Monday, May 4, 2015
Sunday, May 3, 2015
10 sea Creatures You Won't Believe Exist
https://www.youtube.com/watch?v=pGBNLxPMhhI
some times we believe things by naked eyes. But some times we do not accept without evidence.
some times we believe things by naked eyes. But some times we do not accept without evidence.
10 sea Creatures You Won't Believe Exist
https://www.youtube.com/watch?v=pGBNLxPMhhI
some times we believe things by naked eyes. But some times we do not accept without evidence.
some times we believe things by naked eyes. But some times we do not accept without evidence.
15 Things You Didn't Know About Earth
https://www.youtube.com/watch?v=u9A_HSO1TnA
It is nature. man then tries to change it every minute, but finally nature wins over man.
It is nature. man then tries to change it every minute, but finally nature wins over man.
15 Things You Didn't Know About Earth
https://www.youtube.com/watch?v=u9A_HSO1TnA
It is nature. man then tries to change it every minute, but finally nature wins over man.
It is nature. man then tries to change it every minute, but finally nature wins over man.
Planet Earth 100 Million Years In The Future - What will happen to our world?
https://www.youtube.com/watch?v=uQ91AxUqHck&sns=tw
watch carefully and think about the ways that we follow to save world to be lived long long years.
give a contribution by your activities make the world to be lived long days healthy.
watch carefully and think about the ways that we follow to save world to be lived long long years.
give a contribution by your activities make the world to be lived long days healthy.
Planet Earth 100 Million Years In The Future - What will happen to our world?
https://www.youtube.com/watch?v=uQ91AxUqHck&sns=tw
watch carefully and think about the ways that we follow to save world to be lived long long years.
give a contribution by your activities make the world to be lived long days healthy.
watch carefully and think about the ways that we follow to save world to be lived long long years.
give a contribution by your activities make the world to be lived long days healthy.
Saturday, May 2, 2015
Drugs that activate brain stem cells may reverse multiple sclerosis
NIH-funded study identifies over-the-counter compounds that may replace damaged cells
Two drugs already on the market — an antifungal and a steroid — may potentially take on new roles as treatments for multiple sclerosis. According to a study published in Nature today, researchers discovered that these drugs may activate stem cells in the brain to stimulate myelin producing cells and repair white matter, which is damaged in multiple sclerosis. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.
An artist’s representation of the study. Scientists found that certain drugs were able to promote remyelination in mouse models of multiple sclerosis. Image courtesy of Case Western Reserve University; Illustrator: Megan Kern
Specialized cells called oligodendrocytes lay down multiple layers of a fatty white substance known as myelin around axons, the long “wires” that connect brain cells. Myelin acts as an insulator and enables fast communication between brain cells. In multiple sclerosis there is breakdown of myelin and this deterioration leads to muscle weakness, numbness and problems with vision, coordination and balance.
“To replace damaged cells, the scientific field has focused on direct transplantation of stem cell-derived tissues for regenerative medicine, and that approach is likely to provide enormous benefit down the road. We asked if we could find a faster and less invasive approach by using drugs to activate native nervous system stem cells and direct them to form new myelin. Our ultimate goal was to enhance the body’s ability to repair itself,” said Paul J. Tesar, Ph.D., associate professor at Case Western Reserve School of Medicine in Cleveland, and senior author of the study.
It is unknown how myelin-producing cells are damaged, but research suggests they may be targeted by malfunctioning immune cells and that multiple sclerosis may start as an autoimmune disorder. Current therapies for multiple sclerosis include anti-inflammatory drugs, which help prevent the episodic relapses common in multiple sclerosis, but are less effective at preventing long-term disability. Scientists believe that therapies that promote myelin repair might improve neurologic disability in people with multiple sclerosis.
