(HealthDay News) -- The latest chapter in the debate over whether childhood vaccines can cause autism was written Wednesday with release of a study that showed the controversial mercury-containing preservative thimerosal is rapidly excreted from babies' bodies and can't build up to toxic levels.
"Thimerosal has been used for decades, but the surge in vaccinations caused fear that possible accumulations of ethyl mercury, the kind in thimerosal, might exceed safe levels -- at least, when based on the stringent risk guidelines applied to its better-understood chemical cousin, methyl mercury, which is associated with eating fish," lead researcher Dr. Michael Pichichero, professor of microbiology/immunology, pediatrics and medicine at the University of Rochester, said in a prepared statement.
"One of the unanswered questions when this first popped up as a controversy was, when you got thimerosal as an injection, how long would it stay in your blood," co-author Dr. John Treanor, a professor of medicine at the University of Rochester Medical Center, said in an interview.
The new research, he added, showed that "the levels of thimerosal don't go very high and they go down right away. By the time it's time for the next dose of vaccine, the levels are right back to where they were at the beginning."
For their study, Pichichero's team tracked 216 infants from R. Gutierrez Children's Hospital in Buenos Aires, Argentina, where thimerosal is still routinely used in vaccines. Use of thimerosal in childhood vaccines was discontinued in the United States after a joint decision in 1999 by U.S. health officials, pediatricians and vaccine manufacturers.
The infants in the study were put into three age groups and their blood-mercury levels were tested both before and after vaccinations were given to newborns, and at their two- and six-month checkups.
Pichichero's group found that for all three age groups, the half-life of ethyl mercury in the blood -- the time it takes for the body to get rid of half the mercury, and then another half, and so on -- was 3.7 days. That's significantly less than the half-life of methyl mercury, the kind found in fish, at 44 days.
"Until recently, that longer half-life was assumed to be the rule for both types of mercury. Now it's obvious that ethyl mercury's short half-life prevents toxic build-up from occurring. It's just gone too fast," Pichichero said.
"If you thought thimerosal was responsible for autism, you would be looking at mercury levels that were far below anything anyone's previously thought as being toxic," Treanor added.
"Though it's reassuring to affirm that these immunizations have always been safe, our findings really have greater implications for world health," Pichichero said. "Replacing the thimerosal in vaccines globally would put these vaccines beyond what the world community could afford for its children."
The study findings were to be released Monday in the February issue of the journal Pediatrics. But they were released early by the American Academy of Pediatrics, which is requesting that the ABC network cancel the premiere episode of a new show Thursday dealing with the thimerosal-autism controversy.
The new findings also follow a recent report from the California Department of Health that rates of autism continue to climb there even after thimerosal was removed from childhood vaccines.
And they follow a series of studies, including a large-scale U.S. Institute of Medicine review in 2004, that failed to uncover a link between childhood vaccines and autism. The first report of a possible connection appeared in British study in the late 1990s and has since been discredited.
Current estimates by the U.S. National Institutes of Health say that one American child in 150 has been diagnosed with autism, although experts wonder if that increase owes to better diagnoses and a broader definition of the disorder.
Still, at least one vaccine critic worries that inoculations are making children prone to autism, a developmental disorder characterized by impaired social interaction, communication problems, and unusual, repetitive, or severely limited activities and interests. And if it's not thimerosal, then it must be some other vaccine-related interaction, said Barbara Loe Fisher, co-founder and president of the National Vaccine Information Center.
"There are many biological mechanisms involved in vaccine-induced brain and immune system changes that could quite well lead to autism," she said.
"Mercury doesn't belong in any product," Fisher added. "Mercury doesn't belong in vaccines whether it's proven or not proven that mercury is a problem in vaccines."
In ABC's new TV series Eli Stone, the premiere Thursday focuses on a lawyer arguing that a vaccine caused a child's autism. While the show includes statements that science has refuted a link between autism and vaccines, the program reinforces the connection as the jury awards the mother $5.2 million, according to the AAP.
