目的:探讨应用血必净注射液对严重烧伤患者休克期并发脓毒症的治疗效果。方法:依据脓毒症感染诊断标准,对44例严重烧伤患者休克期并发脓毒症的患者,随机分为2组,对照组22例给予常规治疗,治疗组22例,加用血必净注射液,疗程7日。分别观察2组患者治疗前后体温(T)、心率(HR)、白细胞计数(WBC)、中性粒细胞率、血小板记数(PLT)及病死率。结果:血必净注射液治疗后,治疗组的HR、WBC、PLT与对照组比较有显曹改善(Plt;005);病死率较对照组显著降低(Plt;001)。结论:烧伤后早期应用血必净注射液是防治休克期烧伤脓毒症的重要措施,对烧伤脓毒症起到早期保护组织、防治MODS的作用。
Objective To detect the expression of heat shock protein 47 mRNA in pathological scar tissue by using real-time fluorescent quantitative reversetranscription-polymerase chain reaction (RT-PCR). Methods The tissues of normal skin(n=6), hypertrophic scar(n=6) and keloid(n=6) were adopted, which were diagnosised by Pathology Department. Based on fluorescent TaqMan methodology, the real-time fluorescent quantitative RT-PCR were adopted to detect the expression ofheat shock protein 47 mRNA. Results Compared with normal skin tissue（0.019±0.021）×105, the expressions of heat shock protein47 cDNA of hypertrophic scar tissue（1.233±1.039）×105 and keloid tissue（1.222±0.707）×105 were higher， being significant differences（Plt;0.05）. Conclusion A fluorescent quantitative method was successfully applied to detecting the expression of heat shock protein 47 mRNA. Heat shock protein 47 may play an important role in promoting the formation of pathological scar tissue.
Objective To study the effects of heat shock proteins (HSPs) in the course of hepatic ischemia reperfusion injury (HIRI), and analyze its mechanism. Methods The relationship between HSPs and HIRI was studied by reviewing literatures. Results HSPs was a kind of stress protein induced after cell was sitmulated by the stress. It could improve body′s tolerance to tough situation. Though hepatic ischemia reperfusion usually results in serious hepatic injury, at the same time it could induce can increase the production of HSPs that can protect liver from and lessen ischemia reperfusion injury. Conclusion HSPs can improve the tolerance to HIRI and lessen injury. In addition, HSPs is thought to be markers of HIRI, and can be used as a efficient indicator to test the level of hepatic injury and assess prognosis.
Cardiogenic shock (CS) describes a physiological state of end-organ hypoperfusion characterized by reduced cardiac output in the presence of adequate intravascular volume. Mortality still remains exceptionally high. Veno-arterial extracorporeal membrane oxygenation (VA ECMO) has become the preferred device for short-term hemodynamic support in patients with CS. ECMO provides the highest cardiac output, complete cardiopulmonary support. In addition, the device has portable characteristics, more familiar to medical personnel. VA ECMO provides cardiopulmonary support for patients in profound CS as a bridge to myocardial recovery. This review provides an overview of VA ECMO in salvage of CS, emphasizing the indications, management and further direction.
ObjectiveTo investigate the influence of heat shock protein A2 (HSPA2) on the biological behavior of pancreatic adenocarcinoma cells and its mechanism. MethodsThe expressions of HSPA2 were determined in the human pancreatic adenocarcinoma cell lines (PANC-1, BxPC-3, and AsPC-1) using the Western blot. Subsequently, the cells with the lowest and highest HSPA2 expressions among these three lines were selected for conducting overexpression and knockdown experiments targeting HSPA2, respectively. The cellular proliferation, cell clonogenesis, migration, and invasion capabilities were assessed using MTT, clonogenic assay, and Transwell assay, respectively. Additionally, the impact of HSPA2 on the expression of key markers of epithelial-mesenchymal transition (EMT) was examined using the Western blot. The potential target molecules of HSPA2 were identified through immunoprecipitation assay and mass spectrometry. The rescue experiments further explored the regulatory relation between the HSPA2 and its target molecules. The influence of HSPA2 on pancreatic adenocarcinoma growth was investigated through establishment of xenograft tumor model in nude mice. ResultsThe HSPA2 exhibited the lowest expression in the PANC-1 cells and the highest expression in the AsPC-1 cells among the three cell lines. Subsequent functional studies demonstrated that the overexpression of HSPA2 in the PANC-1 cells markedly promoted proliferation, cell clonogenesis, migration, and invasion, while the knockdown of HSPA2 expression in the AsPC-1 cells markedly inhibited these processes. The Western blot analysis further showed that the HSPA2 overexpression downregulated E-cadherin expression and upregulated N-cadherin and Vimentin expressiones, whereas the HSPA2 knockdown produced opposite effects. The rescue experiments indicated that the HSPA2 promoted the EMT in pancreatic adenocarcinoma cells by upregulating Yes associated protein (YAP). The subcutaneous xenograft tumor experiments in the nude mice showed that the HSPA2 knockdown inhibited tumor growth. ConclusionThe results of this study suggest that HSPA2 promotes EMT via upregulating YAP, which facilitates proliferation, migration, and invasion of pancreatic adenocarcinoma cells.
目的 探讨特发性结肠穿孔的治疗方法及成因。方法 结合文献分析2001～2009年期间我院收治的特发性结肠穿孔患者的诊治经过。结果 共收治特发性结肠穿孔9例，占同期结肠穿孔患者的28.1%（9/32），其中5例穿孔（5/9）发生在乙状结肠。修剪破口后直接缝合者2例，行结肠双腔造瘘者7例。术后死亡3例。结论 特发性结肠穿孔好发于乙状结肠，与其解剖和生理上的特点有关。不明原因结肠穿孔的患者要想到本病的可能。及时、合理的手术治疗，仔细周到的术后管理是治疗成功的关键。