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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
41

Neuroprotective effects of adiponectin in focal cerebral ischemia

Ng, Kit-ying, 吳潔瑩 January 2007 (has links)
published_or_final_version / abstract / Medicine / Master / Master of Philosophy
42

The association of adiponectin with cardiovascular disease and endothelial progenitor cell

Li, Mingfang, 酈明芳 January 2009 (has links)
published_or_final_version / Medicine / Doctoral / Doctor of Philosophy
43

Regulation of adipose tissue function by bone morphogenic protein 8b

Peirce, Vivian Julia January 2015 (has links)
No description available.
44

Midthigh adipose tissue infiltration in children with cerebral palsy

Johnson, David L. January 2007 (has links)
Thesis (M.S.)--University of Delaware, 2007. / Principal faculty advisor: Christopher M. Modlesky, Dept. of Health, Nutrition, and Exercise Sciences. Includes bibliographical references.
45

Regulation and function of Skp2 in mediating p27 degradation during adipocyte hyperplasia

Auld, Corinth Andrews. January 1900 (has links) (PDF)
Thesis (Ph. D.)--University of North Carolina at Greensboro, 2006. / Advisor: Ron Morrison; submitted to the School of Human Environmental Sciences. Includes bibliographical references.
46

The association of adiponectin with cardiovascular disease and endothelial progenitor cell

Li, Mingfang, January 2009 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2010. / Includes bibliographical references (leaves 118-145). Also available in print.
47

Regulation of vascular integrity by eNOS and adiponectin: a novel role of endothelial progenitor cells

Chang, Junlei., 畅君雷. January 2011 (has links)
Background and objectives: Circulating endothelial progenitor cells (EPCs) play an essential role in maintaining vascular integrity and preventing endothelial dysfunction. Decreased circulating EPC levels are frequently observed in various cardiovascular risks, including aging and diabetes. Endothelial nitric oxide synthase (eNOS) and adiponectin exert their vasculo-protective effects by directly targeting the key components of the vascular system, such as endothelial cells and smooth muscle cells. Both eNOS and adiponectin have been implicated in the mobilization and in vitro functions of EPCs. However, whether and how circulating EPCs are involved in eNOS and adiponectin-mediated vascular protection remain unclear. The objective of this study is to investigate the role of circulating EPCs in eNOS and adiponectin-mediated regulation of vascular integrity after arterial injury under both physiological and pathophysiological conditions, and to elucidate the underlying mechanisms involved. Key findings: 1. Modulation of eNOS activity in vivo by replacing the serine 1176 (S1176) with an aspartate (S1176D mutation or Dki) to mimic phosphorylation or with an alanine (S1176A mutation or Aki) to render it unphosphorylatable altered reendothelialization and subsequent endothelial function after arterial injury in mice. 2. eNOS S1176D mutation increased the number of circulating EPCs and their incorporation into regenerated endothelium, whereas eNOS S1176A or knockout (KO) impaired the mobilization and reendothelializing capacity of circulating EPCs after injury. 3. eNOS S1176D elevated circulating EPCs by promoting the proliferation and differentiation of bone marrow hematopoietic stem cells (HSCs) into EPCs and by inhibiting apoptosis of circulating EPCs. 4. Adiponectin deficiency in mice resulted in progressive decrease of circulating EPCs with aging. Systemic administration of recombinant adiponectin reversed the decreased EPCs number in adiponectin KO mice. In db(-/-) diabetic mice, adiponectin deficiency further reduced circulating EPCs number and subsequent reendothelialization after injury. Rosiglitazone (Rosi), an antidiabetic drug, induced an upregulation of EPCs number and improved reendothelialization, which were partially abolished in the absence of adiponectin. 5. In cultured EPCs, adiponectin significantly inhibited high glucose-induced premature senescence, whereas its effects on proliferation and apoptosis were not evident. High glucose instigated EPCs senescence by increasing the intracellular accumulation of reactive oxygen species (ROS), activation of p38 MAPK and expression of p16INK4A, whereas all these changes could be abolished by adiponectin through adenosine monophosphate (AMP)-activated protein kinase (AMPK) and cyclic AMP (cAMP)/protein kinase A (PKA)-dependent pathways. 6. Compared to cells from db(-/-) diabetic mice, bone marrow EPCs isolated from db(-/-) plus adiponectin double KO (DKO) mice were more susceptible to high glucose-evoked senescence, which were abrogated by adiponectin in vitro. Importantly, chronic administration of adiponectin or the anti-oxidant N-acetylcysteine (NAC) prevented both aging and diabetes-associated elevation of p16INK4A and decline of circulating EPCs in DKO mice. Conclusions: Collectively, the current study demonstrates that circulating EPCs are actively involved in the vasculo-protective effects of both eNOS and adiponectin under physiological and pathological conditions. These findings enrich our knowledge of the versatile functions of eNOS and adiponectin in vascular protection and provide solid scientific evidence supporting the use of eNOS and adiponectin as possible therapeutic targets for cardiovascular diseases. / published_or_final_version / Medicine / Doctoral / Doctor of Philosophy
48

In vitro modelling of proximal insulin signalling defects in adipocytes : insights into monogenic human disorders

Groeneveld, Matthijs Pieter January 2013 (has links)
No description available.
49

The role of lipid accumulation and insulin signaling in adipose tissue macrophage polarization

Mok, Crystal Yin Lam January 2013 (has links)
No description available.
50

Effects of dietary fatty acid composition and energy restriction on adipose tissue obese mRNA, fatty acid composition and serum leptin levels

Hynes, Geoffrey Ronald January 2002 (has links)
Dietary fatty acid (FA) composition and energy restriction (ER) independently affect serum leptin levels; however it is not known whether this correlates with changes in obese (ob) gene expression. Herein, we assessed whether dietary FA composition and ER influence white adipose tissue (WAT) ob mRNA by Northern analysis. Animals consumed diets containing tallow (BT), safflower oil (SO) or fish oil (FO) ad libitum or at 60% ad libitum intakes. Serum leptin values were not different between levels of energy intake. ER decreased weight gain and WAT weights, which positively correlated with serum leptin values. WAT ob mRNA levels were in the rank order: FO > SO > BT in depots of all groups with ER showing a lower level of ob mRNA. Data show similarity in ob mRNA levels between depots with discordance in circulating leptin levels. These data suggest that energy restriction exerts greater control over leptin production than dietary fat source.

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