Vitamin C can help protect DNA damage of skin cells

Washington, Sept 10 (ANI): Researchers at the University of Leicester and Institute for Molecular and Cellular Biology in Portugal have found that vitamin C can help protect DNA damage of skin cells and lead to better skin regeneration.

Previous research has shown that DNA repair is upregulated in people consuming vitamin C supplements.

In the new study, the researchers have provided some mechanistic evidence.

The researchers used affymetrix microarray, for looking at gene expression, and the ‘Comet’ assay to study DNA damage

“The exposure to solar ultraviolet radiation increases in summer, often resulting in a higher incidence of skin lesions. Ultraviolet radiation is also a genotoxic agent responsible for skin cancer, through the formation of free radicals and DNA damage,” said lead researcher Tiago Duarte, formerly of the University of Leicester, and now at the Institute for Molecular and Cellular Biology in Portugal.

“Our study analysed the effect of sustained exposure to a vitamin C derivative, ascorbic acid 2-phosphate (AA2P), in human dermal fibroblasts.

“We investigated which genes are activated by vitamin C in these cells, which are responsible for skin regeneration.

“The results demonstrated that vitamin C may improve wound healing by stimulating quiescent fibroblasts to divide and by promoting their migration into the wounded area. Vitamin C could also protect the skin by increasing the capacity of fibroblasts to repair potentially mutagenic DNA lesions,” Duarte added.

The researchers hope that the results will be of great relevance to the cosmetics industry.

“The study indicates a mechanism by which vitamin C could contribute to the maintenance of a healthy skin by promoting wound healing and by protecting cellular DNA against damage caused by oxidation,” said Dr Marcus S. Cooke from the Department of Cancer Studies and Molecular Medicine and Department of Genetics, at the University of Leicester.

“These findings are particular importance to our photobiology interests, and we will certainly be looking into this further,” Cooke added.

The findings have been published in the journal Free Radical Biology and Medicine. (ANI)

How females control sperm storage to pick the best dad

Washington, Sept 9 (ANI): University of Exeter researchers have found new evidence to explain how female insects can influence the father of their offspring, even after mating with up to ten males.

In the study, boffins found that female crickets are able to control the amount of sperm that they store from each mate to select the best father for their young.

According to researchers, the females may be using their abdominal muscles to control the amount of sperm stored from each mate.

The study has been published in the journal Molecular Ecology.

Female crickets mate with several different males, including their closest relatives. In general, offspring produced with close relatives are more likely to have genetic disorders.

Different animals employ a range of behaviours to avoid this, such as not mating other animals from the group they grow up in. Crickets do not avoid mating with relatives, but this research shows that they produce more offspring fathered by males that are unrelated to them.

In order to reach the conclusion, researchers bred field crickets in the laboratory. They used new DNA-based techniques to determine the quantity stored by each the female. hey found that the females stored a higher content of sperm from unrelated males. They then tested young crickets to determine their paternity.

The results showed that, regardless of the order in which they had mated, an unrelated mate was more likely to become a father. This must have been under female control, because the methods the team used meant that males could not influence the amount of sperm they passed to the female.

Though the study focused on field crickets, the findings are likely to be relevant in other insect species and possibly other sections of the animal kingdom.

Lead author Dr Amanda Bretman of the University of Exeter said: “Our study shows that even after mating, female insects control who fathers their offspring. We’re only really just beginning to understand the reasons for the different mating strategies in the insect world and that is thanks to new techniques.” (ANI)

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

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)

Novel device to wash away bedsores, chronic ulcers

Washington, Aug 27 (ANI): Researchers at Tel Aviv University have developed a unique device, called Dermastream, which could heal bedsores and chronic ulcers in bedridden elderly and infirm.

When ill, such people are prone to painful and dangerous pressure ulcers, and diabetics are susceptible to wounds caused by a lack of blood flow to the extremities.

“The problem is chronic,” said Prof. Amihay Freeman of TAU’s Department of Molecular Microbiology and Biotechnology.

And thus, he developed Dermastream, that uses a solution to whisk away dead tissue, bathing the wound while keeping dangerous bacteria away.

