be electrostatically
attracted to anionic GAGs to provide a more sensitive technique for imaging cartilage. And
they focused on using the more widely accessible CT equipment because it can image
cartilage and bone simultaneously, enable rapid three-dimensional reconstruction of the
tissue and achieve higher spatial resolution over shorter acquisition times compared to
MRI systems.
DNA mutations linked to diabetes
Genes that regulate the energy consumption of cells have a different structure and
expression in type II diabetics than they do in healthy people, according to a new study
from the Swedish medical university Karolinska Institutet published in Cell Metabolism.
The researchers believe that these epigenetic modifications might have a key part to play
in the development of the disease.Type II diabetes is characterised by a lower sensitivity
to insulin in muscles and organs, and a reduced ability to consume energy in the form of
glucose. Heredity and environmental factors (e.g. exercise) are both involved in the
disease pathogenesis, but scientists are still unclear as to the mechanisms behind it. A
research group at Karolinska Institutet has now shown that genes in the muscle cells of
diabetics are chemically modified through what is known as DNA methylation. They found
that in muscles cells taken from patients with early-onset diabetes, a gene designated as
PGC-1alpha was modified and had reduced expression. PGC-1alpha controls other genes that
regulate the metabolism of glucose by the cell.
Sustainable fertilizer - Urine and
wood ash produce large harvest
Results of the first study evaluating the use of human urine mixed with wood ash as a
fertilizer for food crops has found that the combination can be substituted for costly
synthetic fertilizers to produce bumper crops of tomatoes without introducing any risk of
disease for consumers. The study appears in the current issue of ACS' Journal of
Agricultural and Food Chemistry, a bi-weekly publication. In the study, Surendra Pradhan
and colleagues point out that urine, a good source of nitrogen, has been successfully used
to fertilize cucumber, corn, cabbage, and other crops. Only a few studies, however, have
investigated the use of wood ash, which is rich in minerals and also reduces the acidity
of certain soils. Scientists have not reported on the combinaton of urine and wood ash,
they say. The new study found that plants fertilized with urine produced four times more
tomatoes than nonfertilized plants and as much as plants given synthetic fertilizer. Urine
plus wood ash produced almost as great a yield, with the added benefit of reducing the
acidity of acid soils. "The results suggest that urine with or without wood ash can
be used as a substitute for mineral fertilizer to increase the yields of tomato without
posing any microbial or chemical risks," the report says.
Diesel exhaust is linked to cancer
development
Scientists here are the first to demonstrate that the link between diesel fume exposure
and cancer lies in the ability of diesel exhaust to induce the growth of new blood vessels
that serve as a food supply for solid tumors. The researchers found that in both healthy
and diseased animals, more new blood vessels sprouted in mice exposed to diesel exhaust
than did in mice exposed to clean, filtered air. This suggests that previous illness
isn’t required to make humans susceptible to the damaging effects of the diesel
exhaust. The tiny size of inhaled diesel particles, most less than 0.1 microns in
diameter, potentially enables them to penetrate the human circulatory system, organs and
tissues, meaning they can do this damage just about anywhere in the body. A micron is one
millionth of a meter.
A breath of fresh air could improve
drug toxicity screening
A team led by Massachusetts General Hospital (MGH) researchers has developed an innovative
way to culture liver cells for drug toxicity screening. In a report to be published in
Proceedings of the National Academy of Sciences that has been released online, the
investigators describe how liver cells grown in a high-oxygen environment and in a culture
medium free of animal-derived serum quickly begin to function as they do within the liver.
Better and faster ways to screen drugs for toxic side effects could significantly reduce
the cost and expense of bringing new drugs to market, along with reducing unexpected
adverse events that can occur when new agents move from the clinical trial stage into
wider use, the authors note. Since the liver plays a key role in the metabolism and
clearance of drugs, screening for liver toxicity is an essential step in assuring the
safety of new agents. But studies in animals are not always successful in predicting toxic
liver effects, and freshly cultured liver cells quickly lose their metabolic competence
under standard culture methods. "Finding a better way to culture liver cells has been
a major stumbling block in the development of predictive drug-discovery tools," says
Yaakov Nahmias, PhD, of the MGH Center for Engineering in Medicine (CEM), the paper's
senior author. "We needed to develop an environment in which liver cells behave as
they do in the body." Earlier studies by the CEM team and others suggested that
animal-derived serum, commonly used in cell cultures, may interfere with the metabolism of
cultured liver cells. Since one of the key stresses involved in moving cells from an in
vivo environment into culture is a tenfold drop in oxygen levels, the researchers
theorized that a high-oxygen, serum-free culture environment might be the answer.
Study Results Promise Faster
Recovery from Life-Threatening Blood Cell Shortages
A key compound resupplies bone marrow with fast-acting stem cells that can more quickly
rekindle blood cell production, according to a study published online today in the journal
Blood. While the study was in mice, in the study authors say it has the potential to
increase survival among patients with life-threatening blood cell shortages. Thanks to
stem cells, humans develop from one cell into a complex being with as many as 400 cell
types.
Biotransformed blueberry juice
fights fat and diabetes
Juice extracted from North American lowbush blueberries, biotransformed with bacteria from
the skin of the fruit, holds great promise as an anti-obesity and anti-diabetic agent. The
study, published in the International Journal of Obesity, was conducted by researchers
from the Université de Montréal, the Institut Armand-Frappier and the Université de
Moncton who tested the effects of biotransformed juices compared to regular blueberry
drinks on mice. "Results of this study clearly show that biotransformed blueberry
juice has strong anti-obesity and anti-diabetic potential," says senior author Pierre
S. Haddad, a pharmacology professor at the Université de Montréal's Faculty of Medicine.
"Biotransformed blueberry juice may represent a novel therapeutic agent, since it
decreases hyperglycemia in diabetic mice and can protect young pre-diabetic mice from
developing obesity and diabetes." The scientists tested the effect of biotransformed
blueberry juice on a group of mice prone to obesity, insulin resistance, diabetes and
hypertension. Incorporating biotransformed blueberry juice into the water of mice reduced
their food intake and their body weight. "These mice were an excellent model that
closely resembles obesity and obesity-linked type 2 diabetes in humans," says Dr.
Haddad, who is also director of the CIHR Team in Aboriginal Anti-Diabetic Medicines at the
Université de Montréal. Biotransformation of the blueberry juice was achieved with a new
strain of bacteria isolated from the blueberry flora, specifically called Serratia
vaccinii, which increases the fruit's antioxidant effects. "The identification of the
active compounds in biotransformed blueberry juice may result in the discovery of
promising new antiobesity and antidiabetic molecules," says Dr. Haddad. As for the
impact of blueberry products on diabetes, says Tri Vuong, lead author and recent PhD
graduate from the Université de Montréal's Department of Pharmacology: "Consumption
of fermented blueberry juice gradually and significantly reduced high blood glucose levels
in diabetic mice. After three days, our mice subjects reduced their glycemia levels by 35
percent."