"If parents watch this program and choose to deny their children immunizations, ABC will share in the responsibility for the suffering and deaths that occur as a result. The consequences of a decline in immunization rates could be devastating to the health of our nation's children," AAP President Dr. Renee R. Jenkins said in a prepared statement.
More information
For more on thimerosal and autism, visit the The Children's Hospital of Philadelphia.
Thursday, January 31, 2008
Monday, January 28, 2008
Alzheimers Research Target May Be a Dead End
(HealthDay News) -- A once-promising pathway for research into preventing and treating Alzheimer's disease may have been derailed by a surprise chemical finding, researchers report.
Scientists in laboratories around the world have been investigating drug candidates called amyloid inhibitors, which many experts believed could keep proteins such as amyloid-beta from sticking together in brain tissue.
This type of "sticky" protein plaque build-up is a hallmark of Alzheimer's disease. It also characterizes brain illnesses such as Huntington's disease and "mad cow" disease.
But the new study, published Jan. 27 in the journal Nature Chemical Biology, may sound an unexpected death knell for amyloid inhibitor research.
In the study, a team of chemists at the University of California, San Francisco, found that these candidate drugs form large, unwieldy clumps themselves, rendering them useless as targeted therapy against amyloid in the brain.
High-tech research in the lab is revealing that typical amyloid inhibitors "seem to act not in the way people expect them to and want them to," explained study senior author Brian Shoichet, professor of pharmaceutical chemistry at UCSF.
Once these drugs aggregate into clumps, "they no longer have the right pharmacology, they won't cross the [brain's] membrane barriers, and they inhibit everything -- any protein will bind with them," he said.
In other words, the drugs lose their ability to migrate to the brain to fight amyloid plaque. They also give up their targeted specificity against amyloid, Shoichet said. "They end up inhibiting everything -- any protein that sees them will be sequestered by them," he said. This molecular clumping process is largely inevitable, Shoichet added.
His advice to neuroscientists investigating these agents as potential Alzheimer's therapies: "They should stop."
Another expert agreed.
David Lynn is a Howard Hughes Institute investigator and professor of biological chemistry at Emory University in Atlanta. "I think that Brian's paper argues that [scientists] have been missing the boat here," he said. "It's not clear that you are ever going to get the concentrations that you need of these agents at the right site to be able to have any therapeutic intervention."
On the level of basic chemistry, attacking Alzheimer's and other protein-clumping diseases by preventing amyloid from concentrating has "always been a long shot," Lynn said. That's because amyloid proteins are incredibly "sticky," chemically speaking.
"To find things that will competitively stick and stop them from assembling is theoretically hard to imagine," Lynn said. It was thought that individual molecules of amyloid inhibitors might do so, but the new finding -- that the molecules inevitably bind together in a more impractical mass -- renders them therapeutically useless.
But other avenues of Alzheimer's research remain promising, Lynn said.
"There are certainly other strategies that have potential," he noted, including antibody-focused strategies aimed at eliminating plaques, or treatments focused on easing the downstream effects of amyloid buildup.
Both scientists stressed that it's still not certain whether protein plaques even cause Alzheimer's and other brain diseases, or whether they are merely byproducts of the disease process. "That's really another open area of research," Shoichet said.
"The problem with these diseases is that it is such a moving target," Lynn said. "And so, different people are looking at different things."
More information
There's much more on Alzheimer's disease at the Alzheimer's Association.
Scientists in laboratories around the world have been investigating drug candidates called amyloid inhibitors, which many experts believed could keep proteins such as amyloid-beta from sticking together in brain tissue.
This type of "sticky" protein plaque build-up is a hallmark of Alzheimer's disease. It also characterizes brain illnesses such as Huntington's disease and "mad cow" disease.
But the new study, published Jan. 27 in the journal Nature Chemical Biology, may sound an unexpected death knell for amyloid inhibitor research.
In the study, a team of chemists at the University of California, San Francisco, found that these candidate drugs form large, unwieldy clumps themselves, rendering them useless as targeted therapy against amyloid in the brain.
