161 |
Biochemical and physiological characterization of the human myometrial corticotropin-releasing hormone receptor : a role in the control of parturition?Grammatopoulos, Dimitris Kyriakou January 1995 (has links)
No description available.
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162 |
The role of nitric oxide in cervical ripeningLedingham, Marie Anne January 2000 (has links)
No description available.
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163 |
The energy requirements of pregnant rural Thai womenThongprasert, K. January 1986 (has links)
No description available.
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164 |
The peripheral venous system in health and diseaseStainer, Karen Louise January 1989 (has links)
No description available.
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165 |
Progesterone and fertility in the dairy cowStarbuck, Gareth Robert January 2000 (has links)
No description available.
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166 |
Trophoblast-endothelial cell interactions in the maternal syndrome of pre-eclampsiaSmarason, Alexander Kristinn January 1993 (has links)
No description available.
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167 |
Syncytiotrophoblast microvillous membrane deportation in the pathogenesis of pre-eclampsiaKnight, Marian January 1997 (has links)
No description available.
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168 |
Cortico steroid metabolism by human intra-uterine tissues in relation to parturitionLopez Bernal, A. January 1984 (has links)
No description available.
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169 |
Heightened maternal inflammation is linked to placental oxidative and nitrosative stress associated with fetal growth restriction in the ratSperou, Arissa 05 July 2013 (has links)
Deficient trophoblast invasion and spiral artery remodeling are associated with pregnancy complications such as pre-eclampsia (PE) and fetal growth restriction (FGR). Using a model in which pregnant Wistar rats are given daily, low-dose, injections of bacterial lipopolysaccharide (LPS; 10 – 40 µg/kg) on gestational days (GD) 13.5 – 16.5, our group has shown that abnormal maternal inflammation is causally linked to shallow trophoblast invasion, deficient spiral artery remodeling, and altered utero-placental hemodynamics leading to FGR/PE; these alterations were shown to be mediated by TNF-a. The present research evaluated certain consequences of decreased placental perfusion; this was accomplished by examining placental alterations indicative of decreased placental perfusion. Additionally, the role of glyceryl trinitrate (GTN) was determined as a potential therapeutic to prevent the consequences of decreased placental perfusion. Results indicated that dams experiencing heightened maternal inflammation showed significantly greater expression of hypoxia-inducible factor-1a (HIF-1a) and nitrotyrosine, both of which are markers of decreased perfusion and oxidative/nitrosative stress. Contrary to expectations, inflammation did not appear to affect nitric oxide (NO) bioavailability, as revealed by a lack of change in placental or plasma levels of cyclic guanosine monophosphate (cGMP). However, continuous transdermal administration of GTN (25 µg/hr) on GD 12.5 – 16.5 prevented the accumulation of HIF-1a and nitrotyrosine in placentas from LPS-treated rats. These results support the concept that maternal inflammation contributes to placental hypoxia and oxidative/nitrosative stress. Additionally, they indicate that GTN has potential applications in the treatment and/or prevention of pregnancy complications associated with abnormal maternal inflammation. / Thesis (Master, Anatomy & Cell Biology) -- Queen's University, 2013-07-05 14:37:05.15
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Use of red palm oil in vitamin A deficiency : studies on its analysis, stability and field applicationLietz, Georg January 2000 (has links)
No description available.
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