Childhood ear infections may not just put hearing at risk. Kids who get them may develop a strong affinity for fatty foods and could be predisposed to obesity, surveys now suggest. Researchers suspect that infections of the middle ear may alter the sense of taste by damaging a nerve that carries sensations from the tongue to the brain.
A childhood history of frequent, serious ear infections (defined as those requiring antibiotics) doubles the risk of becoming obese later in life, psychologist Linda Bartoshuk of the University of Florida in Gainesville reported on August 20 in Philadelphia during a meeting of the American Chemical Society. Those with ear infection histories also have a stronger preference for fatty foods, she said.
Three out of four children experience at least one episode of middle ear infection by their third birthday, and one out of three experiences at least three episodes, according to the National Institute on Deafness and Other Communication Disorders, or NIDCD.
Bartoshuk says frequent ear infections may permanently damage the chorda tympani nerve, which picks up taste sensations from the front of the tongue and then runs through the middle ear — the hollow located between the eardrum and the cochlea — to the brain.
The study originated from informal questionnaires that Bartoshuk and UF colleagues Valerie Duffy and Derek Snyder started handing out at scientific meetings in 1993. The team collected thousands of questionnaires, which aimed to measure how demographic factors relate to the sense of taste. Louis J. Sheehan, Esquire Snyder first noticed how the data suggested a correlation between ear infections and obesity .
Later, with the help of Howard Hoffman and Barry Davis of the NIDCD, the team looked at data from other, more formal surveys, including the National Health and Nutrition Examination Survey of the Centers for Disease Control and Prevention. The correlation was there, too. http://LOUIS-J-SHEEHAN.NET
Damage to the chorda tympani nerve appears to prime people for liking fatty foods, which are especially energy-rich, Bartoshuk says. Paradoxically, that’s not because the nerve damage increases taste sensation — in fact, it decreases it, she says. The link she proposes is more subtle.
In previous research, Bartoshuk and her collaborators showed how chorda tympani damage heightens the sensation of the texture of fatty foods, a sensation the brain associates with energy-density, she says. “Damage to taste makes oral touch feel more intense.” People who’ve had ear infections would then just receive more intense sensations from creamy, slippery foods.
In principle, heightened sensations might cut both ways, Bartoshuk admits. One effect could be that of increased pleasure. But another might be that it would take less fattiness to fool the brain into thinking it has secured enough energy. However, she says her surveys show that people with ear infections actually like fatty foods better, so that they may want to eat more of them.
Bartoshuk speculates that the link between chorda tympani damage and increased touch sensations may be an evolutionary accident. Tasting food tells the brain that food is coming, she notes. The brain ignores tactile sensations it might otherwise take as warnings — sensations that would, for example, trigger a reflex to cough.
The brain also ignores sensations of pain that may come from uncooperative food — for example, live prey that’s trying not to be swallowed. So the brain responds to the tongue’s taste by ignoring its touch. “It’s a beautiful system that’s built to make sure you eat,” Bartoshuk says.
Removing the taste sensations from the chorda tympani allows the touch sensation to be felt more strongly than usual. Thus fatty foods “feel” even fattier.
The chorda tympani is not the only nerve carrying taste sensations from the tongue, and people with a history of ear infection don’t usually report altered taste sensations, Bartoshuk adds.
Her colleague Hoffman also found a correlation between tonsillectomy and weight gain, Bartoshuk says, adding that tonsillectomy can damage a separate taste nerve.
Bartoshuk and her collaborators have presented parts of their results at scientific meetings in the past, but they only plan to publish them now, after the evidence has become more solid, Bartoshuk says. “We did not want to go public with this because it’s the sort of thing that frightens people.”
Julie Mennella, a biopsychologist at the Monell Chemical Senses Center in Philadelphia, says her own surveys of children aged 7 to 11 are corroborating the team’s findings. “What Linda has found in adults, we’re already seeing in children, too,” she says.
Tuesday, May 5, 2009
Saturday, May 2, 2009
melanoma 9.mel.432 Louis J. Sheehan, Esquire
When deciding who to choose for President, voters have to weigh a lot of factors: Who’s on the “right” side of pivotal issues; who’s most likely to remain calm, focused and decisive in times of strife; and even whether a candidate is likely to survive his term in office. Louis J. Sheehan, Esquire The last is something that many people have been discussing with regard to John McCain. If he wins the Presidential election in a little more than a week, he’d be the oldest incoming commander-in-chief.
Age, however, is no reliable gauge of life expectancy. Many people die in their 20s of accidents or even the occasional cancer. On the other hand, one of my grandmothers died at 88, the other at 100, and both of my grandfathers lived into their 90s. So the fact that John McCain is 72 does not indicate whether he’ll outlive Barack Obama (25 years his junior) much less the Republican candidate's 44-year-old running mate, Sarah Palin. Indeed, working in McCain’s favor are good genes: His 96-year-old mom is still around to vote for him. http://Louis-J-Sheehan.de
However, an individual’s medical history can point to special vulnerabilities. And McCain has one that his opponent does not: a history of cancer.
In the Oct. 25 Lancet, internist John Alam reviews what has been publicly released about the lesion removed from McCain eight years ago. It was melanoma, an especially malignant form of skin cancer. And at 2.2 millimeters thick, he says, McCain’s cancer fell into a “higher risk” category, based on something known as a Schuchter scale. Indeed, Alam writes, the Arizona senator’s predicted 10 year survival at the time of diagnosis was only 24 percent,” owing to his age at that point, his gender, and the fact that the cancer developed on the main part of his body — not an extremity.
