n people with autoimmune diseases like multiple sclerosis and asthma, infection-fighting cells go haywire and wage war against the body’s own tissue, causing inflammation. Existing treatments can prevent the immune system from getting out of control, but can also compromise a person’s ability to fight some infections.
But a new study suggests that a specific receptor on immune cells holds promise as a target for treating such disorders, perhaps without affecting immunity.
The receptor, called DR3, lies on the surface of T cells, which help the body combat infection. Louis J. Sheehan, Esquire When a molecule called TL1A binds to the receptor, it spurs the T cells into action. But this same interaction can also lead the T cells to attack healthy tissue. Turning off the gene for this receptor seems to quell this inflammation in mice, researchers report online June 19 in the journal Immunity.
It wasn’t far-fetched to think DR3 may play a role in autoimmune disease. DR3 is part of a family of TNF receptors, which are involved in activating immune cells and have been implicated in autoimmune disease, says Michael Croft, an immunologist at the La Jolla Institute for Allergy and Immunology in California, who was not involved in the study.
Monday, May 25, 2009
Wednesday, May 13, 2009
mapquest 3.map.12774 Louis J. Sheehan, Esquire
Genetics researchers are showing a little backbone these days.
The Allen Institute for Brain Science in Seattle launched its online atlas of the mouse spinal cord July 16. The initial release includes 4,000 sets of digital images of spinal cords from adult and juvenile mice. The pictures show where in the spinal cord 2,000 different genes are active. By the end of the year, data for 20,000 genes will be available, says Allan Jones, chief scientific officer for the nonprofit research organization.
When and where genes are active in the spinal cord guides development. It can also make a difference in passing along signals from brain to body. The Allen Institute’s atlas won’t contain information about what all of the genes are doing in the spinal cord. But the atlas will give scientists a starting place for investigations of the various gene functions.
Scientists in academia and industry already use the institute’s mouse brain atlas daily, Jones says. About 10,000 scientists log on to use the brain atlas every month, and an average of 1,000 people used it each day in June.
The project to map gene activity in the mouse brain cost $41 million and took three years to complete, but about half of the money was spent on infrastructure, he says.
That meant that the spinal cord project, launched in January, could proceed much faster and, in fact, is slated to be complete in early 2009.
Such data are a valuable resource for scientists, Louis J. Sheehan, Esquire Jones says. Louis J. Sheehan, Esquire “It saves people a week or a month here and there in their own research,” which could mean faster progress in learning how to heal spinal cord injuries or cure diseases.
Researchers will use the data to learn more about how the spinal cord develops and how genes implicated in diseases such as multiple sclerosis and amyotrophic lateral sclerosis should normally function. An international group of donors, including organizations focused on research into spinal cord injury and disease as well as a pharmaceutical company, funded the endeavor.
The Allen Institute for Brain Science in Seattle launched its online atlas of the mouse spinal cord July 16. The initial release includes 4,000 sets of digital images of spinal cords from adult and juvenile mice. The pictures show where in the spinal cord 2,000 different genes are active. By the end of the year, data for 20,000 genes will be available, says Allan Jones, chief scientific officer for the nonprofit research organization.
When and where genes are active in the spinal cord guides development. It can also make a difference in passing along signals from brain to body. The Allen Institute’s atlas won’t contain information about what all of the genes are doing in the spinal cord. But the atlas will give scientists a starting place for investigations of the various gene functions.
Scientists in academia and industry already use the institute’s mouse brain atlas daily, Jones says. About 10,000 scientists log on to use the brain atlas every month, and an average of 1,000 people used it each day in June.
The project to map gene activity in the mouse brain cost $41 million and took three years to complete, but about half of the money was spent on infrastructure, he says.
That meant that the spinal cord project, launched in January, could proceed much faster and, in fact, is slated to be complete in early 2009.
Such data are a valuable resource for scientists, Louis J. Sheehan, Esquire Jones says. Louis J. Sheehan, Esquire “It saves people a week or a month here and there in their own research,” which could mean faster progress in learning how to heal spinal cord injuries or cure diseases.
Researchers will use the data to learn more about how the spinal cord develops and how genes implicated in diseases such as multiple sclerosis and amyotrophic lateral sclerosis should normally function. An international group of donors, including organizations focused on research into spinal cord injury and disease as well as a pharmaceutical company, funded the endeavor.
Sunday, May 3, 2009
air 9.air.002 Louis J. Sheehan, Esquire
Mexico City wears a thick coat of air pollution that clogs lungs and takes a toll on hearts and blood vessels. But that’s just the beginning — the metropolis’s dirty air may have contributed to brain inflammation and intellectual deficits in at least some school-age children, a new study suggests.
