非典型布鲁杆菌脊柱炎的诊断与治疗

目的：探讨非典型布鲁杆菌脊柱炎的诊断与治疗,以进一步提高临床医师对该病的认识水平及诊治能力。方法回顾分析19例布鲁杆菌脊柱炎患者,病变节段位于腰椎17例、颈椎2例。14例有羊、牛接触史。19例均行 X 线检查,16例行 CT 检查,11例行 MRI 检查,所有患者标准血清试管凝集试验（SAT）滴度均＞1∶160,虎红平板凝集试验（RBP）均为阳性。均采用规范抗菌治疗,3例患者行手术治疗。结果患者均获随访,时间3～12个月,经规范抗菌治疗后治愈18例,治愈率18／19。3例手术患者术后恢复良好。末次随访时,ESR （10．5±5．1）mm／1h,CRP （4．3±2．5）mg／L,VAS 评分（0．9±0．7）分、JOA 评分（25．0±1．8）分,JOA下腰痛评分治疗改善率78．9％;ESR、VAS 及 JOA 评分与治疗前比较差异均有统计学意义（P ＜0．05）,而 CRP与治疗前比较差异无统计学意义（P ＝0．442）。结论布鲁杆菌脊柱炎易被误诊误治,对可疑患者宜早期行血清学检验,一经确诊应规范、联合、长期、足量抗菌治疗,必要时采用手术治疗,可取得良好效果。     

华蟾素片联合SOX方案治疗晚期胃癌的临床研究

目的探讨华蟾素片联合SOX方案(奥沙利铂+替吉奥)治疗晚期胃癌的临床疗效。方法选取2015年1月—2017年12月涟水县人民医院收治的60例晚期胃癌患者作为研究对象,根据不同的治疗方式将患者分为对照组和治疗组,每组各30例。对照组患者采用SOX方案治疗:静滴注射用奥沙利铂130 mg/(m~2·d),用10%葡萄糖注射液500 mL稀释后静滴3 h,21 d给药1次;同时餐后用温水送服替吉奥胶囊,80 mg/(m~2·d),2次/d,连续14 d,停药7 d。治疗组在对照组基础上口服华蟾素片,3片/次,3次/d。21 d为1个周期,两组患者均进行2个周期的治疗。观察两组患者的临床疗效,同时比较两组治疗前后的血清肿瘤指标水平、疼痛评分(VAS)和生活质量综合评定问卷评分。结果治疗后,治疗组的总有效率(RR)和肿瘤控制率(DCR)分别为63.3%、83.3%,均明显高于对照组的36.7%、60.0%,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者的癌胚抗原(CEA)和糖类抗原19-9(CA19-9)水平均显著降低,同组治疗前后比较差异具有统计学意义(P0.05),且治疗后治疗组血清肿瘤指标均明显低于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者VAS评分均明显降低,同组治疗前后比较差异具有统计学意义(P0.05);且治疗后治疗组的VAS评分明显低于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者的社会功能、心理功能、功能和物质生活评分均明显提高,同组治疗前后比较差异具有统计学意义(P0.05),且治疗后治疗组生活质量水平显著高于对照组,两组比较差异具有统计学意义(P0.05)。结论华蟾素片联合SOX化疗方案治疗晚期胃癌具有较好的临床疗效,在不增加化疗副反应的情况下,可有效缓解患者的癌性疼痛状况并可改善患者的预后,值得临床推广应用。     

