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Week 32


 

Bcl6 gene sculpts helper T cell to boost antibody production

Expression of a single gene programs an immune system helper T cell that fuels rapid growth and diversification of antibodies in a cellular structure implicated in autoimmune diseases and development of B cell lymphoma, scientists at The University of Texas M. D. Anderson Cancer Center reported today in Science Express, the advance online publication of the journal Science. The gene is Bcl6, which the team found plays the crucial role in differentiating a naïve T cell into a T follicular helper cell (Tfh). "Tfh cells were first noticed in structures called germinal centers found in the lymphoid system - in lymph nodes and the spleen," said senior author Chen Dong, Ph.D., professor in M. D. Anderson's Department of Immunology. Germinal centers are powerful machines that churn out lots of antibodies. In the adaptive immune system, B cells present an antigen - a distinctive piece of an invading bacterium or virus - to T cells. The bound antigen converts a naïve T cell to a helper T cell that secretes cytokines which help the B cells expand and produce a large volume of antibodies to destroy an intruder. Tfh cells are concentrated with B cells in germinal centers, where they play a helper T cell's traditional role in B cell proliferation and antibody development. "In germinal centers, the B cells not only proliferate but they also undergo hypermutation in their immunoglobulin genes so they can produce a diverse class of antibodies," Dong said. "These mutations also allow production of antibodies with stronger affinity for their target antigens." There are pitfalls to this process. Tfh cells and germinal centers have been implicated in antibody-mediated autoimmune diseases such as lupus and rheumatoid arthritis, Dong noted. In these diseases, the germinal centers are likely producing the wrong type of antibody at great volume. Genetic hypermutation among B cells in germinal centers creates a hotbed of genomic instability, which gives rise to some types of B cell lymphoma, Dong said.


Bone from Blood - Circulating Cells Form Bone Outside the Normal Skeleton, Penn Study Finds

The accepted dogma has been that bone-forming cells, derived from the body’s connective tissue, are the only cells able to form the skeleton. However, new research shows that specialized cells in the blood share a common origin with white blood cells derived from the bone marrow and that these bloodstream cells are capable of forming bone at sites distant from the original skeleton. This work, published online this month in the journal Stem Cells, represents the first example of how circulating cells may contribute to abnormal bone formation.


Human cells secrete cancer-killing protein, UK study finds

Human cells are able to secrete a cancer-killing protein, scientists at the University of Kentucky's Markey Cancer Center have found. Researchers led by Vivek Rangnekar, UK professor of radiation medicine, have determined that the tumor-suppressor protein Par-4, initially thought to be active only within cells expressing the Par-4 gene, is in fact secreted by most human and rodent cells and can target large numbers of cancer cells by binding to receptors on the cell surface. This discovery, published today in the leading journal Cell, makes Par-4 a very attractive molecule for future research aimed at developing new cancer treatments. "It was a pleasant surprise, when we noticed that Par-4 protein is secreted by cells," Rangnekar said. "This new finding means it is not necessary to make genetic modifications, or to employ recombinant viruses, to deliver the Par-4 gene to cancer cells, and it significantly expands the potential applications of Par-4 to selectively kill cancer cells." Funded by several grants from the National Institutes of Health, Rangnekar's study found that when the Par-4 molecule binds to its receptor GRP78 on the surface of a tumor cell, it triggers a biological process called apoptosis or "cell suicide." Consistent with previous research by Rangnekar's laboratory with intracellular Par-4, the newly discovered secreted Par-4 acts selectively against cancer cells, leaving healthy cells unharmed. Few other molecules are known to exhibit such selectivity.


Sticky protein helps reinforce fragile muscle membranes

A new study by scientists at the University of Iowa shows why muscle membranes don't rupture when healthy people exercise. The findings shed light on a mechanism that appears to protect cells from mechanical stress. The study, which appears online July 20-24 in Proceedings of the National Academy of Sciences (PNAS) Early Edition, also helps explain why muscle damage is so severe when this mechanism is disrupted, which occurs in certain congenital and limb-girdle muscular dystrophies. Specifically, the team identified a protein called alpha dystroglycan as the "glue" that binds muscle membranes to a tough layer of extracellular proteins called the basal lamina. Just as a piece of sticky tape can prevent a pin from bursting a balloon, the sturdy basal lamina reinforces muscle cell membranes and keeps small tears from bursting open -- but only if the dystroglycan "glue" affixing the basal lamina to the membrane is working. "This study helps us understand how membrane structure is designed to protect cells, which is a universally important process," said senior study author Kevin Campbell, Ph.D., professor and head of molecular physiology and biophysics at the UI Roy J. and Lucille A. Carver College of Medicine and a Howard Hughes Medical Institute investigator. "The findings may also have clinical implications for muscular dystrophies that are caused by abnormal dystroglycan." These congenital muscular dystrophies include Fukuyama Congenital Muscular Dystrophy, Walker-Warburg Syndrome and Muscle-Eye-Brain disease and limb-girdle muscular dystrophy 2I. In these so-called dystroglycanopathies, too few sugar groups are added to alpha dystroglycan, leading to a version of the protein that does not attach properly to the basal lamina. Detachment of the basal lamina from the muscle membrane appears to be a common feature of these conditions, and patients develop a very severe muscular dystrophy. Working with a mouse model of these diseases, the researchers, including Renzhi Han, Ph.D., a UI research scientist and the first author of the study, found that injecting functional dystroglycan into muscle that lacks this component restored muscle membrane integrity and protected the muscles from damage.


The Alzheimer's Project: Momentum in Science


Council On Foreign Relations - One World Government

Although the Council doesn´t seem to admit what it´s final goal is, the truth behind it is becoming more obvious, when we see who´s participating, and how the council gains more and more control over the media, when a man like Rupert Murdoch, who is a valuable member, is in control of mainstream media in the USA and beyond. Media is crucial to influence public opinion in order to protect the very interests of the organization, which would be more influence and power, of course.


Percy Schmeiser in Salzburg, Austria


Monsanto Harassing and Sueing Farmers Over Seed Patents


Protein excreted in urine may be help in diagnosing kidney disease caused by HIV

New data collected at Columbia University Medical Center and by the Mount Sinai School of Medicine are helping researchers understand the extent to which a certain protein – NGAL – can play a significant role in marking chronic kidney disease resulting from HIV while at the same time distinguishing nephropathy from more common causes such as diabetes and hypertension. It's well-known that Human Immunodeficiency Virus-associated nephropathy (HIVAN) is an important cause of kidney disease in HIV-infected patients. Antiretroviral therapy plays an important role in the treatment of HIVAN, yet despite advances in understanding HIVAN, current recommendations for treatment have largely been based on observational data and can only definitively made after a kidney biopsy. The current study, spearheaded by Columbia University's Jonathan Barasch, M.D., Ph.D., along with Ali Gharavi M.D., Ph.D., Neal Paragas M.S., Thomas Nickolas M.D., M.S., and Vivette D'Agati M.D., together with Paul Klotman, M.D., Christina Wyatt M.D., and Susan Morgello M.D., of the Mount Sinai School of Medicine and Landino Allegri in Parma, Italy, and Prasad Devarajan in Cincinnati Childrens Hospital, represents the examination of data from human cohorts in New York and Parma, and from mouse models created by Dr. Klotman. The team noted that NGAL, or Neutrophil Gelatinase Associated Lipocalin, a protein they previously discovered in damaged kidneys, was prominently expressed in kidney tissue and in the urine of humans and in mouse models of HIVAN. The high levels of the urine protein were out of proportion to the degree of chronic renal failure, for example that typifies patients with other types of chronic glomerular diseases of both mice and humans. Most strikingly, Paragas, Barasch, and Gharavi noticed that the rise in urinary NGAL levels was in conjunction with the development of a specific type of lesion, namely tubular cysts that typify HIVAN. The association with these cysts consequently may justify their biopsy or an aggressive treatment with antiretroviral drugs when high levels of urine NGAL are discovered. "From what we can tell, NGAL is unexpectedly expressed in great abundance by kidney cysts allowing the clinician to potentially identify HIVAN among other types of chronic kidney diseases and hopefully to intervene to prevent a kidney from ultimately dying from what physicians refer to as ESRD, or 'end-stage renal disease,'" Dr. Barasch says. Dr. Barasch cautions that studying a much larger human cohort would be needed in order to determine the precise relationship of NGAL to HIVAN and whether the protein is a good enough predictor of tubular cysts, but he finds the results of the study unexpected and intriguing.


Leukemia cells evade immune system by mimicking normal cells, Stanford studies show

Human leukemia stem cells escape detection by co-opting a protective molecular badge used by normal blood stem cells to migrate safely within the body, according to a pair of studies by researchers at Stanford University Medical School."We call it the 'Don't eat me signal,'" said Ravindra Majeti, MD, PhD, assistant professor of hematology at the medical school and the co-first author of one of the studies, which focused on acute myeloid leukemia. Patients whose cancer stem cells express higher levels of the molecule have a poorer prognosis than those whose cells express lower levels, and masking its presence makes the human cancer cells less deadly and more vulnerable to destruction when injected into mice. The results indicate that the molecule may serve both as a prognostic factor and a valuable therapeutic target for patients with the cancer. "When we blocked this signal in mice with established human leukemia, the cancer cells were more easily removed by the body's natural defenses," Majeti said. The researchers are now moving ahead with plans to test a similar treatment in humans and have filed for a patent for the potential therapy. Irving Weissman, MD, the Virginia & D.K. Ludwig Professor for Clinical Investigation in Cancer Research at the medical school, is the senior author of both studies, which will be published together in the July 24 issue of the journal Cell. Majeti shares his first authorship with Mark Chao, an MD and PhD student in the cancer biology program at the medical school. Both Majeti and Weissman are members of Stanford's Cance Center.Together, the researchers of the studies found that the molecule, CD47, protects the leukemia stem cells from macrophages — part of a roving cellular army tasked with finding and engulfing diseased or dying cells — by binding to a molecule on the macrophage's surface. The interaction between the two proteins inhibits the macrophage's killing instinct and allows the marauding cancer cells to escape unscathed. The current research sprang from an earlier study in Weissman's lab that showed CD47 expression was expressed at significantly higher levels in mouse leukemia cells. "At the time, we didn't know what role CD47 played in leukemia," said Siddhartha Jaiswal, an MD and PhD student at the medical school who is the first author of the second study. "But it was clearly important." It all fell into place, according to Weissman, when another group showed that red blood cells expressing CD47 were bypassed by macrophages, but those without CD47 were eaten. "Our discovery that leukemia cells in mice also expressed CD47 led us to propose that this signal might be appropriated by the leukemia stem cells as part of their leukemic progression," said Weissman.


New breast pumping approach helps preemies' moms to improve milk supply, says Packard/Stanford study

Mothers of premature infants shouldn’t rely solely on breast pumps to establish and maintain their breast milk supply, researchers at Lucile Packard Children’s Hospital and the Stanford University School of Medicine have found. Moms already have a simple, safe and free tool for assisting breast milk production: their own hands. In the study, 67 new mothers of premature infants learned how to combine an electric breast pump with hand-expression techniques to extract milk. Unlike prior research showing poor milk production in preemies’ moms, the subjects who used both hands and pump established plentiful milk supplies. By the end of the eight-week study, their average milk production exceeded the amount needed to feed a healthy 3-month-old, even though none of the women studied could nurse when their babies were born. The findings could have implications for women who have full-term infants, too. “When I saw the data, I realized, oh, my gosh, this is impressive,” said Jane Morton, MD, who led the study. Morton was the director of the breast-feeding medicine program at Packard Children’s when the study, which appeared online July 2 in the Journal of Perinatology, was conducted. “We were worried about mothers of preterm babies establishing any milk supply, much less an average-or-better supply,” said William Rhine, MD, a neonatologist at Packard Children’s and the study’s senior author. The findings contradict widely held assumptions that premature delivery lessens the hormone signals needed to establish breast-feeding.


