Genome Research is publishing three papers related to the genome of the gray short-tailed opossum, Monodelphis domestica, a small, nocturnal marsupial found in South America. The papers will appear online, concomitant with the publication of the opossum genome sequence in the journal Nature.
1. A fresh start for immune-related genes
Like all marsupials, opossums are born without a functioning immune system; they develop immunological tissues, organs, and the ability to produce antibodies outside the shelter of the mother's body. The genome sequence of the opossum--the first for any marsupial--provided Dr. Katherine Belov and her colleagues the opportunity to compare immune-related genes in opossums with those in humans.
Belov's team aligned 1528 human immune-related proteins to the opossum genome, and found that the genetic constituents of the human and opossum "immunomes" were quite similar. "Given the similarities, opossums would make an ideal model organism for developmental immunology studies in mammals, including humans," says Belov.
Contact:
Katherine Belov, Ph.D.
University of Sydney, Australia
Reference:
Belov, K., Sanderson, C.E., Deakin, J.E., Wong, E.S.W., Assange, D., McColl, K.A., Gout, A., de Bono, B., Speed, T.P., Trowsdale, J., and Papenfuss, A.T. 2007. Characterization of the opossum immune genome provides insights into the evolution of the mammalian immune system. Genome Res.
doi:10.1101/gr.6121807
2. New functions for ancient DNA
Transposable elements (TEs) are mobile, repetitive DNA sequences that can provide insight into evolutionary processes. "The opossum genome has been bombarded by TEs," explains Dr. Andrew Gentles, the first author on a paper that describes the first comprehensive survey of TEs in any marsupial. "TEs cover around 52% of the opossum genome, which is higher than any other amniotic lineage studied to date."
Gentles and his colleagues also discovered ancient TEs that appear to have been recruited for specific biological activities. For example, they identified MER131, a non-protein coding sequence that is highly conserved in the human, chicken, and opossum genomes but absent from zebrafish and frogs. They suggest that MER131 acquired a new function--possibly in regulating gene expression--about 300 million years ago, before the evolutionary divergence of birds and marsupials.
"MER131 is one of many non-coding DNA sequences that are conserved across an amazing variety of species, covering several hundred million years of evolution," says Gentles. "As more genomes are sequenced, we will find more pieces of these molecular jigsaw puzzles that can help us trace the influence of TEs in the development and function of modern genomes."
Contact:
Andrew J. Gentles, Ph.D.
Stanford University, Stanford, CA, USA
Reference:
Gentles, A.J. Wakefield, M.J., Kohany, O., Gu, Wanjun, Batzer, M.A., Pollock, D.D., and Jurka, J. 2007. Evolutionary dynamics of transposable elements in the short-tailed opossum Monodelphis domestica. Genome Res.
doi:10.1101/gr.6070707
3. Colonizing colossal chromosomes
The opossum autosomes (non-sex chromosomes) are unusually large--up to three times longer than the largest human chromosome. When Dr. Leo Goodstadt and his colleagues scrutinized these chromosomes, they discovered that genes situated near the edges of the chromosomes were better at removing mutations that may lead to disease.
"Where a gene lives matters," says Goodstadt. "Genes that lie in the middle of chromosomes are less likely to be shuffled before being passed on to the next generation. So evolution has been pretty good at getting rid of mutations when they're near the ends of chromosomes, but rather poor at doing so in their middles."
In addition, Goodstadt's group identified 2,733 genes that have duplicated in the opossum lineage since its divergence from humans ~170-190 million years ago. These genes contribute to unique physiological and behavioral characteristics in the opossum, including nocturnal foraging, pheromonal communication, immunity, and adaptation to dietary changes.
Contact:
Leo Goodstadt, D.Phil.
University of Oxford, UK
Reference:
Goodstadt, L., Heger, A., Webber, C., and Ponting, C.P. 2007. An analysis of the gene complement of a marsupial, Monodelphis domestica: evolution of lineage-specific genes and giant chromosomes. Genome Res.
doi:10.1101/gr.6093907
ABOUT GENOME RESEARCH:
Genome Research (genome/) is an international, monthly, peer-reviewed journal published by Cold Spring Harbor Laboratory Press. Launched in 1995, it is one of the five most highly cited primary research journals in genetics and genomics.
ABOUT COLD SPRING HARBOR LABORATORY PRESS:
Cold Spring Harbor Laboratory Press is an internationally renowned publisher of books, journals, and electronic media located on Long Island, New York. It is a division of Cold Spring Harbor Laboratory, an innovator in life science research and the education of scientists, students, and the public. For more information, visit cshlpress/.
Contact: Maria Smit
Cold Spring Harbor Laboratory
суббота, 2 июля 2011 г.
пятница, 1 июля 2011 г.
Potential New "Twist" In Breast Cancer Detection
Working with mice, scientists at Johns Hopkins publishing in the December issue of Neoplasia have shown that a protein made by a gene called "Twist" may be the proverbial red flag that can accurately distinguish stem cells that drive aggressive, metastatic breast cancer from other breast cancer cells.
Building on recent work suggesting that it is a relatively rare subgroup of stem cells in breast tumors that drives breast cancer, scientists have surmised that this subgroup of cells must have some very distinctive qualities and characteristics.
