Decaf coffee, nicotine-free tobacco may offer Parkinson”s protection

April 24, 2010 By Leave a Comment

London, Apr 24(ANI): In a new study, researchers found that coffee and cigarettes could protect the brain of flies with a form of Parkinson’s disease, but the benefit was not because of caffeine and nicotine.

Leo Pallanck, a neuroscientist at the University of Washington in Seattle, whose team led the new study, said that if they could identify the compounds that put up this brain defence, they could offer a preventive Parkinson”s treatment where none currently exists.

“We think that there”s something else in coffee and tobacco that”s really important,” New Scientist quoted him as saying.

Epidemiological studies have suggested that coffee-drinkers and smokers are less likely to develop Parkinson”s than abstainers.

“A lot of the field has gravitated to the idea that it”s caffeine and nicotine [that protects their brains],” said Pallanck.

To see if ingredients other than caffeine and nicotine might be providing the benefit, Pallanck”s team turned to fruit flies with a condition similar to Parkinson”s disease.

The flies have mutations that kill off dopamine-producing neurons, which causes them to develop movement and cognitive problems like those characteristic of Parkinson”s in people.

The same mutations are linked to hereditary forms of Parkinson”s in humans.

The researchers prepared several fly foods spiced up with normal coffee, decaffeinated coffee, smokeless “dipping” tobacco designed to allow nicotine absorption via the mouth, or a commercial nicotine-free tobacco.

Then the researchers raised groups of flies on the various diets.

Normally, dopamine-producing neurons in the mutant flies die off as they age.

However, a diet featuring coffee and tobacco kept the neurons alive in all the flies tested at 20 days old, whether or not their food contained caffeine or nicotine.

In addition, when pure caffeine or nicotine were added to the meals of other groups of flies, their dopamine neurons died off – just like those of flies whose food had no additive at all.

“We didn”t see any protective effects at all of caffeine and nicotine,” said Pallanck.

His team went on to identify a compound found in both decaf and normal coffee called cafestol that seems partially responsible for its neuro-protective effects.

Cafestol activates a protein produced by flies called Nrf2, and the team found that blocking Nrf2 diminished coffee”s protective effect on dopamine neurons.

Blocking Nrf2 in flies fed tobacco also reduced its protective effects.

And now, the scientists are searching for tobacco ingredients that activate Nrf2 – and other ones that do the same in coffee.

These compounds might one day be given to people to protect against Parkinson”s.

Alternatively, new drugs could mimic the protective neural processes triggered by coffee and cigarettes.

The study was published in the Journal of Neuroscience. (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

Gene responsible for Duchenne muscular dystrophy can be repaired

April 16, 2010 By Leave a Comment

Washington, Apr 16 (ANI): It is possible to repair the defective gene responsible for Duchenne muscular dystrophy, claim researchers from Université Laval”s Faculty of Medicine and the CHUQ Research Center.

The team, led by Professor Jacques P. Tremblay, is presenting its new therapeutic approach in an article published in the online version of the scientific journal Gene Therapy.

Duchenne muscular dystrophy is a hereditary disease. It causes progressive muscle degeneration that begins in early childhood and causes death by age 25 in most people afflicted. The disease is caused by mutations that affect a protein called “dystrophin.” The mutations alter the normal nucleotide sequences of this protein”s gene and stop its synthesis.

Professor Tremblay”s team partnered with Cellectis, a French firm specializing in genome engineering, in order to design enzymes—called meganucleases—with the ability to correct the dystrophin gene. During in vitro testing, the researchers inserted genes coding for a variety of meganucleases into human muscle cells.

They repeated the experiment in vivo with mice carrying the mutation that causes the illness. Both series of testing showed that the meganucleases can lead to a restoration of the normal nucleotide sequences of the dystrophin gene and its expression in muscle cells. (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

Mutations in single gene leads to many cancers

March 30, 2010 By Leave a Comment

Washington, Mar 30 (ANI): Specific mutations in an important gene, that normally protects the body against cancer, can itself cause a variety of cancers, according to a study.

Researchers at the Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute examined mutations in a gene called PTEN.

People who inherit a mutated copy of this gene have Cowden syndrome— a condition that carries a high risk of cancer in a number of organs, including the breast, thyroid and ovary.

In addition, PTEN is frequently mutated in normal body cells leading to prostate, lung and pancreatic cancers.

