By KATIE MOISSE May 5, 2011
Karen Butler is from Oregon, not England. When asked where she got her accent, she says from her dental surgeon.
In 2009 Butler, a 56-year-old tax consultant in Toledo, Ore., awoke from denture implant surgery with an accent that’s a bit British with a Transylvanian twang, and it just sort of stuck.
“I had just had surgery, so at first we assumed it was because of all of the swelling,” said Butler. “But within a week the swelling went down and the accent stayed.”
Butler has foreign accent syndrome — a condition so rare that only about 60 cases have been documented worldwide. Often preceded by a small stroke, the new drawl is thought to stem from a minor injury to a tiny area of the brain responsible for language pattern and tone.
“This is a very small part of the brain that controls the articulation and the intonation of speech that’s affected, and that’s why it’s so rare,” said Dr. Ted Lowenkopf, a neurologist and medical director of Providence Stroke Center in Portland, Ore., in an interview with ABC News affiliate KATU. “The chances to hit such a small area are more than a million to one in a stroke.”
Because certain blood vessels in the brain are more prone to blockages, a stroke often damages parts of the brain responsible for language production and comprehension.
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“Stroke happens in very predictable ways,” said Dr. Julius Fridriksson, an associate professor of neuroscience at the University of South Carolina, who has seen many stroke patients but only a couple with foreign accent syndrome. “This type of damage is out of the ordinary.”
Butler said she was never tested for a stroke because she felt fine.
“I appear to be completely normal otherwise,” Butler said, adding that she never felt any pain or had neurological symptoms other than the change in her speech. “And I’m quite OK with [the accent].”
Nevertheless, Butler endures her fair share of teasing — mostly from her family. She struggles with the letter “W,” which she pronounces like a “V.” So her daughter once asked her to say, “I vant to suck you blood” and recorded it with her cell phone as a ring tone.
But Butler brushes it all off.
“With a sense of humor, you can face anything,” she said.
Not everyone with foreign accent syndrome is so lighthearted.
“It’s very much related to a person’s coping ability,” said Fridriksson. “Some people become isolated because they’re so self-conscious about it.”
Although Butler’s accent sounds vaguely British — Welsh, even — it’s purely coincidental.
“Although we think it sounds like a British accent, if you had a language expert listening to her, they would say that’s not an English accent,” Lowenkopf told KATU. “It’s sort of an amalgam of different-sounding speech that sounds like a foreign accent. But it’s not truly typical of any one foreign accent.”
Because her accent flipped between tax seasons, Butler was forced to start many phone conversations explaining to her clients that she was indeed still Karen Butler, their tax consultant from Oregon. Her husband Glen does his share of explaining too.
“[People] have wanted to know where I met her,” he told KATU with a smile.
The accidental accent is usually fleeting and goes away within weeks or months, Lowenkopf said. But the longer it lasts, the more likely it is to stick for good.
Butler kept her voicemail greeting from before the surgery to remind her and others of her once-Oregonian sound. And although speech therapy could help her get it back, she said she’s used to her new “foreign” accent.
“I used to be painfully shy, and now there’s always something to talk about,” she said. Copyright © 2011 ABC News Internet Ventures. By KATIE MOISSE May 5, 2011
September 14, 2012 · Posted in Ebola Virus
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Ebola outbreak kills one in Uganda, more cases seen
Sat May 14, 2011 2:01pm GMT
The girl from Luwero district, 75 km north of Kampala, died on May 6, Anthony Mbonye, Uganda government’s commissioner for community health told journalists.
“Laboratory investigations have confirmed Ebola to be the primary cause of the illness and death. So there is one case reported but we expect other cases,” said Mbonye.
The last outbreak in 2007 killed 37 people. (Reporting by Barry Malone; Writing by James Macharia)
Some protozoa infect the brain of their host, shaping its behavior in ways most suited to the pathogen, even if it leads to the suicide of the host
By Christof Koch | Tuesday, May 17, 2011 | 3
The ancient debate surrounding the existence of free will appears unresolvable, a metaphysical question that generates much heat yet little light. Common sense and volumes of psychological and neuroscientific research reveal, however, that we are less free than we think we are. Our genes, our upbringing and our environment influence our behaviors in ways that often escape conscious control. Understanding this influence, the advertisement industry spent approximately half a trillion dollars worldwide in 2010 to shape the buying decisions of consumers. And extreme dictatorships, such as that in North Korea, remain in power through the effective use of insidious and all-pervasive forms of propaganda. Yet nothing approaches the perfidy of the one-celled organism Toxoplasma gondii, one of the most widespread of all parasitic protozoa. It takes over the brain of its host and makes it do things, even actions that will cause it to die, in the service of this nasty hitchhiker. It sounds like a cheesy Hollywood horror flick, except that it is for real.