Adult brains contain oligodendrocyte progenitor cells (OPCs), which are stem cells that generate myelin-producing cells. OPCs are found to multiply in the brains of multiple sclerosis patients as if to respond to myelin damage, but for unknown reasons they are not effective in restoring white matter. In the current study, Dr. Tesar wanted to see if drugs already approved for other uses were able to stimulate OPCs to increase myelination.
OPCs have been difficult to isolate and study, but Dr. Tesar and his colleagues, in collaboration with Robert Miller, Ph.D., professor at George Washington University School of Medicine and Health Sciences in Washington, D.C., developed a novel method to investigate these cells in a petri dish. Using this technique, they were able to quickly test the effects of hundreds of drugs on the stem cells.
The compounds screened in this study were obtained from a drug library maintained by NIH’s National Center for Advancing Translational Sciences (NCATS). All are approved for use in humans. NCATS and Dr. Tesar have an ongoing collaboration and plan to expand the library of drugs screened against OPCs in the near future to identify other promising compounds.
Dr. Tesar’s team found that two compounds in particular, miconazole (an antifungal) and clobetasol (a steroid), stimulated mouse and human OPCs into generating myelin-producing cells.
Next, they examined whether the drugs, when injected into a mouse model of multiple sclerosis, could improve re-myelination. They found that both drugs were effective in activating OPCs to enhance myelination and reverse paralysis. As a result, almost all of the animals regained the use of their hind limbs. They also found that the drugs acted through two very different molecular mechanisms.
“The ability to activate white matter cells in the brain, as shown in this study, opens up an exciting new avenue of therapy development for myelin disorders such as multiple sclerosis,” said Ursula Utz, Ph.D., program director at the NINDS.
Dr. Tesar and his colleagues caution that more research is needed before miconazole and clobetasol can be tested in multiple sclerosis clinical trials. They are currently approved for use as creams or powders on the surfaces of the body but their safety administered in other forms, such as injections, in humans is unknown.
“Off-label use of the current forms of these drugs is more likely to increase other health concerns than alleviate multiple sclerosis symptoms. We are working tirelessly to ready a safe and effective drug for clinical use,” Dr. Tesar said.
This work was supported by the NINDS (NS085246, NS030800, NS026543), the New York Stem Cell Foundation and the Myelin Repair Foundation, New York City.
The NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.
The National Center for Advancing Translational Sciences is a distinctly different entity in the research ecosystem. Rather than targeting a particular disease or fundamental science, NCATS focuses on what is common across diseases and the translational process. The Center emphasizes innovation and deliverables, relying on the power of data and new technologies to develop, demonstrate and disseminate advancements in translational science that bring about tangible improvements in human health. For more information, visit http://www.ncats.nih.gov.
Drugs that activate brain stem cells may reverse multiple sclerosis
NIH-funded study identifies over-the-counter compounds that may replace damaged cells
Two drugs already on the market — an antifungal and a steroid — may potentially take on new roles as treatments for multiple sclerosis. According to a study published in Nature today, researchers discovered that these drugs may activate stem cells in the brain to stimulate myelin producing cells and repair white matter, which is damaged in multiple sclerosis. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.
An artist’s representation of the study. Scientists found that certain drugs were able to promote remyelination in mouse models of multiple sclerosis. Image courtesy of Case Western Reserve University; Illustrator: Megan Kern
Specialized cells called oligodendrocytes lay down multiple layers of a fatty white substance known as myelin around axons, the long “wires” that connect brain cells. Myelin acts as an insulator and enables fast communication between brain cells. In multiple sclerosis there is breakdown of myelin and this deterioration leads to muscle weakness, numbness and problems with vision, coordination and balance.
“To replace damaged cells, the scientific field has focused on direct transplantation of stem cell-derived tissues for regenerative medicine, and that approach is likely to provide enormous benefit down the road. We asked if we could find a faster and less invasive approach by using drugs to activate native nervous system stem cells and direct them to form new myelin. Our ultimate goal was to enhance the body’s ability to repair itself,” said Paul J. Tesar, Ph.D., associate professor at Case Western Reserve School of Medicine in Cleveland, and senior author of the study.