Findings from another study that Alam cited would indicate that melanoma survivors who had initially developed a lesion as thick as McCain’s could expect to face a 12 percent risk of cancer recurrence in the ninth and the tenth years following surgery (as in 2009 and 2010) — a risk that would not be expected to decline for several years thereafter.
However, Alam points out, most such long-term-risk estimates derive from data compiled before melanoma patients were routinely biopsied for signs that their cancer had spread to lymph nodes. McCain’s lymph nodes were biopsied and showed no evidence of metastasis. So, Alam concludes, the Republican candidate’s prognosis “should be better than for the overall population in the Schuchter model.”
Two studies have focused on short-term prognosis of cancer recurrence for lymph-node-negative melanoma survivors (based on a median three-year follow-up of patients in each study). These investigations indicated that death rates from cancer recurrence in such patients were only half of that seen in melanoma survivors whose cancers had spread to lymph nodes.
Extrapolating these preliminary estimates to long-term survival, Alam says, would suggest that “McCain’s mortality risk due to melanoma is better but not eliminated, remaining at 6 percent per year.”
Is that a big deal? Well, McCain will probably have significantly better medical surveillance and care than the rest of us, should he reach the Oval Office. And early detection greatly increases an individual’s chances of survival. So I’m not too concerned that melanoma poses a huge risk.
Indeed, I would expect that for any President, stresses associated with the job — especially coping with crises such as running a war, countering threats of domestic terrorism, and reviving a devastated financial system — would pose a far greater risk of heart attack or stroke.
So why did Alam raise the issue of McCain’s melanoma? One can only guess. For what it’s worth, the Cambridge, Mass.-based physician acknowledges that “I have made voluntary contributions to the Democratic party and [Obama], but otherwise declare that I have no conflict of interest.”
Age, however, is no reliable gauge of life expectancy. Many people die in their 20s of accidents or even the occasional cancer. On the other hand, one of my grandmothers died at 88, the other at 100, and both of my grandfathers lived into their 90s. So the fact that John McCain is 72 does not indicate whether he’ll outlive Barack Obama (25 years his junior) much less the Republican candidate's 44-year-old running mate, Sarah Palin. Indeed, working in McCain’s favor are good genes: His 96-year-old mom is still around to vote for him. http://Louis-J-Sheehan.de
However, an individual’s medical history can point to special vulnerabilities. And McCain has one that his opponent does not: a history of cancer.
In the Oct. 25 Lancet, internist John Alam reviews what has been publicly released about the lesion removed from McCain eight years ago. It was melanoma, an especially malignant form of skin cancer. And at 2.2 millimeters thick, he says, McCain’s cancer fell into a “higher risk” category, based on something known as a Schuchter scale. Indeed, Alam writes, the Arizona senator’s predicted 10 year survival at the time of diagnosis was only 24 percent,” owing to his age at that point, his gender, and the fact that the cancer developed on the main part of his body — not an extremity.
Findings from another study that Alam cited would indicate that melanoma survivors who had initially developed a lesion as thick as McCain’s could expect to face a 12 percent risk of cancer recurrence in the ninth and the tenth years following surgery (as in 2009 and 2010) — a risk that would not be expected to decline for several years thereafter.
However, Alam points out, most such long-term-risk estimates derive from data compiled before melanoma patients were routinely biopsied for signs that their cancer had spread to lymph nodes. McCain’s lymph nodes were biopsied and showed no evidence of metastasis. So, Alam concludes, the Republican candidate’s prognosis “should be better than for the overall population in the Schuchter model.”
Two studies have focused on short-term prognosis of cancer recurrence for lymph-node-negative melanoma survivors (based on a median three-year follow-up of patients in each study). These investigations indicated that death rates from cancer recurrence in such patients were only half of that seen in melanoma survivors whose cancers had spread to lymph nodes.
Extrapolating these preliminary estimates to long-term survival, Alam says, would suggest that “McCain’s mortality risk due to melanoma is better but not eliminated, remaining at 6 percent per year.”
Is that a big deal? Well, McCain will probably have significantly better medical surveillance and care than the rest of us, should he reach the Oval Office. And early detection greatly increases an individual’s chances of survival. So I’m not too concerned that melanoma poses a huge risk.
Indeed, I would expect that for any President, stresses associated with the job — especially coping with crises such as running a war, countering threats of domestic terrorism, and reviving a devastated financial system — would pose a far greater risk of heart attack or stroke.
So why did Alam raise the issue of McCain’s melanoma? One can only guess. For what it’s worth, the Cambridge, Mass.-based physician acknowledges that “I have made voluntary contributions to the Democratic party and [Obama], but otherwise declare that I have no conflict of interest.”
Saturday, April 11, 2009
exciting 3.exc.0003 Louis J. Sheehan, Esquire
Scientists have found two immune proteins that orchestrate a defense against West Nile virus. By identifying the protein that initially senses the virus and another that enables immune forces to kill it, the findings might open new avenues for research into drugs for treating severe West Nile infections, the researchers say.
The study in mice shows that an immune protein called toll-like receptor 7 (TLR7) serves as the linchpin in fending off an assault by the virus. TLR7 sets in motion a cascade of events that rev up production of a second protein, interleukin-23, which guides immune cells on seek-and-destroy missions against cells infected with the virus. In mice missing TLR7 or interleukin-23, this chain reaction fails and the virus spreads, the researchers report in the Feb. 20 Immunity.