The device provides an enzyme-based solution that flows continuously over the wound, offering an alternative treatment to combat a problem for which current treatments are costly and labour-intensive.

Freeman said that Dermastream has already passed clinical trials in Israeli hospitals and may be available in the U.S. within the next year.

Dermastream employs a special solution developed at Freeman’s TAU laboratory, thus offering a new approach to chronic wound care- a specialty known as “continuous streaming therapy.”

“Our basic idea is simple. We treat the wound by streaming a solution in a continuous manner. Traditional methods require wound scraping to remove necrotic tissue. That is expensive, painful and extremely uncomfortable to the patient.

And while active ingredients applied with bandages on a wound may work for a couple of hours, after that the wound fights back. The bacteria build up again, creating a tedious and long battle,” said Freeman.

Dermastream “flows” under a plastic cover that seals the wound, providing negative pressure that promotes faster healing.

The active biological ingredient, delivered in a hypertonic medium, works to heal hard-to-shake chronic wounds.

Freeman said that while traditional bandaging methods may take months to become fully effective, Dermastream can heal chronic wounds in weeks.

Dermastream is intended for use in hospitals, nursing homes, outpatient clinics and homecare.

Freeman has founded a company that is currently collaborating with a Veterans Association hospital in Tucson, AZ, to bring the technology to the U.S. market.

“My solution helps doctors regain control of the chronic wound, making management more efficient, and vastly improving the quality of their patients’ lives,” concluded Freeman. (ANI)

Scientists establish new link between pre-eclampsia and diet

Washington, August 26 (ANI): A new study has shown that pregnant women with pre-eclampsia have unusually high levels of a chemical compound called ‘ergothioneine’, which is found in unpasteurised food, in the red blood cells.

The finding made by scientists at the University of Leeds attains significance because they suggest that ergothioneine is an indicator of pre-eclampsia, and may help scientists to understand the cause of the condition, which is currently unknown.

The researchers took blood samples from a group of 37 pregnant women, and compared the red blood cells from women with pre-eclampsia with those from women with no symptoms.

Writing about their findings in the journal Reproductive Sciences, the researchers said that they found a significantly higher concentration of the ergothioneine – a compound made by fungi – in the red blood cells of the women with pre-eclampsia.

Ergothioneine is already well known to be made by micro-organisms that are commonly found in foods like unpasteurised dairy products. Since humans cannot synthesise it, the compound finds its way into human cells exclusively through our diet.

Pregnant women are not advised against eating fungi or foods such as unpasteurised dairy products which contain ergothioneine producing fungi. In fact, scientific studies on animals highlight the benefit of ergothioneine.

“These results suggest that a higher level of ergothioneine is an indicator of pre-eclampsia,” says lead researcher Dr. Julie Fisher, a chemist at the University of Leeds.

“I would not recommend that pregnant women stop eating fungi. However, the high concentration of ergothioneine in the red blood cells of women with pre-eclampsia is a very interesting finding – the more we know about the chemicals involved in the disease the closer we get to understanding what causes it,” says Professor James Walker, Professor of Obstetrics at the Leeds Institute of Molecular Medicine (LIMM), and a co-author of the research.

The symptoms of pre-eclampsia include high blood pressure, protein in urine and fluid retention and affects almost 10 per cent of pregnancies after 20 weeks. If left untreated, the condition can cause a range of problems, such as growth restriction in babies and even foetal and maternal mortality. There is no known cause of the condition.

“Ergothioneine is known as an antioxidant and antioxidants have been proposed to be helpful in reducing the risk of preeclampsia. It is therefore very interesting that we have found it to be in excess for women with the condition,” says Dr. Fisher.

The researchers used a technique that is based on the same science as MRI scans, but which operates on fluids taken from the body, to identify chemicals in the red blood cells of pregnant women.

They say that the amount of these chemicals was found to depend on whether the women were healthy or whether they were suffering from pre-eclampsia.

They previously found that chemical markers for pre-eclampsia also exist in blood plasma. (ANI)

Regulation of ‘short stature’ gene crucial for growth in kids

Washington, August 26 (ANI): A team of researchers in Germany have found that not only a gene called SHOX is involved in the development of short stature, but sequences of genetic material on the X and Y chromosome that regulate it are also crucial for growth in children.

