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Stem cell transplantation may correct rare genetic disorder in kids

September 19, 2009 By admin Leave a Comment

Washington, Sep 18 (ANI): Scripps Research Institute scientists have offered new hope for parents whose children suffer from the rare genetic disorder ‘cystinosis’ by showing through an experiment on mice that stem cell transplantation can successfully correct the defect.

“After meeting the children who suffer from this disease, like an 18-year-old who has already had three kidney transplants, and the families who are desperately searching for help, our team is committed to moving toward a cure for cystinosis, a lysosomal storage disorder. This study is an important step toward that goal,” said principal investigator Stephanie Cherqui.

In the study, the researchers used bone marrow stem cell transplantation to address symptoms of cystinosis in a mouse model.

The procedure virtually halted the cystine accumulation responsible for the disease, and the cascade of cell death that follows.

Cystine is a by-product of the break down of cellular components the body no longer needs in the cell’s “housekeeping” organelles, called lysosomes.

Normally, cystine is shunted out of cells, but in cystinosis a gene defect of the lysosomal cystine transporter causes it to build up, forming crystals that are especially damaging to the kidneys and eyes.

Cystinosis is a rare but devastating disease affecting children as young as six months, who begin to suffer renal dysfunction, which grows progressively worse with time. Other symptoms include diabetes, muscular disease, neurological dysfunction, and retinopathy.

The only available drug to treat cystinosis, cysteamine, while slowing the progression of kidney degradation, does not prevent it, and end-stage kidney failure is inevitable.

In the new study, the researchers found that transplanted bone marrow stem cells carrying the normal lysosomal cystine transporter gene abundantly engrafted into every tissue of the experimental mice.

This led to an average drop in cystine levels of about 80 percent in every organ.

Not only it prevented kidney dysfunction, there was less deposition of cystine crystals in the cornea, less bone demineralization, and an improvement in motor function.

“The results really surprised and encouraged us. Because the defect is present in every cell of the body, we did not expect a bone marrow stem cell transplant to be so widespread and effective,” says Cherqui.

Cherqui said that adult bone marrow stem cell therapy is particularly well suited as a potential treatment for cystinosis because these cells target all types of tissues.

In addition, stem cells reside in the bone marrow for the duration of a patient’s life, becoming active as needed, a particular benefit for a progressive disease like cystinosis.

The study has been published in the journal Blood. (ANI)

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Gene linked to male infertility identified

September 17, 2009 By admin Leave a Comment

Washington, Sept 16 (ANI): Scientists from Virginia Commonwealth University have identified a gene that may contribute to male infertility.

The research team hopes that the new findings would lead to new approaches to male contraception.

Sperm are produced in the testicles through a three-step process called spermatogenesis.

During the final stage, known as spermiogenesis, a lot of changes take place, including the packaging of DNA into the sperm head and the formation of the sperm tail, which propels the sperm cell toward the egg.

The study conducted using mouse model showed that mice lacking a protein called meiosis expressed gene 1, or MEIG1, were sterile as a result of impaired spermiogenesis – the process that encompasses changes in the sperm head and the formation of the tail.

The team also found that MEIG1 associates with the Parkin co-regulated gene protein, or PACRG protein, and that testicular PACRG protein is reduced in MEIG1-deficient mice.

PACRG is thought to play a key role in assembly of the sperm tail, and the reproductive phenotype of PACRG -deficient mice mirrors that of the MEIG1-mutant mice.

“We discovered that MEIG1 is essential for male fertility. Moreover, our findings reveal a critical role for the MEIG1/PACRG partnership in the function of a structure that is unique to sperm, the manchette. The absence of a normal manchette in mice lacking MEIG1 totally disrupts the maturation process of sperm,” said Dr Jerome F. Strauss III, dean in the VCU School of Medicine.

“In addition to having an impact on fertility, the discovery identifies a new target for drug discovery for a much needed reversible male method of contraception,” he added.

The study is published in the Early Edition of the Proceedings of the National Academy of Sciences. (ANI)

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Master gene that switches on disease-fighting cells identified

September 14, 2009 By admin Leave a Comment

London, Sep 14 (ANI): British scientists have identified the master gene, called E4bp4, that causes blood stem cells to turn into disease-fighting ‘Natural Killer’ (NK) immune cells.

The discovery, by researchers at Imperial College London, UCL and the Medical Research Council’s National Institute for Medical Research, could one day help scientists boost the body’s production of these frontline tumour-killing cells, creating new ways to treat cancer.

By ‘knocking out’ E4bp4 in a mouse model, the researchers created the world’s first animal model entirely lacking NK cells, but with all other blood cells and immune cells intact.

The breakthrough model should help solve the mystery of the role that Natural Killer cells play in autoimmune diseases, such as diabetes and multiple sclerosis.

