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High risks in 40s if you are obese in 20s
People who are obese and have type 2 diabetes in their 20s will be at higher risk of having a heart attack or stroke in their 40s if they do not change their lifestyle. ""If your blood pressure is 136/88 and you're a man with a waist over 40 or a woman with a waist over 35 it spells trouble," said Dr. Dale J. Hamilton, diabetes clinical services chief at The Methodist Hospital in Houston. "These are two of the five symptoms of metabolic syndrome, a problem that can lead to type 2 diabetes. All you need is three to begin seeing increased atherosclerosis."
High triglyceride levels over 150, insulin resistance and a low LDL (good cholesterol) are factors of metabolic syndrome, along with high blood pressure and central obesity. According to the American Heart Association more than 47 million Americans have it. Many of these patients will end up suffering with type 2 diabetes, which can eventually lead to coronary artery disease and stroke.
"Small changes every day can help curb big problems later on," Hamilton said. "Losing five to 10 pounds will help lower blood pressure. Reducing saturated fats, carbohydrates, and eating about two-thirds the amount you eat now will help you lose weight around the middle. Walk 45 minutes a day instead of 30."
Some experts believe replacing sugar with high fructose corn syrup in processed foods in the United States and Canada in the 1990s has played a role in the rise of type 2 diabetes cases. High fructose corn syrup is made by changing the sugar in corn starch to fructose, another form of sugar. It has become popular because it extends the shelf life of processed foods and is cheaper than sugar. It has also become a popular ingredient in many sodas and fruit-flavored drinks.
"The problem with high fructose corn syrup is that it promotes central obesity," Hamilton said. "Another problem with it is that it fools your body into thinking you are hungry. I don't think you need to eliminate it from your diet, you just need to be aware of how much of it you are consuming on a daily basis because too much can lead to serious weight gain."
Keep in mind, he said, type 2 diabetes symptoms often go untreated because there are few or no symptoms until it is too late.
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"Having three or more of the risk factors associated with type 2 diabetes over an extended period of time is the equivalent of already having a heart attack," Hamilton said. "These risk factors need to be treated aggressively in order to curb the problem and give you a better chance at a longer, healthier life."
Source: Methodist Hospital, Houston.
High triglyceride levels over 150, insulin resistance and a low LDL (good cholesterol) are factors of metabolic syndrome, along with high blood pressure and central obesity. According to the American Heart Association more than 47 million Americans have it. Many of these patients will end up suffering with type 2 diabetes, which can eventually lead to coronary artery disease and stroke.
"Small changes every day can help curb big problems later on," Hamilton said. "Losing five to 10 pounds will help lower blood pressure. Reducing saturated fats, carbohydrates, and eating about two-thirds the amount you eat now will help you lose weight around the middle. Walk 45 minutes a day instead of 30."
Some experts believe replacing sugar with high fructose corn syrup in processed foods in the United States and Canada in the 1990s has played a role in the rise of type 2 diabetes cases. High fructose corn syrup is made by changing the sugar in corn starch to fructose, another form of sugar. It has become popular because it extends the shelf life of processed foods and is cheaper than sugar. It has also become a popular ingredient in many sodas and fruit-flavored drinks.
"The problem with high fructose corn syrup is that it promotes central obesity," Hamilton said. "Another problem with it is that it fools your body into thinking you are hungry. I don't think you need to eliminate it from your diet, you just need to be aware of how much of it you are consuming on a daily basis because too much can lead to serious weight gain."
Keep in mind, he said, type 2 diabetes symptoms often go untreated because there are few or no symptoms until it is too late.
Try these amazing products from no.1 health products, Nutrilite to loose weight.
Loose fat not muscle
Block up to 500 calories per meal
Trim body system kit
"Having three or more of the risk factors associated with type 2 diabetes over an extended period of time is the equivalent of already having a heart attack," Hamilton said. "These risk factors need to be treated aggressively in order to curb the problem and give you a better chance at a longer, healthier life."
Source: Methodist Hospital, Houston.
