Medical College of Georgia researchers are seeking to refine cancer treatment with an anti-inflammatory plant derivative long used in Chinese medicine.
Celastrol, derived from trees and shrubs called celastracaea, has been used for centuries in China to treat symptoms such as fever, chills, joint pain and inflammation. The MCG researchers think it may also play a role in cancer treatment by inactivating a protein required for cancer growth.
That protein, P23, is one of many proteins helping the heat shock protein 90. Scientists are just beginning to realize the potential of controlling inflammation-related diseases, including cancer, by inhibiting HSP90.
"Cancer cells need HSP90 more than normal cells because cancer cells have thousands of mutations," said Dr. Ahmed Chadli, biochemist in the MCG Center for Molecular Chaperones/Radiobiology and Cancer Virology. "They need chaperones all the time to keep their mutated proteins active. By taking heat shock proteins away from cells, the stabilization is taken away and cell death occurs."
But most HSP90 inhibitors lack selectivity, disabling the functions of all proteins activated by HSP90 rather than only the ones implicated in a specific tumor. Those proteins vary from one tumor to another.
Dr. Chadli and colleagues at the Mayo Clinic believe celastrol holds the key to specificity, targeting the HSP90-activated protein required for folding steroid receptors.
"The celastrol induces the protein to form fibrils and clusters it together, which inactivates it," said Dr. Chadli, whose research was published in the January edition of The Journal of Biological Chemistry. "When they are clustered, they're not available for other functions that help cancer grow."
The research was funded by a seed grant from the MCG Cardiovascular Discovery Institute and a Scientist Development Grant from The American Heart Association.
Dr. Chadli envisions future studies on cancer patients using even more potent derivatives of celastrol.
"They can hopefully be used in combination with other therapeutic agents to reduce the probability of cancer resistance," he said.
Source:
Jennifer Hilliard
Medical College of Georgia
четверг, 20 октября 2011 г.
понедельник, 17 октября 2011 г.
Material Created To Repel Liquids
Sculpting a surface composed of tightly packed nanostructures that resemble tiny nails, University of Wisconsin-Madison engineers and their colleagues from Bell Laboratories have created a material that can repel almost any liquid.
Add a jolt of electricity, and the liquid on the surface slips past the heads of the nanonails and spreads out between their shanks, wetting the surface completely.
The new material, which was reported this month in Langmuir, a journal of the American Chemical Society, could find use in biomedical applications such as "lab-on-a- chip" technology, the manufacture of self-cleaning surfaces, and could help extend the working life of batteries as a way to turn them off when not in use.
UW-Madison mechanical engineers Tom Krupenkin and J. Ashley Taylor and their team etched a silicon wafer to create a forest of conductive silicon shanks and non-conducting silicon oxide heads. Intriguingly, the ability of the surface of the structure to repel water, oil, and solvents rests on the nanonail geometry.
"It turns out that what's important is not the chemistry of the surface, but the topography of the surface," Krupenkin explains, noting that the overhang of the nail head is what gives his novel surface its dual personality.
A surface of posts, he notes, creates a platform so rough at the nanoscale that "liquid only touches the surface at the extreme ends of the posts. It's almost like sitting on a layer of air."
Source: Tom Krupenkin
University of Wisconsin-Madison
Add a jolt of electricity, and the liquid on the surface slips past the heads of the nanonails and spreads out between their shanks, wetting the surface completely.
The new material, which was reported this month in Langmuir, a journal of the American Chemical Society, could find use in biomedical applications such as "lab-on-a- chip" technology, the manufacture of self-cleaning surfaces, and could help extend the working life of batteries as a way to turn them off when not in use.
UW-Madison mechanical engineers Tom Krupenkin and J. Ashley Taylor and their team etched a silicon wafer to create a forest of conductive silicon shanks and non-conducting silicon oxide heads. Intriguingly, the ability of the surface of the structure to repel water, oil, and solvents rests on the nanonail geometry.
"It turns out that what's important is not the chemistry of the surface, but the topography of the surface," Krupenkin explains, noting that the overhang of the nail head is what gives his novel surface its dual personality.
A surface of posts, he notes, creates a platform so rough at the nanoscale that "liquid only touches the surface at the extreme ends of the posts. It's almost like sitting on a layer of air."
Source: Tom Krupenkin
University of Wisconsin-Madison
пятница, 14 октября 2011 г.
Journal Of Clinical Investigation Online Early Table Of Contents: June 2, 2008
Molecular changes in brain fluid give insight into brain-damaging disease
Soon after an individual becomes infected with HIV the virus infects cells in the brain and spinal cord (the central nervous system [CNS]). Although this causes no immediate problems, during the late-stages of disease it can cause dementia and encephalitis (acute inflammation of the brain that can cause death). Monkeys infected with a relative of HIV (SIV) also sometimes develop CNS damage and provide a good model of CNS disease in individuals infected with HIV. Insight into the mechanisms of CNS damage in SIV-infected monkeys has now been provided by a team of researchers at The Scripps Research Institute, La Jolla, who developed an approach to identify molecular changes in the fluid bathing the CNS (the CSF). The researchers, who were led by Howard Fox and Gary Siuzdak, hope that similar approaches could be used to provide new information about other neurodegenerative and neuropsychiatric disorders.
In the study, an approach known as global metabolomics was used to assess the levels of molecules known as metabolites in the CSF before and after SIV-induced encephalitis was manifest. The level of a number of metabolites, including some known as fatty acids and phospholipids, was observed to increase during infection. Consistent with this, a protein known to be important in the generation of fatty acids was found to be increased in the brain of monkeys with SIV-induced encephalitis. Further studies will be required to determine the precise role of the increased level of each metabolite, but it should be noted that many of them are known to induce receptor signaling and thereby might be able to further modulate CNS function.
TITLE: Metabolomic analysis of the cerebrospinal fluid reveals changes in phospholipase expression in the CNS of SIV-infected macaques
AUTHOR CONTACT:
Howard S. Fox
The Scripps Research Institute, La Jolla, California, USA.