It is unknown how myelin-producing cells are damaged, but research suggests they may be targeted by malfunctioning immune cells and that multiple sclerosis may start as an autoimmune disorder. Current therapies for multiple sclerosis include anti-inflammatory drugs, which help prevent the episodic relapses common in multiple sclerosis, but are less effective at preventing long-term disability. Scientists believe that therapies that promote myelin repair might improve neurologic disability in people with multiple sclerosis.
Adult brains contain oligodendrocyte progenitor cells (OPCs), which are stem cells that generate myelin-producing cells. OPCs are found to multiply in the brains of multiple sclerosis patients as if to respond to myelin damage, but for unknown reasons they are not effective in restoring white matter. In the current study, Dr. Tesar wanted to see if drugs already approved for other uses were able to stimulate OPCs to increase myelination.
OPCs have been difficult to isolate and study, but Dr. Tesar and his colleagues, in collaboration with Robert Miller, Ph.D., professor at George Washington University School of Medicine and Health Sciences in Washington, D.C., developed a novel method to investigate these cells in a petri dish. Using this technique, they were able to quickly test the effects of hundreds of drugs on the stem cells.
The compounds screened in this study were obtained from a drug library maintained by NIH’s National Center for Advancing Translational Sciences (NCATS). All are approved for use in humans. NCATS and Dr. Tesar have an ongoing collaboration and plan to expand the library of drugs screened against OPCs in the near future to identify other promising compounds.
Dr. Tesar’s team found that two compounds in particular, miconazole (an antifungal) and clobetasol (a steroid), stimulated mouse and human OPCs into generating myelin-producing cells.
Next, they examined whether the drugs, when injected into a mouse model of multiple sclerosis, could improve re-myelination. They found that both drugs were effective in activating OPCs to enhance myelination and reverse paralysis. As a result, almost all of the animals regained the use of their hind limbs. They also found that the drugs acted through two very different molecular mechanisms.
“The ability to activate white matter cells in the brain, as shown in this study, opens up an exciting new avenue of therapy development for myelin disorders such as multiple sclerosis,” said Ursula Utz, Ph.D., program director at the NINDS.
Dr. Tesar and his colleagues caution that more research is needed before miconazole and clobetasol can be tested in multiple sclerosis clinical trials. They are currently approved for use as creams or powders on the surfaces of the body but their safety administered in other forms, such as injections, in humans is unknown.
“Off-label use of the current forms of these drugs is more likely to increase other health concerns than alleviate multiple sclerosis symptoms. We are working tirelessly to ready a safe and effective drug for clinical use,” Dr. Tesar said.
This work was supported by the NINDS (NS085246, NS030800, NS026543), the New York Stem Cell Foundation and the Myelin Repair Foundation, New York City.
The NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.
The National Center for Advancing Translational Sciences is a distinctly different entity in the research ecosystem. Rather than targeting a particular disease or fundamental science, NCATS focuses on what is common across diseases and the translational process. The Center emphasizes innovation and deliverables, relying on the power of data and new technologies to develop, demonstrate and disseminate advancements in translational science that bring about tangible improvements in human health. For more information, visit http://www.ncats.nih.gov.
How to identify drugs that work best for each patient
Implantable device could allow doctors to test cancer drugs in patients before prescribing chemotherapy.
More than 100 drugs have been approved to treat cancer, but predicting which ones will help a particular patient is an inexact science at best.
A new device developed at MIT may change that. The implantable device, about the size of the grain of rice, can carry small doses of up to 30 different drugs. After implanting it in a tumor and letting the drugs diffuse into the tissue, researchers can measure how effectively each one kills the patient’s cancer cells.
Such a device could eliminate much of the guesswork now involved in choosing cancer treatments, says Oliver Jonas, a postdoc at MIT’s Koch Institute for Integrative Cancer Research and lead author of a paper describing the device in the April 22 online edition ofScience Translational Medicine.