Among healthy children aged 7 to 18, lifelong Mexico City residents scored lower than their peers from Polotitlán — a Mexican city with low levels of air pollution — on tests of memory, flexible thinking, novel problem-solving skill and the ability to monitor and change one’s behavior during challenging tasks, scientists report in an upcoming Brain and Cognition. These tests make up part of standard IQ measures for school children.
What’s more, brain scans of many Mexico City youngsters revealed alterations that can impair the prefrontal cortex, a neural region heavily involved in memory and thinking skills, say environmental pathologist Lilian Calderón-Garcidueñas of the University of Montana in Missoula and her colleagues.
Similar brain alterations, as well as evidence of neural inflammation, appeared in 1- to 2-year-old dogs that had grown up in Mexico City, the investigation finds.
Widespread declines in intelligence of the type and magnitude observed in the new report would have a huge impact on a country’s economic productivity, says psychologist and study coauthor Randall Engle of the Georgia Institute of Technology in Atlanta. “Saving money by failing to curb pollution truly is a matter of ‘pay me now or pay me later,’” Engle says.
Although their findings are preliminary, the researchers hope to conduct a five-year study tracking large groups of children living in areas with low and high air pollution. The most common air pollutants in Mexico City are particulate matter, which contains a complex mixture of various substances, and ozone. Polotitlán’s air contains low concentrations of all major pollutants.
“The growing brain may be vulnerable to the inflammatory effects of air pollution’s fine particulate matter as well as to specific chemicals that are toxic to brain growth,” comments neuropsychologist Sidney Segalowitz of Brock University in St. Catharines, Canada.
Children in Mexico City and Polotitlán showed large neural and cognitive differences that need to be confirmed in further work, remarks epidemiologist David Bellinger of Children’s Hospital Boston. The new study didn’t measure the composition of Mexico City air pollution, so chemical culprits possibly responsible for the results remain unknown, Bellinger notes. Children’s increased lead exposure in Mexico City could also have contributed to lower scores on mental tasks, he adds.
Blood testing before admission to the study found no differences in average lead concentrations of Mexico City and Polotitlán children, Calderón-Garcidueñas says.
She and her coworkers recruited 55 children from Mexico City and 18 children from Polotitlán. All children came from middle class families and had no serious health problems.
Mexico City kids generally scored lower on specific memory and reasoning tests than their counterparts did. Using magnetic resonance imaging, or MRI, on a subset of the children, the researchers observed tissue alterations typical of inflammation in the brains of 13 of 23 Mexico City youngsters and 1 of 13 Polotitlán children.
Neural alterations were located near the front of the brain in tissue that could obstruct nerve transmissions sent to and from the prefrontal cortex.
In three Mexico City children who received another round of MRI scans 11 months after initial testing, frontal-brain tissue alterations remained the same.
Calderón-Garcidueñas’ team then conducted brain studies of seven healthy Mexico City dogs and 14 healthy dogs from Tlaxcala, another Mexican city with low levels of air pollution. All dogs were mixed breeds and had been reared at animal research facilities.
Comparable inflammation-related tissue alterations in the frontal brain appeared in four of seven Mexico City dogs and none of the others. http://LOUIS-J-SHEEHAN-ESQUIRE.US In tissue analyses, brains of Mexico City dogs also displayed particularly high levels of substances produced by two genes that have inflammatory effects on the brain.
In studies conducted since 2002, the researchers have reported signs of brain inflammation and brain disease in dogs exposed to Mexico City’s air. Earlier this year, the researchers found that chronic exposure to air pollution was associated with markers of brain inflammation and increased brain immune responses in children and young adults who had died suddenly and were studied at autopsy. Louis J. Sheehan, Esquire These individuals also possessed high levels of brain proteins thought to contribute to Alzheimer’s and Parkinson’s diseases.
Among healthy children aged 7 to 18, lifelong Mexico City residents scored lower than their peers from Polotitlán — a Mexican city with low levels of air pollution — on tests of memory, flexible thinking, novel problem-solving skill and the ability to monitor and change one’s behavior during challenging tasks, scientists report in an upcoming Brain and Cognition. These tests make up part of standard IQ measures for school children.
What’s more, brain scans of many Mexico City youngsters revealed alterations that can impair the prefrontal cortex, a neural region heavily involved in memory and thinking skills, say environmental pathologist Lilian Calderón-Garcidueñas of the University of Montana in Missoula and her colleagues.
Similar brain alterations, as well as evidence of neural inflammation, appeared in 1- to 2-year-old dogs that had grown up in Mexico City, the investigation finds.