New lab test helps predict kidney damage

'Urine NGAL' gives clues to kidney injury in ICU patients and HIV-related kidney disease. Acute kidney injury (AKI) is a frequent complication in patients in intensive care. A new laboratory test called urine neutrophil gelatinase associated lipocalin (NGAL) helps predict if patients will develop acute kidney injury, reports an upcoming study in the Journal of the American Society of Nephrology (JASN). "As a stand-alone marker, urine NGAL performed moderately well in predicting ongoing and subsequent AKI," comments T. Alp Ikizler, MD (Vanderbilt University). Another study, also in JASN, indicates that urine NGAL may also help in diagnosing HIV-related kidney disease affecting African Americans and black Africans. "NGAL was very specifically expressed in renal cysts—generating the new idea that NGAL may control the development of cysts in HIV-associated nephropathy," says Jonathan Barasch, MD, PhD (Columbia University, New York). He adds, "We and Prasad Devarajan, MD, identified NGAL in the kidney 10 years ago and its translation into a clinical entity in such a short time is quite a story. Almost every paper is positive for the association of NGAL and renal dysfunction/disease." In the ICU study, patients with higher urine NGAL levels were more likely to develop acute kidney injury, even after adjustment for other factors. The rise in NGAL was present before any change in the standard test for AKI (serum creatinine level). Without other information, however, urine NGAL was no more effective in predicting AKI than clinical risk factors. Ikizler notes the study was limited by a lack of information on incidence of death or the need for dialysis, and by a lack of information on the patients' initial kidney function level. In the HIV study, levels of urine NGAL were much higher in patients with HIV-associated nephropathy (HIVAN) than in patients with other forms of kidney disease, with or without HIV. HIVAN is an important complication of HIV, occurring mainly in patients of African descent. Studies in mice suggested that NGAL may play an important role in the development of tubular disease and microcysts, which are specific features of HIVAN. Barasch notes that the human component of their study was limited by its small size but highlights the need for larger studies that definitively measure the NGAL monomer. He adds, "If our results are confirmed, measuring urine NGAL might help triage patients into different risk categories."


What Your Doctor Doesn't Know

Here are 3 simple secrets that are unknown (or ignored) by the medical profession and bitterly disputed by Big Pharma that routinely publishes phony research and
myths against them.

1. Plain cheap vitamin C takes all minerals out of the blood by combining with them metabolically. It's cheaper and safer than any other method.
2. The same vitamin C kills viruses - also by combining with them metabolically.
3. The ONLY bad side effect possible using vitamin C is diarrhea.

Few MD's know this because they get little or no vitamin information in med school, and med journals depend on drug advertising for their existence. Any journal that told the truth would go out of business. As the only PhD in the Orthomolecular Medical Society, I could not use EDTA or other chelation drugs to get toxic minerals out of a patient. In 1981, I had my first case of schizophrenia from a high copper/zinc cause. I asked Carl Pfeiffer what to do in such a case. He told me that he thought vitamin C could be used, and referred me to Linus Pauling. Linus spent a half hour of his time mentoring me in the use of vitamin C for this.

After using vitamin C for many years to "cure" mineral toxicity in many cases of schizophrenia (copper/zinc ratio) and depression (mercury toxicity), I KNOW that vitamin C works! I have personally been taking 4000 mg (4 grams) per day for years. And all my mineral analysis results for years have shown either very low levels of all toxic minerals, or actually immeasurable amounts. I know that this safe and cheap method works personally. (A copy of my recent hair analysis is available showing this "proof".) I recently cured the what I believe was the swine flu in myself and my wife in 24 hours using only vitamin C. For the flu, it took 48 grams per day (6 each 1000mg pills every 3 hours) for both my wife and I to beat it.   The RDA of only 75 mg per day allows people to think that this is healthy, not realizing that this small amount is the MINIMUM just to prevent scurvy. Talk to a vet in the zoo who takes care of primates (primates are apes, monkeys and us), and you'll find out that the RDA to keep a 150 pound ape healthy is 4 grams per day for good health. This is the same for you and I - I take 2 grams AM and PM.

The first two FACTS listed above about vitamin C lead to two different therapies related to Autism, and a very important one for virus curing.

1.. That first fact makes for a simple, safe therapy to Prevent Autism by taking toxic minerals (mostly mercury) out of the pregnant woman prior to birth. This leads
to the tiny infant liver being able to handle mercury in toxic amounts, not only from vaccines, but from environmental sources such as mothers milk, and mercury from
every coal burning power plant around. Basically, this simple system has the expectant mother taking at least 2 grams of vitamin C at breakfast and dinner, leaving
other vitamins and minerals for lunch. Increase to 3 grams each time if mother has 6 months or less remaining. Remember that vitamin C takes out good minerals along
with the toxic ones, so it's necessary to put back the good ones. (Details on http://drbate.com)

2. This same fact helps persons with autism remove mercury, lead, and aluminum from the blood, safely, effectively, and cheap! These all can do damage to the
brain. Doing this is essential to any autism "cure". (A complete article on this therapy was featured in the August issue of this magazine, and may be found at
http://drbate.com.)

3. The other fact dictates the use of vitamin C in huge amounts immediately when any sign of a cold or flu shows up. Start taking at least 6 grams of vitamin C pills
every three hours until diarrhea starts. At that point. drop to 6 every 4-5 hours. The idea is to keep high in vitamin C, but not high enough to cause diarrhea. Diarrhea
shows that the bloodstream is finally "saturated", and "overflowing". Until that point, virus cells are increasing by doubling every 20 minutes or so.

See now why phony research about vitamin C and virus using 500 mg to 1 gram is useless? If it even kills off half of the virus cells, in 20 minutes after it's used up, the virus is back to full strength. As one researcher put it, "the only mistake is not using enough vitamin C. For more information, go to http://drbate.com. On the "navigation" section, there are many articles on vitamin C, and using it for the above therapies. Please help me get this Prevent Autism simple safe and cheap information out to pregnant women everywhere. We can stop this epidemic or at least slow it down easily without a lot of cost (a bottle of 500 one gram pills costs less than $20 at Costco or even WalMart.) This is a case of not using Big Pharma's pet phrase "ask your doctor". They simply don't know.


Nanodiamonds deliver insulin for wound healing

Bacterial infection is a major health threat to patients with severe burns and other kinds of serious wounds such as traumatic bone fractures. Recent studies have identified an important new weapon for fighting infection and healing wounds: insulin. Now, using tiny nanodiamonds, researchers at Northwestern University have demonstrated an innovative method for delivering and releasing the curative hormone at a specific location over a period of time. The nanodiamond-insulin clusters hold promise for wound-healing applications and could be integrated into gels, ointments, bandages or suture materials. Localized release of a therapeutic is a major challenge in biomedicine. The Northwestern method takes advantage of a condition typically found at a wound site -- skin pH levels can reach very basic levels during the repair and healing process. The researchers found that the insulin, bound firmly to the tiny carbon-based nanodiamonds, is released when it encounters basic pH levels, similar to those commonly observed in bacterially infected wounds. These basic pH levels are significantly greater than the physiological pH level of 7.4. The results of the study were published online July 26 by the journal Biomaterials.


Blood flow in Alzheimer's disease

Researchers have discovered that the enzyme, endothelin converting enzyme-2 (ECE-2), may cause the decrease in blood flow in the brain seen in Alzheimer's disease and contribute to progression of the disease. The study by Jennifer Palmer, BRACE/Reverend Williams PhD Scholar and colleagues at the University of Bristol's Dementia Research Group is published in the current issue [July 2009] of the American Journal of Pathology. Alzheimer's disease is the most common form of dementia, affecting over half a million people in the UK - a figure expected to double in the next 20 years. A? peptide, which accumulates in the brain of Alzheimer's disease patients, is thought to lead to narrowing of the blood vessels and reduction of blood flood in the brain. ECE-2 may contribute to the disease by converting an inactive precursor to endothelin-1, which constricts blood vessels and further reduces blood flow.


New predictions for sea level rise

Fossil coral data and temperature records derived from ice-core measurements have been used to place better constraints on future sea level rise, and to test sea level projections. The results are published today in Nature Geoscience and predict that the amount of sea level rise by the end of this century will be between 7- 82 cm – depending on the amount of warming that occurs – a figure similar to that projected by the IPCC report of 2007. Placing limits on the amount of sea level rise over the next century is one of the most pressing challenges for climate scientists. The uncertainties around different methods to achieve accurate predictions are highly contentious because the response of the Greenland and Antarctic ice sheets to warming is not well understood.Dr Mark Siddall from the Earth Sciences Department at the University of Bristol, together with colleagues from Switzerland and the US, used fossil coral data and temperature records derived from ice-core measurements to reconstruct sea level fluctuations in response to changing climate for the past 22,000 years, a period that covers the transition from glacial maximum to the warm Holocene interglacial period.


Researchers capture bacterial infection on film

Researchers have developed a new technique that allows them to make a movie of bacteria infecting their living host. Whilst most studies of bacterial infection are done after the death of the infected organism, this system developed by scientists at the University of Bath and University of Exeter is the first to follow the progress of infection in real-time with living organisms. The researchers used developing fruit fly embryos as a model organism, injecting fluorescently tagged bacteria into the embryos and observing their interaction with the insect’s immune system using time-lapse confocal microscopy. The researchers can also tag individual bacterial proteins to follow their movement and determine their specific roles in the infection process. The scientists are hoping to use this system in the future with human pathogens such as Listeria and Trypanosomes. By observing how these bacteria interact with the immune system, researchers will gain a better understanding of how they cause an infection and could eventually lead to better antibacterial treatments.


Scientists track impact of DNA damage in the developing brain

Switching off a key DNA repair system in the developing nervous system is linked to smaller brain size as well as problems in brain structures vital to movement, memory and emotion, according to new research led by St. Jude Children's Research Hospital scientists. The work, published in the August issue of the journal Nature Neuroscience, also provides the first evidence that cells known as cerebellar interneurons are targeted for DNA damage and are a likely source of neurological problems in humans. The cerebellum coordinates movement and balance. The cerebellar interneurons fine tune motor control. "These data will be important for understanding the role the DNA damage response plays in preventing neurological disease," the investigators wrote. The study also marks the first time researchers have switched off a pathway for repairing damaged single DNA strands in an organ system, in this case the mouse brain and nervous system. While the results suggest certain brain cells are particularly vulnerable, investigators report that with time DNA damage accumulates throughout the nervous system. Some mice in the study eventually develop seizures and difficulty walking. Peter J. McKinnon, Ph.D., a member of St. Jude Genetics and Tumor Cell Biology, said the work provides a new model for understanding how single-strand DNA damage affects the nervous system and offers a new focus for tracking the origins of neurological disease.


Percy Schmeiser - David Gegen Monsanto


Bijlmer escape

A group of students project an escape on Bijlmer prison in Amsterdam.


The Omen (movie connection) - You've Got Monsanto In Your Food


We Are What We Eat


Monsanto is killing our bee population with pesticides


Animal mating rituals of giant cuttle fish in the blue Australian ocean waters


Genetic Testing May Be Valuable in Treating Colorectal Cancer

For the 29,000 patients in the United States with metastatic colorectal cancer, chemotherapy with irinotecan is a standard treatment that has been shown to improve survival. But for more than one in 10 of these patients, a variation in their DNA means that this treatment could result in a severe reduction in their white blood cell count, leading to a high risk of bacterial infection and possible subsequent death. A new genetic test can identify those with the variation in order to lower the treatment dose — however, it has been unclear whether the testing is worthwhile. A new cost-effectiveness study led by scientists at Weill Cornell Medical College has determined that so-called pretreatment pharmacogenetic testing is only beneficial if dose-reduced treatment is shown to be nearly as effective as the full dose. If the lower dose is as effective, the test could prevent many cases of severe neutropenia, an abnormally low count of an important type of white blood cells known as neutrophils. It would also mean better life expectancy and lower cost of care. The study appears online in the journal Cancer and is expected in print in the Sept. 1 issue.