“You can use it to test a patient for a range of available drugs, and pick the one that works best,” Jonas says.
The paper’s senior authors are Robert Langer, the David H. Koch Professor at MIT and a member of the Koch Institute, the Institute for Medical Engineering and Science, and the Department of Chemical Engineering; and Michael Cima, the David H. Koch Professor of Engineering at MIT and a member of the Koch Institute and the Department of Materials Science and Engineering.
Putting the lab in the patient
Most of the commonly used cancer drugs work by damaging DNA or otherwise interfering with cell function. Recently, scientists have also developed more targeted drugs designed to kill tumor cells that carry a specific genetic mutation. However, it is usually difficult to predict whether a particular drug will be effective in an individual patient.
In some cases, doctors extract tumor cells, grow them in a lab dish, and treat them with different drugs to see which ones are most effective. However, this process removes the cells from their natural environment, which can play an important role in how a tumor responds to drug treatment, Jonas says.
“The approach that we thought would be good to try is to essentially put the lab into the patient,” he says. “It’s safe and you can do all of your sensitivity testing in the native microenvironment.”
The device, made from a stiff, crystalline polymer, can be implanted in a patient’s tumor using a biopsy needle. After implantation, drugs seep 200 to 300 microns into the tumor, but do not overlap with each other. Any type of drug can go into the reservoir, and the researchers can formulate the drugs so that the doses that reach the cancer cells are similar to what they would receive if the drug were given by typical delivery methods such as intravenous injection.
After one day of drug exposure, the implant is removed, along with a small sample of the tumor tissue surrounding it, and the researchers analyze the drug effects by slicing up the tissue sample and staining it with antibodies that can detect markers of cell death or proliferation.
Ranking cancer drugs
To test the device, the researchers implanted it in mice that had been grafted with human prostate, breast, and melanoma tumors. These tumors are known to have varying sensitivity to different cancer drugs, and the MIT team’s results corresponded to those previously seen differences.
The researchers then tested the device with a type of breast cancer known as triple negative, which lacks the three most common breast cancer markers: estrogen receptor, progesterone receptor, and Her2. This form of cancer is particularly aggressive, and none of the drugs used against it are targeted to a specific genetic marker.
Using the device, the researchers found that triple negative tumors responded differently to five of the drugs commonly used to treat them. The most effective was paclitaxel, followed by doxorubicin, cisplatin, gemcitabine, and lapatinib. They found the same results when delivering these drugs by intravenous injection, suggesting that the device is an accurate predictor of drug sensitivity.
In this study, the researchers compared single drugs to each other, but the device could also be used to test different drug combinations by putting two or three drugs into the same reservoir, Jonas says.
“This device could help us identify the best chemotherapy agents and combinations for every tumor prior to starting systemic administration of chemotherapy, as opposed to making choices based on population-based statistics. This has been a longstanding pursuit of the oncology community and an important step toward our goal of developing precision-based cancer therapy,” says Jose Baselga, chief medical officer at Memorial Sloan Kettering Cancer Center and an author of the paper.
The researchers are now working on ways to make the device easier to read while it is still inside the patient, allowing them to get results faster. They are also planning to launch a clinical trial in breast cancer patients next year.
“This is a stunning advance in the approach to treating complex cancers,” says Henry Brem, a professor of neurosurgery and oncology at Johns Hopkins School of Medicine who was not involved in the research. “This work is transformative in that it now opens the doors to truly personalized medicine with the right drug or drug combination being utilized for each tumor.”
Another possible application for this device is to guide the development and testing of new cancer drugs. Researchers could create several different variants of a promising compound and test them all at once in a small trial of human patients, allowing them to choose the best one to carry on to a larger clinical trial.
How to identify drugs that work best for each patient
Implantable device could allow doctors to test cancer drugs in patients before prescribing chemotherapy.