High-tech research in the lab is revealing that typical amyloid inhibitors "seem to act not in the way people expect them to and want them to," explained study senior author Brian Shoichet, professor of pharmaceutical chemistry at UCSF.
Once these drugs aggregate into clumps, "they no longer have the right pharmacology, they won't cross the [brain's] membrane barriers, and they inhibit everything -- any protein will bind with them," he said.
In other words, the drugs lose their ability to migrate to the brain to fight amyloid plaque. They also give up their targeted specificity against amyloid, Shoichet said. "They end up inhibiting everything -- any protein that sees them will be sequestered by them," he said. This molecular clumping process is largely inevitable, Shoichet added.
His advice to neuroscientists investigating these agents as potential Alzheimer's therapies: "They should stop."
Another expert agreed.
David Lynn is a Howard Hughes Institute investigator and professor of biological chemistry at Emory University in Atlanta. "I think that Brian's paper argues that [scientists] have been missing the boat here," he said. "It's not clear that you are ever going to get the concentrations that you need of these agents at the right site to be able to have any therapeutic intervention."
On the level of basic chemistry, attacking Alzheimer's and other protein-clumping diseases by preventing amyloid from concentrating has "always been a long shot," Lynn said. That's because amyloid proteins are incredibly "sticky," chemically speaking.
"To find things that will competitively stick and stop them from assembling is theoretically hard to imagine," Lynn said. It was thought that individual molecules of amyloid inhibitors might do so, but the new finding -- that the molecules inevitably bind together in a more impractical mass -- renders them therapeutically useless.
But other avenues of Alzheimer's research remain promising, Lynn said.
"There are certainly other strategies that have potential," he noted, including antibody-focused strategies aimed at eliminating plaques, or treatments focused on easing the downstream effects of amyloid buildup.
Both scientists stressed that it's still not certain whether protein plaques even cause Alzheimer's and other brain diseases, or whether they are merely byproducts of the disease process. "That's really another open area of research," Shoichet said.
"The problem with these diseases is that it is such a moving target," Lynn said. "And so, different people are looking at different things."
More information
There's much more on Alzheimer's disease at the Alzheimer's Association.
Tuesday, January 22, 2008
One Strain Behind Epidemic of Staph Infections
(HealthDay News) -- A single strain of an evolving bacterium has been responsible for most of the community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) infections that have spread rapidly in the United States during the past five years, a new government study finds.
Typically, CA-MRSA causes boils, but it can lead to life-threatening conditions that are difficult to treat, according to the study.
The National Institute of Allergy and Infectious Diseases (NIAID) researchers said their findings resolve debate about the molecular evolution of CA-MRSA in the United States and rule out the possibility that multiple strains of USA300 emerged randomly with similar characteristics.
This single strain of USA300, which has spread with "extraordinary transmissibility" in the past five years, was identified by analyzing the genomes of USA300 collected from 10 patients infected in different parts of the United States between 2002 and 2005. Eight of the 10 samples had almost identical genomes, indicating they were from a common strain. The remaining two were related to the other eight, but more distantly.
The researchers also found that two of the eight almost identical USA300 samples caused far fewer deaths in laboratory mice than the other samples. This appears to support an emerging belief that tiny genetic changes among evolving strains have a major impact on disease severity and the potential for development of drug resistance.
The study was published in this week's online issue of the Proceedings of the National Academy of Sciences.
"The USA300 group of strains appears to have extraordinary transmissibility and fitness," research leader Frank R. DeLeo said in a prepared statement. "We anticipate that new USA300 derivatives will emerge within the next several years and that these strains will have a wide range of disease-causing potential."
It's hoped this research will lead to new test that can quickly identify specific MRSA strains.
A second study, led by the same NIAID scientists, discovered new information about how MRSA bacteria -- including the USA300 group -- avoid destruction by the human immune system's white blood cells. The study found that MRSA senses danger and turns the tables, killing the white blood cells.
That study was recently published online in The Journal of Immunology.
