Objective:To investigate the mechanism of dexmetomidine (DEX) in improving lung injury in septic mice.Methods:Male C57BL/6 mice were randomly assigned to the blank group (NC), sham operation group (sham), cecal ligation and puncture group (CLP), and Dex treatment group (CLP+DEX), 36 mice per group. Mice in the CLP group were intraperitoneally injected with 1 mL sterile saline 15 min before CLP, and mice in the CLP + DEX group were intraperitoneally injected with 50 μg/kg DEX 15 min before CLP. The survival rate was recorded within 24 h after CLP. The mice were sacrificed at 0, 3, 6, 12, and 24 h after CLP, and lung tissues were collected. The expression levels of cytokines (IL-6, IL-1β, TNF-α) and lncRNA-HOTAIR in the lung of mice were detected by qPCR. RAW264.7 cell were cultured in vitro, LPS (100 ng/mL) and DEX (1 μ mol/L) were used to establish a cell model for studying the mechanism of Dex, and the expression of cytokines (IL-6, IL-1β, TNF-α) and lncRNA-HOTAIR in RAW264.7 cell model were detected by qPCR. In addition, the effect of lncRNA-HOTAIR on sepsis was explored in vivo and in vitro by knockdown or overexpression of HOTAIR.Results:The survival rate of the CLP+DEX group was higher than that of the CLP group within 24 h after surgery, and the levels of IL-6, IL-1β, and TNF-α in the lungs were significantly lower than those in the CLP group at 6, 12, and 24 h after surgery ( P<0.05). In addition, the level of lncRNA HOTAIR showed that the expression level of lncRNA HOTAIR in the lungs of mice were decreased after Dex treatment, and were decreased 1.1 times ( P<0.05), 4.0 times ( P<0.01) and 3.8 times ( P<0.01) at 6, 12, and 24 h, respectively. Compared with the NC group, knockdown of HOTAIR significantly decreased the levels of IL-1β, IL-6, and TNF-α in septic mice ( P<0.05), and overexpression of HOTAIR significantly increased the levels of IL-1β, IL-6, and TNF-α in septic mice ( P<0.01). Conclusions:DEX can reduce the production of inflammatory factors in the lungs of septic mice and improve the survival rate of septic mice. The mechanism may be related to the inhibition of HOTAIR expression.

Objective:To study the influence of serum triggering receptor expressed on myeloid cells 1(TREM-1)level on prognosis in elderly patients with sepsis and acute respiratory distress syndrome(ARDS).Methods:A total of 100 elderly patients with sepsis were selected as the research objects.All the patients with sepsis were divided into sepsis ARDS group and sepsis non-ARDS group.General data and TREM-1 level were compared between the two groups.The patients with sepsis ARDS were divided into death group and survival group according to the survival status during the 28-day follow-up.TREM-1 level, acute physiology and chronic health evaluation(APACHE)Ⅱ score and SOFA score were compared between the two groups.The correlation between serum TREM-1 level and procalcitonin(PCT), APACHE Ⅱ score and SOFA score was analyzed.The survival rate of high TREM-1 level group and low TREM-1 level group was compared.Results:The age, white blood cell(WBC), PCT, APACHE Ⅱ score, SOFA score and TREM-1 level of sepsis ARDS patients were significantly higher than those of non-ARDS patients( t=2.722, 6.088, 11.55, 6.889, 4.661, 6.122, all P<0.05). The incidence of sepsis ARDS patients with chronic obstructive pulmonary disease was significantly higher than that of non-ARDS patients( χ2=7.895, P<0.05). Serum TREM-1 level, APACHE Ⅱ score and SOFA score of ARDS patients in death group were significantly higher than those in survival group( t=3.293, 6.173, 4.255, all P<0.05). Serum TREM-1 level was positively correlated with PCT, APACHE Ⅱ score and SOFA score( t=0.553, 0.602, 0.636, P<0.001). The Kaplan-Meier survival curve showed that the survival rate of high TREM-1 level group was significantly lower than that of low TREM-1 level group( χ2=3.999, P=0.036). Cox regression analysis showed that TREM-1 level was a risk factor for the prognosis of ARDS patients with sepsis( HR=1.893, 95% CI: 1.049-3.414). Conclusions:Serum TREM-1 level is significantly increased in elderly patients with sepsis ARDS, which is closely related to the prognosis and can be used as a potential prognostic biomarker.

