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AIDS Origin Traced to Chimp Group in Cameroon
darke,look what i got here:
AIDS Origin Traced to Chimp Group in Cameroon
for National Geographic News
May 25, 2006
Chimpanzees living in dense jungles in Africa have been confirmed as the probable source of the HIV virus which caused the human AIDS pandemic.
Researchers have identified simian immunodeficiency virus (SIV) in wild apes for the first time. The virus, which at some point jumped to humans as human immunodeficiency virus (HIV), has been found in chimpanzees in Cameroon, west-central Africa. (Cameroon map and profile)
Scientists have long suspected that HIV had its in origins in wild chimp populations. But previously SIV had been found only in some captive chimps.
The discovery in wild chimps was made by an international research team, which detected SIV antibodies in chimpanzee feces gathered from forests.
The virus was found in chimpanzees in southeastern Cameroon, where SIV infection rates were as high as 35 percent in some chimp populations.
Further genetic analysis linked these chimps to the source of the main strain of HIV-1, the most prevalent form of HIV. The team's findings are to be published tomorrow in the journal Science.
The Cameroonian chimps showed a diversity of SIV strains, with some twice as similar to human HIV strains as any found in captive apes, says study team member Beatrice Hahn, a professor of medicine at the University of Alabama at Birmingham.
"Two clusters [of SIV strains] were very closely related to human strains," she added.
These human strains belong to the M group of HIV-1, the group which has spread among humans worldwide.
The SIV clusters were restricted to communities of the chimpanzee subspecies Pan troglodytes troglodytes.
Origins of AIDS
The team says the findings provide the clearest picture yet of the 70-year-old origins of the current human AIDS pandemic.
"We think it's likely that the cross-species transmission took place locally" in the Cameroon region, Hahn said.
Hunters in the region who caught and ate chimps were probably the first to contract HIV, she adds.
"Based on what we know about the biology of these viruses, you need to be exposed to infectious blood or body fluids," she said. "You don't get it by petting a chimp."
From southeastern Cameroon the virus appears then to have spread south via the Sangha and Congo Rivers.
"Eventually the virus ended up in a major metropolitan area, which would either be Kinshasa [Democratic Republic of the Congo]or Brazzaville [Republic of the Congo]," Hahn added. "That's where we believe the AIDS pandemic really started."
Chimps in turn are thought to have picked up SIV by eating infected monkeys.
A study published in 2003 in Science suggested a chimp strain of SIV arose through repeated transmissions and recombination of similar viruses found in red-capped mangabeys and greater spot-nosed monkeys. (Read a story about this study.)
This previous research was led by Paul Sharp of the Institute of Genetics at the University of Nottingham in England.
"We now know there are more than 30 species of monkeys across Africa which have their own forms of SIVs," said Sharp, who was also involved with the new study
Chimps, however, are the only apes known to be infected.
"The chimp virus is a mosaic of viruses that infect prey monkeys," the University of Alabama's Hahn said. "Chimps had to eat these monkeys first but they have certainly had their infection a lot longer than humans."
She says the diversity of new SIV strains detected in Cameroon chimps raises the possibility that the animals could pass on new types of HIV infection to humans.
This, says Hahn, could hinder the global fight against AIDS.
"Cross-species transmissions could have already occurred and may have gone unrecognized," she added.
Hahn says it's unlikely that further, recently acquired chimp infections have led to AIDS epidemics in humans. But such transmissions could undermine the effectiveness of AIDS vaccines currently under development.
"If we ever had a vaccine that worked and you then bring in a new virus that's 30 or 40 percent different, that's probably not a good thing," she said.
"It might be much more difficult to detect one of these other chimp viruses if it jumped into humans," the University of Nottingham's Sharp added.
On the other hand, further studies of wild chimp populations could help in finding new treatments for AIDS sufferers, Sharp says.
