PEOPLE HAVE continued to evolve since leaving the ancestral homeland in northeastern Africa 50,000 years ago, both through the random process known as genetic drift and through natural selection.
Recent research indicates we have spread globally and evolved locally the human. genome bears many fingerprints in places where natural selection has recently remoulded the human clay, researchers have found, as people on the various continents adapted to new diseases, climates, diets and, perhaps, behavioural demands.
A striking feature of the changes: they are local. The genes found in one continent-based population or race vary from those that occur in others.
These genes so far make up a small fraction of all human genes. The concept of race having a biological basis is controversial, and most geneticists are reluctant to describe it that way.
But a notable instance of recent natural selection is the emergence of lactose tolerance - the ability to digest lactose in adulthood - among the cattle-herding people of northern Europe 5,000 years ago. Lactase is usually switched off after weaning.
Last year, Sarah Tishkoff of the University of Maryland tested 43 ethnic groups in East Africa and found three mutations, all different from the European one, that keep the lactase gene switched on in adulthood.
Researchers studying single genes have found evidence for recent evolutionary change in genes that mediate conditions like skin color, resistance to malaria and salt retention. Variants of two genes involved in hearing have become universal, one in Chinese, the other in Europeans.
Last year, researchers at the University of Chicago searched for genes under natural selection in Africans, Europeans and East Asians. In each race, 200 genes showed signals of selection suggesting that the populations were adapting to local challenges. A study led by S. Williamson of Cornell University in PLoS Genetics found 100 genes under selection in Chinese, African-Americans and European-Americans.
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Wednesday, June 27, 2007
Tuesday, June 19, 2007
Hope of cure for fatal brain diseases
SCIENTISTS HAVE developed a revolutionary new treatment for neurological diseases that uses an injection to tweak the way genes work in the brain.
The research raises hopes for a new era of effective treatments for some of the most debilitating - and so far incurable - brain conditions, including cancer and Alzheimer's disease.
Tests of the therapy at Harvard Medical School in Boston found that a simple injection was able to cure mice of a potentially fatal brain disease. The re- searchers behind the breakthrough are planning further tests and expect to conduct human trials within five years.
The team used a powerfill new technique called RNA interference to silence faulty genes or viruses that cause brain diseases. The principle of gene silencing is simple: scientists build tiny strands of the genetic material called RNA which, when injected into cells, latch on to problematic genes and smother them, effectively shutting them down.
Until now, attempts to use gene silencing to treat brain diseases have been severely hampered for two reasons. First, many drugs injected into the body are barred from getting into the brain by a membrane that protects it from viruses and microbes in the bloodstream.
Because of this, most gene-silencing treatments require nijections directly into the brain - a second serious drawback because it involves a dangerous surgical procedure and only delivers the treatment to the cells at the end of the needle.
The Harvard team, led by Man- junath Swamy, found a simple way around these problems. They made strands of therapeutic RNA in the lab and mixed them with a tiny part of the rabies virus which helps it get into the brain and infect cells. The key-like fragment is harmless on its own.
Researchers squirted some of the mixture on to a dish of nerve cells and found that the strands of RNA they had created were smuggled inside the cells, where they shut down certain genes. The team tested the therapy on mice that had been infected with a fatal brain disease, viral encephalitis. The scientists found that regular injections of RNA mixed with the rabies virus fragment shut down genes in around half of the cells in the animals' brains and stopped the disease from spreading. Of the mice that received injections, 80 per cent were cured, while those that were untreated died, the team reported in Nature.
"We expect this work to move quite fast now, because there is so much interest in this kind of treatment. Potentially, it could be used for a wide variety of neurodegenerative diseases, but also for controlling cancers that spread to the brain," said Professor Swamy.
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The research raises hopes for a new era of effective treatments for some of the most debilitating - and so far incurable - brain conditions, including cancer and Alzheimer's disease.
Tests of the therapy at Harvard Medical School in Boston found that a simple injection was able to cure mice of a potentially fatal brain disease. The re- searchers behind the breakthrough are planning further tests and expect to conduct human trials within five years.