According to many scientists, these diseases are a result of malfunctioning NK cells that turn on the body and attack healthy cells, which cause disease instead of fighting it.

They believe that clarifying NK cells’ role could lead to new ways of treating these conditions.

Natural Killer cells – a type of white blood cell – are a major component of the human body’s innate, quick-response immune system, providing a fast frontline defence against tumours, viruses and bacterial infections.

The gene E4bp4 is the ‘master gene’ for NK cell production, which means it is the primary driver that causes blood stem cells in the bone marrow to differentiate into NK cells.

Led by Dr Hugh Brady, the researchers are hoping to progress with a drug treatment for cancer patients which reacts with the protein expressed by their E4bp4 gene, causing their bodies to produce a higher number of NK cells than normal, to increase the chances of successfully destroying tumours.

“If increased numbers of the patient’s own blood stem cells could be coerced into differentiating into NK cells, via drug treatment, we would be able to bolster the body’s cancer-fighting force, without having to deal with the problems of donor incompatibility,” Nature quoted Brady as saying.

The researchers proved the pivotal role E4bp4 plays in NK production when they knocked the gene out in a mouse model.

Without E4bp4 the mouse produced no NK cells whatsoever but other types of blood cell were unaffected.

“Now finally, with our discovery of the NK cell master gene and subsequent creation of our mouse model, we will be able to find out if the progression of these diseases is impeded or aided by the removal of NK cells from the equation. This will solve the often-debated question of whether NK cells are always the ‘good guys’, or if in certain circumstances they cause more harm than good,” said Brady.

The study has been published in Nature Immunology. (ANI)

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Missing protein in rare genetic brain disorder restored

September 7, 2009 By admin Leave a Comment

Washington, Sep 7 (ANI): By using protease inhibitors, researchers at the University of California-San Francisco (UCSF) have restored to normal levels a key protein that is involved in early brain development, and causes the rare brain disorder lissencephaly.

Reduced levels of the protein called LIS1 have been shown to cause lissencephaly, which is characterized by brain malformations, seizures, severe mental retardation and very early death in human infants.

The findings in mice offer a proof-of-principle that the genetic equivalent to human lissencephaly, also known as “smooth brain” disease, can be treated during pregnancy and effectively reversed to produce more normal offspring.

The researchers are hoping that this approach could also be used to treat other defects in utero, or even those manifesting after birth, when caused by a partial deficiency in one gene, according to Dr. Anthony Wynshaw-Boris.

“Researchers have not considered it possible to treat such a pervasive, early developmental brain disorder as lissencephaly. Not only were we able to show a clear cellular effect from using these protease inhibitors, but also were able to treat the disorder in utero,” Nature quoted Wynshaw-Boris as saying.

The work is the culmination of 15 years of collaborative research into the cause and mechanisms of lissencephaly, which is caused by a deletion or loss of one copy of the LIS1 gene, and affects an estimated one in 50,000-100,000 infants.

In 1998, the researchers reported of producing a mouse with the same mutation that displayed defective brain development.

The current research used these mice, and found that the protein calpain degrades the LIS1 protein to less than half its normal levels near the surface of the cells.

The team then used a specific small-molecule protease inhibitor of calpain in these mice.

At a cellular level, the protease inhibitors enabled LIS1 protein to be expressed at near-normal levels.

The team then gave daily injections of a calpain inhibitor to pregnant mice whose foetuses had the mouse-model of this defect.

They observed that the resulting offspring had more normal brains and showed no sign of mental retardation.

“This study is really a proof-of-principle not only for treating complex developmental brain disorders, but also for any disorder with reduced protein levels where proteases normally play some role in breaking down that protein. This will be much more difficult to apply to humans, because of the safety issues involved, but it could lead to new therapies that might be effective for a wide range of developmental disorders,” said the researchers.

The findings have been published in the journal Nature Medicine. (ANI)

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‘Master switch’ gene may help control obesity

September 4, 2009 By admin Leave a Comment

Washington, Sept 4 (ANI): Scientists from University of Michigan claim to have discovered a gene, which when switched off, can control obesity in mice and help them remain thin.

According to Alan Saltiel, the Mary Sue Coleman Director of the U-M Life Sciences Institute, deleting the gene, called IKKE, appears to protect mice against conditions that, in humans, lead to Type 2 diabetes, which is associated with obesity.

He said that if follow-up studies confirm IKKE is tied to obesity in humans, the gene and the protein it will be prime targets for the development of drugs to treat obesity and diabetes.

“We’ve studied other genes associated with obesity – we call them ‘obesogenes’ – but this is the first one we’ve found that, when deleted, stops the animal from gaining weight,” said Saltiel, senior author of a paper.