Boosting brain power with magnesium supplements
New research finds that an increase in brain magnesium improves learning and memory in young and old rats. The study, published in the January 28th issue of the journal Neuron, suggests that increasing magnesium intake may be a valid strategy to enhance cognitive abilities and supports speculation that inadequate levels of magnesium impair cognitive function, leading to faster deterioration of memory in aging humans.
Diet can have a significant impact on cognitive capacity. Identification of dietary factors which have a positive influence on synapses, the sites of communication between neurons, might help to enhance learning and memory and prevent their decline with age and disease. Professor Guosong Liu, Director of the Center for Learning and Memory at Tsinghua University in Beijing, China, led a study examining whether increased levels of one such dietary supplement, magnesium, boosts brain power.
"Magnesium is essential for the proper functioning of many tissues in the body, including the brain and, in an earlier study, we demonstrated that magnesium promoted synaptic plasticity in cultured brain cells," explains Dr. Liu. "Therefore it was tempting to take our studies a step further and investigate whether an increase in brain magnesium levels enhanced cognitive function in animals."
Because it is difficult to boost brain magnesium levels with traditional oral supplements, Dr. Liu and colleagues developed a new magnesium compound, magnesium-L-threonate (MgT) that could significantly increase magnesium in the brain via dietary supplementation. They used MgT to increase magnesium in rats of different ages and then looked for behavioral and cellular changes associated with memory.
"We found that increased brain magnesium enhanced many different forms of learning and memory in both young and aged rats," says Dr. Liu. A close examination of cellular changes associated with memory revealed an increase in the number of functional synapses, activation of key signaling molecules and an enhancement of short- and long-term synaptic processes that are crucial for learning and memory.
The authors note that the control rats in this study had a normal diet which is widely accepted to contain a sufficient amount of magnesium, and that the observed effects were due to elevation of magnesium to levels higher than provided by a normal diet.
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"Our findings suggest that elevating brain magnesium content via increasing magnesium intake might be a useful new strategy to enhance cognitive abilities," explains Dr. Liu. "Moreover, half the population of industrialized countries has a magnesium deficit, which increases with aging. This may very well contribute to age-dependent memory decline; increasing magnesium intake might prevent or reduce such decline."
Source: Cell Press/Eurekalert.
Diet can have a significant impact on cognitive capacity. Identification of dietary factors which have a positive influence on synapses, the sites of communication between neurons, might help to enhance learning and memory and prevent their decline with age and disease. Professor Guosong Liu, Director of the Center for Learning and Memory at Tsinghua University in Beijing, China, led a study examining whether increased levels of one such dietary supplement, magnesium, boosts brain power.
"Magnesium is essential for the proper functioning of many tissues in the body, including the brain and, in an earlier study, we demonstrated that magnesium promoted synaptic plasticity in cultured brain cells," explains Dr. Liu. "Therefore it was tempting to take our studies a step further and investigate whether an increase in brain magnesium levels enhanced cognitive function in animals."
Because it is difficult to boost brain magnesium levels with traditional oral supplements, Dr. Liu and colleagues developed a new magnesium compound, magnesium-L-threonate (MgT) that could significantly increase magnesium in the brain via dietary supplementation. They used MgT to increase magnesium in rats of different ages and then looked for behavioral and cellular changes associated with memory.
"We found that increased brain magnesium enhanced many different forms of learning and memory in both young and aged rats," says Dr. Liu. A close examination of cellular changes associated with memory revealed an increase in the number of functional synapses, activation of key signaling molecules and an enhancement of short- and long-term synaptic processes that are crucial for learning and memory.
The authors note that the control rats in this study had a normal diet which is widely accepted to contain a sufficient amount of magnesium, and that the observed effects were due to elevation of magnesium to levels higher than provided by a normal diet.
Check these brain boosting organic supplements (Energize & Memory) from Nutrilite.
"Our findings suggest that elevating brain magnesium content via increasing magnesium intake might be a useful new strategy to enhance cognitive abilities," explains Dr. Liu. "Moreover, half the population of industrialized countries has a magnesium deficit, which increases with aging. This may very well contribute to age-dependent memory decline; increasing magnesium intake might prevent or reduce such decline."