Progress made in traumatic brain
injury treatment and diagnosis
New research on traumatic brain injury (TBI) is being presented this week at the Military
Health Research Forum (MHRF), a scientific meeting hosted by the Department of Defense
(DOD) Congressionally Directed Medical Research Programs (CDMRP). Service men and women
are particularly susceptible to TBI given the nature of combat.TBI is a condition
affecting a significant number of active-duty soldiers. The incidence of TBI among wounded
military personnel is estimated at 20 percent. Often called the "signature
injury" of the Iraqi war, TBI can lead to a range of symptoms, including headache,
confusion, behavior change, memory trouble, repeated vomiting, convulsions, slurred speech
and numbness in the extremities. Studies on topics such as brain tissue regeneration,
driving problems after mild TBI (mTBI), and the use of biomarkers to determine the extent
of TBI are funded by the Psychological Health and Traumatic Brain Injury Research Program
(PH/TBIRP) or by the Peer Reviewed Medical Research Program, both of which are programs
within the CDMRP. The PH/TBIRP aims to prevent, mitigate, and treat the effects of
traumatic stress and TBI on function, wellness, and overall quality of life for service
members as well as their caregivers and families. "We hope this research will address
the nuances of combat-related TBI among our troops and offer physicians better tools for
diagnosis and treatment of this unique population," says Captain E. Melissa Kaime,
M.D., Director of the CDRMP. "Furthermore, the scope of this research could improve
medical care for TBI in the civilian population."
Scientists identify gene that
predicts post-surgical survival from brain metastasis of breast cancer patients
Researchers at the National Cancer Institute have identified a gene that may play a role
in breast cancer metastasis to the brain, according to a report in Molecular Cancer
Research, a journal of the American Association for Cancer Research. Diane Palmieri,
Ph.D., a staff scientist at the NCI, said Hexokinase 2 overexpression was more highly
expressed in brain metastasis in patients with breast cancer than in primary breast
tumors. "Importantly, this study was conducted in human tissue rather than animal
models, so we are able to extrapolate data without the problems inherent in animal
studies," said Palmieri. Brunhilde Felding-Habermann, Ph.D., an associate professor
at The Scripps Research Institute, said the findings are a major step forward in potential
breast cancer treatments. "Improvements in breast cancer therapy have made prognoses
like brain metastasis a growing problem, and this research points to a potential target
for future therapies," said Felding-Habermann. Researchers performed analyses on both
primary tumors and brain metastases. They found higher levels of Hexokinase 2 in brain
metastases compared with unlinked primary tumors. Among resected brain metastases, these
higher levels of Hexokinase 2 were linked with worse survival. The median survival for
patients with high levels of Hexokinase 2 expression in their brain metastasis was 9.6
months compared with 17.5 months for those with lower expression. Palmieri said that
Hexokinase 2 plays a key role in glucose metabolism, which provides the energy tumors need
to grow. It also impacts the cell survival process, apoptosis. "Potential therapies
would need to turn off this gene and thus starve the tumor of its growth potential,"
said Palmieri.
A new molecule to combat diabetes
and obesity
Type 2 diabetes, the most common form of diabetes, is increasing at an alarming state with
more than 180 million people affected worldwide. With the rising incidence of obesity, a
major risk factor for the onset of type 2 diabetes, this metabolic disorder represents a
major health concern. A group from the Ecole Polytechnique Fédérale de Lausanne, now
shows that there may exist new ways to fight these disorders. The study, published in the
current issue of the scientific journal Cell Metabolism (September 2, 2009), demonstrates
that activation of the protein -TGR5- can treat type 2 diabetes and reduce weight gain. In
collaboration with Prof. Roberto Pellicciari and his team at the University of Perugia
(Italy), and Intercept Pharmaceuticals (New York, USA; Perugia, Italy), the group at the
EPFL, led by Dr Kristina Schoonjans and Prof. Johan Auwerx, have characterized the
metabolic properties of a selective TGR5 activator (INT-777), a drug with a promising
future for the treatment of diabetes and obesity. Earlier work from the same group showed
that bile acids (endogenous molecules involved in digestion), via the activation of TGR5
in muscle and brown adipose tissue, are able to boost energy expenditure and to prevent or
reverse diet-induced obesity in mice. In the present study, the group of Dr Kristina
Schoonjans and Prof. Johan Auwerx went further in studying the role of TGR5 in the gut
where TGR5 is expressed in cells specialized in the production of gut-derived hormones.
The authors found that in these so-called enteroendocrine cells TGR5 controls the
secretion of the hormone Glucagon-Like Peptide 1 (GLP-1), which plays a critical role in
the control of pancreatic function and the regulation of blood sugar levels. In addition
to this discovery and in collaboration with Prof. Roberto Pellicciari, who designed the
novel potent and selective TGR5 activator, INT-777, under a longstanding collaboration
with Intercept Pharmaceuticals, the group at the EPFL has shown that under laboratory
conditions this compound can effectively treat diabetes and reduce fat mass. The authors
have furthermore demonstrated that these effects were related to the increase in both
GLP-1 secretion and energy expenditure.
Monsanto GMOs - The Truth
Does WiFi pose a danger to some
people?
Velma Lyrae believes that Wifi is a threat
to the well being of some people.She discusses her viewpoint at Climate Camp 2009.
I know what I saw (Trailer)
Martin Sheen: Shining the Light on
Social Causes
Martin Sheen - Star of television's The
West Wing and social activist, Martin Sheen has been a prolific performer since the late
1960s. He landed his first major role on Broadway in The Subject Was Roses, which later
became a movie. A young, intense leading man, he has played over 70 roles, many of which
were in well-known films such as Apocalypse Now, Badlands, Wall Street, The American
President, Gandhi and Catch Me If You Can, to name a few. His most recent films include
the Academy Award-winning movie The Departed; Bordertown and Bobby, a film written and
directed by his son, Emilio Estevez. Martin Sheen is also no stranger to politics, both
professionally and in real life. He has played U.S. President John F. Kennedy in the
mini-series, Kennedy: The Presidential Years; Robert F. Kennedy in Missiles of October;
The White House Chief of Staff in The American President; and is perhaps best-known as
President Josiah Bartlet in the acclaimed television drama The West Wing, for which he
received a Golden Globe award. Martin Sheen is also known for his robust support of
political causes and has remained a staunch activist throughout his life.
Censoring You: The Limits of What
You See and Hear
Saturated fats build healthy
The Importance of Saturated Fats for
Biological Functions. The scientific evidence, honestly evaluated, does not support the
assertion that "artery-clogging" saturated fats cause heart disease. Actually,
evaluation of the fat in artery clogs reveals that only about 26% is saturated. The rest
is unsaturated, of which more than half is polyunsaturated. Saturated 18-carbon stearic
acid and 16-carbon palmitic acid are the preferred foods for the heart, which is why the
fat around the heart muscle is highly saturated. The heart draws on this reserve of fat in
times of stress. The Eskimos had no carbohydrates and no fiber in their diets but suffered
no detectable health effects. In fact, their health was excellent with absolutely no
dental caries, no heart disease, no cancer and excellent bone health. Price traveled
the world over in order to study isolated human groups, including sequestered villages in
Switzerland, Gaelic communities in the Outer Hebrides, Eskimos and Indians of North
America, Melanesian and Polynesian South Sea Islanders, African tribes, Australian
Aborigines, New Zealand Maori and the Indians of South America. Wherever he went, Dr.