In experiments designed to identify those special qualities, the Hopkins team focused on the gene "Twist" (or TWIST1) named for its winding shape because of its known role as the producer of a so-called transcription factor, or protein that switches on or off other genes. Twist is an oncogene, one of many genes we are born with that have the potential to turn normal cells into malignant ones.
"Our experiments show that Twist is a driving force among a lot of other players in causing some forms of breast cancer," says Venu Raman, Ph.D., associate professor of radiology and oncology, Johns Hopkins University School of Medicine. "The protein it makes is one of a growing collection of markers that, when present, flag a tumor cell as a breast cancer stem cell."
Previous stem cell research identified a Twist-promoted process known as epithelial-to-mesenchymal transition, or EMT, as an important marker denoting the special subgroup of breast cancer stem cells. EMT essentially gets cells to detach from a primary tumor and metastasize. The new Hopkins research shows that the presence of Twist, along with changes in two other biomarkers CD 24 and CD44 even without EMT, announces the presence of this critical sub-group of stem cells.
"The conventional thinking is that the EMT is crucial for recognizing the breast cancer cell as stem cells, and the potential for metastasis, but our studies show that when Twist shows up in excess or even at all, it can work independently of EMT," says Farhad Vesuna, Ph.D., an instructor of radiology in the Johns Hopkins University School of Medicine. "EMT is not mandatory for identifying a breast cancer stem cell."
Working with human breast cancer cells transplanted into mice, all of which had the oncogene Twist, the scientists tagged cell surface markers CD24 and CD44 with fluorescent chemicals. Following isolation of the subpopulation containing high CD44 and low CD24 by flow cytometry, they counted 20 of these putative breast cancer stem cells. They then injected these cells into the breast tissue of 12 mice. All developed cancerous tumors.
"Normally, it takes approximately a million cells to grow a xenograft, or transplanted tumor," Vesuna says. "And here we're talking just 20 cells. There is something about these cells something different compared to the whole bulk of the tumor cell that makes them potent. That's the acid test if you can take a very small number of purified "stem cells" and grow a cancerous tumor, this means you have a pure population."
Previously, the team showed that 65 percent of aggressive breast cancers have more Twist compared to lower-grade breast cancers, and that Twist-expressing cells are more resistant to radiation.
Twist is what scientists refer to as an oncogene, one that if expressed when and where it's not supposed to be expressed, causes oncogenesis or cancer because the molecules and pathways that once regulated it and kept it in check are gone.
This finding that Twist is integral to the breast cancer stem cell phenotype has fundamental implications for early detection, treatment and prevention, Raman says. Some cancer treatments may kill ordinary tumor cells while sparing the rare cancer stem cell population, sabotaging treatment efforts. More effective cancer therapies likely require drugs that kill this important stem cell population.
This study was supported by the Maryland Stem Cell Research Foundation.
In addition to Vesuna and Raman, authors of the paper include Ala Lisok and Brian Kimble, also of Johns Hopkins.
Source: Johns Hopkins Medicine
Building on recent work suggesting that it is a relatively rare subgroup of stem cells in breast tumors that drives breast cancer, scientists have surmised that this subgroup of cells must have some very distinctive qualities and characteristics.
In experiments designed to identify those special qualities, the Hopkins team focused on the gene "Twist" (or TWIST1) named for its winding shape because of its known role as the producer of a so-called transcription factor, or protein that switches on or off other genes. Twist is an oncogene, one of many genes we are born with that have the potential to turn normal cells into malignant ones.
"Our experiments show that Twist is a driving force among a lot of other players in causing some forms of breast cancer," says Venu Raman, Ph.D., associate professor of radiology and oncology, Johns Hopkins University School of Medicine. "The protein it makes is one of a growing collection of markers that, when present, flag a tumor cell as a breast cancer stem cell."
Previous stem cell research identified a Twist-promoted process known as epithelial-to-mesenchymal transition, or EMT, as an important marker denoting the special subgroup of breast cancer stem cells. EMT essentially gets cells to detach from a primary tumor and metastasize. The new Hopkins research shows that the presence of Twist, along with changes in two other biomarkers CD 24 and CD44 even without EMT, announces the presence of this critical sub-group of stem cells.
"The conventional thinking is that the EMT is crucial for recognizing the breast cancer cell as stem cells, and the potential for metastasis, but our studies show that when Twist shows up in excess or even at all, it can work independently of EMT," says Farhad Vesuna, Ph.D., an instructor of radiology in the Johns Hopkins University School of Medicine. "EMT is not mandatory for identifying a breast cancer stem cell."
Working with human breast cancer cells transplanted into mice, all of which had the oncogene Twist, the scientists tagged cell surface markers CD24 and CD44 with fluorescent chemicals. Following isolation of the subpopulation containing high CD44 and low CD24 by flow cytometry, they counted 20 of these putative breast cancer stem cells. They then injected these cells into the breast tissue of 12 mice. All developed cancerous tumors.
"Normally, it takes approximately a million cells to grow a xenograft, or transplanted tumor," Vesuna says. "And here we're talking just 20 cells. There is something about these cells something different compared to the whole bulk of the tumor cell that makes them potent. That's the acid test if you can take a very small number of purified "stem cells" and grow a cancerous tumor, this means you have a pure population."
