archive-org.com » ORG » I » IMGS.ORG

Total: 854

Choose link from "Titles, links and description words view":

Or switch to "Titles and links view".
  • 18th International Mouse Genome Conference (2004)
    University of Michigan Ann Arbor United States 2 Vollum Institute Oregon Health and Science University Portland United States Gastrin deficient G mice develop severe metaplastic changes in the gastric mucosa in response to hypochlorhydria bacterial overgrowth and inflammation Gastrin is a known trophic hormone for the gastric epithelium Sonic hedgehog Shh a morphogenic peptide produced by murine parietal and chief cells maintains normal gastric mucosal architecture but the mechanism is unknown The present study investigates the role of gastrin in the regulation of Shh protein expression and processing using the G mouse model Compared to 12 month old wild type WT and hypergastrinemic somatostatin deficient SOM mice the hypochlorhydric G mice developed parietal cell atrophy antral inflammation and metaplasia 60 of the G mice developed gastric tumors that showed loss of the tumor suppressor gene RUNX3 in isolated tissue To confirm that the tumors in the G mice were malignant cells dissociated from tumors alone grew in soft agar Immunofluorescence revealed co localization of Shh with the parietal cells in the WT animals However Shh expression was decreased in the G mice coincident with loss of parietal cells Gastrin infusion in G mice restored Shh peptide in the parietal cells

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file222.shtml (2016-02-17)
    Open archived version from archive

  • 18th International Mouse Genome Conference (2004)
    University of Nebraska Lincoln United States 2 NCI NIH Bethesda United States Genetic predisposition to complex traits results from interactive combinations of relatively small effects of genetic variations within a large number of primarily unidentified polygenes known as quantitative trait loci QTL Given the growing evidence that obesity may increase the risk of susceptibility to certain forms of cancer we have created a population of F 2 mice cosegregating obesity QTL and the MMTV PyMT transgene with a primary objective of determining how polygenic obesity influences age at mammary tumor onset tumor number and severity The F 2 population n 600 resulted from a cross between the polygenic obesity model M16i and FVB NJ TgN MMTV PyMT 634Mul which develop synchronously appearing multifocal tumors involving all of the mammary glands with more than 85 of the animals developing pulmonary metastases by 100 days of age At four weeks of age all F 2 individuals were randomly assigned to either a high fat 45 calories from fat or a matched normal fat 10 calories from fat synthetic diet Body weights are being recorded at periodic intervals while body composition will be analyzed at pre and post tumor ages using DEXA All

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file223.shtml (2016-02-17)
    Open archived version from archive

  • 18th International Mouse Genome Conference (2004)
    RESPONSIBLE FOR MOUSE ACHONDROPLASIA Tsuji T Kunieda T Okayama University Okayama Japan The achondroplastic cn cn mouse is a spontaneous mutant found in the AKR J colony at the Jackson Laboratory which is characterized by an achondroplastic dwarfism with short limbs and tail due to disturbed chondrogenesis in the endochondral ossification The cn locus has been mapped to mouse chromosome 4 but precise localization has not yet been determined In this study we preciously mapped the cn locus by linkage analysis and identified the causative gene for the cn cn mutant By linkage analysis using 115 affected mice of F 2 progeny the cn locus was mapped on a 0 8 cM region of chromosome 4 We found that Npr2 gene localized in this region was most potent candidate gene The sequence analysis of the gene revealed a T to G transversion leading to an amino acid substitution of highly conserved Leu to Arg in the guanylyl cyclase catalytic domain of NPR2 Npr2 gene encodes a receptor for C type natriuretic peptide CNP which positively regulates longitudinal bone growth by intracellular cGMP production No significant increase of intracellular cGMP level in response to CNP stimulus was observed in the chondrocytes

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file224.shtml (2016-02-17)
    Open archived version from archive

  • 18th International Mouse Genome Conference (2004)
    Incao A Chen A Zerfas P Bryant MA Schwartzberg P Biesecker LG Pavan WJ 1 National Human Genome Research Institute NIH Bethesda United States 2 Diagnostic and Research Services Branch Veterinary Resources Program NIH Bethesda United States Pequeño is inherited in an autosomal recessive pattern and is a mouse model for exocrine pancreatic insufficiency The pequeño phenotype is caused by a transgene insertion and 210kb deletion mutation on chromosome 3 Pequeño mice exhibit progressive postnatal apoptosis of pancreatic acinar cells with nearly complete exocrine acinar cell loss at 8 weeks while islets and ductal tissue remain present Homozygous animals are about 1 3 smaller than heterozygous or wildtype littermates at weaning have an average lifespan of 4 months under standard housing conditions and have immunodeficiency Dietary supplementation pancreatic enzymes can correct the body size weight immunodeficiency and increase the lifespan of pq pq mice suggesting that malnutrition is a major cause of the phenotype BAC transgenic rescue crosses have identified a single transcript present in the deletion that is responsible for the pancreatic insufficiency The pequeño phenotype is similar to that of Shwachman Diamond syndrome SDS in humans SDS is characterized by short stature pancreatic lipomatosis neutropenia and increased risk