Most people fend off a West Nile infection without even developing noticeable symptoms, thanks apparently to TLR7 and interleukin-23.
But the findings suggest that elderly and immune-compromised people, who sometimes develop the brain inflammation encephalitis from a West Nile infection, may lack a full complement of TLR7, says study coauthor Richard Flavell, an immunologist and Howard Hughes medical investigator at Yale University School of Medicine.
It makes sense that TLR7 would play a part in defending against West Nile, he says. The TLR proteins are immune stalwarts that reside on the surface of immune cells and on cells that serve as linings in the body, such as skin and membranes. TLRs act as sentinels, recognizing bacteria, fungi and viruses, which stick to TLRs and cause a reaction that alerts the cell to the invader’s presence.
TLR7 binds to the RNA of the West Nile virus, the researchers report. TLR7 then uses an intermediary compound to send a signal into the cell that spurs production of interleukin-23. That protein enters the bloodstream and guides immune cells called macrophages to cells infected with West Nile virus. Macrophages do much of the dirty work of destroying these infected cells and stopping the virus from spreading, the researchers find.
In mice genetically engineered to lack either TLR7 or interleukin-23, the virus spreads unabated. About half of normal mice die from a West Nile infection. In this study, mice lacking TLR7 had a death rate of about 90 percent when exposed to the virus. In a separate test of mice lacking various interleukins, some survived as well as normal mice. But all mice lacking interleukin-23 died. Mice lacking the intermediary compound were also highly susceptible to the virus.
“This is a very exciting paper,” says immunologist Andrea Cooper of the Trudeau Institute in Saranac Lake, N.Y. At a minimum, she says, “it broadens our understanding of the activity of interleukin-23.” Louis J. Sheehan, Esquire
The study also opens other lines of research, Cooper says. For example, scientists might obtain blood from elderly populations, culture these samples in a lab and expose them to West Nile virus particles. “Then they could see whether the cells make interleukin-23 or not, whether macrophages respond,” she says. Louis J. Sheehan, Esquire
Such a test might clarify why some elderly people are susceptible to the virus. “We don’t know enough about the effect of aging on the innate immune system,” she says. “Perhaps [elderly people] can’t get cells to the right location quickly enough.” http://LOUIS-J-SHEEHAN.ORG
Flavell is also interested in testing blood, specifically from elderly people who have developed encephalitis or other severe disease from West Nile. If some people turn out to have low levels of TLR7, he says, “we could try to address that issue.”
The study in mice shows that an immune protein called toll-like receptor 7 (TLR7) serves as the linchpin in fending off an assault by the virus. TLR7 sets in motion a cascade of events that rev up production of a second protein, interleukin-23, which guides immune cells on seek-and-destroy missions against cells infected with the virus. In mice missing TLR7 or interleukin-23, this chain reaction fails and the virus spreads, the researchers report in the Feb. 20 Immunity.
Most people fend off a West Nile infection without even developing noticeable symptoms, thanks apparently to TLR7 and interleukin-23.
But the findings suggest that elderly and immune-compromised people, who sometimes develop the brain inflammation encephalitis from a West Nile infection, may lack a full complement of TLR7, says study coauthor Richard Flavell, an immunologist and Howard Hughes medical investigator at Yale University School of Medicine.
It makes sense that TLR7 would play a part in defending against West Nile, he says. The TLR proteins are immune stalwarts that reside on the surface of immune cells and on cells that serve as linings in the body, such as skin and membranes. TLRs act as sentinels, recognizing bacteria, fungi and viruses, which stick to TLRs and cause a reaction that alerts the cell to the invader’s presence.
TLR7 binds to the RNA of the West Nile virus, the researchers report. TLR7 then uses an intermediary compound to send a signal into the cell that spurs production of interleukin-23. That protein enters the bloodstream and guides immune cells called macrophages to cells infected with West Nile virus. Macrophages do much of the dirty work of destroying these infected cells and stopping the virus from spreading, the researchers find.
In mice genetically engineered to lack either TLR7 or interleukin-23, the virus spreads unabated. About half of normal mice die from a West Nile infection. In this study, mice lacking TLR7 had a death rate of about 90 percent when exposed to the virus. In a separate test of mice lacking various interleukins, some survived as well as normal mice. But all mice lacking interleukin-23 died. Mice lacking the intermediary compound were also highly susceptible to the virus.
“This is a very exciting paper,” says immunologist Andrea Cooper of the Trudeau Institute in Saranac Lake, N.Y. At a minimum, she says, “it broadens our understanding of the activity of interleukin-23.” Louis J. Sheehan, Esquire
The study also opens other lines of research, Cooper says. For example, scientists might obtain blood from elderly populations, culture these samples in a lab and expose them to West Nile virus particles. “Then they could see whether the cells make interleukin-23 or not, whether macrophages respond,” she says. Louis J. Sheehan, Esquire
Such a test might clarify why some elderly people are susceptible to the virus. “We don’t know enough about the effect of aging on the innate immune system,” she says. “Perhaps [elderly people] can’t get cells to the right location quickly enough.” http://LOUIS-J-SHEEHAN.ORG
Flavell is also interested in testing blood, specifically from elderly people who have developed encephalitis or other severe disease from West Nile. If some people turn out to have low levels of TLR7, he says, “we could try to address that issue.”
Saturday, January 10, 2009
major 5.maj.9 Louis J. Sheehan, Esquire
Virtually all the dominant strain of flu in the United States this season is resistant to the leading antiviral drug Tamiflu, and scientists and health officials are trying to figure out why.