"As far as we know, the chimps don't get any type of AIDS-like disease," he said. "That's part of the reason for being very interested in the infection of chimps, because chimps and humans are very similar genetically."
also,take a look at:
-AIDS origins (Cod. A 27112005)
ACE inhibitors may pose more birth defect risks
June 9, 2006
by Carole Bartoo
The Food and Drug Administration is looking at evidence examined by researchers at the Monroe Carell Jr. Children's Hospital at Vanderbilt to determine if new warnings need to be put on common blood pressure medications regarding an increased risk of birth defects for babies whose mothers take the medications during the first trimester of pregnancy.
William Cooper, M.D., M.P.H., associate professor of Pediatrics, was first author of a study in the New England Journal of Medicine, along with colleagues from the departments of Pediatrics, Preventive Medicine and Biostatistics. Cooper and co-authors found that infants born to mothers who took angiotensin converting enzyme inhibitors (ACE inhibitors) during the first trimester of pregnancy had an increased risk of major birth defects compared with infants whose mothers did not take these medications.
We knew ACE inhibitors were a possible cause of adverse fetal outcomes when exposure occurred later in pregnancy, but it has not been well studied in the first trimester, Cooper said.
We were very surprised that even after controlling for other risk factors, the TennCare records we examined showed a clear increase in a broad range of birth defects following first trimester-only exposures.
This research is important because the number of women of childbearing age who develop high blood pressure and are prescribed ACE inhibitors is increasing in this country, according to other data included in the study.
ACE inhibitors already carry a warning stating that they can cause injury and even death to the developing fetus when used during the second and third trimesters of pregnancy.
The warning states that use of ACE inhibitors should be discontinued as soon as possible when pregnancy is detected.
Cooper and his co-authors performed the research within the Child and Adolescent Health Research Unit at Children's Hospital.
The study was jointly funded by the FDA and Vanderbilt's Center for Education and Research on Therapeutics, which is funded through the Department of Health and Human Services' Agency for Healthcare Research and Quality. Results were published in the June 8 issue of the New England Journal of Medicine.
Scientists Unlock More Secrets Of HIV And SARS
Source: Biotechnology and Biological Sciences Research Council
10 may 2006
UK scientists have cracked one of the key biological processes used by viruses such as HIV and SARS when they replicate according to a paper published in the journal Nature tomorrow (11 May). Viruses are able to interfere with the host cell processes that our bodies use to replicate cells, and protein synthesis is often one of their targets. For the first time, researchers at the Universities of Cambridge and Oxford have witnessed virus-induced "frameshifting" in action and have been able to identify the crucial role of particular elements. The research, funded by the Biotechnology and Biological Sciences Research Council (BBSRC), the Medical Research Council (MRC), The Royal Society and The Wellcome Trust, brings us another step closer to understanding the fundamental workings of these devastating viruses.
The scientists have revealed the workings of the process known as 'ribosomal frameshifting' that forces a mis-reading of the genetic code during protein synthesis. The correct expression of most genes depends upon accurate translation of the 'frame' of the genetic code, which has a three nucleotide periodicity. Viruses such as HIV and SARS bring into the cell a special signal that forces the ribosome to back up by one nucleotide, pushing it into another 'frame' and allowing synthesis of different viral proteins. These are exploited by viruses and help them to survive and multiply.
The British researchers successfully imaged frameshifting in action and for the first time observed how a virus encoded element called an RNA pseudoknot interferes with the translation of the genetic code to allow viruses like HIV and SARS to express their own enzymes of replication.
Dr Ian Brierley, the project leader at the University of Cambridge, said: "This collaborative project was set up with Dr Robert Gilbert's team in Oxford to investigate the structure of a frameshifting ribosome using electron microscopy. The images we obtained give us an insight into how a virus-encoded RNA pseudoknot can induce frameshifting and may be useful in designing new ways to combat virus pathogens that use this process."
Professor Julia Goodfellow, Chief Executive of the Biotechnology and Biological Sciences Research Council, which was one of the main funders, said: "This is exciting and valuable research and demonstrates clearly why investment in fundamental science is so important. The treatments and therapies that we now take for granted are based on decades of work by scientists furthering our understanding of natural processes. The work to explore fundamental biology today is laying the foundation for potential medical applications over the next twenty years."
original source: http://www.sciencedaily.com/release...60510191609.htm
Use Embryonic Stem Cells To Awaken Latent Motor Nerve Repair (1)
Source: Johns Hopkins Medical Institutions
Posted: June 26, 2006
Hopkins Scientists Use Embryonic Stem Cells, New Cues To Awaken Latent Motor Nerve Repair
In a dramatic display of stem cells potential for healing, a team of Johns Hopkins scientists reports that theyve engineered new, completed, fully-working motor neuron circuits -- neurons stretching from spinal cord to target muscles -- in paralyzed adult animals.