Gary Siuzdak
The Scripps Research Institute, La Jolla, California, USA.
It's not a level playing field, your genes determine your levels of glucose
In individuals with type 2 diabetes, the way the level of glucose (the sugar molecule that is our main source of energy) in the body while not eating (fasting glucose level) is regulated fails and fasting glucose levels increase dramatically. New insight into genetic variations that have an impact on the fasting glucose levels of nondiabetic individuals has now been provided by a team of researchers from the Istituto Nazionale Ricovero E Cura Anziari, Italy, and the University of Southern California. Specifically, an association between one defined genetic variation and increased fasting glucose levels was observed in nondiabetic individuals. This variation was located between two genes known as G6PC2 and ABCB11. As G6PC2 carries the information for making a protein expressed by the cells that become dysfunctional in individuals with type 2 diabetes, the authors suggest that the genetic variation probably affects fasting glucose levels by altering the expression of this gene.
TITLE: Variations in the G6PC2/ABCB11 genomic region are associated with fasting glucose levels
AUTHOR CONTACT:
Angelo Scuteri
Istituto Nazionale Ricovero E Cura Anziari, Rome, Italy.
Richard M. Watanabe
Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.
Pinning down a cause of disease in a model of psoriasis
Psoriasis is a chronic skin disease that affects approximately 2-3% of individuals in the Western world. New data, generated by Karin Scharffetter-Kochanek and colleagues, at the University of Ulm, Germany, have indicated that a subset of immune cells known as Tregs (which act to prevent other immune cells from responding inappropriately) are dysfunctional in a mouse model of psoriasis and that this dysfunction contributes substantially to the development of disease.
Mice that express a reduced amount of the protein CD18 (Cd18hypo mice) develop a skin disease that resembles the symptoms of individuals with psoriasis. In the study, Tregs isolated from Cd18hypo mice failed to suppress the proliferation of disease-causing immune cells because they secreted lower levels of the soluble factor TGF-beta than normal Tregs. This was also important for their inability to control disease in vivo, as transplantation of normal Tregs into Cd18hypo mice resulted in a substantial improvement in the psoriasis-like disease, whereas if these cells were transplanted in the presence of antibodies that neutralized TGF-beta there was no improvement in disease. The authors therefore conclude that psoriasis-like disease in Cd18hypo mice is caused mainly by a defect in Treg function and suggest that maintaining CD18 levels is important for ensuring that Tregs function optimally.
TITLE: TGF-beta-dependent suppressive function of Tregs requires wild-type levels of CD18 in a mouse model of psoriasis
AUTHOR CONTACT:
Karin Scharffetter-Kochanek
University of Ulm, Ulm, Germany.
HSN2 mutations lose touch with pain and heat perception
Hereditary sensory and autonomic neuropathy type II, abbreviated to HSANII, is a poorly understood genetic disorder wherein affected patients lose the ability to feel touch, pain, and heat. Although it has been shown to be caused by mutations in a region of DNA known as HSN2, it was not known exactly what this region of DNA was for. In a new study, Guy Roulaeu and colleagues, at the University of Montreal, Canada, have discovered that HSN2 is part of the gene WNK1, but it is only used to generate a protein in the nervous system; in other parts of the body, the gene WNK1 does not use the information in the HSN2 region of DNA to make protein. Further analysis showed that the protein made using information contained in the HSN2 region of DNA (WNK1/HSN2) was found in mouse nerve cells that are vital for relaying sensory inputs such as touch and pain to the brain. Future studies will focus on determining the molecular mechanisms by which WNK1/HSN2 is important for sensing touch, pain, and heat, the very senses lost in individuals with HSANII.
TITLE: Mutations in the nervous system-specific HSN2 exon of WNK1 cause hereditary sensory neuropathy type II
AUTHOR CONTACT:
Guy A. Rouleau
University of Montreal, Montreal, Quebec, Canada.
Linking genes to decreased survival in lung cancer patients
New data, generated by Hongbing Shen and colleagues, at the Cancer Center of Nanjing Medical University, People's Republic of China, has identified a genetic variation that seems to help predict survival in individuals with non-small cell lung cancer (NSCLC).
A systematic screen of the DNA carrying the information for generating regulatory RNA molecules known as a microRNAs identified a specific genetic variant that was associated with decreased survival in individuals with NSCLC. The specific genetic variation resulted in increased levels of expression of the functional miRNA molecule. This was not because more of the miRNA was made but because more of the precursor form of the functional molecule was processed to become functional. The functional miRNA molecule generated by the genetic variation also had different functional properties. The authors hope that further characterization of genetic variations that modify miRNA expression and/or function will uncover other indicators of survival and opportunities for developing new therapeutics.
TITLE: Genetic variants of miRNA sequences and non-small cell lung cancer survival
AUTHOR CONTACT:
Hongbing Shen
Cancer Center of Nanjing Medical University, Nanjing, People's Republic of China.
Blood vessel growth kept under control by the protein LIF
Uncontrolled blood vessel growth is a key feature of many pathological conditions, including the degenerative diabetic eye disease known as diabetic retinopathy. Understanding the factors involved in the process is vital to developing treatments for the disease. In a new study, a team of researchers at Keio University, Japan, has revealed a role for the protein LIF in blood vessel growth in mice.
Specifically, mice lacking LIF were observed to have increased blood vessel growth in many regions of the body, but as this study was focused on the eye, the authors homed in on the increased blood vessel growth in the retina of the eye. Further analysis showed that mice lacking LIF developed more aberrant blood vessels in a model of retinopathy. Mechanistically, LIF was found to inhibit the proliferation of brain cells known as astrocytes as well as inhibit their production of a factor known to promote blood vessel growth, VEGF. It therefore seems that LIF is an important part of the communication between tissues and developing blood vessels, meaning that LIF and the signaling pathway it triggers might serve as a target for new treatment approaches for preventing diabetic retinopathy and other diseases that are associated with uncontrolled blood vessel growth, such as cancer.