The team used a powerfill new technique called RNA interference to silence faulty genes or viruses that cause brain diseases. The principle of gene silencing is simple: scientists build tiny strands of the genetic material called RNA which, when injected into cells, latch on to problematic genes and smother them, effectively shutting them down.
Until now, attempts to use gene silencing to treat brain diseases have been severely hampered for two reasons. First, many drugs injected into the body are barred from getting into the brain by a membrane that protects it from viruses and microbes in the bloodstream.
Because of this, most gene-silencing treatments require nijections directly into the brain - a second serious drawback because it involves a dangerous surgical procedure and only delivers the treatment to the cells at the end of the needle.
The Harvard team, led by Man- junath Swamy, found a simple way around these problems. They made strands of therapeutic RNA in the lab and mixed them with a tiny part of the rabies virus which helps it get into the brain and infect cells. The key-like fragment is harmless on its own.
Researchers squirted some of the mixture on to a dish of nerve cells and found that the strands of RNA they had created were smuggled inside the cells, where they shut down certain genes. The team tested the therapy on mice that had been infected with a fatal brain disease, viral encephalitis. The scientists found that regular injections of RNA mixed with the rabies virus fragment shut down genes in around half of the cells in the animals' brains and stopped the disease from spreading. Of the mice that received injections, 80 per cent were cured, while those that were untreated died, the team reported in Nature.
"We expect this work to move quite fast now, because there is so much interest in this kind of treatment. Potentially, it could be used for a wide variety of neurodegenerative diseases, but also for controlling cancers that spread to the brain," said Professor Swamy.
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Saturday, June 16, 2007
Rules of sleep hygiene
Do not go to bed until you are drowsy. Most insomniacs go to bed before they are sleepy in an attempt to catch up on lost sleep time and to relieve their sense of tiredness and fatigue. However, typically, when they go to bed they don't sleep, but worry about issues in their daily lives and, in particular, their anticipated poor sleep ahead. This worry causes emotional arousal that prevents the passive sleep process from occurring. Some insomniacs have difficulty distinguishing between fatigue and drowsiness, and may need help in making the distinction between these two states, so that they will go to bed when Delaying going to bed until drowsy not only increases the chances of falling asleep, but also strengthens the association between bed and sleepiness.
Get up at the same time each morning, including weekends:
Insomniacs should always place the alarm clock away from the bed so that the sleeper must get up to turn it off. Maintaining a reasonably early awakening time is one of the important time cues for the 24-hour circadian sleep-wake rhythm. Breaking this rule causes sleep disruption in both good and poor sleepers. The common experience of "Sunday night insomnia, Monday morning blues" is caused by ignoring this rule. The sleeper goes to bed at progressively later times during the weekend, and sleeps in the following morning. By Sunday night, the adapted circadian rhythm is expecting to begin the sleep period beginning at, say, 1:00 am and end at 9:00 am. However, on Sunday night the sleeper wants to go to sleep at 11:00 pm and awaken for work at 7:00 but is unable to fall asleep until the reset time of 1:00 am. Thus, he or she awakens, relatively sleep deprived, at 7:00 with "the blues." read more.....
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Get up at the same time each morning, including weekends:
Insomniacs should always place the alarm clock away from the bed so that the sleeper must get up to turn it off. Maintaining a reasonably early awakening time is one of the important time cues for the 24-hour circadian sleep-wake rhythm. Breaking this rule causes sleep disruption in both good and poor sleepers. The common experience of "Sunday night insomnia, Monday morning blues" is caused by ignoring this rule. The sleeper goes to bed at progressively later times during the weekend, and sleeps in the following morning. By Sunday night, the adapted circadian rhythm is expecting to begin the sleep period beginning at, say, 1:00 am and end at 9:00 am. However, on Sunday night the sleeper wants to go to sleep at 11:00 pm and awaken for work at 7:00 but is unable to fall asleep until the reset time of 1:00 am. Thus, he or she awakens, relatively sleep deprived, at 7:00 with "the blues." read more.....
