心脏机械膜瓣置换术后血浆蛋白C和蛋白S活性变化及其与INR的关系

目的:探讨机械瓣膜置换术后口服华法令抗凝的患者血浆蛋白C(PC)、蛋白S(PS)活性改变的意义及其与国际标准IL比值(INR)的关系。方法:动态监测15例心脏机械瓣膜置换术后口服抗凝药初期患者服药1-2 d、3~10 d及1个月的PC、PS活性及INR值。结果:患者组PC、PS活性低于正常对照组(P<0.05),特别是术后3-10 d PC、PS活性明显低于正常对照组(P<0.01),已下降到正常的50％左右,而此时INR尚未达到治疗范围,提示口服抗凝药治疗初期在人体凝血功能未下调时,抗凝系统功能已经开始下降,有发生血栓的倾向;并且,随着抗凝强度的增高(INR低于1.5-高于2.5),PC、PS活性明显下降。结论:口服华法令抗凝患者在监测INR的同时,需要进行血浆PC、PS活性监测,以更好地预防血栓的发生。     

Effect of Group A Streptococcal Cysteine Protease on Invasion of Epithelial Cells

Cysteine protease of group A streptococci (GAS) is considered an important virulence factor. However, its role in invasiveness of GAS has not been investigated. We demonstrated in this study that two strains of protease-producing GAS had the ability to invade A-549 human respiratory epithelial cells. Isogenic protease mutants were constructed by using integrational plasmids to disrupt the speB gene and confirmed by Southern hybridization and Western immunoblot analyses. No extracellular protease activity was produced by the mutants. The mutants had growth rates similar to those of the wild-type strains and produced normal levels of other extracellular proteins. When invading A-549 cells, the mutants had a two- to threefold decrease in activity compared to that of the wild-type strains. The invasion activity increased when the A-549 cells were incubated with purified cysteine protease and the mutant. However, blockage of the cysteine protease with a specific cysteine protease inhibitor, E-64, decreased the invasion activity of GAS. Intracellular growth of GAS was not found in A-549 cells. The presence or absence of protease activity did not affect the adhesive ability of GAS. These results suggested that streptococcal cysteine protease can enhance the invasion ability of GAS in human respiratory epithelial cells.     

益活清下法为主治疗重症急性胰腺炎胰外器官损害与死亡原因分析附:235例病例报告

目的：探讨益活清下法治疗重症急性胰腺炎（ＳＡＰ）的疗效及其原理。方法：于１９９０年～１９９７年采用益活清下法治疗ＳＡＰ２３５例,分为存活组和死亡组,分析两组胰外器官损害与死亡原因。结果：在休克、ＡＲＤＳ、氮质血症、心衰、胰性脑病、感染以及营养不良等胰外器官损害方面,两组比较有显著性差异;死亡原因为病程早期以休克或因休克等因素所致的急性肾衰和ＡＲＤＳ为主,后期以全身衰竭、继发感染伴ＭＯＦ为主。结论：益活清下法为主的非手术综合疗法治疗ＳＡＰ疗效显著,病死率明显降低,为９．７９％。     

转化生长因子-α和myc癌基因蛋白在卵泡发育与黄体形成及退化中的表达

目的：探讨转化生长因子（ＴＧＦ）－α和ｍｙｃ癌基因蛋白（ｍｙｃ蛋白）对人卵巢卵泡发育的局部调控机理。方法：收集３６例月经规则、因不同妇科情况切除的子宫及卵巢标本，采用免疫组织化学方法，研究ＴＧＦ－α和ｍｙｃ蛋白在卵巢组织中的表达。结果：卵母细胞在始基卵泡阶段，ＴＧＦ－α和ｍｙｃ蛋白的表达呈强阳性，随着卵泡的发育与成熟表达逐渐减弱。在颗粒细胞中，ＴＧＦ－α和ｍｙｃ蛋白表达均出现在窦前卵泡阶段，随卵泡的增大与成熟，ＴＧＦ－α表达逐渐增强。闭锁卵泡中ＴＧＦ－α和ｍｙｃ蛋白表达仅限于卵泡膜细胞。在晚期退化的黄体中，ＴＧＦ－α和ｍｙｃ蛋白表达均局限于黄体中央瘢痕周围的黄体膜细胞。结论：ＴＧＦ－α和ｍｙｃ蛋白作为卵巢内局部的调节因子，通过自分泌和旁分泌途径，协同参与人卵母细胞最初的生长、卵泡细胞的增殖分化和黄体细胞凋亡的过程。     

