New role for zebrafish in human studies

Washington, May 20 (ANI): Zebrafish – an important animal model in disease and environmental studies – could eventually help scientists in revealing the function of a mysterious enzyme linked to the steroid cortisol, and found in the human brain, found a researcher at the University of California, San Diego School of Medicine.

In people and other vertebrates, steroids like cortisol perform a variety of diverse duties, including regulating immune response, bone formation and brain activity.

However, too much cortisol is unhealthy. High levels of the steroid have been linked to type 2 diabetes and may impair the brain”s ability to store memories.

The human body regulates cortisol by employing an enzyme called 11 beta-hydroxysteroid dehydrogenase-type 1 or 11beta-HSD1, which catalyzes the synthesis of cortisol in liver and fat cells.

A related enzyme known as 11 beta-HSD-type3 or 11 beta-HSD3 is expressed in the brain, though its utility remains unknown.

In new findings, Dr. Michael E. Baker has reported that 11 beta-HSD3 (but not 11 beta-HSD1) is present in zebrafish, where it appears to serve an important role in fish endocrine physiology.

This makes the fish a potentially useful analog for cortisol studies, including discovering the purpose and function of 11 beta-HSD3 in human brains, which may be an evolutionary precursor to 11 beta-HSD1.

Interestingly, Baker found that the genomes of mice and rats do not contain 11 beta-HSD3.

This means that inserting the appropriate gene for the enzyme in these animal models could provide additional avenues of investigation.

The study will be published in the latest issue of FEBS Letters. (ANI)

Protein that spurs spread of prostate cancer discovered

Washington, May 20 (ANI): Scientists have discovered that Stat5, a signaling protein previously found to be key to survival of prostate cancer, is also involved in metastasis.

The study, conducted by researchers from the Kimmel Cancer Center at Jefferson, demonstrates in both laboratory and animal models that nuclear Stat5 over-expression leads to a deadly spread of the cancer.

They add that their work with mice was unique in that it was the first time Stat5 was associated with prostate cancer metastasis processes in an animal model.

“Until now, we thought that Stat5 was involved in primarily promoting tumor growth, but this study indicates it could be one of the key players in pushing prostate cancer to spread,” said Marja Nevalainen, associate professor of Cancer Biology, Urology and Medical Oncology at Jefferson Medical College of Thomas Jefferson University.

“This seminal paper is sure to open up a new avenue of research, including investigation of therapies that could target Stat5 expression. Fresh approaches are needed since there are no effective therapies for prostate cancer that has metastasized,” Nevalainen added.

The study has been published in the online edition of Endocrine-Related Cancer. (ANI)

Hormone therapies ”up breast cancer metastasis risk in post-menopausal women”

Washington, May 7 (ANI): A University of Missouri study has found that hormone therapies not just increase the risk of breast cancer in post-menopausal women, they can also increase the chance of the cancer metastasising.

After menopause, women take hormone therapies, which are often a combination of estrogen and progestin, to replace hormones lost from inactive ovaries.

Progestin is a hormone that is used to counteract the potentially negative effects of estrogen therapy on the uterus.

Previous studies have shown that estrogen and progestin in hormone therapies increase the risk of breast cancer in post-menopausal women.

Now, the new study has demonstrated that progestins can also increase the chance of the cancer metastasizing, or spreading to the lymph nodes.

“In our study, we found that progestins increase the number of blood vessels that are responsible for transporting existing cancer cells,” said Salman Hyder, the Zalk Endowed Professor in Tumour Angiogenesis and professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Center.

“The more the blood vessels increase, the higher the chance of cancer cell metastasizing. Progestins could even be more harmful to women who have functionally abnormal p53, a protein that acts as a tumour suppressor. In the absence of p53, progestins increase the release of a protein from tumour cells that allows formation of new blood vessels within tumours.”

In the study, researchers compared the effects of several types of commonly used progestins on breast cancer tumours in an animal model. Researchers found that all types of progestin tested act in the same way and increased the risk of metastasis.

Also, results showed that estrogen and progestin acted the same way whether taken together or separately. Although Hyder said that the study was independent of whether or not the ovaries were intact, it”s still unclear whether progestins have the same effects in pre-menopausal women.

“Especially if there”s a family history of breast cancer, it”s advisable not to take progestins. It”s a difficult call that must be made on an individual basis by a physician,” Hyder said.