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Thursday, June 14, 2007
The Hepatitis C virus (HCV)
The Hepatitis C virus (HCV) is a small (50 nm in size), enveloped, single-stranded, positive sense RNA virus in the family Flaviviridae. HCV mainly replicates within hepatocytes in the liver, although there is controversial evidence for replication in lymphocytes or monocytes. Circulating HCV particles bind to receptors on the surfaces of hepatocytes and subsequently enter the cells. Two putative HCV receptors are CD81 and human scavenger receptor class B1 (SR-BI). However, these receptors are found throughout the body. The identification of hepatocyte-specific cofactors that determine observed HCV liver tropism are currently under investigation.
HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, HCV also has an exceptionally high mutation rate, a factor that may help it elude the host's immune response.
Early studies of viral loads in eleven asymptomatically infected viral carriers (blood donors in 1989, prior to implementation of blood bank screening for HCV, and from whom the donated blood units were rejected because of elevated alanine transaminase (ALT) liver enzyme levels) indicated that asymptomatic viral loads in blood plasma varied between 100/mL and 50,000,000/mL.
Although hepatitis A, hepatitis B, and hepatitis C have similar names (because they all cause liver inflammation), these are distinctly different viruses both genetically and clinically. Unlike hepatitis A and B, there is no vaccine to prevent hepatitis C infection.
read more…..
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HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, HCV also has an exceptionally high mutation rate, a factor that may help it elude the host's immune response.
Early studies of viral loads in eleven asymptomatically infected viral carriers (blood donors in 1989, prior to implementation of blood bank screening for HCV, and from whom the donated blood units were rejected because of elevated alanine transaminase (ALT) liver enzyme levels) indicated that asymptomatic viral loads in blood plasma varied between 100/mL and 50,000,000/mL.
Although hepatitis A, hepatitis B, and hepatitis C have similar names (because they all cause liver inflammation), these are distinctly different viruses both genetically and clinically. Unlike hepatitis A and B, there is no vaccine to prevent hepatitis C infection.
read more…..
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Sunday, June 10, 2007
Ecstasy impairs memory
Ecstasy can cause lasting damage to the human brain, even if the drug is only taken for a short time. The memory of ecstasy users who were asked to remember lists of words was impaired.
Researchers compared the performance of the subjects before and after they first tried the drug and concluded that even low doses of the drug could have lasting effects on the brain.
The ideal experiment to investigate the effect of ecstasy on human memory would be to give the drug or a placebo to different participants at random. That would be unethical, so the next best thing would be to test non-drug users first, and then again if they decide to take the drug.
Research on animals has shown that ecstasy can cause long-lasting damage to neurons involved in processing serotonin, a chemical involved in controlling learning, memory, mood and other functions. In several studies a brain region called the hippocampus which is known to be involved in memory has shown up as being particularly badly affected.
A team led by Ben Schmand at the University of Amsterdam recruited 188 volunteers who had never tried the drug, but who said they would probably soon do so. The team tested their performance in a battery of psychological exercises, including tests of attention and memory.
Months later, the team went back to their volunteers and tested 58 who had since taken at least one ecstasy tablet. These subjects were matched against a similar number of controls of a similar age and history of drug use. On average, the subjects who had started to use the drug had taken around three pills in total.
Despite this low dosage, the researchers found a small but statistically significant drop in the volunteers' ability to remember words. This test involved reciting a list of 15 words and remembering the list 20 minutes later. Their performance in other tests was not hampered.
"Our data indicate that low doses of ecstasy are associated with decreased verbal memory function, which is suggestive for ecstasy-induced neurotoxicity," the authors write in the journal Archives of General Psychiatry.
"The main underlying factor seems to be a depletion of serotonin in ecstasy users, a depletion that might be reversible. Serotonin is involved in several cognitive functions, but might be especially relevant to learning and memory."
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Researchers compared the performance of the subjects before and after they first tried the drug and concluded that even low doses of the drug could have lasting effects on the brain.
The ideal experiment to investigate the effect of ecstasy on human memory would be to give the drug or a placebo to different participants at random. That would be unethical, so the next best thing would be to test non-drug users first, and then again if they decide to take the drug.
Research on animals has shown that ecstasy can cause long-lasting damage to neurons involved in processing serotonin, a chemical involved in controlling learning, memory, mood and other functions. In several studies a brain region called the hippocampus which is known to be involved in memory has shown up as being particularly badly affected.
