经枕下乙状窦后锁孔入路治疗听神经瘤的临床体会

目的 总结经枕下乙状窦后锁孔入路切除听神经瘤的手术经验. 方法 采用经枕下乙状窦后锁孔入路对38例听神经瘤进行切除手术.距乙状窦后缘内侧1.5 cm做一小直切口,形成直径2.5～3.0 cm大小骨窗,术毕骨瓣复位固定. 结果本组听神经瘤全切33例,次全切5例;35例面神经解剖保留,2例听力保留;无死亡病例,脑脊液漏1例,术中无一例输血,无皮下积液.结论 经枕下乙状窦后锁孔入路可提供足够的手术空间进行听神经瘤切除,明显减少了医源性损伤,切口愈合好,具备微创性、安全性和有效性.     

吗啡的呼吸抑制作用与中枢胆碱能系统的关系

本文以兔呼吸频率、通气量和血气作为指标,观察到iv吗啡0.5～4.0mg/kg产生剂量依赖性呼吸抑制。icv匹鲁卡品2.5mg/kg能完全逆转这一抑制效应。icv 4—氨基吡啶(4—AP),1.5μg/kg兴奋呼吸,并使吗啡量效曲线右移。用利血平耗竭儿茶酚胺后,吗啡仍能抑制呼吸,4—AP可消除之。表明吗啡抑制呼吸与中枢胆碱能系统有关,且可能系它抑制Ach释放所致。     

玻璃体视网膜界面疾病

玻璃体视网膜交界面的状态与许多临床疾病有紧密联系；诱导完全性的玻璃体后脱离对许多疾病的发生、治疗以及预后起重要作用，可以减少玻璃体切割手术中对视网膜的损伤。本研究就玻璃体视网膜疾病以及诱导完全性玻璃体后脱离的方法做一综述。     

国内丙型肝炎病毒感染与肝细胞癌关系的19个病例对照研究的 Meta 分析

本文对国内１９个有关丙型肝炎病毒（ＨＣＶ）感染与肝细胞癌（ＨＣＣ）关系的病例对照研究进行Ｍｅｔａ分析。经齐性检验表明，１９个研究中有１７个研究结果是一致的。对此１７个研究结果加权合并，累积ＨＣＣ病例１５７７例，ＨＣＶ感染率为２３．０％，累积对照１９８０例，ＨＣＶ感染率为４．０％；合并ＯＲ值为６．７。结果表明，国内ＨＣＶ感染与ＨＣＣ关系密切，ＨＣＶ感染是ＨＣＣ发生的一个危险因素。     

高脂血症患者C—反应蛋白含量的变化及氟伐他汀对它的影响

OBJECTIVE: To observe the changes of C-reactive protein (CRP) level and its relationship with blood lipids, and the effects of fluvastatin on CRP and the lipids in patients with hyperlipidemia. METHODS: Serum levels of cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C) and lipoprotein(a)[Lp(a)] were measured by enzyme assay, and plasma CRP level by immunonephelometry before and after fluvastatin treatment (20 mg/d for 4 weeks) in patients with hyperlipidemia. RESULTS: CRP levels were above normal in 90.3% hyperlipidemia cases in spite of the various accompanying diseases. Fluvastatin treatment significantly reduced TC (-7.49%), TG (-14.32%), LDL (-13.88%), VLDL (-18.48%) and TC/HDL(-13.50%) levels (P<0.01), and also brought down Lp(a) concentration (-13.81%). CRP levels was very effectively reduced after the treatment (-15.92%, P<0.001). No association between basal CRP levels and basal lipids and Lp(a) concentrations was observed. Positive correlation of CRP, however, was observed after fluvastatin treatment with TC/HDL (r=0.62, P=0.041) and Lp(a) (r=0.320, P=0.011), while inverse relations were noted between CRP and HDL (r=-0.288, P=0.023). CONCLUSION: CRP levels increases markedly in patients with hyperlipidemia, a fact that is independent of the accompanying diseases. In addition to modulating blood lipid levels, fluvastatin also reduces CRP level, the latter possibly serving as an independent predictive factor for atherosclerotic cardiovascular diseases and also as an indicator for estimating the effectiveness of the treatment.     

利培酮对氯氮平血浓度影响的研究

目的　了解利培酮对氯氮平血浓度的影响及二药合用的疗效与不良反应。方法　对 5 0例原服用氯氮平治疗的难治性精神分裂症患者合并利培酮治疗 ,分别于合并治疗前及后 1月、2月、3月测定氯氮平血浓度 ,同时评定PANSS ,TESS量表。结果　合用利培酮后 ,氯氮平血浓度无明显升高 ,PANSS评分明显降低(P <0 .0 1) ,TESS评分有所增加。结论　利培酮对氯氮平血浓度无明显影响 ,二药合用能增加疗效 ,不良反应有所增加。     

静脉输液回血问题研究

在静脉输液操作中常常遇到许多静脉输液穿刺成功后无回血情况。由于一次性输液管壁弹性差、管腔内径小，又因液体静压及重力的作用，容易造成回血不畅。尤其是老年人、婴幼儿、休克和脱水病人，因穿刺后无回血无法判断穿刺是否成功，而反复穿刺。这样既增加了病人痛苦，又增加了护士工作量。利用负压原理和局部血管扩张法，[第一段]     

Neurodegeneration in the Central Nervous System of apoE-Deficient Mice

Apolipoprotein E (apoE) is involved in the development and regeneration of the central nervous system (CNS). ApoE may also be necessary to maintain the integrity of the synapto-dendritic complexity. We analyzed the synaptic alterations in the CNS of apoE-deficient (knockout) mice during the aging process. In apoE-deficient homozygous mice, there was an age-dependent 15 to 40% loss of synaptophysin-immunoreactive nerve terminals and microtubule-associated protein 2-immunoreactive dendrites in the neocortex and hippocampus, when compared to controls. Dendritic alterations were observed as early as 4 months of age. Ultrastructural analysis revealed extensive dendritic vacuolization and disruption of the endomembrane system and cytoskeleton in apoE-deficient homozygous mice. Further immunocytochemical studies of the neuronal cytoskeleton showed that in apoE-deficient mice there was a decrease in the immunoreactivity of α and β tubulin (but not kinesin) in the cell bodies and processes. These results support the contention that apoE might play an important role in maintaining the stability of the synapto-dendritic apparatus and that altered or deficient functioning of this molecule could underlie the synaptic and cytoskeletal alterations in Alzheimer's disease.