Hans J. Hedrich

Medizinische Hochschule Hannover

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Dirk Wedekind

Universitätsmedizin Göttingen

André Bleich

Medizinische Hochschule Hannover

Michael Mähler

Nova Medical (United States)

Martina Dorsch

Medizinische Hochschule Hannover

Anna Smoczek

Medizinische Hochschule Hannover

M.‐L. Enss

Medizinische Hochschule Hannover

Siegfried Wagner

University of Alberta

Klaus Gärtner

University of Lisbon

U. Schmidt-Wittig

Medizinische Hochschule Hannover

Kenji Kamino

Medizinische Hochschule Hannover

Cooperative Institutions

Medizinische Hochschule Hannover

123

Giessen School of Theology

Kerckhoff Klinik

University of Massachusetts Chan Medical School

Max Planck Institute for Biophysical Chemistry

University of Veterinary Medicine Hannover, Foundation

Heidelberg University

University of Göttingen

National Institutes of Health

University of Tübingen

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Genetic identification of multiple susceptibility genes involved in the development of endometrial carcinoma in a rat model

International Journal of Cancer (2001)

Leyla Roshani Dirk Wedekind Josiane Szpirer Ziad Taïb Claude Szpirer

There are clear indications that inheritance plays an essential role in certain cases of human endometrial cancer, and there are at least 2 forms of early-onset heritable endometrial adenocarcinomas (EACs). Females of the BDII inbred rat strain are known to be genetically predisposed to endometrial carcinoma, and we have performed a genetic analysis of susceptibility to endometrial cancer in this strain. F2 populations were generated by crossing BDII females with males from 2 different strains with a low incidence of EAC, and the occurrence of endometrial cancer was studied. Three chromosome regions associated to EAC susceptibility were identified, and the susceptibility genes in these regions were designated Ecs1, Ecs2 and Ecs3. Our results indicate that the genes affecting susceptibility to EAC are different in the 2 crosses, suggesting that the genes behind the susceptibility in BDII animals may interact with different genes in different genetic backgrounds. © 2001 Wiley-Liss, Inc.

Genetic predisposition

Inbred strain

Inheritance

Identification

10.1002/ijc.1553

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Citations (26)

Mo1782 Disruption of the TLR4 Pathway Leads to Dysfunction of the Intestinal Barrier in an Escherichia coli Nissle Monoassociation Model - Implication for Experimental Inflammatory Bowel Disease Susceptibility

Gastroenterology (2012)

Marijana Basic Lydia M. Keubler Anna Smoczek Andrea Liese Hans J. Hedrich

10.1016/s0016-5085(12)62636-5

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Citations (0)

Histological Examination in a Blind-deafness Rat Mutant – A Rodent Model for Usher Syndrome Phenotype 1

Investigative Ophthalmology & Visual Science (2003)

S. Lindemann Kenji Kamino Dirk Wedekind Hans J. Hedrich R M Winter

Rodent model

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Citations (2)

Management of immunocompromised and infected animals

Methods in microbiology (2002)

Horst Mossmann Werner Nicklas Hans J. Hedrich

Isolation

Best practice

Constructive

10.1016/s0580-9517(02)32093-2

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Citations (1)

Localization of the Pfkfb 2 gene on rat Chromosome 13

Mammalian Genome (1996)

Michael Pape C.-M. Prokop Hans J. Hedrich

Human genetics

10.1007/s003359900288

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Citations (3)

The circling behavior of the deafblind LEW- ci2 rat is linked to a segment of RNO10 containing Myo15 and Kcnj12

Mammalian Genome (2003)

Wojciech T. Chwalisz Bernd Koelsch Andrea Kindler-R�hrborn Hans J. Hedrich Dirk Wedekind

Human genetics

10.1007/s00335-003-3009-x

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Citations (11)

Taxonomy and Stocks and Strains

Elsevier eBooks (2006)

Hans J. Hedrich

Congenic

Inbred strain

Strain (injury)

Laboratory rat

Laboratory mouse

10.1016/b978-012074903-4/50006-6

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Citations (23)

Analysis of Cd14 as a genetic modifier of experimental inflammatory bowel disease (IBD) in mice

Inflammatory Bowel Diseases (2009)

Maike F. de Buhr Hans J. Hedrich Astrid M. Westendorf Florian Obermeier Claudia Hofmann