“The next step for this research is finding a type of progestin that does not cause tumor progression but still protects the uterus. Also, we”re trying to see if it”s possible to give patients something in addition to estrogen and progestin that can protect the breast,” Hyder added.

The study has been accepted for publication in the Journal Menopause. (ANI)

New discovery to help diabetics with slow-to-heal wounds

Washington, Apr 17 (ANI): With a new discovery about wound-healing process, scientists could offer better treatments to diabetics and other patients who have wounds that take time to heal.

Loyola University Health System researchers found that certain immune system cells slow the wound-healing process.

Thus, it might be possible to improve healing by inactivating these immune system cells, said Dr. Elizabeth Kovacs, who heads the laboratory team that made the discovery.

In the study, the immune system cells that impeded the healing process are called natural killer T (NKT) cells.

NKT cells perform beneficial functions such as killing tumour cells and virus-infected cells.

However, researchers discovered that NKT cells also migrate to wound sites and impede the healing process.

The researchers used an animal model to examine the effects of NKT cells on healing.

Healing was significantly slower in normal mice that had NKT cells than it was in a special breed of mice that lacked NKT cells.

“We demonstrated that early wound closure was accelerated in the absence of NKT cells. Importantly, we also made the novel observation that NKT cells themselves are a constituent of the early wound inflammatory infiltrate,” wrote the researchers.

Certain conditions, such as diabetes and infections, can slow or prevent wounds from healing.

Researchers don”t know how NKT cells slow healing, but they believe it is possible to inactivate NKT cells using an antibody.

They are testing this prediction in a follow-up study.

The findings are reported online, in advance of print, in the Journal of Surgical Research. (ANI)

First biomarker for multiple sclerosis found

London, March 29 (ANI): Scientists have discovered the first biomarker for multiple sclerosis (MS) that might predict which patients will respond to a standard therapy and which will not.

Researchers at the University of Alabama at Birmingham (UAB), along with researchers at Stanford University, found that patients with a particular type of T helper immune cells responded well to interferon-ß, the usual first-line therapy for the disease, while those with a different T helper immune-cell type either did not respond or experienced worsening symptoms.

“Interferon-ß is typically the first therapeutic choice for most MS patients, but there is a subset of about 30 percent of patients for whom it does not work and may make the patient worse,” said Chander Raman, associate professor in the Division of Clinical Immunology and Rheumatology and lead investigator of the study.

“Our findings, in both animal and human models, indicate that the type of T helper cell present is the determining factor in predicting whether interferon-ß will be effective,” Raman added.

Raman suggests this might be another rung on the ladder leading to personalized medicine, in which therapies are based on an individual’s physiology and genetic makeup and the nature of disease.

“When our findings are verified in an expanded human trial, a simple blood test could be used to determine which type of T helper cell is predominantly responsible for the disease in an MS patient, enabling clinicians to provide the proper therapy from the beginning of treatment and eliminate the guesswork,” Raman said.

The researchers examined T helper Type 1 cells and T helper Type 17 cells in an animal model for multiple sclerosis. Both Th1 and Th17 cells are major initiators of MS and important in disease severity. The researchers found that interferon-ß was effective in mice with disease initiated by Th1 cells, but worsened disease initiated by Th17 cells.

The findings were replicated with striking consistency in analysis of human-patient serum with relapsing-remitting multiple sclerosis, the most common form of the disease.

“This research reinforces the concept that diseases have certain signatures that help define their origin and give us glimpses of how they manifest in our bodies. The more we understand these signatures, the more likely we will be able to intervene at a critical junction and design and provide therapies that lessen or cure disease,” said Raman.

The findings have been published online March 28 in Nature Medicine. (ANI)

Sunlight may play a bigger role than vitamin D in controlling multiple sclerosis

Washington, Mar 23 (ANI): Ultraviolet portion of sunlight plays a bigger role than vitamin D in controlling multiple sclerosis (MS), according to researchers at University of Wisconsin-Madison.

For more than 30 years, scientists have known that multiple sclerosis (MS) is much more common in higher latitudes than in the tropics.

Because sunlight is more abundant near the equator, many researchers have wondered if the high levels of vitamin D engendered by sunlight could explain this unusual pattern of prevalence.

Vitamin D may reduce the symptoms of MS, but it is the ultraviolet portion of sunlight that has a major role in controlling MS, according to Hector DeLuca.