Professor Gudrun Rappold, the Director of the Department of Human Molecular Genetics at Heidelberg University Hospital, points out that these gene regulators determine how frequently a gene is copied, and, thus, how effective it is.

In many cases, she says, the mutation of one regulatory sequence of the SHOX gene is sufficient to give rise to the full-blown syndrome.

Publishing their results in the Journal of Medical Genetics, she and her colleagues have said that their findings may open up new possibilities for diagnosing the cause of short stature, and initiating treatment before it is too late.

According to background information in the report, the SHOX gene (short stature homeobox gene) is responsible for the normal growth of bones, and is often mutated in short-stature patients-no more than 160 cm of final height in men, and 150 cm in women.

Hormone disorders, malnutrition, chronic disease, or a genetic disorder are some of the causes of short stature. If, in addition to short stature, other symptoms such as short forearms and lower legs or other bone malformations also occur, it is considered a syndrome.

However, often no exact cause can be determined and other typical features are lacking – this is then known as idiopathic short stature.

In 2007, a research team led by Professor Rappold found that in over 4 percent of children with idiopathic short stature, the trigger for the disorder was a mutation in the SHOX gene. er latest study has shown that not only the gene itself, but its regulators as well can be crucial for developing the disease.

During the study, the researchers examined the genetic material from a total of 893 subjects.

About 5 percent of the patients with idiopathic short stature, and 80 percent of the patients with Leri-Weill syndrome, had mutations in the segment either including or around the SHOX gene.

The researchers said that some patients had an intact SHOX gene, but an unexpectedly high number of mutations in its enhancer sequences: for 26 percent of patients with SHOX deficiency and idiopathic short stature and for 45 percent of patients with SHOX deficiency and Leri-Weill syndrome, the disease could be attributed solely to a genetic mutation of the enhancer sequence.

“The astounding thing is that this enhancer mutation is quite far away from the affected gene and yet it still leads to the exact same clinical symptoms as a mutation in the gene itself,” said Professor Rappold.

The researchers hope that their results will give them a better understanding of the causes of the disease, and allow them to optimise the diagnostic possibilities for patients with SHOX gene mutations.

“Patients who suffer from their short stature often have a great need to be able to name the cause. Even if it is not possible to treat the cause, patients with mutations of the SHOX gene can benefit from a treatment of the symptoms with growth hormones,” said Professor Rappold. (ANI)

Schizophrenia linked to specific DNA region

London, July 9 (ANI): An international group of researchers have for the first time come up with genetic evidence linking schizophrenia to a specific region of DNA – on chromosome 6.

Lead researcher Nancy Buccola, Assistant Professor of Clinical Nursing at LSU Health Sciences Center New Orleans, says that this is the same area where key genes for immune function are located.

The researchers recruited study participants, people with diagnoses of schizophrenia or schizoaffective disorder, as well as controls from the general population.

They analysed data collected and also conducted a meta-analysis of data from the Molecular Genetics of Schizophrenia, International Schizophrenia Consortium and SGENE data sets – thousands of DNA samples.

The team point out that while a single gene does not appear to be the source of the development of schizophrenia, variations on chromosome 6 appeared to be associated with higher risk.

According to them, these variations were found most often in people with schizophrenia, leading the scientists to believe that these common variations contribute to the development of schizophrenia.

They further said that the area of chromosome 6, in the same area where genes important to the immune system function, provokes questions about whether or not treatments for autoimmune disorders might also be helpful in treating schizophrenia.

“Schizophrenia can be a devastating disease, and while treatments are improving, there are still people who do not respond or only partially respond,” Nature magazine quoted Buccola, principal investigator on the LSUHSC study, as noting.

“Understanding the underpinnings of this illness will open doors to new and potentially better treatments,” the researcher added.

The research was supported by funding from the National Institute of Mental Health and the National Alliance for Research on Schizophrenia and Depression.

