Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Surfactant proteins A (SP-A) and D (SP-D) are "collectins": proteins with collagen-like region and lectin domain that bind carbohydrates in a calcium-dependent manner. Mannose-binding protein, a serum collectin, is an acute-phase protein. We hypothesized that SP-A and SP-D would respond to an acute stress, such as lung inflammation, in the same manner as does mannose-binding protein, with increased messenger ribonucleic acid (mRNA) and protein production. Rats received intratracheal lipopolysaccharide (LPS; 0.5 mg/kg) or vehicle and were killed 1, 6, 24, and 72 h later. Their lungs were lavaged and the lung tissue homogenized and analyzed for SP-A, SP-D, and phospholipids. Tissue levels of SP-A were increased by 6 h, peaked at 24 h, and were still elevated at 72 h in LPS-treated animals as compared with those given vehicle. SP-A and SP-D levels in lavage fluid were significantly elevated at 72 h. Message levels for SP-A and SP-D, but not SP-B, were significantly increased at 24 h. Lavage phospholipid levels first increased, then decreased in both the control and LPS-treated animals, and significantly less phospholipid was recovered in the lavage fluid of the LPS-treated animals than in that of controls at 72 h. Although other mechanisms, including altered surfactant metabolism, may be involved, these data are consistent with our hypothesis that SP-A and SP-D are upregulated by an acute inflammatory stress in a manner analogous to that of the structurally and functionally related serum acute-phase reactant, mannose-binding protein. We speculate that this upregulation may be a protective response for the lungs.
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PMID:Surfactant proteins A and D increase in response to intratracheal lipopolysaccharide. 887 85

We have investigated the influence of regulative peptides (oxytocin, pituitrin, thyroid-releasing hormone and SNC) on the expression of mannose-containing membrane structures (MCMS) of lymphocytes and neutrophils in acute stress (3-hour immobilization on the back). MCMS were assayed by the indirect lectin-peroxidase test. We have found that MCMS-expression of lymphocytes significantly decreased but neutrophil MCMS-expression changed in different directions. SNC and thyroid-releasing hormone decreased and MCMS expression increased, respectively. Acute stress activated MCMS expression of lymphocytes. This activation was uncorrectable by the investigated peptides, MCMS expression of neutrophils was corrected by oxytocin, thyroid-releasing hormone and pituitrin. Thus, MCMS expression of leukocytes changed as a multimodal system by acute stress and peptide administration. This system may take part in pathogenesis of the stress reaction.
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PMID:[Effects of regulator peptides on expression of mannose-containing membrane structures in leukocytes in acute stress]. 1124 29

Bilateral common carotid artery occlusion (BCCAO) produces moderate levels of ischemia in the retina of rats, which may simulate the inflow disturbances in severe carotid artery disease. ERG changes following acute BCCAO have been well described, but the effects of chronic BCCAO on the histopathology of the retina remain to be characterized in a reproducible model. Chronic BCCAO was induced in halothane-anaesthetized male Wistar rats and the retina fixed after 3, 6, or 24 hr, 1 week, and 2, 4, or 6 months. Cell counts and measurements of retinal layers were performed in H&E stained paraffin sections. Immunohistochemistry with a panel of fourteen antibodies served to examine the survival of different retinal cell class, astrocytic reactions and the expression of acute stress response proteins. A lectin method was used to label activated microglial cells. Microglial activation, heme oxygenase-1 upregulation and caspase-3 cleavage occurred during the first 24hr in the absence of overt cell death of retinal ganglion cells (RGC). Three waves of neurodegeneration followed. RGCs were affected after 1 week, followed by neurons in the inner nuclear layer at 2 months, and finally photoreceptors at 4 months. Immunomarkers indicated acute damage to horizontal cells and prolonged survival of amacrine cells. In conclusion, chronic BCCAO produced delayed neuronal death in the retina of adult male Wistar rats. The window of moderate changes of at least 1 day may facilitate molecular studies on retinal ganglion cell loss.
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PMID:Complex neurodegeneration in retina following moderate ischemia induced by bilateral common carotid artery occlusion in Wistar rats. 1635 64