The ultraviolet (UV) portion of sunlight stimulates the body to produce vitamin D, and both vitamin D and UV can regulate the immune system and perhaps slow MS.

But researchers were not clear of the immune regulation result directly from the UV, indirectly from the creation of vitamin D, or both.

The study was designed to distinguish the role of vitamin D and UV light in explaining the high rate of MS away from the equator, said DeLuca, a world authority on vitamin D.

“Since the 1970s, a lot of people have believed that sunlight worked through vitamin D to reduce MS. It”s true that large doses of the active form of vitamin D can block the disease in the animal model. That causes an unacceptably high level of calcium in the blood, but we know that people at the equator don”t have this high blood calcium, even though they have a low incidence of MS. So it seems that something other than vitamin D could explain this geographic relationship,” says DeLuca.

Using mice that are genetically susceptible to MS-like disease, the researchers triggered the disease by injecting a protein from nerve fibers.

Then the mice were exposed to moderate levels of UV radiation for a week. After they initiated disease by injecting the protein, they irradiated the mice every second or third day.

The UV exposure (equivalent to two hours of direct summer sun) did not change how many mice got the MS-like disease, but it did reduce the symptoms of MS, especially in the animals that were treated with UV every other day, said DeLuca.

The team also found that although the UV exposure did increase the level of vitamin D, that effect, by itself, could not explain the reduced MS symptoms.

In some situations, radiation does reduce immune reactions, but it”s not clear what role that might play in the current study.

“We are looking to identify what compounds are produced in the skin that might play a role, but we honestly don”t know what is going on. Somehow it makes the animal either tolerate what”s going on, or have some reactive mechanism that blocks the autoimmune damage,” said DeLuca. (ANI)

Master gene that switches on disease-fighting cells identified

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)

Scientists developing probiotics to ambush disease-causing gut bacteria

Washington, Sept 8 (ANI): Scientists from University of Adelaide are working on developing diversionary tactics in a bid to fool disease-causing gut bacteria that often lead to infections, such as cholera.

According to Professor James Paton, bacteria produce toxins that damage human tissues when they bind to complex sugar receptors displayed on the surface of cells in the host’s intestine.

In the new study, researchers have shown how they had added molecular mimics of these host cell receptors onto the surface of harmless bacteria capable of surviving in the human gut.

If given during an infection caused by a toxin-producing bacterium, these “receptor-mimic probiotics” will bind the toxins in the gut very strongly, thereby preventing the toxins from interacting with receptors on host intestinal cells and causing disease.

An advantage of this approach to treatment is that the pathogenic bacteria are unlikely to develop a resistance to it, as that would destroy the basic mechanism by which they cause disease.

Moreover, receptor-mimic bacteria bind toxins more strongly than previous technologies.

They are also more cost effective, as the bacteria can be grown cheaply in large-scale fermenters.

“We initially developed this technology to prevent disease caused by strains of E. coli bacteria that produce Shiga toxin. These include the infamous E. coli O157 strain, which causes outbreaks of severe bloody diarrhoea and the potentially fatal haemolytic uraemic syndrome,” said Paton.

“Our prototype receptor mimic probiotic provided 100% protection against otherwise fatal E. coli disease in an animal model. We have also developed similar receptor mimic probiotics that are capable of preventing cholera and travellers’ diarrhoea.

“As well as being able to treat disease, these probiotics could be given to vulnerable populations following natural disasters to help prevent outbreaks of diseases like cholera,” he added.

The findings were presented at the Society for General Microbiology’s meeting at Heriot-Watt University, Edinburgh. (ANI)

Turmeric root cuts breast cancer risk in postmenopausal women

Washington, July 14 (ANI): Curcumin, a popular Indian spice derived from the turmeric root, can help reduce cancer risk among postmenopausal women exposed to hormone replacement therapy, according to University of Missouri researchers.

Studies conducted in the past have suggested that a combined oestrogen and progestin hormone replacement therapy increases postmenopausal women’s risk of developing progestin-accelerated breast tumours.

“The results of our study show that women could potentially take curcumin to protect themselves from developing progestin-accelerated tumours,” said Salman Hyder, the Zalk Endowed Professorship in Tumor Angiogenesis and professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Centre.

The study conducted using animal model showed that curcumin delayed the first appearance, decreased incidence and reduced multiplicity of progestin-accelerated tumours.