While it is not known why people with Cowden syndrome develop different cancers, or cancers that are more severe in some than in others, the cause is often attributed to the natural genetic differences that exist between individuals.

However, this animal study linked specific mutations in the gene to distinct kinds of cancer in organs targeted by the syndrome.

“We showed that the mutations themselves play a critical role in driving the cancers that occur in certain organs in people with Cowden syndrome. Together, our findings demonstrate that specific inherited PTEN mutations have a strong influence in the variable predisposition to cancer of patients with Cowden syndrome,” said principal investigator Gustavo Leone.

The findings suggest that testing for specific PTEN mutations might predict the kind and severity of cancer that will develop in people with the syndrome.

In addition, because PTEN is the second most commonly mutated gene in human cancer overall, the same mutations might predict severity in sporadic tumours, as well.

“Mutations in this gene also play a role in developmental disabilities and perhaps in autism, so this mouse model might be useful for studies in those conditions, as well,” said co-principal investigator Michael Ostrowski.

The researchers are now investigating why patients may experience differences in cancer severity even when they have the same mutation.

The study has been published in the latest issue of the Proceedings of the National Academy of Sciences of the United States of America. (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

Anaesthesia ups risk of developing Alzheimer’s-like symptoms

March 25, 2010 By Leave a Comment

Washington, Mar 25 (ANI): Repetitive anaesthesia with isoflurane (one of the most common anaesthetics by inhalation) increases the risk of developing Alzheimer”s disease (AD) like symptoms in patients with genetic risk factors for the disease, according to a rodent study.

Spanish researchers coordinated by Doctors Maria Angeles Mena and Justo Garcia de Yebenes, from CIBERNED (Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas), found that anaesthesia is safe for normal mice but potentially harmful for mice with mutations of the amyloid precursor protein (APP).

The findings suggest a possible mechanism of developing Alzheimer.

Some epidemiological studies have shown an increased prevalence of AD in patients undergoing anaesthesia and surgery.

“Before surgery requiring anesthesia, it may be ideal to know the genetic background of the patients so that the drugs used and the pattern of anaesthesia may be personalized accordingly,’ said de Yebenes.

The linkage between the repetitive use of isoflurane anaesthesia and the development of AD changes in mice with mutations indicates the advisability of testing for genetic risk factors for AD in patients prior to surgery.

The researchers concluded that anaesthesia is safe for normal mice but risky for asymptomatic carriers of mutations, which produce AD.

The research has been based on the application of anaesthesia twice a week during three months in normal mice and in mice with mutations (7-10 months old) that produce AD (known as APPswe).

The results show alterations produced in the brain of mice with mutations very similar to those observed in patients that have already developed Alzheimer”s disease.

It was found that application of repetitive anaesthesia in genetically altered mice increased their death rate.

Mutant mice showed less reactivity after anaesthesia was over. Their time for recovery after anaesthesia was also increased.

Repetitive anaesthesia produced persistent disorders affecting behavior of mutant mice.

Neuronal death increased in brain areas critical for cognition.

There was an increase in inflammatory response and deposition of beta-amyloid peptides.

Isoflurane anaesthesia of mutant mice altered the levels of chaperones (proteins which regulate the processing of abnormal proteins)

The work has been published in the Journal of Alzheimer”s Disease. (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

New gene linked to progressive hearing loss identified

September 4, 2009 By Leave a Comment

Washington, Sept 4(ANI): Scientists from The Scripps Research Institute have discovered a gene responsible for progressive hearing loss.

The has team found a gene, called Loxhd1, which is necessary for maintaining proper functioning hair cells in the inner ear.

However, mutations in this gene can lead to degradation of the hair cells and a disruption of the process that enables hearing.

“It is thought that mutations in several hundred genes can lead to deafness,” said team leader Ulrich Mueller, a professor in the Department of Cell Biology and member of the Skaggs Institute for Chemical Biology at Scripps Research.

“However, for many forms of deafness, we don’t know what effects the genes have. In this new research, we have linked a previously uncharacterized gene to deafness, first in mice and then in humans,” said Mueller.

During the study, researchers used a technique called forward genetics in their quest to better understand the genetic basis of hearing and hearing loss.

In forward genetics, scientists make mutations at random in germ cells, screen the resulting models for physical characteristics of interest (in this case hearing impairment), then amplify these traits through the breeding of several generations.