TITLE: Leukemia inhibitory factor regulates microvessel density by modulating oxygen-dependent VEGF expression in mice
AUTHOR CONTACT:
Yoshiaki Kubota
Keio University, Tokyo, Japan.
Toshio Suda
Keio University, Tokyo, Japan.
Repairing the damage to DNA from chronic inflammation protects against cancer
Individuals who have health conditions associated with chronic inflammation are often at increased risk of developing cancer at the site of the chronic inflammation. For example, individuals with inflammatory bowel disease and those who are chronically infected with the bacterium Helicobacter pylori are at increased risk of colon cancer and stomach cancer, respectively. New insight into the mechanisms by which chronic inflammation can contribute to the development cancer has been generated in mice by Leona Samson and colleagues, at Massachusetts Institute of Technology, Boston.
Using mice lacking the protein Aag, which is involved in the repair of DNA damaged by inflammation-associated molecules known as reactive oxygen and nitrogen species (RONS), it was shown that Aag-mediated DNA repair limits cell damage in a mouse model of episodic inflammatory bowel disease and reduces the severity of the colon cancer that develops in the mice experiencing episodic bowel inflammation. In addition, in a mouse model of Helicobacter pylori infection, Aag-deficient mice were found to exhibit more severe cell damage and the damaged area of the stomach resembled that observed prior to the development of stomach cancer. The authors therefore conclude that repair of DNA damage caused by RONS seems to be important for protection against chronic inflammation-induced cancer.
TITLE: DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice
AUTHOR CONTACT:
Leona D. Samson
Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Source: Karen Honey
Journal of Clinical Investigation
Soon after an individual becomes infected with HIV the virus infects cells in the brain and spinal cord (the central nervous system [CNS]). Although this causes no immediate problems, during the late-stages of disease it can cause dementia and encephalitis (acute inflammation of the brain that can cause death). Monkeys infected with a relative of HIV (SIV) also sometimes develop CNS damage and provide a good model of CNS disease in individuals infected with HIV. Insight into the mechanisms of CNS damage in SIV-infected monkeys has now been provided by a team of researchers at The Scripps Research Institute, La Jolla, who developed an approach to identify molecular changes in the fluid bathing the CNS (the CSF). The researchers, who were led by Howard Fox and Gary Siuzdak, hope that similar approaches could be used to provide new information about other neurodegenerative and neuropsychiatric disorders.
In the study, an approach known as global metabolomics was used to assess the levels of molecules known as metabolites in the CSF before and after SIV-induced encephalitis was manifest. The level of a number of metabolites, including some known as fatty acids and phospholipids, was observed to increase during infection. Consistent with this, a protein known to be important in the generation of fatty acids was found to be increased in the brain of monkeys with SIV-induced encephalitis. Further studies will be required to determine the precise role of the increased level of each metabolite, but it should be noted that many of them are known to induce receptor signaling and thereby might be able to further modulate CNS function.
TITLE: Metabolomic analysis of the cerebrospinal fluid reveals changes in phospholipase expression in the CNS of SIV-infected macaques
AUTHOR CONTACT:
Howard S. Fox
The Scripps Research Institute, La Jolla, California, USA.
Gary Siuzdak
The Scripps Research Institute, La Jolla, California, USA.
It's not a level playing field, your genes determine your levels of glucose
In individuals with type 2 diabetes, the way the level of glucose (the sugar molecule that is our main source of energy) in the body while not eating (fasting glucose level) is regulated fails and fasting glucose levels increase dramatically. New insight into genetic variations that have an impact on the fasting glucose levels of nondiabetic individuals has now been provided by a team of researchers from the Istituto Nazionale Ricovero E Cura Anziari, Italy, and the University of Southern California. Specifically, an association between one defined genetic variation and increased fasting glucose levels was observed in nondiabetic individuals. This variation was located between two genes known as G6PC2 and ABCB11. As G6PC2 carries the information for making a protein expressed by the cells that become dysfunctional in individuals with type 2 diabetes, the authors suggest that the genetic variation probably affects fasting glucose levels by altering the expression of this gene.
TITLE: Variations in the G6PC2/ABCB11 genomic region are associated with fasting glucose levels
AUTHOR CONTACT:
Angelo Scuteri
Istituto Nazionale Ricovero E Cura Anziari, Rome, Italy.
Richard M. Watanabe
Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.
Pinning down a cause of disease in a model of psoriasis
Psoriasis is a chronic skin disease that affects approximately 2-3% of individuals in the Western world. New data, generated by Karin Scharffetter-Kochanek and colleagues, at the University of Ulm, Germany, have indicated that a subset of immune cells known as Tregs (which act to prevent other immune cells from responding inappropriately) are dysfunctional in a mouse model of psoriasis and that this dysfunction contributes substantially to the development of disease.
Mice that express a reduced amount of the protein CD18 (Cd18hypo mice) develop a skin disease that resembles the symptoms of individuals with psoriasis. In the study, Tregs isolated from Cd18hypo mice failed to suppress the proliferation of disease-causing immune cells because they secreted lower levels of the soluble factor TGF-beta than normal Tregs. This was also important for their inability to control disease in vivo, as transplantation of normal Tregs into Cd18hypo mice resulted in a substantial improvement in the psoriasis-like disease, whereas if these cells were transplanted in the presence of antibodies that neutralized TGF-beta there was no improvement in disease. The authors therefore conclude that psoriasis-like disease in Cd18hypo mice is caused mainly by a defect in Treg function and suggest that maintaining CD18 levels is important for ensuring that Tregs function optimally.
TITLE: TGF-beta-dependent suppressive function of Tregs requires wild-type levels of CD18 in a mouse model of psoriasis
AUTHOR CONTACT:
Karin Scharffetter-Kochanek
University of Ulm, Ulm, Germany.