Curcumin also prevented the appearance of gross morphological abnormalities in the mammary glands.

The research team previously showed that progestin accelerates the development of certain tumors by increasing production of a molecule called VEGF that helps supply blood to the tumour.

And blocking the production of VEGF could potentially reduce the proliferation of breast cancer cells.

Hyder said that curcumin inhibits progestin-induced VEGF secretion from breast cancer cells.

“Curcumin and other potential anti-angiogenic compounds should be tested further as dietary chemopreventive agents in women already exposed to hormone replacement therapy containing estrogen and progestin in an effort to decrease or delay the risk of breast cancer associated with combined hormone replacement therapy,” Hyder said.

The study has been published in Menopause, a journal of the North American Menopause Society. (ANI)

Swine flu can travel to the lungs and gut

London, July 3 (ANI): The deadly swine flu virus has the potential to reach deep into the respiratory system, and even as far as the intestines, according to two new studies on ferrets.

The above findings could explain why the disease’s symptoms are different from those of seasonal flu.

The studies were conducted by two separate groups that have been using ferrets to investigate how harmful A(H1N1) influenza virus is, and how easily it is transmitted.

One of the studies was led by Terrence Tumpey at the Centers for Disease Control and Prevention in Atlanta, Georgia, whose colleagues put droplets of three different swine flu viruses, and one ‘seasonal’ flu virus, into the noses of ferrets.

Some ferrets shared cages with other uninfected ferrets, and some were placed in cages next to other ferrets, sharing nothing but the air they breathed.

It was found that the ferrets with swine flu strains lost more weight than those with normal flu, and that the swine flu reached lower down into the lungs of some of the ferrets than normal seasonal flu, penetrating the intestines in some cases.

This tallies with observations in humans that some patients suffered vomiting and diarrhoea.

In a second study, led by Ron Fouchier at the Erasmus University Medical Center, Rotterdam, the Netherlands, it was found that the virus could penetrate the lungs.

“This is the first indication of how pathogenic [swine flu] really is. In the field that conclusion is hard to draw,” Nature magazine quoted Fouchier as saying.

Ferrets have long been used as an animal model for flu because they show similar symptoms to humans, and tend to last the same amounts of time in both species.

The studies showed that the virus wasn’t transmitted between animals as efficiently as the seasonal flu, but Fouchier’s results indicated that the virus was transmitted just as efficiently as seasonal flu.

The studies have been published in Science. (ANI)

Scientists suggest new animal model to test carcinogen risk

Washington, June 19 (ANI): Researchers at Oregon State University have suggested a new and improved method to test carcinogen risk.

They said that trout can be a superior animal model than laboratory rats, and other traditional methods of assessing the risk of carcinogens.

“The whole foundation of modern toxicology is that the dose makes the poison,” said George Bailey, an OSU distinguished professor emeritus of molecular and environmental toxicology.

“You can die from eating a few tablespoons of ordinary table salt at one time, but that doesn’t mean that table salt is a poison at the doses that humans normally consume.

“With compounds that we know can cause cancer, the real question is how much is too much.

“What we have found is that traditional approaches to making that evaluation, which are almost always based on studies done at very high doses with laboratory rodents, may not always give us answers that are reasonably accurate,” he added.

Researchers are usually trying to determine what can cause cancer at levels considered unacceptable.

However, the age-old problem they have faced is the cost and laboratory logistics making it virtually impossible to test millions of rats.

“When using rodents, it simply was not possible to study larger numbers of animals, the cost was too prohibitive,” said Linus Pauling Institute at OSU.

The Oregon State University researchers have revealed that rainbow trout may for many purposes be as or more accurate in determining what compounds, at what levels, can pose a risk of human cancer.

They have pioneered the use of trout for studies of this type for 40 years, and researchers believe that it may now be time to greatly expand the use of that research.

“We can do experiments with trout in large numbers at very low cost, about 5 percent of what a rodent study would cost,” she said.

“For most studies of carcinogens, exposing 2,000 rodents would be a huge project. For us, working with 2,000 trout is a pilot study,” she added.

The OSU scientists recently completed the largest study ever done with animals in toxicology, exposing 40,800 trout to what’s considered an “ultra-low” dose of dibenzo-a,l-pyrene, a chemical that can cause liver cancer and is part of a broad field of toxic compounds called polycyclic aromatic hydrocarbons, or PAHs.