The gene responsible for the trait is then identified through positional cloning.

In this case, the scientists were able to generate a new mouse line with hearing impairment that they called samba and then clone the gene responsible, Loxhd1, which had never before been associated with deficits in hearing.

When the mice inherited two copies of the mutated gene, they were profoundly deaf shortly after birth.

This is the third hearing-related gene that the Mueller lab has discovered.

“In humans, the prevailing difficulty is progressive hearing loss,” he said.

“As you age, you lose your hearing slowly. Since this mutation can lead to progressive hearing loss, it provides us with more information on the genetic underpinnings of this condition and gives us clues as to how it might be corrected,” he added.

The study appears in American Journal of Human Genetics, a publication of Cell Press. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , ,

Hepatitis B virus mutations may help predict liver cancer risk

July 3, 2009 By Leave a Comment

Washington, July 3 (ANI): Scientists from Second Military Medical University in Shanghai have revealed that mutations in the DNA of hepatitis B virus (HBV) might help predict which patients are at increased risk of developing liver cancer,

HBV infection is a known cause of hepatocellular carcinoma (HCC), the most common form of liver cancer.

During the research, the team analysed 43 studies with a total of 11,582 HBV-infected participants, of whom 2,801 had HCC.

They found that certain mutations were associated with development of HCC, and more prevalent as chronic HBV infection progressed from the asymptomatic state to liver cirrhosis or HCC.

“Frequent examination of patients with chronic HBV infections for the presence of these mutations may be useful for identifying which patients require preventive antiviral treatment and for the prediction of HCC,” wrote the authors.

The study appears in Journal of the National Cancer Institute. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

New gene linked to familial testicular cancer identified

June 30, 2009 By Leave a Comment

Washington, June 30 (ANI): Scientists at the National Institutes of Health claim to have identified the second gene that can increase a man’s risk of familial, or inherited, testicular germ-cell cancer.

Men with a family member who had a testicular germ cell cancer are at three-to six-fold greater risk than other men of developing testicular cancer.

Although a family history of testicular cancer probably accounts for less than five percent of all testicular cancers, the careful study of rare familial cancer clusters has often led to important new understanding of the non-familial versions of the same cancer.

“This study contributes to our understanding of why testicular germ cell cancer appears to run in families,” said Dr Raynard Kington, Acting NIH Director.

“The findings may also lead to new ways to identify men at high risk, as well as more effective ways to prevent and treat testicular germ cell cancer,” Kington added.

According to researchers, the key pathway in this disease is the cyclic AMP pathway, which regulates how cells respond to such signals as hormones.

Drugs that affect the cyclic AMP pathway are widely available, and, in theory, could affect progression of testicular cancer.

The researchers found that seven different mutations in the gene in question, PDE11A, created abnormal versions of the PDE11A enzyme that slowed down the enzyme’s destruction of cyclic AMP.

“The mutations don’t cause cancer directly, but instead appear to increase an individual’s susceptibility to developing a tumour,” said the study’s senior author, Dr Constantine Stratakis, D.Sc., chief of NICHD’s Section on Endocrinology and Genetics.

“Almost one out of every five families we studied had a variation in the gene that affected its functioning,” Stratakis added.

Stratakis and his colleagues analyzed the portion of the DNA from 95 familial testicular cancer patients that contains the PDE11A gene.

They found seven mutations in the cancer patients, and noted that the rate at which they were detected was much higher than that seen in the DNA of people without testicular cancer.

Stratakis said that learning how disruptions in the PDE11A enzyme lead to an increased risk of tumor formation may help researchers identify other proteins that also play a role.

The study appears in the Cancer Research. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , ,

Enzyme destroys mutated protein to cause inherited Parkinson’s disease

June 27, 2009 By Leave a Comment

Washington, June 27 (ANI): Scientists have identified a naturally occurring enzyme in the brain, which helps in the destruction of the mutated protein that is the most common cause of inherited Parkinson’s disease.

Led by researchers at UT Southwestern Medical Center, the study used human cells and offered a focus for further research into halting the action of the mutated protein.

One of the most famous carriers of the mutation is Google co-founder Sergey Brin, who wrote about it on his blog in 2008.

Dr. Matthew Goldberg, assistant professor of Neurology and Psychiatry and senior author of the paper said: “There are currently enormous efforts to identify potential therapies based on inhibiting this mutated protein.”