Previously, the team showed that 65 percent of aggressive breast cancers have more Twist compared to lower-grade breast cancers, and that Twist-expressing cells are more resistant to radiation.
Twist is what scientists refer to as an oncogene, one that if expressed when and where it's not supposed to be expressed, causes oncogenesis or cancer because the molecules and pathways that once regulated it and kept it in check are gone.
This finding that Twist is integral to the breast cancer stem cell phenotype has fundamental implications for early detection, treatment and prevention, Raman says. Some cancer treatments may kill ordinary tumor cells while sparing the rare cancer stem cell population, sabotaging treatment efforts. More effective cancer therapies likely require drugs that kill this important stem cell population.
This study was supported by the Maryland Stem Cell Research Foundation.
In addition to Vesuna and Raman, authors of the paper include Ala Lisok and Brian Kimble, also of Johns Hopkins.
Source: Johns Hopkins Medicine
четверг, 30 июня 2011 г.
News From The Journal Of Biological Chemistry
Nicotine's Effects are Receptor Specific
Following chronic nicotine exposure, nicotine receptors increase in number, an upregulation that contributes to nicotine's addictive properties. While a current belief is that this process is independent of the type of nicotine receptor, researchers have now uncovered this is not the case: the transient and prolonged changes in the nicotine levels of smokers each affect a specific receptor subtype.
The predominant subtype of nicotine receptor in the brain is known as A4B2; these receptors upregulate as nicotine levels gradually rise in the blood. Generally, they start increasing about 2-3 hours following exposure and peak after about 20 hours.
Due to lower prevalance, the upregulation, if any, of minor nicotine receptor subtypes has been difficult, but William Green and colleagues successfully developed cells expressing A6B2 nicotine receptors. They then demonstrated this class also undergoes nicotine upregulation, but at a much faster rate; A6B2 receptors increase within minutes of exposure and peak after only 2 hours.
These receptors also required about 10 times as much nicotine to stimulate as A4B2 receptors, a level that would only be reached during the brief spikes in nicotine levels occurring during smoking. These results offer new insights into the different phases of smoking, highlighting that separate receptors modulate the immediate and long term effects of nicotine.
Corresponding Authors: William Green, Department of Neurobiology, University of Chicago, Illinois
Two-protein Complex Protects Nerve Cells
Since its discovery as a protein that gets specifically released in response to brain injury, ciliary neurotrophic factor (CNTF) has prompted much interest as a potential therapeutic agent. However, numerous experiments have met with limited success, until now; a research team shows that co-administrating CNTF with its receptor promotes the growth and survival of neurons.
While the receptor for CNTF is normally tied to the surface of neurons, this tether is frequently chopped off during trauma, which led Mark Ozog, Christian Naus and colleagues to suspect that CNTF and the free-floating receptor might act in a complex.
They treated mouse neurons with CNTF, its receptor (CNTFR), or both and then exposed the cells to massive amounts of the neurotransmitter glutamate, enough to kill the neurons by over-stimulating them. CNTF or CNTFR alone did not protect the neurons, but the two complexed together could. In addition, the complex could foster increased growth of nerve cells.
Ozog, Naus and colleagues next ran a microarray analysis of the CNTF complex and found that it altered the expression of 47 genes associated with nerve growth and survival, suggesting it protects neurons through multiple direct and indirect mechanisms and thus making it a strong therapeutic candidate.
Corresponding Author: Christian Naus, Department of Cellular & Physiological Sciences, The University of British Columbia, Vancouver, CA
The American Society for Biochemistry and Molecular Biology is a nonprofit scientific and educational organization with over 11,900 members in the United States and internationally. Most members teach and conduct research at colleges and universities. Others conduct research in various government laboratories, nonprofit research institutions and industry. The Society's student members attend undergraduate or graduate institutions.
Founded in 1906, the Society is based in Bethesda, Maryland, on the campus of the Federation of American Societies for Experimental Biology. The Society's purpose is to advance the science of biochemistry and molecular biology through publication of the Journal of Biological Chemistry, the Journal of Lipid Research, and Molecular and Cellular Proteomics, organization of scientific meetings, advocacy for funding of basic research and education, support of science education at all levels, and promoting the diversity of individuals entering the scientific work force.
For more information about ASBMB, see the Society's Web site at asbmb/.
Source: Nick Zagorski
American Society for Biochemistry and Molecular Biology
Following chronic nicotine exposure, nicotine receptors increase in number, an upregulation that contributes to nicotine's addictive properties. While a current belief is that this process is independent of the type of nicotine receptor, researchers have now uncovered this is not the case: the transient and prolonged changes in the nicotine levels of smokers each affect a specific receptor subtype.
The predominant subtype of nicotine receptor in the brain is known as A4B2; these receptors upregulate as nicotine levels gradually rise in the blood. Generally, they start increasing about 2-3 hours following exposure and peak after about 20 hours.
Due to lower prevalance, the upregulation, if any, of minor nicotine receptor subtypes has been difficult, but William Green and colleagues successfully developed cells expressing A6B2 nicotine receptors. They then demonstrated this class also undergoes nicotine upregulation, but at a much faster rate; A6B2 receptors increase within minutes of exposure and peak after only 2 hours.