We know that illness in general can slow us down, incapacitate us and, in the worst case, kill us. Yet this organism is much more specific. Natural selection has given rise to pathogens that infiltrate the nervous system and change that system’s wiring to achieve its ultimate purpose, replication—like a computer virus that reprograms an infected machine.
Such is the case with T. gondii. It sexually reproduces only in the intestines of cats yet can maintain itself indefinitely in any warm-blooded animal. Infected cats shed millions of their oocysts in their feces. Taken up by all kinds of animals, including dogs, rodents and humans, they infect muscle and the brain to escape attacks by the host’s immune system. Hidden away, they remain dormant as cysts, surrounding themselves with a tough cell wall. Yet this quiet stage of infection, called toxoplasmosis, is deceptive. Violating all rules of good hospitality, these invaders make the host’s brain do things counterproductive to its own survival.
Toxoplasmosis has been most thoroughly studied in rats and mice. Both species have a deep-seated, innate fear of cats for obvious reasons. Spray a bit of cat urine into a corner, and the rodent will avoid this location, well, like the plague. In contrast, an infected animal loses its innate fear of cats. By some measures, it even appears to be mildly attracted to the smell of felines. This is an unfortunate turn of events for the rodent, because it is now more likely to be successfully hunted by a cat. On the other hand, this is a great deal for T. gondii. When the cat devours the sick critter and its contaminated brain, T. gondii moves into its final host, where it reproduces, completing its life cycle. Not quite what the romantics have in mind when they write about “the circle of life”!
The behavioral manipulation induced by T. gondii is quite specific. The infected rodent doesn’t look sick; its weight is normal; it moves about normally, possibly a bit more frantically than other mice; it grooms itself; and it interacts routinely with its conspecifics. Think how different this case is from what happens in rabies, another nasty infection. The animal loses its instinctual shyness, aggressively attacking others (the proverbial mad dog), thereby spreading the rabies virus through its bite. But because T. gondii can reproduce only in felines, it wants its host to be eaten by cats, not by just any carnivore. And because cats hunt live prey and do not eat carrion, T. gondii must not immediately kill its temporary host.
Rodents Aren’t Superheroes How does T. gondii effect its insidious changes in the host? Experiments by Joanne P. Webster of Imperial College London, Robert Sapolsky of Stanford University and others have shown that infected rats or mice do not turn into the murine equivalent of Siegfried, the hero of Wagner’s Ring who knew no fear. No, they still avoid open spaces, remain nocturnal creatures, retain their aversion to the urine of other predators and learn to fear a tone associated with a foot shock. Might the protozoa have stunted their smell? After all, if they cannot smell anything anymore, they would not know how to avoid places smelling of cat urine. But infected mice still avoid food if it smells different—an aversion that arose partly because for centuries humans have been trying to control rodents by poison. The infected mice also respond appropriately to the smell of their littermates.
Clues about how the parasites affect the animal come from several observations. First, the density of cysts in the amygdala is almost double that in other brain structures involved in odor perception. Parts of the amygdala have been linked to anxiety and the sensation of fear. Second, the genome of T. gondii contains two genes related to mammalian genes involved in the regulation of dopamine, the molecule associated with reward and pleasure signals in the brain, including in ours. So perhaps the creepy protozoa makes suicidal activities, such as hanging around places frequented by cats, feel more pleasurable for the infected rodent?
What elevates this vignette about evolution and life in the wild to epic proportions for humanity is that about a tenth of the U.S. population is infected by T. gondii (in some countries, such as France, the infection rate is seven to eight times higher, possibly because of the widespread consumption of uncooked and undercooked meat). Human toxoplasmosis is usually considered to be symptom-free (what doctors refer to as asymptomatic). Exceptions are patients with a weakened immune system and the unborn (hence the need for pregnant women to avoid cleaning cat-litter boxes).
