Scientists studying biology and geography may seem worlds apart, but together they have answered a question that has defied explanation about the spread of the HIV-1 epidemic in Africa.
Writing in the September issue of AIDS, a research team led by scientists at the University of Florida explained why two subtypes of HIV-1 - the virus that causes acquired immunodeficiency syndrome, or AIDS - held steady at relatively low levels for more than 50 years in west central Africa before erupting as an epidemic in east Africa in the 1970s.
Essentially, the explanation for the HIV explosion - obscured until now - involves the relative ease with which people can travel from city to city in east Africa as opposed to the difficulties faced by people living in the population centers of the Democratic Republic of Congo, the point where HIV emerged from west central Africa in its spread to the east.
Later, as the epidemic raged in the east, cities in the Democratic Republic of Congo - a vast country almost as big as all of Western Europe - remained disconnected and isolated, explaining why the virus affected only about 5 percent of the country's population, a level that has not changed much since the 1950s.
"We live in a world that is more interconnected every day, and we have all seen how pathogens such as HIV or the swine flu virus can arise in a remote area of the planet and quickly become a global threat," said Marco Salemi, an assistant professor of pathology, immunology, and laboratory medicine at the UF College of Medicine and senior author of the study. "Understanding the factors that can lead to a full-scale pandemic is essential to protect our species from emerging dangers."
Investigators used databases, including GenBank from the National Center for Biotechnology Information, as well as actual DNA samples, including samples recently collected in Uganda - the vicinity where HIV entered east Africa - to follow the virus' molecular footprints since its emergence in the 1920s.
"HIV mutates rapidly," said Rebecca Gray, a postdoctoral associate in the department of pathology, immunology and laboratory medicine. "This is a successful strategy for the virus, because it evolves quickly and develops drug resistance. But we can use these changes in the genome to follow it over time and develop a history of its progress."
Researchers wanted to know why, the virus smoldered during the 1950s and `60s, before spreading like wildfire through east Africa in the 1970s.
A fateful piece of the puzzle came in the form of geographic information system data, which uses satellite imagery and painstakingly takes into account the availability and navigability of roads between population centers, transportation modes, elevation, climate, terrain and other factors that influence travel.
"We were able to use geographic data to interpret the genetic data," said Andrew J. Tatem, Ph.D., an assistant professor of geography in the College of Liberal Arts and Sciences and a member of UF's Emerging Pathogens Institute. "Genetic data showed once HIV moved out of the Democratic Republic of Congo, it expanded fast and moved rapidly across Uganda, Kenya and Tanzania, all while staying at low levels in the DRC. What was happening was the virus was circulating at stable levels in the urban centers of the DRC, but these centers were isolated. Once it hit east Africa, connectivity between population centers combined with better quality transportation networks, and higher rates of human movement caused HIV to spread exponentially."
HIV was prevalent in about 15 percent of the population in Kenya in 1997, although it has since dropped to about 7 percent, according to the Kaiser Family Foundation. As of 2007, an estimated 22 million people were living with HIV/AIDS in sub-Saharan Africa. About 1.1 million Americans have HIV or AIDS, and an estimated 5.1 million people in India are HIV-positive. In Eastern Europe, HIV infections more than doubled from 420,000 in 1998 to 1 million in 2001.
"If we can predict the specific routes of an epidemic, we can find the geographic regions more at risk and target these areas with medical intervention and strategies for prevention," Salemi said. "In terms of health-care applications, coupling genetic analysis with geographic information systems can give us a powerful tool to understand the spread of pathogens and contain emerging epidemics."
Working with Maureen M. Goodenow, Ph.D., the Stephany W. Holloway university chair for AIDS research at the UF College of Medicine, UF researchers collaborated with an array of scientists hailing from the National Institute of Allergy and Infectious Diseases, the Rakai Health Sciences Program and Makerere University of Uganda, and the Johns Hopkins University. They refer to the combination of techniques that led to the discovery as "landscape phylodynamics."
"It is the first study that has given us a clear picture of epidemic history of HIV in east Africa, including the geographic routes and the time scale that it occurred," said Oliver Pybus, Ph.D., a researcher in the department of zoology at Oxford University who did not participate in the study. "Genetic analysis of the HIV genome provides the family tree of the virus, combined with spatial analysis of high-resolution data of land use, topology and other factors. There is a huge potential in doing that kind of analysis, but it requires a rare combination of specialists in different fields to come together."
Source:
John Pastor
University of Florida
воскресенье, 13 ноября 2011 г.
четверг, 10 ноября 2011 г.