These receptors also required about 10 times as much nicotine to stimulate as A4B2 receptors, a level that would only be reached during the brief spikes in nicotine levels occurring during smoking. These results offer new insights into the different phases of smoking, highlighting that separate receptors modulate the immediate and long term effects of nicotine.
Corresponding Authors: William Green, Department of Neurobiology, University of Chicago, Illinois
Two-protein Complex Protects Nerve Cells
Since its discovery as a protein that gets specifically released in response to brain injury, ciliary neurotrophic factor (CNTF) has prompted much interest as a potential therapeutic agent. However, numerous experiments have met with limited success, until now; a research team shows that co-administrating CNTF with its receptor promotes the growth and survival of neurons.
While the receptor for CNTF is normally tied to the surface of neurons, this tether is frequently chopped off during trauma, which led Mark Ozog, Christian Naus and colleagues to suspect that CNTF and the free-floating receptor might act in a complex.
They treated mouse neurons with CNTF, its receptor (CNTFR), or both and then exposed the cells to massive amounts of the neurotransmitter glutamate, enough to kill the neurons by over-stimulating them. CNTF or CNTFR alone did not protect the neurons, but the two complexed together could. In addition, the complex could foster increased growth of nerve cells.
Ozog, Naus and colleagues next ran a microarray analysis of the CNTF complex and found that it altered the expression of 47 genes associated with nerve growth and survival, suggesting it protects neurons through multiple direct and indirect mechanisms and thus making it a strong therapeutic candidate.
Corresponding Author: Christian Naus, Department of Cellular & Physiological Sciences, The University of British Columbia, Vancouver, CA
The American Society for Biochemistry and Molecular Biology is a nonprofit scientific and educational organization with over 11,900 members in the United States and internationally. Most members teach and conduct research at colleges and universities. Others conduct research in various government laboratories, nonprofit research institutions and industry. The Society's student members attend undergraduate or graduate institutions.
Founded in 1906, the Society is based in Bethesda, Maryland, on the campus of the Federation of American Societies for Experimental Biology. The Society's purpose is to advance the science of biochemistry and molecular biology through publication of the Journal of Biological Chemistry, the Journal of Lipid Research, and Molecular and Cellular Proteomics, organization of scientific meetings, advocacy for funding of basic research and education, support of science education at all levels, and promoting the diversity of individuals entering the scientific work force.
For more information about ASBMB, see the Society's Web site at asbmb/.
Source: Nick Zagorski
American Society for Biochemistry and Molecular Biology
среда, 29 июня 2011 г.
Key Developmental Pathway Activates Lung Stem Cells
Researchers from the University of Pennsylvania School of Medicine found that the activation of a molecular pathway important in stem cell and developmental biology leads to an increase in lung stem cells. Harnessing this knowledge could help develop therapies for lung-tissue repair after injury or disease. The investigators published their findings online last week in advance of print publication in Nature Genetics.
"The current findings show that increased activity of the Wnt pathway leads to expansion of a type of lung stem cell called bronchioalveolar stem cells," says senior author Edward Morrisey, Ph.D., Associate Professor of Medicine and Cell and Developmental Biology.
"This information will give us a more extensive basic understanding of Wnt signaling in adult tissue repair in the lung and other tissues and also start to help us determine whether pharmacological activation or inhibition of this pathway can be utilized for treatments," explains Morrisey, who is also the Scientific Director of the Penn Institute for Regenerative Medicine.
Activation of the Wnt signaling pathway leads to expansion, or increase in number, of bronchioalveolar stem cells in the lung. A protein called GATA6 inhibits Wnt signaling by directly regulating the expression of another protein in the Wnt pathway called frizzled 2 (Fzd2).
Wnt signaling is a major pathway in stem cell biology. The finding that GATA6 negatively regulates Wnt signaling and that GATA6 has been shown to play important roles in embryonic stem cell replication and differentiation suggests that these two pathways are linked not only in lung stem cells but in other tissues where they play important roles including the heart, gut, and pancreas.
"We were surprised by the robust activation of Wnt signaling after loss of GATA6 expression in the lung," says Morrisey. "Such a robust activation is rarely observed."
Wnt signaling can be pharmacologically modulated with compounds, including lithium, already approved by the FDA. Use of such compounds, both known and newly identified through ongoing screens, could allow for forced expansion and differentiation of key stem cell populations in the lung and other tissues for adult tissue repair after injury or disease.
Future directions of the Morrisey lab include not only a more extensive basic understanding of Wnt signaling in adult-tissue repair in the lung and other tissues, but also starting to determine whether pharmacological activation or inhibition of this pathway can really be utilized for treatments.
Penn co-authors are Yuzhen Zhang, Ashley M. Goss, Ethan David Cohen, Rachel Kadzik, John J. Lepore, Karthika Muthukumaraswamy. Jifu Yang, and Michael Parmacek. This work was funded by the National Institutes of Health.
PENN Medicine is a $3.5 billion enterprise dedicated to the related missions of medical education, biomedical research, and excellence in patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System.
Penn's School of Medicine is currently ranked #4 in the nation in U.S.News & World Report's survey of top research-oriented medical schools; and, according to most recent data from the National Institutes of Health, received over $379 million in NIH research funds in the 2006 fiscal year. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.