Science has known for a long time that schizophrenic patients are two to three times more likely to carry antibodies to T. gondii than are controls who are not schizophrenic. Furthermore, antipsychotic drugs that block the action of dopamine, such as haloperidol, commonly used in the treatment of schizophrenia, are also effective in combating toxoplasmosis in both rats and people. And some infected adults go on to develop psychotic symptoms similar to schizophrenia. Little is known about the mode or site of action of this pathogen in the human brain. The exact link between T. gondii and psychiatric diseases is tantalizing but remains murky.
Recent claims go so far as to argue for a role of T. gondii in shaping distinct cultural habits, depending on the rate of infection in the population. A prospective study tracking the road safety in Czech recruits during their 18 months of compulsory military draft found a rate of accidents six times higher in affected drivers. Are the young men with toxoplasmosis infection simply slowed down? Or do they drive more aggressively?
In my November 2009 column, I described the discovery by cognitive neuroscientists that the feeling of freely willing an action (called authorship or agency) is a subjective, conscious sensation no different, in principle, from the conscious awareness of seeing the azure blue sky or feeling the sharp pain of a toothache. When I engage in a dangerous pursuit, such as taking the end of the rope on a steep section of a granite wall in Yosemite Valley while climbing, I feel as if “I freely decided” to do so, whatever this might mean in a metaphysical sense. Yet my action is most likely caused by an inexhaustible multiplicity of factors not accessible to my conscious introspection, including, yes, possibly some tiny single-celled parasites lodging in my brain and making me act out their silent commands. The wonder of it all.
By OLIVIA KATRANDJIAN June 4, 2011
The rapidly developing European E. coli outbreak that has killed 18 people and sickened thousands, including four suspected cases in the United States, has become the deadliest outbreak of E. coli in modern history. Where exactly people are being infected with the disease is still unknown, although 17 people fell ill after eating in the northern German city of Luebeck in May, according to the local media. Researchers from Germany’s national disease control center are inspecting the restaurant in question.
Other health experts suspect the disease first spread last month at a festival in the northern German city of Hamburg that was visited by 1.5 million people. But as of yet, there is no concrete proof that either site is the cause of the outbreak.
In a briefing Friday, the U.S. Centers for Disease Control and Prevention said the four suspected cases in the United States are all people who likely contracted the infection while in northern Germany in May and brought it back to the United States. Three of the victims are hospitalized with hemolytic-uremic syndrome and the fourth reported bloody diarrhea consistent with the outbreak strain of E. coli.
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Two American military service members stationed in Germany are also suspected cases. The CDC said both of them have a similar diarrheal illness.
Government officials stressed that the outbreak has not affected the United States directly.
The Food and Drug Administration is monitoring lettuce, tomatoes and cucumbers from Spain and Germany based on information it has received from European investigators. Produce from those countries accounts for less than 0.2 percent of produce imported into the United States every year.
The FDA says it is also stepping up its food safety regulations.
Hygiene Key to Avoiding Spread
While the outbreak hasn’t hit U.S. soil yet and the infection isn’t easily spread, there are ways to be sure that any illness that may be caused by the outbreak isn’t spread.
In addition to avoiding contaminated food, good hygiene is the most important way to minimize transmission, according to Dr. Maria Alcaide, an assistant professor of infectious diseases at the University of Miami’s Miller School of Medicine.
“It’s also spread through contaminated feces,” Alcaide said. “Anyone who is sick should wash their hands, and their caregivers should as well.”
Anyone who starts noticing any symptoms should get to a doctor.
“If anybody gets very bad, bloody diarrhea, they should get medical care immediately, and providers should also be aware of what’s going on with the situation,” Alcaide said.
ABC News’ Kim Carollo contributed to this report.
Plague is an infectious disease that affects animals and humans. It is caused by the bacterium Yersinia pestis. This bacterium is found in rodents and their fleas and occurs in many areas of the world, including the United States.
Y. pestis is easily destroyed by sunlight and drying. Even so, when released into air, the bacterium will survive for up to one hour, although this could vary depending on conditions.