New Potential To Treat Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) is defined by emphysema and/or chronic bronchitis. It destroys the normal architecture of the lung and inhibits the mechanical aspects of breathing, which prevents necessary gas exchange. Patients suffer from coughing fits, wheezing, and increased incidence of lung infections. These symptoms are associated with changes in the architecture of the lung. The air sacs, which usually inflate with air during breathing as they loose their elasticity, becoming rigid and unable to inflate. The lung becomes inflamed and increases its mucus production, which further inhibits gas exchange, and prevents the patient's ability to be physically active.
Although COPD is a leading cause of morbidity and mortality worldwide, there is currently no cure for the disease. Providing patients with concentrated oxygen therapy and instruction on breathing techniques increases survival rates.
In a new study published in Disease Models & Mechanisms (DMM), dmm.biologists, collaborative findings by European researchers demonstrate that an antioxidant protein, sestrin, triggers molecular pathways that induce some of the critical lung changes associated with COPD. By genetically inactivating this protein, they were able to improve the elastic features of the lung in a mouse model of emphysema. These authors believe that by inhibiting the antioxidant sestrin protein, they prevent the accelerated degradation of elastic fibers within the lung. This suggests that patients with COPD could benefit from treatment with drugs that block sestrin function.
Although sestrin is an antioxidant protein, the authors found that this characteristic of the protein is not likely to influence its effects on COPD progression in the lung. The negative effects of sestrin on lung elasticity results from its suppression of genes whose products maintain elastin. Elastin makes the lung flexible so that it can expand and contract. Without elastin fibers, the lung becomes rigid and increasingly unable to provide for gas exchange.
The report, titled 'Inactivation of sestrin 2 induces TGF-beta signalling and partially rescues pulmonary emphysema in a mouse model of COPD' was Frank Wempe, Silke De-Zolt, Thorsten Bangsow and Harald von Melchner at the University of Frankfurt Medical School, Nirmal Parajuli, Rio Dumitrascu and Norbert Weismann at the University of Giessen Lung Center, Anja Sterner-Kock at the Institute of Veterinary Pathology in Germany and Katri Koli and Jorma Keski-Oja at the University of Helsinki in Finland. The study will be published in the March/April issue of 2010 (Vol 3/Issue 3-4) of the research journal, Disease Models & Mechanisms (DMM), published by The Company of Biologists, a non-profit based in Cambridge, UK.
Source:
Kristy Kain
The Company of Biologists
Although COPD is a leading cause of morbidity and mortality worldwide, there is currently no cure for the disease. Providing patients with concentrated oxygen therapy and instruction on breathing techniques increases survival rates.
In a new study published in Disease Models & Mechanisms (DMM), dmm.biologists, collaborative findings by European researchers demonstrate that an antioxidant protein, sestrin, triggers molecular pathways that induce some of the critical lung changes associated with COPD. By genetically inactivating this protein, they were able to improve the elastic features of the lung in a mouse model of emphysema. These authors believe that by inhibiting the antioxidant sestrin protein, they prevent the accelerated degradation of elastic fibers within the lung. This suggests that patients with COPD could benefit from treatment with drugs that block sestrin function.
Although sestrin is an antioxidant protein, the authors found that this characteristic of the protein is not likely to influence its effects on COPD progression in the lung. The negative effects of sestrin on lung elasticity results from its suppression of genes whose products maintain elastin. Elastin makes the lung flexible so that it can expand and contract. Without elastin fibers, the lung becomes rigid and increasingly unable to provide for gas exchange.
The report, titled 'Inactivation of sestrin 2 induces TGF-beta signalling and partially rescues pulmonary emphysema in a mouse model of COPD' was Frank Wempe, Silke De-Zolt, Thorsten Bangsow and Harald von Melchner at the University of Frankfurt Medical School, Nirmal Parajuli, Rio Dumitrascu and Norbert Weismann at the University of Giessen Lung Center, Anja Sterner-Kock at the Institute of Veterinary Pathology in Germany and Katri Koli and Jorma Keski-Oja at the University of Helsinki in Finland. The study will be published in the March/April issue of 2010 (Vol 3/Issue 3-4) of the research journal, Disease Models & Mechanisms (DMM), published by The Company of Biologists, a non-profit based in Cambridge, UK.
Source:
Kristy Kain
The Company of Biologists
понедельник, 7 ноября 2011 г.
Transfer Of Biological Electron Captured In Real Time
Two research teams led by Dr. Michael Verkhovsky and Prof. Marten Wikstrom of the Institute of Biotechnology of the University of Helsinki have for the first time succeeded in monitoring electron transfer by Complex I in real time. In the future, this work might, for example, have medical relevance, because most of the maternally inherited so-called mitochondrial diseases are caused by dysfunction of Complex I.
