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  • Duke University Department of Molecular Genetics & Microbiology
    stroke infarct volume is highly variable and strain dependent but the natural genetic determinants responsible for this difference remain unknown After permanent distal middle cerebral artery occlusion MCAO infarct volume was determined for 16 inbred mouse strains chromosome substitution strains and for two intercross cohorts F2 B6xBALB c and F2 B6xSWR J Infarct volume varied up to 30 fold between strains with heritability estimated at 0 88 To identify genetic determinants modulating infarct tissue damage we performed quantitative trait locus QTL analysis of surgically induced cerebral infarct volume We have identified multiple quantitative trait loci QTL that modulate infarct volume with a major locus Civq1 on chromosome 7 accounting for over 50 of the variation with a combined LOD score of 21 7 Measurement of infarct volume in chromosome substitution strains CSS and two additional intercrosses validate that Civq1 on chromosome 7 is present in multiple inbred strains Interval specific ancestral SNP haplotype analysis for Civq1 results in 5 candidate genes A causative gene underlying Civq1 may regulate collateral artery formation and genetic variations in the gene may result in the differential outcome of cerebral infarction Interestingly Civq1 appears to be identical to Lsq1 a locus conferring limb salvage and reperfusion in hindlimb ischemia The identification of the genes underlying these loci may uncover novel genetic and physiological pathways that modulate cerebral infarction and provide new targets for therapeutic intervention in ischemic stroke and possibly other human vascular occlusive diseases A locus mapping to mouse chromosome 8 determines infarct volume in a mouse model of ischemic stroke Chris Bennett In an established mouse model of focal cerebral ischemia infarct volume is highly variable and strain dependent but the natural genetic determinants remain unknown To identify these genetic determinants regulating ischemic neuronal damage and to dissect apart the role of individual

    Original URL path: http://mgm.duke.edu/news/keum_bennett.html (2014-06-13)
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  • Duke University Department of Molecular Genetics & Microbiology
    the scientists performed an experiment that made the smaller spores grow into larger spores We found in that case the smaller spore that became large acted like the larger spores Lee said We believe that this spore bypassed the natural growth stage of isotropic growth and that was how it becomes more virulent This means we might be able to find a way to arrest them in the smaller stage before they grow into more virulent larger spores he said Interestingly other scientists have recently published related findings about the dual cell sizes in another virulent fungal pathogen Cryptococcus neoformans in which gigantic cells form in the lungs of infected animals and patients Normally immune cells called macrophages engulf and destroy dangerous fungal spores Small spores can be contained by macrophages but the larger spores switch too quickly to hyphal growth and thereby can destroy the macrophage When the macrophages a first line defense split open they undergo cell death and are unable to protect an infected human or other host animal This finding shows another example of adaptation through fungal cell gigantism which lets pathogenic fungi establish infection in the hosts particularly those that are immune compromised said Joseph Heitman MD PhD co senior author and chair of the Duke Department of Molecular Genetics and Microbiology We used a diabetic model of mice which is also an immunocompromised type of animal We found the fungal subspecies that we studied is highly virulent in mice which correlates well with this subspecies frequent occurrence in clinical human specimens Heitman said the hope is to find a way to arrest the isotropic growth stage Clinically these mucor infections are reasonably common in diabetic patients transplant patients and lung cancer chemotherapy patients he said Having a high blood glucose level is immunosuppressive and

    Original URL path: http://mgm.duke.edu/news/lee_soo_chan.html (2014-06-13)
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  • Duke University Department of Molecular Genetics & Microbiology
    how fungal and other microbial pathogens evolve and emerge to cause disease and outbreaks said Heitman The work on Cryptococcus is becoming increasingly important as harmful and new forms of the fungus have emerged outside of the tropics causing an ongoing outbreak in Canada and the Pacific Northwest in the US Globally Cryptococcus causes more than one million infections annually including more than 600 000 attributable deaths and nearly one third of all AIDS associated deaths Heitman s genetic and evolutionary findings on this pathogen serve as a model to further our understanding of other fungi and parasites causing human infections augmenting the recent discoveries of same sex mating of Candida albicans by Richard Bennett and colleagues at Brown University and selfing in outbreaks of Toxoplasma gondii revealed by Michael Grigg and co workers at the NIH This R37 MERIT Award recognizes the transformative insights that Dr Heitman s work has provided on the evolutionary origins of sexual reproduction from his work on fungi said Arturo Casadevall MD PhD a globally recognized authority on infectious diseases and Chair of the Department of Microbiology and Immunology at the Albert Einstein College of Medicine in New York City Heitman said he was humbled and honored at the news that this grant application had achieved a perfect score and was chosen for a MERIT Award This is a terrific reflection of our robust institutional environment for studies on microbial pathogenesis and genetics and also on the partnership among investigators in basic science departments and physician scientists in the clinical departments at Duke said Heitman This award in many ways can be attributed to the tremendous long term collaboration I have had with John Perfect MD Professor in the Division of Infectious Diseases and the Department of Medicine and other clinical colleagues as well