Colon capsule endoscopy diagnoses 64% of total polyps detected by conventional colonoscopy

Capsule endoscopy for exploring the colon in a minimally invasive manner diagnoses 64% of all lesions located by means of conventional colonoscopy. According to a study published in The New England Journal of Medicine – the specialised medical journal with greatest international impact -, the new device would need technical improvements to achieve similar efficacy to the conventional procedure undertaken with a colonoscopy and to date considered a “gold standard” technique for this medical discipline, given that this is what currently provides the most reliable results. It has to be added that, moreover, conventional colonoscopy enables the undertaking of a diagnosis of the colon as well as practicing therapeutic procedures, such as the in situ extirpation of polyps during exploration or the obtaining of a biopsy when required. Capsule endoscopy of the colon explores the large intestine in a minimally invasive manner, not being necessary to admit patients to hospital, nor to sedate or anaesthesise them; neither is any tube or air needed nor radiation. A total of eight European hospitals took part in the research, amongst these being the University Hospital of Navarra, the only hospital throughout Spain involved and the one contributing most patients for the study – 63 from a total of 328.


Altered gene expression in the placenta of mice may help explain links between assisted reproductive techniques and metabolism of offspring.

Research to be presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that assisted reproductive techniques alter the expression of genes that are important for metabolism and the transport of nutrients in the placenta of mice. The results underscore the need for greater understanding of the long-term effects of new assisted reproductive techniques in humans. Millions of children, comprising roughly 1-2% of all births in the U.S. and Europe, have been born to couples experiencing fertility problems through the use of assisted reproductive techniques such as in vitro fertilization (IVF). However, relatively little research has been conducted to evaluate the long term effects of assisted reproductive techniques. It is suggested that children born following some assisted reproductive techniques have increased incidence of metabolic problems, such as increased blood pressure, higher fasting glucose level and more body fat. Mice generated through IVF show similar problems, and new research suggests that this may be linked to altered expression of genes in the placenta that are important for fetal growth and development before birth. “Our preliminary data suggest that transfer of nutrients or growth factors from mother to fetus may be changed by assisted reproductive techniques, and this change may contribute to increased body weight and decreased glucose tolerance in the adult offspring”, said the lead author of the study, Kellie Tamashiro.


U of T team helps to "barcode" the world's plants

An international team of scientists, including botanists from the University of Toronto, have identified a pair of genes which can be used to catalogue the world's plants using a technique known as DNA barcoding — a rapid and automated classification method that uses a short genetic marker in an organism's DNA to identify it as belonging to a particular species. "Barcoding provides an efficient means by which we can discover the many undescribed species that exist on earth," says Spencer Barrett, a professor of ecology and evolutionary biology at the University of Toronto and the head of the Canadian plant barcoding working group. "This discovery is important because understanding biodiversity is crucial to long-term human existence on the planet." DNA barcoding has been widely used to identify animal species since its invention five years ago. But its use for plants was delayed because of the complex nature of plant genetics and disagreements over the appropriate DNA regions to use.


Study finds significant number of kids experience family homelessness

A new multisite study by UCLA and RAND Corp. researchers and colleagues has found that 7 percent of fifth-graders and their families have experienced homelessness at some point in their lives and that the occurrence is even higher — 11 percent — for African American children and those from the poorest households. The study also found that children who had experienced homelessness at some point during their lives were significantly more likely to have an emotional, behavioral or developmental problem; were more likely to have witnessed serious violence with a knife or a gun; and were more likely to have received mental health care. The research is the first population-based study to describe the lifetime prevalence of family homelessness among children and its association with health and health care. The findings will be published in the August issue of the American Journal of Public Health and are currently available online by subscription.


ISU researchers find possible treatment for Spinal Muscular Atrophy

Spinal Muscular Atrophy is the second-leading cause of infant mortality in the world. Ravindra Singh, associate professor in biomedical sciences at Iowa State University's College of Veterinary Medicine, would like to see Spinal Muscular Atrophy lose its high ranking and even slide off the list altogether. Most Spinal Muscular Atrophy sufferers -- more than 95 percent -- have a mutated or deleted gene called Survival Motor Neuron 1 (SMN1) that doesn't correctly do its job of creating functional SMN proteins. Singh's solution is to replace that poor-performing gene with another gene. Humans need a certain level of SMN protein to ward off Spinal Muscular Atrophy. When SMN1 fails to create functioning proteins, Spinal Muscular Atrophy is the result.


Researchers Develop “Brain-Reading” Methods To Uncover A Person’s Mental State

It is widely known that the brain perceives information before it reaches a person’s awareness. But until now, there was little way to determine what specific mental tasks were taking place prior to the point of conscious awareness. That has changed with the findings of scientists at Rutgers University in Newark and the University of California, Los Angeles who have developed a highly accurate way to peer into the brain to uncover a person’s mental state and what sort of information is being processed before it reaches awareness. With this new window into the brain, scientists now also are provided with the means of developing a more accurate model of the inner functions of the brain. As reported in a forthcoming (Oct. 2009) issue of Psychological Science, the findings obtained by Stephen José Hanson, psychology professor at Rutgers; Russell A. Poldrack, professor at UCLA, and Yaroslav Halchenko, (now a post-doctoral student at Dartmouth College), have provided direct evidence that a person’s mental state can be predicted with a high degree of accuracy through functional magnetic resonance imaging (fMRI). The research also suggests that a more comprehensive approach is needed for mapping brain activity and that the widely held belief that localized areas of the brain are responsible for specific mental functions is misleading and incorrect. The research was funded with grants from the U.S. Office of Naval Research, the James S. McDonnell Foundation and National Science Foundation. The McDonnell Foundation recently awarded Hanson another $1 million for ongoing studies in this area.


Molecule Plays Early Role In Nonsmoking Lung Cancer

The cause of lung cancer in never-smokers is poorly understood, but a study led by investigators at the Ohio State University Comprehensive Cancer Center and at the National Cancer Institute has identified a molecule believed to play an early and important role in its development. The findings, published online recently in the Proceedings of the National Academy of Sciences, may lead to improved therapy for lung cancer in both never-smokers and smokers, including those with tumors resistant to targeted drugs such as gefitinib. The study examined lung tumors from people who had never smoked and found high levels of a molecule called miR-21. The levels were even higher in tumors that had mutations in a gene called EGFR, a common feature of lung cancer in never-smokers. “Several important lung cancer drugs target EGFR mutations, but these agents are ineffective in about 30 percent of cases in which the mutation is present,” says co-principal investigator Dr. Carlo M. Croce, professor of molecular virology, immunology and medical genetics at the Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove Research Institute. “Our study suggests that developing agents to inhibit miR-21 might improve these anti-EGFR therapies.”


Where is the money?


"Cognitive Dysfunction in Disease" (HD) at DMM2008, Karolinska

"Cognitive Dysfunction in Disease" (HD) at DMM2008, Karolinska from Trevor Marshall on Vimeo.

This is a High Definition version of the video which chronicles the presentations made by Prof.Trevor Marshall, Director Meg Mangin RN, and Bacteriality.com 's Amy Proal during the 'Days of Molecular Medicine' conference, April 2008, at the Karolinska Institutet in Stockholm. The conference theme was "Cognitive Dysfunction in Disease."


'MP Study Results,' Cpt. Tom Perez's Porto Presentation

'MP Study Results,' Cpt. Tom Perez's Porto Presentation from Trevor Marshall on Vimeo.

This is the HD video of Cpt. Tom Perez's presentation at the 6th International Congress on Autoimmunity, in Porto, Portugal, Sept 10-14, 2008, titled:  "Bacteria Induced Vitamin D Receptor Dysfunction in Autoimmune Disease: Theoretical and practical Implications for Interpretation of Serum Vitamin D Metabolite Levels"

A written transcript of this presentation is available from URL:
http://AutoimmunityResearch.org/transcripts/ICA2008_Transcript_TomPerez.pdf


Is Cardio Sabotaging Your Weight Loss Program?


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Does Milk help vitamin D levels?


Maternal, paternal genes' tug-of-war may last well into childhood

An analysis of rare genetic disorders in which children lack some genes from one parent suggests that maternal and paternal genes engage in a subtle tug-of-war well into childhood, and possibly as late as the onset of puberty.This striking new variety of intra-family conflict, described this week in the Proceedings of the National Academy of Sciences, is the latest wrinkle in the two-decades-old theory known as genomic imprinting, which holds that each parent contributes genes that seek to nudge his or her children's development in a direction most favorable, and least costly, to that parent. "Compared to other primates, human babies are weaned quite early, yet take a very long time to reach full nutritional independence and sexual maturity," says author David Haig, George Putnam Professor of Organismic and Evolutionary Biology in Harvard University's Faculty of Arts and Sciences. "Human mothers are also unusual among primates in that they often care for more than one child at a time. Evidence from disorders of genomic imprinting suggests that maternal and paternal genes may skirmish over the pace of human development." Previous research has offered evidence of a genetic struggle for supremacy only during fetal development: In the womb, some genes of paternal origin have been shown to promote increased demands on mothers, leading to fetal overgrowth, while genes of maternal origin tend to have the opposite effect. This new work suggests maternal and paternal genes continue to engage in internal genetic conflict past childbirth. "This analysis suggests that human life history, and especially humans' unusual extended childhood, may reflect a compromise between what's best for mothers, fathers, and the offspring themselves," Haig says.


Common household pesticides linked to childhood cancer cases in Washington area

A new study by researchers at the Georgetown's Lombardi Comprehensive Cancer Center finds a higher level of common household pesticides in the urine of children with acute lymphoblastic leukemia (ALL), a cancer that develops most commonly between three and seven years of age. The findings are published in the August issue of the journal Therapeutic Drug Monitoring. Researchers caution that these findings should not be seen as cause-and-effect, only that the study suggests an association between pesticide exposure and development of childhood ALL. "In our study, we compared urine samples from children with ALL and their mothers with healthy children and their moms. We found elevated levels of common household pesticides more often in the mother-child pairs affected by cancer," says the study's lead investigator, Offie Soldin, PhD, an epidemiologist at Lombardi. Soldin cautions, "We shouldn't assume that pesticides caused these cancers, but our findings certainly support the need for more robust research in this area." The study was conducted between January 2005 and January 2008 with volunteer participants from Lombardi and Children's National Medical Center who live in the Washington metropolitan area. It included 41 pairs of children with ALL and their mothers (cases), and 41 pairs of healthy children and their mothers (controls). For comparison purposes, the case pairs were matched with control pairs by age, sex and county of residence. Previous studies in agricultural areas of the country have suggested a relationship between pesticides and childhood cancers, but researchers say this is the first study conducted in a large, metropolitan area.


Chicago team uses artificial intelligence to diagnose metastatic cancer

When doctors are managing care for women with breast cancer, the information available to them profoundly influences the type of care they recommend. Knowing whether a woman's cancer has metastasized, for instance, directly affects how her doctors will approach treatment -- which may in turn influence the outcome of that treatment. Determining whether a tumor has metastasized is not always straightforward, however. Radiologists often start by using diagnostic ultrasound to non-invasively probe the nearby lymph nodes -- tissues where cancer cells first migrate once they metastasize. But in the early stages of cancer, lymph nodes often appear completely normal even if the cancer has metastasized. Now a team of researchers at the University of Chicago has designed a computer program that uses artificial intelligence to analyze the features of ultrasound images in order to help doctors predict earlier whether a woman's cancer has metastasized. The team will discuss the first preclinical results obtained using this program at the upcoming meeting of the American Association of Physicists in Medicine (AAPM), which takes place from July 26 - 30, 2009 in Anaheim, California. Currently there are no automated methods approved by the Food and Drug Administration for diagnosing cancer, but on Wednesday the team will report the results of a preliminary pilot study that retrospectively reanalyzed the diagnostic ultrasounds of 50 women with suspected breast cancer who all had lymph nodes that appeared normal in the ultrasound -- suggesting that their cancers had not metastasized.


