颈性眩晕的分型治疗及疗效分析

目的 将颈性眩晕分为上、下颈性眩晕，采取不同治疗方法并与常规治疗方法的疗效比较，以寻求更好的治疗方法。方法 将135例颈性眩晕随机分为试验组和对照组，对其治愈率及治疗时间进行统计学分析。结果 试验组的治愈率高于对照组，而试验组的治疗时间短于对照组，均有统计学意义。结论 对颈性眩晕进行分型并采用不同的治疗方法能提高治愈率，缩短治疗时间。     

关于我国体外诊断试剂监督管理改革的建议

本文综述了美国、欧盟、日本、中国目前对体外诊断产品（试剂）监督管理的现状以及我国存在的问题。并根据我国具体情况提出了对体外诊断试剂监督管理的改革建议。     

循环内皮细胞水平与糖尿病肾病的相关性及银杏达莫的干预作用

目的:探讨外周血循环内皮细胞(CEC)和糖尿病肾病(DN)的相关性,以及银杏达莫注射液在DN防治中的可能作用。方法:检测65例2型糖尿病患者24h尿白蛋白排泄率(UAER)及CEC数,分析两者的相关性。将UAER为30~300mg·d-1的45例患者随机分为两组,常规治疗组22例,进行常规降血糖、控制血压等治疗;银杏达莫治疗组23例,在常规治疗基础上静脉滴注银杏达莫注射液2周。比较两组治疗前后血糖、血压、UAER及CEC水平的变化。结果:单纯糖尿病(SDM)组和早期糖尿病肾病(EDN)组的外周血CEC水平比对照组(NC)显著性升高,并呈逐渐增高的趋势(P<0.01)。UAER与收缩压(SBP)、外周血CEC水平呈正相关(P<0.01)。EDN组中,银杏达莫治疗后UAER及CEC明显降低(P<0.01);而常规治疗组无明显变化。线性多元逐步回归分析表明,银杏达莫治疗后UAER的改变与CEC数的变化成正相关(P<0.01)。结论:血管内皮细胞(VEC)损伤在DN发生发展中起重要作用,银杏达莫对VEC的保护作用可能是其延缓DN发展的重要机制。     

cNO头颈鳞癌哨位淋巴结示踪法的研究进展

颈部哨位淋巴结是头颈部鳞癌最早发生转移的淋巴结,其所在位置及有无转移或微转移,是决定是否行区域性颈淋巴清扫的一个重要指标.对于哨位淋巴结阴性的cNO患者,为减少过度治疗,精确定位哨位淋巴结十分重要.目前多采用示踪法检测哨位淋巴结,本文就其判断cNO头颈鳞癌隐匿性转移的研究进展作一综述.     

小脑后下动脉动脉瘤的诊断和治疗

目的探讨小脑后下动脉动脉瘤的临床特征、诊断、鉴别诊断和治疗。方法回顾性分析12例小脑后下动脉瘤的临床表现、影像学特征、手术效果及诊治过程中存在的相关问题。结果12例中有11例因动脉瘤破裂出血而发病,单纯第四脑室出血4例,全脑室系统出血2例,小脑半球出血3例,小脑蚓部伴第四脑室出血1例,侧脑室伴第三脑室出血1例,以后颅窝占位病变表现1例。8例术前行DSA检查明确诊断,4例术中明确诊断。12例均行后颅窝开颅显微手术治疗,其中动脉瘤颈夹闭9例,孤立切除2例,动脉瘤加固术1例,术后2例因脑积水加重行脑室-腹腔分流术。12例中除1例术后留有轻偏瘫外,其余11例恢复良好。结论小脑后下动脉瘤多以第四脑室出血发病,少数以小脑半球或蚓部出血发病,及早治疗效果满意。手术方式应尽量夹闭动脉瘤颈,对于小脑后下动脉末端动脉瘤,可以采用孤立切除术。     