“Scientists have been looking for schizophrenia susceptibility genes since the early 1900s. This study shows that these genes can be found and sets the stage for future research,” says Buccola. (ANI)

20 cholesterol-regulating genes identified

Washington, July 8 (ANI): Scientists at the European Molecular Biology Laboratory (EMBL) and the University of Heidelberg, Germany, have identified 20 genes that play a vital role in maintaining cholesterol balance.

The researchers believe that the newly identified genes may help uncover the mechanisms that regulate cholesterol levels, and lead to new treatments for cholesterol-related diseases.

“This finding may open new avenues for designing targeted therapies, for example by looking for small molecules that could impact these genes,” said Heiko Runz, whose group at the University Clinic Heidelberg carried out the research together with Rainer Pepperkok’s lab at EMBL.

High levels of cholesterol in the bloodstream are a major risk factor for atherosclerosis and coronary heart disease.

During the study, the researchers deprived isolated human cells of cholesterol, and then looked at the whole genome to find the genes that react to changes in cholesterol levels by altering their expression.

With a microscope, they then observed what effect switching off different genes had both on cholesterol uptake and on the total amount of cholesterol inside cells.

Of the 20 genes the scientists identified as involved in regulating cholesterol levels and uptake, 12 were previously unknown.

The scientists are now trying to discover exactly how the novel genes regulate cholesterol levels inside cells, as well as looking at patients to determine whether these genes (or alterations in them) do constitute risk factors, and investigating if and how they could be useful drug targets.

The study appears in journal Cell Metabolism. (ANI)

Microscopic ‘beads’ may revolutionise organ transplantation

Washington, July 7 (ANI): If Medical College of Georgia researchers are to be believed, organ transplantation in future may include microscopic beads that create “designer” immune cells so that patients may tolerate their new organ.

Dr. Anatolij Horuzsko, reproductive immunologist at the MCG Center for Molecular Chaperone/Radiobiology and Cancer Virology, has already used this approach successfully in mice with skin grafts.

“It’s absolutely natural,” says the researcher.

The degradable microparticles deliver the most powerful known form of HLA-G, a natural suppressor of the immune response, straight to dendritic cells, which typically show the immune system what to attack.

The microparticles are given right after a transplant, just as dendritic cells are giving the immune system a heads up to get busy attacking the new organ.

Dr. Horuzsko says that microparticle therapy likely would be needed for just a few weeks, until the dendritic cells have learned instead to ignore it.

“It’s like a calming effect and once tolerance is established, we don’t need it any more,” he says.

His team compared the success of HLA-G microparticles with the dendritic cell marker to those without a marker, those with were much more efficient at getting where needed and acting.

He says that those without direction likely were consumed by garbage eaters called macrophages.

“We want to create in kidney transplant patients, the same tolerance to the new kidney,” says Dr. Horuzsko, who reckons that HLA-G microparticles could be doing just that within five years.

He presented the patented process along with his other latest HLA-G findings during an opening lecture of the 5th International Conference on HLA-G in Paris, July 6-8.

Dr. Horuzsko believes that marked microparticles also have treatment potential in diseases where the immune system attacks normal tissue, such as arthritis, multiple sclerosis and inflammatory bowel disease.

He is currently working in collaboration with Dr. Laura Mulloy, chief of the Section of Nephrology, Hypertension and Transplantation Medicine in the MCG School of Medicine, to find out whether higher natural levels of HLA-G already are giving some transplant patients an edge, by comparing HLA-G expression in those who keep and reject their transplanted kidneys. (ANI)

Scientists unveil prostate cancer ‘homing device’ for drug delivery

Washington, July 7 (ANI): Purdue University researchers have come up with a new prostate cancer “homing device” that can improve detection, and allow for the first targeted treatment of the disease.

The researchers have revealed that they have synthesized a molecule that finds and penetrates prostate cancer cells, and created imaging agents and therapeutic drugs that can link to the molecule and be carried with it as cargo.

Philip Low, the Ralph C. Corley Distinguished Professor of Biochemistry who led the team, said that a targeted treatment could be much more effective in treating cancer and would greatly reduce the harmful side effects associated with current treatments.