More than 100 drugs have been approved to treat cancer, but predicting which ones will help a particular patient is an inexact science at best.
A new device developed at MIT may change that. The implantable device, about the size of the grain of rice, can carry small doses of up to 30 different drugs. After implanting it in a tumor and letting the drugs diffuse into the tissue, researchers can measure how effectively each one kills the patient’s cancer cells.
Such a device could eliminate much of the guesswork now involved in choosing cancer treatments, says Oliver Jonas, a postdoc at MIT’s Koch Institute for Integrative Cancer Research and lead author of a paper describing the device in the April 22 online edition ofScience Translational Medicine.
“You can use it to test a patient for a range of available drugs, and pick the one that works best,” Jonas says.
The paper’s senior authors are Robert Langer, the David H. Koch Professor at MIT and a member of the Koch Institute, the Institute for Medical Engineering and Science, and the Department of Chemical Engineering; and Michael Cima, the David H. Koch Professor of Engineering at MIT and a member of the Koch Institute and the Department of Materials Science and Engineering.
Putting the lab in the patient
Most of the commonly used cancer drugs work by damaging DNA or otherwise interfering with cell function. Recently, scientists have also developed more targeted drugs designed to kill tumor cells that carry a specific genetic mutation. However, it is usually difficult to predict whether a particular drug will be effective in an individual patient.
In some cases, doctors extract tumor cells, grow them in a lab dish, and treat them with different drugs to see which ones are most effective. However, this process removes the cells from their natural environment, which can play an important role in how a tumor responds to drug treatment, Jonas says.
“The approach that we thought would be good to try is to essentially put the lab into the patient,” he says. “It’s safe and you can do all of your sensitivity testing in the native microenvironment.”
The device, made from a stiff, crystalline polymer, can be implanted in a patient’s tumor using a biopsy needle. After implantation, drugs seep 200 to 300 microns into the tumor, but do not overlap with each other. Any type of drug can go into the reservoir, and the researchers can formulate the drugs so that the doses that reach the cancer cells are similar to what they would receive if the drug were given by typical delivery methods such as intravenous injection.
After one day of drug exposure, the implant is removed, along with a small sample of the tumor tissue surrounding it, and the researchers analyze the drug effects by slicing up the tissue sample and staining it with antibodies that can detect markers of cell death or proliferation.
Ranking cancer drugs
To test the device, the researchers implanted it in mice that had been grafted with human prostate, breast, and melanoma tumors. These tumors are known to have varying sensitivity to different cancer drugs, and the MIT team’s results corresponded to those previously seen differences.
The researchers then tested the device with a type of breast cancer known as triple negative, which lacks the three most common breast cancer markers: estrogen receptor, progesterone receptor, and Her2. This form of cancer is particularly aggressive, and none of the drugs used against it are targeted to a specific genetic marker.
Using the device, the researchers found that triple negative tumors responded differently to five of the drugs commonly used to treat them. The most effective was paclitaxel, followed by doxorubicin, cisplatin, gemcitabine, and lapatinib. They found the same results when delivering these drugs by intravenous injection, suggesting that the device is an accurate predictor of drug sensitivity.
In this study, the researchers compared single drugs to each other, but the device could also be used to test different drug combinations by putting two or three drugs into the same reservoir, Jonas says.
“This device could help us identify the best chemotherapy agents and combinations for every tumor prior to starting systemic administration of chemotherapy, as opposed to making choices based on population-based statistics. This has been a longstanding pursuit of the oncology community and an important step toward our goal of developing precision-based cancer therapy,” says Jose Baselga, chief medical officer at Memorial Sloan Kettering Cancer Center and an author of the paper.
The researchers are now working on ways to make the device easier to read while it is still inside the patient, allowing them to get results faster. They are also planning to launch a clinical trial in breast cancer patients next year.