Source: Cell Press/Eurekalert.
Parkinson's patients develop abnormalities long before symptoms
Scientists who have identified brain networks damaged in Parkinson's disease have new evidence that these systems become abnormal a few years before symptoms appear. And what's more, parts of the network appear to respond in a last ditch attempt to rescue the brain.
"We were surprised," said Chris Tang, MD, PhD, a Parkinson's investigator at The Feinstein Institute for Medical Research in Manhasset, NY, and an author of the study, published this month in the Journal of Neuroscience. The Feinstein scientists have been following people with Parkinson's disease for decades. They have had a unique opportunity to take snapshots of the brain over the course of four years in 15 patients and an equal number of normal volunteers. The group initially identified two discrete abnormal networks, one that was involved in mediating the motor symptoms of Parkinson's disease, and the other that regulates the cognitive dysfunction that develops in many patients with this illness.
Symptoms of Parkinson's disease initially occur on one side of the body, which provided scientists with a unique opportunity to study the brain scans at multiple times and compare the symptoms to changes in the brain networks over time. The idea for the latest study was to watch the activity of the network on the side of the brain that controls the side of the body that's free of symptoms. As the disease progresses, both sides of the body ultimately become involved.
The motor network that governed the side of the body with initial symptoms was the first to become abnormal. Scientists under the direction of David Eidelberg, MD, head of the Feinstein's Center for Neurosciences, found that the motor network on the other side of the brain was also abnormal, even though symptoms appeared only two years later. The brain network that governs cognition began showing abnormalities after two more years had passed, which was four years after their diagnosis. The average age of the patients in the study is 58 and no one has yet to develop cognition problems.
The brain scans measure glucose and dopamine, the chemical that is depleted during the disease process. By using these scans to understand what the brain is doing before symptoms emerge, investigators are characterizing new therapeutic targets to slow or actually prevent the onset of clinical disability in Parkinson's disease and related neurological illnesses.
"We were surprised," said Chris Tang, MD, PhD, a Parkinson's investigator at The Feinstein Institute for Medical Research in Manhasset, NY, and an author of the study, published this month in the Journal of Neuroscience. The Feinstein scientists have been following people with Parkinson's disease for decades. They have had a unique opportunity to take snapshots of the brain over the course of four years in 15 patients and an equal number of normal volunteers. The group initially identified two discrete abnormal networks, one that was involved in mediating the motor symptoms of Parkinson's disease, and the other that regulates the cognitive dysfunction that develops in many patients with this illness.
Symptoms of Parkinson's disease initially occur on one side of the body, which provided scientists with a unique opportunity to study the brain scans at multiple times and compare the symptoms to changes in the brain networks over time. The idea for the latest study was to watch the activity of the network on the side of the brain that controls the side of the body that's free of symptoms. As the disease progresses, both sides of the body ultimately become involved.
The motor network that governed the side of the body with initial symptoms was the first to become abnormal. Scientists under the direction of David Eidelberg, MD, head of the Feinstein's Center for Neurosciences, found that the motor network on the other side of the brain was also abnormal, even though symptoms appeared only two years later. The brain network that governs cognition began showing abnormalities after two more years had passed, which was four years after their diagnosis. The average age of the patients in the study is 58 and no one has yet to develop cognition problems.
The brain scans measure glucose and dopamine, the chemical that is depleted during the disease process. By using these scans to understand what the brain is doing before symptoms emerge, investigators are characterizing new therapeutic targets to slow or actually prevent the onset of clinical disability in Parkinson's disease and related neurological illnesses.
Cognitive science research to revolutionize the legal system
What if a jury could decide a man's guilt through mind reading? What if reading a defendant's memory could betray their guilt? And what constitutes 'intent' to commit murder? These are just some of the issues debated and reviewed in the inaugural issue of WIREs Cognitive Science, the latest interdisciplinary project from Wiley-Blackwell, which for registered institutions will be free for the first two years. In the article "Neurolaw," in the inaugural issue of WIREs Cognitive Science, co-authors Walter Sinnott-Armstrong and Annabelle Belcher assess the potential for the latest cognitive science research to revolutionize the legal system.