Pneumonic plague is one of several forms of plague. Depending on circumstances, these forms may occur separately or in combination:
•Pneumonic plague occurs when Y. pestis infects the lungs. This type of plague can spread from person to person through the air. Transmission can take place if someone breathes in aerosolized bacteria, which could happen in a bioterrorist attack. Pneumonic plague is also spread by breathing in Y. pestis suspended in respiratory droplets from a person (or animal) with pneumonic plague. Becoming infected in this way usually requires direct and close contact with the ill person or animal. Pneumonic plague may also occur if a person with bubonic or septicemic plague is untreated and the bacteria spread to the lungs.
•Bubonic plague is the most common form of plague. This occurs when an infected flea bites a person or when materials contaminated with Y. pestis enter through a break in a person’s skin. Patients develop swollen, tender lymph glands (called buboes) and fever, headache, chills, and weakness. Bubonic plague does not spread from person to person.
• Septicemic plague occurs when plague bacteria multiply in the blood. It can be a complication of pneumonic or bubonic plague or it can occur by itself. When it occurs alone, it is caused in the same ways as bubonic plague; however, buboes do not develop. Patients have fever, chills, prostration, abdominal pain, shock, and bleeding into skin and other organs. Septicemic plague does not spread from person to person.
Symptoms and Treatment
With pneumonic plague, the first signs of illness are fever, headache, weakness, and rapidly developing pneumonia with shortness of breath, chest pain, cough, and sometimes bloody or watery sputum. The pneumonia progresses for 2 to 4 days and may cause respiratory failure and shock. Without early treatment, patients may die.
Early treatment of pneumonic plague is essential. To reduce the chance of death, antibiotics must be given within 24 hours of first symptoms. Streptomycin, gentamicin, the tetracyclines, and chloramphenicol are all effective against pneumonic plague.
Antibiotic treatment for 7 days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.
A plague vaccine is not currently available for use in the United States.
Facts about Pneumonic Plague
Escherichia coli Infection
( E. coli Infection, Escherichia coli O157:H7)
by Krisha McCoy, MS
En Español (Spanish Version)
- Risk Factors
Escherichia coli ( E. coli ) infection is caused by a bacteria. It is the leading cause of bloody diarrhea. This type of infection may need medical attention. Contact your doctor if you think you may have it.
This infection is caused by some types of the E. coli bacterium. Most E. coli infections are caused by:
- Eating undercooked beef, especially ground beef
- Drinking contaminated water
- Drinking unpasteurized milk
- Working with cattle
Digestive Pathway Through Stomach and Intestines
© 2011 Nucleus Medical Media, Inc.
The following factors increase your chance of developing E. coli infection:
- Age: children and older people
- People with another illness
- Working with cattle
- Living in northern states
- Abdominal cramps
- Watery diarrhea
- Bright red, bloody stools
- Mild fever
- Nausea or vomiting
Your doctor will ask about your symptoms and medical history. A physical exam will be done. Tests may include:
- Stool culture—to find out if you have E. coli O157:H7 in your intestines
Talk with your doctor about the best plan for you. Treatment options include:
Fluid Replacement and Monitoring
Most people will get better in 5-10 days. They rarely need a specific treatment. Avoid medicine that stops diarrhea. Drink plenty of water and fluids. Fluids through an IV line may be needed in cases of severe dehydration .
Treatment for Hemolytic Uremic Syndrome (HUS)
HUS is a life-threatening condition. It occurs in some people with E. coli infection. HUS may need to be treated withblood transfusions and kidney dialysis . Symptoms may include:
- Pallor, tiredness, and irritability
- Small, unexplained bruises, or bleeding from the nose or mouth—caused by problems in the body’s clotting mechanism
© 2011 Nucleus Medical Media, Inc.
If you are diagnosed with an E. coli infection, follow your doctor’s instructions .
To help prevent E. coli infection:
- Cook all ground beef and hamburger thoroughly.
- Avoid eating undercooked hamburger or other ground beef.
- Keep raw meats separate from ready-to-eat foods.
- Wash hands, counters, and utensils with hot soapy water after they are exposed to raw meat.
- Drink only pasteurized milk, juice, and cider.
- Wash fruits and vegetables under running water.
- Drink municipal water that has been treated with a disinfectant (eg, chlorine).
- Wash hands after bowel movements and after changing soiled diapers.