The study determined that a tolerable threshold for human exposure to this toxic chemical would be 500 to 1,500 times higher than is outlined by the Environmental Protection Agency.(ANI)

How high glucose levels damage blood vessels

Washington, May 12 (ANI): Medical College of Georgia researchers have gained fresh insights into how elevated glucose levels, which occur in diabetes, damage blood vessels.

The mechanism can lead to novel strategies for blocking the destruction.

High glucose levels reduce the levels of the powerful vasodilator nitric oxide in blood vessels, a shortfall that increases the risk of high blood pressure and eventual narrows down the vessels.

Rita C. Tostes, physiologist in the MCG School of Medicine, found that decreased ability of blood vessels to relax resulted from increased activity of a natural mechanism for altering protein form and function.

The researchers suspect that increased modification of proteins by a glucose-derived molecule is a player in vascular problems associated with hypertension, stroke and obesity as well.

“We know diabetes is a major risk factor for cardiovascular disease and we think this is one of the reasons,” said Tostes.

In the study conducted over healthy mice, the researchers found that there was an increased activity by O-GlcNAc in the blood vessels, which competes with another mechanism for modifying proteins called phosphorylation.

In blood vessels, phorphorylation modifies the enzyme that produces nitric oxide, called nitric oxide synthase, so that it makes more of the blood vessel dilator.

O-GlcNAc seems to beat phosphorylation to the punch so there is the opposite result.

The longer O-GlcNAc levels were high, the worse the resulting problem, said Victor Lima, a graduate student at the University of Sao Paulo working with Dr. Tostes.

An animal model of hypertension confirmed the finding that the more O-GlcNAc, the more blood vessels contract because these animals had higher O-GlcNAc levels.

“Now we are trying to see why this is happening and what comes first. Is increased blood pressure leading to changed O-GlcNAc or are augmented levels of O-GlcNAc contributing to the change we see in the vasculature of hypertensives?” said Dr. Tostes.

“If we know how this changes vascular function, we can understand some of the dysfunction that we see in diabetes,” she added.

The study was presented at American Society of Hypertension 24th Annual Scientific Program in San Francisco. (ANI)

How a single gene causes severe mental retardation

London, May 11 (ANI): Experiments on mice conducted by scientists at Duke University Medical Center and the University of North Carolina have significant insights into how a single disrupted gene can cause a form of severe mental retardation, Angelman syndrome.

The researchers have found that the UBE3A gene is key to the formation of neurons in the brain, and the adjustment of their connections to other neurons for storing sensory information.

The researchers also observed that when the mice were deprived of sensory stimulation, the brain connections could be recovered.

They said that that finding indicated a pharmaceutical or behavioural treatment might be possible in future.

“We wanted to look at an animal model to learn if this experience-dependent reorganization of the cortex was abnormal in animals that were missing the gene,” Nature magazine quoted Dr. Michael Ehlers, a Duke professor of neurobiology and co-senior author of the study, as saying.

“We looked at the visual cortex, because in this well-studied model, we could precisely control the sensory stimulus and study the mice in the light or the dark. We speculated that similar deficits may be happening in areas of the cortex that are important for language, cognition and emotion, all of which are quite abnormal in Angelman syndrome patients,” he added.

The study showed that brains cells in Angelman syndrome mice lacked the ability to appropriately strengthen or weaken in the cortex, an area of the brain important for cognitive abilities.

“Instead of studying a complex learning model, we studied how connections between brain cells change in visual areas of mice exposed to light or kept in darkness. This approach revealed that brain cells in normal mice can modify their connections in response to changes in visual experiences, while the brain cells in Angelman syndrome mice could not,” said Dr. Koji Yashiro, a former University of North Carolina graduate student and lead author of the study.

According to the researchers, the inability of brain cells to encode information from experiences in the Angelman syndrome model suggested that it was the basis for the profound learning difficulties in these patients.

They were surprised to see that the plasticity of the cellular connections could be restored in visual areas of the brain after brief periods of visual deprivation.

“By showing that brain plasticity can be restored in Angelman syndrome model mice, our findings suggest that brain cells in Angelman syndrome patients maintain a latent ability to express plasticity. We are now collaborating to find a way to tap into this latent plasticity, as this could offer a treatment, or even a cure, for Angelman syndrome,” said Dr. Ben Philpot, a University of North Carolina professor in Cell and Molecular Physiology and co-senior author of the study.

