Disease relevance of Anoxia

• In 18 patients with intention myoclonus due to anoxia or other brain damage, 11 derived more than 50% overall improvement during treatment with L-5HTP and carbidopa [1].
• The ethanol-induced impairment of umbilical circulation produced severe hypoxia and acidosis in the fetus; recovery occurred during the succeeding hour [2].
• Elastin synthesis was studied in blood vessels from newborn calves with severe pulmonary hypertension induced by alveolar hypoxia in order to investigate the cellular stimuli that elicit changes in pulmonary arterial connective tissue production [3].
• Cell-cycle-related proteins, such as cyclins or cyclin-dependent kinases, are re-expressed in neurons committed to death in response to a variety of insults, including excitotoxins, hypoxia and ischemia, loss of trophic support, or beta-amyloid peptide [4].
• Here, we show that anoxia reduces expression of thrombospondin-1 (TSP-1), a natural inhibitor of angiogenesis, in glioblastoma cells [5].

Psychiatry related information on Anoxia

• The piracetam-like nootropics are capable of achieving reversal of amnesia induced by, e.g., scopolamine, electroconvulsive shock and hypoxia [6].
• OBJECTIVES: We sought to determine whether long-term hypoxia/reoxygenation events in mice result in NADPH oxidase activation and whether NADPH oxidase is essential for the proinflammatory response and hypersomnolence [7].
• A previous case report has suggested an association with mild-to-moderate deficiency of arylsulfatase A. We describe a 36-year-old man who recovered completely from an episode of hypoxia related to drug overdose, and 2 weeks later progressed from a confusional state to deep coma [8].
• During wakefulness, hypoxia increased the slope of the ventilatory response to CO2 and shifted the response slightly to the left [9].
• From days 14-21, plasma ACTH and corticosterone levels increased significantly after exposure to ether stress, hypoxia, and, to a lesser extent, electroshocks [10].

High impact information on Anoxia

• Tissue damage-associated deep hypoxia, hypoxia-inducible factors, and hypoxia-induced accumulation of adenosine may represent one of the most fundamental and immediate tissue-protecting mechanisms, with adenosine A2A receptors triggering "OFF" signals in activated immune cells [11].
• In yeast and bacteria, regulatory operons coordinate expression of genes responsible for adaptive responses to hypoxia and hyperoxia [12].
• HCP 1 mRNA was highly expressed in duodenum and regulated by hypoxia [13].
• Microarray analysis revealed that Sre1 activates sterol biosynthetic enzymes as in mammals, and, surprisingly, Sre1 also stimulates transcription of genes required for adaptation to hypoxia [14].
• Siah2 null mice subjected to hypoxia displayed an impaired hyperpneic respiratory response and reduced levels of hemoglobin [15].

Chemical compound and disease context of Anoxia

• Peak titers of RSV-IgE and concentrations of histamine correlated significantly with the degree of hypoxia (P less than 0.001) [16].
• Arnt-/- ES cells also failed to respond to a decrease in glucose concentration, indicating that ARNT is crucial in the response to hypoxia and to hypoglycaemia [17].
• During anoxia, release of arachidonic acid could severely compromise glutamate uptake and thus contribute to neuronal death [18].
• Hypoxia increases the kinase activity of pp60c-src and its phosphorylation on tyrosine 416 but does not activate Fyn or Yes [19].
• This finding links tissue hypoxia, hemoglobin allostery and nitrite bioactivation [20].

Biological context of Anoxia

• A nitric oxide (NO)/cyclic GMP (cGMP) signaling pathway is thought to play an important role in mammalian vasodilation during hypoxia [21].
• The p53 tumour suppressor is a transcription factor that regulates the progression of the cell through its cycle and cell death (apoptosis) in response to environmental stimuli such as DNA damage and hypoxia [22].
• Similar to VEGF, EG-VEGF possesses a HIF-1 binding site, and its expression is induced by hypoxia [23].
• Interaction of HIF-1 alpha transactivation domains with coactivators is induced by hypoxia [24].
• We hypothesize that EPAS1 expressed in the OZ senses hypoxia during mid-gestational development and translates this signal into an altered pattern of gene expression, leading to increases in circulating catecholamine levels and proper cardiac function [25].

Anatomical context of Anoxia

• Siah2 null fibroblasts exhibit prolonged PHD3 half-life, resulting in lower levels of HIF1alpha expression during hypoxia [15].
• In addition, Vegf165 promoted survival of motor neurons during hypoxia through binding to Vegf receptor 2 and neuropilin 1 [26].
• Specifically, we demonstrate that S-nitrosocysteinyl glycine (CGSNO) and S-nitroso-l-cysteine (l-CSNO)-but not S-nitroso-d-cysteine (d-CSNO)-reproduce the ventilatory effects of hypoxia at the level of the nucleus tractus solitarius (NTS) [27].
• Erythropoietin (Epo), the hormone that stimulates red blood cell production, is synthesized in the kidney and liver in response to hypoxia [28].
• These observations raise the possibility that EPAS1 may represent an important regulator of vascularization, perhaps involving the regulation of endothelial cell gene expression in response to hypoxia [29].

Gene context of Anoxia

• Hypoxia-inducible factor 1 (HIF-1) is a transcriptional activator of vascular endothelial growth factor (VEGF) and is critical for initiating early cellular responses to hypoxia [30].
• Thus, the control of PHD1/3 by Siah1a/2 constitutes another level of complexity in the regulation of HIF1alpha during hypoxia [15].
• VEGF induction by hypoxia in c-src(-) cells is impaired, although there is a compensatory activation of Fyn [19].
• During terminal branching, FGF expression is regulated by hypoxia, ensuring that tracheal structure matches cellular oxygen need [31].
• These results indicate that amplification of normal HIF-1-dependent responses to hypoxia via loss of p53 function contributes to the angiogenic switch during tumorigenesis [32].

Analytical, diagnostic and therapeutic context of Anoxia

• VEGF messenger RNA levels are dramatically increased within a few hours of exposing different cell cultures to hypoxia and return to background when normal oxygen supply is resumed [33].
• Because ischemic hypoxia is often followed by reperfusion and reactive oxygen intermediate (ROI) generation, we examined the potential role of ROI in the control of VEGF gene expression [34].
• Hypoxia induced by a low rate of perfusion led to near anoxia confined to centrilobular regions of the liver lobule [35].
• Immediately after treatment with O2- or repetitive, brief anoxia, O2- production was increased in myocytes [36].
• Measurements were performed under resting conditions, during a 10-minute period of hypoxia (12.5% O2/87.5% N2) and during a 3-minute mental stress test [37].

References