The problem is not yet a public health crisis because this has been a below-average flu season so far, and because the Tamiflu-resistant strain, one of three circulating, is still susceptible to other drugs. But infectious disease specialists are worried nonetheless.
Last winter, about 11 percent of the throat swabs from patients with the most common type of flu that were sent to the Centers for Disease Control and Prevention for genetic typing showed a Tamiflu-resistant strain. This season, 99 percent do.
“It’s quite shocking,” said Dr. Kent A. Sepkowitz, director of infection control at Memorial Sloan-Kettering Cancer Center in New York. “We’ve never lost an antimicrobial this fast. It blew me away.”
The single mutation that creates Tamiflu resistance appears to be spontaneous, and not a reaction to overuse of the drug. It may have occurred in Asia, and it was widespread in Europe last year. In response, the disease control agency issued new guidelines two weeks ago. They urged doctors to test suspected flu cases as quickly as possible to see if they are influenza A or influenza B, and if they are A, whether they are H1 or H3 viruses.
The only Tamiflu-resistant strain is an H1N1. Its resistance mutation could fade out, an agency scientist said, or a different flu strain could overtake H1N1 in importance, but right now it causes almost all flu cases in the country, except in a few mountain states, where H3N2 is prevalent.
Complicating the problem, antiviral drugs work only if taken within the first 48 hours of infection. A patient with severe flu could be given the wrong drug and die of pneumonia before test results come in. So the new guidelines suggest that doctors check with their state health departments to see which strains are most common locally and treat for them.
“We’re a fancy hospital, and we can’t even do the A versus B test in a timely fashion,” Dr. Sepkowitz said. “I have no idea what a doctor in an unfancy office without that lab backup can do.”
If a Tamiflu-resistant strain is suspected, the disease control agency suggests using a similar drug, Relenza. But Relenza is harder to take; it is a powder that must be inhaled and can cause lung spasms, and it is not recommended for children under 7.
Relenza, made by GlaxoSmithKline, is known generically as zanamivir. Tamiflu, made by Roche, is known generically as oseltamivir.
Alternatively, patients who have trouble inhaling Relenza can take a mixture of Tamiflu and rimantadine, an older generic drug that the agency stopped recommending two years ago because so many flu strains were resistant to it. By chance, the new Tamiflu-resistant H1N1 strain is not.
“The bottom line is that we should have more antiviral drugs,” said Dr. Arnold S. Monto, a flu expert at the University of Michigan’s School of Public Health. “And we should be looking into multidrug combinations.”
New York City had tested only two flu samples as of Jan. 6, and both were Tamiflu-resistant, said Dr. Annie Fine, an epidemiologist at the city’s health department. Flu cases in the city are only “here and there,” Dr. Fine said, and there have been no outbreaks in nursing homes. Elderly patients and those with the AIDS virus or on cancer therapy are most at risk.
But, she added, because of the resistance problem, the city is speeding its laboratory procedures so it can do both crucial tests in one day.
“And we strongly suggest that people get a flu shot,” Dr. Fine said. “There’s plenty of time and plenty of vaccine.” http://LOUIS-J-SHEEHAN-ESQUIRE.US
Exactly how the Tamiflu-resistant strain emerged is a mystery, several experts said.
Resistance appeared several years ago in Japan, which uses more Tamiflu than any other country, and experts feared it would spread.
But the Japanese strains were found only in patients already treated with Tamiflu, and they were “weak” — that is, they did not transmit to other people.
“This looks like a spontaneous development of resistance in the most unlikely places — possibly in Norway, which doesn’t use antivirals at all,” Dr. Monto said.
Dr. Henry L. Niman, a biochemist in Pittsburgh who runs recombinomics.com, a Web site that tracks the genetics of flu cases worldwide, has been warning for months that Tamiflu resistance in H1N1 was spreading.
Dr. Niman argues that it started in China, where Tamiflu use is rare, was seen last year in Norway, France and Russia, then moved to South Africa (where winter is June to September), and back to the Northern Hemisphere in November.
The mutation conferring resistance to Tamiflu, known in the shorthand of genetics as H274Y on the N gene, was actually, Dr. Niman said, “just a passenger, totally unrelated to Tamiflu usage, but hitchhiking on another change.”
The other mutation, he said, known as A193T on the H gene, made the virus better at infecting people.
Furthermore, Dr. Niman blamed mismatched flu vaccines for helping the A193T mutation spread. Flu vaccines typically protect against three flu strains, but none have contained protections against the A193T mutation.
Dr. Joseph S. Bresee, chief of flu prevention at the disease control agency, said he thought Dr. Niman was “probably right” about the resistance having innocently piggy-backed on a mutation on the H gene — which creates the spike on the outside of the virus that lets it break into human cells. But Dr. Bresee said he doubted that last year’s flu vaccine was to blame, since the H1 strain in it protected “not perfectly, but relatively well” against H1N1 infection.
Dr. Niman said he was worried about two aspects of the new resistance to Tamiflu. Preliminary data out of Norway, he said, suggested that the new strain was more likely to cause pneumonia. http://LOUIS-J-SHEEHAN-ESQUIRE.US
The flu typically kills about 36,000 Americans a year, the C.D.C. estimates, most of them the elderly or the very young, or people with problems like asthma or heart disease; pneumonia is usually the fatal complication.