The research, in which mouse embryonic stem (ES) cells were injected into rats whose virus-damaged spinal cords model nerve disease, shows that such cells can be made to re-trace complex pathways of nerve development long shut off in adult mammals, the researchers say.
This is proof of the principle that we can recapture what happens in early stages of motor neuron development and use that to repair damaged nervous systems, says Douglas Kerr, M.D., Ph.D., a neurologist who led the Hopkins team.
Its a remarkable advance that can help us understand how stem cells can begin to fulfill their great promise, says Elias A. Zerhouni, director of the National Institutes of Health. Demonstrating restoration of function is an important step forward, though we still have a great distance to go.
The researchers created what amounts to a cookbook recipe to restore lost nerve function, Kerr explains. The approach could one day repair damage from such diseases as ALS (Lou Gehrigs disease), multiple sclerosis or transverse myelitis or from traumatic spinal cord injury, the researchers say. With small adjustments keyed to differences in nervous system targets, Kerr says, the approach may also apply to patients with Parkinson's or Huntingtons disease.
In a report on the study, to be released online June 26 in the Annals of Neurology, the Hopkins team says 11 of the 15 treated rats gained significant, though partial, recovery from paralysis after losing motor neurons to an aggressive infection with Sindbis virus -- one that, in rodents, specifically targets motor neurons and kills them. The animals recovered enough muscle strength to bear weight and step with the previously paralyzed hind leg.
Kerr likens the approach to electrical repair. Paralysis is like turning on a light switch and the light doesnt go on. The connectivity is messed up but you dont know where. Weve asked stem cells to go where needed to fix the circuit.
For a brief period after a nerve dies, it leaves behind whats essentially an empty shell, with some scaffolding and non-nerve substances remaining. But with ES injections at the right time and place, and by adding the right cues, weve learned to restore the biological memory for growing neurons, which is clearly still in place, he added.
The motor circuit engineering combines recent discoveries on stem cell differentiation, a growing understanding of early development of the nervous system, and insights into behavior of the nervous system in traumatic injury, Kerr notes.
As adults, our cells no longer respond to early developmental cues because those cues are usually gone, says Kerr. Thats why we dont recover well from severe injuries. But thats what we believe we have changed. We asked what was there when motor neurons were born, and specifically what let motor neurons extend outward. Then we tried to bring that environment back, in the presence of adaptable, receptive stem cells.
In the study, Kerrs team first pre-treated cultures of mouse embryonic stem cells with growth factors that both increase survival and prompt specialization into motor neurons. Adding retinoic acid and sonic hedgehog protein -- agents that direct cells in the first weeks of life to assume the proper places in the spinal cord -- readied the conditioned ES cells for the motor neuron circuit that starts in the spinal cord. Then, stem cells were fed into the paralyzed rats spinal cords.
Use Embryonic Stem Cells To Awaken Latent Motor Nerve Repair (2)
Extending new motor neurons in an adult nervous system, however, meant overcoming hurdles. One involved myelin, the fatty material that insulates mature motor neurons. Like the coating on electrical wire, myelin prevents weakening of the traveling electrical impulse and lets it continue long distances. In humans, the myelinated sciatic nerve, for example, exits the spinal cord and extends to the leg muscles it activates, carrying impulses several feet.
Once laid down, however, myelin inhibits further nerve growth -- natures way to discourage excessive wiring in the nervous system. We had to overcome inhibition from myelin lingering in the dead nerve pathways, Kerr explains. Two recently-developed agents, rolipram and dbcAMP enabled that.
The assorted treatments let the new motor neurons survive, grow through the spinal cord and extend slightly into the outlying nervous system. A second hurdle remained in getting the neurons to skeletal muscle targets.