He added: “Our paper is a major advance because we identify a protein that binds to the mutated protein and promotes its breakdown.”

The particular mutation examined in the study affects a protein whose function is not well understood, but in its normal form, it appears to have multiple sites where other molecules can attach themselves, like a space station with many docking areas.

Named LRRK2, the protein is vulnerable to several mutations, some of which can cause Parkinson’s disease.

For the study, the researchers used cultured human kidney cells and found that LRRK2 and a protein called CHIP “robustly” associated with each other.

On further testing, it was found that CHIP and LRRK2 could bind to each other in two different ways, either directly or indirectly by a third molecule that acted as a bridge.

The researchers observed that when CHIP bound to either the normal or mutant form of LRRK2, levels of LRRK2 in the cell decreased. This occurred because the cells increased the rate at which they destroyed LRRK2.

“CHIP may be a useful therapeutic target for treatments to break down LRRK2 in people with Parkinson’s,” said Goldberg.

He added: “Our next step is to identify cellular mechanisms that signal LRRK2 to be degraded by CHIP or by other mechanisms. Because LRRK2 mutations are believed to cause Parkinsonism by increasing the activity of LRRK2, enhancing the normal mechanisms that target LRRK2 for degradation by CHIP may be therapeutically beneficial.”

The study has been published in the journal Public Library of Science. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , ,

Evolution in animals is faster in regions with warmer climates

June 27, 2009 By Leave a Comment

London, June 25 (ANI): In a new study, scientists have found out that evolution in animals is faster in regions with warmer climates, which could help explain why the warm topics are so species-rich.

According to a report by BBC News, researchers have found that among pairs of mammals of the same species, the DNA of those living in warmer climates changes at a faster rate.

These mutations, where one letter of the DNA code is substituted for another, are a first step in evolution.

DNA can mutate and change imperceptibly every time a cell divides and makes a copy of itself.

But, when one of these mutations causes a change that is advantageous for the animal, for example, rendering it resistant to a particular disease, it is often “selected for”, or passed down to the next few generations of that same species.

Such changes, which create differences within a population but do not give rise to new species, are known as “microevolution”.

The idea that microevolution happens faster in warmer environments is not new. But, this is the first time the effect has been shown in mammals, which regulate their own body temperature.

“The result was unexpected,” said Len Gillman from Auckland University of Technology, who led the study.

“We have previously found a similar result for plant species and other groups have seen it in marine animals. But, since these are ‘ectotherms’ – their body temperature is controlled directly by the environment – everyone assumed that the effect was caused by climate altering their metabolic rate,” he added.

Scientists believe that this link between temperature and metabolic rate means that, in warmer climates, the germ cells that eventually develop into sperm and eggs divide more frequently.

“An increase in cell division provides more opportunities for mutations in the population over a given time,” explained Dr Gillman.

“This increases the probability of advantageous mutations that are selected for within the species,” he said.

“We suspected the same effect might be happening in mammals, because seasonal changes affect the animals’ activity,” Dr Gillman told BBC News.

In the DNA study, it was found that at higher latitudes where environments are colder and less productive, animals often conserve their energy – hibernating or resting to reduce their metabolic activity.

“In warmer climates annual metabolic activity is likely to be greater, so this will lead to more total cell divisions per year in the germline,” said Dr Gillman.

These results support the idea that high tropical biodiversity is caused by faster rates of evolution in warmer climates. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Grey hair may give protection against cancer

June 22, 2009 By Leave a Comment

London, June 22 (ANI): Experiments on mice suggest that having grey hair may tender protection against cancer, say researchers.

Emi Nishimura, of Tokyo Medical and Dental University in Japan, points out that melanocytes are the cells that produce the pigments that colour hair, and that their numbers are kept topped up by stem cells.

According to Nishimura, hair goes grey when the number of stem cells in hair follicles declines.

The researcher says that a new study conducted at the university has now revealed what causes this decline in mice.

During the study, the researchers exposed mice to radiation and chemicals that harm DNA, and found that damaged stem cells transformed permanently into melanocytes.

Nishimura and colleagues say that that eventually led to fewer melanocytes, meaning that there were fewer stem cells capable of topping up the melanocyte pool.

Writing about their findings in the journal Cell, the researchers have revealed that the mice also went grey.