This achievement required developing and building of a special device by which the enzyme-catalysed electron transfer could be captured at different time points by stopping the reaction at liquid nitrogen temperatures, on a microsecond (one millionth of a second) time scale. The electrons are very small elementary particles, which is why their transfer is very fast. This work is published this week in the prestigious journal of the American National Academy of Sciences (Proc. Natl. Acad. Sci.). The results give certain hints of the function of Complex I at the molecular level.
Electron transfer is central to many chemical reactions in the cell. It has particular functional importance in cell respiration, which in eukaryotes takes place in the inner mitochondrial membrane, and in the cell membrane of prokaryotes. In cellular respiration molecules stemming from food are oxidised to carbon dioxide, and the electrons liberated in the process are "fed" into the so-called respiratory chain, which consists of three successive membrane-bound enzyme complexes, finally to react with the oxygen we breathe, which is reduced to water using these electrons.
The purpose of electron transfer in cellular respiration is to release the major part of the energy of foodstuffs and to conserve it in a suitable form, ATP (adenosine triphosphate), which the cell may use in its energy-requiring reactions (e.g. biosynthesis, active transport, mechanical work), which are essential e.g. during fetal development and growth, in neural and kidney function, muscle contraction, etc. The energy captured in cellular respiration is transduced to ATP in two phases. The role of the respiratory chain is to couple electron transfer to the translocation of positively charged protons across the membrane, so that the mitochondrial membrane (or the cell membrane in bacteria) becomes electrically polarised, just like charging up a battery. In the second phase, the voltage difference of the battery is used to drive the protons back across the membrane, coupled to the synthesis of ATP by very special molecular machinery.
The first enzyme complex of the respiratory chain is called Complex I. High-energy electrons are fed into this complex in the form of a reduced coenzyme, NADH (nicotinamide adenine dinucleotide), which is oxidised to NAD+ having donated its two electrons. After this, the electrons are transferred along several protein-bound iron/sulphur centres in Complex I until they reach their destination, a molecule of ubiquinone, which is thus reduced to ubiquinol. This reaction, as catalysed by Complex I, is linked to proton translocation across the membrane and thus leads to "charging the battery". At a later stage ubiquinol donates its electrons further in the respiratory chain (ultimately to oxygen), by which it is oxidised back to ubiquinone to allow continuation of Complex I function.
Source: Marten Wikstrom
University of Helsinki
This achievement required developing and building of a special device by which the enzyme-catalysed electron transfer could be captured at different time points by stopping the reaction at liquid nitrogen temperatures, on a microsecond (one millionth of a second) time scale. The electrons are very small elementary particles, which is why their transfer is very fast. This work is published this week in the prestigious journal of the American National Academy of Sciences (Proc. Natl. Acad. Sci.). The results give certain hints of the function of Complex I at the molecular level.
Electron transfer is central to many chemical reactions in the cell. It has particular functional importance in cell respiration, which in eukaryotes takes place in the inner mitochondrial membrane, and in the cell membrane of prokaryotes. In cellular respiration molecules stemming from food are oxidised to carbon dioxide, and the electrons liberated in the process are "fed" into the so-called respiratory chain, which consists of three successive membrane-bound enzyme complexes, finally to react with the oxygen we breathe, which is reduced to water using these electrons.
The purpose of electron transfer in cellular respiration is to release the major part of the energy of foodstuffs and to conserve it in a suitable form, ATP (adenosine triphosphate), which the cell may use in its energy-requiring reactions (e.g. biosynthesis, active transport, mechanical work), which are essential e.g. during fetal development and growth, in neural and kidney function, muscle contraction, etc. The energy captured in cellular respiration is transduced to ATP in two phases. The role of the respiratory chain is to couple electron transfer to the translocation of positively charged protons across the membrane, so that the mitochondrial membrane (or the cell membrane in bacteria) becomes electrically polarised, just like charging up a battery. In the second phase, the voltage difference of the battery is used to drive the protons back across the membrane, coupled to the synthesis of ATP by very special molecular machinery.
The first enzyme complex of the respiratory chain is called Complex I. High-energy electrons are fed into this complex in the form of a reduced coenzyme, NADH (nicotinamide adenine dinucleotide), which is oxidised to NAD+ having donated its two electrons. After this, the electrons are transferred along several protein-bound iron/sulphur centres in Complex I until they reach their destination, a molecule of ubiquinone, which is thus reduced to ubiquinol. This reaction, as catalysed by Complex I, is linked to proton translocation across the membrane and thus leads to "charging the battery". At a later stage ubiquinol donates its electrons further in the respiratory chain (ultimately to oxygen), by which it is oxidised back to ubiquinone to allow continuation of Complex I function.
Source: Marten Wikstrom
University of Helsinki
пятница, 4 ноября 2011 г.
