NO及NO合成酶与感染性休克

感染性休克病理生理学过程十分复杂。NO在其中的作用既具有有害的一面，同时也存在有利的一面。受内毒素、细胞因子等诱导，iNOS表达上调并产生大量NO，引起循环衰竭、组织细胞损伤以及通过调节炎症介质基因表达扩大全身炎症反应。另一方面，eNOS所产生的NO对机体具有保护作用。然而，感染性休克时，eNOS蛋白质合成及其功能受到损害，反而成为血管内皮功能失常、诱发多器官功能障碍的重要原因。     

Production of tumour necrosis factors by human T cells stimulated by a superantigen,toxic shock syndrome toxin-1

The capacity of human T cell subsets, CD4⁺ or CD8⁺ T cells, to produce tumour necrosis factors (TNF-α and TNF-β) upon stimulation with toxic shock syndrome toxin-l (TSST-I) and the requirement for MHC ctass II molecules on accessory cells (AC) in the response were investigated. The capacity of CD4⁺ T cells was much higher than that of CD8⁺ T cells in TSST-1-induced production of TNF-α and TNF-β. The expression of MHC class II molecules on AC was required in the response.     

Increased production of tumor necrosis factor during endotoxin shock in mice presensitized with serum of mice with tumors or with tumor cell factors

Laboratory of Cellular Immunopathology and Biotechnology, Research Institute of Human Morphology, Academy of Medical Sciences of the USSR, Moscow (Presented by Academician of the Academy of Medical Sciences of the USSR N. K. Permyakov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 7, pp. 78–80, July, 1991.     

Heat shock protein 60 (HSP60) immunoreactivity in gastric epithelium associated with Helicobacter pylori infection: a pitfall in immunohistochemically interpreting HSP60-mediated autoimmune responses

Previous studies have suggested that heat shock proteins (HSP) of Helicobacter pylori (H. pylori) are involved in the induction of autoimmunity mediated gastritis. In the present report, the cross-reactivity between H. pylori-related HSP60 and gastric epithelial cells was investigated by the indirect immunoperoxidase method using two monoclonal antibodies (mAb) against H. pylori-derived HSP60, H9 and H20. H9 is reactive with an epitope common to bacterial HSP60, while H20 is specific to H. pylori HSP60. A total of 70 paraffin-embedded gastric biopsy specimens were analyzed after heat-induced epitope retrieval. Both mAb were cross-reactive with the gastric epithelial cells, with a higher frequency seen for the H9-reactive epitope. The frequency of positive epithelial decoration was not significantly different between H. pylori-positive and H. pylori-negative gastric mucosae. A variety of epithelial and non-epithelial cells were immunostained with mAb H9, while mAb H20 was cross-reactive only with small intestinal epithelia. Reactivity was mainly located in the Golgi area and rarely in the cytoplasm. These results suggest a noteworthy pitfall in immunohistochemical interpretations of HSP60-associated autoimmune reactions in the gastric mucosa.     

Induction of heat shock proteins in lymphocytes increases with mitogen stimulation

The effect of the growth state of a cell on the ability of hyperthermia to induce the synthesis of heat shock proteins (HSPs) was studied in resting and concanavalin A (ConA)-stimulated lymphocytes. Hyperthermia induced the synthesis of hsp 110, hsp 90, hsc 70, and hsp 70 in both resting and ConA-stimulated lymhocytes, and ConA-treatment induced the synthesis of the hsp 90 and hsc 70 at normal temperature. The induction of the synthesis of hsp 110 and hsp 70 by hyperthermia was 3- to 6-fold higher for lymphocytes cultured with ConA for 12 and 24 h than in non-stimulated lymphocytes. Thus, lymphocytes induced to undergo proliferation showed a greater response to hyperthermia than resting lymphocytes.     

LHRH messenger RNA in neurons in the intact and castrate male rat forebrain,studied by in situ hybridization

Summary The slow potential change (spc) accompanying spreading depression (SD) was studied in rats and in a seizure-sensitive strain of Mongolian gerbil under three different experimental paradigms, each involving the use of naloxone. Gerbils undergoing electroconvulsive shock treatment displayed SD during the post-ictal phase, which was blocked by the intraperitoneal (i.p.) administration of naloxone (20–50 mg kg^-1). Topical application of naloxone to the exposed cortex of the anaesthetized gerbil and rat blocked the spc of SD evoked by KCl. Microiontophoretic ejection of naloxone during extracellular recordings reversed cell refractoriness following the spc, demonstrated by the observation of a maintained sensitivity to iontophoretic pulses of glutamate. The results suggest a possible involvement of naloxone-sensitive processes in the mechanism responsible for cortical SD.     

ESWL实际焦点位置的理论和数值分析

从理论和数值模拟两个方面分析了ESWL中的非线性的动力学焦点和实际焦点的位置 ,给出三种典型的动力学焦点的数值结果 ,说明非线性动力学焦点和实际焦点一般不是几何焦点 ,指出正确确定实际焦点在ESWL技术中的重要性。     

Heat shock proteins HSP25, HSP60, HSP72, HSP73 in isoosmotic cortex and hyperosmotic medulla of rat kidney

The distribution of heat shock proteins (HSP) HSP60, HSP73, HSP72 and HSP25 in the isoosmotic cortex and the hyperosmotic medulla of the rat kidney was investigated using Western blot analysis and immunohistochemistry. HSP73 was homogeneously distributed throughout the whole kidney. The level of HSP60 was high in the renal cortex and low in the medulla. HSP25 and HSP72 were present in large amounts in the medulla. Only low levels of HSP25 and almost undetectable amounts of HSP72 were found in the cortex. HSP25 exists in one nonphosphorylated and several phosphorylated isoforms. Western blot analysis preceded by isoelectric focussing showed that HSP25 predominates in its nonphosphorylated form in the outer medulla but in its phosphorylated form in cortex and inner medulla. Although this intrarenal distribution pattern was not changed during prolonged anaesthesia (thiobutabarbital sodium), a shift from the nonphosphorylated to the phosphorylated isoforms of HSP25 occurred in the medulla. The characteristic intrarenal distribution of the constitutively expressed HSPs (HSP73, HSP60, HSP25) may reflect different states of metabolic activity in the isoosmotic (cortex) and hyperosmotic (medulla) zones of the kidney. The high content of inducible HSP72 in the medulla most likely is a consequence of the osmotic stress imposed upon the cells by the high urea and salt concentrations in the hyperosmotic medullary environment.     

Prevention of endotoxin shock by an antibody against leukocyte integrin {beta}2 through inhibiting production and action of TNF

Septic shock remains a serious disorder associated with highmortality. Accumulating evidence indicates that TNF is a majorand essential mediator of endotoxin shock. We report here thatadministration of an antibody against CD18 dramatically reducedendotoxin-induced shock inrabbits as revealed by preventionof severe hypotension, metabolic acidosis and a pathologicalchange suggestive of disseminated intravascular coagulationwith concomitant inhibition of elevation of plasma TNF activity.The anti-CD18 antibody also inhibited the hypotension inducedby administering recombinant TNF. Furthermore, an antibody againsta ligand for CD18 complexes, intercellular adhesion molecule-1,also prevented TNF-induced shock as well as endotoxin shockinrabbits. These observations suggest that adhesion of leukocytesto endothelium may be of primary importance in the action ofTNF as well as in the production of TNF in vivo and that theantibody against adhesion molecules could be of therapeuticbenefit in life-threatening septic shock in humans.