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alkaline phosphatase/hypoxie

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Expression of muscle capillary alkaline phosphatase is affected by hypoxia.

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Hypoxia stimulates angiogenesis in some microvascular beds, but no clear angiogenic effect of hypoxia has yet been demonstrated in adult skeletal muscle. In this study the distribution of alkaline phosphatase (APase) was compared with a novel microvascular marker, Griffonia simplicifolia I (GSI), to
Hypoxia cooperates with endocrine signaling to maintain the symmetric self-renewal proliferation and migration of embryonic germline stem cells (GSCs). However, the lack of an appropriate in vitro cell model has dramatically hindered the understanding of the mechanism underlying this cooperation.

Effect of beta-interferon on vascular density, mitochondrial metabolism and alkaline phosphatase in normoxia and hypoxia.

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[Behavior of histochemically detected alkaline phosphatase and 5-nucleotidase in oxygen deficiency and renal infarction].

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Organisms at all levels of evolutionary complexity react to hypoxic stress. To clarify the effects of acute hypoxia on physiological and biochemical responses of Larimichthys crocea, we measured the activity levels of the antioxidant enzymes superoxide dismutase and catalase, hemoglobin
Hypoxia inducible factor 2α (HIF-2α) is critical for primordial germ cell (PGC) survival as knockout of HIF-2α (HIF-2α(-/-)) decreases both expression of Oct-4 and PGC number in genital ridge. Hypoxia is known to stabilize HIF-2α protein from proteasomal degradation. However, little is known about

Hypoxia alleviates dexamethasone-induced inhibition of angiogenesis in cocultures of HUVECs and rBMSCs via HIF-1α

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Background and aim: Inadequate vascularization is a challenge in bone tissue engineering because internal cells are prone to necrosis due to a lack of nutrient supply. Rat bone marrow-derived mesenchymal stem cells (rBMSCs) and human
Orthodontic tooth movement can lead to temporary hypoxia of periodontal tissues. Periodontal ligament cells (PDLCs) react to hypoxia, releasing various biological factors to promote periodontal tissue reconstruction. Hypoxia-inducible factor-1α (HIF-1α) is one of the most sensitive factors involved
Mesenchymal stem or stromal cells (MSCs) derived from the induced pluripotent stem cells (iPSCs) have uniform biological activity, which makes the clinical application of MSCs in bone repair possible. Culturing the iPSC-MSCs onto osteoconductive materials is a promising tissue

Hypobaric-hypoxia induces alteration in microbes and microbes-associated enzyme profile in rat colonic samples.

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Present study deals with the straight impact of hypobaric hypoxia on the quantity and composition of some predominant fecal microflora and its functional aspects. For that, isolated fecal contents of rat were exposed to two different simulated air pressures (70 kPa and 40 kPa) for different time

[Effect of acute hypobaric hypoxia on renal function and structure in rats].

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OBJECTIVE To observe renal damage due to acute hypobaric hypoxia. METHODS Thirty-six male wistar rats were randomly divided into three groups A, B and C (n = 12 for each). Group A served as control, while groups B and C were exposed to 5000 m altitude for 30 min. Sample of serum and renal tissues

Stratified control of IGF-I expression by hypoxia and stress hormones in osteoblasts.

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Bone cells respond to the integrated effects of local and systemic regulation. Here we show that hypoxia and the stress hormones PGE2 and glucocorticoid interact in complex ways in osteoblasts, converging on insulin like growth factor I (IGF-I) expression. Whereas hypoxia alone rapidly increased
In an attempt to elucidate the specificity of pathways from environmental stress to cellular outcome via mitogen activated protein kinases (MAPKs) activation, we examined the responsiveness of cultured human osteoblastic periodontal ligament (PDL) cells to epidermal growth factor (EGF), hypoxia, and

Intestinal alkaline phosphatase to treat necrotizing enterocolitis.

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BACKGROUND Intestinal alkaline phosphatase (IAP) activity is decreased in necrotizing enterocolitis (NEC), and IAP supplementation prevents NEC development. It is not known if IAP given after NEC onset can reverse the course of the disease. We hypothesized that enteral IAP given after NEC induction
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