Price found that beautiful straight teeth, freedom from decay, stalwart bodies, resistance
to disease and fine characters were typical of primitives on their traditional diets, rich
in essential food factors. And every group had a high intake of fat soluble vitamins.
Mothers with a vegetarian diet in the first half of pregnancy had a 4.99 times greater
risk of having a boy with hypospadias compared with mothers who included meat in their
diets, the researchers report. In addition, mothers who took iron supplements had double
the normal risk of having a boy with hypospadias, and influenza during the first 3 months
of pregnancy increased the risk of by just over three times. BJU International January
2000;85:107-113 Does a vegetarian diet contributed to cancer? Certainly the evidence
points to it.
Some deny there's a link but the rate of
autism is many times higher than 25 years ago. The number of inoculations kids receive is
more than 4 times higher than the early 80s. Now the gov't is trying to rush through a new
vaccine for the H1N1 Swine flu. Will they try to force us all to get it?
H1N1 vaccines under threat
Swine Flu Vaccinations Coast to
Coast
Dr. Len Horowitz commented on the Swine
Flu, which a White House panel has warned could kill as many as 90, 000 Americans. He
believes the greater danger stems from "toxic" vaccinations that will be foisted
upon the public. For more, see his website www.FluScam.com.
From fat to chronic inflammation
Researchers may have found a key ingredient in the recipe that leads from obesity to
chronic low-grade inflammation, according to a report in the September issue of Cell
Metabolism, a Cell Press publication. Chronic inflammation within fat tissue is now
recognized as a contributor to the many ill health consequences that come with obesity,
from diabetes to cardiovascular disease, explains Yuichi Oike of Kumamoto University in
Japan. The new discovery may therefore point to a targeted therapy designed to limit the
health impact of the obesity epidemic, the researchers say. The new culprit Oike's team
identifies is a fat-derived protein called angiopoietin-like protein 2 (Angptl2). In mice,
Angptl2 levels are elevated in many organs, but especially in fat tissue, they show. Those
levels increase further under the oxygen-deprived conditions typically found within obese
fat tissue. In humans, too, they find higher Angptl2 levels in the blood of people with
higher body mass index and insulin levels. Obese mice lacking Angptl2 show less
inflammation in their fat tissue and are less insulin resistant, they report. Likewise,
otherwise healthy mice made to have higher than normal Angptl2 levels in their fat tissue
develop inflammation and insulin resistance. They also showed additional details of what
Angptl2 does. The protein starts an inflammatory cascade, causing blood vessels to remodel
and attracting immune cells called macrophages. The researchers conclude that Angptl2 is a
key adipocyte-derived inflammatory mediator linking obesity to systemic insulin resistance
and identify it as a new molecular target that could be used to improve the diagnosis and
treatment of obesity and related metabolic diseases. Oike says he thinks drugs that would
act on Angptl2 not only have considerable promise, but are also likely to come with
limited side effects.
Dynamic changes in DNA linked to
human diabetes
A study in the September issue of Cell Metabolism, a Cell Press publication, may give new
meaning to the adage, "You are what you eat." The DNA isolated from the muscles
of people with diabetes bears chemical marks not found in those who respond normally to
rising blood sugar levels, according to the report. The epigenetic marks in question are
specifically found on a gene that controls the amount of fuel, in the form of glucose or
lipids, that cells burn. Those marks also show up in the skeletal muscle of people with
prediabetes, suggesting that the DNA modification might be an early event in the
development of the disease. Those changes rapidly reprogram the gene's activity without
altering the underlying DNA sequence at all. They suggest a way that environmental
factors—what we eat or how active we are—may perhaps influence our genes, for
better or for worse. Indeed, the researchers show that the hypermethylation of the gene
known as PGC-1? for short (peroxisome proliferator-activated receptor ? [PPAR?]
coactivator-1?) also takes place in isolated muscle fiber cells when they are exposed to
an inflammatory factor or to free fatty acids. "These changes take place when you
expose muscle to systemic factors that mimic the diabetic condition," said Juleen
Zierath of the Karolinska Institutet in Sweden. Such changes to the epigenetic imprint
have been seen before, explain Zierath and Romain Barrès, the study's first author. For
instance, chemical modification of genes are responsible for developmental changes that
take place as cells differentiate. They are the reason that keratin is produced in the
skin but not in blood, for instance. In contrast, the changes they've now revealed take
place in cells of the body that are fully mature. "It's a much more dynamic process
than we thought," Zierath said. "The genetic causes of diabetes are important,
but this shows us that epigenetic changes, which take place on top of our genes, can alter
our physiology in critical ways." Evidence that dietary factors might influence
epigenetic gene control in diabetes had been suggested previously by a generational study
in humans, which showed that the nutritional status of the grandparent is closely linked
to an increased risk of diabetes-associated mortality in their grandkids. In mice,
researchers have demonstrated the crossgenerational effects of nutrition on DNA
methylation status directly.
Chemotherapy for breast cancer is
associated with disruption of sleep-wake rhythm in women
A study in the Sept.1 issue of the journal Sleep shows that the sleep-wake activity
rhythms of breast cancer patients are impaired during the administration of chemotherapy.
Results indicate that the first cycle of chemotherapy is associated with a temporary
disruption of these rhythms, while repeated administration of chemotherapy results in
progressively worse and more enduring impairments. During week one of the first cycle of
chemotherapy, participants switched from low to high activity about 30 minutes later in
the day and decreased their level of activity about 50 minutes earlier at night,
suggesting that their days were shorter. During the first week of the fourth cycle of
chemotherapy, the women increased their level of activity about 37 minutes later in the
day and switched from high to low activity about 34 minutes earlier at night. Although
most variables returned to baseline levels in the second and third weeks of the first
cycle of chemotherapy, circadian impairments were maintained on several variables in the
second and third weeks of cycle four. Principal investigator, Sonia Ancoli-Israel, PhD,
professor of psychiatry at the University of California San Diego, said that the findings
were not surprising. Sleep disturbances are common in cancer patients, with 30 percent to
50 percent reporting symptoms of insomnia. Previous studies also have shown that both
sleep and fatigue get worse with chemotherapy, so it was expected that circadian rhythms
would deteriorate. "Results of this study suggest that our biological clocks are
affected by chemotherapy. Our biological clock, or circadian rhythm (24-hour cycles) help
keep our bodies in sync with the Environment," said Ancoli-Israel. "During
chemotherapy, our biological clock gets out of sync, especially after the first cycle of
treatment. The clock seems to regulate itself after only one cycle, but with repeated
administration of chemotherapy, it becomes more difficult for the biological clock to
readjust." The study involved 95 women with a mean age of 50.72 years who were
scheduled to receive neoadjuvant or adjuvant anthracycline-based chemotherapy for stage
I-III breast cancer.
