肺炎支原体感染69例临床特点分析

目的分析肺炎支原体感染的临床特点,探讨诊断策略并评价大环内酯类与喹诺酮类抗生素联合治疗的疗效。方法回顾性分析我院69例肺炎支原体感染患者的临床资料,统计治疗前后实验室检查及X线胸片检查的情况。结果 69例患者治疗后显效率为100%,X线胸片复查显示肺部病变完全吸收,胸腔积液消失,24 h内体温降至37℃以下,对69例患者进行随访,均未见复发。结论肺炎支原体为呼吸道感染的主要原因体之一,临床诊断时应结合影像学表现和血清学检查结果综合进行判断。     

脑梗死患者医院感染因素分析及护理干预

目的探讨降低脑梗死患者医院内感染发生率的护理干预措施。方法对1 945例脑梗死患者住院期间发生医院内感染的资料进行回顾性分析。结果采取护理干预前脑梗死患者972例发生医院内感染114例次,医院内感染发生率为11.6%,发生的首要部位是下呼吸道、泌尿道和上呼吸道;护理干预组脑梗死患者973例,感染73例次,感染率7.4%,明显低于护理干预前(P<0.01)。结论有效的护理干预可减少脑梗死患者医院内感染的发生。     

痛宁胶囊对硝酸甘油型偏头痛大鼠血浆NO和5-HT浓度的影响

目的 观察痛宁胶囊对偏头痛大鼠血浆一氧化氮(NO)和5-羟色胺(5- HT)浓度的影响,探讨痛宁胶囊治疗偏头痛的神经学机制.方法 SD大鼠随机分成6组:空白对照组、模型对照组、阳性药物对照组、研究药物组(痛宁胶囊高、中、低剂量组).除空白对照组外,其余各组采用皮下注射硝酸甘油法复制大鼠偏头痛模型.30 min后研究药物组给予痛宁胶囊高、中、低剂量药液灌胃.阳性药物对照组按照6 mg/kg给予琥珀酸舒马普坦溶液灌胃.空白对照组和模型对照组予以等容积的蒸馏水灌胃.造模4h后腹主动脉采血,NO采用硝酸还原酶法测定,5- HT采用酶联免疫吸附法(ELISA)测定.结果 与模型对照组比较,阳性药物对照组及痛宁胶囊高、中剂量组均能显著降低偏头痛大鼠血浆NO的浓度,且能明显升高血浆5- HT的浓度(P＜0.05).与阳性药物对照组比较,高剂量组降低NO浓度及升高5- HT浓度无统计学意义(P＞0.05).结论 病宁胶囊可以调节偏头痛大鼠血管活性物质和神经递质的水平,可能是痛宁胶囊治疗偏头痛的作用机制之一.     

miR-92a/DUSP10/JNK signalling axis promotes human pancreatic cancer cells proliferation

Pancreatic cancer is one of the most common types of cancers in the whole world with a poor prognosis. Finding out how the cancer form and develop is the most important way to cure this cancer. miRNAs, 21–22 nucleotides regulatory small non-coding RNAs, have been found to be critical involved in the growth of pancreatic cancer. In this study, we found that miR-92a was up regulated in three kinds of human pancreatic cancer cell lines. There is a correlation between miR-92a and malignant degree of human pancreatic cancer cell lines. Then we found that miR-92a was essential for promoting cell proliferation in human pancreatic cancer. Inhibition of the function of miR-92a repressed the proliferation of pancreatic cancer cells. Further, we found that miR-92a enhanced the activation of JNK signalling pathway by directly targeting the JNK signalling inhibitor DUSP10. DUSP10 is responsible for miR-92a induced JNK signalling and cell proliferation. Altogether, our study showed a miR-92a/DUSP10/JNK signalling pathway that plays an important role in regulating the proliferation of pancreatic cancer cells.     

Targeting AMCase reduces esophageal eosinophilic inflammation and remodeling in a mouse model of egg induced eosinophilic esophagitis

Studies of AMCase inhibition in mouse models of lung eosinophilic inflammation have produced conflicting results with some studies demonstrating inhibition of eosinophilic inflammation and others not. No studies have investigated the role of AMCase inhibition in eosinophilic esophagitis (EoE). We have used a mouse model of egg (OVA) induced EoE to determine whether pharmacologic inhibition of AMCase with allosamidin reduced eosinophilic inflammation and remodeling in the esophagus in EoE. Administration of intra-esophageal OVA for 6 weeks to BALB/c mice induced increased levels of esophageal eosinophils, mast cells, and features of esophageal remodeling (fibrosis, basal zone hyperplasia, deposition of the extracellular matrix protein fibronectin). Administration of intraperitoneal (ip) allosamidin to BALB/c mice significantly inhibited AMCase enzymatic activity in the esophagus. Pharmacologic inhibition of AMCase with ip allosamidin inhibited both OVA induced increases in esophageal eosinophilic inflammation and OVA induced esophageal remodeling (fibrosis, epithelial basal zone hyperplasia, extracellular matrix deposition of fibronectin). This inhibition of eosinophilic inflammation in the esophagus by ip allosamidin was associated with reduced eotaxin-1 expression in the esophagus. Oral allosamidin inhibited eosinophilic inflammation in the epithelium but did not inhibit esophageal remodeling. These studies suggest that pharmacologic inhibition of AMCase results in inhibition of eosinophilic inflammation and remodeling in the esophagus in a mouse model of egg induced EoE partially through effects in the esophagus on reducing chemokines (i.e. eotaxin-1) implicated in the pathogenesis of EoE.     