Widespread declines in intelligence of the type and magnitude observed in the new report would have a huge impact on a country’s economic productivity, says psychologist and study coauthor Randall Engle of the Georgia Institute of Technology in Atlanta. “Saving money by failing to curb pollution truly is a matter of ‘pay me now or pay me later,’” Engle says.
Although their findings are preliminary, the researchers hope to conduct a five-year study tracking large groups of children living in areas with low and high air pollution. The most common air pollutants in Mexico City are particulate matter, which contains a complex mixture of various substances, and ozone. Polotitlán’s air contains low concentrations of all major pollutants.
“The growing brain may be vulnerable to the inflammatory effects of air pollution’s fine particulate matter as well as to specific chemicals that are toxic to brain growth,” comments neuropsychologist Sidney Segalowitz of Brock University in St. Catharines, Canada.
Children in Mexico City and Polotitlán showed large neural and cognitive differences that need to be confirmed in further work, remarks epidemiologist David Bellinger of Children’s Hospital Boston. The new study didn’t measure the composition of Mexico City air pollution, so chemical culprits possibly responsible for the results remain unknown, Bellinger notes. Children’s increased lead exposure in Mexico City could also have contributed to lower scores on mental tasks, he adds.
Blood testing before admission to the study found no differences in average lead concentrations of Mexico City and Polotitlán children, Calderón-Garcidueñas says.
She and her coworkers recruited 55 children from Mexico City and 18 children from Polotitlán. All children came from middle class families and had no serious health problems.
Mexico City kids generally scored lower on specific memory and reasoning tests than their counterparts did. Using magnetic resonance imaging, or MRI, on a subset of the children, the researchers observed tissue alterations typical of inflammation in the brains of 13 of 23 Mexico City youngsters and 1 of 13 Polotitlán children.
Neural alterations were located near the front of the brain in tissue that could obstruct nerve transmissions sent to and from the prefrontal cortex.
In three Mexico City children who received another round of MRI scans 11 months after initial testing, frontal-brain tissue alterations remained the same.
Calderón-Garcidueñas’ team then conducted brain studies of seven healthy Mexico City dogs and 14 healthy dogs from Tlaxcala, another Mexican city with low levels of air pollution. All dogs were mixed breeds and had been reared at animal research facilities.
Comparable inflammation-related tissue alterations in the frontal brain appeared in four of seven Mexico City dogs and none of the others. http://LOUIS-J-SHEEHAN-ESQUIRE.US In tissue analyses, brains of Mexico City dogs also displayed particularly high levels of substances produced by two genes that have inflammatory effects on the brain.
In studies conducted since 2002, the researchers have reported signs of brain inflammation and brain disease in dogs exposed to Mexico City’s air. Earlier this year, the researchers found that chronic exposure to air pollution was associated with markers of brain inflammation and increased brain immune responses in children and young adults who had died suddenly and were studied at autopsy. Louis J. Sheehan, Esquire These individuals also possessed high levels of brain proteins thought to contribute to Alzheimer’s and Parkinson’s diseases.
Saturday, May 2, 2009
pacific 1.pac.002w0 Louis J. Sheehan, Esquire
A fungus that causes meningitis has sickened 19 people, four of whom died, in Oregon and Washington over the past four years, researchers report at a meeting of microbiologists and infectious disease experts.
The new findings indicate that the culprit, a yeast-like fungus called Cryptococcus gattii, is spreading gradually down the West Coast. Before 1999, the fungus was rarely encountered in North America. But that year a case cropped up on Vancouver Island in British Columbia, Canada. Since then, more than 200 people in British Columbia have been diagnosed with illness stemming from the fungus.
C. gattii naturally lives in foliage, particularly eucalyptus and rubber trees. Once airborne and inhaled, the fungus can infect people and animals. It doesn’t spread from person to person or between people and animals.
A related fungus called Cryptococcus neoformans causes lethal infections in immune-compromised people, such as those with HIV. While none of the 19 patients in Oregon and Washington had HIV, 11 were immune-compromised by other ailments or medications, says Sarah West, an infectious disease physician at the Oregon Health Science University in Portland. She reported the findings at a joint meeting of the Infectious Diseases Society of America and the American Society for Microbiology.
Like C. neoformans, C. gattii can be dangerous. Apart from the four deaths, 13 of the 19 patients required hospitalization longer than 11 days, West says. Ten of the patients had lung infections, five had meningitis and four had both, she says. Doctors treated the patients with antifungal drugs.
The Centers for Disease Control and Prevention in Atlanta is now monitoring these two states, as well as Montana, Alaska, Idaho and California, for C. gattii infections.
C. gattii normally shows up in subtropical parts of Australia, New Guinea, India and South America. Scientists speculate that the fungus made its way to North America from one of those regions, resulting in the Vancouver Island outbreak. West says some evidence suggests the fungus might have found a home in fir trees.