HSN2 mutations lose touch with pain and heat perception
Hereditary sensory and autonomic neuropathy type II, abbreviated to HSANII, is a poorly understood genetic disorder wherein affected patients lose the ability to feel touch, pain, and heat. Although it has been shown to be caused by mutations in a region of DNA known as HSN2, it was not known exactly what this region of DNA was for. In a new study, Guy Roulaeu and colleagues, at the University of Montreal, Canada, have discovered that HSN2 is part of the gene WNK1, but it is only used to generate a protein in the nervous system; in other parts of the body, the gene WNK1 does not use the information in the HSN2 region of DNA to make protein. Further analysis showed that the protein made using information contained in the HSN2 region of DNA (WNK1/HSN2) was found in mouse nerve cells that are vital for relaying sensory inputs such as touch and pain to the brain. Future studies will focus on determining the molecular mechanisms by which WNK1/HSN2 is important for sensing touch, pain, and heat, the very senses lost in individuals with HSANII.
TITLE: Mutations in the nervous system-specific HSN2 exon of WNK1 cause hereditary sensory neuropathy type II
AUTHOR CONTACT:
Guy A. Rouleau
University of Montreal, Montreal, Quebec, Canada.
Linking genes to decreased survival in lung cancer patients
New data, generated by Hongbing Shen and colleagues, at the Cancer Center of Nanjing Medical University, People's Republic of China, has identified a genetic variation that seems to help predict survival in individuals with non-small cell lung cancer (NSCLC).
A systematic screen of the DNA carrying the information for generating regulatory RNA molecules known as a microRNAs identified a specific genetic variant that was associated with decreased survival in individuals with NSCLC. The specific genetic variation resulted in increased levels of expression of the functional miRNA molecule. This was not because more of the miRNA was made but because more of the precursor form of the functional molecule was processed to become functional. The functional miRNA molecule generated by the genetic variation also had different functional properties. The authors hope that further characterization of genetic variations that modify miRNA expression and/or function will uncover other indicators of survival and opportunities for developing new therapeutics.
TITLE: Genetic variants of miRNA sequences and non-small cell lung cancer survival
AUTHOR CONTACT:
Hongbing Shen
Cancer Center of Nanjing Medical University, Nanjing, People's Republic of China.
Blood vessel growth kept under control by the protein LIF
Uncontrolled blood vessel growth is a key feature of many pathological conditions, including the degenerative diabetic eye disease known as diabetic retinopathy. Understanding the factors involved in the process is vital to developing treatments for the disease. In a new study, a team of researchers at Keio University, Japan, has revealed a role for the protein LIF in blood vessel growth in mice.
Specifically, mice lacking LIF were observed to have increased blood vessel growth in many regions of the body, but as this study was focused on the eye, the authors homed in on the increased blood vessel growth in the retina of the eye. Further analysis showed that mice lacking LIF developed more aberrant blood vessels in a model of retinopathy. Mechanistically, LIF was found to inhibit the proliferation of brain cells known as astrocytes as well as inhibit their production of a factor known to promote blood vessel growth, VEGF. It therefore seems that LIF is an important part of the communication between tissues and developing blood vessels, meaning that LIF and the signaling pathway it triggers might serve as a target for new treatment approaches for preventing diabetic retinopathy and other diseases that are associated with uncontrolled blood vessel growth, such as cancer.
TITLE: Leukemia inhibitory factor regulates microvessel density by modulating oxygen-dependent VEGF expression in mice
AUTHOR CONTACT:
Yoshiaki Kubota
Keio University, Tokyo, Japan.
Toshio Suda
Keio University, Tokyo, Japan.
Repairing the damage to DNA from chronic inflammation protects against cancer
Individuals who have health conditions associated with chronic inflammation are often at increased risk of developing cancer at the site of the chronic inflammation. For example, individuals with inflammatory bowel disease and those who are chronically infected with the bacterium Helicobacter pylori are at increased risk of colon cancer and stomach cancer, respectively. New insight into the mechanisms by which chronic inflammation can contribute to the development cancer has been generated in mice by Leona Samson and colleagues, at Massachusetts Institute of Technology, Boston.
Using mice lacking the protein Aag, which is involved in the repair of DNA damaged by inflammation-associated molecules known as reactive oxygen and nitrogen species (RONS), it was shown that Aag-mediated DNA repair limits cell damage in a mouse model of episodic inflammatory bowel disease and reduces the severity of the colon cancer that develops in the mice experiencing episodic bowel inflammation. In addition, in a mouse model of Helicobacter pylori infection, Aag-deficient mice were found to exhibit more severe cell damage and the damaged area of the stomach resembled that observed prior to the development of stomach cancer. The authors therefore conclude that repair of DNA damage caused by RONS seems to be important for protection against chronic inflammation-induced cancer.
TITLE: DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice
AUTHOR CONTACT:
Leona D. Samson
Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Source: Karen Honey
Journal of Clinical Investigation
вторник, 11 октября 2011 г.
Biologist Andrew Hendry And Psychologist Karim Nader Take Two Of Six National Canadian Fellowships
Two McGill researchers have been named as 2009 recipients of E.W.R. Steacie Memorial Fellowships. Dr. Andrew P. Hendry an associate professor with McGill's Department of Biology and the Redpath Museum, and Dr. Karim Nader, an associate professor and Willam Dawson Chair in the Department of Psychology, will both receive the prestigious fellowships from the Natural Sciences and Engineering Research Council of Canada (NSERC).
It is somehow appropriate that as we mark in 2009 the 150th anniversary of the publication of Charles Darwin's The Origin of the Species and the 200th anniversary of Darwin's birth, that an evolutionary expert like Andrew Hendry is recognized. Dr. Hendry heads McGill's Hendry Lab in Eco-Evolutionary Dynamics and is a leading investigator into the interface between ecological and evolutionary processes and their influence on biodiversity. Most recently, he co-authored a much-cited study about a rarely seen pattern of "disruptive natural selection" leading to the creation of new species among the famous finches of the Galapagos Islands, originally studied by Darwin.
