肺间质纤维化大鼠肺组织基质金属蛋白酶及其组织抑制因子含量变化

观察肺纤维化形成过程中基质金属蛋白酶（Matrix Metallo proteinas简称MMPs)及其组织抑制因子（Tissue inhibitors of Metallo proteinases简称TIMPs)含量的变化,探讨其在肺纤维化发病中的作用。将Wistar大鼠60只,随机均分为对照组及模型组,气管内注入博莱霉素A5 5mg/kg,制备肺间质纤维化动物模型,观察注药后1、3、7、14及28d肺脏病理变化,利用酶谱法及免疫印记法分析肺组织MMP－2、MMP－9、TIMP－1的含量变化。结果显示各模型组pro-MMP-2、MMP－2、TIMP－1蛋白含量均较对照组增加,尤其7、14及28d组MMP－2较前明显增多。而MMP－9变化不很明显。提示在肺纤维化形成过程中,pro-MMP-2、MMP－2及TIMP－1都有所增高,MMP／TIMP比例失衡是最终导致肺间质纤维化形成的重要因素。     

应用两性霉素B治疗ICU念珠菌感染临床观察

目的 评价近年来静脉应用两性霉素B治疗念珠菌感染的疗效及不良反应.方法 回顾性分析40例念珠菌感染患者静脉应用两性霉素B的疗效、治疗过程中的不良反应及相应防治措施.结果 除1例因不良反应明显而中途停药外,其余39例患者病原学监测真菌均已清除.应用两性霉素B治疗过程中,低钾血症的发生率最高(80.0%),肾功能损害、血红蛋白下降、血小板下降、寒战、心电图改变、肝功能损害的发生率分别为32.5%、20.0%、5.0%、17.5%、17.5%、10.0%.结论 两性霉素B疗效显著,虽然应用过程中不良反应发生率较高,但只要密切监测病情变化,采取相关措施,仍可用于念珠菌感染的治疗.     

右中叶肺癌术后合并急性呼吸窘迫综合征救治体会

ARDS作为多脏器功能障碍综合征(MODS)的组成部分,其发病机制错综复杂.病死率较高.临床早期诊断及干预治疗对提高患者生存率非常重要.我科成功救治1例肺癌术后并发ARDS的患者,并随访至今,现将治疗体会总结如下.     

锌指蛋白A20对Toll样受体信号途径的负反馈调控及其对机体的保护作用

Toll-like receptors (TLRs) recognize pathogens and initiate innate immune responses at the early stage of virus invasion, promoting the maturation and differentiation of immune cells, regulating immune respon-ses,and triggering inflammatory responses. Lipopolysaccharide (LPS) activates the TLR4 signaling pathways which result in the activation of NFκB and JNK/SAPK and the expression of large amounts of inflammatory fac-tors,leading to systemic inflammatory response and multiple organ failure. A20, a NFκB-dependant cytosolic protein, via a negative feedback loop blocks NFκB activation and participates in the regulation of inflammatory responses and the inhibition of apptosis;therefore, it provides protective effect on the body.     

心脏结节病致三度房室传导阻滞1例

正1病例资料患者,女,61岁,2015年12月以"活动后胸闷、气促3年余,再发加重1个月"为主诉入院。既往体健。患者3年前无明显诱因反复出现活动后胸闷、气促,不影响日常生活。1年前出现胸骨后及心前区胀痛,可放射至后背,伴心悸、乏力、多汗,持续半小时缓解。半年前胸闷、气促症状较前加重,轻微活动后即可出现,夜间不能平卧,伴咳嗽、咳白痰。入院后体检:双肺呼吸音粗,可闻及散在湿性     

锌指蛋白A20对Toll样受体信号途径的负反馈调控及其对机体的保护作用

Toll-like receptors (TLRs) recognize pathogens and initiate innate immune responses at the early stage of virus invasion, promoting the maturation and differentiation of immune cells, regulating immune respon-ses,and triggering inflammatory responses. Lipopolysaccharide (LPS) activates the TLR4 signaling pathways which result in the activation of NFκB and JNK/SAPK and the expression of large amounts of inflammatory fac-tors,leading to systemic inflammatory response and multiple organ failure. A20, a NFκB-dependant cytosolic protein, via a negative feedback loop blocks NFκB activation and participates in the regulation of inflammatory responses and the inhibition of apptosis;therefore, it provides protective effect on the body.     

锌指蛋白A20对Toll样受体信号途径的负反馈调控及其对机体的保护作用

Toll-like receptors (TLRs) recognize pathogens and initiate innate immune responses at the early stage of virus invasion, promoting the maturation and differentiation of immune cells, regulating immune respon-ses,and triggering inflammatory responses. Lipopolysaccharide (LPS) activates the TLR4 signaling pathways which result in the activation of NFκB and JNK/SAPK and the expression of large amounts of inflammatory fac-tors,leading to systemic inflammatory response and multiple organ failure. A20, a NFκB-dependant cytosolic protein, via a negative feedback loop blocks NFκB activation and participates in the regulation of inflammatory responses and the inhibition of apptosis;therefore, it provides protective effect on the body.     

锌指蛋白A20对Toll样受体信号途径的负反馈调控及其对机体的保护作用

Toll-like receptors (TLRs) recognize pathogens and initiate innate immune responses at the early stage of virus invasion, promoting the maturation and differentiation of immune cells, regulating immune respon-ses,and triggering inflammatory responses. Lipopolysaccharide (LPS) activates the TLR4 signaling pathways which result in the activation of NFκB and JNK/SAPK and the expression of large amounts of inflammatory fac-tors,leading to systemic inflammatory response and multiple organ failure. A20, a NFκB-dependant cytosolic protein, via a negative feedback loop blocks NFκB activation and participates in the regulation of inflammatory responses and the inhibition of apptosis;therefore, it provides protective effect on the body.     

非霍奇金淋巴瘤致重度溶血性贫血一例

患者男，53岁，因感冒后乏力、尿黄半个月，加重伴发热4d于2005年10月3日入院。既往高血压史2年。感冒后出现咽痛，应用青霉素1200万单位每日1次静脉输注，咽痛好转。体格检查：体温38．2℃，血压140／70mmHg，脉搏92次／min，呼吸18次／min，精神萎靡，皮肤巩膜黄染，左颈部扪及一枚1cm×1cm淋巴结，无触痛。睑结膜苍白，双肺呼吸音清，心率92次／min。血常规：血红蛋白（Hb）由125g／L迅速下降至86g／L，白细胞7．8×10^9／L，血小板215×10^9／L，并见红细胞有自身凝集现象。Coombs直接和间接试验C3和IgG阳性，血浆游离Hb 0．1065g／L。