阻塞性睡眠呼吸暂停综合征相关高血压病的临床特点

探讨阻塞性睡眠呼吸暂停综合征相关性高血压病 (obstructive sleep apnea associated hypertension,OSAAHT)的临床特点。对照分析 2 4例 OSAAHT和年龄及病期相匹配的 2 2例原发性高血压病患者 ,比较症状、体重指数、治疗前睡眠前后血压变化及 2 4h血压动态监测等指标。结果发现 OSAAHT患者白天明显过度困倦 ,睡眠监测呼吸紊乱指数 (AHI)为 (4 5 .1± 15 .3)次 / h,体重指数高于对照组 [(2 7.9± 2 .5 ) kg/ m2比 (2 3.9± 1.7) kg/ m2 ,P<0 .0 1]。OSAAHT睡前血压 (137.1± 10 .5 ) / (88.4± 6 .6 ) mm Hg,清晨血压 (15 5 .9± 14.4) / (10 1.8± 4.9) m m Hg;原发性高血压病组睡前血压 (149.2± 12 .5 ) / (91.7± 6 .2 ) mm Hg,清晨血压 (140 .7± 9.4) / (83.4± 5 .9) mm Hg;两组睡前收缩压及清晨收缩压和舒张压均有差异 ,P<0 .0 1。OSAAHT夜间血压下降率明显小于原发性高血压病对照组[(13.3± 4.9) %比 (4 .5± 1.6 ) % ,P<0 .0 1]。提示 OSAAHT除了睡眠呼吸障碍外 ,还具有以下临床特点 :清晨睡醒时血压较高 ,夜间血压下降幅度变小 ,白天过度困倦以及肥胖等     

脂质体介导人β-神经生长因子基因转染培养肌母细胞的表达研究

目的　了解含 β-神经生长因子 (β- NGF)基因的表达质粒 PSVCEP NGF- CAT在培养肌母细胞中的表达及 L ipofect AMINE阳离子脂质体介导的转染效率。方法　将表达质粒 PSVCEP NGF- CAT经 L ipofectAMINE转染至培养成的肌母细胞中 ,用免疫细胞化学方法检测基因在肌母细胞内的表达。结果　培养肌母细胞在转染 6小时吞噬脂质体最显著 ,转染 48小时后约 40 %的肌母细胞胞质内有β- NGF基因表达。结论　含β- NGF基因的表达质粒 PSVCEP NGF- CAT可以在培养肌母细胞中表达 ,脂质体转染的方法简便、有效     

胸腰段脊柱脊髓损伤减压与固定相关问题探讨（附166例报告）

目的 对胸腰段脊柱脊髓，马尾神经损伤患者的外科治疗及几种内固定方法的疗效进行探讨。方法 对166例患者的治疗进行回顾分析。该组患者中椎体爆裂性骨折37例，椎体压缩骨折超二分之一109例，椎体骨折脱位14例，多节段或跳跃骨折6例，脊髓损伤按Frankel分级，A级59例，B级46例，C级42例，D级19例，治疗采用后路减压复位122例，前路减压复位，髂骨植骨融合44例。结果 术后123例获3-18个月随访，随访患者中随4例RF钉断裂，5例Harrington上钩脱落，6例棍断裂，其余患者内固定稳固，脊髓，马尾神经恢复，除35例仍为A级外，余脊髓神经功能恢复1-3个级别。结论 各种不同内固定可保持或增强脊柱的稳定，胸腰段脊柱脊髓损伤的外科治疗应根据骨折类型，脊髓及马尾神经损伤程度选择手术入路及内固定材料。     

二乙基亚硝胺诱导大鼠肝细胞癌过程中明胶酶的动态变化

目的：观察肝癌形成过程中明胶酶表达（蛋白及mRNA水平）的动态变化，探索明胶酶在肝癌生长浸润中的作用。方法：应用免疫组化法、明胶酶谱法和RT-PCR法对大鼠肝癌形成过程中各期明胶酶表达情况进行观察，并与正常对照组进行比较分析。结果：正常肝组织及肝硬化组织内明胶酶有表达，肝癌形成后主要在癌细胞内表达；明胶酶原在正常肝组织中有低表达，诱癌过程中呈持续增高趋势；明胶酶-2mRNA与其酶蛋白表达趋向一致。结论：在肝癌形成过程中明胶酶转录和翻译水平均呈持续增高趋势。     

ABO血型与肝炎病毒感染关系的探讨

目的：探讨ABO血型与肝炎病毒感染的关系，方法：应用疾病关联分析方法对HBsAg和,抗－HCV阳性献血者与同期健康献血者的ABO血型资料进行比较分析。结果：ABO血型与HBsAg和抗－HCV阳性率之间无显著性相关关系（P＞0．05），结论：乙型肝炎和丙型肝炎病毒感染与ABO血型无显著性相关。     