Neurolaw, also known as legal neuroscience, builds upon the research of cognitive, psychological, and social neuroscience by considering the implications for these disciplines within a legal framework. Each of these disciplinary collaborations has been ground-breaking in increasing our knowledge of the way the human brain operates, and now neurolaw continues this trend.
One of the most controversial ways neuroscience is being used in the courtroom is through 'mind reading' and the detection of mental states. While only courts in New Mexico currently permit traditional lie detector, or polygraph, tests there are a number of companies claiming to have used neuroscience methods to detect lies. Some of these methods involve electroencephalography (EEG), whereby brain activity is measured through small electrodes placed on the scalp. This widely accepted method of measuring brain electrical potentials has already been used in two forensic techniques which have appeared in US courtrooms: brain fingerprinting and brain electrical oscillations signature (BEOS).
Brain fingerprinting purportedly tests for 'guilty knowledge,' or memory of a kind that only a guilty person could have. Other forms of guilt detection, using functional magnetic resonance imaging (fMRI), are based on the assumption that lying and truth-telling are associated with distinctive activity in different areas of the brain. These and other potential forms of 'mind reading' are still in development but may have far-reaching implications for court cases.
"Some proponents of neurolaw think that neuroscience will soon be used widely throughout the legal system and that it is bound to produce profound changes in both substantive and procedural law," conclude the authors. "Other leaders in neurolaw employ a less sanguine tone, urging caution so as to prevent misuses and abuses of neuroscience within courts, legislatures, prisons, and other parts of the legal system. Either way we need to be ready to prevent misuses and encourage legitimate applications of neuroscience and the only way to achieve these goals is for neuroscientists and lawyers to work together in the field of neurolaw."
As this paper shows, WIREs Cognitive Science takes an original interdisciplinary approach to understanding the key issues surrounding state-of-the-art cognitive research. Disciplines featured in the inaugural issue include topics as diverse as cognitive biology, computer science, linguistics, neuroscience, philosophy and psychology.
Neurolaw, also known as legal neuroscience, builds upon the research of cognitive, psychological, and social neuroscience by considering the implications for these disciplines within a legal framework. Each of these disciplinary collaborations has been ground-breaking in increasing our knowledge of the way the human brain operates, and now neurolaw continues this trend.
One of the most controversial ways neuroscience is being used in the courtroom is through 'mind reading' and the detection of mental states. While only courts in New Mexico currently permit traditional lie detector, or polygraph, tests there are a number of companies claiming to have used neuroscience methods to detect lies. Some of these methods involve electroencephalography (EEG), whereby brain activity is measured through small electrodes placed on the scalp. This widely accepted method of measuring brain electrical potentials has already been used in two forensic techniques which have appeared in US courtrooms: brain fingerprinting and brain electrical oscillations signature (BEOS).
Brain fingerprinting purportedly tests for 'guilty knowledge,' or memory of a kind that only a guilty person could have. Other forms of guilt detection, using functional magnetic resonance imaging (fMRI), are based on the assumption that lying and truth-telling are associated with distinctive activity in different areas of the brain. These and other potential forms of 'mind reading' are still in development but may have far-reaching implications for court cases.
"Some proponents of neurolaw think that neuroscience will soon be used widely throughout the legal system and that it is bound to produce profound changes in both substantive and procedural law," conclude the authors. "Other leaders in neurolaw employ a less sanguine tone, urging caution so as to prevent misuses and abuses of neuroscience within courts, legislatures, prisons, and other parts of the legal system. Either way we need to be ready to prevent misuses and encourage legitimate applications of neuroscience and the only way to achieve these goals is for neuroscientists and lawyers to work together in the field of neurolaw."
As this paper shows, WIREs Cognitive Science takes an original interdisciplinary approach to understanding the key issues surrounding state-of-the-art cognitive research. Disciplines featured in the inaugural issue include topics as diverse as cognitive biology, computer science, linguistics, neuroscience, philosophy and psychology.