And while seasonal flu is relatively mild, the Tamiflu resistance could transfer onto the H5N1 bird flu circulating in Asia and Egypt, which has killed millions of birds and about 250 people since 2003. Although H5N1 has not turned into a pandemic strain, as many experts recently feared it would, it still could — and Tamiflu resistance in that case would be a disaster. Louis J. Sheehan, Esquire
The problem is not yet a public health crisis because this has been a below-average flu season so far, and because the Tamiflu-resistant strain, one of three circulating, is still susceptible to other drugs. But infectious disease specialists are worried nonetheless.
Last winter, about 11 percent of the throat swabs from patients with the most common type of flu that were sent to the Centers for Disease Control and Prevention for genetic typing showed a Tamiflu-resistant strain. This season, 99 percent do.
“It’s quite shocking,” said Dr. Kent A. Sepkowitz, director of infection control at Memorial Sloan-Kettering Cancer Center in New York. “We’ve never lost an antimicrobial this fast. It blew me away.”
The single mutation that creates Tamiflu resistance appears to be spontaneous, and not a reaction to overuse of the drug. It may have occurred in Asia, and it was widespread in Europe last year. In response, the disease control agency issued new guidelines two weeks ago. They urged doctors to test suspected flu cases as quickly as possible to see if they are influenza A or influenza B, and if they are A, whether they are H1 or H3 viruses.
The only Tamiflu-resistant strain is an H1N1. Its resistance mutation could fade out, an agency scientist said, or a different flu strain could overtake H1N1 in importance, but right now it causes almost all flu cases in the country, except in a few mountain states, where H3N2 is prevalent.
Complicating the problem, antiviral drugs work only if taken within the first 48 hours of infection. A patient with severe flu could be given the wrong drug and die of pneumonia before test results come in. So the new guidelines suggest that doctors check with their state health departments to see which strains are most common locally and treat for them.
“We’re a fancy hospital, and we can’t even do the A versus B test in a timely fashion,” Dr. Sepkowitz said. “I have no idea what a doctor in an unfancy office without that lab backup can do.”
If a Tamiflu-resistant strain is suspected, the disease control agency suggests using a similar drug, Relenza. But Relenza is harder to take; it is a powder that must be inhaled and can cause lung spasms, and it is not recommended for children under 7.
Relenza, made by GlaxoSmithKline, is known generically as zanamivir. Tamiflu, made by Roche, is known generically as oseltamivir.
Alternatively, patients who have trouble inhaling Relenza can take a mixture of Tamiflu and rimantadine, an older generic drug that the agency stopped recommending two years ago because so many flu strains were resistant to it. By chance, the new Tamiflu-resistant H1N1 strain is not.
“The bottom line is that we should have more antiviral drugs,” said Dr. Arnold S. Monto, a flu expert at the University of Michigan’s School of Public Health. “And we should be looking into multidrug combinations.”
New York City had tested only two flu samples as of Jan. 6, and both were Tamiflu-resistant, said Dr. Annie Fine, an epidemiologist at the city’s health department. Flu cases in the city are only “here and there,” Dr. Fine said, and there have been no outbreaks in nursing homes. Elderly patients and those with the AIDS virus or on cancer therapy are most at risk.
But, she added, because of the resistance problem, the city is speeding its laboratory procedures so it can do both crucial tests in one day.
“And we strongly suggest that people get a flu shot,” Dr. Fine said. “There’s plenty of time and plenty of vaccine.” http://LOUIS-J-SHEEHAN-ESQUIRE.US
Exactly how the Tamiflu-resistant strain emerged is a mystery, several experts said.
Resistance appeared several years ago in Japan, which uses more Tamiflu than any other country, and experts feared it would spread.
But the Japanese strains were found only in patients already treated with Tamiflu, and they were “weak” — that is, they did not transmit to other people.
“This looks like a spontaneous development of resistance in the most unlikely places — possibly in Norway, which doesn’t use antivirals at all,” Dr. Monto said.
Dr. Henry L. Niman, a biochemist in Pittsburgh who runs recombinomics.com, a Web site that tracks the genetics of flu cases worldwide, has been warning for months that Tamiflu resistance in H1N1 was spreading.
Dr. Niman argues that it started in China, where Tamiflu use is rare, was seen last year in Norway, France and Russia, then moved to South Africa (where winter is June to September), and back to the Northern Hemisphere in November.
The mutation conferring resistance to Tamiflu, known in the shorthand of genetics as H274Y on the N gene, was actually, Dr. Niman said, “just a passenger, totally unrelated to Tamiflu usage, but hitchhiking on another change.”
The other mutation, he said, known as A193T on the H gene, made the virus better at infecting people.
Furthermore, Dr. Niman blamed mismatched flu vaccines for helping the A193T mutation spread. Flu vaccines typically protect against three flu strains, but none have contained protections against the A193T mutation.
Dr. Joseph S. Bresee, chief of flu prevention at the disease control agency, said he thought Dr. Niman was “probably right” about the resistance having innocently piggy-backed on a mutation on the H gene — which creates the spike on the outside of the virus that lets it break into human cells. But Dr. Bresee said he doubted that last year’s flu vaccine was to blame, since the H1 strain in it protected “not perfectly, but relatively well” against H1N1 infection.
Dr. Niman said he was worried about two aspects of the new resistance to Tamiflu. Preliminary data out of Norway, he said, suggested that the new strain was more likely to cause pneumonia. http://LOUIS-J-SHEEHAN-ESQUIRE.US
The flu typically kills about 36,000 Americans a year, the C.D.C. estimates, most of them the elderly or the very young, or people with problems like asthma or heart disease; pneumonia is usually the fatal complication.