George Thompson, a physician at the University of Texas Health Sciences Center at San Antonio, says the key to controlling C. gattii will be to raise the level of suspicion surrounding the fungus. In North America, he says, “I think people just don’t look for it” as a possible explanation for troubling symptoms.
C. gattii can cause a prolonged cough, headache, fever, chest pain and other nondescript symptoms. Of the 19 Washington and Oregon patients, 12 went more than a week before being properly diagnosed.
C. gattii causes disease in people only sporadically. Most of those who come into contact with either form of cryptococcus don’t become ill, says Jeremy Farrar, an Oxford University physician based in Ho Chi Minh City, Vietnam. An HIV infection and other forms of immune suppression clearly place people at risk. But other people who get lung infections or meningitis from either form of cryptococcus might just be unlucky, he says.
“My guess is that in some very tiny way, these people have some defect in their immune system that makes them susceptible to crypto,” he says. http://LOUIS-J-SHEEHAN.INFO That flaw is likely to be hardwired into a person’s innate immunity and not in the immune cells and proteins that make antibodies in response to specific pathogens, he says.
Since no such specific immune flaw has been identified, predicting who might be naturally susceptible remains a puzzle, he says.
How the fungus moves from place to place is equally mysterious, and existing antifungal drugs are sometimes inefficient in stopping an infection, says Thompson. He has developed a mouse model of the disease and is testing drugs against C. gattii in the animals.
“I think we may have seen only the tip of the iceberg with C. gattii-caused infections in the United States,” he says. Louis J. Sheehan, Esquire
The new findings indicate that the culprit, a yeast-like fungus called Cryptococcus gattii, is spreading gradually down the West Coast. Before 1999, the fungus was rarely encountered in North America. But that year a case cropped up on Vancouver Island in British Columbia, Canada. Since then, more than 200 people in British Columbia have been diagnosed with illness stemming from the fungus.
C. gattii naturally lives in foliage, particularly eucalyptus and rubber trees. Once airborne and inhaled, the fungus can infect people and animals. It doesn’t spread from person to person or between people and animals.
A related fungus called Cryptococcus neoformans causes lethal infections in immune-compromised people, such as those with HIV. While none of the 19 patients in Oregon and Washington had HIV, 11 were immune-compromised by other ailments or medications, says Sarah West, an infectious disease physician at the Oregon Health Science University in Portland. She reported the findings at a joint meeting of the Infectious Diseases Society of America and the American Society for Microbiology.
Like C. neoformans, C. gattii can be dangerous. Apart from the four deaths, 13 of the 19 patients required hospitalization longer than 11 days, West says. Ten of the patients had lung infections, five had meningitis and four had both, she says. Doctors treated the patients with antifungal drugs.
The Centers for Disease Control and Prevention in Atlanta is now monitoring these two states, as well as Montana, Alaska, Idaho and California, for C. gattii infections.
C. gattii normally shows up in subtropical parts of Australia, New Guinea, India and South America. Scientists speculate that the fungus made its way to North America from one of those regions, resulting in the Vancouver Island outbreak. West says some evidence suggests the fungus might have found a home in fir trees.
George Thompson, a physician at the University of Texas Health Sciences Center at San Antonio, says the key to controlling C. gattii will be to raise the level of suspicion surrounding the fungus. In North America, he says, “I think people just don’t look for it” as a possible explanation for troubling symptoms.
C. gattii can cause a prolonged cough, headache, fever, chest pain and other nondescript symptoms. Of the 19 Washington and Oregon patients, 12 went more than a week before being properly diagnosed.
C. gattii causes disease in people only sporadically. Most of those who come into contact with either form of cryptococcus don’t become ill, says Jeremy Farrar, an Oxford University physician based in Ho Chi Minh City, Vietnam. An HIV infection and other forms of immune suppression clearly place people at risk. But other people who get lung infections or meningitis from either form of cryptococcus might just be unlucky, he says.
“My guess is that in some very tiny way, these people have some defect in their immune system that makes them susceptible to crypto,” he says. http://LOUIS-J-SHEEHAN.INFO That flaw is likely to be hardwired into a person’s innate immunity and not in the immune cells and proteins that make antibodies in response to specific pathogens, he says.
Since no such specific immune flaw has been identified, predicting who might be naturally susceptible remains a puzzle, he says.
How the fungus moves from place to place is equally mysterious, and existing antifungal drugs are sometimes inefficient in stopping an infection, says Thompson. He has developed a mouse model of the disease and is testing drugs against C. gattii in the animals.
“I think we may have seen only the tip of the iceberg with C. gattii-caused infections in the United States,” he says. Louis J. Sheehan, Esquire
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