Ehlers believes that perhaps some of these developmental brain disorders are a form of social and cognitive blindness. In a condition known as amblyopia, or cortical blindness, the eye can function normally, but past a critical period, the brain cannot process the sensory input correctly.

“We think that children with Angelman syndrome may have a condition in which sensory experience dampens down plasticity and affects learning. One important aspect of our findings is that sensory manipulations recovered plasticity, suggesting that the underlying substrates for plasticity are intact in mice. If the same thing holds true for the human disease, there may be a chance to improve brain function,” Ehlers said.

A research article on the study has been published in the journal Nature Neuroscience. (ANI)

Novel animal model provides sciatica insights

Washington, Apr 30 (ANI): Duke University bioengineers and surgeons have developed a new animal model for the painful nerve condition, known as sciatica, which could offer insights to help researchers diagnose and treat it.

Sciatica is characterised by numbness or pain from the lower back to the feet, radiating leg pain or difficulty in controlling the leg.

It is often caused by compression, or pinching, of any of the five nerve roots that combine to make up the sciatic nerve. These roots are the parts of the nerve that pass through openings in the spine to the spinal cord.

Dr. Mohammed Shamji, a neurosurgery resident, led the surgical simulation of nerve compression in rats, and observed that the animals’ gait became asymmetric, and that they over-responded to temperature changes and touch in their limbs after the surgery.

And for the first time, they found that the physical symptoms experienced by the affected animals were apparently linked to an increase in levels of interleukin-17 (IL-17)-a protein involved in regulating the inflammatory response.

Already, increased IL-17 levels have been implicated in such autoimmune diseases as rheumatoid arthritis and asthma.

“This finding suggests a possible role for immune system activation in contributing to symptoms of sciatica. This offers new insight into the pathophysiology of the disease, and may also identify novel therapeutic targets to treat it,” said Shamji.

“If immune system activation is involved, and it turns out to be an important part of the condition, it is possible that existing or new drugs that can block this immune response could offer relief to patients. This new model should help us find answers for a disorder that has few good treatments,” said a co-author of the study.

The results of the study were published online in the journal Spine. (ANI)

Indian scientists complete full genome sequencing of the striped Zebra fish

With the consistent, almost two months-long efforts of the scientists at the Institute of Genomics and Integrative Biology (IGIB), New Delhi, a striped ‘Zebra fish,’ picked up from a rivulet in Assam, has become the first vertebrate in India to have its whole genome sequenced.

The Indian scientists sequenced nearly 1.7 billion genetic alphabets that make up the full genome of the Zebra fish. Along with being native to Indian rivers, the barely four centimeter long striped fish is popular in household aquariums and is widely considered an ideal organism for studying human genes, as it has blood, eye, heart, kidney and other biological processes similar to the human system.

Talking about the significance of having worked out the genome sequence, Dr. Vinod Scaria, IGIB’s research team member, said: “After the mouse, the zebrafish is the most favoured animal model for human diseases. The zebrafish may be used to study the mechanics of a variety of human diseases – cardiovascular diseases, genetic disorders, blood disorders, muscle and bone diseases.”

In order to complete the Zebra fish sequence, high-speed sequencers and computers were used by the researchers, who have now embarked on the next phase of the research called ‘Project Kaurava’, by launching the world’s first endeavor towards comparison of genetic variations in 100 siblings from a single parent zebrafish.

Lipoic acid supplements can reduce heart attack risk

Washington, Mar 31 (ANI): A new study has shown that dietary supplementation with lipoic acid, a natural compound found at low levels in red meat and green leafy vegetables, can significantly reduce triglycerides, a key risk factor in cardiovascular disease.

While experimenting on rats, the researchers found that supplements of lipoic acid lowered triglyceride levels up to 60 percent.

“The extent of triglyceride reduction was really dramatic, we didn’t expect it to be this profound,” said Regis Moreau, an assistant professor with the Linus Pauling Institute at Oregon State University.

“The potential is good that this could become another way to lower blood triglycerides and help reduce the risk of atherosclerosis. It’s pretty exciting,” he added.

The researchers found that supplements of lipoic acid appeared to affect triglyceride levels through two pathways.

They said that lipoic acid supplementation increased the rate of disappearance of triglycerides in the bloodstream, and reduced the genetic expression of enzymes in the liver that synthesize triglycerides.