“Currently none of the drugs available to treat prostate cancer are targeted, which means they go everywhere in the body as opposed to only the tumour, and so are quite toxic for the patient,” said Low, who is a member of the Purdue Cancer Center.

“By being able to target only the cancer cells, we could eliminate toxic side effects of treatments. In addition, the ability to target only the cancer cells can greatly improve imaging of the cancer to diagnose the disease, determine if it has spread or is responding to treatment,” Low added.

The Purdue team say that the molecule they have created attaches to prostate-specific membrane antigen (PSMA), a protein that is found on the membrane of more than 90 percent of all prostate cancers.

Low points out that it is also found on the blood vessels of most solid tumours, and may provide a way to cut off the tumour blood supply.

“A lot of new drugs are being designed to destroy the vasculature of solid tumours, and, if they could be linked to this new targeting molecule, we could have a two-pronged attack for prostate cancer. We could not only kill the prostate cancer cells directly, we could also destroy the vasculature that feeds the tumours,” he said.

The researcher says that there also is potential for the targeting molecule to be used to attack the vasculature of solid tumours of other types of cancers.

Animal studies carried out by the researchers have shown an ability to eliminate human prostate cancer cells in mice, without any collateral toxicity in normal tissue.

“The molecule acts like a homing device for prostate cancer. PSMA, which is found only on prostate cancer cells and tumor blood vessels, acts as the homing signal that the molecule targets. The molecule and its cargo go only to cancerous tissue, leaving healthy tissue unharmed,” says Sumith Kularatne, a graduate student in Purdue’s chemistry department and first author of both papers who compared the targeting molecule to a homing device.

He has revealed that the molecule is designed with a specific shape that fits with the protein like a key to a lock. The molecule and its cargo are then carried inside the cell with the protein as it goes through its normal cycle.

A radioimaging application used for body scans is expected to enter clinical trials this fall, and an optical imaging application used to measure prostate cancer cells in blood samples is already in clinical trials.

The findings of the researchers have been described in two research articles published in the journal Molecular Pharmaceutics. (ANI)

Keanu Reeves thinking of turning a trained chef

Washington, July 4 (ANI): Keanu Reeves has apparently set his sights on a new career, for the actor wants to get trained to become a chef.

The ‘Speed’ star was so impressed with a cookbook by famed French chef Herve This that he says that it has changed his life.

This, who uses science to perfect his culinary skills, has written the book ‘Molecular Gastronomy: Exploring the Science of Flavour’.

After reading the tome, Reeves has been spending his spare time experimenting with recipes.

“I’m dabbling in it and looking at becoming a chef. He is fantastic. I didn’t really cook before but this book may be changing my life,” Contactmusic quoted him as saying. (ANI)

Scientists use genetic engineering to make virus-resistant grapevines

Washington, July 3 (ANI): Scientists are making certain plants resistant to the “Grapevine fanleaf virus” GFLV by genetic engineering.

Extremely hot or rainy periods can destroy entire crops, not to mention the wide variety of pests that can appear on the scene.

Bugs such as the vine louse or the rust mite, fungi such as mildew, or viruses such as the GFLV can give the vines a hard time.
he GFLV infects the grapevine and causes fanleaf disease, resulting in deformed and very yellowed leaves, smaller grapes and crop loss.

Now, with the help of genetic engineering, researchers at the Fraunhofer Institute for Molecular Biology and Applied Ecology IME in Aachen in Germany, are making certain plants resistant to GFLV.

“Our modified plants produce antibodies,” explained Dr. Stefan Schillberg, head of department at the IME. “These antibodies ‘recognize’ the viruses and prevent them from spreading in the plant and causing damage,” she added.

To enable the plant to produce the antibodies, the scientists have to modify its genotype and channel genetic information for the antibodies into it.

This task is performed by tiny helpers called agrobacteria, which genetic engineers have been using for over twenty years.

These are soil bacteria that inherently transfer parts of their own genome to that of the plant.

Using simple routine processes, the researchers introduce the antibody gene into the bacteria, which then act as a transport vehicle and carry it over to the vine.