肠康方对肠易激综合征内脏高敏感模型大鼠的作用

[目的]探讨肠康方对肠易激综合征(IBS)内脏高敏感模型大鼠的作用.[方法]制备肠易激综合征内脏高敏感模型,将72只Sprague-Dawley大鼠随机分为6组,即模型组,空白对照组,阳性药物对照组,肠康方高、中、低剂量组.在造模第60天开始灌胃给药或0.9％氯化钠溶液共10d,干预后通过腹肌回缩反射(AWR)半定量评分测定大鼠内脏敏感性.[结果]不同压力下模型组AWR评分显著高于空白对照组,肠康方高、中、低剂量组治疗后AWR评分均显著低于模型组(P＜0.05或P＜0.01).[结论]肠康方可通过改善内脏高敏感治疗IBS.     

放化疗结合中医药治疗食管癌的临床研究进展

食管癌的非手术治疗手段目前有放疗、化疗、中医药治疗.放疗及化疗都有其局限性和不足之处:放疗过程中不可避免会出现放射性食管炎、放射性肺炎等不良反应;化疗的不良反应,尤其是消化系反应、骨髓抑制、肝肾功能损害等,使部分肿瘤患者生活质量降低,甚至造成化疗疗程中断,影响治疗效果.中医药能明显减轻放化疗治疗的不良反应、提高患者生存质量、延长生存期.本文就近年来放化疗结合中医药治疗食管癌的临床研究作一综述.     

清肺活血方对AECOPD患者凝血、纤溶活性影响

目的观察慢性阻塞性肺病急性加重期(AECOPD)患者应用清肺活血方对其凝血和纤溶活性的干预作用。方法将48例AECOPD患者随机分成治疗组和对照组,两组均给予常规治疗,治疗组(24例)在常规治疗基础上加用清肺活血中药,治疗10 d,治疗前后均检测凝血和纤溶活性指标。结果对照组治疗前后凝血功能指标略有改善,但无显著性差异(P0.05),显示常规治疗虽能使患者病情得到改善,但无法有效改善患者血液的高粘、高凝状态;治疗组治疗前后凝血和纤溶活性改善明显(P0.01或P0.05),显示其可有效改善患者血液的高粘、高凝状态。结论对AECOPD患者常规治疗同时配合清肺活血治疗,效果肯定,防止血栓形成起着重要的作用。     

VEGFR-1抗体对肺癌A549细胞顺铂药物敏感性的影响

目的观察血管内皮生长因子受体-1(VEGFR-1)抗体影响人肺腺癌A549细胞对顺铂(CDDP)的药物敏感性。方法将VEGFR-1抗体与顺铂单独及联合作用于A549细胞,72 h后用MTT法,克隆形成法检验化疗药物的敏感性。结果VEGFR-1抗体(30μmol/L)和顺铂(10μg/mL)联用组抑制A549细胞生长均显著强于VEGFR-1抗体与顺铂单独用药组。结论VEGFR-1抗体能显著增强顺铂抑制人肺癌细胞A549细胞生长的作用,可能是很有潜力化疗增敏剂。     

前列腺炎患者前列腺按摩液320例病原体分析及其与血清PSA的关系

目的:分析前列腺按摩液病原体感染及药敏情况,并探讨其与血清前列腺特异性抗原(PSA)的相关性,为系统、规范地诊断和治疗前列腺炎提供依据。方法:320例前列腺炎患者,每例采集前列腺按摩液并一式3份:其中1份做细菌培养及鉴定,另1份做支原体培养及药敏,第3份用胶体金法测衣原体。在采集前列腺按摩液前抽取静脉血供PSA检测。结果:320例前列腺按摩液标本,分离出病原菌244株,其中细菌188株,以葡萄球菌为主;支原体和衣原体44株,以解脲脲原体(UU)为主。革兰阳性球菌对万古霉素、利奈唑烷较敏感;UU主要对交沙霉素和强力霉素敏感;病原菌培养阳性组的血清PSA水平[(6.98±0.56)μg/L]较阴性组[(2.32±0.12)μg/L]明显升高,差异有统计学意义(P0.05)。结论:前列腺炎可引起血清PSA水平升高,其感染的病原体对不同的抗菌谱耐药性差异很大,应在正确的病原学诊断和药敏试验指导下,选择合适以及个性化的抗生素治疗方案。