As suggested by earlier work by team member Ahmet Hoke on repair in the outlying, peripheral nervous system, the researchers applied GDNF, a powerful stimulator of neuron growth, to the remains of the newly-dead sciatic nerve at a point near its former leg muscle contacts. GDNF attracted the extending motor neurons, luring them to the muscles. To ensure a continuous supply of GDNF, the researchers relied on injected fetal mouse neural stem cells, a known source of the molecule.
Of some 4,100 new motor neurons created in the spinal cord, roughly 200 exited the cord and 120 reached skeletal muscle, forming typical nerve-muscle junctions, with appropriate, typical chemical markers. Microscopically, the neurons and their muscle associations appear identical to natural ones in healthy animals.
Fifty of the new neurons were found to carry electrical impulses. (Because such testing is time and labor intensive, only a small area of leg muscle was assayed. The improved ability of treated rats, however, suggests more functional neurons are likely.) The rats gained weight, were more mobile in their cages and measures of muscle strength increased.
Animals treated without even one component of the cocktail experienced no such recovery. Novel ways of tracing the neurons back to their source assured the scientists that they indeed had come from the injected stem cells, not from lingering host neurons.
Research begins this summer to see how well the technique applies to human nerve recovery, using federally-approved human ES cells in larger mammals like pigs, Kerr says. Each of six academic institutions in a new collaboration will tackle a different major question of safety and effectiveness. Questions of tumor-formation, often a concern with ES cells, of the safety of surgery and of the ES cells ability to form healthy motor circuits are major questions to answer. Several years of testing and thorough data evaluation would occur before applying to the FDA to approve human clinical trials. The study was supported by Families of SMA, Andrews Buddies/Fight SMA, the ALS Association and The Robert Packard Center for ALS Research at Johns Hopkins, the Muscular Dystrophy Association, Wings Over Wall Street, and a grant from the NIH.
Kerr is a grantee of The Packard Center for ALS Research at Johns Hopkins. He also directs Project RESTORE, a Hopkins-based undertaking to advance therapies for transverse myelitis and multiple sclerosis.
Avoiding Punishment Is Its Own Reward
12 july 2006
To give your child an incentive to take out the garbage, you might offer to buy her a treat, or you might threaten to withhold her regular allowance. Does the child respond the same way to reward as it does to avoiding punishment? Psychologists have evidence from certain kinds of behavioral experiments to believe that avoiding punishment is itself a reward.
In a new study published online in the open-access journal PLoS Biology , Hackjin Kim, Shinsuke Shimojo, and John O'Doherty investigated this question by scanning the brains of humans performing a simple instrumental conditioning task. A brain area called the medial orbitofrontal cortex (OFC) has been linked to reward-related stimuli, particularly when the reward involves money. The researchers found that the OFC is also activated for avoidance learning, supporting the hypothesis that these cognitive processes share neural mechanisms.
Sixteen people participated in the study, during which they could either lose or win one dollar in an instrumental choice task. During the experimental trials, participants selected one of two fractal images presented on a screen. After a fractal was chosen, it became brighter, and four seconds later the participant got one of four types of feedback: reward (a picture of a dollar bill and the message, You win!), negative outcome (same image, with the text, You lost!), neutral (a scrambled bill with the text, No change), or nothing (a blank screen). During reward trials, the choice led to a high or low probability of reward (earning a dollar); during avoidance trials, the choice led to a high or low probability of avoiding a negative outcome (losing a dollar).
Over time, participants learned to choose fractals associated with a greater probability of reward and a lower probability of a negative outcome. And, as predicted, the medial OFC showed a higher response when participants chose an option that resulted in not losing the dollar or in winning it. Conversely, when participants' choices resulted in negative outcomes and when there was no reward offered OFC activity declined. Compared to neutral trials, reward and avoidance events produced significantly greater brain activity, while negative outcomes and neutral events linked to no chance of reward resulted in significantly decreased activity. Kim et al. argue that these functional magnetic resonance imaging (fMRI) results provide direct evidence that avoiding bad outcomes and receiving a reward provoke a similar response in the medial OFC.