They believe that the same process leads to the reduction in stem cells in the follicles of older people, especially as DNA damage accumulates with the as they age.

David Fisher, a cancer researcher at Harvard Medical School, thinks that such processes may discourage the proliferation of stem cells with damaged DNA, which could pass on mutations, and thereby protect people against cancer.

“One likely beneficial effect is the removal of potentially dangerous cells that may contain pre-cancerous capabilities,” New Scientist magazine quoted him as saying. (ANI)

Filed Under: Health News Tagged With: , , , , , , , , , , , , , , , , , , ,

Zebrafish may help explain how skin cancer spreads

May 26, 2009 By Leave a Comment

Washington, May 26 (ANI): Scientists claim that zebrafish can help explain how aggressive human skin cancer, melanoma, grows and spreads.

The pigmented cells in zebrafish helped scientists tease out how oncogenes that are know to contribute to cancer, influence the formation and regulation of melanoma.

Inside the cell, signals are delivered that direct the cell on whether to divide, migrate or even die. In cancer, cells divide, grow and migrate when they should not, therefore resulting in an aggressive disease that can spread throughout the body.

A key molecule in this signalling pathway is RAS, and mutations in it are known to lead to cancer.

During the study, the University of Manchester in England and the University Hospital Zurich in Switzerland generated several zebrafish with changes in RAS or other RAS-regulated proteins to create a useful model that can be used to study and understand human melanoma.

The tumours created from the pigmented cells of zebrafish, known as melanocytes, are easy to see against their thin, light colored bodies.

The researchers say that these fish may be a useful experimental tool for human disease.

Many of the changes they made caused melanoma in the zebrafish, indicating that zebrafish respond similarly to changes in these signals as do humans.

The study is published in Disease Models and Mechanisms. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Genes behind ageing process identified

May 26, 2009 By Leave a Comment

London, May 26 (ANI): British scientists have identified genes that control the ageing process.

The finding could lead to new drugs to prevent illnesses from heart disease to Alzheimer’s.

In the laboratory, researchers have found that mutations could extend the lifespan of animals such as worms, fruit flies and mice, and appear to play the same role in humans.

Professor Linda Partridge, director of the Institute of Healthy Ageing at University College London, has said that the research could help in the treatment or delay of many diseases simultaneously with medication.

She added that tackling the very causes of ageing, instead of treating the symptoms, could be the best way of dealing with the diseases that result from it.

In her opinion, such scientific advances are offering up hope to improve health during ageing in humans and inspiring a new wave in ageing research.

“Research on the diseases associated with ageing is generally done by separate communities of research workers who read different journals, attend different conferences and generally do not communicate with each other,” The Telegraph quoted Partridge as saying.

She added: “But by tacking the causes of ageing itself we could treat, or at least delay, a broad spectrum of conditions simultaneously.”

Drugs, which inhibit the nutrient pathways in humans, could replicate the effects of a healthy diet.

And thus, they can act not only to increase lifespan but also to target a broad range of ageing related diseases such as cardiovascular disease, cancers, diabetes and Alzheimer’s.

Partridge said that the research indicates a new approach to the treatment of age-related conditions.

“The major burden of ill health is in the older section of the population. The new discoveries about ageing have raised the prospect of increasing the number of years that people enjoy in good health, with broad-spectrum preventative medicines for the diseases of ageing,” said Linda.

She will present the findings at a public lecture at the Royal Society in London. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , ,

HIV’s ‘hide and seek’ could make it weaker

May 9, 2009 By Leave a Comment

Melbourne, May 9 (ANI): HIV usually plays a game of hide and seek to dodge the immune system, but a new study has claimed that such playfulness actually makes the deadly virus vulnerable at times, according to an Australian study.

The finding could offer insights into the treatment of HIV during the early stages of infection.

At the time of entering a new host, HIV includes a form that researchers call escape mutant.

Although the escape mutant virus is better at evading our immune system, it is weaker and replicates slower than the wild-type form.

“When HIV infects a new host it needs to adapt to this new environment,” ABC News quoted lead author and PhD student Liyen Loh, of the Department of Immunology and Microbiology at The University of Melbourne, as saying.

She added: “The mutations often revert to the original wild-type virus, allowing the virus to regain a fitter state, or the changes may be retained, depending on the individual’s immune system. This explains why some individuals have better clinical outcomes than others.”