3D images of communication between neurons
A team of researchers from the Max Planck Institute of Biochemistry, in Germany, led by the Spanish physicist Rubén Fernández-Busnadiego, has managed to obtain 3D images of the vesicles and filaments involved in communication between neurons. The method is based on a novel technique in electron microscopy, which cools cells so quickly that their biological structures can be frozen while fully active.
"We used electron cryotomography, a new technique in microscopy based on ultra-fast freezing of cells, in order to study and obtain three-dimensional images of synapsis, the cellular structure in which the communication between neurons takes place in the brains of mammals" Rubén Fernández-Busnadiego, lead author of the study which features on the front cover of this month's Journal of Cell Biology and a physicist at the Max Planck Institute of Biochemistry, in Germany, said.
During synapsis, a presynaptic cell (emitter) releases neurotransmitters to another post-synaptic one (recipient), generating an electric impulse in it, thereby allowing nervous information to be transmitted. During this study, the researchers focused on the tiny vesicles (measuring around 40 nanometres in diameter), which transport and release the neurotransmitters from the presynaptic terminals.
"Thanks to the use of certain pharmacological treatments and the advanced 3D imaging analysis method we have developed, it is possible to observe the huge range of filamentous structures that are within the presynaptic terminal and interact directly with the synaptic vesicles, as well as to learn about their crucial role in responding to the electrical activity of the brain," explains Fernández-Busnadiego.
The filaments connect the vesicles and also connect them with the active area, the part of the cellular membrane from which the neurotransmitters are released. According to the Spanish physicist, these filamentous structures act as barriers that block the free movement of the vesicles, keeping them in their place until the electric impulse arrives, as well as determining the ease with which they will fuse with the membrane.
Sub-zero images
The technique upon which these discoveries are based, electron cryotomography, makes it possible to obtain three-dimensional images of the inside of cells and to minimise any changes to their structure. This is possible because the cells are not fixed with chemical reagents, but are vitrified -- in other words they are frozen so fast that the water inside them does not have time to crystallise, and remains in solid state.
These samples, which are always maintained at liquid nitrogen temperatures (below -140 ºC), can be viewed using specially-equipped microscopes. In addition, this method does not require any kind of additional staining, meaning the density of the biological structures can be observed directly.
"We used electron cryotomography, a new technique in microscopy based on ultra-fast freezing of cells, in order to study and obtain three-dimensional images of synapsis, the cellular structure in which the communication between neurons takes place in the brains of mammals" Rubén Fernández-Busnadiego, lead author of the study which features on the front cover of this month's Journal of Cell Biology and a physicist at the Max Planck Institute of Biochemistry, in Germany, said.
During synapsis, a presynaptic cell (emitter) releases neurotransmitters to another post-synaptic one (recipient), generating an electric impulse in it, thereby allowing nervous information to be transmitted. During this study, the researchers focused on the tiny vesicles (measuring around 40 nanometres in diameter), which transport and release the neurotransmitters from the presynaptic terminals.
"Thanks to the use of certain pharmacological treatments and the advanced 3D imaging analysis method we have developed, it is possible to observe the huge range of filamentous structures that are within the presynaptic terminal and interact directly with the synaptic vesicles, as well as to learn about their crucial role in responding to the electrical activity of the brain," explains Fernández-Busnadiego.
The filaments connect the vesicles and also connect them with the active area, the part of the cellular membrane from which the neurotransmitters are released. According to the Spanish physicist, these filamentous structures act as barriers that block the free movement of the vesicles, keeping them in their place until the electric impulse arrives, as well as determining the ease with which they will fuse with the membrane.
Sub-zero images
The technique upon which these discoveries are based, electron cryotomography, makes it possible to obtain three-dimensional images of the inside of cells and to minimise any changes to their structure. This is possible because the cells are not fixed with chemical reagents, but are vitrified -- in other words they are frozen so fast that the water inside them does not have time to crystallise, and remains in solid state.