CT扫描及超声内镜术前评价进展期食管癌

目的比较胸部螺旋CT增强扫描及微探头超声内镜 (MPS)检查在评价进展期食管癌中的价值。方法 :32例进展期食管癌术前行CT扫描和MPS检查并与术后病理学比较。结果 :CT扫描能发现 84 .4 %的食管癌病灶 ,但不能准确诊断癌肿浸润深度 ,诊断纵隔结构受侵准确率 75 % ,发现区域淋巴结转移的敏感性90 .9% ,特异性 81.8% ,对纵隔内远处淋巴结转移诊断准确率 80 %。MPS检查能检出所有病例的进展期食管癌病灶 ,癌肿浸润深度诊断准确率 81.3% ,诊断纵隔结构受侵准确率 5 0 % ,诊断区域淋巴结转移敏感性81.8% ,特异性 72 .7% ,而对纵隔内远处转移的淋巴结均未能探及。结论 :CT扫描在评价进展期食管癌纵隔内结构受侵及远处淋巴结转移的意义较大。而MPS检查在判断癌肿管腔浸润深度的准确率较高。     

Intracellular Ca2+ suppressed a transient potassium current in hippocampal neurons

The effects of intracellular Ca2+ (Ca2+i) on K+ currents in hippocampal cells were examined using acutely isolated cells obtained from adult guinea pigs. Whole-cell voltage-clamp recordings were carried out in a configuration that allowed a continuous perfusion of the intracellular medium. Recording media were made to block inward currents and allowed selective activation of K(+)-dependent outward currents. Voltage-dependent outward currents consisted of an initial rapidly decaying component followed by a sustained component. The time constant of decay of the transient current was about 25 msec, and previous studies (Numann et al., 1987) showed that the kinetic and pharmacological properties of this current closely resembled the A current recorded in invertebrate neurons (Connor and Stevens, 1971; Thompson, 1982). Intracellular perfusion of hippocampal cells with a solution containing elevated Ca2+ (about 4.5 x 10(-4) M) elicited outward currents at the holding potential (-45 to -55 mV) and produced changes in voltage-dependent K+ currents. The transient outward current (IA) activated by depolarization was suppressed with increases in Ca2+i. Delayed, sustained K+ currents were greatly potentiated. Data also showed that, among the 3 effects elicited by Ca2+i, suppression of IA was most sensitive to Ca2+i elevation. Previous results (Numann et al., 1987) showed that IA had a lower threshold (about -45 mV) than sustained currents (about -40 mV). By using low levels of depolarization (-40 mV), IA can be selectively activated, and the suppressive effect of Ca2+i on IA was confirmed on the kinetically isolated IA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Therapy of human cervical carcinoma with monoclonal antibody-Pseudomonas exotoxin conjugates.

Pseudomonas exotoxin A (PE) linked to the F(ab')2 fragment of 1H10, a murine monoclonal antibody recognizing a carbohydrate epitope of a glycoconjugate expressed on the surface of human cervical carcinoma tumor cells, was evaluated for in vitro and in vivo activity. PE can kill cells by ADP-ribosylating elongation factor 2 thus inhibiting protein synthesis. Disulfide- as well as thioether-linked immunotoxins (1H10-PE) killed cervical carcinoma cells in vitro and were 20-160 times more inhibitory to target than to control cells. Cell killing was antibody mediated as demonstrated by the reduction of 1H10-PE growth inhibition to target CaSki cells by free 1H10 F(ab')2. In addition, a control antibody immunotoxin was nontoxic to CaSki cells. Thioether-linked 1H10-PE administered either i.v. or i.p. suppressed the growth of established solid s.c. cervical carcinoma tumors xenografted in nude mice for over 30 days. Treatment with antibody alone or a control immunotoxin had no significant effect on tumor growth. Administration of immunotoxin i.p. was associated with less toxicity than administration i.v., but i.v. injections were more effective at suppressing the growth of established solid tumors.     

Ischemic rat brain extracts induce human marrow stromal cell growth factor production

Intravenous administration of human bone marrow stromal cells (hMSCs) after middle cerebral artery occlusion (MCAo) in rats provides functional benefit. We tested the hypothesis that these functional benefits are derived in part from hMSC production of growth and trophic factors. Quantitative sandwich enzyme‐linked immunosorbent assay (ELISA) of hMSCs cultured with normal and MCAo brain extracts were performed. hMSCs cultured in supernatant derived from ischemic brain extracts increased production of brain‐derived neurotrophic factor (BDNF), nerve growth factor (NGF), vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF). These neurotrophins and angiogenic growth factors increased in a post‐ischemia time‐dependent manner. The hMSC capacity to increase expression of growth and trophic factors may be the key to the benefit provided by transplanted hMSCs in the ischemic brain.