In the study, the researchers from the University of Melbourne and the University of Sydney analysed the evolution of the virus using macaque monkeys by infecting them with different quantities of wild-type SIV (the non-human equivalent of HIV) and escape mutant SIV.

They then measured the growth of the virus for the next three months to find out how much time the escape mutant form took to revert back to its fitter wild-type state.

“In the absence of immune pressure the virus will not stay in its weakened state, because it is not beneficial for the virus,” said Loh.

It was discovered that in animals infected with the escape mutant virus, it took 8 days for wild type to appear and it took 8 weeks for them to outnumber the escape mutant form.

The researchers also found that the genetic makeup of the virus affected how fast the virus adapts in the host.

“If (the macaques) get infected with purely one strain of virus it will take longer to adapt to the new host,” said Loh.

In her opinion, the study only focused on one structural part of the virus that mutates, and also claimed that there are many “other bits” that affect how the HIV evolves in an infected individual.

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

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Swine flu’s first genetic analysis reveals potency

May 3, 2009 By Leave a Comment

London, May 2 (ANI): While swine flu virus H1N1 continues to spread around the world, the first genetic analysis of the efficacy of its transmission from person to person revealed that it spreads barely well enough to keep itself going.

The analysis also suggested that the virus might have started circulating as long ago as January.

However, because of the scarcity of cases to analyse, the calculation is still uncertain, as many believe that the circulation could have started more recently, or as far back as September.

Nicholas Grassly of Imperial College London and Andrew Rambaut of the University of Edinburgh, UK, have analysed the rate of spread.

Their analysis is based on the small mutations that have accumulated in almost two-dozen genetic sequences produced so far, from viruses collected from patients in Mexico and the US.

Unlike H5N1 bird flu, all the genetic sequences of this H1N1 are being posted on bulletin boards like GISAID, so that scientists can access them and compare preliminary analyses.

Scientists who protested that H5N1 sequences were not being made freely available set up the GISAID system in 2006.

“The limited sampling so far gives rise to considerable uncertainty in the estimate,” New Scientist quoted Rambaut as saying.

However, if the rate at which genes mutate is similar for this virus as for other H1N1 viruses, the number of mutations that have accumulated so far have indicated that it has been circulating since January – or even September 2008.

If the new virus spreads from one infected person to the next at about the same speed as ordinary flu, it could give an idea of how many cases there may have been in that time.

A mathematical model permits the calculation of an important variable called R0 – the number of additional people infected, on average, by each case.

If R0 is less than one, an infection dies out.

Also, Grassly cautioned that the estimate is very preliminary.

However, with newly available data, he gets an R0 of 1.16 – enough for the virus to keep going, but only just.

This comes as good news, as epidemiological theory suggests that the lower the R0, the easier it may be to snuff the virus out by further hindering its spread.

And now the onus lies on how quickly the new H1N1 virus from swine adapts to people. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Native Americans descended from a single ancestral group

May 2, 2009 By Leave a Comment

Washington, April 30 (ANI): In a new research, an international team of scientists has determined that the Native Americans, who came to the New World, descended from a single ancestral group.

“Our work provides strong evidence that, in general, Native Americans are more closely related to each other than to any other existing Asian populations, except those that live at the very edge of the Bering Strait,” said Kari Britt Schroeder, a lecturer at the University of California, Davis, and the first author on the paper describing the study.

“While earlier studies have already supported this conclusion, what’s different about our work is that it provides the first solid data that simply cannot be reconciled with multiple ancestral populations,” he added.

The research team, which was headed by Noah Rosenberg at the University of Michigan, scrutinized DNA samples of people from 31 modern-day Asian populations, 19 Native American, one Greenlandic and two western Beringian populations.

The team’s work follows up on earlier studies by several of its members who found a unique variant (an allele), dubbed the “9-repeat allele,” of a genetic marker in the DNA of modern-day Native American people.

They found that in each sample that contained the 9-repeat allele, short stretches of DNA on either side of it were characterized by a distinct pattern of base pairs, a pattern they seldom observed in people without the allele.

“If natural selection had promoted the spread of a neighboring advantageous allele, we would expect to see longer stretches of DNA than this with a similarly distinct pattern,” Schroeder said.