Karim Nader's research group specializes in the esoteric area of memory and trauma. His research has focused on victims of violence, rape and abuse who suffer from post-traumatic stress disorder (PTSD), which can force them to relive their ordeals over and over again, with debilitating consequences. Dr. Nader's experiments suggest that damaging memories can be stripped of their potency by a common blood pressure medication, propranolol. News headlines around the world about this research have often made reference to the fictional Eternal Sunshine of the Spotless Mind.
"McGill is extremely proud of these two outstanding researchers," said Vice-Principal (Research and International Relations) Denis ThГ©rien. "Their work has produced important results on crucial matters related to both the human experience and the natural world. We are grateful to NSERC for recognizing the value of this top-level research."
The NSERC Steacie Fellowships honour the memory of Dr. Edgar William Richard Steacie, an outstanding chemist and research leader who made significant contributions to the development of science in Canada during, and immediately following, World War II. Dr. Steacie believed young researchers are great national assets and should be given every opportunity to develop their own ideas. Through his philosophy, summarized below, he nurtured Canadian talent and drew many promising scientists to Canada.
Every year, NSERC awards up to six Steacie Fellowships that are held for a two-year period. Successful Fellows are relieved of teaching and administrative duties, so they can devote all their time and energy to research. The Fellowships are held at a Canadian university or affiliated research institution.
The Fellowship normally includes a contribution to the university in the amount of $90,000 per year toward the Fellow's salary. As part of the Fellowship agreement, the university is expected to fund a replacement for the Fellow's teaching and administrative responsibilities or to enhance the research environment of the Fellow's department.
Notes:
NSERC is a federal agency whose vision is to help make Canada a country of discoverers and innovators for the benefit of all Canadians. The agency supports some 26,500 university students and postdoctoral fellows in their advanced studies. NSERC promotes discovery by funding more than 11,800 university professors every year and fosters innovation by encouraging more than 1,400 Canadian companies to participate and invest in postsecondary research projects.
ABOUT McGILL UNIVERSITY
McGill University, founded in Montreal, Que., in 1821, is Canada's leading post-secondary institution. It has two campuses, 11 faculties, 10 professional schools, 300 programs of study and more than 34,000 students. McGill attracts students from more than 160 countries around the world. Almost half of McGill students claim a first language other than English - including 6,000 francophones - with more than 6,400 international students making up almost 20 per cent of the student body.
This release is available in French.
Source: Mark Shainblum
McGill University
It is somehow appropriate that as we mark in 2009 the 150th anniversary of the publication of Charles Darwin's The Origin of the Species and the 200th anniversary of Darwin's birth, that an evolutionary expert like Andrew Hendry is recognized. Dr. Hendry heads McGill's Hendry Lab in Eco-Evolutionary Dynamics and is a leading investigator into the interface between ecological and evolutionary processes and their influence on biodiversity. Most recently, he co-authored a much-cited study about a rarely seen pattern of "disruptive natural selection" leading to the creation of new species among the famous finches of the Galapagos Islands, originally studied by Darwin.
Karim Nader's research group specializes in the esoteric area of memory and trauma. His research has focused on victims of violence, rape and abuse who suffer from post-traumatic stress disorder (PTSD), which can force them to relive their ordeals over and over again, with debilitating consequences. Dr. Nader's experiments suggest that damaging memories can be stripped of their potency by a common blood pressure medication, propranolol. News headlines around the world about this research have often made reference to the fictional Eternal Sunshine of the Spotless Mind.
"McGill is extremely proud of these two outstanding researchers," said Vice-Principal (Research and International Relations) Denis ThГ©rien. "Their work has produced important results on crucial matters related to both the human experience and the natural world. We are grateful to NSERC for recognizing the value of this top-level research."
The NSERC Steacie Fellowships honour the memory of Dr. Edgar William Richard Steacie, an outstanding chemist and research leader who made significant contributions to the development of science in Canada during, and immediately following, World War II. Dr. Steacie believed young researchers are great national assets and should be given every opportunity to develop their own ideas. Through his philosophy, summarized below, he nurtured Canadian talent and drew many promising scientists to Canada.
Every year, NSERC awards up to six Steacie Fellowships that are held for a two-year period. Successful Fellows are relieved of teaching and administrative duties, so they can devote all their time and energy to research. The Fellowships are held at a Canadian university or affiliated research institution.
The Fellowship normally includes a contribution to the university in the amount of $90,000 per year toward the Fellow's salary. As part of the Fellowship agreement, the university is expected to fund a replacement for the Fellow's teaching and administrative responsibilities or to enhance the research environment of the Fellow's department.
Notes:
NSERC is a federal agency whose vision is to help make Canada a country of discoverers and innovators for the benefit of all Canadians. The agency supports some 26,500 university students and postdoctoral fellows in their advanced studies. NSERC promotes discovery by funding more than 11,800 university professors every year and fosters innovation by encouraging more than 1,400 Canadian companies to participate and invest in postsecondary research projects.
ABOUT McGILL UNIVERSITY
McGill University, founded in Montreal, Que., in 1821, is Canada's leading post-secondary institution. It has two campuses, 11 faculties, 10 professional schools, 300 programs of study and more than 34,000 students. McGill attracts students from more than 160 countries around the world. Almost half of McGill students claim a first language other than English - including 6,000 francophones - with more than 6,400 international students making up almost 20 per cent of the student body.
This release is available in French.
Source: Mark Shainblum
McGill University
суббота, 8 октября 2011 г.
Replacement Drug For Treating Cocaine Addiction Has Positive Finding In Animal Model
New research in monkeys suggests the feasibility of treating cocaine addiction with a "replacement" drug that mimics the effects of cocaine but has less potential for abuse - similar to the way nicotine and heroin addictions are treated.
Reporting at the annual meeting of the American Society of Pharmacology and Experimental Therapeutics in San Diego, Calif., scientists from Wake Forest University School of Medicine said treating monkeys with amphetamine significantly reduced their self-administration of cocaine for up to a month.