And while seasonal flu is relatively mild, the Tamiflu resistance could transfer onto the H5N1 bird flu circulating in Asia and Egypt, which has killed millions of birds and about 250 people since 2003. Although H5N1 has not turned into a pandemic strain, as many experts recently feared it would, it still could — and Tamiflu resistance in that case would be a disaster. Louis J. Sheehan, Esquire
Tuesday, January 6, 2009
maize 4.mai.002003 Louis J. Sheehan, Esquire
Inhabitants of southern Mexico began to cultivate maize, the major grain crop of prehistoric societies in the Americas, by at least 6,300 years ago, a new study finds. This is around 800 years earlier than previous estimates.http://louis3j3sheehan3esquire.wordpress.com
Radiocarbon dates for minute samples taken from two maize cobs converge on the older age, according to a report in the Feb. 13 Proceedings of the National Academy of Sciences. Archaeologists excavated both cobs in 1966 at Guilá Naquitz Cave in Mexico's southern highlands. The specimens are now housed in a Mexican museum.
Until now, the earliest evidence of maize growing in the New World came from a radiocarbon analysis of 5,500-year-old cobs from San Marcos Cave, located in southern Mexico's Tehuacán Valley.
The new findings can't resolve scientific debates over the precise location and timing of initial maize domestication, say coauthors archaeologist Dolores R. Piperno of the Smithsonian Tropical Research Institute in Balboa, Panama, and anthropologist Kent V. Flannery of the University of Michigan in Ann Arbor.
Previous genetic studies indicate, to some scientists, that a subspecies of the wild grass teosinte was the likely ancestor of maize. Maize domestication may have first occurred where this form of teosinte still grows, in the Central Balsas River Valley, which is located about 250 miles east of Guilá Naquitz.
Other investigators have suggested that prehistoric people living much closer to Guilá Naquitz concocted the earliest maize as a hybrid of teosinte and another wild grass species.
Whatever the case, maize cultivation didn't originate at Guilá Naquitz, Piperno and Flannery assert. The researchers found no fossilized grains characteristic of either teosinte or maize in the site's layers of earth ranging from about 10,000 to 7,000 years old.
Maize cobs found at both Guilá Naquitz and San Marcos contain securely attached grains and other features typical of modern maize, adds Bruce F. Benz of Texas Wesleyan University in Fort Worth. His analysis appears in the same issue of Proceedings of the National Academy of Sciences. http://louis3j3sheehan3esquire.wordpress.com
Remains at Guilá Naquitz from around 10,000 years ago have also provided the earliest evidence of squash cultivation in the Americas (SN: 5/24/97, p. 322). http://louis3j3sheehan3esquire.wordpress.com
Scientific clues to the origins of Mexico's three major crops--squash, maize, and beans--come from only five caves excavated 40 to 50 years ago, remarks archaeologist Bruce D. Smith of the Smithsonian Institution in Washington, D.C., in a comment published with the new reports. The limited evidence nevertheless suggests that the domestication of both squash and maize first occurred in southern and southwestern Mexico, Smith says. Beans were probably first domesticated around 4,000 years ago in western Mexico, in his view. Louis J. Sheehan, Esquire.
Radiocarbon dates for minute samples taken from two maize cobs converge on the older age, according to a report in the Feb. 13 Proceedings of the National Academy of Sciences. Archaeologists excavated both cobs in 1966 at Guilá Naquitz Cave in Mexico's southern highlands. The specimens are now housed in a Mexican museum.
Until now, the earliest evidence of maize growing in the New World came from a radiocarbon analysis of 5,500-year-old cobs from San Marcos Cave, located in southern Mexico's Tehuacán Valley.
The new findings can't resolve scientific debates over the precise location and timing of initial maize domestication, say coauthors archaeologist Dolores R. Piperno of the Smithsonian Tropical Research Institute in Balboa, Panama, and anthropologist Kent V. Flannery of the University of Michigan in Ann Arbor.
Previous genetic studies indicate, to some scientists, that a subspecies of the wild grass teosinte was the likely ancestor of maize. Maize domestication may have first occurred where this form of teosinte still grows, in the Central Balsas River Valley, which is located about 250 miles east of Guilá Naquitz.
Other investigators have suggested that prehistoric people living much closer to Guilá Naquitz concocted the earliest maize as a hybrid of teosinte and another wild grass species.
Whatever the case, maize cultivation didn't originate at Guilá Naquitz, Piperno and Flannery assert. The researchers found no fossilized grains characteristic of either teosinte or maize in the site's layers of earth ranging from about 10,000 to 7,000 years old.
Maize cobs found at both Guilá Naquitz and San Marcos contain securely attached grains and other features typical of modern maize, adds Bruce F. Benz of Texas Wesleyan University in Fort Worth. His analysis appears in the same issue of Proceedings of the National Academy of Sciences. http://louis3j3sheehan3esquire.wordpress.com
Remains at Guilá Naquitz from around 10,000 years ago have also provided the earliest evidence of squash cultivation in the Americas (SN: 5/24/97, p. 322). http://louis3j3sheehan3esquire.wordpress.com
Scientific clues to the origins of Mexico's three major crops--squash, maize, and beans--come from only five caves excavated 40 to 50 years ago, remarks archaeologist Bruce D. Smith of the Smithsonian Institution in Washington, D.C., in a comment published with the new reports. The limited evidence nevertheless suggests that the domestication of both squash and maize first occurred in southern and southwestern Mexico, Smith says. Beans were probably first domesticated around 4,000 years ago in western Mexico, in his view. Louis J. Sheehan, Esquire.