Research shows rates of severe childhood obesity have tripled

Rates of severe childhood obesity have tripled in the last 25 years, putting many children at risk for diabetes and heart disease, according to a report in Academic Pediatrics by an obesity expert at Brenner Children's Hospital, part of Wake Forest University Baptist Medical Center. "Children are not only becoming obese, but becoming severely obese, which impacts their overall health," said Joseph Skelton, M.D., lead author and director of the Brenner FIT (Families in Training) Program. "These findings reinforce the fact that medically-based programs to treat obesity are needed throughout the United States and insurance companies should be encouraged to cover this care." The research was published on-line and will appear in the September print edition. Skelton and colleagues compared data from the National Health and Nutrition Examination Survey (NHANES). They looked at the prevalence of obesity and severe obesity in a study population of 12,384 children, representing approximately 71 million U.S. children ages 2 to 19 years. Severe childhood obesity is a new classification for children and describes those with a body mass index (BMI) that is equal to or greater than the 99th percentile for age and gender. For example, a 10-year-old child with a BMI of 24 would be considered severely obese, Skelton said, whereas in an adult, that is considered a normal BMI. An expert committee convened by the American Medical Association, the Centers for Disease Control and the Department of Health and Human Services proposed the new classification in 2007. The research by Skelton and colleagues is the first of its kind to use the new classification and detail the severity of the problem. They found that the prevalence of severe obesity tripled (from 0.8 percent to 3.8 percent) in the period from 1976-80 to 1999-2004. Based on the data, there are 2.7 million children in the U.S. who are considered severely obese. Increases in severe obesity were highest among blacks and Mexican-Americans and among those below the poverty level. For example, the percentage of Mexican-American children in the severely obese category was 0.9 percent in 1976-80 and 5.2 percent in 1999-2004.


NIST scientists study how to stack the deck for organic solar power

A new class of economically viable solar power cells—cheap, flexible and easy to make—has come a step closer to reality as a result of recent work* at the National Institute of Standards and Technology (NIST), where scientists have deepened their understanding of the complex organic films at the heart of the devices. Organic photovoltaics, which rely on organic molecules to capture sunlight and convert it into electricity, are a hot research area because in principle they have significant advantages over traditional rigid silicon cells. Organic photovoltaics start out as a kind of ink that can be applied to flexible surfaces to create solar cell modules that can be spread over large areas as easily as unrolling a carpet. They'd be much cheaper to make and easier to adapt to a wide variety of power applications, but their market share will be limited until the technology improves. Even the best organic photovoltaics convert less than 6 percent of light into electricity and last only a few thousand hours. "The industry believes that if these cells can exceed 10 percent efficiency and 10,000 hours of life, technology adoption will really accelerate," says NIST's David Germack. "But to improve them, there is critical need to identify what's happening in the material, and at this point, we're only at the beginning." The NIST team has advanced that understanding with their latest effort, which provides a powerful new measurement strategy for organic photovoltaics that reveals ways to control how they form. In the most common class of organic photovoltaics, the "ink" is a blend of a polymer that absorbs sunlight, enabling it to give up its electrons, and ball-shaped carbon molecules called fullerenes that collect electrons. When the ink is applied to a surface, the blend hardens into a film that contains a haphazard network of polymers intermixed with fullerene channels. In conventional devices, the polymer network should ideally all reach the bottom of the film while the fullerene channels should ideally all reach the top, so that electricity can flow in the correct direction out of the device. However, if barriers of fullerenes form between the polymers and the bottom edge of the film, the cell's efficiency will be reduced.


Little-known protein found to be key player

- Italian and U.S. biologists this week report that a little-understood protein previously implicated in a rare genetic disorder plays an unexpected and critical role in building and maintaining healthy cells. Even more surprising, their report in the journal Nature shows that the protein, called "atlastin," does its work by fusing intracellular membranes in a previously undocumented way. "If you'd asked me a year ago whether this was possible, I would have said, 'No,'" said study co-author James McNew, associate professor of biochemistry and cell biology at Rice University. "In fact, that's exactly what I told (co-author) Andrea Daga when we first spoke about the idea a year ago." McNew has spent the past 15 years studying SNARE proteins, a specialized family of proteins that carries out membrane fusion. It's a vital process that happens thousands of times a second in every cell of our bodies. "It is fitting that the discovery of a new protein capable of fusing membranes comes 10 years after the demonstration that SNAREs can fuse lipid bilayers," said Daga, a researcher at the Eugenio Medea Scientific Institute in Conegliano, Italy. In the new study, Daga's and McNew's research teams used fruit flies to study how atlastin functions. The atlastin in fruit flies is very similar to the human version of the protein and serves the same function. "Prior to this, there were only two defined ways in which you could take biological membranes and put them together in a specific way," said McNew, a faculty investigator at Rice's BioScience Resesarch Collaborative. "Atlastin is the third, and it's the only one that requires enzymatic activity, so it's distinctly different." Using a range of tests on purified proteins, live fruit flies and cell cultures, the Italian and U.S. teams examined the effect of both an overabundance and a scarcity of atlastin on cell function and on fruit fly development. They also created mutant versions of the protein to see how it functioned -- or failed to function -- when some parts were disabled.


Diabetes gene raises odds of lower birth weight

Pediatric researchers have found that a gene previously shown to be involved in the development of type 2 diabetes also predisposes children to having a lower birth weight. The finding sheds light on a possible genetic influence on how prenatal events may set the stage for developing diabetes in later childhood or adulthood. Researchers from The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine published the study July 10 in the online version of the journal Diabetes. "It's a bit unusual to find a gene linked to both prenatal events and to a disease that occurs later in life," said study leader Struan F.A. Grant, Ph.D., a researcher at the Center for Applied Genomics of The Children's Hospital of Philadelphia. "This gene variant carries a double whammy, in raising the risk of both lower birth weight and the development of type 2 diabetes in later life." Type 2 diabetes occurs either when the pancreas produces too little insulin or when the body cannot efficiently use the insulin that is produced. Formerly called adult-onset diabetes and still most common in adults, type 2 diabetes has been increasing sharply among children.


Freshly crushed garlic better for the heart than processed

A new study reports what scientists term the first scientific evidence that freshly crushed garlic has more potent heart-healthy effects than dried garlic. Scheduled for the Aug. 12 issue of the Journal of Agricultural and Food Chemistry, it also challenges the widespread belief that most of garlic's benefits are due to its rich array of antioxidants. Instead, garlic's heart-healthy effects seem to result mainly from hydrogen sulfide, a chemical signaling substance that forms after garlic is cut or crushed and relaxes blood vessels when eaten. In the study, Dipak K. Das and colleagues point out that raw, crushed garlic generates hydrogen sulfide through a chemical reaction. Although best known as the stuff that gives rotten eggs their distinctive odor, hydrogen sulfide also acts as a chemical messenger in the body, relaxing blood vessels and allowing more blood to pass through. Processed and cooked garlic, however, loses its ability to generate hydrogen sulfide. The scientists gave freshly crushed garlic and processed garlic to two groups of lab rats, and then studied how well the animals' hearts recovered from simulated heart attacks. "Both crushed and processed garlic reduced damage from lack of oxygen, but the fresh garlic group had a significantly greater effect on restoring good blood flow in the aorta and increased pressure in the left ventricle of the heart," Das said.


Experimental treatment halts hypoxic-ischemic brain injury in newborns

Inhibiting an enzyme in the brains of newborns suffering from oxygen and blood flow deprivation stops a type of brain damage that is a leading cause of cerebral palsy, mental retardation and death, according to researchers at Cincinnati Children's Hospital Medical Center. Reporting their results in the Journal of Neuroscience, the scientists show blocking the brain enzyme, tissue-type plasminogen activator (tPA), prevents progressive brain damage triggered by the lack of oxygen and blood supply. The experimental pre-clinical treatment involved putting a naturally occurring substance called plasminogen activator inhibitor-1 (PAI-1) into the brains of newborn rats, said Chia-Yi Kuan, M.D. PhD, senior investigator on the study and a researcher in the divisions of Developmental Biology and Neurology at Cincinnati Children's. Besides demonstrating the brain's plasminogen activator system plays a pivotal role in neonatal cerebral hypoxic-ischemic brain injury, Dr. Kuan said the study also shows this system may be a promising therapeutic target in infants suffering hypoxic-ischemic encephalopathy (HIE). Identification of a treatment target is a vital step to finding better ways to treat newborns with HIE. "Not only is hypoxic-ischemic encephalopathy an important cause of perinatal mortality and permanent neurological morbidities, but there are no specific medications against HIE in current medical practice," explained Ton J. DeGrauw, M.D., Ph.D., director of Neurology at Cincinnati Children's. "This is why the findings of this study may have important clinical implications because, in a rodent model of HIE, they that show inhibiting plasminogen activators in functional areas of the brain is powerful strategy for brain protection." Earlier studies have pointed to the role certain brain proteases, or enzymes, play in adult brain injury following stroke, but very little has been known about what these enzymes do in neonatal cerebral hypoxic-ischemia, according to the researchers. The enzyme in this case, tPA, normally breaks down proteins and other molecules to eliminate blood clots.


Childhood adversities have a predictive role in peptic ulcer

Helicobacter pylori, nonsteroidal anti-inflammatory drug use and smoking are the most important risk factors for peptic ulcer. Alcohol intake may also play a role in the development of gastric ulcers. Psychological stress may also have an impact on the onset and course of ulcer disease. However, very little is known as to whether childhood adversities involving financial problems, conflicts in the family, problems with alcohol, and matters of personal security are associated with peptic ulcer. A research article to be published on July 21,2009 in the World Journal of Gastroenterology addresses this question. Dr. Markku Sumanen and his colleagues of the Health and Social Support Study (HeSSup) investigated this subject in a nationwide sample of working-aged people in Finland. The participants were asked whether or not a doctor had told them that they have or have had a peptic ulcer. They were also asked to think about their childhood adversities in terms of the following questions: 1) "Did your parents divorce?" 2) "Did your family have long-lasting financial difficulties?" 3) "Did serious conflicts arise in your family?" 4) "Were you often afraid of some member of your family?" 5) "Was someone in the family seriously or chronically ill?" 6) "Did someone in the family have problems with alcohol?" The most common childhood adversities to emerge were long-lasting financial difficulties in the family, serious conflicts in the family and someone in the family having been seriously or chronically ill. All adversities reported were more common among peptic ulcer patients than among other respondents. Alcohol problems in the family and fear of some member of the family were also more common among peptic ulcer patients than among other respondents. With regard to parental divorce there was no statistically significant difference between the two groups. Age- and sex-adjusted odds ratios (ORs) of childhood adversities for peptic ulcer were statistically significant, indicating that participants with childhood adversities had a higher proportional risk of developing peptic ulcer. Adjusting also for smoking, heavy drinking, stress and current NSAID use had no further influence. Long-lasting financial difficulties in the family had the greatest influence.According to the findings there is reason to believe that stress factors during childhood maintain a connection with the development of peptic ulcers. Childhood adversities are not necessarily true risk factors for peptic ulcer, but may play a predictive role in the development of the disease. A more comprehensive understanding of peptic ulcer patients is worth aspiring to.


Humans "damaging the oceans"

Mounting evidence that human activity is changing the world’s oceans in profound and damaging ways is outlined in a new scientific discussion paper released today. Man-made carbon emissions “are affecting marine biological processes from genes to ecosystems over scales from rock pools to ocean basins, impacting ecosystem services and threatening human food security,” the study by Professor Mike Kingsford of the ARC Centre of Excellence for Coral Reef Studies and James Cook University and colleague Dr Andrew Brierley of St Andrews University, Scotland, warns. Their review, published in the latest issue of the journal Current Biology, says that rates of physical change in the oceans are unprecedented in some cases, and change in ocean life is likely to be equally quick. These include changes in the areas fish and other sea species can inhabit, invasions, extinctions and major shifts in marine ecosystems. “In the past, the boundaries between geological ages are marked by sudden losses of species. We may now be entering a new age in which climate change and other human-caused factors such as fishing are the major threats for the oceans and their life,” Andrew and Mike say. “Given how essential the oceans are to how our entire planet functions it is vital that we intervene before more tipping points are passed and the oceans go down the sort of spiral of decline we have seen in the world’s tropical forests and rangelands, for example.”


