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  • 17th International Mouse Genome Conference (2003)
    F 2 INTERCROSS BETWEEN THE 129P3 J AND C57BL 6BYJ MOUSE STRAINS Li X Monell Chemical Senses Center Co Authors 1 Bachmanov A A 1 McDaniel AH 2 Lu K 2 Li S 1 Tordoff M G 2 Price R A 1 Reed D R Institutions 1 Monell Chemical Senses Center 2 University Pennsylvania Mice have proved to be a powerful model organism for understanding obesity in humans Single gene mutants and genetically modified mice have been used to identify obesity genes and the discovery of loci for polygenic forms of obesity in the mouse is an important next step To pursue this goal the inbred mouse strains 129P3 J 129 and C57BL 6ByJ B6 which differ in body weight body length and adiposity were used in an F 2 cross to identify loci affecting these phenotypes Linkages were determined in a two phase process In the first phase 169 randomly selected F 2 mice were genotyped for 134 markers that covered all autosomes and the X chromosome Significant linkages were found for body weight and body length on chromosome 2 In addition we detected several suggestive linkages on chromosomes 2 adiposity 9 body weight body length and adiposity and

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file151.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Imaging The Genetics and Genomics of Infectious Disease Verne Chapman Memorial Lecture Table of Contents Sponsor Exhibitor List Awards Photographs POSTER 104 RETINAL COLOBOMA IN FLS MICE Matsuura T Setsunan University Co Authors 1 Kodama Y 1 Ozaki K 2 Hirasawa S 1 Narama I Institutions 1 Setsunan University 2 Shionogi Co Ltd A new type of morphological anomalies of the retina were detected in a new strain of mouse named FLS fatty liver Shionogi derived from the dd strain In this study eyes of FLS mice during lactation period were investigated morphologically Animals postpartum days 7 21 and 35 were fixed by perfusion of solution containing 4 paraformaldehyde and 2 glutaraldehyde Then both eyeballs were enucleated and the cornea was removed along a horizontal line between the cornea and conjunctiva Under a binocular stereoscope the fundus was carefully observed then they were dehydrated and embedded in paraffin and subjected to histological examination by light microscopy Macroscopic observation of the fundus revealed that incidence of retinal coloboma with retina fold was clearly high more than 70 in males and females of FLS mice Light microscopically disarrangement or rosette formation of retinal layers was noted and almost whole retinal layers disappeared

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file152.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    CharalambousM 2 Bennett W R 1 KellyS M 3 DellG 1 Ward A Institutions 1 University of Bath Centre for Regenerative Medicine Department of Biology and Biochemistry 2 University of Manchester UK Centre for Tissue Engineering 3 University of Bristol Department of Biochemistry The Igf2 gene is imprinted at most sites of its expression but escapes imprinting in the choroid plexus and leptomeninges of the brain Imprinting of Igf2 has been shown to be dependent upon a differentially methylated imprinting control region ICR that lies in the 5 flank of the neighbouring H19 gene and acts as an insulator to block enhancers that are situated further downstream We have found that enhancers for brain specific expression of Igf2 reside within a 2kb region located centrally between Igf2 and H19 These elements permit bi allelic expression of Igf2 because of their location upstream of the ICR avoiding its influence on the maternal as well as the paternal chromosomes Consistent with this proposal we have shown that the ICR maintains differential allelic methylation in the choroid plexus To further address potential roles played by epigenetic factors we have developed in vitro culture systems for choroid plexus epithelial tissue In addition it appears

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file153.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    PURIFICATION FROM MOUSE TAILS Mulrooney C Tepnel Life Sciences PLC Co Authors Howe S Oultram J Robinson J Maloney S Sayle J Institutions Tepnel Life Sciences PLC The extraction of high quality genomic DNA is the first and often limiting step in the process of mouse tail genotyping Tail snips are difficult samples to work with and most of the chemistries and systems available on the market today fail to

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file154.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    of Contents Sponsor Exhibitor List Awards Photographs POSTER 107 PANCREAS ANOMALY AND INTESTINAL TUMORS IN THE MOUSE SMALL EYE MUTANTS PAX6 SEY3H AND PAX6 SEY4H Nitta Y Hiroshima University Co Authors 2 Yoshida K 3 Nakagata N Institutions 2 National Institute for Radiological Science 3 Kumamoto University Deletions of the chromosome 2 middle regions are associated with the radiation induced mouse acute myeloid leukemias while murine small eye mutants delete the chromosome 2 middle regions genetically Expecting the predisposition to acute myeloid leukemia the tumorigenicity of the two small eye mutants Pax6Sey3H and Pax6Sey4H was examined The commonly deleted region of the two small eye mutants was the segment of 3 2Mb between 106 0Mb and 109 2Mb from the centromere where the Wilm s tumor 1 Wt1 Reticulocarbin Rcn Paired box gene 6 Pax6 Elongation protein homolog 4 Elp4 and other fourteen novel genes located The two mutants produced glucagon in the islets however they impaired to elevate the blood glucose level up when loaded with insulin Morphological anomaly of the Wirsung duct chronic pancreatitis or fatty degeneration of the pancreas was observed with age Both mutants developed intestinal tumors spontaneously 52 0 and 32 0 for the Pax6Sey3H