“This is a stunning advance in the approach to treating complex cancers,” says Henry Brem, a professor of neurosurgery and oncology at Johns Hopkins School of Medicine who was not involved in the research. “This work is transformative in that it now opens the doors to truly personalized medicine with the right drug or drug combination being utilized for each tumor.”
Another possible application for this device is to guide the development and testing of new cancer drugs. Researchers could create several different variants of a promising compound and test them all at once in a small trial of human patients, allowing them to choose the best one to carry on to a larger clinical trial.
Unique UIC Center Will Study Alcohol's Effect on Genes
Newswise — Funded by a five-year, $7 million federal grant, the University of Illinois at Chicago College of Medicine will create a new center, the first of its kind, to study the effect of long-term alcohol exposure on genes.
The National Institute on Alcohol Abuse and Alcoholism, one of the National Institutes of Health, awarded the funding to establish a Center for Alcohol Research in Epigenetics (CARE). Subhash Pandey, UIC professor of psychiatry, will direct the center.
"Epigenetics" refers to chemical changes to DNA, RNA, or specific proteins, that change the activity of genes without changing the genes themselves. Epigenetic changes can occur in response to environmental or even social factors, such as alcohol and stress -- and these changes have been linked to changes in behavior and disease.
Epigenetics plays a role in the development and persistence of neurological changes associated with alcoholism, says Pandey, who is director of neuroscience alcoholism research at UIC and research career scientist at the Jesse Brown VA Medical Center.
The CARE researchers will investigate how alcohol-related epigenetic changes influence gene expression and "synaptic remodeling" -- the networking of nerve cells to each other. They will also look closely at how these changes correlate with behavior, such as anxiety and depression, and whether epigenetics may play a role in the withdrawal symptoms that make abstinence difficult.
“This award will allow the College of Medicine to build on Professor Pandey’s exemplary research on chronic alcohol use and alcoholism in addition to bolstering our leadership in understanding the causes of alcoholism as well as finding new ways to treat this devastating disease,” said Dr. Dimitri Azar, dean of the University of Illinois College of Medicine.
In a recent study using an animal model, Pandey and colleagues at UIC found that epigenetic changes resulting from exposure to alcohol during adolescence were associated with abnormal brain development and anxiety and alcohol preference in adulthood. In earlier work, the researchers were able to show that reshaping of the DNA scaffolding that supports and controls the expression of genes in the brain may play a major role in alcohol withdrawal symptoms, particularly anxiety.
Several brain regions play a crucial role in regulating both the positive and negative emotional states associated with alcohol addiction. Pandey said the center will look at the circuitry involved in reward and pleasure, depression, cognition, and anxiety.
CARE researchers will study disease using preclinical animal models and post-mortem examination of human brain. Investigators will also do neuroimaging of patients diagnosed with alcohol abuse and dependence and search for "biomarkers" of alcoholism -- measurable indicators in blood that correlate with alcohol addiction.
There are two causes of dependence on alcohol, said Pandey -- people may drink to get pleasure, or to self-medicate to relieve depression or anxiety. But alcohol addiction may itself cause depression and anxiety, feeding into a cycle.
“Ultimately, we hope these studies may lead to the identification of molecular cellular targets and gene networks which can be used to develop new pharmacotherapies to treat or prevent alcoholism,” Pandey said.
UIC's CARE is the only NIH-funded alcohol research center in Illinois, said Dr. Anand Kumar, Lizzie Gilman Professor and head of psychiatry, and is "well positioned to perform state-of-the-art basic translational and clinical research in alcoholism.”
In addition to its research projects, CARE will provide resources for training and community outreach. Based in the UIC psychiatry department, it includes collaborators from biophysics and physiology, anesthesiology, the Jesse Brown VA Medical Center, and the University of Illinois Urbana-Champaign campus.
Other members of the CARE research team are Alessandro Guidotti, Mark Brodie, Amy Lasek, Rajiv Sharma, Dennis Grayson, Harish Krishnan, David Gavin, Douglas Feinstein, Chunyu Liu, Dulal Bhaumik, Mark Rasenick and Marc Atkins of UIC; and Alvaro Hernandez and Victor Jongeneel from the Roy J. Carver Biotechnology Center at UIUC.