高同型半胱氨酸对高血压大鼠血管平滑肌细胞GRP78和CHOP的表达的影响与血管重构的关系

目的：观察同型半胱氨酸（Homocysteine,Hcy）对高血压大鼠内质网应激因子GRP78和CHOP表达及血管中层厚度变化,探讨Hcy对血管重构的影响。方法：采用腹主动脉缩窄术建立高血压大鼠模型,术后两周采用无创尾套法测量大鼠血压,选取24只成年雄性大鼠[平均动脉压（MAP）〉150mmHg]随机等分为2组,即对照组和蛋氨酸组,每组12只（n=12）。对照组给予普通饮食＋双蒸水灌胃,蛋氨酸组给于30g/L蛋氨酸饮食＋双蒸水灌胃;根据实验结束的时间,又将各组分为4W和8W两个亚组,各亚组6只（n=6）。用同型半胱氨酸检测仪检测血清同型半胱氨酸浓度,用颈动脉插管法测定各组大鼠的MAP,并利用图像分析软件测量血管中层的厚度;HE染色观察大鼠主动脉血管形态学变化;通过免疫组化及Western blot检测大鼠主动脉血管平滑肌细胞（VSMCs）组织中GRP78及CHOP表达水平。结果：①对照组大鼠血清Hcy浓度在正常值范围（〈10μmol／L）;蛋氨酸组大鼠血清Hcy浓度明显高于对照组（P〈0．01）。②两组大鼠MAP均显著增高,4周时两者之间差异不明显,8周时两者差异显著（P〈0．05）;③蛋氨酸组大鼠血管平滑肌中层厚度显著大于对照组（P〈0．05）;④HE染色显示,与对照组相比,蛋氨酸组大鼠主动脉VSMCs显著肥大,管壁显著增厚;⑤两组CRP78和CHOP蛋白表达量增高,与对照组相比蛋氨酸组表达更明显。结论：高同型半胱氨酸可能通过促使高血压大鼠动脉VSMCs内质网应激反应,导致CRP78及CHOP的平衡失调加剧,从而引起血管损伤加重,而发生血管重构加重。     

Anticoagulation therapy prevents portal-splenic vein thrombosis after splenectomy with gastroesophageal devascularization

AIM: To compare the incidence of early portal or splenic vein thrombosis (PSVT) in patients treated with irregular and regular anticoagulantion after splenectomy with gastroesophageal devascularization.METHODS: We retrospectively analyzed 301 patients who underwent splenectomy with gastroesophageal devascularization for portal hypertension due to cirrhosis between April 2004 and July 2010. Patients were categorized into group A with irregular anticoagulation and group B with regular anticoagulation, respectively. Group A (153 patients) received anticoagulant monotherapy for an undesignated time period or with aspirin or warfarin without low-molecular-weight heparin (LMWH) irregularly. Group B (148 patients) received subcutaneous injection of LMWH routinely within the first 5 d after surgery, followed by oral warfarin and aspirin for one month regularly. The target prothrombin time/international normalized ratio (PT/INR) was 1.25-1.50. Platelet and PT/INR were monitored. Color Doppler imaging was performed to monitor PSVT as well as the effectiveness of thrombolytic therapy.RESULTS: The patients’ data were collected and analyzed retrospectively. Among the patients, 94 developed early postoperative mural PSVT, including 63 patients in group A (63/153, 41.17%) and 31 patients in group B (31/148, 20.94%). There were 50 (32.67%) patients in group A and 27 (18.24%) in group B with mural PSVT in the main trunk of portal vein. After the administration of thrombolytic, anticoagulant and anti-aggregation therapy, complete or partial thrombus dissolution achieved in 50 (79.37%) in group A and 26 (83.87%) in group B.CONCLUSION: Regular anticoagulation therapy can reduce the incidence of PSVT in patients who undergo splenectomy with gastroesophageal devascularization, and regular anticoagulant therapy is safer and more effective than irregular anticoagulant therapy. Early and timely thrombolytic therapy is imperative and feasible for the prevention of PSVT.     

VD方案和VAD方案治疗多发性骨髓瘤的疗效观察和比较

目的 探讨VD方案和VAD方案治疗多发性骨髓瘤的临床疗效和安全性.方法 回顾性分析了2008年6月到2011年6月我院收治的59例多发性骨髓瘤患者的临床资料,根据治疗方案将患者分为VD组(38例)和VAD组(21例),VD组接受硼替佐米联合地塞米松治疗,3周为一个疗程,治疗2个疗程;VAD组接受长春新碱、阿霉素联合地塞米松治疗,4周为一疗程,治疗2个疗程.分别对两组疗效和不良反应进行分析.结果 VD组和VAD组治疗缓解率分别为83.78％和59.09％,VD方案优于VAD方案,差异具有统计学意义(P＜0.05).VD组主要不良反应为血液毒性和周围神经病变,症状较轻微,在停药和对症处理后症状消失或缓解.VAD组主要不良反应为感染、脱发和血液毒性等,其中感染多以3～4度为主.结论 VD方案治疗多发性骨髓瘤疗效优于VAD方案,不良反应轻微,患者可耐受,值得临床推广使用.     

A novel protocol for postpartum magnesium sulphate in severe pre-eclampsia: a randomized controlled pilot trial

Objective: Magnesium sulphate is the preferred anticonvulsant used to prevent the development of fits in severe pre-eclampsia; we aim to compare between three different protocols of postpartum magnesium sulphate in the effectiveness of preventing the development of fits in severe pre-eclampsia.

