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Myocardial capillarity in acclimation to hypoxia.
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Capillarity, O2 diffusion distances and fiber cross-sectional growth were measured in the hearts of guinea pigs exposed early during growth to hypobaric hypoxia (PB = 430 torr, PO2 = 90 torr). Twelve 5-week old males were maintained in a hypobaric chamber for 4-14 weeks. Their hearts were
The effects of a graded increase in chronic hypoxia exposure duration on healthy rats at high-altitude.
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To investigate the effects of chronic hypoxia exposure at high altitude on the formation of pulmonary edema in rats, we randomized rats into normoxic control groups and hypoxic 24, 48, and 72-hour exposure groups. In the hypoxic exposure group, the arterial blood gas, wet-dry weight ratio (W/D),
[HYPOXIA INDUCIBLE FACTOR lα/2α GENES EXPRESSION IN CHONDROGENIC DIFFERENTIATION OF HUMAN BONE MARROW MESENCHYMAL STEM CELLS].
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OBJECTIVE
To observe the genes expression of hypoxia inducible factor lα (HIF-1α) and HIF- 2α by inducing chondrogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs) so as to provide a fundamental basis for HIF involving in the mechanism of chondrogenesis.
METHODS
High density
Neuronal and glial alterations due to focal cortical hypoxia induced by direct cobalt chloride (CoCl2) brain injection.
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Ischemic brain injury is a dynamic process that involves oxidative stress, inflammation, and cell death, as well as activation of endogenous adaptive and regenerative mechanisms depending on activation of transcription factors such as hypoxia inducible factor 1-alpha (HIF-1alpha). Because CoCl2
Hypoxia induces caspase-9 and caspase-3 activation without neuronal death in gerbil brains.
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To investigate the in vivo apoptotic machinery in oxygen deprived brain, we examined the expression of caspase-9 and caspase-3 in the hippocampus of Mongolian gerbils subjected to either transient hypoxia (4% O2 for 6 min) or forebrain ischemia (10 min bilateral carotid artery occlusion) followed by
Acute hypoxia and osteoclast activity: a balance between enhanced resorption and increased apoptosis.
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Osteoclasts are the primary mediators of pathological bone resorption in many conditions in which micro-environmental hypoxia is associated with disease progression. However, effects of hypoxia on human osteoclast activity have not been reported. Mature human osteoclasts were differentiated from
Mast cell stabilization with sodium cromoglycate modulates pulmonary vessel wall remodeling during four-day hypoxia in rats.
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OBJECTIVE
In rats, the environment with low content of oxygen induces hypoxic pulmonary hypertension. Remodeling of pulmonary resistance arteries is particularly triggered by the mast cell degranulation products, e.g., rodent-like interstitial collagenase (matrix metalloproteinase 13).
[Comparative study between hypoxia and hypoxia mimetic agents on osteogenesis of bone marrow mesenchymal stem cells in mouse].
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OBJECTIVE
?To compare the effects on the osteogenesis of bone marrow mesenchymal stem cells (BMSCs) between hypoxia and hypoxia mimetic agents dimethyloxalylglycine (DMOG) under normal oxygen condition.
METHODS
?BMSCs were isolated and cultured from healthy 3-4 weeks old Kunming mouse. Cell
Acute and chronic hypoxia as well as 7-day recovery from chronic hypoxia affects the distribution of pulmonary mast cells and their MMP-13 expression in rats.
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Chronic hypoxia results in pulmonary hypertension due to vasoconstriction and structural remodelling of peripheral lung blood vessels. We hypothesize that vascular remodelling is initiated in the walls of prealveolar pulmonary arteries by collagenolytic metalloproteinases (MMP) released from
Effects of hypoxia and ASIC3 on nucleus pulposus cells: From cell behavior to molecular mechanism.
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This study aimed to explore the effects of hypoxia and acid-sensing ion channel 3 (ASIC3) on nucleus pulposus cells from cell behavior to molecular mechanism. Primary rabbit nucleus pulposus cells were isolated and identified by HE, toluidine blue and immunohistochemical staining of collagen II. 2%
Inflammatory reaction patterns of the lung as a response to alveolar hypoxia and their significance for the diagnosis of asphyxiation.
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Providing evidence of asphyxia death is a challenging issue in forensic pathology. Besides helpful macroscopical signs (e.g. strangulation mark, lung edema), recent data from literature indicate that the time of protracted asphyxia suffices to trigger an increase of giant cells and a migration of
Hypoxia enhances chondrogenic differentiation of human adipose tissue-derived stromal cells in scaffold-free and scaffold systems.
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Human adipose-derived stromal cells (hASCs) possess the potential for chondrogenic differentiation. Recent studies imply that this differentiation process may be enhanced by culturing the cells in low oxygen tension in combination with three-dimensional (3D) scaffolds. We report the evaluation of
Hospital treatment of victims exposed to combustion products.
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Combustion toxicology is complex so, although victims exposed to combustion products are mainly treated symptomatically, it is important to identify those situations when specific therapeutic measures might be of importance. Victims presenting respiratory symptoms including severe cough,
Quantitative changes in neuroglia in the white matter of the mouse brain following hypoxic stress.
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Two experimental and one control group of 70-80 day old mice were used in this study. The two experimental groups were subjected to hypoxia for 2 days in a decompression chamber at 390 mmHg. The animals in one experimental group were killed on removal from the chamber (hypoxic group) while those in
Mast cell isolation from the immature rat brain.
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Mast cells are immune cells of hematopoietic origin that circulate as precursor cells prior to migration into vascularized tissues where they mature and undergo terminal differentiation in response to different cytokines within the local environment. Mast cells are well known as important regulators
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