创伤后感染致多器官功能障碍综合征患者血清β-hBD-2、OPN、pro-ADM和NPt水平的变化

目的：探讨多器官功能障碍综合征（multipleorgandysfunctionsyndrome,MODS）患者的炎症感染病理过程中炎性介质水平的变化。方法：血清人类B防御素-2（humanB．defensin-2,β—hBD-2）、骨桥蛋白（osteopontin,OPN）和新蝶呤（neoptefin,NPt）采用酶联免疫分析法（ELISA）测定,肾上腺髓质素前体（pro-adrenomeduUin,pro—ADM）检测采用化学免疫发光法。结果：四项血清标志物测定结果分别显示,对照组和确诊时组B-hBD-2、OPN、pro-ADM、NPt四种血清炎症介质标志水平均显著高于正常人组（P〈0．05,P〈0．01）,出院前组β-hBD-2、OPN水平显著高于正常人组,另两项指标均与正常人组比较无显著性差异（P均〉0．05）;同时确诊时组与对照组比较β—hBD-2、OPN、pro-ADM三项指标水平也显著升高（P〈0．05,P〈0．01）,NPt水平患者组呈略高,但无统计学意义（P〉0．05）;出院前组β-hBD-2、OPN、pro-ADM、NPt四种血清炎症介质标志水平均显著低于确诊时组（P〈0．05,P〈0．01）。结论：MODS患者的炎症感染病理过程中炎性介质水平显著升高,其测定对于临床抗感染治疗提供重要价值。     

Protection against Klebsiella pneumoniae Using Lithium Chloride in an Intragastric Infection Model

Intragastric Klebsiella pneumoniae infections of mice can cause liver abscesses, necrosis of liver tissues, and bacteremia. Lithium chloride, a widely prescribed drug for bipolar mood disorder, has been reported to possess anti-inflammatory properties. Using an intragastric infection model, the effects of LiCl on K. pneumoniae infections were examined. Providing mice with drinking water containing LiCl immediately after infection protected them from K. pneumoniae-induced death and liver injuries, such as necrosis of liver tissues, as well as increasing blood levels of aspartate aminotransferase and alanine aminotransferase, in a dose-dependent manner. LiCl administered as late as 24 h postinfection still provided protection. Monitoring of the LiCl concentrations in the sera of K. pneumoniae-infected mice showed that approximately 0.33 mM LiCl was the most effective dose for protecting mice against infections, which is lower than the clinically toxic dose of LiCl. Surveys of bacterial counts and cytokine expression levels in LiCl-treated mice revealed that both were effectively inhibited in blood and liver tissues. Using in vitro assays, we found that LiCl (5 μM to 1 mM) did not directly interfere with the growth of K. pneumoniae but made K. pneumoniae cells lose the mucoid phenotype and become more susceptible to macrophage killing. Furthermore, low doses of LiCl also partially enhanced the bactericidal activity of macrophages. Taken together, these data suggest that LiCl is an alternative therapeutic agent for K. pneumoniae-induced liver infections.     

Mental Well‐Being Mediates the Relationship between Perceived Stress and Perceived Health

The association between stress and health has been well researched in the past; however, comparatively few mediators have been tested to understand the underlying mechanism. With increasing awareness on mental well‐being, this study evaluated the relationship between perceived stress and perceived health and examined mental well‐being as a mediator. Two‐hundred undergraduates aged 21 to 26 years completed the English Perceived Stress Scale, Health Status Questionnaire and Asian Mental Well‐Being Scale that assess perceived stress, perceived health and mental well‐being, respectively. Factor analysis and structural equation modelling on the Perceived Stress Scale replicated the reported two‐factor structure after excluding an insignificant item. Linear multiple regression analyses indicated that perceived stress was negatively associated with perceived health. Results showed that mental well‐being partially mediated the relationship between perceived stress and perceived health, although it is acknowledged that this association could be bidirectional. Findings from the present study suggest that future research could focus on reducing stress and improving mental well‐being to alleviate the effect of stress on health. Copyright © 2013 John Wiley & Sons, Ltd.