头孢哌酮钠舒巴坦钠联合左氧氟沙星治疗医院获得性肺炎的临床疗效观察

目的：探讨头孢哌酮钠舒巴坦钠联合左氧氟沙星治疗医院获得性肺炎（ hospital acquired pneu-monia,HAP）的临床疗效和不良反应。方法将42例HAP确诊病例随机分为治疗组和对照组,每组21例。治疗组用头孢哌酮钠舒巴坦钠联合左氧氟沙星治疗,对照组用头孢哌酮钠舒巴坦钠治疗,疗程均为7～8d。结果治疗组症状、体征恢复正常的时间为（48.24±7.54）h,对照组为（72.36±10.24）h,两组比较差异有统计学意义（P＜0.01）;治疗组的临床疗效优于对照组（P＜0.05）;两组不良反应发生率比较差异无统计学意义（ P＞0.05）。结论头孢哌酮钠舒巴坦钠联合左氧氟沙星治疗HAP的疗效明显优于单用头孢哌酮钠舒巴坦钠,值得临床推广应用。     

盖髓剂抑菌作用的体外实验观察

本文通过体外抑菌实验观察羟基磷灰石（Ｈｙｄｒｏｘｙａｐａｔｉｔｅ，ＨＡＰ）、氢氧化钙（Ｃａｌｃｉｕｍｈｙｄｒｏｘｉｄｅ，ＣＨ）以及两种盖髓制剂（ＨＡＰ制剂、ＨＡＰ－ＣＨ制剂）对金黄色葡萄球菌、大肠杆菌、化脓性链球菌、变形链球菌、中间普里沃氏菌的抑菌作用。结果显示：ＨＡＰ对各实验菌无抑菌作用，ＣＨ有一定的抑菌作用，ＨＡＰ制剂和ＨＡＰ－ＣＨ制剂具有较强的抑菌作用     

急性脑梗死合并医院内获得性肺炎后血栓调节蛋白变化及其与血浆TNF-α的相关性

目的:观察脑梗死合并医院内获得性肺炎患者血栓调节蛋白含量的变化及其与血浆肿瘤坏死因子的相关性,探讨脑梗死合并医院内获得性肺炎对脑梗死后内皮细胞损伤和凝血机制的影响。方法:初发脑梗塞患者分为单纯脑梗塞组(24例)和脑梗塞合并医院内获得性肺炎组(16例)。健康对照13例。脑梗死发病后第1、3、5、7、14、21天分别采血。血栓调节蛋白(TM)检测采用ELISA法。TNF-α检测采用放免法。结果:1血栓调节蛋白(TM):脑梗死合并医院内获得性肺炎后第1周、14天TM与单纯梗死组相比下降(P<0.05);21天与单纯梗死组无统计学差异但高于健康对照组。2肿瘤坏死因子(TNF-α):单纯脑梗死组与脑梗死合并医院内获得性肺炎组第1天无统计学差异,两组均高于健康对照组。脑梗塞合并医院内获得性肺炎发生第1周和14天TNF-α明显增高,高于单纯脑梗死组(P<0.05);21天虽然HAP已控制TNF-α仍高于单纯梗死组(P<0.05)。3脑梗死合并HAP组TM与TNF-α有相关性。随着TNF-α增高,血栓调节蛋白有下降趋势,两者相关关系以Gompertz曲线拟合满意,在高浓度TNF-α时TM降低较快,而低浓度TNF-α时TM降低较慢。结论:脑梗塞合并医院内获得性肺炎后血浆TNF-α增高,可能导致脑血管内皮细胞的损伤和抗凝机制的抑制,表现为血栓调节蛋白的下调。这可能是获得?     

头孢哌酮／舒巴坦治疗医院内获得性肺炎临床分析

目的评价头孢哌酮／舒巴坦治疗HAP的疗效。方法87例HAP患者随机分为头孢哌酮／舒巴垣治疗组和头孢他啶对照组，治疗前后行痰培养。结果治疗组与对照组总有效率、细菌清除率分别为93．19％和90．48％、72．09％和61．91％，差异有统计学意义。结论头孢哌酮／舒巴坦可以作为HAP的经验治疗用药。     

Are People With Joint Hypermobility Syndrome Slow to Strengthen?

ObjectivesTo investigate whether the rate of change of muscle strength in people with joint hypermobility syndrome (JHS) who have anterior knee pain (AKP) differs when compared to 2 control groups who have AKP and to evaluate the relationship between strength and pain as well as the effect of strength upon activity and knee function.DesignA cohort study, with 3 groups: JHS with AKP, generalized joint hypermobility with AKP (GJH), and normal flexibility with AKP (control group [CG]). Follow-up appointments were performed every 2 weeks for 16 weeks.SettingThe physiotherapy outpatient department within a London (United Kingdom) hospital.ParticipantsA total of 102 people, aged between 18 and 55 years, were recruited between July 2014 and March 2016; 47 JHS, 29 GJH, and 26 CG (N=102). After 16 weeks, 31, 20, and 21 participants completed the study, respectively. Participants were recruited from support groups, a London hospital group and university, local sports centers, and clubs.InterventionsIndividualized leg exercises for 16 weeks.Main Outcome MeasureMuscle torque generated from the lower limb, every 2 weeks for 16 weeks.ResultsThere was no difference in the rate of change of concentric muscle strength between the JHS group and the CG or GJH group (P>.88 and P>.97). There was no difference in the rate of change of eccentric muscle strength between the JHS group and the CG or GJH group (P>.60 and P>.94). However, people with JHS were significantly weaker than the other 2 groups, taking 3 to 4 months to reach the baseline strength of the GJH group.ConclusionPeople with JHS can strengthen at the same rate as other people in pain.     

Neuroanatomical distribution of Huntingtin-associated protein 1-mRNA in the male mouse brain

Huntingtin-associated protein 1 (HAP1) was identified as an interactor of the gene product (Huntingtin) responsible for Huntington's disease and found to be a core component of the stigmoid body. Even though HAP1 is highly expressed in the brain, detailed information on HAP1 distribution has not been fully described. Focusing on the neuroanatomical analysis of HAP1-mRNA expression using in situ hybridization histochemistry, the present study clarified its detailed regional distribution in the entire mouse brain. Mouse HAP1 (Hap1)-mRNAs were abundantly expressed in the limbic-related forebrain regions and midline/periventricular brainstem regions including the olfactory bulb, limbic-associated cortices, hippocampus, septum, amygdala, bed nucleus of the stria terminalis, preoptico-hypothalamic regions, central gray, raphe nuclei, locus coeruleus, parabrachial nuclei, nucleus of the solitary tract, and area postrema. In contrast, little expression was detected in the striatum and thalamus, implying that Hap1 is associated with neurodegeneration-sparing regions rather than target lesions in Huntington's disease. The distribution pattern, resembling that of the stigmoid body, suggests that HAP1 and the stigmoid body are implicated in protection from neuronal death rather than induction of neurodegeneration in Huntington's disease, and that they play an important role in integrating instinct behaviors and underlying autonomic, visceral, arousal, drive, memory, and neuroendocrinergic functions, particularly during extensive homeostatic or emotional processes. These data will provide an important morphological base for a future understanding of functions of HAP1 and the stigmoid body in the brain.