“The fact that you can disrupt all the effects of a high-fat diet by deleting this one gene in mice is pretty interesting and surprising,” Saltiel added.

During the study, the high-fat-diet mice were fed a lard-like substance with 45 percent of its calories from fat. Control mice were fed standard chow with 4.5 percent of its calories from fat.

The gene IKKE produces a protein kinase also known as IKKE. The IKKE protein kinase appears to target proteins, which, in turn, control genes that regulate the mouse metabolism.

When the high-fat diet is fed to a normal mouse, IKKE protein-kinase levels rise, the metabolic rate slows, and the animal gains weight. In that situation, the IKKE protein kinase acts as a brake on the metabolism.

The new study showed that knockout mice placed on the high-fat diet did not gain weight, apparently because deleting the IKKE gene releases the metabolic brake, allowing it to speed up and burn more calories, instead of storing those calories as fat.

The new study is published in the journal Cell. (ANI)

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Vitamin C deficiency may impair newborn babies’ mental development

September 3, 2009 By admin Leave a Comment

Washington, Sept 3 (ANI): A new study has revealed that vitamin C deficiency may impair the mental development of newborn babies.

The study showed that guinea pigs, which lack vitamin C, have 30 per cent less hippocampal neurones and significantly worse spatial memory.

According to lead researcher Jens Lykkesfeldt, like guinea pigs, human beings are dependent on getting vitamin C through their diet.

He speculates that vitamin C deficiency in pregnant and breast-feeding women may also lead to impaired development in foetuses and new-born babies.

This vitamin seems quite important to brain activity.

Tests have shown that mouse foetuses that were not able to transport vitamin C develop severe brain damage, which resembles the ones found in premature babies and which is linked to learning and cognitive disabilities later in life.

In some areas in the world, vitamin C deficiency is very common – population studies in Brazil and Mexico have shown that 30 to 40 per cent of the pregnant women have too low levels of vitamin C, and the low level is also found in their foetuses and new-born babies.

“We may thus be witnessing that children get learning disabilities because they have not gotten enough vitamin C in their early life,” said Lykkesfeldt, from Faculty of Life Sciences at University of Copenhagen.

“This is unbearable when it would be so easy to prevent this deficiency by giving a vitamin supplement to high-risk pregnant women and new mothers,” Lykkesfeldt added.

The researchers are currently studying how early in pregnancy vitamin C deficiency affects the embryonic development of guinea pigs and whether the damage may be reversed after birth.

The study appears in American Journal of Clinical Nutrition. (ANI)

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Indian-origin scientists find novel therapeutic target for autoimmune diseases

September 2, 2009 By admin Leave a Comment

London, Sept 2 (ANI): A research team led by Indian-origin scientists from University of Michigan have discovered a new mechanism that would help in future therapies for conditions ranging from autoimmune diseases to organ transplants to cancer.

U-M biochemistry professor Ruma Banerjee and her colleagues have identified a mechanism that keeps a check on aggressive immune cells that can attack the body’s own cells.

They found that immune system’s regulatory T cells influence aggressive immune cells by regulating the chemical environment between cells.

“Now we know that the redox environment outside the cell is a very important dynamic. It regulates cell function,” Nature quoted Banerjee as saying.

The processes known as redox chemistry are fundamental to the way cells derive and consume energy.

She said that regulatory T cells appear to alter the chemical environment around their aggressive cousins, known as autoreactive T cells, which either curb them or cause them to proliferate.

This mechanism is likely to be involved in inflammatory bowel disease (IBD) and ulcerative colitis.

The study conducted over live mouse immune cells showed that important redox communication occurs between dendritic cells, which are the first immune cells to detect a foreign agent, and autoreactive T cells.

Dr Sanjay Garg, a research investigator in the U-M Department of Biological Chemistry, said that the dendritic cells alter the chemical environment outside cells in a way that promotes activation of the T cells.

But then T regulatory cells “intervene in the redox chatter” and suppress that effect.

Banerjee insists that she needs to conduct more study to fully understand the process before they can use their insights to block or encourage T regulatory cell activity in animal studies of IBD or another autoimmune disease.

The study appears in Nature Chemical Biology. (ANI)

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New, improved zebrafish cloning method may further human health research

September 1, 2009 By admin Leave a Comment

London, August 31 (ANI): In what may eventually prove very useful in human health research, scientists at Michigan State University have come up with a more efficient method to clone zebra fish.

What makes this work an important achievement is the fact that zebra fish, which have served as an excellent model for understanding normal development and birth defects for more than 20 years, are quickly becoming the animal of choice for many researchers.

“After the mouse, it is the most commonly used vertebrate in genetic studies. It is used in cancer research and cardiovascular research because they have many of the same genes we have,” Nature magazine quoted Jose Cibelli, an MSU professor of Animal Science, as saying.