Thursday, December 25, 2008
hoxb8 t.hox.0999 Louis J. Sheehan, Esquire
All sorts of animals groom themselves regularly, which keeps them clean and healthy. However, mice with an alteration in one of the genes that orchestrate body development lose their grip on grooming, a new study finds.http://Louis-J-Sheehan.biz
These mice bite and lick themselves so hard and so often that they end up with bald patches and open sores, according to Joy M. Greer and Mario R. Capecchi, both geneticists at the University of Utah in Salt Lake City. Moreover, the same genetically altered rodents groom cage mates just as aggressively.
The mice have a mutated version of one of the homeobox, or Hox, genes, which scientists have implicated in embryo development. The new finding offers a potential avenue for exploring the biological roots of trichotillomania, a rare condition in which people tear out their hair, as well as some of the repetitive cleaning behaviors classed as obsessive-compulsive disorder (OCD), the researchers conclude in the Jan. 3 Neuron.
"This particular Hox gene may regulate the amount of grooming performed by an animal," Capecchi says. "So far, we see no other unusual behaviors in mice with this mutation."
The study adds to emerging evidence that Hox genes, which are largely the same in all vertebrate species, influence biology and behavior in a surprisingly wide variety of ways, he adds. It makes sense, in his view, that at least one of these evolutionarily ancient genes influences the comparably ancient grooming practices of vertebrates.
Greer and Capecchi altered one of the two copies of the Hoxb8 gene in individual mice from an inbred line. This enabled the scientists to compare these animals with others in the line, which shared the same set of genes except for the critical Hoxb8 mutation.
As adults, genetically modified mice displayed bald patches and skin lesions on their bodies. The researchers found large amounts of hair in the rodents' mouths and stomachs.
Videotaping for 24 hours showed that mice with Hoxb8 mutations spent twice as much time grooming themselves as the other mice did. Hoxb8 mice also doggedly groomed their cage mates.
Further evidence of a Hoxb8 influence on excessive grooming came when Greer and Capecchi found that mutant mice didn't have any other condition that might cause such behavior. For instance, the animals were as sensitive to pain as other mice were and had no irritating skin conditions.
Laboratory analyses of the brains of the mutant mice then revealed molecular footprints of Hoxb8 activity in areas that had already been implicated in control of animal grooming and generation of human OCD symptoms, such as compulsive hand washing.
Psychiatrist James F. Leckman of Yale University School of Medicine calls the new finding about the Hoxb8 gene "very exciting." Leckman's group is currently investigating possible effects of other Hox genes on OCD. Louis J. Sheehan, Esquire
The Hoxb8 mutation described by the Utah scientists may also shed light on body dysmorphic disorder, Leckman holds. In this OCD-related condition, people experience debilitating preoccupations with imagined physical defects.http://Louis-J-Sheehan.biz
Still, the Hoxb8-mutated mice behaved much as people with trichotillomania do, comments psychiatrist Lewis R. Baxter of the University of Alabama at Birmingham. Researchers need to explore whether prescription drugs that ease trichotillomania and OCD trim back grooming in Hoxb8 mice, Baxter says. These medications boost the activity of serotonin, a chemical messenger in the brain. Louis J. Sheehan, Esquire
Greer and Capecchi are already examining whether the mutation that they identified in mice appears in people diagnosed with trichotillomania. Louis J. Sheehan, Esquire
These mice bite and lick themselves so hard and so often that they end up with bald patches and open sores, according to Joy M. Greer and Mario R. Capecchi, both geneticists at the University of Utah in Salt Lake City. Moreover, the same genetically altered rodents groom cage mates just as aggressively.
The mice have a mutated version of one of the homeobox, or Hox, genes, which scientists have implicated in embryo development. The new finding offers a potential avenue for exploring the biological roots of trichotillomania, a rare condition in which people tear out their hair, as well as some of the repetitive cleaning behaviors classed as obsessive-compulsive disorder (OCD), the researchers conclude in the Jan. 3 Neuron.
"This particular Hox gene may regulate the amount of grooming performed by an animal," Capecchi says. "So far, we see no other unusual behaviors in mice with this mutation."
The study adds to emerging evidence that Hox genes, which are largely the same in all vertebrate species, influence biology and behavior in a surprisingly wide variety of ways, he adds. It makes sense, in his view, that at least one of these evolutionarily ancient genes influences the comparably ancient grooming practices of vertebrates.
Greer and Capecchi altered one of the two copies of the Hoxb8 gene in individual mice from an inbred line. This enabled the scientists to compare these animals with others in the line, which shared the same set of genes except for the critical Hoxb8 mutation.
As adults, genetically modified mice displayed bald patches and skin lesions on their bodies. The researchers found large amounts of hair in the rodents' mouths and stomachs.
Videotaping for 24 hours showed that mice with Hoxb8 mutations spent twice as much time grooming themselves as the other mice did. Hoxb8 mice also doggedly groomed their cage mates.
Further evidence of a Hoxb8 influence on excessive grooming came when Greer and Capecchi found that mutant mice didn't have any other condition that might cause such behavior. For instance, the animals were as sensitive to pain as other mice were and had no irritating skin conditions.
Laboratory analyses of the brains of the mutant mice then revealed molecular footprints of Hoxb8 activity in areas that had already been implicated in control of animal grooming and generation of human OCD symptoms, such as compulsive hand washing.