Duke scientists create airway spheres to study lung diseases

Using both animal and human cells, Duke University Medical Center scientists have demonstrated that a single lung cell can become one of two very different types of airway cells, which could lead to a better understanding of lung diseases. From this single "basal" cell, a small, squat stem cell that divides to replenish the lung lining layer, scientists created 3-D hollow spheres that were lined inside with both ciliary and secretory cells. This 3-D model can be used to study dynamic processes underlying lung diseases, including cancer, said Brigid Hogan, Ph.D., chair of the Duke Department of Cell Biology and senior researcher of the study, which was published in PNAS Early Edition. "Now that we have this 3-D model and information about the gene expression 'signature' of basal cells, we are in a strong position to see what happens when lung-cell behavior goes awry," Hogan said. "We might, for example, be able to activate an oncogene (a cancer-causing gene) or other factors to see how lung cancer might develop in the airways. Amazingly, almost nothing is known about lung basal cells, which are so important to health and make up nearly a third of the cells in the human airways."Normally, basal stem cells maintain the airways by turning over slowly into new ciliated cells and secretory cells. Ciliated cells resemble waving brooms that sweep along particles and distribute secretions that are needed in the airways, and secretory cells provide the antibacterial and lubricating secretions. These two types of cells are neatly arranged in equal proportions in healthy lung airways. However, when lungs are affected by maladies like cancer, chemical damage, cystic fibrosis or asthma, the balance of these cells can be thrown off. By learning the role these basal cells play in maintaining the airway tissue, the scientists were able to create an entirely new way to study them.


Risø DTU develops magnetic Curie valve that does not require power!

Christian Bahl is a Senior Scientist in the Fuel Cells and Solid State Chemistry Division and works mainly with magnetic refrigeration. Magnetic refrigeration is an energy-efficient cooling technique that could help save substantially on electricity consumption in the long term. Through this, Christian Bahl has knowledge of the Curie temperature of different substances. At the Curie temperature the material switches between being magnetic and non magnetic. And precisely this property inspired the group to create a shunt valve controlled by magnets. "If you imagine in your house at home that you had one of our valves connected to the hot water circulation, running through your radiators, then the valve would be able to lead the water through the radiators again, provided the water is hot enough. The rest would go to reheating, "explains Dan Eriksen who was employed on this project as a Development Engineer in July 2008. The idea behind this new type of valve is that the liquid flows past a material with a certain Curie temperature. When the liquid temperature falls below this temperature, the material is attracted by a magnet outside the valve. If the temperature rises again, the material is less attracted to the magnet, and is pushed back to its starting position by a spring. This movement is used to activate the valve.


Stress signals link pre-existing sickness with susceptibility to bacterial infection

Mitochondrial diseases disrupt the power generating machinery within cells and increase a person's susceptibility to bacterial infection, particularly in the lungs or respiratory tract. A new study published in Disease Models & Mechanisms (DMM), shows that infection with the pneumonia causing bacteria Legionella, is facilitated by an increased amount of a signaling protein that is associated with mitochondrial disease. Patients with mitochondrial disease exhibit a wide range of symptoms including diabetes, blindness, deafness, stroke-like episodes, epilepsy, ataxia, muscle weakness and kidney disease. The metabolic abnormalities that cause these effects also induce a stress signal intended to help the body overcome its energy deficit. The stress-signal induces the production of more mitochondria, the energy generating 'powerplants' of the body, in the hopes that more mitochondria will result in a better power supply. Researchers now show that the stress-signal associated with mitochondrial disease facilitates the growth and reproduction of the lung-infecting bacteria, Legionella. Cells with mitochondrial disease increase their production of a signaling protein called AMP-activated protein kinase (AMPK), to promote the generation of more energy producing mitochondria. Infectious bacteria, like Legionella, target the mitochondria and might use them to supplement their own needs and survival requirements. By manipulating AMPK levels, scientists were able to directly influence the ability of bacteria to replicate inside of the single-celled organism, Dictyostelium.


High calcium level in arteries may signal serious heart attack risk

Researchers may be able to predict future severe cardiac events in patients with known, stable coronary artery disease (CAD) using coronary calcium scoring, according to a study published in the online edition of Radiology."The amount of calcium in the coronary vessels, as measured by CT, is of high predictive value for subsequent serious or fatal heart attack in these patients, independent of the patient's age, sex and other coronary risk factors," said the study's lead author, Marcus Hacker, M.D., resident physician in the Department of Nuclear Medicine, leader of the research unit for nuclear cardiology and assistant medical director at Ludwig Maximilians University in Munich, Germany. CAD is the most common type of heart disease. According to the National Heart, Lung and Blood Institute, it is the leading cause of death in the U.S. for both men and women, killing more than 500,000 Americans each year. CAD is a condition in which plaque, consisting of cholesterol, calcium, fat and other substances, builds up inside the arteries that supply blood to the heart. When plaque builds up in the coronary arteries, blood flow to the heart is reduced and may lead to arrhythmia, heart attack or heart failure. Single photon emission computed tomography (SPECT) myocardial perfusion imaging is a nuclear medicine diagnostic procedure that provides excellent three-dimensional images of the coronary arteries to assist in the diagnosis and treatment of CAD. Currently, calcium scoring—measuring the amount of calcium in the arteries—is used as a screening exam and in cases of suspected CAD, but not in cases of known CAD.


Shark Alert! Species Struggle


Psychiatry Industry Of Death


8 Foot Alien on CCTV Cameras 3 Police Cars Trapped in Reverse BigBrother Surveillance


Scientists Question Mass Vaccinations SwineFlu


Stand By Me / Beautiful Girls - The Choir


Life-saving research in to stem cells

A look at life-saving research scientists are doing in to stem cell therapy. Interesting video from BBC show Life Blood. Watch more high quality videos on the Explore YouTube channel from BBC Worldwide here: http://www.youtube.com/bbcexplore


Wild Herbs - What to Eat Now Preview


Discovery to aid in future treatments of third-world parasites

Schistosomiasis, one of the most important of the neglected tropical diseases, is caused by infection with parasitic helminths of the genus Schistosoma. These parasites are long lived (>10 years) and dwell within blood vessels, where they produce eggs that become the focus of intense, chronic inflammatory responses. In severe cases, this inflammation is associated with life-threatening liver disease. No vaccine is currently available to prevent schistosomiasis. Options for treating the disease are largely limited to one drug, Praziquantel. Rates of re-infection in drug-treated individuals are high, and it is feared that widespread use may foster the emergence of drug-resistant variants, such as has seen with drug-resistant strains of tuberculosis. The body's immune response to schistosome infection, as with all immune responses, is coordinated by cytokines, small proteins secreted by immune cells. Due to their fundamental importance, cytokine research is a significant focus of research at the Trudeau Institute. Because cytokines travel through the body to relay critical information, it is difficult to identify the cells that produce them and to learn about their role. Trudeau investigators have devised cytokine "reporter mice" for tracking cells that produce the signature cytokine of the so-called "Th2" immune response mounted against infections with parasitic worms, interleukin-4 (IL-4). While it was previously known that the complex mixture of proteins released by schistosome eggs induce Th2 responses and the production of IL-4, the specific molecule(s) responsible for these effects were unknown. Research from the laboratories of Markus Mohrs of the Trudeau Institute and Gabriele Schramm of the Research Centre Borstel in Germany had previously shown that a protein called alpha-1 can support Th2 responses but is unable to initiate them.


Placenta-derived stem cells may help sufferers of lung diseases

An Italian research team, publishing in the current issue of Cell Transplantation (18:4), which is now available on-line without charge at http://www.ingentaconnect.com/content/cog/ct, has found that stem cells derived from human placenta may ultimately play a role in the treatment of lung diseases, such as pulmonary fibrosis and fibrotic diseases caused by tuberculosis, chemical exposure, radiation or pathogens. These diseases can ultimately lead to loss of normal lung tissue and organ failure. No known therapy effectively reverses or stops the fibrotic process. Placenta-derived stem cells are known to be able to engraft in solid organs, including the lungs. Human term placenta stem cells also demonstrate characteristics of high plasticity and low immunogenicity. "The potential application of fetal membrane-derived cells as a therapeutic tool for disorders characterized by inflammation and fibrosis is supported in previous studies," says Dr. Ornella Parolini, the study's lead author. "In line with the hypothesis that cells derived from the amniotic membrane have immunomodulatory properties and have been used as an anti-inflammatory agent, we set out to evaluate the effects of fetal membrane-derived cell transplantation in chemically-treated (bleomycin) mice." According to Dr. Parolini, cells delivered via intra-peritoneal transplant, regardless of the cells being allogenic or xenogenic (host's own cells or from another individual respectively), the procedure resulted in a significant anti-fibrotic effect on the lab animals. A "consistent" reduction in lung fibrosis, says Dr. Parolini, "provides convincing proof" that placenta-derived cells do confer benefits for bleomycin-induced lung injury. While the severity of inflammation did not show an overall reduction, there was a marked reduction in neutrophil (white blood cell) infiltration after both xeno-and-allo-transplantation. "It is worth noting," says Dr. Parolini," that the presence of neutrophils is associated with poor prognosis for several lung diseases. However, the mechanism by which placenta-derived cells might affect infiltration by neutrophils is not known." The researchers speculated that these cells may produce soluble factors that induce anti-inflammatory effects.


Mines could provide geothermal energy

Mine shafts on the point of being closed down could be used to provide geothermal energy to local towns. This is the conclusion of two engineers from the University of Oviedo, whose research is being published this month in the journal Renewable Energy. The method they have developed makes it possible to estimate the amount of heat that a tunnel could potentially provide. "One way of making use of low-intensity geothermal energy is to convert mine shafts into geothermal boilers, which could provide heating and hot water for people living nearby", Rafael Rodríguez, from the Oviedo Higher Technical School of Mining Engineering, tells SINC. This type of energy, which is hardly used in Spain, is obtained from the internal heat of the Earth. The engineer and his colleague María Belarmina Díaz have developed a "semi-empirical" method (part mathematical and part experimental) to calculate the amount of heat that could be produced by a mine tunnel that is due to be abandoned, based on studies carried out while it is still in use. "When the mine is still active one can access the tunnels easily in order to gather data about ventilation and the properties of the rocks, as well as to take samples and design better circuits, and even programme the closure of some sections in order to use them for geothermal energy production", says the engineer, who stresses that, although geothermal energy can be made use of once the mine is closed, "it is no longer possible by that stage to make any modifications, or to gather any useful data to evaluate and improve the system".


Dopamine-related activity of food reward circuits in the brain and weight gain

Research to be presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that women who possess genetic modifications associated with low activity of the reward neurotransmitter dopamine in the brain when they imagine eating appetizing foods are more prone to weight gain. Functional Magnetic Resonance Imaging (fMRI) scans of brain activity revealed that women who had lower activity in food reward regions of the brain and who had genetic modifications associated with lower dopamine activity showed the greatest weight gain after one year. Eric Stice from the Oregon Research Institute says, “These findings provide some of the first prospective evidence that people who experience blunted reward from food may compensate by overeating, increasing risk for unhealthy weight gain.” Overconsumption of appetizing foods may occur in an attempt to increase brain reward in less responsive systems. The results of this study highlight the need for further research into the role that neural reward systems play in the development of obesity. “It may be useful for individuals who show low food-related reward to increase their physical activity, which not only promotes activity the same reward circuitry but also reduces unhealthy weight gain from overeating” says Stice.


Weight loss improves mood in depressed people

Research to be presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that after a 6-month behavioral weight loss program, depressed patients not only lost 8% of their initial weight but also reported significant improvements in their symptoms of depression, as well as reductions in triglycerides, which are a risk factor for heart disease and stroke. The results of this study highlight the need for further research into the effects of weight loss in individuals suffering from psychiatric disorders. “This research is novel because clinically depressed individuals are not usually included in weight loss trials due to concerns that weight loss could worsen their depression,” said Dr. Lucy Faulconbridge, lead author of the study. “These concerns, however, are not based on empirical evidence, and the practice of excluding depressed individuals from clinical weight loss trials means that we are learning nothing about this high-risk population.” The latest findings suggest that depressed, obese individuals can indeed lose clinically significant amounts of weight, and that weight loss can actually reduce symptoms of depression. Fifty-one depressed and non-depressed subjects were recruited into the study to follow a supervised weight loss program that included lifestyle modification and meal replacements. Both depressed and non-depressed subjects lost significant amounts of weight, with depressed individuals losing 8% of their initial body weight, compared with 11% loss by non-depressed individuals. After 6 months on the weight loss program, depressed subjects also showed significant improvement of their depressive symptoms, based on a questionnaire. Additional significant improvements in glucose, insulin and high density lipoprotein (HDL) cholesterol were observed in both depressed and non-depressed subjects, and depressed individuals showed reduced levels of triglycerides in the blood, which have been linked to risk of heart disease and stroke. “Depression and obesity are independently associated with increased risk of heart disease and stroke, and so reductions in both body weight and symptoms of depression are likely to improve long-term health outcomes” said Faulconbridge.