The researchers are still testing this process on model plants, and the first results show that their modified versions are up to 100 percent resistant to the virus.
“The antibody is produced very effectively inside the plants,” said Schillberg. “The next step on the agenda is to test the method on actual grapevines and then to carry out field tests,” he added. (ANI)

Bone marrow extract therapy after heart attack improves cardiac function

Washington, June 30 (ANI): A new study has found that an extract derived from bone marrow cells is as effective as therapy using bone marrow stem cells for improving cardiac function after a heart attack.

The study was conducted in mice using a novel stem cell delivery method developed by researchers to show that the extract from bone marrow cells is as beneficial to cardiac function as are intact, whole cells.

Both the cell and cell extract therapies resulted in the presence of more blood vessels and less cardiac cell death, or apoptosis, than no therapy.

The study also showed that heart function benefitted despite the finding that few of the injected cells remained in the heart at one month after therapy.

“Peer-reviewed medical literature is controversial as to whether bone marrow cells differentiate into cardiomyocytes, or cardiac muscle cells, but there is general agreement that stem cell therapy with these cells results in some level of functional improvement after a heart attack. The exact mechanism for this is not yet clear,” said Yerem Yeghiazarians, MD, study author, cardiologist and director of UCSF’s Translational Cardiac Stem Cell Development Program.

“Our results confirm that whole cells are not necessarily required in order to see the beneficial effects of bone marrow cell therapy,” Yeghiazarians added.

Researchers are investigating these new therapies to improve cardiac function after heart attack in an effort to prevent heart failure.

“Current therapies improve symptoms but do not replace scar tissue. Our hope is to use stem cells to decrease the scar, minimize the loss of cardiac muscle and maintain or even improve the cardiac function after a heart attack,” Yeghiazarians said.

The researchers are conducting further studies to evaluate bone marrow cell and extract therapies in order to identify the proteins and factors within the extract and gain insight into the possible mechanisms of cardiac functional improvement.

The findings were published online and in the July 2009 issue of the Journal of Molecular Therapy. (ANI)

How eating less can help boost lifespan

London, June 25 (ANI): Scientists have long known that a restricted diet extends life. Now, researchers at the Salk Institute for Biological Studies have identified two enzymes that provide a new molecular explanation for how eating less leads to living longer.

Howard Hughes Medical Institute investigator Andrew Dillin and colleagues identified two proteins, WWP-1 and UBC-18, that link dietary restriction to longevity in roundworms.

Dillin says when researchers removed the two enzymes from the test animals, the benefits of a restricted diet disappeared.

And when those enzymes were enhanced, longevity and disease resistance increased.

The scientists say understanding how these molecules influence longevity could have implications for developing new treatments for age-related diseases.

“The only other known factor regulating longevity in response to diet restriction operates at the very end of the signaling cascade,” said Howard Hughes Medical Investigator and senior author Andrew Dillin, Ph.D., an associate professor in the Molecular and Cell Biology Laboratory.

“These two enzymes are further up the ladder, bringing us closer to the receptor that receives the signal for throwing the switch to promote a healthy lifespan,” Dillin added.

The study has been published in the June 24, 2009, advance online edition of the journal Nature. (ANI)

Rats are loyal to their neighbourhoods

Washington, May 27 (ANI): In what may have important implications for controlling diseases that spread from rats to humans, Johns Hopkins scientists have found that rodents spend the majority of their lives close to their homes.

The researchers have also observed that some rodents may, in the face of danger, travel as far as seven miles to repopulate abandoned areas.

Wild Norway rats-also called wharf rats, sewer rats or brown rats-can weigh nearly 2 pounds and transmit a variety of diseases to humans.

Even though expensive eradication efforts have been made in Baltimore, point out the researchers, the number of rats there has remained unchanged over the past 50 years.

With a view to finding out why such drives have failed to eradicate rats from Baltimore, the researchers trapped about 300 rats from 11 residential areas and conducted genetic studies to see how the rats were related.

They found that East Baltimore rats are separated from their unrelated West-side counterparts by a large waterway known as the Jones Falls. Within these hemispheres, rat families form smaller communities of about 11 city blocks.

Each community is further divided into neighborhoods that span little more than the length of an average alley. And to a city rat, this is home sweet home.

