Thesis (Ph. D.)--Michigan State University. Dept. of Animal Science, 2006. / Title from PDF t.p. (viewed on Nov. 16, 2008) Includes bibliographical references. Also issued in print.

Thesis (M.Sc.)--York University, 2006. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 66-88). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR19754

Thesis (Ph. D.)--University of Texas at Austin, 2006. / Vita. Includes bibliographical references.

Thesis (M. Phil.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 118-130) Also available in print.

Thesis (doctoral)--Karolinska Institutet, Stockholm, 1993. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (doctoral)--Karolinska Institutet, Stockholm, 1993. / Added t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (Ph. D.)--Ohio State University, 2006. / Title from first page of PDF file. Includes bibliographical references (p. 77-90).

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

I have used a molecular genetic approach to study early events in the gene network that precede apoptotic commitment in glucocorticoid-induced thymocyte apoptosis. A panel of recessive, apoptotic-deficient (Apt⁻) mutants were isolated that are cross resistant to several diverse apoptotic treatments. These results indicated that the signal pathways initiated by glucocorticoids, gamma radiation, and c-AMP analog treatment converge to a common apoptotic pathway. Complementation analysis of Apt⁻ cell lines has defined five independent complementation groups that appear to represent mutations in genes that are required for apoptotic commitment. In addition, I have characterized induced gene expression patterns characteristic of dexamethasone (dex)-induced apoptosis and have found that glutathione-s-transferase (GST), Dag8 (a gene of unknown function) and calmodulin (Cam) transcript levels are elevated following dex treatment. Dex-treatment of Apt⁻ cell lines does not change GST or Cam transcript levels which suggests that these cell lines are blocked in early steps of the apoptotic pathway. In contrast, the dominant oncogene, Bcl-2, blocks apoptosis and appears to affect a relatively late event in the apoptotic pathway since the pattern of dex-induced gene expression is normal in cells that express this protein. Since the Apt⁻ cells contain wild type levels of functional glucocorticoid receptor (GR), GST and Cam do not appear to be primary GR target genes, but seem to respond to cellular events that occur prior to apoptotic commitment. In support of this conclusion, it was found that GST transcript levels increase in calcium ionophore-induced apoptotic cells. In contrast, Dag8, transcript levels increased in dex-treated Apt⁻ cells indicating that Dag8 is most likely a primary GR target gene. Furthermore, Dag8 expression was found to be restricted to thymocyte containing tissues and its locus was mapped to the H2 complex of chromosome 17, a region that is known to contain many immunologically important genes. Finally, a model is presented to describe a common apoptotic pathway in murine thymocytes and proposes that an increase in oxidative stress precedes calcium mobilization in response to glucocorticoid treatment.

Charles University Faculty of Pharmacy in Hradec Králové Department of Pharmacology & Toxicology Student: Katarína Tripská Supervisor: prof. PharmDr. Petr Pávek, Ph.D. Title of diploma thesis: miRNAs as diagnostic markers after treatment with glucocorticoids in rheumatology MicroRNAs are important class of non-coding RNAs that play important role in modulation of expression of multiple genes at a post-transcriptional level. Their deregulation contributes to many immune disorders including rheumatoid arthritis, systemic lupus erythematosus and systemic sclerosis. This thesis represents the most recent knowledge about functions of microRNAs in pathogenesis of these disorders and results were obtained by review of scientific literature published on PubMed database. The most perspective microRNAs in rheumatoid arthritis seem to be miR-16, miR-21, miR- 146a, miR-150 a miR-223. In lupus miR-148, miR-126, miR-21, miR-155, miR-125a a miR- 146 will probably find their useage as biomarkers. Systemic sclerosis is less examined diseases and we know most about miR-29 in the disease. Since the research of microRNA as diagnostic biomarkers is only at the beginning, it is most likely, that with the time there will be more and more of new microRNAs helping us clarify pathogenesis of each disorder. We can suppose...