"Scientists are pressing ahead quickly to learn more about how some MRSA strains evade the immune system and spread quickly. The information presented in these two studies adds important new insights into that expanding knowledge base," NIAID Director Dr. Anthony S. Fauci said in a prepared statement.
More information
The U.S. Centers for Disease Control and Prevention has more about MRSA.
Typically, CA-MRSA causes boils, but it can lead to life-threatening conditions that are difficult to treat, according to the study.
The National Institute of Allergy and Infectious Diseases (NIAID) researchers said their findings resolve debate about the molecular evolution of CA-MRSA in the United States and rule out the possibility that multiple strains of USA300 emerged randomly with similar characteristics.
This single strain of USA300, which has spread with "extraordinary transmissibility" in the past five years, was identified by analyzing the genomes of USA300 collected from 10 patients infected in different parts of the United States between 2002 and 2005. Eight of the 10 samples had almost identical genomes, indicating they were from a common strain. The remaining two were related to the other eight, but more distantly.
The researchers also found that two of the eight almost identical USA300 samples caused far fewer deaths in laboratory mice than the other samples. This appears to support an emerging belief that tiny genetic changes among evolving strains have a major impact on disease severity and the potential for development of drug resistance.
The study was published in this week's online issue of the Proceedings of the National Academy of Sciences.
"The USA300 group of strains appears to have extraordinary transmissibility and fitness," research leader Frank R. DeLeo said in a prepared statement. "We anticipate that new USA300 derivatives will emerge within the next several years and that these strains will have a wide range of disease-causing potential."
It's hoped this research will lead to new test that can quickly identify specific MRSA strains.
A second study, led by the same NIAID scientists, discovered new information about how MRSA bacteria -- including the USA300 group -- avoid destruction by the human immune system's white blood cells. The study found that MRSA senses danger and turns the tables, killing the white blood cells.
That study was recently published online in The Journal of Immunology.
"Scientists are pressing ahead quickly to learn more about how some MRSA strains evade the immune system and spread quickly. The information presented in these two studies adds important new insights into that expanding knowledge base," NIAID Director Dr. Anthony S. Fauci said in a prepared statement.
More information
The U.S. Centers for Disease Control and Prevention has more about MRSA.
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Saturday, January 19, 2008
Combo Therapy Shows Promise in Treating Brain Tumors
(HealthDay News) -- Implantation of radioactive seeds and chemotherapy wafers following surgery shows promise in treating malignant brain tumors, a new study finds.
The early-phase clinical trial, led by researchers at The Neuroscience Institute at the University of Cincinnati and University Hospital, included 34 patients who had the combination therapy after surgery to remove recurrent glioblastoma multiforme (GBM).
The study, designed to assess the safety and effectiveness of simultaneous use of radioactive seeds and chemotherapy wafers, found that median patient survival was 69 weeks. Almost 25 percent (eight) of the patients survived two years. Patients with recurrent GBM who receive conventional treatment (chemotherapy) have a median survival of about 26 weeks.
About 25 percent of patients developed brain tissue death, which was treated with surgery or hyperbaric oxygen and did not affect survival. That rate of brain tissue death appeared to be higher than what's seen in patients treated with either seeds or wafers alone.
"Treatment of recurrent GBM presents a major challenge to neurosurgeons and neuro-oncologists," study author Dr. Ronald Warnick, a professor of neurosurgery, said in a prepared statement.
"Glioblastoma is an aggressive, highly malignant tumor with unclear boundaries. Because of its diffuse nature, surgeons are unable to remove it completely, and it regrows in the majority of patients. Our aim is to find a way to keep the infiltrating glioblastoma cells from growing into adjacent, health tissue," he said.
The radiation seeds, each about the size of a grain of rice, deliver radiation to the targeted area for six months. The chemotherapy wafers, which are about the size of a nickel, are placed along the surface of the brain.
Compared with the use of either one alone, the combination of the seeds and wafers appeared to further delay disease progression and increase length of patient survival, Warnick said.