While previous methods of cloning zebra fish have had very low success rates, the MSU researchers say that their novel method can increase the number of cloned fish that can be obtained from an adult fin cell or an embryonic tail clip increased by 2 percent to 13 percent, respectively.

What makes zebra fish so useful in research is their eggs are transparent and the fish’s development is easy to follow.

Improving on the techniques of zebra fish cloning also is important because currently only the mouse remains the best model for gene targeting.

“So far the mouse is the only one from which you can delete genes in a reliable fashion. What researchers do is mutate a gene, abolish its function completely, and then study the consequences,” Cibelli said.

A research article describing the novel technique has been published in the journal Nature Methods. (ANI)

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Gerard Butler takes to playing ‘cat and mouse game’ with paparazzi

September 1, 2009 By admin Leave a Comment

Washington, Aug 31 (ANI): Scottish actor Gerard Butler is so harried by the paparazzi following him that he has taken to playing a cat and mouse game with them.

Butler, 39, has become a well-known star, and with rumours of a romance with actress Jennifer Aniston, he has become the hot target for celebrity photographers.

But the actor has revealed that he is not happy with the attention he is getting, especially because the photographers try to catch him in compromising positions.

He was recently caught dining outside a restaurant by a photographer determined to get a snap of him eating, and Butler was equally determined not to let the photog succeed.

“It was almost like holding out a (stick) for a dog. Every time I got my fork, he picked his camera up, so I put it down again and he put his camera down. Then I’d pick it up again,” Contactmusic quoted him as saying.

“The only time I could eat was when a bus went past or a truck. Then literally the truck would stop and I go boom, boom, boom and I’d shovel the food in,” he added. (ANI)

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Novel method to make safer human stem cells uses just one gene

August 29, 2009 By admin Leave a Comment

London, Aug 29 (ANI): Inching closer to curing diseases like Parkinson’s using cells generated from a patient’s own body, researchers have successfully reprogrammed human nerve cells back to an embryo-like state by using just a single gene.

It is known that embryonic stem cells are pluripotent – they can develop into any of the body’s cell types.

But such cells are not available in large numbers, as they can only be harvested from a donated egg or embryo, and, for ethical reasons, most countries have laws restricting their use.

In 2006, Shinya Yamanaka and his colleagues at Kyoto University in Japan successfully made mouse cells pluripotent by reprogramming skin cells into a state like embryo cells.

They did so by using retroviruses to insert four genes – known as “factors” – into the cells’ DNA.

They repeated the trick a year later with human cells.

However, using genes and retroviruses in this way increases the risk of the cell becoming cancerous, not just because tinkering with DNA has that effect, but also because two of the four factors are known to cause cancer.

In a bid to make these promising cells in a safe way, Hans Scholer’s team at the Max Planck Institute for Molecular Biomedicine in Münster, Germany, has been working to achieve pluripotency using fewer factors.

Last year, they did this with the two factors that do not cause cancer, and now they have simplified the recipe further, doing it with just one.

“Remarkably, it turns out that three of these four essential factors are already expressed in human neural stem cells – although not in skin cells – so we only needed to add one factor, OCT4,” New Scientist quoted Boris Greber, a member of the team, as saying.

He said that the cells from neural tissue are much easier to reprogram than skin cells, and are less prone to mutations.

It is much harder to get a sample of neural stem cells than skin cells, as it can be done via extracting the cells from the dental pulp of teeth, said Greber.

Inserting even one gene into the chromosome of a cell still permanently modifies its DNA, which is why the new method will remain a lab tool instead of being allowed in the clinic.

However, the researchers are hoping that it will help them improve methods for producing embryonic stem cells.

“Ideally, we will be able to find a chemical that does the same job of expressing the factor without the need for a gene,” said Greber.

Earlier this year, researchers in California managed just that when they reprogrammed mouse fibroblasts using a cocktail of proteins.

That technique did not involve inserting genes, and, thus, shouldn’t raise the cancer risk. But that was far less efficient.

“Without stable intervention using viruses, the frequency of reprogramming goes down and you have to wait a long time. We don’t have the perfect method yet,” said Greber.

The study has been published in the journal Nature. (ANI)

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‘Thick’ blood causes as well as protects from heart attack, stroke

August 25, 2009 By admin Leave a Comment

Washington, Aug 25 (ANI): Animal studies carried out by researchers at Heidelberg University Hospital have shown that “thick” blood can not only cause heart attack and stroke, but also prevent them.

In their study report, the scientists say that mice with a greater tendency to form blood clots have larger plaques in their vessels, but they are more stable.

Thus, there is less risk that these plaques will rupture and obstruct circulation.

Usually, the more blood coagulates, the greater is the risk of vascular obstruction, and anticoagulants are used to protect against these complications.