Novel Genomic Alterations Not Seen Before Revealed By Melanoma Transcriptome
Melanoma, the most deadly form of skin cancer, afflicts more than 50,000 people in the United States annually and the incidence rate continues to rise. In a study published online in Genome Research (genome), scientists have delved deeper than ever before into the RNA world of the melanoma tumor and identified genomic alterations that could play a role in the disease.
The latest high-throughput DNA sequencing technologies are ushering in a new era of discovery in cancer genomics that promises to reveal molecular mechanisms of the disease. Beyond cataloging the genetic mutations present in tumors, application of high-throughput sequencing to the RNA "transcriptome" can uncover other genomic alterations missed by DNA sequencing and identify potential targets for therapy.
For example, two adjacent genes can be transcribed together in a single "chimeric" RNA transcript. This RNA message is then translated into a protein with an altered or new function. In addition, rearrangements of the genome can cut and paste genes together, creating "gene fusions." These events occur in normal cells, but they also have the potential to cause disease. Recently these alterations have been detected a few tumor types, and it is very likely that more will be found in other cancers such as melanoma.
To capture the full spectrum of genomic alterations present in the expressed genes of melanoma, a team of researchers in the United States and Switzerland performed an integrative analysis of melanoma tumors using RNA sequencing and structural genomic data. The group identified 11 novel gene fusions involving several common cancer-related genes, and 12 cases of chimeric transcripts. "This is the first direct evidence for these types of genetic alterations in melanoma," said Michael Berger, a research scientist at the Broad Institute and first author of the report.
A particularly interesting finding was that a recurrent chimeric transcript was found involving the CDK2 gene, known to be required for melanoma cell proliferation. The authors suggest that the functional role of the aberrant CDK2 transcript is an attractive target of future investigation. In addition to novel gene fusions and chimeric transcripts, the research group also identified many other alterations in the melanoma tumors, including novel mutations, alternative splice variants, and expression changes.
Berger noted that this type of cancer transcriptome analysis is very appealing, as it complements common DNA-based genomic sequencing and characterization approaches to capture a more complete picture of the cancer genome. "Such studies should help reveal the cancer RNA world," added Levi Garraway, an Assistant Professor at Harvard Medical School/Dana-Farber Cancer Institute and the study's senior author, "thereby nominating many new genetic targets relevant to tumor biology and drug discovery."
Scientists from the Broad Institute of MIT and Harvard (Cambridge, MA), the Dana-Farber Cancer Institute (Boston, MA), the University of Zurich (Zurich, Switzerland), Massachusetts General Hospital (Boston, MA), the Massachusetts Institute of Technology (Cambridge, MA) and Harvard Medical School (Boston, MA) contributed to this study.
This work was supported by the Starr Cancer Consortium, the Melanoma Research Alliance, the Novartis Institutes of Biomedical Research, and the Adelson Medical Research Foundation.
Source:
Peggy Calicchia
Cold Spring Harbor Laboratory
The latest high-throughput DNA sequencing technologies are ushering in a new era of discovery in cancer genomics that promises to reveal molecular mechanisms of the disease. Beyond cataloging the genetic mutations present in tumors, application of high-throughput sequencing to the RNA "transcriptome" can uncover other genomic alterations missed by DNA sequencing and identify potential targets for therapy.
For example, two adjacent genes can be transcribed together in a single "chimeric" RNA transcript. This RNA message is then translated into a protein with an altered or new function. In addition, rearrangements of the genome can cut and paste genes together, creating "gene fusions." These events occur in normal cells, but they also have the potential to cause disease. Recently these alterations have been detected a few tumor types, and it is very likely that more will be found in other cancers such as melanoma.
To capture the full spectrum of genomic alterations present in the expressed genes of melanoma, a team of researchers in the United States and Switzerland performed an integrative analysis of melanoma tumors using RNA sequencing and structural genomic data. The group identified 11 novel gene fusions involving several common cancer-related genes, and 12 cases of chimeric transcripts. "This is the first direct evidence for these types of genetic alterations in melanoma," said Michael Berger, a research scientist at the Broad Institute and first author of the report.
A particularly interesting finding was that a recurrent chimeric transcript was found involving the CDK2 gene, known to be required for melanoma cell proliferation. The authors suggest that the functional role of the aberrant CDK2 transcript is an attractive target of future investigation. In addition to novel gene fusions and chimeric transcripts, the research group also identified many other alterations in the melanoma tumors, including novel mutations, alternative splice variants, and expression changes.
Berger noted that this type of cancer transcriptome analysis is very appealing, as it complements common DNA-based genomic sequencing and characterization approaches to capture a more complete picture of the cancer genome. "Such studies should help reveal the cancer RNA world," added Levi Garraway, an Assistant Professor at Harvard Medical School/Dana-Farber Cancer Institute and the study's senior author, "thereby nominating many new genetic targets relevant to tumor biology and drug discovery."