"This suggests the possibility of developing an amphetamine-like drug for treating cocaine addiction," said Paul Czoty, Ph.D., lead author and assistant professor of physiology and pharmacology. "The research also demonstrates the usefulness for conducting studies in monkeys to test potential treatments."
Czoty said the quest to develop a treatment for cocaine addiction has been ongoing for decades with little success. "While we have medications for heroin and tobacco abuse, there is no FDA-approved treatment for cocaine," he said.
With both heroin and tobacco, there are treatments to replace the addictive drug with a drug that has similar effects on the body, but with less potential for abuse.
"With this strategy in mind, clinical researchers have turned to drugs currently available, including amphetamines," said Czoty. "While it's unlikely that amphetamine itself will turn out to be the best treatment, these drugs allow us to prove the concept of using a replacement drug to combat cocaine addiction."
Amphetamines have been used in clinical studies with some success, said Czoty. His research in monkeys may help identify the best dose and schedule for administering a replacement drug - as well as evaluate potential treatment candidates and estimate potential side effects.
For the study, a monkey was taught to press levers multiple times to obtain food or a cocaine injection. With each injection, the number of required lever presses increased so that the animal had to work harder for the cocaine.
"This procedure measures the strength of the reinforcing effects of drugs," said Czoty. "Each injection requires more and more work and eventually it gets to the point where it's not worth it to the monkey because more than 1,000 presses are required."
Access to cocaine was then removed and the monkey was treated intravenously with an amphetamine 24 hours per day. When re-exposed to cocaine one week later, a dramatic decrease in responding for cocaine was observed. They tested three different doses of amphetamine and found that a moderate dose was most effective. Although the treatment also decreased lever-pressing for food - which could be predictive of side effects in humans - this effect disappeared within one week while the effect on responding for cocaine injections persisted for up to one month.
"This was a very positive finding - exactly what we had hoped to see," said Czoty. "Cocaine use was significantly reduced - by about 60 percent."
The researchers are currently repeating the study in additional animals. They hope it could eventually lead to identifying a slightly different drug that will obtain the same results as amphetamines.
Czoty said the study is significant because it and other similar studies in monkeys duplicate what has been found in small studies in humans, which suggests that the animal model can be used to test other treatments. The researchers, for example, plan to test topiramate (Topamax®), an anti-convulsant drug that is sometimes used to treat epilepsy and may be effective in treating alcoholism.
"We have found a model we can use to test new drugs and have an idea of what positive or negative effects would look like," said Czoty.
The research was funded by the National Institute on Drug Abuse and was part of Wake Forest's Center for the Neurobiological Investigation of Drug Abuse. Co-researchers were graduate student Jenn Martelle, and Professor Mike Nader, Ph.D., both in the Department of Physiology and Pharmacology.
Wake Forest University Baptist Medical Center (wfubmc/) is an academic health system comprised of North Carolina Baptist Hospital, Brenner Children's Hospital, Wake Forest University Physicians, and Wake Forest University Health Sciences, which operates the university's School of Medicine and Piedmont Triad Research Park. The system comprises 1,154 acute care, rehabilitation and long-term care beds and has been ranked as one of "America's Best Hospitals" by U.S. News & World Report since 1993. Wake Forest Baptist is ranked 32nd in the nation by America's Top Doctors for the number of its doctors considered best by their peers. The institution ranks in the top third in funding by the National Institutes of Health and fourth in the Southeast in revenues from its licensed intellectual property.
Source: Karen Richardson
Wake Forest University Baptist Medical Center
View drug information on Topamax.
Reporting at the annual meeting of the American Society of Pharmacology and Experimental Therapeutics in San Diego, Calif., scientists from Wake Forest University School of Medicine said treating monkeys with amphetamine significantly reduced their self-administration of cocaine for up to a month.
"This suggests the possibility of developing an amphetamine-like drug for treating cocaine addiction," said Paul Czoty, Ph.D., lead author and assistant professor of physiology and pharmacology. "The research also demonstrates the usefulness for conducting studies in monkeys to test potential treatments."
Czoty said the quest to develop a treatment for cocaine addiction has been ongoing for decades with little success. "While we have medications for heroin and tobacco abuse, there is no FDA-approved treatment for cocaine," he said.
With both heroin and tobacco, there are treatments to replace the addictive drug with a drug that has similar effects on the body, but with less potential for abuse.
"With this strategy in mind, clinical researchers have turned to drugs currently available, including amphetamines," said Czoty. "While it's unlikely that amphetamine itself will turn out to be the best treatment, these drugs allow us to prove the concept of using a replacement drug to combat cocaine addiction."
Amphetamines have been used in clinical studies with some success, said Czoty. His research in monkeys may help identify the best dose and schedule for administering a replacement drug - as well as evaluate potential treatment candidates and estimate potential side effects.
For the study, a monkey was taught to press levers multiple times to obtain food or a cocaine injection. With each injection, the number of required lever presses increased so that the animal had to work harder for the cocaine.
"This procedure measures the strength of the reinforcing effects of drugs," said Czoty. "Each injection requires more and more work and eventually it gets to the point where it's not worth it to the monkey because more than 1,000 presses are required."
Access to cocaine was then removed and the monkey was treated intravenously with an amphetamine 24 hours per day. When re-exposed to cocaine one week later, a dramatic decrease in responding for cocaine was observed. They tested three different doses of amphetamine and found that a moderate dose was most effective. Although the treatment also decreased lever-pressing for food - which could be predictive of side effects in humans - this effect disappeared within one week while the effect on responding for cocaine injections persisted for up to one month.
"This was a very positive finding - exactly what we had hoped to see," said Czoty. "Cocaine use was significantly reduced - by about 60 percent."
The researchers are currently repeating the study in additional animals. They hope it could eventually lead to identifying a slightly different drug that will obtain the same results as amphetamines.