However, clinical studies have thus far not proven that an increased clotting tendency also has a detrimental effect for plaque development.

Led by Dr. Berend Isermann, the researchers examined mice with elevated blood fat levels, and a genetic defect that leads to an increase in blood clotting.

They found that the mice developed larger plaques than those without the genetic defect, but the plaques were more stable.

In addition, no vascular obstruction was observed, as the vascular wall expanded to adapt to the new situation.

The negative effect of larger plaques on circulation was compensated by the positive effect of stability and a greater vessel diameter.

However,the long-term use of anticoagulants (in this case, low molecular weight heparin) reversed these advantages- the size of the plaques was reduced, but stability was lost, increasing the risk of complications.

“Our findings were made on mice, but they confirm the results of clinical studies on humans. In addition, in vitro studies show that human cells react similarly to mouse cells,” said Isermann.

The team assumed that the results could be transferred to humans and recommends weighing the advantages and disadvantages of anticoagulants carefully before administering them to a patient.

“Currently, there is no indication that these new observations also apply to drugs that inhibit the function of platelets,” said Isermann.

When deciding on therapy, the cause of the coagulation disorder and the degree of already existing atherosclerosis should be taken into consideration.

Additionally, the researchers recommended using anticoagulants that inhibit specific coagulation factors in order to preserve the positive effects on plaque stability.

Various new drugs that inhibit specific coagulation factors are currently being studied in clinical trials.

“It is important that plaque stability and the influence on atherogenesis are also studied in these trials,” said Isermann.

The study has been published in the journal Circulation. (ANI)

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Cheap BP drug could help treat multiple sclerosis

August 18, 2009 By admin Leave a Comment

Washington, Aug 18 (ANI): A cheap blood pressure drug could help keep multiple sclerosis at bay, claim researchers at the Stanford University School of Medicine.

The study’s boffins came to the conclusion after finding a link, in mice and in human brain tissue, between high blood pressure and multiple sclerosis.

While neurology professor Lawrence Steinman, MD, senior author of the new study, cautioned that extensive clinical trial work is needed to determine if the drug, known as lisinopril, can do in humans what it does in mice, he is excited that “we were able to show that all the targets for lisinopril are there and ready for therapeutic manipulation in the multiple-sclerosis lesions of human patients. Without that, this would be just another intriguing paper about what’s possible in the mouse.”

The paper has been published online Aug. 17 by the Proceedings of the National Academy of Sciences.

Multiple sclerosis is a chronic and occasionally lethal autoimmune disease in which the body’s immune system mounts recurring assaults on the myelin sheathing of nerve cells in the brain.

This causes nerves to malfunction and can lead to blindness and paralysis. Both multiple sclerosis and atherosclerosis involve inflammatory processes.

Drugs currently used to treat MS are of limited effectiveness. Some cost up to 15,000 pounds a year.

Lisinopril, in contrast, costs as little as 2p per pill.

Research by Steinman indicated that the chemical, called angiotensinconverting enzyme, also played a role in the inflammation responsible for the damage caused by MS.

Steinman, of Stanford University in the U.S., showed that samples of brain tissue from MS patients had high levels of angiotensin-converting enzyme.

He then gave Lisinopril to mice before giving them a chemical that normally causes an MS-like illness in mice.

The creatures remained healthy, suggesting the blood pressure drug was holding MS at bay.

Strikingly, when he gave Lisinopril to mice after giving them the MS-causing chemical, paralysis was reversed.

Tests showed that Lisinopril boosted production of immune cells called regulatory T cells. These protect against autoimmune diseases such as MS by dampening down the rogue immune response that damages the body. (ANI)

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High-fat diets ‘make us lazy, forgetful’

August 13, 2009 By admin Leave a Comment

Washington, Aug 13 (ANI): Eating hotdogs and French fries might be a great treat, however, these high fat diets can significantly reduce our exercising ability and lead to short term memory loss, reveals a new study.

The research conducted using mouse model showed that in less than 10 days of eating a high-fat diet, rats had a decreased ability to exercise and experienced significant short-term memory loss.

“Western diets are typically high in fat and are associated with long-term complications, such as obesity, diabetes, and heart failure, yet the short-term consequences of such diets have been given relatively little attention,” said Andrew Murray, co-author of the study and currently at the University of Cambridge in the United Kingdom.

“We hope that the findings of our study will help people to think seriously about reducing the fat content of their daily food intake to the immediate benefit of their general health, well-being, and alertness,” he added.

Study leader Murray fed rats with low-fat diet (7.5 percent of calories as fat) and high-fat diet (55 percent of calories as fat).

He discovered that the muscles of the rats eating the high-fat diet for four days were less able to use oxygen to make the energy needed to exercise, causing their hearts to worker harder-and increase in size.

