Inaug.-diss.--Greifswald. / Lebenslauf. At head of title: Romanische philologie. "Literatur": p. [120]-125.

Mémoire (M.A.)--Université du Québec à Trois-Rivières, 2003. / Bibliogr.: f.[170]-182.

A company’s ability to support its business strategy with it’s Human Capital is an important indication of the company’s future business performance. No standard or framework to enable the inclusion of Human Capital information in company reporting to demonstrate the effect on performance currently exists. Traditional HR metrics fail to report on the level of performance, knowledgebase or value of Human Capital, making it virtually impossible for stakeholders or valuators of companies to take this most important asset into account in valuing the company against it’s competitors. This exploratory study has been commissioned to add new theory which would span further research with the objective of improving the reporting systems and/or methodologies to value Human Capital for South African industry. The study poses the following questions: 1. What insight should investors and other external stakeholders have into the Human Capital employed by a specific organisation? 2. How best to ensure that Human Capital is reported and the information is trusted by investors and other stakeholders as seen as relevant, reliable and consistent, adding value to shareholders? 3. Which Human Resource Management components can form a basis for comparative external reporting on Human Capital (if any)? The study created an innovative framework for reporting which, is viewed as an improved, practical and theoretical approach and method relating to Human Capital and value creation for Human Assets. Triangulation was used to include a number of different metrics used by HR, linked to a framework that allows those who uses it to link quantitative calculations to Human Capital dimensions. Further testing may be required due to the limited insight and knowledge of current practitioners which may have skewed some of the results. This framework also links to a number of business questions and metrics which in turn, link to broader HR strategic themes and recommendations for reporting as part of company annual reports and which Human Capital aspects should be included as standard in such a report. The study provides Human Resource practitioners with the ability to counter the one-sidedness of viewing people as purely costs, demonstrating the value of Human Assets in quantitative terms. / Thesis (PhD (Organisational Behaviour))--University of Pretoria, 2006. / Human Resource Management / unrestricted

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

<p>Hypoxia-reoxygenation (H-R) injury is an important clinical phenomenon in patients with coronary artery disease (CAD). Endothelial injury is a critical step in the initiation and progression of atherosclerosis. Therefore, endothelial and cardiomyocyte protection has been considered an effective step in prevention and treatment of CAD.</p><p>To investigate the cardioprotective effect of tocopherols, omega-3 fatty acid [eicosapentaenoic acid (EPA)] and transforming growth factor-β₁ (TGF-β₁) during H-R, calcium tolerant myocytes isolated from adult rats were cultured and subjected to hypoxia for 24 hrs followed by reoxygenation of 3 hrs. All strategies, including tocopherol preparations, EPA and TGF-β₁, showed attenuation of H-R-induced myocyte injury indicated by reduction of lactate dehydrogenase (LDH) release. Both a-tocopherol and a mixed- tocopherols (α-, γ-, and δ-) decreased the effects of H-R on iNOS expression and SOD activity in cultured myocytes. The mixed-tocopherols was more potent than a-tocopherol alone. EPA inhibited H-R-induced lipid peroxidation, MMP-1 expression and p38MAPK phosphorylation. TGF-β₁ blocked the increase in iNOS and PKB phosphorylation as well as the decrease in eNOS expression in cultured myocytes exposed to H-R.</p><p> To further investigate the protective effect of omega-3 fatty acids [docosahexaenoic acid (DHA) and EPA] and TGF-β₁, the cultured endothelial cells were exposed to oxidant injury mediated by oxidized low-density lipoprotein (ox-LDL). Ox-LDL markedly reduced TGF-β₁ release, increased the expression of TGF-β₁ receptors, upregulated the expression of adhesion molecules, P-selectin and ICAM-1, enhanced the adhesion of monocytes to endothelial cells, and decreased protein kinase B (PKB) activation. Both DHA and EPA blocked these effects of ox-LDL on endothelial cells. Exogenous recombinant TGF-β₁ also ameliorated ox-LDL-induced expression of adhesion molecules and monocytes adhesion, which were blocked by antibodies to the TGF-β₁ type 2, but not to the type 3 receptor.</p><p>These observations provide mechanistic insights into H-R and oxidant injury and tissue protection by three different strategies.</p>

Hypoxia-reoxygenation (H-R) injury is an important clinical phenomenon in patients with coronary artery disease (CAD). Endothelial injury is a critical step in the initiation and progression of atherosclerosis. Therefore, endothelial and cardiomyocyte protection has been considered an effective step in prevention and treatment of CAD. To investigate the cardioprotective effect of tocopherols, omega-3 fatty acid [eicosapentaenoic acid (EPA)] and transforming growth factor-β1 (TGF-β1) during H-R, calcium tolerant myocytes isolated from adult rats were cultured and subjected to hypoxia for 24 hrs followed by reoxygenation of 3 hrs. All strategies, including tocopherol preparations, EPA and TGF-β1, showed attenuation of H-R-induced myocyte injury indicated by reduction of lactate dehydrogenase (LDH) release. Both a-tocopherol and a mixed- tocopherols (α-, γ-, and δ-) decreased the effects of H-R on iNOS expression and SOD activity in cultured myocytes. The mixed-tocopherols was more potent than a-tocopherol alone. EPA inhibited H-R-induced lipid peroxidation, MMP-1 expression and p38MAPK phosphorylation. TGF-β1 blocked the increase in iNOS and PKB phosphorylation as well as the decrease in eNOS expression in cultured myocytes exposed to H-R. To further investigate the protective effect of omega-3 fatty acids [docosahexaenoic acid (DHA) and EPA] and TGF-β1, the cultured endothelial cells were exposed to oxidant injury mediated by oxidized low-density lipoprotein (ox-LDL). Ox-LDL markedly reduced TGF-β1 release, increased the expression of TGF-β1 receptors, upregulated the expression of adhesion molecules, P-selectin and ICAM-1, enhanced the adhesion of monocytes to endothelial cells, and decreased protein kinase B (PKB) activation. Both DHA and EPA blocked these effects of ox-LDL on endothelial cells. Exogenous recombinant TGF-β1 also ameliorated ox-LDL-induced expression of adhesion molecules and monocytes adhesion, which were blocked by antibodies to the TGF-β1 type 2, but not to the type 3 receptor. These observations provide mechanistic insights into H-R and oxidant injury and tissue protection by three different strategies.

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