Scientists from the Broad Institute of MIT and Harvard (Cambridge, MA), the Dana-Farber Cancer Institute (Boston, MA), the University of Zurich (Zurich, Switzerland), Massachusetts General Hospital (Boston, MA), the Massachusetts Institute of Technology (Cambridge, MA) and Harvard Medical School (Boston, MA) contributed to this study.
This work was supported by the Starr Cancer Consortium, the Melanoma Research Alliance, the Novartis Institutes of Biomedical Research, and the Adelson Medical Research Foundation.
Source:
Peggy Calicchia
Cold Spring Harbor Laboratory
вторник, 1 ноября 2011 г.
CRi Oosight Imaging System A Key To Breakthrough Gene Replacement Method With Potential To Prevent Inherited Mitochondrial Diseases
U.S. researchers using CRi's Oosight(TM) imaging system have developed a gene transfer technique that has potential to prevent inherited diseases passed on from mothers to their children through mutated DNA in cell mitochondria. The research, which demonstrated the technique in rhesus monkeys, appears in the Aug. 26 issue of the journal Nature.
The group, headed by Dr. Shoukhrat Mitalipov of the Oregon National Primate Research Center and the Oregon Stem Cell Center, extracted the nuclear DNA from the mother's egg, guided by the Oosight system, and transplanted it into another egg that had the nucleus removed. The technique allowed the mother to pass along her nuclear genetic material to her offspring without her mitochondrial DNA. The eggs were fertilized and transplanted into surrogate mothers, resulting in the birth of four apparently healthy monkeys. Defects in DNA of mitochondria, the cell's "power plants," are associated with a wide range of human diseases.
The Oosight system solved a key problem in avoiding damage to the nuclear DNA during the transfer procedure by providing a non-invasive imaging technique for visualizing the genetic material. Traditional visualization methods employ a stain or involve exposure to ultraviolet light, either of which can damage DNA. The Oregon team had used the Oosight system in previous research, published in Nature in 2007, that provided a foundation for the current study. In that research, they cloned rhesus monkey embryos and used them to create embryonic stem cells.
The Oosight system uses polarized light to generate high-contrast, real-time images of biological features such as the spindle apparatus housing the chromosomes and other filamentous structures within the egg, such as the multi-layer zona pellucida, without the addition of toxic stains or labels, while simultaneously generating useful quantitative data of their structural composition. Two of the four offspring, Spindler and Spindy, were named after the spindle, which is what the Oosight system is used to visualize.
"This study underscores the potential of the Oosight system to advance reproductive medicine and highlights the enabling capabilities or our polarized light technology," said George Abe, president and CEO of CRi.
"With this advance, the Oosight imaging system, which is already widely used in fertility clinics, has offered new insights and possibilities into reproductive health and medicine," said Gary Borisy, director and CEO of the Marine Biological Laboratory (MBL) in Woods Hole, MA. The Oosight system is based on imaging technology originally developed by MBL scientists Rudolf Oldenbourg and Michael Shribek, working in collaboration with David Keefe, M.D., of the University of South Florida College of Medicine.
In in vitro fertilization (IVF) the Oosight system is used as an aid to intracytosplasmic sperm injection (ICSI). The system not only provides assurance that the genetic material is not damaged by the injection needle, but it can also be used as a measurement tool to assess egg viability in both fresh and frozen eggs. Data show that an egg with a weak or malformed spindle and inner layer zona as measured with the system is much less likely to result in pregnancy.
Other scientists have welcomed news of the advance. Mitochondria-expert Douglas Wallace of the University of California, Irvine, said "results were exciting" and the technique is "potentially very interesting." Although he did caution that "there are safety issues that are going to need to be addressed before one could think about it in humans."
The Nature article reported that 15 embryos were transplanted into nine surrogate mothers; three became pregnant, one with twins, and four offspring were born (only three of these offspring have been reported in the Nature paper) The success rate is similar to that of conventional in vitro fertilization.
Cambridge Research & Instrumentation, Inc. (CRi) is a leader in biomedical imaging, and is dedicated to providing comprehensive solutions that analyze disease-specific information from biological and clinical samples in the combined physiological, morphological, and biochemical context of intact tissues and organisms for a variety of applications. With over 80 patents pending and issued, CRi's award-winning innovations are being utilized around the world to enable our customers to perform leading research and provide better healthcare.