    Original URL path: http://mgm.duke.edu/news/heitman_8.html (2014-06-13)
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  • Duke University Department of Molecular Genetics & Microbiology
    stroke research by providing research assistance and training Tang received a Postdoctoral Fellowship which helps trainees initiate careers in cardiovascular and stroke research while obtaining significant research results under the supervision of a sponsor or mentor Ciotti works in the laboratory of Raphael Valdivia PhD Associate Professor and Director of Graduate Programs in the Department of Molecular Genetics and Microbiology McDonald and Tang work in the laboratory of Doug Marchuk

    Original URL path: http://mgm.duke.edu/news/aha_2011.html (2014-06-13)
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  • Duke University Department of Molecular Genetics & Microbiology
    Duke University Medical Center was selected by the American Society for Microbiology ASM to receive the 2011 ICAAC Young Investigator Award Supported in part by an unrestricted educational grant from Merck U S Human Health Division since 1983 the ICAAC Young Investigator Awards recognize and reward early career scientists for research excellence and potential in microbiology and infectious diseases Coers has demonstrated outstanding creativity in the study of mouse genetics

    Original URL path: http://mgm.duke.edu/news/coers_1.html (2014-06-13)
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  • Duke University Department of Molecular Genetics & Microbiology
    He joined the Heitman lab in 2008 to study the population genetics of C neoformans and C gatti as well as characterize the mating type MAT locus in some fungal genomes Mitchell works in the laboratory of Sue Jinks Robertson Professor in the Department of Molecular Genetics and Microbiology She joined the Jinks Robertson lab in 2008 and is using a transformation based gap repair assay to examine the mechanisms

    Original URL path: http://mgm.duke.edu/news/delill_nasser_2011.html (2014-06-13)
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  • Duke University Department of Molecular Genetics & Microbiology
    Dr DeRisi is currently a Howard Hughes Medical Institute HHMI Investigator and a Professor and Vice Chairman of the Department of Biochemistry and Biophysics at the University of California San Francisco UCSF with a joint appointment at the California Institute for Quantitative Biomedical Research QB3 Dr DeRisi s best known achievements are his work on profiling gene expression throughout the lifecycle of the malaria causing protozoan Plasmodium falciparum and his

    Original URL path: http://mgm.duke.edu/news/mcginnis_lecture_2011.html (2014-06-13)
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  • Duke University Department of Molecular Genetics & Microbiology
    new PhD graduate the opportunity to address the difficult questions in cancer biology The transformation of this self described shy boy from a small town in rural China to Associate Professor of Molecular Biology at Princeton University and Member of the Cancer Institute of New Jersey is bracketed between those two vastly different circumstances Born in 1973 in Fujian Province Dr Kang s scientific skills were apparent early As a student of the Experimental Science Class in Peking University High School he won the top prizes in the National Chemistry Competition But chemistry gave way to genetics when as an undergraduate at Fudan University in Shanghai Dr Kang recalls first being fascinated by the potential power of genetics to tackle human diseases His research direction chosen in 1995 Dr Kang turned toward the West for his graduate studies Enrolling first at Michigan State University he transferred a year later to Duke University where he worked in the laboratory of renowned virologist Dr Bryan Cullen As the only graduate student in the group Dr Kang proved early he could hold his own among his colleagues all highly successful postdocs Dr Kang completed his graduate studies in less than four years and as part of his thesis work solved an important problem in virology relating to the export of viral genomic RNA His success in studying virus host interactions inspired him to tackle an even more difficult question How do tumor cells turn against their hosts and eventually kill the cancer patients It was now 2000 and the genomic revolution was underway Dr Kang joined the lab of Dr Joan Massagué at the Sloan Kettering Institute Dr Massagué gave his ambitious new colleague free rein to pursue the molecular mechanism of cancer metastasis even though no research of this sort had ever

    Original URL path: http://mgm.duke.edu/news/kang.html (2014-06-13)
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