高血压家系802人的高血压患病率、知晓率、治疗和控制状况调查

目的了解高血压家系人群高血压患病率、治疗率和控制率特点。方法用整群随机抽样调查的方法调查高血压家系高血压的流行和控制情况，分析比较相关指标的差异。结果家系成员高血压患病率为55．86％，存在危险因素聚集现象。高血压的知晓率、治疗率、控制率分别为79．46％、62．72％、19．64％。结论该地区高血压家系高血压患病率较高，遗传因素是重要原因。虽高血压控制水平较高，但需加强高血压的一级预防。     

阿昔洛韦联合胸腺肽抗乙肝病毒疗效观察

本文报道了阿昔洛韦联合胸腺肽对慢性乙型肝炎抗病毒疗效，阿昔洛韦１０ｇ，胸腺肽１６ｍｇ静滴，每日一次，连续治疗２月，共治疗３３例，治疗结束后，治疗组ＨＢｅＡｇ阴转１６例，阴转率５５１７％，ＨＢＶ ＤＮＡ阴转１８例，阴转率５４５４％。对照组ＨＢｅＡｇ阴转率９５２％（２／２５），ＨＢＶ ＤＶＡ阴转率９０９％（１／２５），两组比较有显著性差异（ｐ＜００１），表明阿昔洛韦联合胸腺肽是一种有效、价廉、使用方便的抗乙型肝炎病毒药物。     

促甲状腺素释放激素类似物YM14673对小鼠学习记忆的影响

采用小鼠跳台法评价促甲状腺素释放激素类似物ＹＭ１４６７３（ｉｐ１ｍｇ·ｋｇ－１）对正常成年小鼠被动回避学习记忆成绩的影响．结果表明ＹＭ１４６７３对东莨菪碱，氯霉素和乙醇造成的小鼠记忆获得，巩固及再现障碍均有明显的改善作用．     

组织扩张术皮肤胶原的代谢改变

目的：研究常规扩张（ＩＴＥ）和持续快速扩张（ＣＴＥ）对皮肤胶原代谢的影响。方法用白色小家猪制作组织扩张术动物模型，用Ｇｏｒｄｅｌａｄｚｅ法测定血清和扩张组织的羟脯氨酸（ＨＰ）含量，藻酸盐印模材膜片法测量标记区面积；光镜测量真皮厚度。结果：ＩＴＥ组血清ＨＰ含量升高，０．８倍，ＣＴＥ组升高１．２倍，ＩＴＥ和ＣＴＥ组皮肤含量与正常皮肤相同，组织中ＨＰ总量均明显升高，持续扩张皮瓣组（ＣＴＥＦ）术后４ｗｋ皮     

Distribution of glutathione and glutathione-related enzyme systems in mitochondria and cytosol of cultured cerebellar astrocytes and granule cells

The cellular and regional distribution of glutathione (GSH) and GSH-related enzyme systems involved in cellular defense against reactive oxygen species and electrophilic xenobiotics in the nervous system has been extensively studied. However, little is known about the subcellular distribution of GSH systems in brain tissue and cultured neural cells. The present study investigates the distribution of mitochondrial and cytosolic GSH and GSH-related enzymes in cultured cerebellar astrocytes and granule cells, and compares them with levels in the adult rat cerebellum. Cytosolic GSH levels and cytosolic activities of glutathione reductase (GR), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) in astrocytes were 57, 153, 245, and 92% higher than those found in granule cells, respectively. In contrast, granule cells contained significantly higher mitochondrial GSH levels than astrocytes. Granule cells also demonstrated comparable mitochondria/cytosolic concentrations of GSH and GR, GPX and GST activities to those observed in the cerebellar tissue, whereas ratios in astrocytes were markedly lower. Although in vitro treatments with 100 μM ethacrynic acid depleted both cytosolic and mitochondrial GSH in cultured astrocytes and granule cells in a time-dependent fashion, cellular GSH in granule cells was more resistant to the GSH-depleting agent than astrocytes. These results suggest that although GSH and GSH-related enzymes are abundant in cytosolic compartments of astrocytes, mitochondrial pools are relatively small. Since brain mitochondria are sites of significant hydrogen peroxide generation, the mitochondrial localization of GSH and its associated enzymes in neural cells provide important defenses against toxic oxygen species in the nervous system. Differences in subcellular distribution of GSH systems in individual neural cell types may provide a basis for selective cellular and/or subcellular expression of neurotoxicity.