A team led by Ben Schmand at the University of Amsterdam recruited 188 volunteers who had never tried the drug, but who said they would probably soon do so. The team tested their performance in a battery of psychological exercises, including tests of attention and memory.
Months later, the team went back to their volunteers and tested 58 who had since taken at least one ecstasy tablet. These subjects were matched against a similar number of controls of a similar age and history of drug use. On average, the subjects who had started to use the drug had taken around three pills in total.
Despite this low dosage, the researchers found a small but statistically significant drop in the volunteers' ability to remember words. This test involved reciting a list of 15 words and remembering the list 20 minutes later. Their performance in other tests was not hampered.
"Our data indicate that low doses of ecstasy are associated with decreased verbal memory function, which is suggestive for ecstasy-induced neurotoxicity," the authors write in the journal Archives of General Psychiatry.
"The main underlying factor seems to be a depletion of serotonin in ecstasy users, a depletion that might be reversible. Serotonin is involved in several cognitive functions, but might be especially relevant to learning and memory."
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Friday, June 01, 2007
How the brain grows Experts take a peek
Living Can you get smarter than a fifth-grader? Of course, but new research suggests some of the brain's basic building blocks for learning are nearing adult levels by age 11 or 12. It is the first finding from a study of how children's brains grow. The most interesting results are yet to come.
About 500 super-healthy newborns to teenagers, recruited from super-healthy families, are having periodic MRI scans of their brains as they grow up. They also get a battery of age-appropriate tests of such abilities as IQ, language skills and memory. The project, funded by the National Institutes of Health, is tricky work.
Move during an MRI, and the image blurs. Because scientists cannot sedate healthy children, they are having to get crafty to keep their subjects still. Tired toddlers are put in the scanners at naptime; mom squeezes in for a cuddle and earplugs help block the machines' noisy banging. Six-year-olds wear earphones and watch favourite videos beamed into the scanner.
The MRI images measure how different parts of the brain grow and reorganise throughout childhood. Overlap them with the children's shifting behavioural and intellectual abilities at each age, and scientists expect to produce a long-sought map of normal brain development in children representative of the diverse US population. On Friday, scientists were publishing a sneak peek at some surprising early results.
Performance on a variety of cognitive tasks — working memory, vocabulary, spatial recognition, reasoning, and calculation— rapidly improves between age 6 and 10, but then levels off. Children's Hospital Boston, who led the analysis published in the Journal of the International Neuropsychological Society. This is a snapshot of 6- to 18-year-olds' abilities during their first study visit. Results may change after researchers observe each child's progress with age and compare their MRI scans.
The adolescent brain is still growing. Indeed, the region responsible for things such as impulse control and moral judgment is the last to mature, sometime in the early 20s, said of the NIH's National Institute of Neurological Disorders and Stroke.
The study did not evaluate those kinds of skills. "It's an incomplete picture," But the age finding does make sense, suggesting a foundation necessary for higher learning is in place by puberty, said an expert from the University of North Carolina School of Medicine."
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About 500 super-healthy newborns to teenagers, recruited from super-healthy families, are having periodic MRI scans of their brains as they grow up. They also get a battery of age-appropriate tests of such abilities as IQ, language skills and memory. The project, funded by the National Institutes of Health, is tricky work.
Move during an MRI, and the image blurs. Because scientists cannot sedate healthy children, they are having to get crafty to keep their subjects still. Tired toddlers are put in the scanners at naptime; mom squeezes in for a cuddle and earplugs help block the machines' noisy banging. Six-year-olds wear earphones and watch favourite videos beamed into the scanner.
The MRI images measure how different parts of the brain grow and reorganise throughout childhood. Overlap them with the children's shifting behavioural and intellectual abilities at each age, and scientists expect to produce a long-sought map of normal brain development in children representative of the diverse US population. On Friday, scientists were publishing a sneak peek at some surprising early results.
