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glyceraldehyde 3 phosphate/oedeem

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LidwoordKlinische proevenOctrooien
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Metabolic myopathy produced by acute inhibition of glyceraldehyde-3-phosphate dehydrogenase with ortho-iodosobenzoic acid.

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A previously developed model of exercise-induced muscle contracture using iodoacetate to inhibit glyceraldehyde-3-phosphate dehydrogenase in rat hindlimb muscles produced selective type II myofiber damage. Utilizing a modification of the same model system, rats were given intra-aortic
OBJECTIVE To investigate the expressions of hypothalamic arginine vasopressin (AVP) mRNA, renal AVP V2 receptor mRNA, and AVP-dependent aquaporin-2 (AQP2) mRNA in rats with adriamycin-induced nephrotic syndrome. Effects of Chinese herb Astragalus membranaceus (AM) were also

Early response of C2C12 myotubes to a sub-cytotoxic dose of hemorrhagic metalloproteinase HF3 from Bothrops jararaca venom.

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Manifestations of local tissue damage, such as hemorrhage and myonecrosis, are among the most dramatic effects of envenomation by viperid snakes. Snake venom metalloproteinases (SVMPs) of the P-III class are main players of the hemorrhagic effect due to their activities in promoting blood vessel
Extracellular glutathione peroxidase (E-GPx) is a selenoenzyme that reduces hydrogen peroxide and organic peroxides. All plasma glutathione peroxidase (GPx) activity in humans is attributable to E-GPx. The gastrointestinal (GI) tract also synthesizes and secretes E-GPx into the extracellular milieu.
Menadione (MQ), a quinone used with cancer chemotherapeutic agents, causes cytotoxicity to endothelial cells (EC). Previous studies have suggested that MQ induces an oxidative stress and dysfunction in EC by either increasing hydrogen peroxide (H(2)O(2)) production or depleting intracellular

The megencephaly mouse has disturbances in the insulin-like growth factor (IGF) system.

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Megencephaly, enlarged brain, is a major sign in several human neurological diseases. The mouse model for megencephaly, mceph/mceph, has an enlarged brain and a lowered body weight. In addition, it displays several neurological and motoric disturbances. Previous studies suggest that the brain

The anti-cancer drug, doxorubicin, causes oxidant stress-induced endothelial dysfunction.

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The anticancer drug doxorubicin (DOX) is toxic to target cells, but also causes endothelial dysfunction and edema, secondary to oxidative stress in the vascular wall. Thus, the mechanism of action of this drug may involve chemotoxicity to both cancer cells and to the endothelium. Indeed, we found
Impaired macroautophagy/autophagy has been implicated in experimental and human pancreatitis. However, the transcriptional control governing the autophagy-lysosomal process in pancreatitis is largely unknown. We investigated the role and mechanisms of TFEB (transcription factor EB), a master
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