Source: Cambridge Research & Instrumentation, Inc
The group, headed by Dr. Shoukhrat Mitalipov of the Oregon National Primate Research Center and the Oregon Stem Cell Center, extracted the nuclear DNA from the mother's egg, guided by the Oosight system, and transplanted it into another egg that had the nucleus removed. The technique allowed the mother to pass along her nuclear genetic material to her offspring without her mitochondrial DNA. The eggs were fertilized and transplanted into surrogate mothers, resulting in the birth of four apparently healthy monkeys. Defects in DNA of mitochondria, the cell's "power plants," are associated with a wide range of human diseases.
The Oosight system solved a key problem in avoiding damage to the nuclear DNA during the transfer procedure by providing a non-invasive imaging technique for visualizing the genetic material. Traditional visualization methods employ a stain or involve exposure to ultraviolet light, either of which can damage DNA. The Oregon team had used the Oosight system in previous research, published in Nature in 2007, that provided a foundation for the current study. In that research, they cloned rhesus monkey embryos and used them to create embryonic stem cells.
The Oosight system uses polarized light to generate high-contrast, real-time images of biological features such as the spindle apparatus housing the chromosomes and other filamentous structures within the egg, such as the multi-layer zona pellucida, without the addition of toxic stains or labels, while simultaneously generating useful quantitative data of their structural composition. Two of the four offspring, Spindler and Spindy, were named after the spindle, which is what the Oosight system is used to visualize.
"This study underscores the potential of the Oosight system to advance reproductive medicine and highlights the enabling capabilities or our polarized light technology," said George Abe, president and CEO of CRi.
"With this advance, the Oosight imaging system, which is already widely used in fertility clinics, has offered new insights and possibilities into reproductive health and medicine," said Gary Borisy, director and CEO of the Marine Biological Laboratory (MBL) in Woods Hole, MA. The Oosight system is based on imaging technology originally developed by MBL scientists Rudolf Oldenbourg and Michael Shribek, working in collaboration with David Keefe, M.D., of the University of South Florida College of Medicine.
In in vitro fertilization (IVF) the Oosight system is used as an aid to intracytosplasmic sperm injection (ICSI). The system not only provides assurance that the genetic material is not damaged by the injection needle, but it can also be used as a measurement tool to assess egg viability in both fresh and frozen eggs. Data show that an egg with a weak or malformed spindle and inner layer zona as measured with the system is much less likely to result in pregnancy.
Other scientists have welcomed news of the advance. Mitochondria-expert Douglas Wallace of the University of California, Irvine, said "results were exciting" and the technique is "potentially very interesting." Although he did caution that "there are safety issues that are going to need to be addressed before one could think about it in humans."
The Nature article reported that 15 embryos were transplanted into nine surrogate mothers; three became pregnant, one with twins, and four offspring were born (only three of these offspring have been reported in the Nature paper) The success rate is similar to that of conventional in vitro fertilization.
Cambridge Research & Instrumentation, Inc. (CRi) is a leader in biomedical imaging, and is dedicated to providing comprehensive solutions that analyze disease-specific information from biological and clinical samples in the combined physiological, morphological, and biochemical context of intact tissues and organisms for a variety of applications. With over 80 patents pending and issued, CRi's award-winning innovations are being utilized around the world to enable our customers to perform leading research and provide better healthcare.
Source: Cambridge Research & Instrumentation, Inc
суббота, 29 октября 2011 г.
DNA Conclusive Yet Still Controversial, Carnegie Mellon Professor Says
Although the odds that DNA evidence found at a crime scene will match by chance the DNA of a person who was not there are infinitesimal, controversy continues about DNA identification and its use in criminal investigations, says Carnegie Mellon University Statistics Professor Kathryn Roeder. Roeder will present a historical overview of the use of DNA identification on Tuesday, April 25, during the Annual Symposia of the National Academy of Sciences in Washington, D.C.
Almost 28,000 cases nationwide have been prosecuted with help from the FBI's data bank of DNA profiles, while at least 170 people have seen their convictions overturned on appeal thanks to DNA evidence. Nonetheless, the use of DNA evidence in appeals has been impeded by political considerations and legal uncertainties, according to Roeder. "After all other legal avenues have been tried, the hope of any innocent person is that biological evidence from their cases still exists and can be subjected to DNA testing. But DNA's value to free the wrongfully convicted can be attained only if political leaders allow its full application," Roeder said. "Thousands currently await the evaluation of their cases."
In the early phases, technical disputes among scientists impeded the use of DNA evidence, Roeder said. One of the earliest controversies to erupt over DNA testing was the magnitude of genetic diversity among people of different ancestry.