By combining QTL and gene expression analyses, we have previously identified Cd14 as a potential candidate gene contributing to the differential IBD susceptibility of C3H/HeJBir (C3/J)-Il10(-/-) mice [carrying IBD-resistance alleles at this QTL (Cdcs6)] and C57BL/6J (B6)-Il10(-/-) mice, corroborating studies that showed an association of a CD14-promoter polymorphism with Crohn's disease and ulcerative colitis. The aim of the present study was to analyze the molecular mechanisms leading to differential intestinal expression of Cd14 and its contribution to IBD development.Intestinal CD14 expression was assessed by FACS, immunohistochemistry, and ELISA on supernatants of primary epithelial cell and tissue cultures. RAW264.7 cells were stimulated with LPS and PGN in the presence or absence of CD14. Cd14 alleles were sequenced and promoters cloned for luciferase assays in transfected RAW264.7 cells. The severity of typhlocolitis between Cd14(-/-) and wild-type mice was compared in 2 distinct mouse models of IBD (acute DSS and Il10(-/-) ).In the gut, CD14 was detected mainly in its soluble form (sCD14), with higher expression in C3/J-Il10(-/-) mice. Polymorphisms in C3/J mice caused higher activity of the Cd14 promoter (luciferase assays). Intestinal sCD14 concentrations influenced the LPS and PGN responses of RAW264.7 cells. In vivo, genetic deletion of Cd14 aggravated colitis in both mouse models of IBD.Our study shows that Cd14-promoter polymorphisms affect CD14 expression and confirms the protective effect of CD14 against experimental IBD, potentially mediated by TLR2- and TLR4-dependent effects on intestinal barrier function. These findings support the concept that human CD14-promoter polymorphisms contribute to disease development.

10.1002/ibd.21030

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Citations (24)

Experimental middle ear surgery in rabbits: a new approach for reconstructing the ossicular chain

Laboratory Animals (2009)

Martin Stieve Hans J. Hedrich R.-D. Battmer Peter Behrens Peter Müller

This experimental animal study aimed at evaluating a new prosthesis to replace the ossicular chain; we developed a new technique for surgical implantation into the middle ear of rabbits. The rabbit middle ear is, owing to the relative anatomical dimensions involved, an ideal environment for implantation procedures involving the ossicles, as the surgical conditions are similar to those of the human middle ear. This study included a total of 34 approximately six-month-old female white rabbits (New Zealand) weighing between 3.2 and 4.4 kg. The implants used were constructed of ceramic materials (titania, TiO(2)) of various pore sizes. Directly prior to implanting the total ossicular reconstruction prostheses (TORPs), as well as at 28, 84 and 300 days after implantation, electric response audiometry was used to determine the hearing thresholds of the animals (bone conduction; click stimulus nHL). An erbium:YAG laser was used to excise the original ossicular chain. Following implantation, we were unable to detect any stenosis of the outer ear canal or perforation of the tympanic membrane. The conductive hearing threshold was in the range of 4.21 +/- 6.68 dB nHL (n = 131). The hearing level showed no significant difference before and after surgery (P < 0.05).

Ossicles

Bone conduction

Conductive hearing loss

10.1258/la.2008.007152

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Citations (15)

Re-evaluation of LG V of the rat and assignment of 12 carboxylesterases to two gene clusters

Journal of Heredity (1987)

Hans J. Hedrich O. v. Deimling

Examining the strain distribution pattern of the recombinant Inbred strain series LXB and DXE and of backcross progeny of (LEW×LE) F1 × LEW, (LEW×BN) F1 × LEW, and (LEW×BN) F1 × BN for esterase markers, including three carboxylesterase allozymes (ES-15, ES-16, ES-18), hitherto not studied genetically, revealed the existence of two esterase gene clusters within LG V: cluster 1, containing Es-2, Es-8, Es-10, Es-3, Es-7, Es-9, and separated by 8.8 ± 1.3 cM from cluster 2, containing Es-1, Es-14 (formerly Es-SI), Es-15, Es- 16, and Es-18. Analyses of 93 inbred strains of rats showed only 12 and 6 haplotypes for cluster 1 and cluster 2, respectively, Indicating a strong linkage disequilibrium. These data and serotyping results of one backcross population for the RT2 blood group system lead to a re-evaluation of linkage group V. Including literature data the following gene order is suggested: RT2 – (7.1 ± 1.8) Es-2, Es-4, Es-8, Es-10 (2.7 ± 0.7) Es-3, Es-7, Es-9 (8.8 ± 1.3) Es-7, Es-14, Es-15, Es-16, Es-18.

Carboxylesterase

Linkage Disequilibrium

Esterase

Inbred strain

Gene cluster

10.1093/oxfordjournals.jhered.a110343

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Citations (22)