Just expecting a tasty food activates brain reward systems

Research to be presented at the Annual Meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, shows that exposing rats to a context associated with eating chocolate activates a part of the brain’s reward system known as the orexin system. This finding helps explain why eating can be triggered by environmental cues even in the absence of hunger. The results have implications for the development of new drug treatments for overeating. The rate of obesity continues to rise within the United States and abroad, and overconsumption of tasty food is an obvious culprit. Little is known regarding how palatable foods affect the brain, but it seems that especially tasty foods elicit brain responses similar to those elicited by drugs of abuse such as cocaine and nicotine, pointing to a general involvement of the brain’s “reward” system. A common factor may be activation of orexin neurons in the brain, which are recruited during of rewards such as a tasty food or a dose of cocaine. “Our research program is focused on identifying brain systems that are activated by palatable food intake. The hypothalamic orexin system is known to promote wakefulness and arousal; however, it is now clear that this system also participates in the regulation of reward-related behaviors, including overconsumption of palatable foods,” says Derrick Choi, lead author. Because reward anticipation is a contributing factor to relapse to drug use, Choi hypothesizes that orexin is an ideal candidate system that may underlie the rewarding aspects of eating highly palatable foods, which clearly can lead to obesity. In their current study, the researchers trained rats to expect a piece of Hershey’s milk chocolate in a unique environment. After training, rats were placed into the same environment, where no chocolate was present. The researchers found that the expectation of chocolate alone activated brain orexin systems. The results could explain why individuals tend to overeat in contexts associated with prior experiences of eating good food. “It entirely possible that future treatments for obesity will involve a combination of lifestyle changes as well as pharmacological therapies aimed at orexin and other brain systems, to regulate food reward-related behaviors,” said Choi.


High fat, high sugar foods alters brain receptors

Overconsumption of fatty, sugary foods leads to changes in brain receptors, according to new animal research at Johns Hopkins University School of Medicine. The new research results are being presented at the 2009 annual meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior. The results have implications for understanding bulimia and other binge eating disorders. Dr. Bello and colleagues report that either continuous eating or binge eating a high fat, high sugar diet alters opioid receptor levels in an area of the brain that controls food intake. Opioids are a family of chemicals with actions similar to those of morphine; however, opioids exist naturally in the brain and have been linked to feelings of pleasure and euphoria. “These results are interesting because we saw changes in opioid receptor gene expression in a brain area that controls how much we eat during a meal”, said Bello. The new findings suggest that overconsumption of highly palatable foods maintains bingeing by enhancing opioids in the brain, and that increased opioids could be a factor involved in binge eating disorders. These findings may help to understand the biological basis of eating disorders.


Cancer's distinctive pattern of gene expression could aid early screening and prevention

Distinctive patterns of genes turned off – or left on – in healthy versus cancerous cells could enable early screening for many common cancers and maybe help avoid them, Medical College of Georgia scientists say. Researchers are comparing chemical alterations, called DNA methylation, in the body's basic building block in healthy colon, breast, brain and lymphatic cells and their cancerous counterpart to find telltale patterns that could one day be detected in the blood, urine or feces. The patterns could give patients a heads up that lifestyle changes, or more severe intervention, is in order, says Dr. Kapil Bhalla, director of the MCG Cancer Center, Cecil F. Whitaker Jr., M.D./Georgia Research Alliance Eminent Scholar in Cancer and Georgia Cancer Coalition Scholar. DNA methylation is a piece of a relatively new research field called epigenetics that looks more globally at which genes are turned off and on with an eye on early identification of some of the aberrant adjustments that enable cancer cells to thrive. Epigenetic changes actually are more common than the genetic mutations long known to put people at risk for cancer and other diseases and they are probably inherited as well, Dr. Bhalla says. The early and apparently significant role of epigenetics in cancer has made the field a focal point for centers such as the MCG Cancer Center, which recently recruited two new epigenetics researchers with the help of the Georgia Cancer Coalition. The second floor of the three-year-old Cancer Research Center building, which is being finished with the help of $3.5 million from the Georgia Research Alliance, will house the Georgia Genomics/Epigenomics Center. In early 2008, the National Institutes of Health established an epigenomics program to coordinate such efforts to better understand how this method of gene regulation fits into normal development, aging, learning and memory as well as its role in cancer, obesity, depression and other disease. DNA methylation inhibitors already are under study at MCG and other centers for a variety of cancers and blood disorders. Because tumor cells that result from aberrant changes shed their DNA into bodily fluids, non-invasive screening for a wide range of cancers could result be another result of this initiative, Dr. Bhalla says.


Teasing apart T helper cells

The cytokine IL-9 promotes a multiple sclerosis-like disease in mice, according to a new study by Nowak et al. published online on July 13th in the Journal of Experimental Medicine. In a related Commentary, Richard Locksley discusses the molecular and genetic regulation of cytokine production by CD4+ T helper (Th) cells and the plasticity among different Th subsets. The Commentary will be published online in the Journal of Experimental Medicine on Monday, July 27th. Since the late 1980s, when the concept of Th1 and -2 were first introduced, several new subsets have arisen, including Th17 cells and regulatory T (T reg) cells. Recent attention has focused on a putative new Th cell subset with the propensity to secrete IL-9. But whether these "Th9" cells are truly a unique subset or whether many Th cell subsets can produce IL-9 under the right circumstances has been a matter of debate. Nowak and colleagues now show that a Th17-driven CNS disease was blunted in mice lacking IL-9. In vitro studies showed that IL-9 was produced primarily by Th17 and T reg cells—subsets that depend on TGF-beta for their differentiation. Thus IL-9 production may go hand-in-hand with the presence of TGF-beta rather than with a defined Th cell subset.


Study finds acceptable levels of anxiety among men living with early, untreated prostate cancer

Men with early stages of prostate cancer who delay radical treatment in favor of an approach of "expectant management" do not have high levels of anxiety and distress. That is the conclusion of a new study published in the September 1, 2009 issue of Cancer, a peer-reviewed journal of the American Cancer Society. The study's results suggest that living with untreated cancer is not upsetting for many patients with early prostate cancer. The rapid increase in the use of screening using prostate specific antigen (PSA) testing has led to a large number of men diagnosed with prostate cancer, many of who do not require treatment. In these cases, close clinical monitoring—or active surveillance—is often recommended. If progression of the cancer occurs during active surveillance, patients may undergo radical therapy. While active surveillance may delay or even avoid the possible adverse side effects of radical treatment, it could also cause psychological harm in patients because they must live with untreated cancer. Data on the levels of such potentially negative emotions among men on active surveillance are lacking, however. Roderick van den Bergh, (MD), of the Erasmus Medical Center, in Rotterdam, the Netherlands, and colleagues assessed levels of anxiety and distress in a group of recently diagnosed prostate cancer patients on active surveillance. They sent 150 men questionnaires to gauge uncertainty about their treatment decision, as well as levels of depression and anxiety among these men. A total of 129 questionnaires were completed and returned an average of 2.7 months after diagnosis. More than 80 percent of the 129 respondents scored favorably low on the parameters measured. Patients' scores were comparable or favorable to scores of men (reported in other studies) who underwent treatment for early prostate cancer. Certain men in the study—such as men with neurotic personalities and those who were in poor physical health—exhibited more anxiety and distress than others. These findings indicate that besides cancer-specific factors, mental and physical patient-specific factors are important aspects to take into account when selecting men for active surveillance. The results also suggest that psychological support may be indicated in certain patients undergoing active surveillance. While this study's findings are useful, Dr. van den Bergh noted that longer-term analyses are needed on the psychological effects of active surveillance in men with early prostate cancer. His research team is currently conducting such a study.


E-Cigarettes Contain Toxins, FDA Analysis Shows

Electronic cigarettes, or e-cigarettes, contain carcinogens and toxic chemicals, according to a new analysis by the Food and Drug Administration (FDA). One sample even included diethylene glycol, a toxic ingredient found in antifreeze. E-cigarettes are often sold as a way to quit smoking or to get nicotine in places where smoking isn't allowed, but they aren't currently regulated by the FDA. "The FDA is concerned about the safety of these products and how they are marketed to the public,” said Margaret A. Hamburg, M.D., commissioner of food and drugs. E-cigarettes, first produced in China in 2004, are battery-operated devices designed to look and feel like cigarettes, right down to the glowing tip. They contain cartridges which are filled with chemicals and varying doses of nicotine, from high doses to no nicotine at all. They’re available in different flavors, such as chocolate and mint, which make them appealing to kids and teens. These products are also easy for kids and teens to buy – they’re readily available online and in shopping malls. And at this time, e-cigarettes do not contain any health warnings, such as those on FDA-approved nicotine replacement products or conventional cigarettes. The FDA looked at 18 samples of cartridges from 2 leading e-cigarette brands. Half the samples contained cancer-causing substances. They found other impurities, as well, including diethylene glycol.


Researchers rapidly turn bacteria into biotech factories

High-throughput sequencing has turned biologists into voracious genome readers, enabling them to scan millions of DNA letters, or bases, per hour. When revising a genome, however, they struggle, suffering from serious writer's block, exacerbated by outdated cell programming technology. Labs get bogged down with particular DNA sentences, tinkering at times with subsections of a single gene ad nauseam before moving along to the next one.A team has finally overcome this obstacle by developing a new cell programming method called Multiplex Automated Genome Engineering (MAGE). Published online in Nature on July 26, the platform promises to give biotechnology, in particular synthetic biology, a powerful boost. Led by a pair of researchers in the lab of Harvard Medical School Professor of Genetics George Church, the team rapidly refined the design of a bacterium by editing multiple genes in parallel instead of targeting one gene at a time. They transformed self-serving E. coli cells into efficient factories that produce a desired compound, accomplishing in just three days a feat that would take most biotech companies months or years."We initiated the project to close the gap between DNA sequencing technology and cell programming technology," explains graduate student Harris Wang, the paper's co-first author. "The goal was to use information gleaned from genetics and genomics to rapidly engineer new functions and improve existing functions in cells," adds postdoctoral researcher Farren Isaacs, the other first author. "We wanted to develop a new tool and demonstrate how to apply it; we were determined to hand labs a hammer and a nail."


An 'eye catching' vision discovery

Nearly all species have some ability to detect light. At least three types of cells in the retina allow us to see images or distinguish between night and day. Now, researchers at the Johns Hopkins School of Medicine have discovered in fish yet another type of cell that can sense light and contribute to vision. Reporting in this week's Nature, the team of neuroscientists shows that retinal horizontal cells, which are nerve cells once thought only to talk to neighboring nerve cells and not even to the brain, are light sensitive themselves. "This is mind-boggling," says King-Wai Yau, Ph.D., a professor of neuroscience at the Solomon H. Snyder Department of Neuroscience at Johns Hopkins. "For more than 100 years, it's been known that rod cells and cone cells are responsible for sensing light, and therefore, vision," says Yau. "Then, about seven years ago, another light sensor was discovered in the retina, revealing a third type of light-sensitive cells in mammals, so we set out to look at whether this was true in other vertebrates as well." Focusing their efforts on the melanopsin light sensor, which is responsible for sensing day and night but barely involved — in mammals, at least — in seeing images, Yau's team looked for melanopsin-containing cells in other vertebrates, and found some in the retinal horizontal cells in goldfish and catfish.