However, he noted that the effectiveness of the combination therapy is not definitive, because this study did not include a control group.
The study was published in the February issue of the Journal of Neurosurgery.
More information
The U.S. National Cancer Institute has more about brain tumors.
The early-phase clinical trial, led by researchers at The Neuroscience Institute at the University of Cincinnati and University Hospital, included 34 patients who had the combination therapy after surgery to remove recurrent glioblastoma multiforme (GBM).
The study, designed to assess the safety and effectiveness of simultaneous use of radioactive seeds and chemotherapy wafers, found that median patient survival was 69 weeks. Almost 25 percent (eight) of the patients survived two years. Patients with recurrent GBM who receive conventional treatment (chemotherapy) have a median survival of about 26 weeks.
About 25 percent of patients developed brain tissue death, which was treated with surgery or hyperbaric oxygen and did not affect survival. That rate of brain tissue death appeared to be higher than what's seen in patients treated with either seeds or wafers alone.
"Treatment of recurrent GBM presents a major challenge to neurosurgeons and neuro-oncologists," study author Dr. Ronald Warnick, a professor of neurosurgery, said in a prepared statement.
"Glioblastoma is an aggressive, highly malignant tumor with unclear boundaries. Because of its diffuse nature, surgeons are unable to remove it completely, and it regrows in the majority of patients. Our aim is to find a way to keep the infiltrating glioblastoma cells from growing into adjacent, health tissue," he said.
The radiation seeds, each about the size of a grain of rice, deliver radiation to the targeted area for six months. The chemotherapy wafers, which are about the size of a nickel, are placed along the surface of the brain.
Compared with the use of either one alone, the combination of the seeds and wafers appeared to further delay disease progression and increase length of patient survival, Warnick said.
However, he noted that the effectiveness of the combination therapy is not definitive, because this study did not include a control group.
The study was published in the February issue of the Journal of Neurosurgery.
More information
The U.S. National Cancer Institute has more about brain tumors.
Wednesday, January 16, 2008
MS Drug Tysabri Approved for Crohn's Disease
(HealthDay News) -- Tysabri, a controversial drug used to treat multiple sclerosis, may also be used for patients with a moderate to severe form of another autoimmune illness, Crohn's disease, the U.S. Food and Drug Administration announced Monday.
But the drug also comes with a rare but serious risk of a potentially deadly brain infection, as well as other side effects, so it must be used carefully, the FDA said in a press teleconference.
"With the addition of Tysabri to the treatment options of sufferers of Crohn's disease, we make an important step in the armamentarium for treatment, but one that carries serious risks," said Dr. Joyce Korvick, deputy director of the division of gastroenterology products at the FDA's Office of New Drugs.
Crohn's is a serious, often painful, inflammatory bowel disorder that affects about 600,000 people in the United States. It can involve intestinal bleeding, diarrhea, weight loss, arthritis, skin problems, fever and anemia.
Tysabri (natalizumab), a monoclonal antibody used to treat MS, has been under a cloud of controversy for some time. The drug works by attaching itself to white blood cells called lymphocytes and preventing them from entering the brain, where they do damage that causes the disabling symptoms of MS.
But the drug has a checkered past. It first received U.S. Food and Drug Administration approval in November 2004, only to be pulled from the market three months later after several patients in clinical trials developed a rare but deadly viral infection of the brain called progressive multifocal leukoencephalopathy (PML).
In June 2006, the FDA allowed the drug to return to the market but with strict conditions. According to the new guidelines, Tysabri can only be administered by approved doctors, at infusion sites and pharmacies that register and comply with a patient-safety program called CD Touch, designed by Biogen Idec, the maker of Tysabri, and approved by the FDA.
Last August, an FDA advisory panel voted 12-3 in favor of the use of the drug for Crohn's disease during a joint meeting of the Gastrointestinal Drugs Advisory Committee and the Drug Safety and Risk Management Advisory Committee.
At the time, the panel found that Tysabri could help ease the symptoms of the disease in patients who don't respond to standard therapies such as steroids or immunosuppressants.
