心肺复苏机与徒手心肺复苏临床疗效的研究

目的 分析使用心肺复苏机与徒手心肺复苏抢救心脏呼吸骤停患者的临床疗效.方法 选取来院心脏呼吸骤停的87例患者为研究对象,其中49例均采用CPR model 心肺复苏,为实验组;其余38例采用徒手心肺复苏,为对照组.结果 实验组平均动脉压、血氧分压、血氧饱和度、有效率均显著优于对照组(P<0.05),并发症发生率显著低于对照组(P<0.05),而两组间复苏成功率无显著性差异(P>0.05).结论 心肺复苏机比徒手心肺复苏能更好的改善心脏呼吸骤停患者的平均动脉压、血氧分压、血氧饱和度,但不能挽救更多的患者生命.     

螨性过敏性疾病的免疫治疗研究进展

尘螨分布广泛,其蜕皮、尸体,尤其是代谢产物都是强烈致敏原,是引起各类过敏性疾病的重要病因之一,其中最主要的是引起过敏性哮喘。螨性过敏性疾病在全球的发生及其严重程度正日渐受到关注。免疫治疗作为一种针对螨性过敏性疾病的对因治疗,受到人们越来越多的重视。本文对螨性过敏性疾病免疫治疗方法,如特异性免疫治疗（SIT）、DNA-变应原免疫疗法、抗IgE单克隆抗体免疫疗法、抗CD11a单克隆抗体免疫疗法、趋化因子受体拮抗剂免疫疗法和抗FcγRⅠ单克隆抗体免疫疗法等进行了综述。     

脑安胶囊对320例卒中高危患者的干预效果

目的评价脑安胶囊对卒中高危患者的中长期干预效果。方法在门诊与住院患者中,筛选出有高血压、心脏病、糖尿病、血脂异常、卒中家族史等危险因素,同时年龄≥40岁、脑血管血流动力学参数（CVHP）积分〈75分者320例,按随机数字法分为脑安胶囊组162例及阿司匹林组158例。脑安胶囊组口服脑安胶囊,2次/d,2粒/次;阿司匹林组口服拜阿司匹林,100mg/次,1次/d。干预时间均为24～36个月。每年随访1次,随访内容为血压、血脂、CVHP积分的水平以及卒中的发病率及病死率。结果①脑安胶囊组累积随访470人年,卒中发生率和病死率分别为1.915%和0.851%;阿司匹林组累积随访460人年,卒中发生率和病死率分别为4.130%和2.391%。脑安胶囊组卒中综合发生率及病死率均低于阿司匹林组（P〈0.05）。②脑安胶囊组干预前、后,收缩压为（162±11）、（130±7）mmHg,舒张压为（101±9）、（83±6）mmHg,CVHP积分值为（49±13）、（82±9）;阿司匹林组干预前、后,收缩压为（161±10）、（137±5）mmHg,舒张压为（99±7）、（90±4）mmHg,CVHP积分值为（49±12）、（70±11）。两组干预后收缩压、舒张压及CVHP积分值差异均有统计学意义（P〈0.01）。结论脑安胶囊可以降低卒中的发生率和病死率,改善脑血管功能。在卒中高危人群一级预防中长期疗效优于阿司匹林。     

慢性乙型肝炎抗病毒用药临床要点

对慢性乙型肝炎患者来说,干扰素α仍然是抗乙型肝炎病毒(HBV)的主要药物,但使用不方便、不良反应较大,不宜用于失代偿期肝硬化患者.而所有已经上市的以及正处于研发或临床试验阶段的核苷(酸)类似物抗病毒制剂均是以持续抑制病毒复制发挥其抗病毒作用,还难以达到彻底清除病毒,需要长期治疗达到最大限度地抑制HBV复制.联合用药目前处于探索研究中.医生需要根据病毒的特点、患者的个体对抗HBV治疗的应答、耐受性以及心理健康等拟定出更科学的个体化抗病毒治疗方案.     

宠物仓鼠胃肠道寄生虫感染情况调查

用饱和蔗糖溶液漂浮法、改良抗酸染色法和卢戈碘液染色法对郑州某宠物市场金色仓鼠（Mesocricetus auratus）、黑线毛足鼠（Phodopus sungorus）、坎氏毛足鼠（P. campbelli）和小毛足鼠（P. roborovskii）共153份粪便样品进行检查, 寄生虫感染阳性率分别为70.7%（41/58）、96.7%（59/61）、83.9%（26/31）和100%（3/3）, 平均阳性率为84.3%。共检出8种寄生虫, 分别为隐孢子虫（15.0％）、贾第虫（22.2％）、球虫（2.0%）、短膜壳绦虫（31.4％）、长膜壳绦虫（25.5%）、管状线虫（41.8％）、四翼无刺线虫（7.2%）和毛尾目未定种类（18.3%）。表明宠物仓鼠可感染和传播多种人兽共同感染的寄生虫。     