The University of Pennsylvania Health System includes three hospitals - its flagship hospital, the Hospital of the University of Pennsylvania, rated one of the nation's "Honor Roll" hospitals by U.S.News & World Report; Pennsylvania Hospital, the nation's first hospital; and Penn Presbyterian Medical Center - a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice.
Source: Karen Kreeger
University of Pennsylvania School of Medicine
"The current findings show that increased activity of the Wnt pathway leads to expansion of a type of lung stem cell called bronchioalveolar stem cells," says senior author Edward Morrisey, Ph.D., Associate Professor of Medicine and Cell and Developmental Biology.
"This information will give us a more extensive basic understanding of Wnt signaling in adult tissue repair in the lung and other tissues and also start to help us determine whether pharmacological activation or inhibition of this pathway can be utilized for treatments," explains Morrisey, who is also the Scientific Director of the Penn Institute for Regenerative Medicine.
Activation of the Wnt signaling pathway leads to expansion, or increase in number, of bronchioalveolar stem cells in the lung. A protein called GATA6 inhibits Wnt signaling by directly regulating the expression of another protein in the Wnt pathway called frizzled 2 (Fzd2).
Wnt signaling is a major pathway in stem cell biology. The finding that GATA6 negatively regulates Wnt signaling and that GATA6 has been shown to play important roles in embryonic stem cell replication and differentiation suggests that these two pathways are linked not only in lung stem cells but in other tissues where they play important roles including the heart, gut, and pancreas.
"We were surprised by the robust activation of Wnt signaling after loss of GATA6 expression in the lung," says Morrisey. "Such a robust activation is rarely observed."
Wnt signaling can be pharmacologically modulated with compounds, including lithium, already approved by the FDA. Use of such compounds, both known and newly identified through ongoing screens, could allow for forced expansion and differentiation of key stem cell populations in the lung and other tissues for adult tissue repair after injury or disease.
Future directions of the Morrisey lab include not only a more extensive basic understanding of Wnt signaling in adult-tissue repair in the lung and other tissues, but also starting to determine whether pharmacological activation or inhibition of this pathway can really be utilized for treatments.
Penn co-authors are Yuzhen Zhang, Ashley M. Goss, Ethan David Cohen, Rachel Kadzik, John J. Lepore, Karthika Muthukumaraswamy. Jifu Yang, and Michael Parmacek. This work was funded by the National Institutes of Health.
PENN Medicine is a $3.5 billion enterprise dedicated to the related missions of medical education, biomedical research, and excellence in patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System.
Penn's School of Medicine is currently ranked #4 in the nation in U.S.News & World Report's survey of top research-oriented medical schools; and, according to most recent data from the National Institutes of Health, received over $379 million in NIH research funds in the 2006 fiscal year. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.
The University of Pennsylvania Health System includes three hospitals - its flagship hospital, the Hospital of the University of Pennsylvania, rated one of the nation's "Honor Roll" hospitals by U.S.News & World Report; Pennsylvania Hospital, the nation's first hospital; and Penn Presbyterian Medical Center - a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice.
Source: Karen Kreeger
University of Pennsylvania School of Medicine
вторник, 28 июня 2011 г.
Tree Of Life Award Received By Jefferson Doctor
Edith P. Mitchell, M.D., clinical professor, Department of Medical Oncology at Jefferson Medical College of Thomas Jefferson University and associate director of Diversity Programs for the Kimmel Cancer Center at Jefferson, was recently honored with a 'Tree of Life' award from The Wellness of You, a local nonprofit health education and resource organization.
The Tree of Life award recognizes health professionals who are committed to making a difference in community health. Recipients of this coveted award have made extraordinary contributions to health management in both the local and global community. Recipients include educators, physicians, authors, community activists, and masters of various disciplines such as martial arts and feng shui.
"I am honored to accept this award from The Wellness of You organization whose purpose is to help individuals in medically underserved areas realize that simple changes in lifestyle can have a dramatic impact on one's health," said Dr. Mitchell. "Their mission matches my own in regards to the importance of community outreach especially to those individuals who may not have the means to seek out more conventional medical advice."
Dr. Mitchell received a bachelor of science in Biochemistry "with distinction" from Tennessee State University and her medical degree from the Medical College of Virginia in Richmond. In 1973, while attending medical school, Dr. Mitchell entered the Air Force and received a commission through the Health Professions Scholarship Program. She entered active duty after completion of her internship and residency in Internal Medicine at Meharry Medical College and a fellowship in Medical Oncology at Georgetown University.
Dr. Mitchell's research in pancreatic cancer and other GI malignancies involves new drug evaluation and chemotherapy, development of new therapeutic regimens, chemoradiation strategies for combined modality therapy, patient selection criteria and supportive care for patients with gastrointestinal cancer. She travels nationally and internationally teaching and lecturing on the treatment of gastrointestinal malignancies.
Dr. Mitchell has authored and co-authored more than 100 articles, book chapters, and abstracts on cancer treatment, prevention, and cancer control. As a distinguished researcher, she has received 21 Cancer Research and Principal Investigator Awards, and serves on the National Cancer Institute Review Panel and the Cancer Investigations Review Committee.