Last reviewed September 2010 by David L. Horn, MD, FACP
Please be aware that this information is provided to supplement the care provided by your physician. It is neither intended nor implied to be a substitute for professional medical advice. CALL YOUR HEALTHCARE PROVIDER IMMEDIATELY IF YOU THINK YOU MAY HAVE A MEDICAL EMERGENCY. Always seek the advice of your physician or other qualified health provider prior to starting any new treatment or with any questions you may have regarding a medical condition.
Copyright © 2011 EBSCO Publishing. All rights reserved.
August 25, 2012 · Posted in HIV Virus
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by Mary Carmichael
How It Began – HIV Before The Age Of Aids
As soon as HIV was identified in 1983, scientists started trying to understand where it had come from, when it had arisen, and why it had spread. Were they too late? To answer most of their questions, they would have had to witness the virus’s evolution. Scientists can track new pathogens such as SARS and avian flu because they produce obvious symptoms almost immediately. But HIV is a stealth virus that takes as many as 10 years to present symptoms; by the time researchers knew enough to wonder about its origins, those origins were in the distant past.
For the last 23 years, scientists have been trying to peer into that past. Jon Cohen, a correspondent for Science who has written extensively about the virus, compares the work to fossil hunting, using a few precious shreds of evidence to construct a possible history. “Everybody’s always looking for certainty. It doesn’t exist [in this field],” he says. “In a sense it’s all theory.”
Nonetheless, the theory rests on facts, and at least a few of them are undisputed — including, most significantly, HIV’s family tree. There are two species of the virus, HIV-1 and HIV-2. The first evolved from a simian immunodeficiency virus (SIV) found in chimpanzees, while the second came from an SIV in a type of monkey called the sooty mangabey.
Part One: Chapter Four Scientific Breakthroughs
HIV-1, which is responsible for the vast majority of AIDS cases worldwide, is divided into three groups — the “major” group M, and the much rarer “outlier” group O and “new” group N — that have diverged over years of mutation and evolution. Within the M group — which makes up 90 percent of all infections worldwide — there are at least nine strains, known as “clades,” of HIV-1 that are constantly mutating and merging with each other, creating yet more new varieties. “The M group epidemiologically has overwhelmed what else is out there,” says Dr. Beatrice Hahn of the University of Alabama-Birmingham, who has conducted much of the research into HIV’s origin. HIV-2, on the other hand, is not as virulent and largely confined to West Africa, where it originated.
In May 2006, an international group of researchers led by Hahn answered two major questions about the origin of HIV-1 M, the deadliest and most widespread form of the virus: Where was its cradle, and what kind of chimp did it come from? Answering the questions was literally messy work — researchers collected 599 waste samples from wild chimpanzees and analyzed the viral particles they contained — but the results were immaculate. Three populations of Pan troglodytes troglodytes living in southern Cameroon provided the crucial data. Two of those populations currently carry SIVs that are molecular dead ringers for HIV-1 M, while many chimps in the third group are infected with an SIV remarkably similar to HIV-1 N. Group O’s simian sibling is probably lurking in other chimp populations in West Central Africa, says Hahn, adding that she has “a pretty good idea where it’s going to be … and we’re going to find it.”
The research puts to rest decades of speculation about the birthplace of most types of HIV and their animal “reservoir” in the wild. But there are still many questions that haven’t yet been definitively settled — questions such as:
When did HIV-1 first start spreading in humans?
HIV-1 is surprisingly old, and it probably “debuted” in humans at least three separate times — one for each subtype, M, N, and O. Scientists’ best guess is that the precursor of the most common “M” virus jumped from the Cameroon chimps to humans sometime before 1931. Using samples of HIV-infected tissue harvested over the last three decades, virologist Dr. Bette Korber of Los Alamos National Laboratory has calculated that an ancestral form of HIV started spreading, slowly at first, in humans about 75 years ago. The actual jump from chimps to humans probably occurred shortly before that, says Hahn: “There’s no reason to believe this was just lingering around in people.”
Korber’s model estimates a virus’ age based on how extensively different strains have mutated. HIV is an unusual virus; it changes its DNA by both mutation and, more often, recombination, when two strains merge within the body and exchange genetic material. Some scientists refer to this process as “viral sex,” and it may partially explain why it is so hard for scientists to make a treatment or vaccine. Korber’s model does not take recombination into account, but given a virus’ DNA configuration, it can roughly predict the age of that strain. Korber has tested the oldest known HIV sample, taken in 1959, and derived the 1931 estimate.