Carbon monoxide linked to heart
problems in elderly
Exposure to carbon monoxide, even at levels well below national limits, is associated with
an increased risk of hospitalization for the elderly with heart problems, according to a
study published today in Circulation: Journal of the American Heart Association. The
nationwide study of 126 urban communities, funded by the Environmental Protection Agency
(EPA) and the National Institute of Environmental Health Sciences, found that an increase
in carbon monoxide of 1 part per million in the maximum daily one-hour exposure is
associated with a 0.96 percent increase in the risk of hospitalization from cardiovascular
disease among people over the age of 65. This link holds true even when carbon monoxide
levels are less than 1 part per million, which is well below the EPA's National Ambient
Air Quality Standard of 35 parts per million. This finding suggests an under-recognized
health risk to seniors. Currently, the EPA is evaluating the scientific evidence on the
link between carbon monoxide and health to determine whether the health-based standard
should be modified. "This evidence indicates that exposure to current carbon monoxide
levels may still pose a public health threat," said Michelle Bell, the study's lead
investigator and associate professor of environmental health at the Yale School of
Forestry & Environmental Studies. "Higher levels of carbon monoxide were
associated with higher risk of hospitalizations for cardiovascular heart disease."
Bell and researchers from the Johns Hopkins Bloomberg School of Public Health and the
University of Southern California's Keck School of Medicine based their findings on an
analysis of hospital records for 9.3 million Medicare recipients and data on air pollution
levels and weather gathered between 1999 and 2005. Their analysis took into account the
health effects of other traffic-related pollutants, including nitrogen dioxide, fine
particles and elemental carbon. "We found a positive and statistically significant
association between same-day carbon monoxide levels and an increased risk of
hospitalization for cardiovascular disease in general, as well as for multiple, specific
cardiovascular disease outcomes, including ischemic heart disease, heart rhythm
disturbances, heart failure and cerebrovascular disease," Bell said. Carbon monoxide
is a tasteless, odorless gas that is a component of automobile exhaust. The researchers
acknowledged that additional research is needed to investigate whether carbon monoxide or
a combination of it and other traffic-related pollutants are the cause of the increased
risk of cardiovascular hospitalizations in seniors.
Study reveals how a common virus
eludes the immune system
Viruses have numerous tricks for dodging the immune system. In the September 7, 2009 issue
of the Journal of Cell Biology, Stagg et al. reveal a key detail in one of these
stratagems, identifying a protein that enables cyto¬megalovirus to shut down an antiviral
defense (online August 31). Cytomegalovirus, which most people contract at some point in
their lives, eludes immune system surveillance by targeting the protein MHC I. When we're
sick, MHC I captures bits of viral proteins and presents them to cytotoxic T cells, which
respond by killing cells that harbor the virus, stanching the infection. However, two
cytomegalovirus genes dupe cells into ubiquitinating MHC I and demolishing it in the
proteasome, the cellular garbage disposal. To trigger MHC I ubiquitination, the genes
co-opt a cellular protein called the E3 ligase. Researchers haven't been able to pin down
the identity of this protein, which could be one of several hundred enzymes. Stagg et al.
sifted 373 candidates by depleting them one by one with RNAi. Knocking down a ligase
called TRC8 spared MHC I from destruction, the team found. Mutant versions of TRC8 that
curtail ubiquitination allow MHC I to return to duty. Researchers know little about the
function of the protein except that it is mutated in some rare hereditary and sporadic
kidney tumors. That result suggests that one of the normal targets of TRC8 helps spur
cancer.
NIH study reveals new genetic
culprit in deadly skin cancer
Drawing on the power of DNA sequencing, National Institutes of Health researchers have
identified a new group of genetic mutations involved in the deadliest form of skin cancer,
melanoma. This discovery is particularly encouraging because some of the mutations, which
were found in nearly one-fifth of melanoma cases, reside in a gene already targeted by a
drug approved for certain types of breast cancer. In the United States and many other
nations, melanoma is becoming increasingly more common. A major cause of melanoma is
thought to be sun exposure; the ultraviolet radiation in sunlight can damage DNA and lead
to cancer-causing genetic changes within skin cells. In work published in the September
issue of Nature Genetics, a team led by Yardena Samuels, Ph.D., of the National Human
Genome Research Institute (NHGRI) sequenced the protein tyrosine kinase (PTK) gene family
in tumor and blood samples from people with metastatic melanoma. The samples were
collected by the study's coauthor Steven Rosenberg, M.D., Ph.D., a leading expert on
melanoma and chief of surgery at the National Cancer Institute (NCI). The PTK family
includes many genes that, when mutated, promote various types of cancer. However,
relatively little had been known about roles played by PTK genes in human melanoma. The
NIH study was among the first to use large-scale DNA sequencing to systematically analyze
all 86 members of the PTK gene family in melanoma samples. The team's initial survey,
which involved samples from 29 melanoma patients, identified mutations in functionally
important regions of 19 PTK genes, only three of which had been previously implicated in
melanoma. The researchers then conducted more detailed analyses of those 19 genes in
samples from a total of 79 melanoma patients.
No evidence for the routine use of
aspirin in people with asymptomatic vascular events
he routine use of aspirin for the primary prevention of vascular events in people with
asymptomatic disease cannot be supported, according to results from the Aspirin for
Asymptomatic Atherosclerosis (AAA) study. The study is the first placebo-controlled
randomised trial designed to determine the effect of aspirin in asymptomatic
atherosclerosis as reflected by a low ankle brachial index (ABI). Results found no
statistically significant difference in primary endpoint events between those subjects
allocated to aspirin or placebo (HR 1•03, 95% CI 0•84-1•27). Joint first
author Professor Gerry Fowkes from the Wolfson Unit for Prevention of Peripheral Vascular
Diseases in Edinburgh said: "It is possible that in the general population, aspirin
could produce a smaller reduction in vascular events than this trial was designed to
detect, but it is questionable whether such an effect, together with aspirin related
morbidity, would justify the additional resources and health care requirements of an ABI
screening programme." The benefits of antiplatelet therapy in the prevention of
future cardio- and cerebrovascular events is well established in patients with a clinical
history of arterial vascular disease (secondary prevention); however, evidence in primary
prevention is limited, with studies suggesting that any benefit of aspirin must be weighed
against the risk of bleeding. The aim of the AAA trial was to determine the effectiveness
of aspirin in preventing events in people with asymptomatic atherosclerosis detected by
ABI screening. The study recruited 28,980 men and women aged 50 to 75 years who were free
of clinically evident cardiovascular disease in central Scotland; all were given an ABI
screening test. Those with a low ABI (3350 subjects, ?0•95 ABI) were entered into the
trial and randomised to once daily 100 mg aspirin or placebo. Participants were followed
up for a mean of 8•2 years and outcomes ascertained by annual contact, general
practitioner records, linkage to discharges from Scottish hospitals, and death
notification. The primary endpoint was a composite of initial fatal or non-fatal coronary
event or stroke, or revascularisation. There were two secondary endpoints: all initial
vascular events defined as a composite of a primary endpoint event or angina, intermittent
claudication or transient ischaemic attack; and all-cause mortality.