Pulse Wave Velocity as a Marker of Severity of Coronary Artery Disease

To determine whether pulse wave velocity (PWV) as a measure of arterial stiffness is a marker of coronary artery diseases (CAD), the authors did a cross-sectional study in 92 patients undergoing coronary angiography for suspected CAD. Arterial stiffness was assessed through recording PWV from the left carotid–right femoral arteries using an automated machine. The mean PWV was higher in patients with CAD than in those without CAD (11.13±0.91 vs 8.14±1.25 m/sec; P< .001). When the severity of CAD was expressed as 1-, 2-, and multiple-vessel disease, there was a significant association between the severity of CAD and PWV. PWV differed significantly with different categorical severity of CAD even when age and total cholesterol were controlled for. In a univariable analysis, PWV was higher with higher systolic blood pressure (P< .004). The authors conclude that arterial stiffness measured through PWV is an independent and complementary cardiovascular risk marker.     

Primary human herpesvirus 8 infection generates a broadly specific CD8(+) T-cell response to viral lytic cycle proteins

Human herpesvirus 8 (HHV-8) is a recently discovered gammaherpesvirus that is the etiologic agent of Kaposi sarcoma (KS). The natural history of primary HHV-8 infection, including clinical outcome and host immune responses that may be important in preventing disease related to HHV-8, has not been elucidated. The present study characterized the clinical, immunologic, and virologic parameters of primary HHV-8 infection in 5 cases detected during a 15-year longitudinal study of 108 human immunodeficiency virus type 1 seronegative men in the Multicenter AIDS Cohort Study. Primary HHV-8 infection was associated with mild, nonspecific signs and symptoms of diarrhea, fatigue, localized rash, and lymphadenopathy. There were no alterations in numbers of CD4(+) or CD8(+) T cells or CD8(+) T-cell interferon gamma (IFN-gamma) production to mitogen or nominal antigen. CD8(+) cytotoxic T-lymphocyte precursor (CTLp) and IFN-gamma reactivity were detected during primary HHV-8 infection, with broad specificity to 5 lytic cycle proteins of HHV-8 encoded by open reading frame 8 (ORF 8; glycoprotein B homolog of Epstein-Barr virus), ORF 22 (gH homolog), ORF 25 (major capsid protein homolog), ORF 26 (a minor capsid protein homolog), or ORF 57 (an early protein homolog), in association with increases in serum antibody titers and appearance of HHV-8 DNA in blood mononuclear cells. CD8(+) T-cell responses to HHV-8 decreased by 2 to 3 years after primary infection. This antiviral T-cell response may control initial HHV-8 infection and prevent development of disease.     

Mutant G protein alpha subunit activated by Gbeta gamma: a model for receptor activation?

How receptors catalyze exchange of GTP for GDP bound to the Galpha subunit of trimeric G proteins is not known. One proposal is that the receptor uses the G protein's betagamma heterodimer as a lever, tilting it to pull open the guanine nucleotide binding pocket of Galpha. To test this possibility, we designed a mutant Galpha that would bind to betagamma in the tilted conformation. To do so, we excised a helical turn (four residues) from the N-terminal region of alpha(s), the alpha subunit of G(S), the stimulatory regulator of adenylyl cyclase. In the presence, but not in the absence, of transiently expressed beta(1) and gamma(2), this mutant (alpha(s)Delta), markedly stimulated cAMP accumulation. This effect depended on the ability of the coexpressed beta protein to interact normally with the lip of the nucleotide binding pocket of alpha(s)Delta. We substituted alanine for an aspartate in beta(1) that binds to a lysine (K206) in the lip of the alpha subunit's nucleotide binding pocket. Coexpressed with alpha(s)Delta and gamma(2), this mutant, beta(1)-D228A, elevated cAMP much less than did beta(1)-wild type; it did bind to alpha(s)Delta normally, however, as indicated by its unimpaired ability to target alpha(s)Delta to the plasma membrane. We conclude that betagamma can activate alpha(s) and that this effect probably involves both a tilt of betagamma relative to alpha(s) and interaction of beta with the lip of the nucleotide binding pocket. We speculate that receptors use a similar mechanism to activate trimeric G proteins.     

氟乙酰胺中毒92例临床分析

现将我院１３年来内儿科收治的氟乙酰胺中毒９２例临床资料分析如下。临床资料一般资料男５４例,女３８例,１～１０岁４２例,１１～１８岁３２例,＞１８岁１８例。服毒到住院时间最短２０ｍｉｎ,最长７ｈ。中毒量０．１５～１ｇ。以临床症状分度［１］,轻度中毒３０...