目的 本文研究羟基红花黄色素A(Hydroxysaffior yellow A,HSYA)对重症急性胰腺炎(severe acute pancreatitis,SAP)相关肺损伤的保护作用及其机制.方法 50只小鼠随机数字法分成5组(每组10只):假手术组,SAP组和不同剂量(20,40和80 mg/kg)HSYA预处理组.在SAP诱导前24 h,采用HSYA预处理小鼠,并在造模72 h后分离胰腺和肺组织用于组织病理学检查,并收集支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)用于生化分析.结果 与对照组相比,SAP组血清淀粉酶活性、肺损伤病理评分和BALF蛋白浓度均显著增高[(2120.44±354.5)U/L vs.(226.72±20.84)U/L;(6.91±0.28)vs.(0.53±0.18);(2563.25±348.22)μ g/mL vs.(345.62±56.35)μ g/mL,均P＜0.05];炎性因子 tumor necrosis factor(TNF)-α 和 interleukin(IL)-6 水平和髓过氧化物酶(myeloperoxidase,MPO)活性升高[(120.5±14.25)pg/mL vs.(31.5±4.82)pg/mL;(214.72±10.62)pg/mL vs.(39.26±5.66)pg/mL;(4.52±0.34)Units/mg vs.(1.03±0.17)Units/mg].与SAP组相比,HSYA预处理显著减轻SAP相关胰腺和肺组织损伤以及BALF中炎性因子TNF-α、IL-6和MPO活性.此外,HSYA促进抗氧化蛋白血红素氧合酶l(heme oxygenase-1,HO-1)表达,并阻断NF-κB信号通路激活.结论 HSYA可以发挥抗炎和抗氧化活性从而抑制SAP相关肺损伤,表明HSYA可能是SAP诱导肺损伤的潜在治疗药物.

目的:探讨血清中介素对脓毒症合并肝损伤患者预后的影响.方法:选择2017年1月～2020年6月中日友好医院收治的90例脓毒症合并肝损伤患者作为研究对象,另选择40例单纯脓毒症患者和40例健康体检者作为对照.比较各组的中介素水平.根据入院后28d内的生存状态将患者分为死亡组和生存组,采用多因素回归分析脓毒症合并肝损伤患者预后的影响因素.结果:脓毒症合并肝损伤组的中介素水平显著高于脓毒症组(P＜0.05).血清中介素水平在轻度、中度和重度肝损伤脓毒症组的差异均有统计学意义(P＜0.05).死亡组的重度肝损伤程度和意识障碍的发生率、中介素水平和APACHE Ⅱ评分均显著高于生存组,BMI显著低于生存组.重度肝损伤、意识障碍、高中介素水平、高APACHE Ⅱ评分是脓毒症合并肝损伤患者死亡的危险因素(P＜0.01).结论:血清中介素水平与脓毒症合并肝损伤患者临床预后密切相关,可作为评估预后的潜在指标.

每年一到盛夏,老年人中署送医院急救的屡见不鲜.天气“炎值”持续爆表,老年人由于身体机能减弱、体温调节功能下降,再加上汗腺开始萎缩散热不畅,极易发生中暑.又是一年“三伏天”,老年朋友,防暑您真的准备好了吗?

如今全球变暖愈发明显,再加上城市热岛效应,原本酷热难耐的夏天愈发不好过,气温更是屡创新高!空调无疑成了人们最好的消暑利器. ”命是空调给的,病也是空调吹的”.空调给人们带来舒爽的同时,也带来了一系列疾病.从高温环境进入空调屋,或从低温的空调室内来到户外时都会引发人体的不适.与此同时,长期待在空调房里,因空气不流通,会出现鼻塞、头昏、头痛、打喷嚏等症状,以及一些皮肤过敏症状如皮肤发紧发干、皮肤变差等.这类现象在现代医学上统称为“空调综合征”,也叫“空调病”.

目的:总结过度换气综合征患者的临床表现和治疗体会.方法:回顾性分析急诊科2009年5月～2012年6月共110例过度换气综合征患者的临床资料.结果:110例患者均具有不同程度的情绪紧张、焦虑等典型症状,多为负面情绪诱发,并排除其他器质性疾病;78例患者经过心理疏导和呼吸管理治疗痊愈,32例患者同时辅以药物镇静、对症治疗痊愈.结论:对于过度换气综合征患者,应该准确识别,以心理疏导、呼吸管理为主,根据个体情况辅以药物治疗,大多数患者可得到迅速、有效的缓解.

回顾性分析2例Peutz-Jeghers综合征患者的临床资料,并结合相关文献探讨其临床特征及诊断与治疗,提示内镜下息肉电切术为治疗有效方法,同时此类患者发生肿瘤的危险性较高,应加强术后随访,定期复查内镜和筛查肿瘤.

<正>患者女性,64岁,因咳嗽、胸闷憋气1周,加重1d,于2011年10月15日入院。查体:端坐体位,双肺呼吸音粗,双肺底少量细湿罗音,心律齐,未及杂音,双下肢无可凹性浮肿;血液化验:丙氨酸转氨酶(ALT)2690 IU/L,天冬氨酸转氨酶(AST)6640 IU/L,总胆红素(TBIL)20.91μmol/L,直