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file225.shtml (2016-02-17)
    Open archived version from archive

  • 18th International Mouse Genome Conference (2004)
    MOUSE MUTANTS REVEAL NEW GENES INVOLVED IN PIGMENTATION McGowan K Van Raamsdonk C Aradhya S Fitch K Barsh G Stanford University Stanford United States Melanocytes undergo a series of stereotypic behaviors as they move from the neural crest to their final resting position in the skin including migration proliferation programmed cell death and differentiation Recently large scale mutagenesis projects in mice have enabled our lab to use forward genetics to study a novel class of pigmentation mutants identified by dark skin Dsk One class of Dsk mutants represented by Dsk3 Dsk4 Dsk6 and Dsk11 is characterized by increased epidermal pigment in non hairy skin Each mutant can be identified at weaning age While Dsk3 Dsk4 and Dsk6 homozygotes die early in embryogenesis Dsk11 homozygotes expire within minutes of birth In addition Dsk11 homozygotes are born with an open eye phenotype and exhibit gross and histologic abnormalities consistent with pulmonary hypoplasia Using melanocyte specific markers we have shown that Dsk3 animals have an increased number of epidermal melanocytes in the tail and footpad skin whereas Dsk4 Dsk6 and Dsk11 animals have dark skin based on mechanisms independent of pigment cell number Each mutant maps to a unique location in the genome

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file226.shtml (2016-02-17)
    Open archived version from archive

  • 18th International Mouse Genome Conference (2004)
    the bone formation dominates the bone resorption until the age of twenties when the bone mass reaches a maximum The bone mass remains stable for years and starts to decrease after a certain age Balance between formation and resorption is regulated by multiple complex systems which include growth factors hormones and vitamins Although defects in bone remodeling in humans such as osteoporosis cause deterioration of quality of life in old age its mechanisms remain incompletely understood In a large scale mouse ENU mutagenesis project we use 49 visible morphological parameters for mutant screening So far 260 dysmorphological mutant lines have been isolated and confirmed To identify mouse models for human bone diseases we have started a secondary screening of existing mutant lines in the dysmorphology module of the German Mouse Clinic Additional bone related parameters include x ray radiography dual energy x ray absorptiometry DEXA micro computer tomography and physiological analysis We selected mutant lines showing bone related phenotypes for this screening One mutant line Ali14 abnormal limb mutant mice showed decreased bone mass density p 0 001 weight p 0 001 fat and lean mass p 0 001 and body size p 0 001 were detected Ali14 is a

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file227.shtml (2016-02-17)
    Open archived version from archive

  • 18th International Mouse Genome Conference (2004)
    Laboratory Bar Harbor United States The Center for New Mouse Models of Heart Lung Blood and Sleep Disorders was established in 2000 as a National Heart Lung and Blood Institute Program for Genomic Applications Our goal is to provide the scientific community with new mouse models in these disease areas We are conducting high throughput primary phenotyping of third generation ENU mutagenized pedigrees derived from background strain C57BL 6J A battery of non invasive phenotypic screens is performed on mature mice over the course of a 9 week protocol and includes challenge with a high fat high cholesterol diet Testing of each animal includes the following plasma coagulation factor profile fibrinogen antithrombin III Factor VII standard whole blood count plasma total and HDL cholesterol triglycerides and glucose metabolic cage monitoring including a novel method for assessment of sleep behavior whole body plethysmography dual energy x ray absorptiometry for obesity and evaluation of cardiac function by echocardiography and unanesthetized electrocardiography To date we have identified over 350 phenotypic deviants of which more than 60 have proven heritable Heritability testing and colony development of more than 100 additional lines is ongoing for all phenotypes Breeding pairs of all proven heritable mutants are

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file228.shtml (2016-02-17)
    Open archived version from archive

  • 18th International Mouse Genome Conference (2004)
    PESTICIDES DURING DEVELOPMENT ROLE OF PARAOXONASE PON1 Pettan Brewer C Cole TB Walter BJ Fisher JC Richter RJ Burbacher TM Costa LG Furlong CE University of Washington Seattle United States Paraoxonase PON1 is an HDL associated enzyme involved in the metabolism of organophosphorous pesticides We demonstrate that infants have very low PON1 levels and a variable onset of expression reaching a plateau at 6 24 mo To assess the importance of PON1 for protecting against the developmental toxicity of chlorpyrifos oxon CPO PON1 knockout PON1 and wild type WT mice were exposed chronically PN4 to PN21 to low levels of CPO Endpoints included cholinesterase activity histopathology gene expression and behavior As early as PN4 PON1 mice were more sensitive to inhibition of brain cholinesterase by CPO At PN22 and persisting as long as 4 months chronic developmental exposure to 0 18 mg kg d or 0 25 mg kg d CPO resulted in perinuclear vacuolization of cells in a discrete area of the neocortex with an increase in the number of affected cells at 0 25 mg kg d Surprisingly none of the behaviors chosen for assessment were affected However from PN16 19 mice exposed to 0 18 or 0

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file229.shtml (2016-02-17)
    Open archived version from archive



  •