These samples, which are always maintained at liquid nitrogen temperatures (below -140 ºC), can be viewed using specially-equipped microscopes. In addition, this method does not require any kind of additional staining, meaning the density of the biological structures can be observed directly.
Better understanding of schizophrenia from mouse model
Scientists have created what appears to be a schizophrenic mouse by reducing the inhibition of brain cells involved in complex reasoning and decisions about appropriate social behavior. Findings by Medical College of Georgia scientists, published Dec. 28 in the Proceedings of the National Academy of Sciences, elucidate the critical balance between excitation and inhibition of these cells that appears to go awry in schizophrenia. They also provide the first animal model for studying the disabling psychiatric disorder that affects about 1 percent of the population.
"We believe the mouse, which exhibits some of the same aberrant behavior as patients with this disorder, will help identify better therapies," said Dr. Lin Mei, a developmental neurobiologist who directs MCG's Institute of Molecular Medicine and Genetics. "We are doing testing to see if antipsychotic drugs already on the market are effective in treating the mouse."
Scientists at the Medical College of Georgia have created what appears to be a schizophrenic mouse by reducing the inhibition of brain cells involved in complex reasoning and decisions about appropriate social behavior. Pictured is Dr. Lin Mei, a developmental neurobiologist who directs MCG's Institute of Molecular Medicine and Genetics. (Credit: Medical College of Georgia).
MCG scientists made the mouse by deleting a candidate gene for schizophrenia, ErbB4, from interneurons, which are brain cells that help shower larger decision-making neurons, called pyramidal cells, with inhibition.
In their earlier work, they identified how ErbB4 and another candidate gene, neuregulin-1, work together to balance the activity of these pyramidal cells. They reported in Neuron in May 2007 that the two help keep a healthy balance between excitation and inhibition by increasing release of GABA, a major inhibitory neurotransmitter in the inhibitory synapses of the brain's prefrontal cortex. Seven years earlier, they showed the two also put a damper on excitatory synapses, communication points between neurons where the neurotransmitter glutamate excites cells to action.
To further test these findings, this time they altered the natural check and balance in cells directly involved with supplying pyramidal neurons with the inhibitor GABA. They did this by knocking out the ErbB4 gene in nearby chandelier and basket interneurons that supply GABA to pyramidal cells. "If we take out ErbB4 in these two interneurons, the neuregulin should have no effect because it can't promote GABA," Dr. Mei, Georgia Research Alliance Eminent Scholar in Neuroscience, said.
His postulation played out in the behavior of the mouse, who exhibited schizophrenia-like behavior including increased movement and impaired short-term memory. The scientists are still gathering data on the manic aspect of schizophrenia in their mice.
For example, both the normal and knockout mice learned they would find a food pellet in each arm of an eight-armed chamber but that if they went to the same arm for seconds, there were none. But the knockouts took longer to learn and finish the task. Knockouts also spent a lot more time sniffing and snooping around and revisiting empty arms.
In another test, knockouts couldn't -- or wouldn't -- make the connection that a relatively low noise would be followed by a slightly louder one. When they treated the knockouts with diazepam, an anti-anxiety medication, they responded similarly to the normal mice: the first sound prepared them for the second.
Dr. Mei suspects that if he could look at the chandelier and basket interneurons in the prefrontal cortex of schizophrenics, he would also find something wrong with their usual role of sensing the need for the inhibitor GABA and supplying it to the pyramidal cells. "In schizophrenia, the baseline of the excitatory neurotransmitter is probably high," he said.
The research was funded by the National Institutes of Health and the National Alliance for Research on Schizophrenia and Depression, for which he is a distinguished investigator.
Co-authors include MCG scientists Drs. Wen-Cheng Xiong, Alvin Terry and Almira Vazdarjanova and postdoctoral fellows Drs. Lei Wen, Yi-Sheng Lu and Xin-Hong Zhu.
Source: Medical College of Georgia.
