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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.
11

The development of Interleukin-6 specific peptide antagonists

Bailey, Louise Lyn January 1999 (has links)
No description available.
12

Manipulation and control of thermoregulation in the newborn lamb

Clark, Lynne January 1994 (has links)
No description available.
13

Studies on ovine adipocyte precursor cells in vitro

Cryer, Jennifer January 1993 (has links)
No description available.
14

Mammary development and the role of leptin

Ong, Eddie January 2002 (has links)
No description available.
15

Some factors affecting the stability of skin tissue fat

Wingerd, Winston Harold. January 1949 (has links)
LD2668 .T4 1949 W52 / Master of Science
16

The role of Dlk1 in in vivo adipogenesis

Cassidy, Fearon January 2018 (has links)
Misregulation of Dlk1, a paternally expressed imprinted gene, is known to cause adipose phenotypes in both mice and humans. It is now known that the type of fat a person has, the location of and type of expansion are all important factors for the epidemic of obesity-related diseases, yet there is little understanding of the factors that influence which depots expand, and how. This project investigates how Dlk1, expressed primarily during embryogenesis, effects adulthood adiposity, which has shed light on the mechanism by which embryonic insults affect adulthood adipose physiology and resultant metabolic disease. Much previous work has been done on the role of Dlk1 in adipogenesis in vitro, however little is known of its role in this process in vivo. To achieve an in vivo investigation of its role in adipogenesis, adipose tissue has been measured in mice with deleted Dlk1 from embryo through early life and into adulthood. Gross measurement has been supported by mechanistic interrogation of adipose expandability using a triple transgenic adipocyte labelling mouse model, results from which are the most comprehensive to date in a wild type context and reveal insight into the Dlk1 knock-out phenotype. Results indicate a complex and dynamic role of Dlk1 that is interlinked with overall growth in mice. Moreover new evidence is presented here for tissue specific c imprinting of Dlk1 in some adipose cell types with consequential growth and adipose alterations in Dlk1 heterozygote mice that do not follow the expected phenotype of imprinted gene knock-out models.
17

The Therapeutic Efficacy of Adipose Stromal Cells in a Model of Multiple Sclerosis

January 2017 (has links)
acase@tulane.edu / Multiple sclerosis (MS) is a common neurodegenerative disease and remains an unmet clinical challenge. In MS, an autoimmune response leads to immune cell infiltration, inflammation, demyelination, and lesions in central nervous system (CNS) tissues resulting in tremors, fatigue, and progressive loss of motor function. These pathologic hallmarks are effectively reproduced in the murine experimental autoimmune encephalomyelitis (EAE) model. Using the EAE mouse, we have defined critical time points during the disease progression that have correlative immunopathology with those that occur in MS. As promising therapeutic alternatives to treat MS, we investigated the fresh, heterogeneous population of cells from adipose called the stromal vascular fraction (SVF), which contains adipose-derived stromal/stem cells (ASCs). With these studies, we evaluated the therapeutic efficacies of fresh SVF cells and culture-expanded ASCs at early and late stage EAE disease after intraperitoneal (i.p.) administration. At early stage EAE disease, autoimmune reactions and inflammation are prevalent in the periphery lead to CNS damage by the infiltration of cells that generate inflammatory and demyelinating lesions. We demonstrated that at this time, treatment with SVF cells and ASCs were incapable of attenuating CNS pathology. However, the potency of SVF cells to suppress the autoimmune reactions in the periphery was strong enough to partially ameliorate motor impairments. Furthermore, we revealed the altered gene expressions of the SVF cells and ASCs when exposed to this pathogenic milieu in vitro. Not only did we show that the majority of the helper T (TH) cells contained within the SVF are of the TH2 phenotype, but the most enhanced cytokines in response to the inflammatory milieu were interleukin-10 (IL-10) and transforming growth factor-β (TGFβ) which promote regulatory T cells (Tregs). The most dominant increase detected in ASCs was interleukin-6 (IL-6) which correlates with the inability of ASCs to suppress the activities of the pathogenic T cells at early stage disease. At late stage disease, we showed the greatest improvements in SVF-treated EAE mice that led to amelioration to pathology in CNS tissues and partial restoration of motor function. The most pronounced changes following SVF treatment were the high levels of IL-10 in the peripheral blood, lymphoid and CNS tissues along with the induction of regulatory T cells in the lymph nodes which indicated potent immunomodulatory effects. These effects were not as robust following ASC treatment. A deeper investigation into the potential mechanisms showed phenotypes of T cells and macrophages skewed towards favorable phenotypes. SVF treatment shifted the TH cell subsets away from the effector TH1 and TH2 and toward the Tregs which promote immune tolerance and anti-inflammatory effects. Furthermore, the Treg-associated effects involve the induction of the alternative activation phenotype of macrophages, or M2, which were evidenced in the spleens and CNS tissues of SVF-treated EAE mice. Moreover, we determined that i.p. injected ASCs, and more so, SVF cells were still present in the spleens of EAE mice after 5 days. Together, we investigated a novel modality for treating an inflammatory, autoimmune disease. By comparison with ASC treatment, we demonstrated potential mechanisms of SVF treatment at early and late stage EAE disease that are translational to the inflammatory and demyelinating phases MS disease, respectively. We determined that the timing of administration is most critical, and once active immune activities subside, SVF treatment provides robust and comprehensive effects for improving CNS damage. Additionally, these mechanisms may translate and help explain the favorable effects with current clinical applications such as cell-assisted liposuction that uses SVF cells for improving fat grafting yet mechanisms are still unclear. / 1 / Annie C. Bowles
18

Adipose related signaling in syndromic obesity /

Zheng, Yue, January 2009 (has links)
Thesis (M.S.) in Biochemistry--University of Maine, 2009. / Includes vita. Includes bibliographical references (leaves 44-48).
19

Percent body fat and fat distribution are not associated with carotid artery intima-media thickness in healthy middle-aged women /

Goff, Kayleen Adams, January 2008 (has links) (PDF)
Thesis (M.S.)--Brigham Young University. Dept. of Exercise Sciences, 2008. / Includes bibliographical references.
20

Association of adiponectin gene variants and adiponectin level with ischemic stroke in a Chinese cohort

Lam, Ka-yan, 林嘉茵 January 2009 (has links)
published_or_final_version / Medicine / Master / Master of Philosophy

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