glyceraldehyde/hemorrhage

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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

Novel roles of nitric oxide in hemorrhagic shock.

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The aim of the current article is to overview the recent developments in the field of hemorrhagic shock research, as it relates to the roles of nitric oxide (NO) in the pathogenesis of this condition. The first part of the review focuses on the roles of peroxynitrite, a reactive oxidant produced

Simple hemorrhage induces tissue factor mRNA in the liver.

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Thrombogenic responses are sometimes seen after a large hemorrhage, but the precise mechanisms whereby this phenomenon occurs still remain unknown. We recently showed that plasminogen activator inhibitor-1 rises after a 20-ml/kg hemorrhage in rats and suggested that this change may be one of the

Identification of early markers for symptomatic vasospasm in human cerebral microdialysate after subarachnoid hemorrhage: preliminary results of a proteome-wide screening.

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A major complication of aneurysmal subarachnoid hemorrhage (SAH) is symptomatic vasospasm, a complex syndrome consisting of neurological deterioration and exclusion of other sources of ischemia. Approximately 30% of SAH patients are affected. Although symptomatic vasospasm is associated with high

Association between expression of MMP-2 and MMP-9 genes and pathogenesis of intracranial hemorrhage in severe coagulation factor XIII deficiency.

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Background Matrix metalloproteinases (MMPs) play a key role in the degradation of basement membrane and extracellular matrix in tissue remodeling, and are involved in pathogenesis of intracranial hemorrhage (ICH). Despite replacement therapy, ICH is by far the main cause of bleeding-related death

Induction of housekeeping gene expression after subarachnoid hemorrhage in dogs.

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Changes in gene expression are commonly assessed relative to the expression of housekeeping genes, which are assumed to remain unchanged. We tested this assumption in cerebral arteries obtained from dogs 4 and 7 days after subarachnoid hemorrhage (SAH) had been created using the double hemorrhage

Multifactorial modulation of susceptibility to l-lysine in an animal model of glutaric aciduria type I.

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Glutaric aciduria type I is an inherited defect in L-lysine, L-hydroxylysine and L-tryptophan degradation caused by deficiency of glutaryl-CoA dehydrogenase (GCDH). The majority of untreated patients presents with accumulation of neurotoxic metabolites - glutaric acid (GA) and 3-hydroxyglutaric acid

[Value of the study of various erythrocyte enzymes in determining the nature of cerebral stroke in the acute period].

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Activities of catalase, superoxide dismutase, glyceraldehyde phosphatedehydrogenase and glucose-6-phosphate dehydrogenase implicated in the process of hemoglobin oxygenation were studied and compared in 40 patients with ischemic and in 30 patients with hemorrhagic brain strokes in the most acute

Nitro-arginine methyl ester, a non-selective inhibitor of nitric oxide synthase reduces ibuprofen-induced gastric mucosal injury in the rat.

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Ibuprofen is a commonly used non-steroidal anti-inflammatory drug. Gastrointestinal adverse drug reactions from ibuprofen usage include gastric mucosal ulcers and bleeding. The mechanism by which ibuprofen induces gastric mucosal damage is not clear. The present study is an attempt to examine the

[Relationship between PMI and relative expression of myocardial various RNAs in rats died of different causes].

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OBJECTIVE To observe the changes of relative expression of myocardial various RNAs in rats died of different causes and their relationship with PMI. METHODS The rat models were established in which the rats were sacrificed by broken neck, asphyxia, and hemorrhagic shock. Total RNAs were extracted

The pathophysiological role of peroxynitrite in shock, inflammation, and ischemia-reperfusion injury.

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Peroxynitrite is a reactive oxidant produced from nitric oxide (NO) and superoxide, which reacts with proteins, lipids, and DNA under conditions of inflammation and shock. Here we overview the role of peroxynitrite in circulatory shock and inflammation. Immunohistochemical and biochemical evidence

P-selectin mRNA is maintained in platelet concentrates stored at 4 degrees C.

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BACKGROUND Platelets (PLTs) contain mRNA and synthesize proteins in response to activation. Most guidelines for PLT concentrates (PCs) recommend ambient temperature for storage but the impact of the storage temperature on PLT mRNA content has not yet been investigated. METHODS Ten leukoreduced

Oxygen-Glucose Deprivation (OGD) Modulates the Unfolded Protein Response (UPR) and Inflicts Autophagy in a PC12 Hypoxia Cell Line Model.

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Hypoxia is the lack of sufficient oxygenation of tissue, imposing severe stress upon cells. It is a major feature of many pathological conditions such as stroke, traumatic brain injury, cerebral hemorrhage, perinatal asphyxia and can lead to cell death due to energy depletion and increased free

Pathophysiological roles of peroxynitrite in circulatory shock.

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Peroxynitrite is a reactive oxidant produced from nitric oxide and superoxide, which reacts with proteins, lipids, and DNA, and promotes cytotoxic and proinflammatory responses. Here, we overview the role of peroxynitrite in various forms of circulatory shock. Immunohistochemical and biochemical

The effect of probiotics and organic acids on Shiga-toxin 2 gene expression in enterohemorrhagic Escherichia coli O157:H7.

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Probiotics are known to have an inhibitory effect against the growth of various foodborne pathogens, however, the specific role of probiotics in Shiga-toxin-producing Escherichia coli (STEC) virulence gene expression has not been well defined. Shiga toxins are members of a family of highly potent

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