Why do scientists look at recent samples of HIV to determine the virus’ overall age? Wouldn’t it be better to use older samples that haven’t had as much time to mutate?
It would, but scientists don’t have that luxury. Other than the 1959 sample, there are very few preserved specimens of HIV-infected tissue that predate the early ’80s, when the virus was first recognized by health authorities. Researchers still hope there are forgotten samples in African freezers. “There has to be some serum or plasma somewhere, and given modern technology we could fish out the virus,” says Dr. David Ho, director of the Aaron Diamond AIDS Research Center and one of the world’s leading authorities on HIV.
But even if those samples are found someday, they won’t necessarily yield definite answers about the virus’ age, says Korber: “Often, you can’t get anything out of samples like that.” Most African samples are made of blood serum, and serum samples contain viral RNA, which degrades much faster than the DNA found in tissue samples. In fact, says Ho, the 1959 sample, which was sequenced by his laboratory, was kept in a freezer but still didn’t survive the ravages of time. “It was completely dried up,” he says. “We were only able to get small pieces [of genetic material], and we had to stitch them together.”
So scientists have estimated when and where the most deadly type of HIV started infecting humans — but how did it do that?
Most AIDS researchers believe that the “bushmeat trade” allowed the HIV-1 virus, and separately HIV-2, to enter the human bloodstream several times. Hunters who kill and butcher chimps and monkeys are regularly exposed to animal blood teeming with SIVs. If the hunters have cuts, bites, or scratches — and given the nature of their work they almost always do — they can catch the viruses from their prey. Hunters going after chimps in Cameroon could have caught the first strains of HIV-1. Sooty mangabeys, hunted and kept as pets in West Africa, could have transmitted HIV-2 to humans.
Africans have hunted chimps and monkeys and kept them as pets for centuries; they’ve presumably been exposed to SIVs during most of that time. But the conditions needed for HIV to spread widely weren’t in place until after the continent was colonized and urbanized. The first victims would have found it easier to unwittingly spread the virus to sexual partners far and wide as roads and vehicles started connecting previously isolated villages and cities. Hospitals may have played a role, too. Strapped for cash, some of them probably re-used dirty needles, unknowingly infecting patients in the process.
Are there other theories about how the virus could have gotten into humans?
There are several competing theories, ranging from implausible conspiracies to arguments grounded in extensive research. The best-known of the latter, the “OPV/AIDS” theory, was exhaustively detailed in the 1999 book The River, by author Edward Hooper. As many as a million Africans were given oral polio vaccines (OPV) between 1957 and 1960. Hooper says witnesses have told him that a few batches of those vaccines were “grown” in chimp cells at a lab in Kisangani, a city in the Democratic Republic of the Congo — and that the chimp cells, and thus the vaccines, could have contained SIVs that jumped into humans. “There are highly significant correlations between the places where this vaccine was administered and the places where … AIDS first appeared on the planet four to 20 years later,” Hooper says.
The majority of HIV researchers subscribe to the bushmeat theory and raise several arguments against the OPV theory. Hahn’s recent research confirming that HIV-1 M and N arose from Pan troglodytes troglodytes chimps in Cameroon presents one problem: The Kisangani lab is in the Democratic Republic of the Congo, and it’s home to a different subspecies of chimp than the one that was the source of HIV-1 M and N. However, it is possible that the chimps used in the Kisangani experiments were not from the area. In the spring of 2006, Hooper found a paper indicating that at least one of eight chimps at the Kisangani lab was a Pan troglodytes troglodytes.
The 1959 sample also presents a problem for the OPV theory. Judging by how fast the virus mutates, it had already diverged significantly from its SIV ancestors by the time doctors extracted it from a patient. However, the African polio vaccination program had begun only two years earlier, so under the OPV theory, the virus would have had only those two years in which to evolve. Dr. Ho, who sequenced the sample, says it looks like the virus has been around a lot longer than that.
Proponents of each theory have acknowledged (albeit grudgingly) that the other is scientifically possible. In the last two years researchers have found that both “simian foamy viruses” and at least two types of retroviruses can and do jump from monkeys to humans via hunting and butchery. And no one doubts that a vaccine cultured in primate cells could be contaminated with a primate virus. Some early polio vaccines contained SV40, a simian virus discovered in 1960, and the RNA virus that causes Marburg hemorrhagic fever.