Czoty said the study is significant because it and other similar studies in monkeys duplicate what has been found in small studies in humans, which suggests that the animal model can be used to test other treatments. The researchers, for example, plan to test topiramate (Topamax®), an anti-convulsant drug that is sometimes used to treat epilepsy and may be effective in treating alcoholism.
"We have found a model we can use to test new drugs and have an idea of what positive or negative effects would look like," said Czoty.
The research was funded by the National Institute on Drug Abuse and was part of Wake Forest's Center for the Neurobiological Investigation of Drug Abuse. Co-researchers were graduate student Jenn Martelle, and Professor Mike Nader, Ph.D., both in the Department of Physiology and Pharmacology.
Wake Forest University Baptist Medical Center (wfubmc/) is an academic health system comprised of North Carolina Baptist Hospital, Brenner Children's Hospital, Wake Forest University Physicians, and Wake Forest University Health Sciences, which operates the university's School of Medicine and Piedmont Triad Research Park. The system comprises 1,154 acute care, rehabilitation and long-term care beds and has been ranked as one of "America's Best Hospitals" by U.S. News & World Report since 1993. Wake Forest Baptist is ranked 32nd in the nation by America's Top Doctors for the number of its doctors considered best by their peers. The institution ranks in the top third in funding by the National Institutes of Health and fourth in the Southeast in revenues from its licensed intellectual property.
Source: Karen Richardson
Wake Forest University Baptist Medical Center
View drug information on Topamax.
среда, 5 октября 2011 г.
Long-Distance Brain Waves Focus Attention
Just as our world buzzes with distractions - from phone calls to e-mails to tweets - the neurons in our brain are bombarded with messages. Research has shown that when we pay attention, some of these neurons begin firing in unison, like a chorus rising above the noise. Now, a study in the May 29 issue of Science reveals the likely brain center that serves as the conductor of this neural chorus.
MIT neuroscientists found that neurons in the prefrontal cortex - the brain's planning center - fire in unison and send signals to the visual cortex to do the same, generating high-frequency waves that oscillate between these distant brain regions like a vibrating spring. These waves, also known as gamma oscillations, have long been associated with cognitive states like attention, learning, and consciousness.
"We are especially interested in gamma oscillations in the prefrontal cortex because it provides top-down influences over other parts of the brain," explains senior author Robert Desimone, director of the McGovern Institute for Brain Research and the Doris and Don Berkey Professor of Neuroscience at MIT. "We know that the prefrontal cortex is affected in people with schizophrenia, ADHD and many other brain disorders, and that gamma oscillations are also altered in these conditions. Our results suggest that altered neural synchrony in the prefrontal cortex could disrupt communication between this region and other areas of the brain, leading to altered perceptions, thoughts, and emotions."
To explain neural synchrony, Desimone uses the analogy of a crowded party with people talking in different rooms. If individuals raise their voices at random, the noise just becomes louder. But if a group of individuals in one room chant together in unison, the next room is more likely to hear the message. And if people in the next room chant in response, the two rooms can communicate.
In the Science study, Desimone looked for patterns of neural synchrony in two "rooms" of the brain associated with attention - the frontal eye field (FEF) within the prefrontal cortex and the V4 region of the visual cortex. Lead authors Georgia Gregoriou, a postdoctoral associate in the Desimone lab, and Stephen Gotts of the National Institute of Mental Health, trained two macaque monkeys to watch a monitor displaying multiple objects, and to concentrate on one of the objects when cued. They monitored neural activity from the FEF and the V4 regions of the brain when the monkeys were either paying attention to the object or ignoring it.
When the monkeys first paid attention to the appropriate object, neurons in both areas showed strong increases in activity. Then, as if connected by a spring, the oscillations in each area began to synchronize with one another. Desimone's team analyzed the timing of the neural activity and found that the prefrontal cortex became engaged by attention first, followed by the visual cortex - as if the prefrontal cortex commanded the visual region to snap to attention. The delay between neural activity in these areas during each wave cycle reflected the speed at which signals travel from one region to the other - indicating that the two brain regions were talking to one another.
Desimone suspects this pattern of oscillation is not just specific to attention, but could also represent a more general mechanism for communication between different parts of the brain. These findings support speculation that gamma synchrony enables far-flung regions of the brain to rapidly communicate with each other - which has important implications for understanding and treating disorders ranging from schizophrenia to impaired vision and attention. "This helps us think about how to approach studying and treating these disorders by finding ways to restore gamma rhythms in the affected brain regions."
Huihui Zhou, a research scientist in the Desimone lab, contributed to this study. The NIH/National Eye Institute and National Institute of Mental Health supported this research.
Source:
Elizabeth Thomson
McGovern Institute for Brain Research
MIT neuroscientists found that neurons in the prefrontal cortex - the brain's planning center - fire in unison and send signals to the visual cortex to do the same, generating high-frequency waves that oscillate between these distant brain regions like a vibrating spring. These waves, also known as gamma oscillations, have long been associated with cognitive states like attention, learning, and consciousness.
"We are especially interested in gamma oscillations in the prefrontal cortex because it provides top-down influences over other parts of the brain," explains senior author Robert Desimone, director of the McGovern Institute for Brain Research and the Doris and Don Berkey Professor of Neuroscience at MIT. "We know that the prefrontal cortex is affected in people with schizophrenia, ADHD and many other brain disorders, and that gamma oscillations are also altered in these conditions. Our results suggest that altered neural synchrony in the prefrontal cortex could disrupt communication between this region and other areas of the brain, leading to altered perceptions, thoughts, and emotions."
To explain neural synchrony, Desimone uses the analogy of a crowded party with people talking in different rooms. If individuals raise their voices at random, the noise just becomes louder. But if a group of individuals in one room chant together in unison, the next room is more likely to hear the message. And if people in the next room chant in response, the two rooms can communicate.