Unique UIC Center Will Study Alcohol's Effect on Genes
Newswise — Funded by a five-year, $7 million federal grant, the University of Illinois at Chicago College of Medicine will create a new center, the first of its kind, to study the effect of long-term alcohol exposure on genes.
The National Institute on Alcohol Abuse and Alcoholism, one of the National Institutes of Health, awarded the funding to establish a Center for Alcohol Research in Epigenetics (CARE). Subhash Pandey, UIC professor of psychiatry, will direct the center.
"Epigenetics" refers to chemical changes to DNA, RNA, or specific proteins, that change the activity of genes without changing the genes themselves. Epigenetic changes can occur in response to environmental or even social factors, such as alcohol and stress -- and these changes have been linked to changes in behavior and disease.
Epigenetics plays a role in the development and persistence of neurological changes associated with alcoholism, says Pandey, who is director of neuroscience alcoholism research at UIC and research career scientist at the Jesse Brown VA Medical Center.
The CARE researchers will investigate how alcohol-related epigenetic changes influence gene expression and "synaptic remodeling" -- the networking of nerve cells to each other. They will also look closely at how these changes correlate with behavior, such as anxiety and depression, and whether epigenetics may play a role in the withdrawal symptoms that make abstinence difficult.
“This award will allow the College of Medicine to build on Professor Pandey’s exemplary research on chronic alcohol use and alcoholism in addition to bolstering our leadership in understanding the causes of alcoholism as well as finding new ways to treat this devastating disease,” said Dr. Dimitri Azar, dean of the University of Illinois College of Medicine.
In a recent study using an animal model, Pandey and colleagues at UIC found that epigenetic changes resulting from exposure to alcohol during adolescence were associated with abnormal brain development and anxiety and alcohol preference in adulthood. In earlier work, the researchers were able to show that reshaping of the DNA scaffolding that supports and controls the expression of genes in the brain may play a major role in alcohol withdrawal symptoms, particularly anxiety.
Several brain regions play a crucial role in regulating both the positive and negative emotional states associated with alcohol addiction. Pandey said the center will look at the circuitry involved in reward and pleasure, depression, cognition, and anxiety.
CARE researchers will study disease using preclinical animal models and post-mortem examination of human brain. Investigators will also do neuroimaging of patients diagnosed with alcohol abuse and dependence and search for "biomarkers" of alcoholism -- measurable indicators in blood that correlate with alcohol addiction.
There are two causes of dependence on alcohol, said Pandey -- people may drink to get pleasure, or to self-medicate to relieve depression or anxiety. But alcohol addiction may itself cause depression and anxiety, feeding into a cycle.
“Ultimately, we hope these studies may lead to the identification of molecular cellular targets and gene networks which can be used to develop new pharmacotherapies to treat or prevent alcoholism,” Pandey said.
UIC's CARE is the only NIH-funded alcohol research center in Illinois, said Dr. Anand Kumar, Lizzie Gilman Professor and head of psychiatry, and is "well positioned to perform state-of-the-art basic translational and clinical research in alcoholism.”
In addition to its research projects, CARE will provide resources for training and community outreach. Based in the UIC psychiatry department, it includes collaborators from biophysics and physiology, anesthesiology, the Jesse Brown VA Medical Center, and the University of Illinois Urbana-Champaign campus.
Other members of the CARE research team are Alessandro Guidotti, Mark Brodie, Amy Lasek, Rajiv Sharma, Dennis Grayson, Harish Krishnan, David Gavin, Douglas Feinstein, Chunyu Liu, Dulal Bhaumik, Mark Rasenick and Marc Atkins of UIC; and Alvaro Hernandez and Victor Jongeneel from the Roy J. Carver Biotechnology Center at UIUC.
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