Failing heart, failing kidney -
Double trouble?
Concomitant kidney dysfunction and/or worsening renal function in patients with heart
failure is a frequent finding and is associated with a poor prognosis. Current treatment
of heart failure has beneficial effects on cardiac function but does not favorably affect
renal function. The possibility to improve renal function and/or obtain kidney protection
with new drugs or devices is still uncertain. Heart failure remains the most important
cause of hospitalisation for patients aged more than 65 years and this proportion is going
to increase because of aging of the general population and improvement in outcomes of most
cardiac diseases. Current treatment has improved the clinical course and prognosis of
chronic heart failure. However, hospitalisations for heart failure continue to be
associated with a poor prognosis with in-hospital mortality rates of 4% to 9%, and
post-discharge mortality and re-hospitalisation rates of 9-15% and 30-45%, respectively,
in the following 6-12 months. Comorbidities and, namely, kidney dysfunction play a major
role in the poor prognosis of heart failure patients. The development, or coexistence, of
kidney dysfunction in patients with heart failure is often defined as cardiorenal syndrome
Current treatment has improved cardiac function but seems to have no effect on concomitant
kidney dysfunction and this has become a major determinant of outcomes. A mild to moderate
impairment of kidney dysfunction is present in 40-50% of the patients admitted for acute
heart failure and 30-40% of the patients develop worsening renal function, generally
defined as an increase in serum creatinine >0.3 mg/dl, during their hospitalisations.
The causes of the frequent coexistence of kidney and cardiac dysfunction are multiple.
First, these two conditions may share common causes, such as hypertension, diabetes,
atherosclerosis, as well as common pathogenetic mechanisms, such neurohormonal and
inflammatory activation and endothelial dysfunction. In addition, heart failure causes
kidney dysfunction through its hemodynamic abnormalities, namely low cardiac output and
increased central venous pressure. Lastly, treatment of heart failure may also favor
kidney dysfunction.
Do women who smoke like men die
like men?
Smoking still kills more men than women, because men started smoking substantial numbers
of cigarettes long before women did. But, because so many men have now quit, male death
rates from smoking are decreasing in many European countries where female death rates from
smoking are still increasing. Taking men and women together, smoking causes about 0.7
million deaths per year in the 27 countries of the present European Union, including 0.3
million deaths per year before age 70 (more than one of five of all deaths before age 70).
Those killed by tobacco before age 70 lose, on average, about 23 years of life (and those
killed by tobacco at older ages lose, on average, about 8 years). Sir Richard Peto,
professor of medical statistics at the University of Oxford, UK, said "In Western
Europe tobacco causes more premature deaths than anything else does, and among both men
and women about a quarter of those who smoke throughout adult life will be killed by
tobacco before they are old, unless they can manage to stop smoking."
High caffeine intake can lead to
arrhythmias
Coffee is routinely consumed in countries within the Mediterranean basin. Coffee, an
infusion of ground, roasted coffee beans, is the most widely consumed behaviourally active
substance in the world. It contains several hundred different substances including,
antioxidants, carbohydrates, lipids, vitamins, minerals, phenolic compounds and alkaloids.
Nevertheless, the effects of coffee on the cardiovascular system have been mainly related
to caffeine. Acute and chronic caffeine intake appears to have only minor negative
consequence on health. However, high levels of caffeine intake have been related to
ventricular arrhythmias. Epidemiologic studies have already underlined the beneficial role
of the Mediterranean dietary pattern on mortality, coronary artery disease, lipid
metabolism and on blood pressure. The diet of people living in Mediterranean area, where
olive oil is the principal source of dietary fat, encompasses all the beneficial dietary
characteristics presented in previous studies. Little information is available on
relationship between adherence to Mediterranean Diet and atrial fibrillation (AF).
"We aimed to investigate the relationship between diets and atrial fibrillation, one
of the most common arrhythmias, and we focused on coffee and caffeine intake"
explained Prof Mattioli from the University of Modena, Italy."We selected patients
presenting with a first detected episode of AF. Nutrition habits were investigated by a
self administered food frequency questionnaire that included 116 items, followed by an
interviewer-administered 24 h diet recall questionnaire." In this population the
adherence to Mediterranean Diet is scarce. In addition, the antioxidant intake from coffee
is higher than antioxidant intake from vegetables and fruits. High antioxidant levels in
coffee were reported in several studies. A major issue is whether the antioxidants from
coffee are bioactive. Many epidemiologic studies found that coffee is associated with
reduced early oxidative stress. Thus, coffee may contain several bioactive compounds, some
of which may be beneficial, whereas others may increase the risk of disease. A second
point is the synergistic and antagonist interactions between food components of diet and
the complex of nutrients intake. "Our study suggests that high intake of coffee
increase the risk of arrhythmias in people without known cardiac disease", concludes
Prof Mattioli.
Think zinc - Molecular sensor could
reveal zinc's role in diseases
Scientists have developed a new molecular sensor that can reveal the amount of zinc in
cells, which could tell us more about a number of diseases, including type 2 diabetes. The
research, published today in Nature Methods, opens the door to the hidden world of zinc
biology by giving scientists an accurate way of measuring the concentration of zinc and
its location in cells for the first time. Zinc is involved in many processes in the body
and five percent of all the proteins made by the body's cells are involved in transporting
zinc. Scientists believe that zinc plays a role in many diseases; for example, it helps
package insulin in pancreas cells and in people with type 2 diabetes, the gene that
controls this packaging is often defective. Previously, researchers used crude chemical
techniques to get a rough idea of the concentration of zinc in cells. However, they could
not produce an accurate picture of how much zinc was present in cells or where it was
within them. In today's study, researchers from Imperial College London and Eindhoven
University of Technology in The Netherlands have developed a molecular sensor using
fluorescence proteins that can measure the distance between zinc ions in individual cells,
showing how much zinc is present. Professor Guy Rutter, one of the authors of the study
from the Division of Medicine at Imperial College London, said: "There has been
relatively little biological work done on zinc compared to other metals such as calcium
and sodium, partly because we didn't have the tools to measure it accurately before now.
Zinc is so important in the body – studies have suggested it has roles in many
different areas, including muscles and the brain." The new sensor, called a
fluorescence resonance energy transfer (FRET)-based sensor, is made up of two jellyfish
proteins called green fluorescent proteins. The researchers altered the first protein to
give off light at a certain wavelength, and altered the second protein to collect that
light. When the proteins attached to zinc ions, the proteins became pushed apart and the
transmission of light between them became weaker. The researchers used a fluorescence
microscope to detect the wavelengths of light emitted by the proteins. This revealed zinc
in the cell, with coloured patches visible where the proteins detected zinc.