“And we would also have expected to see the pattern in a high frequency even among people who do not carry the 9-repeat allele. So we can now consider the positive selection possibility unlikely,” he added.

The results also ruled out the multiple mutations hypothesis.

If that had been the case, there would have been myriad DNA patterns surrounding the allele rather than the identical characteristic signature the team discovered.

“There are a number of really strong papers based on mitochondrial DNA – which is passed from mother to daughter – and Y-chromosome DNA – which is passed from father to son – that have also supported a single ancestral population,” Schroeder said.

“But, this is the first definitive evidence we have that comes from DNA that is carried by both sexes,” he added. (ANI)

Filed Under: Uncategorized Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

How HIV escapes immune system pressure

April 16, 2009 By Leave a Comment

Washington, April 16 (ANI): Studying HIV-infected people with a particular gene, scientists have gained fresh insights into how the virus mutates and evolves in response to the body’s immune pressure.

Dr. Eric Hunter of the Emory Vaccine Center and Oxford University graduate student Hayley Crawford studied people in Zambia and South Africa with one form of the HLA gene that helps the immune system control HIV, called HLA-B*5703.

HLA genes encode molecules that display fragments of viral proteins, known as epitopes, on the surface of infected cells.

When white blood cells known as cytotoxic T lymphocytes (CTLs) spot certain combinations of HLA molecules and viral epitopes, they attack the infected cells.

During the study, the researchers observed that a set of three mutations in HIV’s Gag protein, which makes up the viral core, progressively slow viral replication.

They say that a triple-mutant virus replicates 20 times slower than normal in cell culture.

However, the same mutations effectively eliminate the ability of CTLs to detect the virus, so that in an infected person, once all three mutations are in place, viral abundance shoots upwards.

“In this situation, HIV resembles a thief picking a lock. Once all three mutations are in place, the lock is picked and the virus can thrive because the immune system can’t fight against it,” Hunter says.

The Emory/Oxford researchers followed the mutations’ fate after transmission by studying couples in which one person had infected the other.

They observed that the virus lost the mutations when the recipient lacked HLA-B*5703, as the three handicapping mutations were not useful in evading the new, different immune system.

However, unlucky recipients with the HLA gene, who got the triple-mutant virus from their partners, quickly got sick.

The results demonstrate the importance of CTLs, the white blood cells that attack viral infected cells, in controlling HIV infection.

They also suggest that a successful vaccine will need to induce responses to many epitopes, or combinations of HLA molecule and viral protein.

The study has been published in the Journal of Experimental Medicine. (ANI)

Filed Under: Health News Tagged With: , , , , , , , , , , , , , , , , , , ,

Mutations that hide HIV from immune system weaken its ability to replicate

April 13, 2009 By Leave a Comment

Washington, Apr 13 (ANI): Scientists at University of Oxford have found that mutations that hide HIV from immune system weaken the virus’ ability to replicate.

According to them, when HIV infects a cell, a complex of human immune proteins called HLA (short for human leukocyte antigen) alert killer T cells by displaying bits of the virus on the surface of the cell, in response to which the T-cells trigger immune attack.

They suggest that individuals who have certain types of HLA proteins control infection better than others.

For instance, in people with HLA-B*5703, the virus multiplies less than in people with some other HLA variants likely because killer T cells in these individuals are quick to attack infected cells. However, HIV is tricky.

To get around HLA-B*5703, the virus mutates three amino acids that T cells need to recognize the infected cells, causing the killers to pass by the infected cell unnoticed.

Thus by mutating, the virus becomes invisible to the immune system.

In the new study, lead researcher Hayley Crawford showed that the triple mutant replicated 20 times slower than normal in cell culture.

During the study, the researchers examined Zambian couples in which one HLA-B*5703-expressing person infected with triple-mutant virus passed the infection to a partner who either did or didn’t have the same HLA variant.

When transmitted to a person without HLAB*5703, the virus changed its mutated amino acids back to their original sequence because the benefit of avoiding killer T cells no longer outweighed the cost of reduced replication.

However, when transmitted to another HLA-B*5703-expressing person, the triple-mutated virus came out on top despite its reduced replication. In these individuals, the avoidance of killer T cells allowed the infection to rapidly proceed to clinical illness.

The study has been published in Journal of Experimental Medicine. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , ,

Kids with older fathers ‘are less intelligent’

March 9, 2009 By Leave a Comment

London, Mar 8 (ANI): Are you delaying fatherhood? Well, then you should reconsider your family plan, for a new study has found that kids with older dads perform badly in intelligence tests.

