慢性肺心病急性失代偿性呼吸衰竭静注蛋白营养疗法近期疗效观察

目的　探讨静注蛋白营养疗法对慢性肺心病合并急性失代偿性呼吸衰竭病人近期疗效。方法　治疗组４０ 例静脉输注复方氨基酸、人血白蛋白、血浆,测定治疗前后蛋白电泳、ＰａＣＯ２ 、ＰａＯ２ ,统计病死率,并与４０ 例常规治疗对照组比较。结果　治疗组治疗后血浆白蛋白升高,球蛋白无明显变化;ＰａＣＯ２ 降低,ＰａＯ２ 升高,病死率下降,与对照组相比有统计学意义。结论　慢性肺心病急性失偿性呼衰经静脉蛋白营养治疗可明显改善ＰａＣＯ２ 和ＰａＯ２ 指标,降低住院病死率。     

酒精胎骨移植促进骨愈合的实验研究

目的：通过酒精胎骨移植观察骨愈合情况。方法：用酒精棒状兔胎骨为材料,手术将骨植入兔实验侧骨折端内,对侧不植骨作自身对照,术后进行免疫学、放射学、组织学及生物力学检查。结果：表明植骨不引起明显排斥反应,植骨侧新骨形成多、骨折愈合快、抗弯应力强度大。结论：酒精胎骨移植是一种简便而有效的植骨材料和方法。     

热休克蛋白70抑制大鼠感染性脑水肿炎症因子的研究

为了探讨热休克蛋白７０（ＨＳＰ７０）对大鼠感染性脑水肿的保护作用,该文采用百日咳菌液所致的大鼠感染性脑水肿模型及将大鼠进行热休克处理,观察脑组织中白细胞介素１－β（ＩＬ－１β）、肿瘤坏死因子－α（ＴＮＦ－α）及一氧化氮（ＮＯ）水平的变化,并应用Ｗｅｓｔｅｒｎ印迹分析检测大鼠脑组织的ＨＳＰ７０表达。结果发现感染性脑水肿脑组织ＩＬ－１β、ＴＮＦ－α及ＮＯ浓度均增高,热休克处理可降低以上三者的浓度,Ｗｅ     

E.coli产Ampli Taq DNA聚合酶的分离纯化

将含有Ｔａｑ ＤＮＡ聚合酶基因的Ｅ．ｃｏｌｉ经发酵,细胞培养液经破壁裂解,粗蛋白抽提Ｓｅｐｈａｅｒｙｌ－ｓ－１００,ＣＭ－Ｓｅｐｈａｄｅｘ Ｃ５０柱层析等纯化步骤,可获得电泳纯的重组Ｔａｑ ＤＮＡ聚合酶,用于科研和检测工作。     

胆囊结石患者胆固醇酯转移蛋白基因多态性研究

为揭示胆囊结石病与遗传因素的关系,运用聚合酶链反应技术（ＰＣＲ）和基因限制性片段长度多态性分析法（ＲＦＬＰｓ）对１０４例胆囊结石患者和６８例健康人进行了研究。结果显示：胆囊结石组Ｂ１等位基因频率５２．３％,Ｂ１Ｂ１基因型频率２８．８％,大于对照组Ｂ１等位基因频率３４．６％（Ｐ＜０．０５）,Ｂ１Ｂ１基因型频率１１．７６％（Ｐ＜０．０５）,胆囊结石组Ｂ２等位基因频率４７．７％,Ｂ２Ｂ２基因型频率２４．２％小于对照组Ｂ２等位基因频率６５．４％（Ｐ＜０．０５）,Ｂ２Ｂ２基因型频率４２．６％（Ｐ＜０．０５）。胆囊结石组Ｈ１等位基因频率２０％,Ｈ１Ｈ１基因型频率５％,Ｈ２Ｈ２基因型频率６５％,Ｈ２等位基因频率８０％与对照组Ｈ１等位基因频率１７．９％,Ｈ１Ｈ１基因型频率２％,Ｈ２Ｈ２基因型频率６５．９％,Ｈ２等位基因频率８２．１％比较无显著性差异（Ｐ＞０．０５）。提示：Ｂ１等位基因是胆囊结石患者主导基因。Ｂ２等位基因是对照组的主导基因。Ｈ１及Ｈ２等位基因频率在胆囊结石患者及对照组中分布相同,无显著性差异（Ｐ＞０．０５）。     

大鼠局灶性脑缺血模型及其与C反应蛋白变化的关系

目的 改进大鼠大脑中动脉梗塞法,建立更接近于临床缺血性脑卒中及其再扩灌注的可靠模型,并观察其与血甭Ｃ反应蛋白变化的。方法沿大鼠右颈内动脉插入长２．１￣２．３ｃｍ直径０．２０５ｍｍ的单股尼龙丝,直达大脑中动脉起始部开口,阻断其血流,观察大鼠神经病学改变及脑组织形态学变化,并测定血清Ｃ反应蛋白含量。结果 术后大鼠表现特殊体态及典型追尾征,６ｈ大脑中动脉供血区出现缺血性外观（ＴＴＣ染色）及相应组织学变化     