“We believe that a novel means of controlling triglyceridemia in this animal model has been revealed,” wrote the researchers.

“Given its strong safety record, lipoic acid may have therapeutic applications for the treatment or prevention of hypertriglyceridemia and diabetic dyslipidemia in humans,” they added.

The results appear in the Archives of Biochemistry and Biophysics. (ANI)

Spinal cord stimulator shows promise to treat Parkinson’s disease

Washington, Mar 20 (ANI): A novel device implanted inside the spinal cord might offer an effective treatment against Parkinson’s disease, according to a study.

Researchers at Duke University Medical Centre have developed a prosthetic device, which applies electrical stimulation to the dorsal column in the spinal cord, the main sensory pathway carrying tactile information from the body to the brain.

In an animal study, the team attached the device to the surface of the spinal cord in mice and rats with depleted levels of the chemical dopamine – mimicking the biologic characteristics of someone with Parkinson’s disease along with the impaired motor skills seen in advanced stages of the disease.

When the device was turned on, the dopamine-depleted animals’ slow, stiff movements were replaced with the active behaviours of healthy mice and rats.

The improvement in motor skills was observed within 3.35 seconds after stimulation.

“We see an almost immediate and dramatic change in the animal’s ability to function when the device stimulates the spinal cord,” said senior study investigator Dr Miguel Nicolelis, the Anne W. Deane Professor of Neuroscience at Duke.

“Moreover, it is easy to use, significantly less invasive than other alternatives to medication, such as deep brain stimulation, and has the potential for widespread use in conjunction with medications typically used to treat Parkinson’s disease,” Nicolelis added.

When the device was used without additional medication, Parkinsonian animals were 26 times more active.

However, when stimulation was coupled with medication, only two doses of dopamine replacement therapy were needed to produce movement, compared to five doses when the medication was used by itself.

Nicolelis said that the low frequency seizures, or oscillations, seen in the animal model of Parkinson’s disease had been observed in humans with the condition.

Stimulating the dorsal column of the spinal cord reduces these oscillations, which researchers believe creates the ability to produce motor function.

“Our device works as an interface with the brain to produce a neural state permissive for locomotion, facilitating immediate and dramatic recovery of movement,” said Per Petersson, co-author of the study.

“Following stimulation, the neurons desynchronize, similar to the firing pattern that you would see when a healthy mouse is continuously moving,” Petersson added. The study appears in the journal Science (ANI)

Lab grown transplantable tissue encourages nerve regeneration in animal model

Washington, March 20 (ANI): Scientists at the University of Pennsylvania School of Medicine have announced the creation of transplantable living nerve tissue that encourages and guides regeneration in an animal model.

Dr. Douglas H. Smith, a professor in the Department of Neurosurgery and Director of the Center for Brain Injury and Repair at Penn, says that he and his colleagues have successfully grown, transplanted, and integrated axon bundles that act as “jumper cables” to the host tissue in order to bridge a damaged section of nerve.

This advance attains significance because there are insufficient means for repairing peripheral nerve injuries that, in many cases, result in permanent loss of motor function, sensory function, or both.

Previously, Smith and colleagues have “stretch-grown” axons (nerve fibres) by placing neurons from rat dorsal root ganglia, clusters of nerves just outside the spinal cord, on nutrient-filled plastic plates.

Axons sprouted from the neurons on each plate and connected with neurons on the other plate, which were then slowly pulled apart over a series of days, aided by a precise computer-controlled motor system.

The nerves were elongated to over 1 cm over seven days, after which they were embedded in a protein matrix (with growth factors), rolled into a tube, and then implanted to bridge a section of nerve that was removed in a rat.

“That creates what we call a ‘nervous-tissue construct’. We have designed a cylinder that looks similar to the longitudinal arrangement of the nerve axon bundles before it was damaged. The long bundles of axons span two populations of neurons, and these neurons can have axons growing in two directions – toward each other and into the host tissue at each side,” says Smith.

The researcher said that the constructs were transplanted to bridge an excised segment of the sciatic nerve in rats. Sixteen weeks after the transplantation, the constructs still had their pre-transplant shape, with surviving transplanted neurons at the extremities of the constructs spanned by tracts of axons.

The authors observed that the host axons seemed to use the transplanted axons as a living scaffold to regenerate across the injury.

They found host and graft axons intertwined throughout the transplant region, suggesting a new form of axon-mediated axonal regeneration.