After nine days on a high-fat diet, the rats took longer to complete a maze and made more mistakes in the process than their low-fat-diet counterparts.

The researchers also studied the cellular causes of these problems, particularly in the mitochondria of muscle cells.

They found increased levels of a protein called uncoupling protein 3, which made them less efficient at using oxygen needed to make the energy required for running.

The new research is published online in The FASEB Journal. (ANI)

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Signalling pathway operational in intra-abdominal fat identified

July 15, 2009 By admin Leave a Comment

Washington, July 15 (ANI): Ben-Gurion University of the Negev (BGU) researchers and Germany-based University of Leipzig experts have announced the identification of a signalling pathway that is operational in intra-abdominal fat, the fat depot that is most strongly tied to obesity-related morbidity.

“Fat tissue in obesity is dysfunctional, yet, the processes that cause fat tissue to malfunction are poorly understood-specifically, it is unknown how fat cells ‘translate’ stresses in obesity into dysfunction,” said Dr. Assaf Rudich, senior lecturer from the Department of Clinical Biochemistry at Ben-Gurion University.

Fat tissue is no longer considered simply a storage place for excess calories, but in fact is an active tissue that secretes multiple compounds, thereby communicating with other tissues, including the liver, muscles, pancreas and the brain.

Normal communication is needed for optimal metabolism and weight regulation, but in obesity, fat (adipose) tissue becomes dysfunctional, and mis-communicates with the other tissues.

According to the researchers, this places fat tissue at a central junction in mechanisms leading to common diseases attributed to obesity, like type 2 diabetes and cardiovascular diseases.

The researchers highlight the fact that fat tissue dysfunction is believed to be caused by obesity-induced fat tissue stress: Cells over-grow as they store increasing amounts of fat. They say that this excessive cell growth may cause decreased oxygen delivery into the tissue; individual cells may die (at least in mouse models), and fat tissue inflammation ensues.

Excess nutrients, they add, may also lead to increased metabolic demands, and cause cellular stress.

The BGU and Leipzig teams collected fat tissue samples from people undergoing abdominal surgery, and identified a signalling pathway that is operational in intra-abdominal fat, the fat depot that is most strongly tied to obesity-related morbidity.

They say that the degree of activation of a signalling pathway from these individuals was compared with those of leaner people, those with obesity predominantly characterized by accumulation of “peripheral” fat, and those with obesity with predominant accumulation of fat within the abdominal cavity.

They found that the signalling pathway was more active depending on the amount of fat accumulation in the abdomen, and that it correlated with multiple biochemical markers for increased cardio-metabolic risk.

In their study report, they have revealed that the expression of one of the upstream signaling components, a protein called ASK1, predicts whole-body insulin resistance (an endocrine abnormality that is strongly tied to diabetes and cardiovascular disease), independent of other traditional risk factors.

The researchers have also shown that although non-fat cells within adipose tissue express most of this protein in lean persons, the adipocytes themselves increase its expression by more than four-fold in abdominally-obese persons.

“The importance of this study is not only in contributing to the understanding of adipose tissue dysfunction in obesity, but as a consequence, may provide important leads for novel ways to prevent the dangerous consequences, such as type 2 diabetes, of intra-abdominal fat accumulation,” states Dr. Iris Shai, a BGU researcher at the S. Daniel Abraham International Center for Health and Nutrition and Soroka University Medical Center in Beer-Sheva, Israel.

The study has been published in the Endocrine Society’s the Journal of Clinical Endocrinology and Metabolism. (ANI)

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Single gene mutation behind catastrophic epilepsy

July 8, 2009 By admin Leave a Comment

Washington, July 8 (ANI): Researchers at Baylor College of Medicine have found a mutation in a single gene to be responsible for catastrophic epilepsy – characterized by severe muscle spasms, persistent seizures, mental retardation and sometimes autism.

Dr. Jeffrey Noebels, professor of neurology, neuroscience and molecular and human genetics at BCM and director of the Blue Bird Circle Developmental Neurogenetics Laboratory at BCM, said that the team replicated the defect in mice, developing a mouse model of the disease that could help researchers figure out effective treatments for and new approaches to curing the disease.

“While many genes underlying various forms of childhood epilepsy have been identified in the past decade, most cause a disorder of ‘pure’ seizures,” said Noebels.

Why some children have a more complicated set of disorders beginning with major motor spasms in infancy followed by cognitive dysfunction and developmental disorders such as autism remained a mystery until the discovery by the BCM team that a mutation in only a single gene explains all four features of catastrophic epilepsy.

A gene known as Aristaless-related homeobox or ARX has a specific mutation called a triplet repeat, which means that a particular genetic (in this case, GCG) is repeated many times in the gene.

When the researchers duplicated this particular mutation in specially bred mice, the animals had motor spasm similar to those seen in human infants.