"We believe the mouse, which exhibits some of the same aberrant behavior as patients with this disorder, will help identify better therapies," said Dr. Lin Mei, a developmental neurobiologist who directs MCG's Institute of Molecular Medicine and Genetics. "We are doing testing to see if antipsychotic drugs already on the market are effective in treating the mouse."
Scientists at the Medical College of Georgia have created what appears to be a schizophrenic mouse by reducing the inhibition of brain cells involved in complex reasoning and decisions about appropriate social behavior. Pictured is Dr. Lin Mei, a developmental neurobiologist who directs MCG's Institute of Molecular Medicine and Genetics. (Credit: Medical College of Georgia).MCG scientists made the mouse by deleting a candidate gene for schizophrenia, ErbB4, from interneurons, which are brain cells that help shower larger decision-making neurons, called pyramidal cells, with inhibition.
In their earlier work, they identified how ErbB4 and another candidate gene, neuregulin-1, work together to balance the activity of these pyramidal cells. They reported in Neuron in May 2007 that the two help keep a healthy balance between excitation and inhibition by increasing release of GABA, a major inhibitory neurotransmitter in the inhibitory synapses of the brain's prefrontal cortex. Seven years earlier, they showed the two also put a damper on excitatory synapses, communication points between neurons where the neurotransmitter glutamate excites cells to action.
To further test these findings, this time they altered the natural check and balance in cells directly involved with supplying pyramidal neurons with the inhibitor GABA. They did this by knocking out the ErbB4 gene in nearby chandelier and basket interneurons that supply GABA to pyramidal cells. "If we take out ErbB4 in these two interneurons, the neuregulin should have no effect because it can't promote GABA," Dr. Mei, Georgia Research Alliance Eminent Scholar in Neuroscience, said.
His postulation played out in the behavior of the mouse, who exhibited schizophrenia-like behavior including increased movement and impaired short-term memory. The scientists are still gathering data on the manic aspect of schizophrenia in their mice.
For example, both the normal and knockout mice learned they would find a food pellet in each arm of an eight-armed chamber but that if they went to the same arm for seconds, there were none. But the knockouts took longer to learn and finish the task. Knockouts also spent a lot more time sniffing and snooping around and revisiting empty arms.
In another test, knockouts couldn't -- or wouldn't -- make the connection that a relatively low noise would be followed by a slightly louder one. When they treated the knockouts with diazepam, an anti-anxiety medication, they responded similarly to the normal mice: the first sound prepared them for the second.
Dr. Mei suspects that if he could look at the chandelier and basket interneurons in the prefrontal cortex of schizophrenics, he would also find something wrong with their usual role of sensing the need for the inhibitor GABA and supplying it to the pyramidal cells. "In schizophrenia, the baseline of the excitatory neurotransmitter is probably high," he said.
The research was funded by the National Institutes of Health and the National Alliance for Research on Schizophrenia and Depression, for which he is a distinguished investigator.
Co-authors include MCG scientists Drs. Wen-Cheng Xiong, Alvin Terry and Almira Vazdarjanova and postdoctoral fellows Drs. Lei Wen, Yi-Sheng Lu and Xin-Hong Zhu.
Source: Medical College of Georgia.
Adults exposed to tobacco smoke in childhood more prone to early emphysema
Children regularly exposed to tobacco smoke at home were more likely to develop early emphysema in adulthood. This finding by researchers at Columbia University's Mailman School of Public Health suggests that the lungs may not recover completely from the effects of early-life exposures to tobacco smoke (ETS).The study is published in the December 2009 American Journal of Epidemiology.
This population-based research is the first to examine the association of childhood ETS with early emphysema by CT scan in nonsmokers. Approximately half of the participants in this large multiethnic cohort had at least one regular cigarette smoker in their childhood home. Participants with more childhood ETS exposure had more emphysema-like lung pixels; an average of 20% of scan pixels were emphysema-like for those who lived with two or more smokers as a child, compared with 18% for those who lived with one regular smoker, or 17% for those who said that they did not live with a regular inside smoker as a child.