Researchers identify protein
involved in causing gum disease, osteoporosis, arthritis
Investigators at Hospital for Special Surgery, collaborating with researchers from other
institutions, have contributed to the discovery that a gene called interferon regulator
factor-8 (IRF-8) is involved in the development of diseases such as periodontitis (gum
disease), rheumatoid arthritis and osteoporosis. The study, which will be published online
August 30, ahead of print, in the journal Nature Medicine, could lead to new treatments in
the future. "The study doesn't have immediate therapeutic applications, but it does
open a new avenue of research that could help identify novel therapeutic approaches or
interventions to treat diseases such as periodontitis, rheumatoid arthritis or
osteoporosis," said Baohong Zhao, Ph.D., lead author of the study and a research
fellow in the Arthritis and Tissue Degeneration Program at Hospital for Special Surgery
located in New York City. Dr. Zhao initiated the study while working in the laboratory led
by Drs. Masamichi Takami and Ryutaro Kamijo at Showa University, Tokyo, where much of the
work was performed. Dr. Zhao completed the study and extended the work to human cells
during the past year at Hospital for Special Surgery working with Dr. Lionel Ivashkiv.
Specifically, the researchers discovered that downregulation of IRF-8 (meaning that the
gene produces less IRF-8 protein) increases the production of cells called osteoclasts
that are responsible for breaking down bone. An osteoblast is a type of cell that is
responsible for forming bone and an osteoclast is a type of cell that breaks down bony
tissue (bone resorption). In humans and animals, bone formation and bone resorption are
closely coupled processes involved in the normal remodeling of bone. Enhanced development
of osteoclasts, however, can create canals and cavities that are hallmarks of diseases
such as periodontitis, osteoporosis and rheumatoid arthritis. Previous researchers have
spent time identifying genes that are upregulated during enhanced development of
osteoclasts, such as NFATc1, but few studies have identified genes that are downregulated
in the process. To fill this knowledge gap, scientists at Hospital for Special Surgery,
collaborating with researchers at other institutions, used microarray technology to
conduct a genome-wide screen to identify genes that are downregulated during the formation
of osteoclasts. They found that expression of IRF-8 was reduced by 75 percent in the
initial phases of osteoclast development. The researchers then genetically engineered mice
to be deficient in IRF-8 and gave the animals x-rays and CT (computed tomography) scans to
analyze IRF-8's influence on bone. They found that the mice had decreased bone mass and
severe osteoporosis. Experiments demonstrated that this was due not to a decreased number
of osteoblasts, but because of an increased number of osteoclasts. The researchers
concluded that IRF-8 suppresses the production of osteoclasts.
Can psychosocial stress at work put
at risk of developing rheumatoid arthritis?
A Swedish study published in one of the latest issue of Psychotherapy and Psychosomatics
discloses new relationships between stress at work and development of rheumatoid
arthritis. Psychosocial work stress, in terms of high psychological demands, low decision
latitude or the combination of these stressors (job strain), is associated with an
increased risk of several diseases (e.g. cardiovascular disease), but it has not been
studied in relation to rheumatoid arthritis (RA). However, research on the relationship
between psychosocial work stress and immunological parameters also suggests a possible
association with inflammatory conditions, including RA. In order to investigate whether
high psychological job demands, low decision latitude and job strain are associated with
the risk of developing RA, a group of Swedish investigators used data from EIRA, a large
population-based case-control study with incident cases of RA. The study base comprised
the population, aged 18–65 years, in middle and southern parts of Sweden during
1996–2003. In total, 1,221 cases and 1,454 controls participated.
Scientists develop a new approach
for cancer treatment
A new paradigm in the way we look at cancer with important implications on how we treat it
is about to be published in the British Journal of Cancer1 by Portuguese, Belgian and
American researchers. The group use a mathematical approach to reveal how - by changing
the dynamics of interaction between the cancer cells and those of the affected tissue
– it is possible to control and even potentially cure the disease. Even more
interesting is the fact that this new approach can be used in any number of pathologies
where different cells interact. The work has the potential to revolutionise the way we
look into the treatment of disease and demonstrates the relevance of mathematical models,
not only to improve our understanding of biological systems, but also to find more
effective ways for dealing with problems in them. In cancer, the apparently same disease
and/or treatment can have radically distinct outcomes in different patients, and while it
is easy to understand that the interactions between the cancer cells and the individual
specificities have a major role determining the final outcome, how this happens and,
consequently, how to control it is a major issue in medicine and one very far from being
clear.
Air pollution is reducing the
amount of rain in China
Air pollution in eastern China during the last 50 years has led to a reduction in the
amount of light rainfall of almost a quarter. This is revealed by an international study
conducted with support from the University of Gothenburg, Sweden. There is a risk that the
consequences will be increased drought, reduced harvests and poorer public health.
China’s dramatic growth has also brought about an increase in environmental problems.
At the same time as the population has more than doubled during the last century,
emissions into the atmosphere have increased by 800 percent. The environmental impact has
been particularly pronounced in eastern China, where most of the people live and where the
emissions are greatest: it does not rain in the same way as it did before. In some parts
of eastern China the number of days with rain has diminished by 23 percent in 50 years.
The consequences are increased drought and poorer harvests. A team of climate researchers
from the USA, China and Sweden – including Deliang Chen, Professor of Physical
Meteorology in the Department of Earth Sciences, University of Gothenburg – has now
studied the problem and demonstrated that the reduced amounts of rainfall have a direct
connection with high concentrations of air pollution.
Makers Of the H1N1 Vaccination
Refuse To Take It
Even scientists who helped develop the
vaccine say THEY ARE NOT GOING TO TAKE ITAND URGE THEIR FRIENDS AND FAMILY NOT TO TAKE IT
EITHER, says Wayne Madsen, an investigative journalist and RT contributor. Meanwhile, it
has been reported that vets have found traces of the swine flu virus in birds. It was
detected in turkeys at farms in Chile. So far swine flu has proved to be very contagious,
but not more deadly than the common flu. However, scientists fear it may combine with
avian flu, which is currently very dangerous but hard to pass on.
Dark Clouds - The hidden side of
China's miracle economy
China's economy is exploding and behind the
scenes of this economic miracle is the industrial revolution powered by the cheap labour
that is helping to build and sustain the economy. Coal for power, coal for steel, coal for
cement. Coal and labour are the raw materials, the flip side and the dark side of this
economic juggernaut that is China. But it comes at a heavy price for the country's
environment and its people's health. And now that is has overtaken the US as the biggest
producer of carbon dioxide, China's emission levels will increase anxiety about its role
in driving man-made global warming and will add to pressure on the world's politicians to
reach an agreement on climate change that includes the Chinese economy.
Bottom trawling is laying waste to the
precious ecosystems of the deep sea. Sigourney Weaver calls on delegates of the UN to take
immediate action to stop this destruction.
The Disclosure Project - Alien life
forms
Steven Greer is the founder and
international director of CSETI, the only worldwide organization dedicated to establishing
peaceful and sustainable relations with extraterrestrial life forms. He is a medical
doctor specializing in trauma medicine. He is the former chairman of the Department of
Emergency Medicine at Caldwell Memorial Hospital in North Carolina. He is a lifetime
member of Alpha Omega Alpha, USA's most prestigious academic honor society for physicians.