中药壮骨胶囊治疗Ⅰ型原发性骨质疏松症74例临床研究

目的　探讨中药壮骨胶囊对Ⅰ型原发性骨质疏松症的疗效及其与骨代谢的关系。方法　采用益肾健脾的中药壮骨胶囊治疗７４ 例绝经后妇女原发性骨质疏松症,并与钙尔奇Ｄ 治疗的３１ 例作对照。结果　３ 个月后,其总有效率达９１ ．８９ ％ ,骨质疏松程度、血ＡＬＰ、ＣＴ、Ｅ２ 皆显著改善,且显著优于对照组（ Ｐ＜ ０．０５ ～０．０１）。无明显副反应。结论　绝经后妇女骨质疏松症主要由肾虚所致,采用中药补肾健脾治疗,疗效显著优于补钙、雌激素的替代疗法等。壮骨胶囊有调整骨代谢作用。该药安全可长期服用     

Precision and intersite correlation of bone densitometry at the radius, tibia and femur with peripheral quantitative CT

Objective. To compare the in situ precision of peripheral quantitative CT (pQCT) at the radius, tibia and femur, and to analyze the intersite correlation, in order to determine whether measurements at the lower extremity reproduce results at the radius or are of additional informative value. Design and material. pQCT measurements were performed in 86 elderly cadavers (mean age 80.5 years) at trabecular and cortical locations in the radius, tibia and femur, determining densitometric (bone mineral content and density) as well as geometric parameters (cross-sectional area, cortical thickness, polar moment of inertia and others). In 14 cadavers, repeated measurements were obtained at all sites on four different days. Results and conclusions. At cortical sites, the precision for the densitometric and geometric variables ranged from 0.4% to 4.3%, and was similar for the radius, tibia and femur. At trabecular locations, the reproducibility of the density measurements ranged from 1.8% to 2.5% at the radius, and from 3.2% to 5.9% at the femur and tibia. The intersite correlation of the total bone mineral content ranged from 0.87 and 0.97 at cortical sites, and from 0.63 to 0.85 at trabecular locations. The trabecular density showed a higher similarity between the tibia and femur (r=0.68–0.78) than between the radius and the lower extremity (r=0.41–0.45). The results demonstrate a substantial heterogeneity of trabecular bone in elderly individuals and advocate measurements directly at the site of clinical or scientific interest. Received: 5 July 1999 Revision requested: 12 August 1999 Revision received: 31 August 1999 Accepted: 13 September 1999     

Neuron-specific enolase as an effective immunohistochemical marker for injured axons after fatal brain injury

Recently, it has been reported that a diagnosis of diffuse axonal injury in cases with a short survival period can be made with the use of immunolabelling for β-amyloid precursor protein (APP). We examined whether immunostaining for neuron-specific enolase (NSE) can also be a useful marker for the detection of axonal injury in its early stages. Sections of the corpus callosum from 19 cases of head injury and from 9 cases of no head injury were immunostained for NSE and stained by the standard Holmes’ silver method. For comparison, serial sections from several cases were immunostained for APP. Immunostaining for NSE as well as for APP, labelled injured axons in head injury cases with as early as 1.5 h survival where Holmes’ staining failed to detect any changes of axons. Since NSE and APP labelled only injured axons but not normal axons, the results were readily interpretable. These findings indicate that NSE should be an effective marker for the detection of axonal injury in its early stages. Received: 7 December 1998 / Received in revised form: 11 March 1999     

Axonal cytoskeleton changes in experimental optic neuritis

Axonal loss and degeneration in multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE) have been suggested by brain imaging, pathological and axonal transport studies. Further elucidation of the processes and mechanisms of axonal degeneration in demyelinating diseases is therefore of potential importance in order to alleviate the permanent disabilities of MS patients. However, detailed studies in this area are impeded by the small number of reliable models in which the onset and location of demyelination can be well-controlled. In this study, microinjection of polyclonal rabbit anti-galactocerebroside (anti-Gal C) antibody and guinea pig complement was used to induce local demyelination in the rat optic nerve. We found that treatment with appropriate volumes of the antibody and complement could induce local demyelination with minimal pressure- or trauma-induced damage. Local changes in neurofilaments (NFs) and microtubules (MTs) were examined with both immunohistochemistry (IHC) and electron microscopy (EM). On day 1 after microinjection, we observed moderate NF and MT disassembly in the local demyelinated area, although in most cases, no apparent inflammatory cell infiltration was seen. The NF and MT changes became more apparent on days 3, 5, 7 after microinjection, along with gradually increased inflammatory cell infiltration. These results suggested that acute demyelination itself may induce local cytoskeleton changes in the demyelinated axons, and that the ensuing local inflammation may further enhance the axonal damage. When the lesions were stained with specific antibodies for T lymphocytes, macrophages, and astrocytes, we found that most of the cells were macrophages, suggesting that macrophages may play a greater role in inflammation-related axonal degeneration and axonal loss. These results were confirmed and further characterized on the ultrastructural level.