Some controversy remains concerning the so-called "cold hit" technique, in which investigators search a DNA database to find a match of DNA found at a crime scene and then collect other evidence to build their case -- as opposed to first identifying a suspect through other evidence and then using DNA to confirm their case. Some critics claimed that this practice could snag an innocent person, but Roeder has demonstrated through her own research that the likelihood of a false hit are miniscule -- in one case, for example, it was about 1 in 26 quintillion, a probability so slight it needn't be shared with juries, Roeder said.
"The jury can't handle such small numbers. We would do them a service to simply tell them it matches or it doesn't match," Roeder said.
Roeder began her career as a biologist, and much of her current research is focused on using statistical tools to understand the workings of the human genome and the nature of inherited diseases. She is a member of the Bioinformatics and Statistics Genetics Group, which includes researchers in the departments of Statistics and Biological Sciences at Carnegie Mellon, and the departments of Psychiatry and Human Genetics at the University of Pittsburgh. The group's primary research goal is to develop statistical tools for finding associations between patterns of genetic variation and complex disease.
Contact: Jonathan Potts
Carnegie Mellon University
Almost 28,000 cases nationwide have been prosecuted with help from the FBI's data bank of DNA profiles, while at least 170 people have seen their convictions overturned on appeal thanks to DNA evidence. Nonetheless, the use of DNA evidence in appeals has been impeded by political considerations and legal uncertainties, according to Roeder. "After all other legal avenues have been tried, the hope of any innocent person is that biological evidence from their cases still exists and can be subjected to DNA testing. But DNA's value to free the wrongfully convicted can be attained only if political leaders allow its full application," Roeder said. "Thousands currently await the evaluation of their cases."
In the early phases, technical disputes among scientists impeded the use of DNA evidence, Roeder said. One of the earliest controversies to erupt over DNA testing was the magnitude of genetic diversity among people of different ancestry.
Some controversy remains concerning the so-called "cold hit" technique, in which investigators search a DNA database to find a match of DNA found at a crime scene and then collect other evidence to build their case -- as opposed to first identifying a suspect through other evidence and then using DNA to confirm their case. Some critics claimed that this practice could snag an innocent person, but Roeder has demonstrated through her own research that the likelihood of a false hit are miniscule -- in one case, for example, it was about 1 in 26 quintillion, a probability so slight it needn't be shared with juries, Roeder said.
"The jury can't handle such small numbers. We would do them a service to simply tell them it matches or it doesn't match," Roeder said.
Roeder began her career as a biologist, and much of her current research is focused on using statistical tools to understand the workings of the human genome and the nature of inherited diseases. She is a member of the Bioinformatics and Statistics Genetics Group, which includes researchers in the departments of Statistics and Biological Sciences at Carnegie Mellon, and the departments of Psychiatry and Human Genetics at the University of Pittsburgh. The group's primary research goal is to develop statistical tools for finding associations between patterns of genetic variation and complex disease.
Contact: Jonathan Potts
Carnegie Mellon University
среда, 26 октября 2011 г.
Genome Connects The Dots Between Amphimedon, Animal Descendants
The simple sponge can reveal much about life on Earth. Researchers who have sequenced the genome of one Down Under inhabitant are learning just how common those roots are.
In a paper published online this week in the journal Nature, Rice University's Nicholas Putnam is among a group of scientists who have established a draft genome sequence for Amphimedon queenslandica, a sponge found off the coast of Australia. The genome is helping evolutionary biologists connect the dots as they look for DNA sequences shared by metazoans, or multicelled animals.
Sponges are an ancient group, with fossils dating back at least 650 million years. They are thought to have been the first group of animals to branch from all the others. Therefore, genes shared by sponges and other animals must have been present in the common ancestor of all metazoans. This ancestor would have evolved mechanisms to coordinate cell division, growth, specialization, adhesion and death; this suggests that early sponges already had a developmental set of tools similar to those in metazoans today, said Putnam, an assistant professor of ecology and evolutionary biology.
"What's exciting is the new things we're learning about animal evolution," said Putnam, who got involved with the project while working at the Department of Energy's Joint Genome Institute in 2006. "For example, sponges have embryos, and having the genome helps us look at how they develop and make specific connections to developmental pathways in other animals.
"It's the kind of thing that will lead to a much clearer understanding of what the very first metazoans looked like," he said.
That distant ancestor may well have looked like a sponge. For the paper, Putnam helped compare Amphimedon's draft genome with 13 other complete animal genomes, including a selection of invertebrates, as well as a choanoflagellate. The researchers wrote of a "striking conservation of gene structure and genome organization" that is common to all. "We can now say that the large-scale patterns of genome organization we've seen conserved in other animal groups come from the very root of the animal tree," Putnam said.
The challenge ahead is learning what they do. "The focus of my research is to understand whether patterns that have been around for a billion years have some particular functions -- or if they're hanging around because not enough time has gone by to erase them."