The research, led by John McGrath, of the Queensland Brain Institute at the University of Queensland in Australia, found children with older fathers tended to obtain significantly lower scores in a variety of cognitive tests than those born to younger fathers.

“The offspring of older fathers show subtle impairments on tests of neurocognitive ability during infancy and childhood,” The Times quoted John, as saying.

“In light of the trends to delay fatherhood, the clinical implications and the mechanisms underlying these findings warrant closer scrutiny,” he added.

To reach the conclusion, McGrath analysed data on 33,437 Americans born between 1959 and 1965. All were tested at eight months, four years and seven. The data set, despite its age, remains one of the best resources.

The underlying biological mechanisms are the key questions, according to McGrath. One idea is that as men age the cells that produce sperm suffer increasing numbers of mutations, which are passed on to an offspring. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , ,

Scientists identify gene that plays key role in cancer

March 2, 2009 By Leave a Comment

Washington, February 28 (ANI): Karolinska Institutet scientists have identified a gene that regulates the activity of another gene called p53, which protects against cancer.

Writing about their work in the journal Molecular Cell, the researchers have revealed the newly identified gene as Wrap53.

They have found that Wrap53 gives rise to a molecule, known as antisense RNA, the presence of which is necessary for the production of sufficient quantities of p53 protein in the event of DNA damage.

Marianne Farnebo, a member of the research team, said that the results suggested that damage to Wrap53 could indirectly cause cancer.

She, thus, said that Wrap53 was a new potential target for future cancer therapies.

“Mutations in the p53 gene contribute to about half of all cancer cases. In the remaining half, p53 is probably inactivated in other ways, such as damage to Wrap53 knocking out the production of the p53 protein,” she said.

The researchers also claimed that theirs was one of the first to show how antisense RNA regulates genes in the human body.

It is already a well-known fact that genes often control each other through the influence of their end products – usually proteins – on gene expression.

With antisense regulation, control is effected instead through the production of mutually stabilising or destructive RNA molecules by genes with overlapping sequences, which determines whether or not the RNA molecules form proteins.

“At least 20 per cent of all genes can be regulated by antisense RNA, making it a potentially very common control mechanism. But it’s been difficult to show that antisense RNA really does serve important functions in the body, as we’ve managed to do in this study,” says Dr Farnebo. (ANI)

Filed Under: Health News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

17,00 genes vital to sleep identified

February 23, 2009 By Leave a Comment

London, Feb 23 (ANI): In a study on the need for sleep in animals, scientists at North Carolina State University have identified almost 1,700 genes associated with the variability of sleep in fruit flies.

Led by Dr. Trudy Mackay, the study has shown that the fruit fly is genetically wired to sleep, although the sleep comes in widely variable amounts and patterns.

The researcher believes that understanding the genetics of sleep in model animals could lead to advances in understanding human sleep, and how sleep loss affects the human condition.

During the study, the research group examined the sleep and activity patterns of 40 different wild-derived lines of Drosophila melanogaster, one of the model animals used in scientific studies.

The researchers observed that male fruit flies on average slept longer than females, males slept more during the day than females, and males were more active when awake than females.

The females, in turn, tended to have more frequent bouts of sleep, and thus were disrupted more from sleep, than the males.

The researchers closed down on almost 1,700 genes linked with variability of sleep in fruit flies, most of which were previously not known to affect sleep.

Mackay said that fruit flies within each of the 40 lines were homozygous, or exactly the same genetically, but the lines were completely different from one another.

For the study, the researchers placed small glass tubes containing one fruit fly and some food in a machine, which used infrared sensors to monitor the minute-by-minute activity of the flies.

If at least five minutes passed without any fly activity, it was calculated as sleep.

The study predicted that certain important genes would affect sleep duration, and independent verification with mutations in those genes was found to have an effect on how long fruit flies slept.

The study also discovered teams of genes that appeared to act together to affect some portion of sleep.

“We’re starting to get a glimmer of how groups of correlated genes are overrepresented in different traits, and we now know more about how traits are associated with each other at the molecular level,” Nature magazine quoted Mackay as saying.

The study has been published in the online edition of the journal Nature Genetics. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , ,
« Older Posts