In the Science study, Desimone looked for patterns of neural synchrony in two "rooms" of the brain associated with attention - the frontal eye field (FEF) within the prefrontal cortex and the V4 region of the visual cortex. Lead authors Georgia Gregoriou, a postdoctoral associate in the Desimone lab, and Stephen Gotts of the National Institute of Mental Health, trained two macaque monkeys to watch a monitor displaying multiple objects, and to concentrate on one of the objects when cued. They monitored neural activity from the FEF and the V4 regions of the brain when the monkeys were either paying attention to the object or ignoring it.
When the monkeys first paid attention to the appropriate object, neurons in both areas showed strong increases in activity. Then, as if connected by a spring, the oscillations in each area began to synchronize with one another. Desimone's team analyzed the timing of the neural activity and found that the prefrontal cortex became engaged by attention first, followed by the visual cortex - as if the prefrontal cortex commanded the visual region to snap to attention. The delay between neural activity in these areas during each wave cycle reflected the speed at which signals travel from one region to the other - indicating that the two brain regions were talking to one another.
Desimone suspects this pattern of oscillation is not just specific to attention, but could also represent a more general mechanism for communication between different parts of the brain. These findings support speculation that gamma synchrony enables far-flung regions of the brain to rapidly communicate with each other - which has important implications for understanding and treating disorders ranging from schizophrenia to impaired vision and attention. "This helps us think about how to approach studying and treating these disorders by finding ways to restore gamma rhythms in the affected brain regions."
Huihui Zhou, a research scientist in the Desimone lab, contributed to this study. The NIH/National Eye Institute and National Institute of Mental Health supported this research.
Source:
Elizabeth Thomson
McGovern Institute for Brain Research
воскресенье, 2 октября 2011 г.
A Better Way To Battle Mosquitoes
Protecting ourselves from backyard mosquito bites may come down to leaving the vacuuming for later, a study from York University shows.
Rather than vacuuming the grass clippings out of catch basins before adding treatments to control mosquitoes, municipalities should leave the organic waste in place, the research found.
"Catch basins are a permanent source of mosquitoes on every street. By putting S-methoprene in cleaned catch basins we saw an average of 20 per cent of the mosquito larvae make it to the adult stage over the duration of the study. But that number was reduced to less than 3 per cent just by leaving the organic debris in the catch basins until the fall, when mosquito season is over," says Norman Yan, a professor in York University's Department of Biology.
Yan and former York master's student Stacey Baker co-authored a study published in the current issue of the Journal of the American Mosquito Control Association. They were surprised by the results of the research, conducted by Baker in 2005 on residential streets in the Greater Toronto Area.
"We predicted that S-methoprene would work better in the catch basins that had been cleaned. We found the opposite - that S-methoprene binds to organic material, which holds it in the catch basins longer so that mosquito larvae are exposed to it for longer," says Baker.
The research may have implications not only for our comfort levels, but for disease control, says Yan. The human West Nile Virus rate and the number of positive mosquito pools have been lower in the past two years in Ontario, but it remains a problem in some areas of the United States, and warmer temperatures and a wet season could increase the risk in Ontario. The West Nile Virus is not carried by all mosquitoes but it can lead to severe symptoms and even death.
Public health units in Ontario determine if and when they will larvicide based on their surveillance of the level of risk. S-methoprene, which is used in Canada only for control of West Nile Virus, is still being used in hundreds of thousands of catch basins in the GTA, but there has been no thought given to the cleaning schedule, according to the authors. The study demonstrates that scheduling both the application of S-methoprene and the removal of debris makes sense, they said, and it may be worthwhile to clean the catch basins every two years instead of annually.
"Accumulated Organic Debris in Catch Basins Improves the Efficacy of S-methoprene against Mosquitoes in Toronto, Ontario, Canada" appears in the Journal of the American Mosquito Control Association. York University's Knowledge Mobilization Unit, which seeks to maximize the impact of academic research on public policy and professional practice, has sent a summary of the research findings to Ontario's public health units.
Source:
Janice Walls
York University
Rather than vacuuming the grass clippings out of catch basins before adding treatments to control mosquitoes, municipalities should leave the organic waste in place, the research found.
"Catch basins are a permanent source of mosquitoes on every street. By putting S-methoprene in cleaned catch basins we saw an average of 20 per cent of the mosquito larvae make it to the adult stage over the duration of the study. But that number was reduced to less than 3 per cent just by leaving the organic debris in the catch basins until the fall, when mosquito season is over," says Norman Yan, a professor in York University's Department of Biology.
Yan and former York master's student Stacey Baker co-authored a study published in the current issue of the Journal of the American Mosquito Control Association. They were surprised by the results of the research, conducted by Baker in 2005 on residential streets in the Greater Toronto Area.
"We predicted that S-methoprene would work better in the catch basins that had been cleaned. We found the opposite - that S-methoprene binds to organic material, which holds it in the catch basins longer so that mosquito larvae are exposed to it for longer," says Baker.
The research may have implications not only for our comfort levels, but for disease control, says Yan. The human West Nile Virus rate and the number of positive mosquito pools have been lower in the past two years in Ontario, but it remains a problem in some areas of the United States, and warmer temperatures and a wet season could increase the risk in Ontario. The West Nile Virus is not carried by all mosquitoes but it can lead to severe symptoms and even death.
Public health units in Ontario determine if and when they will larvicide based on their surveillance of the level of risk. S-methoprene, which is used in Canada only for control of West Nile Virus, is still being used in hundreds of thousands of catch basins in the GTA, but there has been no thought given to the cleaning schedule, according to the authors. The study demonstrates that scheduling both the application of S-methoprene and the removal of debris makes sense, they said, and it may be worthwhile to clean the catch basins every two years instead of annually.
"Accumulated Organic Debris in Catch Basins Improves the Efficacy of S-methoprene against Mosquitoes in Toronto, Ontario, Canada" appears in the Journal of the American Mosquito Control Association. York University's Knowledge Mobilization Unit, which seeks to maximize the impact of academic research on public policy and professional practice, has sent a summary of the research findings to Ontario's public health units.
Source:
Janice Walls
York University
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