Based on their observations, the researchers have come to the conclusion that while rats rarely migrate, neighborhood eradication efforts may backfire by encouraging the rodents to repopulate other areas and further spread disease.

They believe that the best solution may be to tackle the problem on a much larger scale-perhaps by targeting entire families at once.

A research article on the study has been published in the journal Molecular Ecology. (ANI)

Genetic link between dental disease, heart attack identified

Washington, May 25 (ANI): Scientists from University of Kiel, Germany have identified a genetic link between dental disease periodontitis and coronary heart disease (CHD).

Dr. Arne Schaefer, of the Institute for Clinical Molecular Biology, University of Kiel, Germany, said that they have discovered a genetic variant situated on chromosome 9, which was shared between the two diseases.

“We studied a genetic locus on chromosome 9p21.3 that had previously been identified to be associated with myocardial infarction, in a group of 151 patients suffering from the most aggressive, early-onset forms of periodontitis, and a group of 1097 CHD patients who had already had a heart attack,” he said.

“The genetic variation associated with the clinical pictures of both diseases was identical,” he added.

The further analysis of 1100 CHD patients and 180 periodontitis patients showed that the genetic risk variant is located in a genetic region that codes for an antisense DNA called ANRIL and that it is identical for both diseases.

Both CHD and periodontitis are propagated by the same risk factors – most importantly smoking, diabetes and obesity – and there is also a gender relationship, with men possibly more liable to these diseases than women.

“These factors already indicated a possible mutual genetic basis underlying the two diseases”, said Schaefer.

“Now we know for sure that there is a strong genetic link, patients with periodontitis should try to reduce their risk factors and take preventive measures at an early stage.

“We hope that our findings will make it easier to diagnose the disease at an early stage, and that in future a greater insight into the specific pathophsyiology might open the way to effective treatment before the disease can take hold,” he added.

The study was presented at the annual conference of the European Society of Human Genetics. (ANI)

Gene linked to autism risk identified

Washington, May 20 (ANI): A new study from University of California, Los Angeles has identified a genetic variant that may increase a child’s risk of developing autism, particularly boys.

The research team has discovered a variant of a gene called CACNA1G that, according to the researchers, that makes boys four times more likely to develop autism, than girls.

“This is a strong finding,” said Dr. Stanley Nelson, professor of human genetics at the David Geffen School of Medicine at UCLA.

“No one has scrutinized the role that CACNA1G plays in autism.

“We found that a common form of the gene occurs more frequently in the DNA of families that have two or more sons affected by autism, but no affected daughters.

“Our study may explain why boys are more susceptible to the disorder than girls,” he added.

Researchers zeroed in on a region of Chromosome 17 that previous studies have tied to autism.

They scoured the DNA of 1,046 members of families with at least two sons affected by autism for common gene variants and identified genetic markers to CACNA1G, which helps move calcium between the cells.

They discovered that the gene has a common variant that appears in the DNA of nearly 40 percent of the population.

“This alternate form of CACNA1G consistently increased the correlation to autism spectrum disorder, suggesting that inheriting the gene may heighten a child’s risk of developing autism,” said Nelson.

“This variant is a single piece of the puzzle. We need a larger sample size to identify all of the genes involved in autism and to solve the whole puzzle of this disease,” he added.

The study appears in journal Molecular Psychiatry. (ANI)

3-D kidney atlas to help researchers, physicians treat renal diseases

Washington, May 16 (ANI): In a bid to diagnose and treat renal diseases early and more successfully, researchers from nine European countries have spent four-and-a half years to create a three-dimensional virtual “Kidney Atlas”, which incorporates the latest research findings on the development and diseases of the kidney.

The Kidney Atlas was part of the European Renal Genome Project (EuReGene), coordinated by the Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch, Germany, which the European Union (EU) funded with more than 10 million euros.

Renal disease not only affects the elderly because of hypertension and diabetes, but also targets children, who are often born with congenital renal anomalies.

Particularly, the increase in the incidence of type 2 diabetes has caused a rise in the number of renal patients.

While the primary aim of the Kidney Atlas is to map genes that play a key role in renal diseases, it also contains other data, for example on anatomy.