Avoiding negative outcomes and receiving rewards amount to the same thing for the brain: achieving a goal. Reward serves as an external signal that reinforces behavior associated with a positive outcome, Kim et al. explain, and punishment amounts to an intrinsic reward signal that reinforces actions linked to avoiding bad outcomes. With fMRI evidence connecting avoidance and reward circuits, researchers can now determine which neuron populations within the OFC contribute to the avoidance "reward response"and perhaps shed light on the neurobiological roots of pathological risk-seeking behavior.
Morning sickness - a form of protection for mother and baby
Published: Wednesday, 12-Jul-2006
As many as 90% of mothers experience nausea during pregnancy, and about half that number vomit.
Although it is more common in the first three months some women are nauseous throughout their pregnancy.
The name "morning sickness" is misleading because nausea can occur at any time of day and in the most serious cases it can become hyperemesis gravidarum, or excess vomiting, which can be fatal.
In research by Liverpool University, where an analysis of 56 previous studies in 21 countries was carried out, the prevalence of nausea and sickness in pregnant women was examined.
Researchers Dr. Gillian Pepper and Dr. Craig Roberts linked these figures to the typical diet in each country and suggest there is a link between nausea and diet.
They say morning sickness might have evolved to ensure pregnant women do not digest too much unhealthy food.
They found evidence that nausea and vomiting in pregnancy is associated with high intake of sugar, alcohol, oils and meat.
For some women even the common smells, particularly fat and fried food, and the sight of food cooking is enough to bring on a wave of nausea.
Another study found that 50% of women developed an aversion to alcohol in their first three months and there appears to be mounting evidence that morning sickness is the body protecting itself against harmful substances in food.
It seems countries with a high intake of sugars, sweeteners, stimulants such as caffeine, vegetables, meats, milk and eggs had more sick pregnant women, and those with high intake of cereals and pulses had lower levels.
The researchers believe that the pregnant human body may have evolved an aversion to foods containing high levels of toxins, and that this may have carried over into modern living.
They suggest that the body might reject meat because of the relatively high risk that it might harbour disease-causing agents while the low level of plant toxins in cereals may make them particularly unlikely to trigger nausea.
But the body's rejection of sugars and oils is less easy to explain.
Lead researcher Dr. Roberts says womens' bodies may be pre-programmed by evolution to avoid particular foodstuffs in the first trimester and the nausea could be nature's way of avoiding problems in pregnancy for both mother and foetus.
Experts say the theory makes sense as morning sickness is always worst in the first three months, which is when the most important part of a foetus's development is happening.
They say it is sensible for a woman to eat healthily in pregnancy, but more important she avoid alcohol, smoking or drugs.
Ne muajin e pare te shtatzanise kam zhvilluar neveri per disa lloj ushqimesh, por kryesisht vezet dhe nje lloj embelsire. Kam vrare shume mendjen ne lidhje me rolin e GCH-se ne kete proces por nuk shihja logjike. Sepse ne mjekesi gjithcka e ka nje arsye madhore, sado qe ne veshtrim te pare duket rastesi ose rrjedhoje e evolucionit (ne te cilin nuk besoj aspak). Tani ky lajm ploteson ne menyre te perkryer mozaikun e kesaj enigme. Faleminderit NS-6.
me vjen mire qe artikulli te paska qene ne ndihme...sic e the,cdo gje e ka nje shpjegim ne mjeksi,dhe keto gjera nuk i lene shume vend rastesise sic thote teorija e evolucionit (qe nuk i besoj fare)...ndoshta ne te ardhmen do ti bej nje analize kesaj teorie tek tema e gjenetikes
ne kete teme,jam duke vendos artikujt qe me duken me interesante nder ato qe me qellon te lexoj here pas here!jane ne pergjithsi lajme te fresketa te marre nga sitet kryesore te lajmeve mjeksore
p.s: darke,sorry about the albanian language here ...Izolda,shkaku i kesaj teme ka qene darke,qe eshte spanjolle dhe nuk ka mundesi qe te kuptoje ato gjera qe ishin ne shqip...kshu qe ketu mund te shohe artikuj ne anglisht
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