Recordings of their brain waves showed that they had several kinds of seizes, included absence epilepsy and general convulsion. They also had learning disabilities and were four times more likely to avoid contact with other mice than their normal counterparts.

This behaviour is similar to that seen in children with autism or similar disorders in the same spectrum.

“The new model is an essential tool to find a cure for the disorder,” said Noebels.

The study appears in the current issue of the Journal of Neuroscience. (ANI)

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Scientists create artificial sperm cells from human embryonic stem cells

July 8, 2009 By admin Leave a Comment

London, July 8 (ANI): Scientists have achieved a major breakthrough in making sperm-like cells from human embryonic stem cells.

Karim Nayernia, of the University of Newcastle Upon Tyne in the UK, has revealed that these cells can swim like sperm do.

He says that his team used the same technique to create sperm-like cells from human embryonic stem cells that he had used in 2006 to produced sperm from mouse embryonic stem cells.

The team labelled embryonic stem cells with a fluorescent marker attached to a particular gene that is expressed during reproductive-cell development, and cultured the cells in a medium that encourages differentiation into sperm cells.

The researchers observed that about three per cent of the resulting cells contained enough DNA for only one set of chromosomes, suggesting that meiosis had occurred.

Some of these cells also formed tails and were motile, they said.

Nayernia and his colleagues have yet to analyse methylation patterns in their sperm-like cells, or conduct a detailed study of the cells’ morphology.

While there work has been hailed by other scientists, the sperm-like cells created by the researchers will still require much more characterization before they can be used as an experimental model for the study of inherited diseases and infertility.

Another hurdle is that, in several countries, it may actually be illegal even if these cells were properly characterised.

Nayernia admits it, but still insists that his team’s work was a “proof-of-principle experiment”.

“We don’t claim that it is fully normal sperm, but they do have some of the right characteristics,” Nature magazine quoted him as saying.

Meanwhile, he and his colleagues have also launched a project to produce sperm cells from induced pluripotent stem cells, which can be generated from adult cells.

The researchers believe that such cells would make it easier to derive sperm cells from many individuals.

“Then we can, for example, see whether environmental factors or genetic factors are affecting fertility, and which step of sperm production has been affected by those factors,” he says. (ANI)

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Antibodies in blood may help prevent Alzheimer’s

July 8, 2009 By admin Leave a Comment

Washington, July 7 (ANI): Stanford University Medical Centre scientists have identified certain antibodies in the blood and cerebrospinal fluid of healthy people that may help prevent Alzheimer’s disease.

They say that the levels of the antibodies found in healthy people decline with age and, in Alzheimer’s patients, with increasing progression of the disease.

Alzheimer’s disease is characterized by the build-up of amyloid plaques in the brain.

These are large aggregations of a protein breakdown product, or peptide, called A-beta. Many experiments have shown that immunization with A-beta can reduce the formation of amyloid plaques.

It is believed that more than the plaques themselves (which are also found in the brains of people with no Alzheimer’s symptoms), it is smaller aggregations of a few A-beta molecules, called oligomers, which are most toxic to neurons.

During the study, the researchers found that the antibodies target many forms and aggregation-states of A-beta in both healthy and diseased subjects’ blood, with antibodies to oligomers showing the most immunoreactivity.

A follow-on experiment showed that the same antibodies, whether isolated from plasma of either Alzheimer’s patients or healthy controls, were able to protect freshly cultured mouse neurons in a dish from destruction by A-beta, which is typically highly toxic to these neurons.

Previous studies conducted on vervet monkeys showed that immunizing with A-beta substantially cleared their plaques.

In this new study, the Stanford team obtained blood samples extracted from those monkeys before and after immunization, and compared levels and diversity of relevant antibodies in pre- and post-inoculation samples

They observed several such antibodies in the pre-immunized samples, as well as significant post-immunization increases in levels of several different antibodies.

“Other studies have found antibodies against A-beta, but nobody has ever done a large-scale analysis using hundreds of different samples and almost a hundred different peptides to look for what’s already in people’s bodies,” said the paper’s first author, Markus Britschgi, PhD, an instructor working as a researcher in the laboratory of Tony Wyss-Coray, PhD.

The study appears in the journal Proceedings of the National Academy of Sciences. (ANI)

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Novel targeted therapy shows promise to eliminate leukaemia stem cells

July 3, 2009 By admin Leave a Comment

Washington, July 3 (ANI): A piece of research has shown that it is possible to eliminate stem cells related to human acute myeloid leukemia (AML), a notoriously treatment-resistant blood cancer, using a new targeted therapy.

Associate Professor Richard Lock, from the Children’s Cancer Institute Australia and the University of New South Wales, has revealed that the new therapeutic approach has been found to selectively attack human cancer cells grown in the lab as well as in animal models of leukaemia.