The FDA is only approving Tysabri for Crohn's patients with moderate to severe symptoms, and this use will be subject to strict controls.
Korvick said that, besides the risk of PML, Tysabri also raises a patient's odds for hypersensitivity reactions, liver injury and severe herpes infections, especially in those on immunosuppressant therapy, so people taking immuno-suppressing drugs should not take Tysabri, Korvick said.
Crohn's patients who begin Tysabri therapy should also taper off their use of steroids, she added.
Side effects from the drug include headache, fatigue, infusion reactions, rash, and joint and limb pain.
"Because of these risks, patients, prescribers, pharmacies and infusion centers must all be enrolled in the [drug makers'] 'CD Touch' program and agree to comply with the company's strict monitoring guidelines," Korvick said. Doctors should also "evaluate Crohn's patients after three months of treatment to determine if they have improved on Tysabri. If not, then patients should be discontinued," she added.
According to the Wall Street Journal, Biogen Idec earlier this month noted that more than 21,000 patients were using Tysabri without any additional reports of PML.
More information
There's more on Crohn's disease at the U.S. National Institute of Diabetes and Digestive and Kidney Diseases.
But the drug also comes with a rare but serious risk of a potentially deadly brain infection, as well as other side effects, so it must be used carefully, the FDA said in a press teleconference.
"With the addition of Tysabri to the treatment options of sufferers of Crohn's disease, we make an important step in the armamentarium for treatment, but one that carries serious risks," said Dr. Joyce Korvick, deputy director of the division of gastroenterology products at the FDA's Office of New Drugs.
Crohn's is a serious, often painful, inflammatory bowel disorder that affects about 600,000 people in the United States. It can involve intestinal bleeding, diarrhea, weight loss, arthritis, skin problems, fever and anemia.
Tysabri (natalizumab), a monoclonal antibody used to treat MS, has been under a cloud of controversy for some time. The drug works by attaching itself to white blood cells called lymphocytes and preventing them from entering the brain, where they do damage that causes the disabling symptoms of MS.
But the drug has a checkered past. It first received U.S. Food and Drug Administration approval in November 2004, only to be pulled from the market three months later after several patients in clinical trials developed a rare but deadly viral infection of the brain called progressive multifocal leukoencephalopathy (PML).
In June 2006, the FDA allowed the drug to return to the market but with strict conditions. According to the new guidelines, Tysabri can only be administered by approved doctors, at infusion sites and pharmacies that register and comply with a patient-safety program called CD Touch, designed by Biogen Idec, the maker of Tysabri, and approved by the FDA.
Last August, an FDA advisory panel voted 12-3 in favor of the use of the drug for Crohn's disease during a joint meeting of the Gastrointestinal Drugs Advisory Committee and the Drug Safety and Risk Management Advisory Committee.
At the time, the panel found that Tysabri could help ease the symptoms of the disease in patients who don't respond to standard therapies such as steroids or immunosuppressants.
The FDA is only approving Tysabri for Crohn's patients with moderate to severe symptoms, and this use will be subject to strict controls.
Korvick said that, besides the risk of PML, Tysabri also raises a patient's odds for hypersensitivity reactions, liver injury and severe herpes infections, especially in those on immunosuppressant therapy, so people taking immuno-suppressing drugs should not take Tysabri, Korvick said.
Crohn's patients who begin Tysabri therapy should also taper off their use of steroids, she added.
Side effects from the drug include headache, fatigue, infusion reactions, rash, and joint and limb pain.
"Because of these risks, patients, prescribers, pharmacies and infusion centers must all be enrolled in the [drug makers'] 'CD Touch' program and agree to comply with the company's strict monitoring guidelines," Korvick said. Doctors should also "evaluate Crohn's patients after three months of treatment to determine if they have improved on Tysabri. If not, then patients should be discontinued," she added.
According to the Wall Street Journal, Biogen Idec earlier this month noted that more than 21,000 patients were using Tysabri without any additional reports of PML.