Performance on a variety of cognitive tasks — working memory, vocabulary, spatial recognition, reasoning, and calculation— rapidly improves between age 6 and 10, but then levels off. Children's Hospital Boston, who led the analysis published in the Journal of the International Neuropsychological Society. This is a snapshot of 6- to 18-year-olds' abilities during their first study visit. Results may change after researchers observe each child's progress with age and compare their MRI scans.
The adolescent brain is still growing. Indeed, the region responsible for things such as impulse control and moral judgment is the last to mature, sometime in the early 20s, said of the NIH's National Institute of Neurological Disorders and Stroke.
The study did not evaluate those kinds of skills. "It's an incomplete picture," But the age finding does make sense, suggesting a foundation necessary for higher learning is in place by puberty, said an expert from the University of North Carolina School of Medicine."
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Thursday, May 31, 2007
Mom's stress harms foetus
STRESS EXPERIENCED by a woman during pregnancy may affect her unborn baby as early as 17 weeks after conception, with potentially harmful effects on brain and development, according to new research.
The study is the first to show that unborn babies are exposed to their mother's stress hormones at such an early stage in pregnancy
The study's authors said they did not wish to "unduly worry pregnant women", but highlighted the need to lead a "healthy balanced lifestyle" to avoid general stress.
The findings come days after the government changed its advice to pregnant women and those trying to conceive, warning them to abstain from drinking alcohol.
Previous guidelines had said they could drink up to two small glasses of wine a week.
The change in advice, which government health advisers said was made to avoid confusion, rather than in response to new medical evidence, prompt- ed claims from some critics that pregnant women are increasingly becoming targets in an obsessively anti-risk culture.
Researchers in the latest study led by Professor Vivette Glover at Imperial College London and the consultant obstetrician Pampa Sarkar, from Wexham Park hospital, Berkshire, UK, measured levels of the stress hormone cortisol in 267 pregnant women.
Cortiso1, which is pumped into the blood when we become anxious, is good in the short term, as it helps the body to deal with a stressful situation, but long-term stress can cause tiredness, depression and make an individual more prone to illness.
Dr Sarkar said further research was needed into how high levels of stress in a mother affect the unborn baby "We are all a product of our developmental history," she added.
"Our research shows that the foetus is exposed to cortiso1 in the maternal blood, and we also demonstrated that at and above 17 weeks, the cortisol in amniotic fluid had a strong positive relationship with cortiso1 in maternal
Dr Sarkar continued, "We found that the strength of this correlation became stronger with increasing gestational age. We now need to carry out further research to unravel the mechanisms by which maternal stress affects the foetus, both during foetal life and through into childhood."
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The study is the first to show that unborn babies are exposed to their mother's stress hormones at such an early stage in pregnancy
The study's authors said they did not wish to "unduly worry pregnant women", but highlighted the need to lead a "healthy balanced lifestyle" to avoid general stress.
The findings come days after the government changed its advice to pregnant women and those trying to conceive, warning them to abstain from drinking alcohol.
Previous guidelines had said they could drink up to two small glasses of wine a week.
The change in advice, which government health advisers said was made to avoid confusion, rather than in response to new medical evidence, prompt- ed claims from some critics that pregnant women are increasingly becoming targets in an obsessively anti-risk culture.
Researchers in the latest study led by Professor Vivette Glover at Imperial College London and the consultant obstetrician Pampa Sarkar, from Wexham Park hospital, Berkshire, UK, measured levels of the stress hormone cortisol in 267 pregnant women.
Cortiso1, which is pumped into the blood when we become anxious, is good in the short term, as it helps the body to deal with a stressful situation, but long-term stress can cause tiredness, depression and make an individual more prone to illness.
Dr Sarkar said further research was needed into how high levels of stress in a mother affect the unborn baby "We are all a product of our developmental history," she added.
"Our research shows that the foetus is exposed to cortiso1 in the maternal blood, and we also demonstrated that at and above 17 weeks, the cortisol in amniotic fluid had a strong positive relationship with cortiso1 in maternal
Dr Sarkar continued, "We found that the strength of this correlation became stronger with increasing gestational age. We now need to carry out further research to unravel the mechanisms by which maternal stress affects the foetus, both during foetal life and through into childhood."
For more details on Mom’s Stress harms visit www.halfvalue.com and www.halfvalue.co.uk
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