AML is a cancer of the white blood cells that has an extremely poor prognosis and does not respond well to conventional chemotherapy.

“The cellular and molecular basis for this dismal picture is unclear. However, previous research has suggested that leukaemia stem cells (LSCs) may lie at the heart of post-treatment relapse and chemoresistance,” says Lock.

LSCs are cells that can initiate AML and are critical for its long-term growth.

Lock and his colleagues exploited the fact that the molecule CD123 is expressed at very high levels on LSCs but not on normal blood cells.

The researchers created a therapeutic antibody that recognized and bound to CD123, hoping that the antibody would selectively interfere with AML-LSC survival.

When AML-LSCs from human patients were transplanted into mice treated with the antibody, called 7G3, cytokine signalling in the tumour cells was blocked.

The research team also observed that 7G3 impaired migration of the AML-LSCs to bone marrow, and activated the innate immune system of the host mouse to destroy the AML-LSCs.

They say that, overall, treatment with 7G3 substantially improved mouse survival when compared with control groups.

Lock and his colleagues are currently using a CD123-targeting antibody in phase 1 clinical trials of advanced AML. They say that there are no signs of treatment-related toxicity.

These results hold substantial promise for future cancer therapeutics.

“The recent characterization of defined populations of cancer stem cells in a range of human malignancies, as well as their relative resistance to conventional chemotherapy and radiotherapy, supports the broad applicability of our approach and provides rationale for the progression of AML-LSC-targeted therapeutics from preclinical evaluation to clinical trials,” concludes Associate Professor Lock.

A research article on the study has been published in the journal Cell Stem Cell. (ANI)

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How to prevent cardiac failure in endurance athletes

June 22, 2009 By admin Leave a Comment

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Washington, June 22 (ANI): Atrial fibrillation still poses a huge death threat to endurance athletes. Now, experts have shed light on how to prevent cardiac arrhythmias and even sudden death in sportspersons./pp
Atrial fibrillation, which represents one of the major cardiovascular reasons for hospital admission, is common among cyclists, marathon runners and other athletes with a long history of endurance training./pp
Dr. Luis Mont, from the Hospital Clmnic de Barcelona in Spain, says that atrial fibrillation is more frequent in middle-aged individuals who formerly took part in competitive sports and continue to be active, or simply in those involved in regular endurance training without having actually participated in competitive sports. /pp
So we have to look at the effects of endurance or athletic training with a more open view, he added./pp
Dr Mont says that circumferential pulmonary vein ablation (CPVA) is a recently introduced technique, which identifies the signals causing the atrial fibrillation, and isolates their source in the pulmonary veins from the left ventricle of the heart./pp
It has been successfully used in routine patients with atrial fibrillation and, according to new data; it is now as effective./pp
Another study using mouse model showed that deconditioning reverses expression of cardiac fibrosis markers in endurance training. /pp
Mont showed that those with a history of arrhythmias following endurance training may benefit from a period of deconditioning following their efforts. /pp
The study showed that endurance exercise causes cardiac structural changes, which may play a role in the development of arrhythmias. /pp
Anti-hypertensive drug losartan might also help in preventing the heart fibrosis induced by endurance exercise. (ANI)/p

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New interferon response could offer early control of bird flu virus

June 20, 2009 By admin Leave a Comment

Washington, June 20 (ANI): The cell-signalling protein, interferon type 1, has the potential to reduce H5N1 influenza virus’ (bird flu virus) replication in mice, and can thus offer protection in the early stages of infection, according to researchers from Georgia.

Highly pathogenic avian influenza H5N1 viruses increasingly pose a serious public health risk, as cases of interspecies transmission from birds to humans continue to rise.

While not much is known about the pathogenic mechanisms of H5N1 influenza viruses, prior research has suggested that their ability to evade innate immune responses within the host, such as the type 1 interferon (IFN-a/B) response, contributes to virulence in mammals.

In the study, they used a mouse model to analyse the role of type 1 interferons in IFN a/ receptor-deficient and wild-type mice challenged with two avian influenza A viruses isolated from humans (HK/483 and HK/486).

The two viruses generally exhibit high and low lethality in mice.

The findings revealed that INF-a/ß receptor-deficient mice lost significantly more weight, and were faster to succumb to death than wild-type mice.

Both the HK/483 and H/K 486 virus caused a similar systemic infection in INF-a/ß receptor-deficient mice.

However, pre-treatment with IFN-a/ß significantly reduced replication of both viruses.

“These results suggest a role for the IFN-a/ß response in the control of H5N1 virus replication both in vivo and in vitro, and as such it may provide some degree of protection to the host in the early stages of infection,” said the researchers.

The findings of the study have been reported in the Journal of Virology. (ANI)

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