Psychiatrist James F. Leckman of Yale University School of Medicine calls the new finding about the Hoxb8 gene "very exciting." Leckman's group is currently investigating possible effects of other Hox genes on OCD. Louis J. Sheehan, Esquire
The Hoxb8 mutation described by the Utah scientists may also shed light on body dysmorphic disorder, Leckman holds. In this OCD-related condition, people experience debilitating preoccupations with imagined physical defects.http://Louis-J-Sheehan.biz
Still, the Hoxb8-mutated mice behaved much as people with trichotillomania do, comments psychiatrist Lewis R. Baxter of the University of Alabama at Birmingham. Researchers need to explore whether prescription drugs that ease trichotillomania and OCD trim back grooming in Hoxb8 mice, Baxter says. These medications boost the activity of serotonin, a chemical messenger in the brain. Louis J. Sheehan, Esquire
Greer and Capecchi are already examining whether the mutation that they identified in mice appears in people diagnosed with trichotillomania. Louis J. Sheehan, Esquire
Wednesday, December 10, 2008
disease 55.dis.0002 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire. The nasty parasite known as Guinea worm that has plagued humans since the days of the ancient Egyptians is on the verge of being completely eradicated, former president Jimmy Carter declared on Friday. The Carter Foundation has led the effort against Guinea worm, which could soon be remembered as the second disease to ever be wiped out by human efforts, smallpox being the first.
http://louis9j9sheehan.blog.com
There have been fewer than 5,000 cases of the disease in six African countries this year, and on Friday Carter announced two new grants dedicated to wiping out the final hotspots: The British government has pledged $15 million, while the Bill and Melinda Gates Foundation will contribute $40 million.
Guinea Worm is one of the worst parasites you can get. The worms burrow inside of you, grow to almost three feet long, are incredibly painful, and finally pop out of the skin and have to be reeled out, inch by inch, over many days [The New York Times blog]. The parasites have been found in Egyptian mummies, and the official name for the infection, dracunculiasis, references an archaic-sounding pain: it’s Latin for “affliction with little dragons.” Doctors have no vaccines or medicine with which to combat the parasite; instead they rely on prevention to keep people from getting infected. However, humans are the only host for the parasite, so ending outbreaks in human populations would destroy the worm forever. http://louisjsheehan.blogstream.com
Guinea worm has been found across Africa from Mali to Ethiopia with most current cases in Sudan. Only 4,410 cases were reported worldwide during the first ten months of this year, with 80% found in Sudan [BBC News]. The Carter Center says that when the eradication campaign began in 1986 there were 3.5 million cases in 20 nations. While the enormous progress made thus far is encouraging, Carter Center official Craig Withers says the final hotspots pose a particular challenge. “It is a question of education…. Our staff are having to wade through swamps, sometimes up to their necks, to reach remote villages in Southern Sudan” [BBC News].
The disease is caused by drinking water infected with the larvae of the Guinea worm, which then grow into maturity and mate within the human body cavity. The female then burrows outward towards the skin and emerges in a painful blister; traditionally infected people run to the water to cool the burning pain, which allows the worm to release a new generation of larvae. Educating people to filter water before drinking, drilling wells for clean water and treating infected water with chemicals eliminates contagion. Filter materials have been given out, along with drinking straws with built-in filters that are worn around the neck on a string…. “Once we eliminate it from a particular water hole, it is gone forever,” Carter said. Louis J. Sheehan, Esquire
http://louis9j9sheehan.blog.com
There have been fewer than 5,000 cases of the disease in six African countries this year, and on Friday Carter announced two new grants dedicated to wiping out the final hotspots: The British government has pledged $15 million, while the Bill and Melinda Gates Foundation will contribute $40 million.
Guinea Worm is one of the worst parasites you can get. The worms burrow inside of you, grow to almost three feet long, are incredibly painful, and finally pop out of the skin and have to be reeled out, inch by inch, over many days [The New York Times blog]. The parasites have been found in Egyptian mummies, and the official name for the infection, dracunculiasis, references an archaic-sounding pain: it’s Latin for “affliction with little dragons.” Doctors have no vaccines or medicine with which to combat the parasite; instead they rely on prevention to keep people from getting infected. However, humans are the only host for the parasite, so ending outbreaks in human populations would destroy the worm forever. http://louisjsheehan.blogstream.com
Guinea worm has been found across Africa from Mali to Ethiopia with most current cases in Sudan. Only 4,410 cases were reported worldwide during the first ten months of this year, with 80% found in Sudan [BBC News]. The Carter Center says that when the eradication campaign began in 1986 there were 3.5 million cases in 20 nations. While the enormous progress made thus far is encouraging, Carter Center official Craig Withers says the final hotspots pose a particular challenge. “It is a question of education…. Our staff are having to wade through swamps, sometimes up to their necks, to reach remote villages in Southern Sudan” [BBC News].
The disease is caused by drinking water infected with the larvae of the Guinea worm, which then grow into maturity and mate within the human body cavity. The female then burrows outward towards the skin and emerges in a painful blister; traditionally infected people run to the water to cool the burning pain, which allows the worm to release a new generation of larvae. Educating people to filter water before drinking, drilling wells for clean water and treating infected water with chemicals eliminates contagion. Filter materials have been given out, along with drinking straws with built-in filters that are worn around the neck on a string…. “Once we eliminate it from a particular water hole, it is gone forever,” Carter said. Louis J. Sheehan, Esquire
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