“Regenerating axons grew across the transplant bridge and became totally intertwined with the transplanted axons,” says Smith.

The constructs survived and integrated without the use of immunosuppressive drugs, challenging the conventional wisdom regarding immune tolerance in the peripheral nervous system.

The researchers suspect that the living nerve-tissue construct encourages the survival of the supporting cells left in the nerve sheath away from the injury site, which further guide regeneration and provide the overall structure of the nerve.

“This may be a new way to promote nerve regeneration where it may not have been possible before,” says co-first author Dr. D. Kacy Cullen, a post doctoral fellow in the Smith lab.

“It’s a race against time – if nerve regeneration happens too slowly, as may be the case for major injuries, the support cells in the extremities can degenerate, blunting complete repair. Because our living axonal constructs actually grow into the host nerve sheath, they may ‘babysit’ these support cells to give the host more time to regenerate,” Cullen added.

A research article on this work has been published in the journal Tissue Engineering. (ANI)

Stressful memories may soon be history

Washington, Mar 18 (ANI): Scientists have suggested a new strategy to treat the distress related to traumatic memories.

Their strategy is based on the study of a drug, RU38486, which blocks the effects of the stress hormone cortisol.

Posttraumatic stress disorder (PTSD) is among the most common and disabling psychiatric casualties of combat and other extremely stressful situations.

People suffering from PTSD often suffer from vivid intrusive memories of their traumas.

Current medications are often ineffective in controlling these symptoms and so novel treatments are needed urgently.

Using an animal model of traumatic memory, researchers at the Mount Sinai School of Medicine has shown that treatment with RU38486 selectively reduces stress-related memories, leaving other memories unchanged.

They also found that the effectiveness of the treatment is a function of the intensity of the initial “trauma.”

Although this particular study was performed in rats, their findings help to set the stage for trials in humans.

Cristina Alberini, Ph.D., co-author of the study, explained how the findings would translate into developing clinical parameters: “First, the drug should be administered shortly before or after recalling the memory of the traumatic event. Second, one or two treatments are sufficient to maximally disrupt the memory.

“Third, the effect is long lasting and selective for the recalled memory. Finally, the time elapsing between the traumatic experience and the treatment seems to be an important parameter for obtaining the most efficacious treatment,” Alberini added.

Alberini said that “these results suggest that carefully designed combinations of behavioral and pharmacological therapies may represent novel, effective treatments for PTSD or other anxiety disorders.”

The study has published in the February 1st issue of Biological Psychiatry. (ANI)

Stem cells may stop osteoporosis, promote bone growth

Washington, Mar 5 (ANI): A new study has shown that tweaking a certain group of multipotent stem cells-mesenchymal stem cells-with a hormone called interferon (IFN) in our bodies, might stop osteoporosis and promote bone growth.

Scientists from the Research Institute of the McGill University Health Centre say that IFN holds great promise to repair bones affected by osteoporosis.

“We have identified a new pathway, centered on IFN gamma, that controls the bone remodelling process both in-vivo and in-vitro.

More studies are required to describe it more precisely, but we are hopeful that it could lead to a better understanding of the underlying causes of osteoporosis, as well as to innovative treatments,” said Dr. Richard Kremer, the study’s lead author and co-director of the Musculoskeletal Axis of the McGill University Health Centre.

He added: “First, we stimulated cultured mesenchymal stem cells to turn into bone cells (osteoblasts) in-vitro. We realised that this differentiation process involved IFN gamma-related genes, but also that these bone cells precursors could both be stimulated by IFN gamma and produced IFN gamma.”

In the next step, the researchers focussed on an animal model where IFN gamma effect is blocked by inactivating its receptor-a model called IFN gamma receptor knock-out.

They later conducted bone density tests, comparable to those used to diagnose people with osteoporosis.

The results revealed that the animals had significantly lower bone mass than their healthy counterparts, and also the mesenchymal stem cells were found to have a decreased ability to make bone.

“These findings confirm that IFN gamma is an integral factor for mesenchymal stem cells’ differentiation into osteoblasts also in-vivo,” said Kremer.

Both in-vitro and in-vivo results proved that IFN gamma was key to the differentiation of mesenchymal cells into bone cells, and to growth process of the bone.

The findings provide hope that IFN gamma itself, or another molecule involved in its pathway, could soon become efficient drug-target for an antidote for osteoporosis.

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