In addition to her medical achievements, Dr. Mitchell is a retired Brigadier General having served as the Air National Guard Assistant to the Command Surgeon for US Transportation command and headquarters Air Mobility Command (AMC) based at the Scott Air Force Base in Illinois. In this capacity she served as the senior medical Air National Guard advisor to the command surgeon and was the medical liaison between the active Air Force and the Air National Guard. Her responsibilities in this role included ensuring maximum wartime readiness and combat support capability of the worldwide patient movement and aero medical evacuation system, the Global Patient Movement Requirements Center and AMC's 52 Air National Guard medical squadrons.
General Mitchell has been awarded over 15 military service medals and ribbons including the Legion of Merit, Meritorious Service Medal, Air Force Achievement and Commendation Medals, National Defense Service Medal, and Humanitarian Service Medal. Dr. Mitchell was selected for inclusion in America's Top Oncologists. Dr. Mitchell is a Fellow of the American College of Physicians and a member of the American Medical Association, the National Medical Association, Aerospace Medical Association, Association of Military Surgeons, and the Medical Society of Eastern Pennsylvania. She is also a member of the Eastern Cooperative Oncology Group, Radiation Therapy Oncology Group, National Surgical Adjuvant Breast and Bowel Project, and the Philadelphia Society of Medicine.
Source: Ed Federico
Thomas Jefferson University
The Tree of Life award recognizes health professionals who are committed to making a difference in community health. Recipients of this coveted award have made extraordinary contributions to health management in both the local and global community. Recipients include educators, physicians, authors, community activists, and masters of various disciplines such as martial arts and feng shui.
"I am honored to accept this award from The Wellness of You organization whose purpose is to help individuals in medically underserved areas realize that simple changes in lifestyle can have a dramatic impact on one's health," said Dr. Mitchell. "Their mission matches my own in regards to the importance of community outreach especially to those individuals who may not have the means to seek out more conventional medical advice."
Dr. Mitchell received a bachelor of science in Biochemistry "with distinction" from Tennessee State University and her medical degree from the Medical College of Virginia in Richmond. In 1973, while attending medical school, Dr. Mitchell entered the Air Force and received a commission through the Health Professions Scholarship Program. She entered active duty after completion of her internship and residency in Internal Medicine at Meharry Medical College and a fellowship in Medical Oncology at Georgetown University.
Dr. Mitchell's research in pancreatic cancer and other GI malignancies involves new drug evaluation and chemotherapy, development of new therapeutic regimens, chemoradiation strategies for combined modality therapy, patient selection criteria and supportive care for patients with gastrointestinal cancer. She travels nationally and internationally teaching and lecturing on the treatment of gastrointestinal malignancies.
Dr. Mitchell has authored and co-authored more than 100 articles, book chapters, and abstracts on cancer treatment, prevention, and cancer control. As a distinguished researcher, she has received 21 Cancer Research and Principal Investigator Awards, and serves on the National Cancer Institute Review Panel and the Cancer Investigations Review Committee.
In addition to her medical achievements, Dr. Mitchell is a retired Brigadier General having served as the Air National Guard Assistant to the Command Surgeon for US Transportation command and headquarters Air Mobility Command (AMC) based at the Scott Air Force Base in Illinois. In this capacity she served as the senior medical Air National Guard advisor to the command surgeon and was the medical liaison between the active Air Force and the Air National Guard. Her responsibilities in this role included ensuring maximum wartime readiness and combat support capability of the worldwide patient movement and aero medical evacuation system, the Global Patient Movement Requirements Center and AMC's 52 Air National Guard medical squadrons.
General Mitchell has been awarded over 15 military service medals and ribbons including the Legion of Merit, Meritorious Service Medal, Air Force Achievement and Commendation Medals, National Defense Service Medal, and Humanitarian Service Medal. Dr. Mitchell was selected for inclusion in America's Top Oncologists. Dr. Mitchell is a Fellow of the American College of Physicians and a member of the American Medical Association, the National Medical Association, Aerospace Medical Association, Association of Military Surgeons, and the Medical Society of Eastern Pennsylvania. She is also a member of the Eastern Cooperative Oncology Group, Radiation Therapy Oncology Group, National Surgical Adjuvant Breast and Bowel Project, and the Philadelphia Society of Medicine.
Source: Ed Federico
Thomas Jefferson University
понедельник, 27 июня 2011 г.
Turning Carbon Nanotubes Into Cellular Probes With Surface Enhanced Raman Spectroscopy
Carbon nanotubes (CNTs) have shown great potential for use as cellular probes. As "nanopipes" they can be used to transport liquids to or from cells and inject solutions or drugs directly into individual cells and individual organelles within the cells. In addition, because of the small diameters of the carbon nanotubes induce little damage to cells upon penetration. By making these probes able to sense within the cells, information about chemical interactions within the cells could be found. Surface-enhanced Raman Spectroscopy (SERS) has this capability.
A journal article just released on the nanotechnology website AZoNano examines making carbon nanotubes SERS active by functionalization with SERS active nanoparticles. This creates the possibility of extremely sensitive study and identification of components of cells. In addition, the nanotubes can be applied to a nanofluidic device where they can serve as an interconnection between a fluid reservoir and the cell, to both deliver and extract fluids. The effects of the fluids on the cells could be studied in situ.