More information
There's more on Crohn's disease at the U.S. National Institute of Diabetes and Digestive and Kidney Diseases.
Friday, January 11, 2008
Gene Plays Role in Risk of Autism
(HealthDay News) -- A gene that appears to play a key role in the development of autism has been identified by three different teams of researchers.
UCLA scientists found that the gene -- contactin-associated protein-like 2 (CNTNAP2) -- is most active in brain regions involved with language and thought and that the presence of the gene may explain speech delays in children with autism.
Their study appears in the Jan. 10 online edition of The American Journal of Human Genetics.
The same issue also features reports from research teams at Johns Hopkins University and Yale University that link the CNTNAP2 gene to autism. Meanwhile, a consortium of autism researchers from the Boston area reported in the Jan. 10 issue of the New England Journal of Medicine that abnormalities on chromosome 16 seemed to raise the risk of a certain kind of autism.
The UCLA scientists noted that the gene they discovered is tied closely to language development.
"This gene not only may predispose children to autism. It also may influence the development of brain structures involved in language, providing a tangible link between genes, the brain and behavior," principal investigator Dr. Daniel Geschwind, a professor of human genetics at UCLA's David Geffen School of Medicine, said in a prepared statement.
In the study, researchers analyzed DNA samples from almost 500 families that had at least one autistic child and found that CNTNAP2 showed up consistently in the samples.
The UCLA team also examined CNTNAP2 presence in early brain tissue and found that the gene was most active in developing brain structures involved in language and thought.
Researcher Brett Abrahams, a postdoctoral fellow, explained the significance of the finding by comparing the brain to a house.
"We know that different rooms in houses serve different purposes. For example, if an item only appears in the kitchen, it makes sense to assume it's involved in cooking. Or if we find an object only in the bedroom, it's likely connected to sleeping," he said in a prepared statement. "The fact that we found CNTNAP2 concentrated in the brain's structures that are involved in higher cognition gives us strong clues about how its disruption might adversely shape brain development, including speech and language."
The UCLA researchers also found that the gene was strongest in families with autistic boys, compared to families with autistic boys and girls or families with autistic girls only.
"Autism strikes boys three times as often as girls," Maricela Alarcon, first study author and an assistant professor in residence of neurology at UCLA, said in a prepared statement. "This finding may partly explain why."
In the Johns Hopkins study, researchers found that a specific variation in the structure of CNTNAP2 makes a child more vulnerable to developing autism. They looked at more than 1,300 children with autism and their parents and found that where a single segment of the genetic code of CNTNAP2 could contain either the chemical base adenine or thymine, children with autism tended to have the thymine variant.
The researchers also found that children with autism were about 20 percent more likely to have inherited the thymine variant from their mothers than from their fathers.
"This is a common variant. People inherit it all the time. Our finding that it's associated with autism more often when it's inherited from mothers is intriguing, but needs to be replicated," Johns Hopkins researcher Aravinda Chakravarti said in a prepared statement.
More information
The U.S. National Institute of Neurological Disorders and Stroke has more about autism.
UCLA scientists found that the gene -- contactin-associated protein-like 2 (CNTNAP2) -- is most active in brain regions involved with language and thought and that the presence of the gene may explain speech delays in children with autism.
Their study appears in the Jan. 10 online edition of The American Journal of Human Genetics.
The same issue also features reports from research teams at Johns Hopkins University and Yale University that link the CNTNAP2 gene to autism. Meanwhile, a consortium of autism researchers from the Boston area reported in the Jan. 10 issue of the New England Journal of Medicine that abnormalities on chromosome 16 seemed to raise the risk of a certain kind of autism.
The UCLA scientists noted that the gene they discovered is tied closely to language development.
"This gene not only may predispose children to autism. It also may influence the development of brain structures involved in language, providing a tangible link between genes, the brain and behavior," principal investigator Dr. Daniel Geschwind, a professor of human genetics at UCLA's David Geffen School of Medicine, said in a prepared statement.
