Thesis (Ph. D.) -- University of Alberta, 2009. / "A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Counselling Psychology, Department of Educational Psychology, University of Alberta." Title from pdf file main screen (viewed on August 31, 2009). Includes bibliographical references.

<p> Age-Related Resistance (ARR) has been observed in numerous plant species, resulting in increased disease resistance as the plant matures. The ARR defective mutant, iap1-1, (important in the ARR Pathway,) was discovered in an ARR mutant screen and EDS1, (enhanced disease susceptibility,) which is involved in other disease resistance pathways, was shown to be required for ARR. lntercellular accumulation of salicylic acid (SA) is required for ARR suggesting that SA may act as an anti-microbial agent. Mature (6 wpg) iap1-1 does not accumulate intercellular or intracellular SA in response to Pst inoculation. lntercellular and intracellular SA accumulation is also partially reduced in young (4 wpg) plants during R gene-mediated resistance to Pst(AvrRpt2) which is partially compromised suggesting that the two pathways share common elements. The novel discovery of the presence of intercellular SA during R gene-mediated resistance suggests that it may act as an antimicrobial agent during R gene-mediated resistance as it is hypothesized to during ARR. The iap1-1 mutation maps to chromosome four between 17,938,268bp and 18,133,423b. The semi-dominant, loss of function nature of the iap1-1 mutation suggests that IAP1 is a positive regulator in the ARR pathway.</p> / Thesis / Doctor of Philosophy (PhD)

Thesis (M.S.)--University of Michigan, 1992.

Thesis (M.S.)--University of Michigan, 1992.

Research project (M.S.N.)--University of North Carolina at Wilmington, 2005. / Includes bibliographical references (leaves: [42]-46)

Thesis (Ph. D.)--University of North Texas, Dec., 2009. / Title from title page display. Includes bibliographical references.

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown aetiology, characterised by the progressive and irreversible scarring of parenchymal lung tissue that leads to respiratory failure and death. The disease is understood to be driven by an impaired and aberrant wound healing response, with an inappropriate reactivation of developmental signalling. The greatest risk factor for the disease is age, which is a process intimately associated with an increase in the burden of senescent cells. Such cells acquire a unique secretory phenotype and are known to have a significant impact on their local micro-environment. It was hypothesised that an alteration in epithelial-mesenchymal secretory communication, due to senescent-like changes in the fibroblast phenotype, may detrimentally contribute to lung homeostasis. An in vitro model of the lung airway was established in which primary human lung fibroblasts (HLFs) were co-cultured with human bronchial epithelial cells (HBECs). HBECs were cultured on a semi-permeable, transwell insert and co-cultured with either normal (NHLF), fibrotic (FHLF) or senescent fibroblasts. Over 72 hrs of co-culture, wound healing was assessed, via an epithelial scratch assay, and epithelial regeneration was measured, via trans-epithelial electrical resistance. Co-culture with NHLFs improves epithelial regeneration, however, FHLFs and senescent cells in co-culture show a diminished ability to promote epithelial regeneration and wound repair. The secretory repertoire of these cells contains elevated levels of IL-6, CXCL8, CXCL1 and GCSF (when assessed at both an RNA and protein level), factors strongly associated with the senescent phenotype. Targeting this secretome via treatment with the JAK 1/2 inhibitor Ruxolitinib attenuates these impairments and may point towards a new therapeutic strategy for the treatment of IPF.

During mitogen-induced transformation of human lymphocytes, phosphoglycerate kinase (PGK) exhibits new electrophoretic forms (pl=8.5-8.9). Electrophoresis and electrofocusing showed that the new forms are not due to expression of the autosomally linked isozyme found in semen (PGK-B; pl=9.7). The multiple electrophoretic forms are the result of protease modification of sex-linked PGK-A isozyme.When peripheral lymphocytes from young persons are stimulated in vitro with phytohemagglutinin, a selective increase in the levels of the glycolytic enzymes occurs concomitantly with blastogenesis. Human lymphocytes from a geriatric population were also subjected to mitogen stimulation. The initial levels of the enzymes were essentially identical in lymphocytes from young and old subjects as were mitogenfree cultured controls. However, during mitogen stimulation the cells from the old subjects failed to increase the glycolytic enzymes. This inability to activate glycolysis may be related to the decline in cell-mediated immunity which occurs with advancing age. Triosephosphate isomerase (TPI) has an increased thermolabile component in skin fibroblasts from patients with progeria (41.4 per cent)and Werner's syndrome (20.1 per cent) when compared with normal fibroblasts (0-3 per cent). The incorporation of various protease inhibitors failed to affect the percentages of heat-labile triosephosphate isomerases. The labile component appears to be identical to the deamidated form of the enzyme which accumulates in other aging cells. Isoelectric focusing demonstrated increased quantities of the deamidated TPI-A form in progeria and Werner's syndrome fibroblasts as compared to normal. The deamidated TPI-A was considerably more labile than the native TPI-B indicating the increased lability of triosephosphate isomerase in premature aging syndrome fibroblasts is due to an accumulation of the deamidated form of the enzyme. The levels of several proteases were found to be diminished in progeria fibroblast extracts as compared to normal. A deamidation mechanism of enzyme degradation plays a key role in the normal cellular catabolism of this enzyme and the mechanism for accumulation of defective forms in aging cells is apparently exacerbated by an impaired proteolytic capacity.

The author in her diploma theses deals with the problem of elderly suicide rates in the helping professionals' point of view in the district of Karlovy Vary. Her two key focus areas are personal experiences of the helping professionals with this particular topic and their knowledgeableness of it. Furthermore, the author validates whether the helping professionals are supported adequately enough to be able to deal with this phenomenon appropriately. In the theoretical part of the study the author presents basic introduction into the issue of suicide itself - briefly outlines the history of suicide rate and the most common motive, causes and forms of suicidal behavior. Moreover, she sketches the specifics of suicide rate among seniors and ways of working with this particular target group. Last but not least she drafts possible preventive techniques of suicide behavior among seniors. In the empirical part of the study the author explains the research methodology and briefly describes the district of Karlovy Vary. Most importantly the author presents findings concerning experience and knowledgeability of suicide rate among seniors by helping professionals gathered by research consisting of semi-structured interviews. She also thoroughly examines the professionals' point of view on individual elements...