目的:观察血清降钙素原( procalcitonin,PCT)对脓毒症的早期诊断、监测病情的临床应用价值及其与急性生理学及慢性健康状况评分 ( acute physiology and chronic health evaluationⅡ,APACHEⅡ评分)之间的相关性.方法:回顾性分析脓毒症组56例和非脓毒症组30例均在入院当天用抗生素前采血检测PCT和C-反应蛋白(CRP)及进行APACHEⅡ评分,在治疗后第1d、3d和7d分别复查,并根据28d病死率将患者分为存活组与死亡组.结果:脓毒症组PCT、CRP水平和APACHEⅡ评分均明显高于非脓毒症组,差异有统计学意义(P<0.05);治疗后第3d开始,存活组PCT、CRP水平随病情好转迅速下降,而死亡组虽有下降趋势,但仍持续高水平,PCT水平和APACHEⅡ评分显著高于存活组(P<0.05),PCT水平与APACHEⅡ评分的相关系数0.66(P<0.05).结论:血清PCT对脓毒症早期诊断、监测病情有重要的临床价值,而APACHEⅡ评分与其有较强的相关性.联合APACHEⅡ评分可作为对脓毒症患者病情严重程度及预后评估的一个可靠指标. 相似文献
Summary: The wavelength‐dependent vacuum ultraviolet (VUV) photolysis of several polymers, low density polyethylene (LDPE), biaxially oriented poly(propylene) (BOPP), atactic polystyrene (PS), and poly(methyl methacrylate) (PMMA), was studied by irradiation in vacuum with the well‐characterized emissions from four different resonant or excimer VUV sources. These lamps comprise radiofrequency (r.f.) discharges in different noble gases, such as krypton, xenon (at low pressures, producing near‐monochromatic resonant line radiations), xenon excimer (at “high” pressure), and a deuterium/argon mixture (producing a broad‐band emission). VUV‐induced mass loss (ablation or etching) was monitored in situ by quartz crystal microbalance measurements. Following irradiation, samples were analysed by ATR‐FTIR and XPS, to evaluate near‐surface structural changes (e.g., creation of unsaturation, cross‐linking) resulting from the VUV‐initiated bond scissions and radical‐creation reactions. PMMA was the most readily ablatable polymer, whereas the mass loss of BOPP was higher than that of LDPE, regardless of the irradiation wavelength, λ. All polymers were found to form double bonds, with the exception of PS, which is rather stable, probably due to energy dissipation by fluorescence.
Formation of double bonds in a) vinyl‐, b) vinylidene‐, and c) vinylene‐like unsaturated groups, as a function of the radiation dose, D, for KrL (?), XeL (?), and D2Ar‐irradiated (?) PMMA. 相似文献
Aim: AQP4 in the brain is involved in the occurrence and development of a variety of encephalopathy. AQPs family changes in kidney were accompanied by altered UTs family. The aim of this study was to observe AQP4 and UT-A3 expression in CNS and to explore their role in the pathogenesis of endotoxemia encephalopathy following peripheral LPS injection in mice. Methods: Endotoxemia was induced in C57Bl/6 mice by intraperitoneal injection of LPS. The expression of UT-A3 and AQP4 in brain were detected by Western blot and immunohistochemistry, the level of cytokines were detected by ELISA, and the content of LDH, AST/ALT, BUN and CREA were detected by colorimetric method. Results: As compared with the control group, in model group, the brain weight/ body weight ratio increased by 13%. Meanwhile, a 2.5 fold increase in LDH and a 1.2 fold increase in AST/ALT were found in peripheral serum (P < 0.05), and also, BUN and CREA increased 2.5 fold (P < 0.01). In addition to severe CNS injury in response to lipopolysaccharide, the contents of cytokines and the expression of AQP4 protein in hippocampal is increased (P < 0.05), while the expression of UT-A3 protein in the hippocampus and cortical astrocytes decreased (P < 0.05). And, in part, Dexa pretreatment attenuated those effects. Conclusions: In endotoxemia encephalopathy, AQPs and UTs which regulate the functions of cell membrane are both altered. We suggested that the molecular mechanisms of regulation in endotoxemia may provide a new strategy for clinical treatment of the disease and drug binding sites. 相似文献