The Kidney Atlas, primarily directed towards both basic researchers and clinicians, also contains information for the general public.

The Atlas is based upon various Genome Projects, and the scientists involved in its creation were pathologists, developmental and molecular biologists as well as geneticists from 14 research groups from non-university institutions, universities and six university clinics.

Project coordinator, Professor Thomas Willnow (MDC), has said that the Kidney Atlas will also be of great significance for the research of metabolic disorders, which lead to kidney damage such as diabetes.

The Kidney Atlas was presented at MDC during a two-day symposium, which was attended by approximately 100 researchers. (ANI)

Why some pregnant women find it difficult to quit smoking

Washington, May 15 (ANI): Scientists from Peninsula Medical School and the University of Bristol have discovered a common genetic variant that might make it difficult for women to quit smoking during pregnancy.

They found that variation in 15q24 nicotinic acetylcholine receptor gene receptor cluster is associated with a reduced ability of women to quit smoking in pregnancy.

For the study, the researchers looked at 7,845 women of European descent from the South West of England.

Using 2,474 women who smoked regularly immediately before they became pregnant, the association between the variant and smoking cessation and smoking quantity during pregnancy was analysed.

When asked about smoking in the first trimester of pregnancy, 28 pct of the women said they had given up.

However, this figure was only 21pct in the group of women with two copies of the smoking addiction gene, whereas in women with two copies of the non-addictive gene, 31pct said they had quit.

In the third trimester, 47pct of women with two copies of the non-addictive gene had stopped smoking, compared with only 34pct of women with two copies of the smoking addiction gene.

“Pregnant women are under considerable health and social pressure to stop smoking, and quitting in such circumstances is influenced by a number of factors including the age of the expectant mother, their education and whether or not their partners smoke,” said Dr. Rachel Freathy from the Peninsula Medical School.

“However, we were keen to investigate whether the genetic variant that influences increased cigarette consumption also had a role to play as an extra hurdle to quitting smoking during pregnancy, and our study suggests that it does,” she added.

The study is published in Human Molecular Genetics. (ANI)

How meningococcal bacteria break through body’s natural defence mechanism

Washington, May 14 (ANI): Scientists at The University of Nottingham claim to have discovered how the deadly meningococcal bacteria avoid the body’s natural defence mechanism and attack the brain.

Their work attains significance because it may pave the way for better treatment and vaccines for meningitis, and eventually save the lives of hundreds of children.

Bacterial meningitis in childhood is almost exclusively caused by the respiratory tract pathogens Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae.

Scientists struggled to understand the mechanism used by these lethal germs to break through the blood brain barrier until the current study.

Lead researcher Dlawer Ala’Aldeen, Professor of Clinical Microbiology and Head of the Molecular Bacteriology and Immunology Group at the Centre for Biomolecular Sciences, says that the research team’s discovery shows that all three pathogens target the same receptor on human cerebrovascular endothelial cells – the specialised filtering system that protects our brain from disease – to enable the organisms to cross the blood-brain barrier.

The researcher says that these findings suggest that disruption or modulation of this interaction of bacterial adhesins with the receptor might offer unexpectedly broad protection against bacterial meningitis, and may provide a therapeutic target for the prevention and treatment of disease.

Professor Ala’Aldeen, who has been studying meningitis and its causes for over 20 years, said: “This is a significant breakthrough which will help us design novel strategies for the prevention and treatment of bacterial meningitis.

Identification of the human receptor and bacterial ligands is like identifying a mysterious key and its lock, which will open new doors and pave the way for new discoveries.”

The research was carried out in collaboration with the Department of Infectious Diseases at St. Jude Children’s Research Hospital in Memphis Tennessee.

It involved students from the University who have been regular and willing volunteers in the research programme.

Professor Ala’Aldeen said: “The ultimate aim is to save lives by protecting the healthy and curing the sick. We are one step closer to new breakthroughs that would prevent disease or its complications. There still is a long way to go before we have the ultimate vaccine and the ultimate treatment of bacterial meningitis.”

The findings of the study have been published in The Journal of Clinical Investigation. (ANI)