He is the father of four girls. He has studied and worked in the U.S., Europe, the
Caribbean and Israel. He served for three years at the World Center of the Baha'i Faith in
Haifa, Israel.
Witnesses
Mr John Callahan FAA head of accidents and investigations Link
Merle Shane McDow: US Navy Atlantic Command
Lance Corporal Jonathan Weygandt: US Marine Corps
Nick Pope: British Ministry of Defense Official
Master Sgt. Dan Morris: US Air Force, NRO Operative
Officer Alan Godfrey: British Police
Dr. Robert Wood: McDonnell Douglas Aerospace Engineer
Dr. Roberto Pinotti: Italian UFO expert
Dr. Paul Czysz: McDonnell Douglas Career Engineer
Astronaut Edgar Mitchell
Neil Daniels: United Airlines Pilot
Lt. Frederick Fox: US Navy Pilot
Astronaut Gordon Cooper
Admiral Lord Hill-Norton: Five-Star Admiral, Former Head of the British Ministry of
Defense
Major-General Vasily Alexeyev: Russian Air Force,
Dr. Alfred Webre: Senior Policy Analyst Stanford Research Institute
Denise McKenzie: Former SAIC employee
Lieutenant Walter Haut: US Navy
Admiral Lord Hill-Norton: Five-Star
Admiral, Former Head of the British Ministry of Defense, July 2000 Lord Hill-Norton is a five-star Admiral and the former Head of the British
Ministry of Defense who was kept in the dark about the UFO subject during his official
capacities. In this short interview, he states that this subject has great significance
and should no longer be denied and kept secret. He emphatically states, "…that
there is a serious possibility that we are being visited — and have been visited for
many years — by people from outer space, from other civilizations; that it behooves
us to find out who they are, where they come from, and what they want. This should
be the subject of rigorous scientific investigation, and not the subject of rubbishing by
tabloid newspapers."
Free Energy
Wouldn't it be great if we could all have
water powered cars?
The Path to New Antibiotics
Researchers at Burnham Institute for Medical Research (Burnham), University of Texas
Southwestern Medical Center and University of Maryland have demonstrated that an enzyme
that is essential to many bacteria can be targeted to kill dangerous pathogens. In
addition, investigators discovered chemical compounds that can inhibit this enzyme and
suppress the growth of pathogenic bacteria. These findings are essential to develop new
broad-spectrum antibacterial agents to overcome multidrug resistance. The research was
published in the Cell journal Chemistry & Biology on August 27.
U-Iowa improves delivery of
cancer-fighting molecules
Small interfering RNA (siRNA), a type of genetic material, can block potentially harmful
activity in cells, such as tumor cell growth. But delivering siRNA successfully to
specific cells without adversely affecting other cells has been challenging. University of
Iowa researchers have modified siRNA so that it can be injected into the bloodstream and
impact targeted cells while producing fewer side effects. The findings, which were based
on animal models of prostate cancer, also could make it easier to create large amounts of
targeted therapeutic siRNAs for treating cancer and other diseases. The study results
appeared online Aug. 23 in the journal Nature Biotechnology. "Our goal was to make
siRNA deliverable through the bloodstream and make it more specific to the genes that are
over expressed in cancer," said the study's senior author Paloma Giangrande, Ph.D.,
assistant professor of internal medicine and a member of Holden Comprehensive Cancer
Center. In previous research completed at Duke University, Giangrande's team showed that a
compound called an aptamer can be combined with siRNA to target certain genes. When the
combined molecule is directly injected into tumors in animal models, it triggers the
processes that stop tumor growth. However, directly injecting the combination into tumors
in humans is difficult. In the new study, the researchers trimmed the size of a prostate
cancer-specific aptamer and modified the siRNA to increase its activity. Upon injection
into the bloodstream, the combination triggered tumor regression without affecting normal
tissues.
Familiar and newly learned words
are processed by the same neural networks in the brain
Our vocabulary continues to grow and expand even in adulthood. Just ten years ago, the
word ‘blog’ did not yet exist – and now we no longer remember when we heard
this word for the first time or when we learned its meaning. At some stage new words
become just as familiar to us as words we have learned earlier. One of the areas of
interest in the Academy of Finland’s Neuroscience Research Programme (NEURO) is how
the process of learning new words is reflected in the function of the brain. The new
research evidence emerging about how the brain processes language and its different levels
has important application among other things in the development of language teaching. In
one of the experiments conducted in the NEURO programme, participants learned the name
and/or purpose of 150 ancient tools. They had never heard these words before. The
subjects’ brain function was measured by means of magnetoencelography during the
naming of the tools, both before and after the learning period.
Finnish scientists discover nerve
growth factor with possible therapeutic potential in Parkinson’s disease
Scientists in the Academy of Finland’s Neuroscience Research Programme have reported
promising new results with potential implications for the treatment of Parkinson’s
disease. They have been studying the impacts of nerve growth factors in the treatment of
PD, and their latest results show that a certain growth factor can be used to halt the
progress of damage brought on by a nerve poison and possibly even restore the function of
damaged cells. The studies on nerve growth factors used an experimental PD model in rats.
Administration of the growth factor reduced motor disturbances in rats. The severe motor
disturbances that are seen in PD are caused by the slow degeneration of dopamine nerves in
the brain. There are treatments that alleviate the symptoms of the disease, such as hand
tremor, but they do not prevent or halt the degeneration of nerve cells. The nerve growth
factors studied to date have slowed nerve cell degeneration to some extent, but they have
had only limited therapeutic effect. Several known nerve growth factors, such as GDNF,
also attach to extracellular tissue, possibly deterring their movement to nerve cells that
require treatment.
Restoring the ecology can boost the
economy
Research co-authored by Bournemouth University (BU) Professor Adrian Newton and published
in the leading journal Science this week shows that ecological restoration in areas of
environmental degradation can help reverse global biodiversity losses, as well as
promoting recovery of ecosystem services. However the research also showed that measures
of biodiversity and ecosystem services are higher in pristine land, freshwater and marine
systems than in restored systems. Examples of ecosystem services include improved water
quality and increased carbon storage, services which benefit human well-being. The
research was carried out by an international team from the University of Alcalá in Spain,
the UK’s Centre for Ecology & Hydrology, and Bournemouth University in the UK.
The Origins of Lactase Persistence
in Europe
Lactase persistence (LP) is common among people of European ancestry, but with the
exception of some African, Middle Eastern and southern Asian groups, is rare or absent
elsewhere in the world. Lactase gene haplotype conservation around a polymorphism strongly
associated with LP in Europeans (?13,910 C/T) indicates that the derived allele is recent
in origin and has been subject to strong positive selection. Furthermore, ancient DNA work
has shown that the ?13,910*T (derived) allele was very rare or absent in early Neolithic
central Europeans. It is unlikely that LP would provide a selective advantage without a
supply of fresh milk, and this has lead to a gene-culture coevolutionary model where
lactase persistence is only favoured in cultures practicing dairying, and dairying is more
favoured in lactase persistent populations. We have developed a flexible demic computer
simulation model to explore the spread of lactase persistence, dairying, other subsistence
practices and unlinked genetic markers in Europe and western Asia's geographic space.