The paper by Alia Sabur from Drexel University has been released as part of the open access journal, AZoJono*. The research found that carbon nanotubes and nanopipes can be used as SERS probes by two different methods that achieved identical results. Combining these SERS active nanotubes with already existing nano-probing techniques could enable the study of cells with single-molecule sensitivity.
Click here to view the article in full.
*AZojono publishes high quality articles and papers on all aspects of nanomaterials and related technologies. All the contributions are reviewed by a world class panel of editors who are experts in a wide spectrum of materials science.
AZojono is based on the patented OARS (Open Access Rewards System) publishing protocol. The OARS protocol represents a unique development in the field of scientific publishing -- the distribution of online scientific journal revenue between the authors, peer reviewers and site operators with no publication charges, just totally free to access high quality, peer reviewed materials science. [See azonano/nanotechnology%20journal.asp and azonano/journal_of_nanotechnology.asp]
Source: Dr. Ian Birkby
AZoNetwork
A journal article just released on the nanotechnology website AZoNano examines making carbon nanotubes SERS active by functionalization with SERS active nanoparticles. This creates the possibility of extremely sensitive study and identification of components of cells. In addition, the nanotubes can be applied to a nanofluidic device where they can serve as an interconnection between a fluid reservoir and the cell, to both deliver and extract fluids. The effects of the fluids on the cells could be studied in situ.
The paper by Alia Sabur from Drexel University has been released as part of the open access journal, AZoJono*. The research found that carbon nanotubes and nanopipes can be used as SERS probes by two different methods that achieved identical results. Combining these SERS active nanotubes with already existing nano-probing techniques could enable the study of cells with single-molecule sensitivity.
Click here to view the article in full.
*AZojono publishes high quality articles and papers on all aspects of nanomaterials and related technologies. All the contributions are reviewed by a world class panel of editors who are experts in a wide spectrum of materials science.
AZojono is based on the patented OARS (Open Access Rewards System) publishing protocol. The OARS protocol represents a unique development in the field of scientific publishing -- the distribution of online scientific journal revenue between the authors, peer reviewers and site operators with no publication charges, just totally free to access high quality, peer reviewed materials science. [See azonano/nanotechnology%20journal.asp and azonano/journal_of_nanotechnology.asp]
Source: Dr. Ian Birkby
AZoNetwork
воскресенье, 26 июня 2011 г.
New Approach For Treatment Of The AIDS Virus?
The AIDS-causing HIV specifically counteracts the mechanisms of human cells that protect these against viral infections - a special viral protein marks protective cellular proteins for their rapid destruction and thus diminishes the cell's supply. A team of researchers in Heidelberg under supervision of virologist Dr. Oliver Keppler demonstrated this mechanism for the first time in cell cultures, thus discovering a target for a novel treatment strategy.
Another important discovery of the Heidelberg virologists - this strategy of the human HIV is not effective in a rat model for AIDS. The protective protein in rats is immune to HIV counteraction. Consequently, HIV cannot propagate itself as easily in the animal model as in humans - one limitation of the current rat model. However, this new knowledge may enable an improvement of the small animal model developed by the Heidelberg researchers. The study was published in the journal Cell Host & Microbe in March 2009.
Newly formed viruses are retained at the cell surface
In addition to the immune system, the body can activate other protective mechanisms to fight or stop virus infections - the infected cells themselves dispose of several proteins that inhibit various steps of virus reproduction. In the presence of the protective protein CD317, newly formed viruses are tethered to the cell surface when they are in the process of leaving the cell and this prevents them from infecting other cells of the body. HIV overcomes this restriction by its protein Vpu by specifically counteracting this protective mechanism, which, interestingly, is effective against many types of viruses.
Dr. Keppler's team of virologists from the Department of Virology at the Hygiene Institute of Heidelberg University Hospital (Medical Director: Professor Dr. Hans-Georg Kräusslich) studied how Vpu disrupts protection by CD317. They determined that in human cells in which Vpu was formed after infection with HIV, the pool of CD317 was reduced to about one quarter of the original amount. "When Vpu is present, CD317 is rapidly degraded by a cellular system. Vpu presumably binds to the CD317 and marks it for rapid destruction," explains Dr. Keppler.
The less CD317 is present in the cell, the more viruses can escape interception. "Disrupting this interaction between Vpu and CD317 to increase the cells' own protective mechanisms could thus be a promising strategy for therapy," says Dr. Keppler.
Rats and mice also have this protective protein; it has the same function and is able to block HIV. However, there is a significant difference - the Heidelberg virologists discovered that in rat cells, Vpu has no effect on CD317. "HIV is adapted to humans and the disruptive mechanism of Vpu does not affect protection against infection in animals," said Dr. Christine Goffinet, first author of the study.
Rat model now to be improved
This detail is important when one wants to imitate and study HIV infection in rats in an animal model - the infection in rats does not follow the same course as in humans, since fewer viruses are released due to the intact protective mechanisms. Based on the new research results, the Heidelberg scientists now hope to improve the current transgenic rat model of HIV infection. The goal is to suppress CD317 in rats through genetic engineering and thus achieve a degree of HIV infection that is more similar to that in humans.
As early as 2007, the researchers in Heidelberg first succeeded in making rats susceptible to HIV infection by specifically modifying their genetic material. They successfully tested drugs against HIV infection in humans in these transgenic rats. Using this small animal model, it is possible to test the efficacy of medications against the AIDS virus HIV rapidly and on a larger scale prior to clinical studies in humans and thus to accelerate the further development of virostatics.