The researchers studied CT scans of 1,781 non-smokers without clinical cardiovascular disease recruited from six communities in the United States, including northern Manhattan and the Bronx, New York. Those reporting childhood ETS exposure were somewhat younger, with an average age of 61; were more likely to be non- Hispanic white; and less likely to have been born outside the United States. These differences were statistically controlled in the analyses.
"We were able to detect a difference on CT scans between the lungs of participants who lived with a smoker as a child and those who did not," observed Gina Lovasi, PhD, MPH, assistant professor of epidemiology at Columbia's Mailman School of Public Health. "Some known harmful effects of tobacco smoke are short term, and this new research suggests that effects of tobacco smoke on the lungs may also persist for decades."
Previous studies have found evidence that childhood ETS exposure affects perinatal and childhood health outcomes, and that adult exposure may affect adult respiratory health outcomes, including lung function and respiratory symptoms.
Although childhood ETS was not associated with adult lung function in this healthy population, this does not contradict the results for early emphysema, since airflow obstruction and anatomic damage are theoretically and clinically distinguishable. "However, emphysema may be a more sensitive measure of damage compared with lung function in this relatively healthy cohort,"
Dr. Lovasi notes. Combined emphysema and chronic obstructive pulmonary disease are projected to become the third leading cause of death worldwide by 2020.
The exposure information in this study does not provide information on the timing of ETS exposure during childhood, making it difficult to distinguish as exposure in utero. "The association between childhood ETS and early emphysema among participants whose mothers did not smoke, suggests that the effect we are detecting is for smoke exposure in the home during childhood rather than in utero exposure alone," observed Dr. Lovasi.
This work was supported by the National Institutes of Health and the Robert Wood Johnson Foundation Health & Society Scholars Program and the National Institutes of Health.
Source: Columbia University's Mailman School of Public Health.
This population-based research is the first to examine the association of childhood ETS with early emphysema by CT scan in nonsmokers. Approximately half of the participants in this large multiethnic cohort had at least one regular cigarette smoker in their childhood home. Participants with more childhood ETS exposure had more emphysema-like lung pixels; an average of 20% of scan pixels were emphysema-like for those who lived with two or more smokers as a child, compared with 18% for those who lived with one regular smoker, or 17% for those who said that they did not live with a regular inside smoker as a child.
The researchers studied CT scans of 1,781 non-smokers without clinical cardiovascular disease recruited from six communities in the United States, including northern Manhattan and the Bronx, New York. Those reporting childhood ETS exposure were somewhat younger, with an average age of 61; were more likely to be non- Hispanic white; and less likely to have been born outside the United States. These differences were statistically controlled in the analyses.
"We were able to detect a difference on CT scans between the lungs of participants who lived with a smoker as a child and those who did not," observed Gina Lovasi, PhD, MPH, assistant professor of epidemiology at Columbia's Mailman School of Public Health. "Some known harmful effects of tobacco smoke are short term, and this new research suggests that effects of tobacco smoke on the lungs may also persist for decades."
Previous studies have found evidence that childhood ETS exposure affects perinatal and childhood health outcomes, and that adult exposure may affect adult respiratory health outcomes, including lung function and respiratory symptoms.
Although childhood ETS was not associated with adult lung function in this healthy population, this does not contradict the results for early emphysema, since airflow obstruction and anatomic damage are theoretically and clinically distinguishable. "However, emphysema may be a more sensitive measure of damage compared with lung function in this relatively healthy cohort,"
Dr. Lovasi notes. Combined emphysema and chronic obstructive pulmonary disease are projected to become the third leading cause of death worldwide by 2020.
The exposure information in this study does not provide information on the timing of ETS exposure during childhood, making it difficult to distinguish as exposure in utero. "The association between childhood ETS and early emphysema among participants whose mothers did not smoke, suggests that the effect we are detecting is for smoke exposure in the home during childhood rather than in utero exposure alone," observed Dr. Lovasi.
This work was supported by the National Institutes of Health and the Robert Wood Johnson Foundation Health & Society Scholars Program and the National Institutes of Health.
Source: Columbia University's Mailman School of Public Health.
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