What's missing is also interesting, he said. The ancestral patterns of genome organization common to other creatures is absent from certain arthropods -- invertebrates that include the likes of centipedes and lobsters -- and nematodes. "If the missing pattern is neutral, you'd say that somewhere along the history of those groups, the rate of (evolutionary) change sped up enough to break the connection," Putnam said. "If it's functional, then somehow those groups overcame whatever constraint is on it in other lineages."
Also puzzling is that while Amphimedon shares key developmental genes with a diverse set of metazoans, its basic structure hasn't changed in 600 million years. Given the same roots, researchers wonder why it didn't evolve more radically, and they are working to identify the differences that gave rise to, say, nerve cells in other creatures but not sponges.
Unlocking the basic mechanisms of multicellularity may also help researchers understand what happens when those mechanisms go wrong and lead to cancer and autoimmune disorders.
Notes:
The paper's senior authors are Daniel Rokhsar of the University of California, Berkeley, and Bernard Degnan of the University of Queensland in Australia.
The work was funded by the Australian Research Council, the Department of Energy Joint Genome Institute, Harvey Karp, the National Science Foundation, the National Institutes of Health/National Human Genome Research Institute, the University of Queensland Postdoctoral Fellowship, the Sars International Center for Marine Molecular Biology, Deutsche Forschungsgemeinschaft, Agricultural and Natural Resources/University of California, the French National Center for Scientific Research, the Gordon and Betty Moore Foundation and Richard Melmon.
Source:
David Ruth
Rice University
In a paper published online this week in the journal Nature, Rice University's Nicholas Putnam is among a group of scientists who have established a draft genome sequence for Amphimedon queenslandica, a sponge found off the coast of Australia. The genome is helping evolutionary biologists connect the dots as they look for DNA sequences shared by metazoans, or multicelled animals.
Sponges are an ancient group, with fossils dating back at least 650 million years. They are thought to have been the first group of animals to branch from all the others. Therefore, genes shared by sponges and other animals must have been present in the common ancestor of all metazoans. This ancestor would have evolved mechanisms to coordinate cell division, growth, specialization, adhesion and death; this suggests that early sponges already had a developmental set of tools similar to those in metazoans today, said Putnam, an assistant professor of ecology and evolutionary biology.
"What's exciting is the new things we're learning about animal evolution," said Putnam, who got involved with the project while working at the Department of Energy's Joint Genome Institute in 2006. "For example, sponges have embryos, and having the genome helps us look at how they develop and make specific connections to developmental pathways in other animals.
"It's the kind of thing that will lead to a much clearer understanding of what the very first metazoans looked like," he said.
That distant ancestor may well have looked like a sponge. For the paper, Putnam helped compare Amphimedon's draft genome with 13 other complete animal genomes, including a selection of invertebrates, as well as a choanoflagellate. The researchers wrote of a "striking conservation of gene structure and genome organization" that is common to all. "We can now say that the large-scale patterns of genome organization we've seen conserved in other animal groups come from the very root of the animal tree," Putnam said.
The challenge ahead is learning what they do. "The focus of my research is to understand whether patterns that have been around for a billion years have some particular functions -- or if they're hanging around because not enough time has gone by to erase them."
What's missing is also interesting, he said. The ancestral patterns of genome organization common to other creatures is absent from certain arthropods -- invertebrates that include the likes of centipedes and lobsters -- and nematodes. "If the missing pattern is neutral, you'd say that somewhere along the history of those groups, the rate of (evolutionary) change sped up enough to break the connection," Putnam said. "If it's functional, then somehow those groups overcame whatever constraint is on it in other lineages."
Also puzzling is that while Amphimedon shares key developmental genes with a diverse set of metazoans, its basic structure hasn't changed in 600 million years. Given the same roots, researchers wonder why it didn't evolve more radically, and they are working to identify the differences that gave rise to, say, nerve cells in other creatures but not sponges.
Unlocking the basic mechanisms of multicellularity may also help researchers understand what happens when those mechanisms go wrong and lead to cancer and autoimmune disorders.
Notes:
The paper's senior authors are Daniel Rokhsar of the University of California, Berkeley, and Bernard Degnan of the University of Queensland in Australia.
The work was funded by the Australian Research Council, the Department of Energy Joint Genome Institute, Harvey Karp, the National Science Foundation, the National Institutes of Health/National Human Genome Research Institute, the University of Queensland Postdoctoral Fellowship, the Sars International Center for Marine Molecular Biology, Deutsche Forschungsgemeinschaft, Agricultural and Natural Resources/University of California, the French National Center for Scientific Research, the Gordon and Betty Moore Foundation and Richard Melmon.
Source:
David Ruth
Rice University
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