Notes:
References:
Christine Goffinet, Hans-Georg Kräusslich, and Oliver T. Keppler: HIV-1 Antagonism of CD317 Is Species Specific and Involves Vpu-Mediated Proteasomal Degradation of the Restriction Factor. Cell Host & Microbe 5, 285-297, March 19, 2009. DOI 10.1016/j.chom.2009.01.009
Heidelberg University Hospital and Medical Faculty:
Internationally recognized patient care, research, and teaching
Heidelberg University Hospital is one of the largest and most prestigious medical centers in Germany. The Medical Faculty of Heidelberg University belongs to the internationally most renowned biomedical research institutions in Europe. Both institutions have the common goal of developing new therapies and implementing them rapidly for patients. With about 7,000 employees, training and qualification is an important issue. Every year, around 500,000 patients are treated on an inpatient or outpatient basis in more than 40 clinics and departments with 1,600 beds. Currently, about 3,100 future physicians are studying in Heidelberg; the reform Heidelberg Curriculum Medicinale (HeiCuMed) is one of the top medical training programs in Germany.
Source:
PD Dr. med. Oliver T. Keppler
University Hospital Heidelberg
Another important discovery of the Heidelberg virologists - this strategy of the human HIV is not effective in a rat model for AIDS. The protective protein in rats is immune to HIV counteraction. Consequently, HIV cannot propagate itself as easily in the animal model as in humans - one limitation of the current rat model. However, this new knowledge may enable an improvement of the small animal model developed by the Heidelberg researchers. The study was published in the journal Cell Host & Microbe in March 2009.
Newly formed viruses are retained at the cell surface
In addition to the immune system, the body can activate other protective mechanisms to fight or stop virus infections - the infected cells themselves dispose of several proteins that inhibit various steps of virus reproduction. In the presence of the protective protein CD317, newly formed viruses are tethered to the cell surface when they are in the process of leaving the cell and this prevents them from infecting other cells of the body. HIV overcomes this restriction by its protein Vpu by specifically counteracting this protective mechanism, which, interestingly, is effective against many types of viruses.
Dr. Keppler's team of virologists from the Department of Virology at the Hygiene Institute of Heidelberg University Hospital (Medical Director: Professor Dr. Hans-Georg Kräusslich) studied how Vpu disrupts protection by CD317. They determined that in human cells in which Vpu was formed after infection with HIV, the pool of CD317 was reduced to about one quarter of the original amount. "When Vpu is present, CD317 is rapidly degraded by a cellular system. Vpu presumably binds to the CD317 and marks it for rapid destruction," explains Dr. Keppler.
The less CD317 is present in the cell, the more viruses can escape interception. "Disrupting this interaction between Vpu and CD317 to increase the cells' own protective mechanisms could thus be a promising strategy for therapy," says Dr. Keppler.
Rats and mice also have this protective protein; it has the same function and is able to block HIV. However, there is a significant difference - the Heidelberg virologists discovered that in rat cells, Vpu has no effect on CD317. "HIV is adapted to humans and the disruptive mechanism of Vpu does not affect protection against infection in animals," said Dr. Christine Goffinet, first author of the study.
Rat model now to be improved
This detail is important when one wants to imitate and study HIV infection in rats in an animal model - the infection in rats does not follow the same course as in humans, since fewer viruses are released due to the intact protective mechanisms. Based on the new research results, the Heidelberg scientists now hope to improve the current transgenic rat model of HIV infection. The goal is to suppress CD317 in rats through genetic engineering and thus achieve a degree of HIV infection that is more similar to that in humans.
As early as 2007, the researchers in Heidelberg first succeeded in making rats susceptible to HIV infection by specifically modifying their genetic material. They successfully tested drugs against HIV infection in humans in these transgenic rats. Using this small animal model, it is possible to test the efficacy of medications against the AIDS virus HIV rapidly and on a larger scale prior to clinical studies in humans and thus to accelerate the further development of virostatics.
Notes:
References:
Christine Goffinet, Hans-Georg Kräusslich, and Oliver T. Keppler: HIV-1 Antagonism of CD317 Is Species Specific and Involves Vpu-Mediated Proteasomal Degradation of the Restriction Factor. Cell Host & Microbe 5, 285-297, March 19, 2009. DOI 10.1016/j.chom.2009.01.009
Heidelberg University Hospital and Medical Faculty:
Internationally recognized patient care, research, and teaching
Heidelberg University Hospital is one of the largest and most prestigious medical centers in Germany. The Medical Faculty of Heidelberg University belongs to the internationally most renowned biomedical research institutions in Europe. Both institutions have the common goal of developing new therapies and implementing them rapidly for patients. With about 7,000 employees, training and qualification is an important issue. Every year, around 500,000 patients are treated on an inpatient or outpatient basis in more than 40 clinics and departments with 1,600 beds. Currently, about 3,100 future physicians are studying in Heidelberg; the reform Heidelberg Curriculum Medicinale (HeiCuMed) is one of the top medical training programs in Germany.
Source:
PD Dr. med. Oliver T. Keppler
University Hospital Heidelberg
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