In the study, researchers analyzed DNA samples from almost 500 families that had at least one autistic child and found that CNTNAP2 showed up consistently in the samples.
The UCLA team also examined CNTNAP2 presence in early brain tissue and found that the gene was most active in developing brain structures involved in language and thought.
Researcher Brett Abrahams, a postdoctoral fellow, explained the significance of the finding by comparing the brain to a house.
"We know that different rooms in houses serve different purposes. For example, if an item only appears in the kitchen, it makes sense to assume it's involved in cooking. Or if we find an object only in the bedroom, it's likely connected to sleeping," he said in a prepared statement. "The fact that we found CNTNAP2 concentrated in the brain's structures that are involved in higher cognition gives us strong clues about how its disruption might adversely shape brain development, including speech and language."
The UCLA researchers also found that the gene was strongest in families with autistic boys, compared to families with autistic boys and girls or families with autistic girls only.
"Autism strikes boys three times as often as girls," Maricela Alarcon, first study author and an assistant professor in residence of neurology at UCLA, said in a prepared statement. "This finding may partly explain why."
In the Johns Hopkins study, researchers found that a specific variation in the structure of CNTNAP2 makes a child more vulnerable to developing autism. They looked at more than 1,300 children with autism and their parents and found that where a single segment of the genetic code of CNTNAP2 could contain either the chemical base adenine or thymine, children with autism tended to have the thymine variant.
The researchers also found that children with autism were about 20 percent more likely to have inherited the thymine variant from their mothers than from their fathers.
"This is a common variant. People inherit it all the time. Our finding that it's associated with autism more often when it's inherited from mothers is intriguing, but needs to be replicated," Johns Hopkins researcher Aravinda Chakravarti said in a prepared statement.
More information
The U.S. National Institute of Neurological Disorders and Stroke has more about autism.
Sunday, January 06, 2008
Health Tip: Get Children Tested for Lead Poisoning
(HealthDay News) - Since exposure to even low amounts of lead among children can cause learning disabilities and behavioral problems, it's important for parents to prevent exposure at home.
The Environmental Protection Agency offers these suggestions:
The Environmental Protection Agency offers these suggestions:
- Have your child tested regularly by a pediatrician.
- If your home was built before 1978, have it tested for lead paint.
- Always have your child wash his or her hands before eating.
- Wash bottles, pacifiers and toys -- and anything else that may be put in the mouth -- frequently.
- Keep floors and window sills clean and free of dust and paint chips.
- Use cold water, not hot, for drinking, cooking and preparing baby formula. Let the water run until it is as cold as possible.
Wednesday, January 02, 2008
Health Tip: Cosmetics Safety
(HealthDay News) - Some cosmetic products can cause irritation, rashes or even infections, especially if shared with others.
Here are some suggestions to prevent problems from using cosmetics, courtesy of the U.S. Department of Health and Human Services:
Here are some suggestions to prevent problems from using cosmetics, courtesy of the U.S. Department of Health and Human Services:
- Never allow other people to borrow your makeup, which can spread bacteria and other germs.
- When trying on makeup at a store, always use a new applicator, or ask the salesperson to clean it with alcohol before using.
- To prevent bacterial growth, keep your makeup closed tightly, and store it in a cool, dry place. Avoid exposing makeup to sun and other forms of direct light and heat.
- If you have an eye infection, stop using makeup until the irritation clears. Discard any makeup you used when you had the infection.
- Throw away old makeup, and any makeup that turns color or develops an odor.
- Try not to inhale powders or aerosol products, which can irritate or damage the lungs.
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Dr. Group's Secret to Health Kit$39.94 Dr. Group's Secret to Health Kit offers simple at-home solutions for cleansing internally and externally thereby reducing toxins, restoring the body's natural healing process, and helping you achieve true health and happiness. |
Advanced Body Cleansing Kit$147.75 Advanced Body Cleansing Kit with Livatrex™, Oxy-Powder®, Latero-Flora™ and two bottles of ParaTrex®. |