Methods: Double-blind randomized controlled pilot trial, done in Cairo university hospital, Cairo, Egypt during 2013–2014, on 240 women with severe pre-eclampsia. Magnesium sulphate intravenous infusion was given in the postpartum period to all the patients, women were randomly allocated to group I (Single loading dose only), group II (12?h abbreviated protocol) or group III (24?h standard protocol) (n?=?80 in each group).

Results: There were no significant difference between the three groups as regards the incidence of eclampsia, elevated liver enzymes and low platelets syndrome, maternal ICU admission and; however The incidence of flushing was significantly higher in group III than group II and I (24 [30%] versus 12 [15%] versus 4 [5%]; p?<?0.001) respectively.

Conclusion: The pilot study demonstrates that the single-loading dose of postpartum magnesium sulphate is a promising alternative to the standard and the abbreviated protocol in preventing eclampsia; however, a large clinical trial is necessary to prove this.     

FOLFOX4联合参麦注射液治疗中晚期肝癌术后存活质量的影响

目的探究FOLFOX4联合参麦注射液治疗中晚期肝癌术后存活质量的影响。方法选取2012年3月~2014年2月我院收治的90例原发性肝癌患者为研究对象,按随机数字表法分为观察组和对照组,每组45例,对照组患者单独给予FOLFOX4方案(奥沙利铂~+亚叶酸钙~+5-氟尿嘧啶)治疗,观察组在对照组基础上联合参麦注射液,治疗2个疗程后评价两组患者治疗疗效,同时分别检测治疗前后患者血液T淋巴细胞亚群(CD3~+、CD4~+、CD8~+)变化情况,比较两组患者治疗前后细胞免疫指标。观察两组患者治疗前后生存质量评分和KPS评分改善程度和毒副反应。结果观察组患者治疗总有效率为57.78%,对照组患者治疗总有效率为35.56%,两组差异具有统计学意义(P0.05)。治疗后两组患者CD3~+、CD4~+、CD8~+、CD4~+/CD8~+细胞免疫指标差异显著,观察组患者CD3~+、CD4~+、CD4~+/CD8~+细胞免疫指标明显明显高于对照组,CD8~+指标明显低于对照组,差异具有统计学意义(P0.05)。治疗后两组患者生活质量评分和KPS评分总改善率差异显著,观察组生活质量评分和KPS评分总改善率显著高于对照组,差异具有统计学意(P0.05)。两组患者在骨髓抑制、神经毒性、肝功能方面等毒副反应差异具有统计学意义(P0.05),而在胃肠道反应、口腔炎上差异不具有统计学意义(P0.05)。结论参麦注射液联合FOLFFOX4方案治疗中晚期原发性肝癌具有良好疗效,能够改善患者免疫力和提高患者生活质量,降低化疗引起的毒副反应,其疗效明显优于单独FOLFFOX4方案治疗。     

Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in Oxidized Low-density Lipoprotein Mediated Induction of Endothelial Apoptosis

Objective PERK/eI F2α/CHOP is a major signaling pathway mediating endoplasmic reticulum(ER) stress related with atherosclerosis.Oxidized LDL(ox-LDL) also induces endothelial apoptosis and plays a vital role in the initiation and progression of atherosclerosis.The present study was conducted to explore the regulatory effect of ox-LDL on PERK/e IF2α/CHOP signaling pathway in vascular endothelial cells.Methods The effects of ox-LDL on PERK and p-e IF2α protein expression of primary human umbilical vein endothelial cells(HUVECs) were investigated by Western blot analysis.PERK gene silencing and selective eI F2α phosphatase inhibitor,salubrinal were used to inhibit the process of ox-LDL induced endothelial cell apoptosis,caspase-3 activity,and CHOP mR NA level.Results Ox-LDL treatment significantly increased the expression of PERK,PERK-mediated inactivation of e IF2α phosphorylation,and the expression of CHOP,as well as the caspase-3 activity and apoptosis.The effects of ox-LDL were markedly decreased by knocking down PERK with stable transduction of lentiviral sh RNA or by selective eI F2α phosphatase inhibitor,salubrinal.Conclusion This study provides the first evidence that ox-LDL induces apoptosis in vascular endothelial cells mediated largely via the PERK/eI F2α/CHOP ER-stress pathway.It adds new insights into the molecular mechanisms underlying the pathogenesis and progression of atherosclerosis.