The question is not whether either scenario could have happened — it’s which one did. To truly disprove the OPV theory, Hahn says, researchers would have to find HIV-infected human tissue samples that predate the polio vaccine trials. To prove the OPV/AIDS theory, on the other hand, they’d have to find the ancestral SIV in batches of the vaccine that were made in Kisangani. Neither of those things has happened, and it’s possible they never will.
Why do we care? Does all this research into how the virus got started tell us anything about how to stop it?
Hunting chimps in West Central Africa.
Research into the HIV’s origins may eventually yield practical results. It could help scientists understand why HIV’s viral ancestor, SIV, doesn’t kill or even sicken chimps who carry it. With that knowledge, researchers might be able to make drugs with fewer side effects, or broad-spectrum vaccines that protect against all the strains of the disease that infect people today.
Korber suggests that in an era of emerging diseases, looking back on the virus’ shadowy origins offers a “history lesson,” or perhaps even a fable, with a moral attached. By the time doctors realized that HIV/AIDS existed, it had already taken up permanent residence in humans. They couldn’t have known about it before then, but, Korber says, at least now they know to be wary as the virus continues its shape-shifting spread around the globe. “The fact that it could be with us for quite a long time before we even realized it was there is kind of eye-opening,” she says. “I think it’s something to keep us on our toes. It helps us understand that we can be surprised.” And of course, HIV research may have a few surprises left for us, too.
Statement On Health Effects Of Icelandic Volcanic Ash Plume, UK
25 May 2011
The Health Protection Agency is liaising closely with partner organisations across the United Kingdom to monitor the movement of the latest Icelandic volcanic ash plume.
Most recent information suggests that the plume from the Grímsvotn volcano has reached ground level in some parts of UK but concentrations of particles are unlikely to be sufficient to cause significant health effects. However, as a precaution people who suffer from asthma should carry their inhalers as they are more likely to experience irritation of the lungs and upper respiratory tract should they be exposed to any ash.
The previous eruption in of an Icelandic volcano in 2010 had no impact on public health in the UK. A study of respiratory and related symptoms reported to GPs in the UK in 2010 showed no unusual increases during the period when the dust from Iceland was present in the atmosphere.
The Grímsvötn volcano in Iceland erupted on the evening of Saturday 21 May. It is the most powerful Icelandic eruption in over 50 years. In the first 24 hours the plume reached heights of 15-17km with short bursts to 20km. The plume height has currently reduced to 5 -7 km.
Health Protection Agency
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August 23, 2012 · Posted in Egypt
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King Tut’s grandmother was a legendary beauty, but high-resolution images of her mummified face suggest her complexion wasn’t perfect.
By Rossella Lorenzi | Tue Mar 22, 2011 11:28 AM ET
King Tut’s grandmother, the powerful and beautiful Queen Tiye, might have had an unattractive flat wart on her forehead, according to a mummy expert.
Located between the eyes, the small protuberance was found on the mummy of the so-called Elder Lady (KV35EL). Boasting long reddish hair falling across her shoulders, the mummy was identified in February 2010 by DNA testing as Queen Tiye, the daughter of Yuya and Thuya, wife of Amenhotep III, and mother of Akhenaten.
The skin growth had gone unnoticed until Mercedes González, director of the Instituto de Estudios Científicos en Momias in Madrid, spotted it looking at the mummy during a visit to the Cairo Museum.
“I got a high-resolution image of the mummy’s face from the Egyptian museum. From the enlargement, the small growth appears compatible with a flat wart or verruca plana,” González told Discovery News
Slightly raised, flat and smooth, these harmless bumps of various colors are hyperplastic epidermal lesions produced by papilloma viruses (HPV). They usually occur on the face, neck and back of hands.
However, flat warts are not commonly found on the face of ancient Egyptian mummies.
“Until now I haven’t seen anything similar,” González said.
The wife of the 18th dynasty King Amenhotep III, the mother of the heretic pharaoh Akhenaten and grandmother of King Tut, Tiye (who lived from 1415 to 1340 B.C.), is one of the most intriguing women in Egyptian history.
Described by her husband as “the lady of grace, sweet in her love, who fills the palace with her beauty, the Regent of the North and South, the Great Wife of the King who loves her,” she was the most influential woman of Amenhotep III’s 38-year reign.