Fluoride can Harm Kidney Patients

The National Kidney Foundation withdrew its support of water fluoridation citing the 2006 National Research Council (NRC) fluoride report (A) indicating that kidney patients are more susceptible to fluoride’s bone and teeth-damaging effects forcing the American Dental Association (ADA) to admit on its web site that fluoride is a concern to kidney patients. The kidney-impaired may retain and store more fluoride in their bones. High bone-fluoride-levels are linked to skeletal fluorosis (a bone weakening disease), fractures and severe tooth damage (enamel fluorosis) which can increase the risk of dental decay, reports the NRC. Chronic kidney disease and bone fracture is already a growing concern. Fluoride is added to US water supplies ostensibly to reduce tooth decay. Fluoride is also in foods, beverages, (1) common antibiotics and dental products. The National Kidney Foundation’s (NKF) (2) former fluoridation position statement also carried surprising cautions. The NKF advised monitoring children’s fluoride intake along with patients with chronic kidney impairment, those with excessive fluoride intake, and those with prolonged disease. But NKF now admits, “exposure from food and beverages is difficult to monitor, since FDA food labels do not quantify fluoride content.”


LSUHSC research shows for 1st time infant inhalation of ultrafine air pollution linked to adult lung disease

Stephania Cormier, PhD, Associate Professor of Pharmacology at LSU Health Sciences Center New Orleans, has shown for the first time that early exposure to environmentally persistent free radicals (present in airborne ultrafine particulate matter) affects long-term lung function. She recently presented her latest research data at the 11th International Congress on Combustion By-Products and Their Health Effects at the Environmental Protection Agency Conference Center in Research Triangle Park, N.C.Dr. Cormier, a 2006 National Institute of Environmental Health Sciences Outstanding New Environmental Scientist awardee, is conducting research to determine how inhalation exposure to environmental factors such as allergens, pollutants, and respiratory viruses during infancy leads to pulmonary inflammatory diseases, such as chronic obstructive pulmonary disease (COPD) and asthma later in life. Using protein profiling techniques, Dr. Cormier’s lab was able to determine that early exposure to these ultrafine pollutants caused genes to produce a number of proteins, including one associated with COPD and steroid-resistant asthma, and also caused proteins to misfold, rendering them dysfunctional. These genetic defects are linked to structural changes in the lung, airflow limitations, and permanent changes in immune responses. “It is no surprise that elevations in airborne particulate matter (PM) are associated with increased hospital admissions for respiratory symptoms including asthma exacerbations,” notes Dr. Cormier. “What has come as a surprise is that early exposure to elevated levels of PM elicits long-term effects on lung function and lung development in children.” These results could be especially important because the US Environmental Protection Agency does not currently regulate ultrafine PM emissions.


Fresh meats often contain additives harmful to kidney disease patients

Uncooked meat products enhanced with food additives may contain high levels of phosphorous and potassium that are not discernable from inspection of food labels, according to a study appearing in an upcoming issue of the Clinical Journal of the American Society Nephrology (CJASN). This can make it difficult for people to limit dietary phosphorous and potassium that at high levels are harmful to kidney disease patients. Kidney disease patients on dialysis must watch their intake of dietary phosphate so that their blood phosphate levels do not rise. This is important because high blood phosphate levels may cause premature death in dialysis patients. Kidney disease patients also must limit their intake of potassium, because high blood potassium levels can cause sudden death. One growing source of dietary phosphorous and potassium is through "enhanced" fresh meat and poultry products. These foods are injected with a solution of water with sodium and potassium salts (particularly phosphates) as well as antioxidants and flavorings. While ingesting phosphates and potassium can be dangerous for dialysis patients, there is no requirement that these ingredients be included in nutrition labels. There also have been no studies on the levels of phosphates and potassium contained in fresh meat and poultry products that have been "enhanced."


HIV infection and chronic drinking have a synergistic, damaging effect on the brain

More than half of clinic patients infected with the human immunodeficiency virus (HIV) report they also drink heavily. While highly active antiretroviral therapy has helped to reduce HIV-related cognitive and motor deficits, neuropsychological deficits may continue and even be exacerbated by alcohol. A study of memory deficits has found that HIV infection and chronic alcoholism have synergistic, damaging effects on brain function. Results will be published in the October issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View. "It has been consistently documented that chronic heavy drinking results in cognitive and motor deficits, particularly impairments in component processes of executive functions, memory, visuospatial abilities, and speed of cognitive processing and motor movements," said Edith V. Sullivan, professor in the department of psychiatry and behavioral sciences at Stanford University School of Medicine and corresponding author for the study. "Chronic heavy drinking co-occurring with HIV infection is highly prevalent, and the separate and combined untoward effects on the brain and its processes can be significant and disruptive of activities of daily living." This prevalence exists despite considerable educational and prevention programs regarding both HIV and alcoholism, added Sara Jo Nixon, a professor in the department of psychiatry at the University of Florida. "Furthermore, their comorbidity constitutes an even greater health concern with implications for treatment adherence, work and interpersonal skill maintenance." Sullivan and her colleagues examined working and episodic memory in four groups (n=164) – 40 individuals with HIV (28 men, 12 women), 38 with chronic alcoholism (24 men, 14 women), 47 with both HIV and chronic alcoholism (38 men; 9 women), and 39 "normal" controls (22 men, 17 women) – at baseline and then again at a one-year follow-up. Measures included accuracy scores, response times, and rate of information processing. "Individuals who are both positive for HIV and have a history of chronic heavy drinking are at greater risk than individuals with only one of these conditions to have trouble learning new information," said Sullivan. "This difficulty in new learning can affect an individual's ability to use information important to the successful completion of personal and work-related activities."


UTMB study identifies women at risk of gaining excessive weight with injectable birth control

Researchers at the University of Texas Medical Branch at Galveston have identified women who are likely to gain weight while using depot medroxyprogesterone acetate, more commonly known as Depo-Provera or the birth control shot. These findings dispel the myth that all women who use DMPA will gain weight and will help physicians to counsel patients appropriately. DMPA users whose weight increased by 5 percent within the first six months of use, called “early gainers,” are at risk of continued, excessive weight gain. While 75 percent of users gained little or no weight, the early gainers averaged weight gain of 24 pounds over three years. “DMPA-related weight gain is linked to increased abdominal fat, a known component of metabolic syndrome, which raises the risk of obesity-related conditions such as cardiovascular disease, stroke and diabetes,” said corresponding author Dr. Abbey Berenson, professor in UTMB’s department of obstetrics and gynecology.


Airway cells use 'tasting' mechanism to detect and clear harmful substances

The same mechanism that helps you detect bad-tasting and potentially poisonous foods may also play a role in protecting your airway from harmful substances, according to a study by scientists at the University of Iowa Roy J. and Lucille A. Carver College of Medicine. The findings could help explain why injured lungs are susceptible to further damage. The study, published online July 23 in Science Express, shows that receptors for bitter compounds that are found in taste buds on the tongue also are found in hair-like protrusions on airway cells. In addition, the scientists showed that, unlike taste cells on the tongue, these airway cells do not need help from the nervous system to translate detection of bitter taste into an action that expels the harmful substance. The hair-like protrusions, called motile cilia, were already known to beat in a wave-like motion to sweep away mucus, bacteria and other foreign particles from the lungs. The study is the first to show that motile cilia on airway cells not only have this "clearing" function, but also use the receptors to play a sensory role. The researchers also found that when the receptors detect bitter compounds, the cilia beat faster, suggesting that the sensing and the motion capabilities of these cellular structures are linked.


Protein That Promotes Cancer Cell Growth Identified

Scientists at Burnham Institute for Medical Research (Burnham) have found that the Caspase-8 protein, long known to play a major role in promoting programmed cell death (apoptosis), helps relay signals that can cause cancer cells to proliferate, migrate and invade surrounding tissues. The study was published in the journal Cancer Research on June 15. The team of scientists, led by Kristiina Vuori, M.D., Ph.D., professor and director of the Cancer Center at Burnham, showed that Caspase-8 caused neuroblastoma cancer cells to proliferate and migrate. For the first time, Caspase-8 was shown to play a key role in relaying the growth signals from epidermal growth factor (EGF) that cause cell division and invasion. The researchers also identified an RXDLL amino acid motif that controls the signaling from the EGF receptor through the protein kinase Src to the master cell proliferation regulator protein, MAPK. This same signaling pathway stimulates neuroblastoma cells to migrate and invade neighboring tissues--a critical process in cancer metastasis. “Caspase-8 has a well defined role in promoting apoptosis, especially in response to activation of the so-called death receptors on the outside of cells,” said Darren Finlay, Ph.D., first author on the paper. “Although Caspase-8 is involved in apoptosis, it is rarely deleted or silenced in tumors, suggesting that it was giving cancer cells a leg up in some other way. Our studies suggest that Caspase-8 does so by activating the MAPK pathway through Src.” Using immuno-blot assays, the scientists showed that EGF signaling was absent in a cancer cell line that is deficient in Caspase-8 and that EGF signaling can be restored by reconstituting the cells with wildtype Caspase-8. Sequence homology studies helped to identify a RXDLL motif in the protein, a sequence that has been shown in other proteins to function in cell signaling. The researchers also used immune-blot assays to demonstrate that reconstituting the Caspase-8 deficient cells with Caspase-8 with mutations in the RXDLL domain did not result in EGF signaling. This suggests that Caspase-8 mediates signaling through the RXDLL domain. The scientists had previously shown in another study that Caspase-8 associates with Src, a protein known to be involved in cancer cell proliferation. In this study they showed that interruption in this association disrupts EGF signaling indicating that Caspase-8 exerts EGF signaling through Src.


Nigel Farage Second Lisbon Treaty vote Conning the Irish


The Union

A very well built documentary about cannabis and drug prohibition. Does the drug prohibition work? Have a look and think for yourself.


War Vaccine Illnesses

Gulf War veterans advocate Joyce Riley discussed soldiers being sickened by vaccines. Ms. Riley is a graduate of the University of Kansas with a Bachelor of Science in Nursing. Her nursing career includes clinical positions of Staff Nurse, Patient Care Systems Analyst, Utilization Review, Nursing Instructor and Director of Nursing of an acute care hospital, long term care facility and home care agency. Her areas of nursing specialty are nursing administration, medical-surgical nursing and organ transplantation. She has presented at the National Institutes of Health, medical legal conferences such as the American Trail Lawyers Association, was host of her own radio talk show "Nurse Talk Radio-The Truth in Health Care", and has guested on over 1500 radio and television shows, including Art Bell, Chuck Harder and Michael Reagan. While employed at Bexar Count Hospital, San Antonio, Ms. Riley became involved in nursing medical malpractice issues after learning that Nurse Genene Jones was responsible for deaths of many babies in the well publicized "Baby Death" case. She has served as consultant and testifying expert for both plaintiff and defense medical malpractice cases for the last ten years. Ms. Riley served as a Captain in the United States Air Force and flew on C-130 missions in support of Operation Desert Storm. She now serves as spokesperson for the American Gulf War Veterans Association who's purpose is to provide education and information for the Gulf War veterans and their families and to seek treatment for the illnesses that thousands of Gulf War veterans now suffer from. The Dept. of Defense is covertly using soldiers as "experimental guinea pigs," for unproven and dangerous vaccines, she declared.


Answers to Autism and Vaccine Damage

Deel 2


Run from the cure - The Rick Simpson Story

Hemp oil is not the same as "hemp seed oil". Although hemp seed oil is extremely nutritious, it does not contain the high concentrations of THC needed to cure cancers. The true story of hemp, as told by Rick Simpson, the man who cured cancer with hemp oil.


Jane Burgermeister interview on Swine Flu

http://www.youtube.com/watch?v=PhGoubc2ygg
http://www.youtube.com/watch?v=FcwNp2ejJLk&feature=related
http://www.youtube.com/watch?v=nVc2vtWgAus&feature=related
http://www.youtube.com/watch?v=cXi1EFSUIiU&feature=related


Barefoot Technology Exposed

David Wolfe over de voordelen van het blootvoets lopen op de aarde.....