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file155.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Molecular Medicine Co Authors 1 Petersson S 1 Johansen J 2 Ingvar M 3 Nilsson J 3 Klement G 3 Århem P 1 Schalling M 1 Lavebratt C Institutions 1 Department of Molecular Medicine 2 Department of Clinical Neuroscience 3 Department of Neuroscience Karolinska Institutet Stockholm Sweden The megencephaly mouse mceph mceph displays dramatically increased brain volume and hypertrophic brain cells Despite overall enlargement the mceph mceph brain appears structurally normal without edema hydrocephaly or leukodystrophy and with only minor astrocytosis Furthermore it presents striking disturbances in expression of trophic and neuromodulating factors within the hippocampus and cortex Using a positional cloning approach we have identified the mceph mutation We show that mceph mceph mice carry an eleven base pair deletion in the gene encoding the Shaker like voltage gated potassium channel subtype 1 Kcna1 The mutation leads to a frame shift and the predicted MCEPH protein is truncated at amino acid 230 out of 495 terminating with six aberrant amino acids The expression of Kcna1 mRNA is increased in the mceph mceph brain The putative MCEPH protein retains only the N terminal domains for channel assembly and may congregate non functional complexes of multiple Shaker like subunits Indeed whereas

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file156.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    GENE BICC1 Price S J Joan C Edwards School of Medicine Marshall University Co Authors 2 Davis K L 2 Guay Woodford L M 1 3 Bryda E C Institutions 1 Joan C Edwards School of Medicine Marshall University 2 University of Alabama at Birmingham 3 University of Missouri Columbia The Bicaudal C Bicc1 gene on mouse Chromosome 10 when mutated causes a severe form of polycystic kidney disease PKD At least two mutant alleles of Bicc1 exist Bicc1 jcpk and Bicc1 bpk These two mutations are predicted to have distinctly different effects on the structure of the Bicc1 protein and in turn may partially explain the different PKD phenotypes observed in Bicc1 jcpk jcpk versus Bicc1 bpk bpk animals Confocal microscopy of cultured cells demonstrates localization of the Bicc1 protein to the primary apical cilia of renal epithelium Interestingly a number of other mouse models exhibiting mutations in the genes encoding cilia proteins not only develop PKD but also exhibit alterations in body plan asymmetry Preliminary analyses of PKD affected Bicc1 jcpk mice have identified a number of laterality defects including dextrocardia and lung isomerism Currently the function of the Bicc1 protein is unknown however several functional domains have

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file157.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    MODELS FOR HUMAN NEPHROPATHIES Rathkolb B Institute of Molecular Animal Breeding and Biotechnology LMU Munich Hackerstrasse 27 85764 Oberschleiβheim Co Authors 1 Tran TV 1 Klempt M 1 Mohr M 2 Soewarto D 2 Hoffmann S 2 Hrabe de Angelis M 1 Wolf E 1 Aigner B Institutions 1 Institute of Molecular Animal Breeding and Biotechnology LMU Munich Hackerstrasse 27 85764 Oberschleiβheim 2 Institute of Experimental Genetics GSF Research Center Ingolstädter Landstrasse 1 85764 Oberschleiβheim Neuherberg Nephropathies include various multifactorial disorders caused by genetic and or environmental factors Chronic renal insufficiencies usually progress to end stage kidney failure irrespective of the initial nephropathy Novel animal models for the evaluation of genetic factors in the development of terminal renal failures in humans are urgently needed Therefore we identified chemically induced mouse mutants showing relevant alterations in clinical chemistry parameters in the Munich ENU mouse mutagenesis program The analysis revealed four independent mutant mouse lines HST001 HST002 HST007 HST009 showing elevated plasma urea levels Disturbances of the excretion of protein metabolites appear as a consequence of markedly reduced renal function In humans this is the main symptom for the subsequent development of clinical nephropathies One additional line UAH001 shows albumin excretion in

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file158.shtml (2016-02-17)
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