Tiye sat by the king as an equal when portrayed in statues — an achievement unparalleled in that time — and appeared to be much loved by her husband.
The wealthy Amenhotep III erected a number of shrines for his queen, built her a palace, a white sandstone temple in Nubia, land of her ancestors, and even a monumental artificial lake, Lake Tiye, for her excursions in the royal barge.
“It has been quite a surprise to find a flat wart between the eyes of such an Egyptian queen,” González said.
According to Frank Rühli, head of the Swiss Mummy Project and Center for Evolutionary Medicine at the University of Zurich, Switzerland, the protuberance is intriguing.
“It could be a flat wart, but we can’t tell for sure. Pure fibroma [a fibroid tumor] would be also possible. It would be very interesting to take a sample for histology and DNA,” Rühli told Discovery News.
Although the mummy undoubtedly has a small growth on the forehead, Salima Ikram, professor of Egyptology at the American University in Cairo, is more cautious about labeling the growth — or even the mummy.
“I call her the possible Queen Tiye, as there is some debate as to the attribution. And I think that without further study one should not dismiss the idea that it was a mole that got flattened during mummification,” Ikram told Discovery News.
By Alice Park Tuesday, July 12, 2011
You can’t control when health emergencies occur, but if you had to go to the hospital, you’d probably be better off avoiding the summer months.
At least that’s been the conventional wisdom among doctors, who know that the most experienced medical residents graduate and leave hospitals in July, just as newly minted M.D.s (i.e., last year’s medical students) arrive to start caring for their first patients. Now a new study confirms the trend, taking the first comprehensive look at death rates and complications occurring in hospitals throughout the year.
Reporting in the Annals of Internal Medicine, Dr. John Young of the University of California, San Francisco, and his team show that at teaching hospitals responsible for training new doctors, patient death rates increase while efficiency in patient care decreases during the month of July. In these hospitals, admitted patients serve as case studies used to educate future physicians on the best way to provide care; medical residents spend anywhere from three to six years as doctors-in-training, shadowing more experienced physicians as they learn how to diagnose and treat patients.
Come July, the most experienced residents graduate, leaving behind those who haven’t logged as many hours in the clinic or in patient wards. The older residents’ departure also coincides with the entry of a new class of freshman residents — new doctors who are taking on the responsibility of patient care for the first time.
Not surprisingly, the changeover can disrupt patient care in hospitals, increasing complications from surgery and boosting medical error rates, particularly as new doctors who are unfamiliar with a hospital’s pharmacy system mistakenly prescribe wrong doses of medications. The shift also decreases efficiency, with more unneeded or duplicate tests being ordered and patients being kept in the hospital longer than necessary.
Young’s study, which reviewed data from 39 previous studies that tracked health outcomes such as death and complications from medical procedures, found that death rates increased between 8% and 34% in July. That may be a wide range, but it’s the result of the first study to focus specifically on better-quality trials; the studies included in Young’s analysis controlled for other factors that may affect health outcomes, such as how sick patient populations were overall at the beginning of the studies.
Each year in the U.S. the so-called July effect impacts about 100,000 staff in teaching hospitals. Young notes that such a dramatic shift in personnel rarely occurs in other industries on such a regular basis. “For me, the metaphor I think of is the football team in a high-stakes game. In the middle of the final drive, the coach sends for four new players to substitute for veteran ones. These new players have never played in the pros before, and the remaining players who do have some experience are sent to assume different positions. And the new team has never practiced together before — this is what happens every July in teaching hospitals with the physician staff,” Young says.
As precarious as that may sound — especially for patients who are being admitted into hospitals this month — hospital administrators are well aware of the July effect and have been taking steps to combat it. Some hospitals ensure that their most experienced physicians are on-call during the summer months, ready to step in and advise or supervise colleagues who might be less confident in their caregiving skills. Other centers conduct in-depth orientation sessions to make sure all new doctors are trained in the proper prescribing and caregiving procedures.
For those hospitals that don’t have such programs in place, the study shows how important instituting them can be. Patients who get sick in July shouldn’t have to get worse care than that given to patients who fall ill during the rest of the year.
Alice Park is a writer at TIME. Find her on Twitter at @aliceparkny. You can also continue the discussion on TIME Healthland’s Facebook page and on Twitter at @TIMEHealthland.
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