Using data on ?13,910*T allele frequency and farming arrival dates across Europe, and
approximate Bayesian computation to estimate parameters of interest, we infer that the
?13,910*T allele first underwent selection among dairying farmers around 7,500 years ago
in a region between the central Balkans and central Europe, possibly in association with
the dissemination of the Neolithic Linearbandkeramik culture over Central Europe.
Furthermore, our results suggest that natural selection favouring a lactase persistence
allele was not higher in northern latitudes through an increased requirement for dietary
vitamin D. Our results provide a coherent and spatially explicit picture of the
coevolution of lactase persistence and dairying in Europe.
Researchers Find High-Dose Therapy
for Liver Disease Not Effective
High-dose ursodeoxycholic acid detrimental for treatment of primary sclerosing cholangitis
Tunnels concentrate air pollution
by up to 1000 times
A toxic cocktail of ultrafine particles is lurking inside road tunnels in concentration
levels so high they have the potential to harm drivers and passengers, a new study has
found. The study, which has been published in Atmospheric Environment, measured ultrafine
particle concentration levels outside a vehicle travelling through the M5 East tunnel in
Sydney. Study co-author and director of Queensland University of Technology's
International Laboratory for Air Quality and Health, Professor Lidia Morawska, said road
tunnels were locations where maximum exposure to dangerous ultrafine particles in addition
to other pollutants occurred. "The human health effects of exposure to ultrafine
particles produced by fuel combustion are generally regarded as detrimental,"
Professor Morawska said. "Effects can range from minor respiratory problems in
healthy people, to acute myocardial infarction (heart attack) in people with existing
heart complaints. Professor Morawska said the study involved more than 300 trips through
the four kilometres of the M5 East tunnel, with journeys lasting up to 26 minutes,
depending on traffic congestion. "What this study aimed to do was identify the
concentration levels found in the tunnel. It generated a huge body of data on the
concentrations and the results show that, at times, the levels are up to 1000 times higher
than in urban ambient conditions," she said.
Collagen-deficient mice show signs
of osteoarthritis
Osteoarthritis (OA) and degenerative disc disease (DDD) are common, chronic
musculoskeletal disorders. Both diseases cause joint pain, loss of function, and decreased
quality of life for the more than 27 million OA and 59 million DDD suffers in the US.
According to a 2003 Medical Expenditure Panel Survey, arthritis such as OA costs the U.S.
economy nearly $128 billion per year in medical care and indirect expenses including lost
wages and productivity. Researchers at Duke University Medical Center, under a grant from
the National Institutes of Health (NIH), conducted a study of mice to determine the effect
of Type IX collagen (Col9a1) deficiency on functional ability. The authors found that mice
with the Col9a1 gene inactivated prematurely develop OA and DDD. Findings of this study
appear in the September issue of Arthritis & Rheumatism, a journal of the American
College of Rheumatology, published by Wiley-Blackwell. Duke University researchers led by
Kyle Allen, Ph.D. compared the behavioral abilities of Col9a1 deficient mice to wild-type
(WT) mice. Mice of advanced age (9-11 months) were selected because they represent an age
at which there is histological evidence of OA and DDD. Functional tests of reflexes,
posture, strength, coordination, balance, sensorimotor skills, and gait were conducted to
measure physical capabilities that could be impaired due to OA or DDD. Symptomatic pain
was assessed through mechanical and thermal withdrawal thresholds. "We observed a
pattern of behavioral changes in the collagen deficient mice that suggests a relationship
to OA- and DDD-like degeneration," stated Dr. Allen. The data shows that mice
deficient in Type IX collagen clearly displayed behavioral characteristics of pain and
functional loss. These mice had delayed righting reflex (ability to regain footing from a
back position), decreased sensorimotor skills, and altered gait compared with WT mice.
Collagen deficient mice also had elevated levels of knee and intervertebral disc
structural changes.
Chemotherapy resistance -
Checkpoint protein provides armor against cancer drugs
Cell cycle checkpoints act like molecular tripwires for damaged cells, forcing them to
pause and take stock. Leave the tripwire in place for too long, though, and cancer cells
will press on regardless, making them resistant to the lethal effects of certain types of
chemotherapy, according to researchers at the Salk Institute for Biological Studies. Their
findings, published in the Aug. 28 issue of Molecular Cell, help explain how the
checkpoint exit is delayed in some cancer cells, helping them to recover and resume
dividing after treatment with DNA-damaging cancer drugs. "A lot of progress has been
made in understanding the molecular details of checkpoint activation," says senior
author Tony Hunter, Ph.D., a professor in the Molecular and Cell Biology Laboratory,
"but checkpoint termination, which is essential for the resumption of cell cycle
progression, is less well understood." The Salk researchers say that a better
understanding of this crucial process may allow them to develop biological markers that
predict clinical resistance to chemotherapy and to design cancer drugs with fewer side
effects by exploiting the molecular mechanism underlying the checkpoint exit. "If we
could screen tumors for markers of chemo-resistance, we could then adjust the treatment
accordingly," hopes first author You-Wei Zhang, Ph.D., formerly a postdoctoral
researcher in Hunter's lab and now an assistant professor at Case Western Reserve
University in Cleveland, Ohio. In response to DNA damage and blocked replication—the
process that copies DNA—eukaryotes activate the DNA damage checkpoint pathway, which
stops the cell cycle, buying time to repair damage and recover from stalled or collapsed
replication forks. If not repaired, these errors can either kill a cell when it attempts
to divide or lead to genomic instability and eventually cancer.
'Fatostatin' is a turnoff for fat
genes
A small molecule earlier found to have both anti-fat and anti-cancer abilities works as a
literal turnoff for fat-making genes, according to a new report in the August 28th issue
of the journal Chemistry and Biology, a Cell Press journal. The chemical blocks a well
known master controller of fat synthesis, a transcription factor known as SREBP. That
action in mice that are genetically prone to obesity causes the animals to become leaner.
It also lowers the amount of fat in their livers, along with their blood sugar and
cholesterol levels. "We are frankly very excited about it," said Salih Wakil of
Baylor College of Medicine. "It goes to the origin of [fat synthesis] – all the
way back to gene expression." Unlike cholesterol-lowering statins in use today, which
block a single enzyme in the pathway, the chemical, which the researchers call fatostatin,
"hits fat from the very beginning," added Motonari Uesugi, who is now at Kyoto
University. In doing so, fatostatin influences many of the genes involved in fat
production and in various aspects of metabolic syndrome – a collection of risk
factors including obesity, high cholesterol and insulin resistance – in one go.
Studies in cell culture showed that fatostatin, previously known only as 125B11,
significantly lowers the activity of 63 genes, including 34 directly associated with fatty
acid or cholesterol synthesis. Many of those were known to be under the control of SREBP.