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Mob Rule - Canada

The Hells Angels illicit drug trade has reached every corner of the city of Vancouver. This organised crime has successfully become a multi billion-dollar business based on their fierce reputation. Local communities are lacking faith in their government, blaming them for allowing these thugs to become so powerful. Why is it that the most open, known, brazen criminal gangs can't be put away? With no dedicated policing, the families of victims feel that the criminals are prioritised over them, a feeling fuelled by claims that these thugs- turned-police informants have made deals with the law. We have promises for secret deals says former drug dealer Jim Boivine. Journalist and activist Julian Sher has followed the rise of the Angels for over 10 years and believes a tougher more direct approach should be used: You can't strut around wearing your biker vests and your bikie patches and think you control our cities. Over 100 members of the Hells Angels gang are now behind bars.

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When Saturday Came - 45min Documentary

As all hell broke loose in Gaza in January a brave production team was on the ground recording for a documentary. Today it has become the definitive account of the dark and deadly days that followed. Combining quality camera work with brave and unshrinking journalism, this is the powerful film that resulted


Knee injuries may start with strain on the brain, not the muscles

New research shows that training your brain may be just as effective as training your muscles in preventing ACL knee injuries, and suggests a shift from performance-based to prevention-based athletic training programs. The ACL, or anterior cruciate ligament, is one of the four major ligaments of the knee, and ACL injuries pose a rising public health problem as well as an economic strain on the medical system. University of Michigan researchers studying ACL injuries had subjects perform one-legged squats to fatigue, then tested the reactions to various jumping and movement commands. Researchers found that both legs—not just the fatigued leg—showed equally dangerous and potentially injurious responses, said Scott McLean, assistant professor with the U-M School of Kinesiology. The fatigued subjects showed significant potentially harmful changes in lower body movements that, when preformed improperly, can cause ACL tears. "These findings suggest that training the central control process—the brain and reflexive responses—may be necessary to counter the fatigue induced ACL injury risk," said McLean, who also has an appointment with the U-M Bone & Joint Injury Prevention Center.


Emphysema severity directly linked to coal dust exposure

Coal dust exposure is directly linked to severity of emphysema in smokers and nonsmokers alike, according to new research from the National Institute for Occupational Safety and Health (NIOSH). "In this study we have shown that coal mine dust exposure is a significant predictor of emphysema severity," said Eileen Kuempel, Ph.D., a senior scientist at NIOSH and lead author of the study. The findings, which were reported in the August 1 issue of the American Thoracic Society's American Journal of Respiratory and Critical Care Medicine (AJRCCM), highlight a health problem related to a growing industry. In the past 25 years, coal production has nearly doubled worldwide. Dr. Kuempel and colleagues compared lung autopsy results from 722 individuals, including 616 coal miners from West Virginia and 106 non-miners from West Virginia and Vermont. Those from West Virginia were collected from consecutive autopsies from 1957 and 1973 at the Beckley Southern Appalachian Regional Hospital as part of a black lung study. Those from Vermont were taken from consecutive autopsies performed at the University of Vermont between 1972 and 1978. Age at death, race, miner/non-miner status and smoking history were established where possible, and individual exposure to coal dust was estimated using work history data and job-specific dust exposure estimates. Pathologists Francis Green, M.D., and Val Vallyathan, Ph.D., two of the coauthors on this study, examined sections of the lungs to determine the presence and extent of emphysema. A smaller subset of the study group had their lung tissue analyzed for dust content. Emphysema was graded for type and severity.


Limited data suggest possible association between Agent Orange exposure

A new report from the Institute of Medicine finds suggestive but limited evidence that exposure to Agent Orange and other herbicides used during the Vietnam War is associated with an increased chance of developing ischemic heart disease and Parkinson's disease for Vietnam veterans. The report is the latest in a congressionally mandated series by the IOM that every two years reviews the evidence about the health effects of these herbicides and a type of dioxin -- TCDD -- that contaminated some of the defoliants. A finding of "limited or suggestive evidence of an association" means that the evidence indicates there could be a link between exposure to a chemical and increased risk for a particular health effect, though conflicting results from studies, problems with how the studies were conducted, or other confounding factors limit the certainty of the evidence. Until now, the cumulative evidence had been inadequate to draw conclusions about whether these two conditions may be associated with veterans' exposures to herbicides or TCDD. Ischemic heart disease -- a condition characterized by reduced blood supply to the heart, which can lead to heart attack and stroke -- is the foremost cause of death among people in industrialized countries. Major risk factors include buildup of cholesterol in the arteries, age, smoking, high blood pressure, and diabetes. The committee that wrote the report reviewed several studies investigating TCDD exposure and heart disease, many of which showed that higher TCDD exposure correlated with greater incidence of disease. The studies had weaknesses; for instance, it is difficult to adjust entirely for the impact of smoking, age, weight, and other common risk factors. But based on the preponderance of the evidence as well as biologic data beginning to show how TCDD can cause this toxic effect, the committee concluded


Scientists discover gene mutation responsible for hereditary neuroendocrine tumor

University of Utah researchers and their colleagues have identified the gene that is mutated in a hereditary form of a rare neuroendocrine tumor called paraganglioma (PGL). The gene, called hSDH5, is required for activation of an enzyme complex that plays a critical role in the chemical reactions that take place within cells to convert biochemical energy into usable energy. This study will be published in the journal Science, to be released online in Science Express on July 23, 2009. Paragangliomas are rare, generally benign tumors that arise from cells called glomus cells, which are located along blood vessels and play a role in regulating blood pressure and blood flow. Approximately 25 percent of paragangliomas are hereditary. Of the four familial PGL syndromes, three forms have previously been associated with mutations in genes of the succinate dehydrogenase (SDH) complex, an enzyme complex involved in the ability of cells to extract energy from nutrients.


Newly Discovered Gene Fusion May Lead to Improved Prostate Cancer Diagnosis

Researchers from NewYork-Presbyterian Hospital/Weill Cornell Medical Center have discovered a new gene fusion that is highly expressed in a subset of prostate cancers. The results may lead to more accurate prostate cancer testing and new targets for potential treatments. Experts believe that gene fusions — a hybrid gene formed from two previously separated genes — may be at the root of what causes cancer cells to grow more quickly than normal cells. The new findings, published in the August issue of the journal Neoplasia, are exciting, because unlike two previous fusions co-discovered by the same Weill Cornell Medical College laboratory group, this fusion, called NDRG1-ERG, produces a protein that may be a potential target for drug therapies. "The prostate cancer gene fusions, and proteins they produce, are important because they serve as a cancer-specific marker," says Dr. Mark A. Rubin, the Homer T. Hirst Professor of Oncology in Pathology, professor of pathology and laboratory medicine, and vice chair for experimental pathology at Weill Cornell Medical College. "Currently, PSA testing is the standard of care, yet it is not accurate enough to predict prostate cancer, because many men may have an elevated PSA level, but have benign conditions such as inflammation of the prostate." It is important to distinguish harmful cancer from non-lethal diseases, such as benign prostatic hyperplasia, or enlarged prostate disease that exhibits similar symptoms to prostate cancer, in order to provide effective care, explains Dr. Rubin. Gen-Probe, a biotechnology diagnostics company, has licensed this technology and is currently working with Dr. Rubin, and his collaborator Dr. Arul Chinnaiyan at the University of Michigan, to develop urine tests to screen for gene fusions as a means of improving upon the current standard PSA test.


Short Stressful Events May Improve Working Memory

Experiencing chronic stress day after day can produce wear and tear on the body physically and mentally, and can have a detrimental effect on learning and emotion. However, acute stress -- a short stressful incident -- may enhance learning and memory.Researchers at the University at Buffalo have shown, in trials using rodents as an animal model, that acute stress can produce a beneficial effect on learning and memory, through the effect of the stress hormone corticosterone (cortisol in humans) on the brain's prefrontal cortex, a key region that controls learning and emotion. Specifically, they demonstrated that acute stress increases transmission of the neurotransmitter glutamate and improves working memory.


Injection reverses heart-attack damage

Injured heart tissue normally can't regrow, but researchers at Children's Hospital Boston have now laid the groundwork for regenerating heart tissue after a heart attack, in patients with heart failure, or in children with congenital heart defects. In the July 24 issue of Cell, they show that a growth factor called neuregulin1 (NRG1), which is involved in the initial development of the heart and nervous system, can spur heart-muscle growth and recovery of cardiac function when injected systemically into animals after a heart attack. After birth, heart-muscle cells (cardiomyocytes) normally withdraw from the cell cycle – meaning they stop dividing and proliferating. But the researchers, led by Bernhard Kühn, MD, and Kevin Bersell of the Department of Cardiology at Children's, were able to restart the cell cycle with NRG1, stimulating cardiomyocytes to divide and make copies of themselves -- even though they are not stem cells. "Although many efforts have focused on stem-cell based strategies, our work suggests that stem cells aren't required and that stimulating differentiated cardiomyocytes to proliferate may be a viable alternative," says Kühn, the study's senior investigator and a practicing pediatric cardiologist at Children's since 2007. When the team injected NRG1 into the peritoneal cavity of live mice after a heart attack, once daily for 12 weeks, heart regeneration was increased and pumping function (ejection fraction, assessed on echocardiograms) improved as compared with untreated controls. The NRG1-injected mice also lacked the left-ventricular dilation and cardiac hypertrophy that typify heart failure; both were seen in the controls. When the researchers also stimulated production of a cellular receptor for NRG1, known as ErbB4, cardiomyocyte proliferation was further enhanced, demonstrating that NRG1 works by stimulating this receptor. They also identified the specific kinds of cardiomyocytes (mononucleated) that are most likely to respond to treatment.


The 'see food' diet

Current research suggests that a diet high in omega-3 fatty acids may help prevent one of the leading causes of legal blindness among the elderly. The related report by Tuo et al, "A high omega-3 fatty acid diet reduces retinal lesions in a murine model of macular degeneration," appears in the August 2009 issue of the American Journal of Pathology.Age-related macular degeneration (AMD), loss of vision in the center of the visual field (macula) due to retinal damage, is one of the leading causes of legal blindness among the elderly. Approximately 10% of people from 66 to 74 years of age will develop some level of macular degeneration, making it difficult for them to read or even recognize faces.A diet high in omega-3 fatty acids has been found to protect against a variety of diseases including atherosclerosis and Alzheimer's disease. Retrospective studies have suggested that diets high in fish oil or omega-3 fatty acids may also contribute to protection against AMD. A group led by Dr. Chi-Chao Chan at the National Eye Institute in Bethesda, MD examined the direct effect of omega-3 fatty acids on a mouse model of AMD. A diet with high levels of omega-3 fatty acids resulted in slower lesion progression, with improvement in some lesions. These mice had lower levels of inflammatory molecules and higher levels of anti-inflammatory molecules, which may explain this protective effect.


Some blood pressure drugs may help protect against dementia, study shows

A particular class of medication used to treat high blood pressure could protect older adults against memory decline and other impairments in cognitive function, according to a newly published study from Wake Forest University School of Medicine. Research suggests that some of the drugs classified as angiotensin-converting enzyme (ACE) inhibitors, specifically those types of ACE inhibitors that affect the brain by crossing the blood-brain barrier, may reduce inflammation that could contribute to the development of Alzheimer's disease, a major cause of dementia. The study appears in the current issue of Archives of Internal Medicine. "High blood pressure is an important risk factor for Alzheimer's disease and vascular dementia," said Kaycee Sink, M.D., M.A.S., lead author of the study, geriatrician and an assistant professor of internal medicine – gerontology. "Our study found that all blood pressure medications may not be equal when it comes to reducing the risk of dementia in patients with hypertension." Dementia is the broad term used to describe conditions in the brain that cause loss of brain function. There are several different causes of dementia, but Alzheimer's disease and strokes are two of the most common. People with dementia begin to lose their memory and may not be able to think well enough to do normal activities, such as getting dressed or eating, may lose their ability to solve problems or control their emotions, may experience personality changes and/or may become agitated or see things that are not there. While memory loss is the hallmark of dementia, it does not, by itself, mean an individual has dementia. People with dementia have serious problems with two or more brain functions, such as memory and problem solving. Someone is diagnosed with dementia every 70 seconds. It is estimated that the number of people in the United States living with dementia will increase to about 13 million by the year 2050. Therefore, delaying the onset of dementia, even by one year, would have a substantial impact on public health.


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