目的:分析行心肺联合移植术的患者术后出现精神障碍的原因,并探讨合理护理对策,改善患者预后.方法:回顾性分析14例行心肺联合移植术患者的临床资料,术后借助SINH精神卫生评价系统(SAS)观察精神障碍发生情况,分析原因并提出护理对策.结果:14例患者术后共计8例出现精神障碍,发生率为57.14％,其中以妄想型精神病占比最高,所有精神障碍经对症治疗及护理,在出监护室其情况明显改善.结论:心肺联合移植术后容易发生精神障碍,需分析具体原因并给予合理护理,促进患者早日康复.

异位静脉曲张(ectopic varices,EV)是指发生于除了胃底食管静脉以外的静脉曲张,它主要由门静脉高压症引起,其破裂出血占所有静脉曲张破裂出血的1％～5％.笔者诊治了1例肝硬化门静脉高压致心膈角静脉曲张破裂大出血的患者,临床上极少见,容易漏诊或误诊;治疗不及时,病死率极高,现报道如下.

Objective To explore stable and functional microRNA (miRNA)-disease relationships using a genome-wide expression profile pattern matching strategy. Methods We applied the ranked microarray pattern matching strategy Gene Set Enrichment Analysis to identify miRNA permutations with similar expression patterns to diseases. We also used quantitative reverse transcription PCR to validate the predicted expression levels of miRNAs in three diseases: inflammatory bowel disease (IBD), oesophageal cancer, and colorectal cancer. Results We found that hsa-miR-200c was upregulated more than 40-fold in oesophageal cancer. The expression of miR-16 and miR-124 was not consistently upregulated in IBD or colorectal cancer. Conclusions Our results suggest that this expression profile matching strategy can be used to identify functional miRNA-disease relationships.

急性胰腺炎（ AP）是消化系统最常见的急腹症之一，发病急、病程长、并发症多，总的病死率约5％［1］，其中重症急性胰腺炎（SAP）的病死率高达36％～50％［2］，因此早期评价AP患者病情的严重程度对患者的治疗和监护具有十分重要的临床意义。2008年提出的AP 床旁严重度指数（ bedside index for severity in AP ， BISAP ）是一种简便、准确的评分系统，已被广泛应用于临床。文献报道红细胞比容（ HCT ）≥44％可作为预测SAP的重要指标［3-4］，入院时HCT升高可以预测AP并发感染［5］。早期快速补液以降低HCT可改善AP患者的预后［6-7］。本研究回顾性分析温州医科大学附属第一医院近2年来资料完整的AP患者586例，分析BISAP评分联合HCT预测SAP患者预后的临床价值。

Pregnant women are usually in a hypercoagulable state;if it is complicated with high risk conditions of thrombosis,such as obesity,pregnancy-induced hypertension,mechanical heart valve replacement,systemic lupus erythematosus and antiphospholipid syndrome,prophylactic anticoagulation therapy with heparin/warfarin will be required.Due to pros and cons of heparin/warfarin,there is a controversy about how to choose anticoagulants.This article reviews the current status and progress of drug prophylaxis for thrombosis disease,and related issues particularly for administration of heparin and warfarin.

目的 探究褪黑素(MLT)联合顺铂(CDDP)对人胃癌AGS细胞的疗效及相关凋亡蛋白表达的影响.方法 将体外培养的人胃癌细胞AGS细胞株分为4组,即AGS对照组、AGS MLT组(2mmol/L)、AGS CDDP组(4μg/ml)和AGS MLT+ CDDP组(2mmol/L MLT和4μg/ml CDDP).采用CCK8试验检测各组细胞增殖的抑制情况,Annexin V FITC/PI凋亡试剂盒检测各组细胞早晚期细胞凋亡情况,Western blot法检测各组细胞凋亡蛋白表达情况.结果 MLT+ CDDP组细胞的生存率明显低于AGS对照组和AGS单药组;流式细胞术检测细胞凋亡情况表明,正常对照组、单药组和联合组细胞的早期凋亡率依次增加;蛋白水平研究表明,相比单药组和正常组,联合组的Bcl-2、原形态caspase-3表达显著降低,Bax及活化态cleaved-caspase-3表达明显增高.结论 与单用顺铂相比,褪黑素联合顺铂能明显抑制胃癌AGS细胞增殖并加强促凋亡能力,这可能与联合药影响相关凋亡蛋白表达有关.

Background/Aims: Melatonin, synthesized by the pineal gland and released into the blood, appears to have antitumour properties; however, the mechanisms of its anti-cancer effects are largely unknown, especially in stomach cancer. Here, we explore the antitumour activity of melatonin in a gastric cancer cell line (AGS) and analyse its molecular mechanisms. Methods: AGS cells were treated with melatonin, and cell viability was assessed using a CCK-8 assay. Flow cytometry was performed to evaluate apoptosis, and protein expression was examined by Western blotting. Results: Melatonin significantly inhibited cell viability, clone formation, and cell migration and invasion and induced apoptosis in AGS cells. Moreover, MAPK pathways (p38, JNK and ERK) were activated by melatonin treatment, which also significantly increased caspase-3 cleavage and Bax protein expression and decreased Bcl-2 protein expression in a time-dependent manner. Our results demonstrate that p38 and JNK inhibitors (SB203580 and SP600125, respectively) prevented melatonin-induced apoptosis; thus, the propensity of p38 MAPK and JNK to promote apoptosis could be at least partly due to the inhibition of NF-κB p65 activation by p38 and JNK. Finally, melatonin was able to strengthen cisplatin-mediated antitumour effects in human gastric carcinoma cells by up-regulating the expression of Bax, down-regulating the expression of Bcl-2 and activating the caspase-dependent apoptotic pathway. Conclusion: Melatonin induced apoptosis in AGS cells by activating the caspase-dependent apoptotic pathway and by inhibiting the nuclear translocation of NF-κB p65, two processes that are regulated by p38 and JNK. Furthermore, melatonin significantly enhanced the anti-tumour effects of cisplatin, with low systemic toxicity. These new findings suggest that melatonin may act as a potent anti-tumour agent and may have great potential as an adjuvant therapy in the future.