颅内肿瘤切除术后颅内感染危险因素分析

目的 探讨颅内肿瘤切除术后颅内感染的危险因素和预防措施。方法 回顾性分析442例颅内肿瘤切除术患者的临床资料。结果 442例颅内肿瘤切除术患者发生颅内感染33例，感染率为7．47％。非脑膜瘤手术颅内感染率为10．04％，高于脑膜瘤术后颅内感染率3．83％（P〈0．05）；手术时间≥4h者颅内感染率为9．87％，高于手术时间〈4h者颅内感染率4．78％（P〈0．05）；有脑脊液漏者颅内感染率为15．00％，高于无脑脊液漏者颅内感染率6．28％（P〈0．05）；引流管留置≥24h者颅内感染率为11．58％，高于未留置或留置〈24h者颅内感染率5．03％（P〈0．05）。结论 手术时间≥4h、引流管留置时间≥24h、存在脑脊液漏是颅内肿瘤切除术后发生颅内感染的危险因素。     

曲尼司特对豚鼠肺组织β肾上腺素受体向下调节的影响

用放射配体结合分析法分别测定了正常组、特布他林组、特布他林十曲尼司特组豚鼠的肺组织β受体最大结合力和解离常数,结果显示:给特布他林后豚鼠肺组织β受体发生明显的向下调节.曲尼司特可预防此向下调节的发生.     

慢性中耳炎的HRCT诊断

探讨慢性中耳炎的ＨＲＣＴ征象，诊断及鉴别诊断。材料与方法；对手术证实的１７例慢性中耳炎患者术前进行ＨＲＣＴ扫描并与手术病理结果对照分析。结果；胆脂瘤８例表现为中耳腔内团块状影，周围低密度环包绕，听骨明显破坏及鬓 扩大，骨缘硬化。４例肉芽肿多呈片状，条索状或网状，听骨破坏较轻。     

111例双黄连过敏反应文献分析

目的:分析临床应用双黄连引致的过敏反应的规律。方法:对2000年1月-2004年3月中国期刊网中收录的111例双黄连过敏反应在性别、年龄、发生时间、给药途径和临床表现进行分析。结果:双黄连过敏与年龄、性别无关,与给药途径有关,注射剂易发生过敏反应。该药过敏的临床表现有:过敏性休克67例(60%),皮肤黏膜症状61例(55%),其他类型过敏反应14例(13%)31例同时出现多种过敏症状。过敏发生时间最短为开始用药1m in以内,最长为用药后72h,97例(87%)在用药过程中发生过敏症状。结论:双黄连的过敏反应以速发型过敏反应(如过敏性休克)为主,应是临床关注的重点。     

银杏竹鼠肌肉成分对小鼠智力、体力的影响

目的：观察银杏竹鼠肌肉成分对小鼠智力体力的影响。方法：小鼠随机分为七组，通过喂饲银杏竹鼠肌肉干粉连续一个月，用小鼠低温游泳存活时间实验，耐缺氧实验及跳台和记忆获得障碍实验分别记录低温游泳存活时间，缺氧存活时间及第一次错误潜伏期和跳台错误次数。结果：各竹肉组小鼠与普通饲料（ＮＳ）组，普肉组，护宝液组比较，均可明显延长小鼠低温游泳存活时间和缺氧存活时间（Ｐ＜０．０５），与洋参丸组相当（Ｐ＞０．０５），竹肉大／超组小鼠跳台错误次数均减少（Ｐ＜０．０５），竹肉超组小鼠第一次错误潜伏期延长（Ｐ＜０．０５），竹肉大组小鼠第一次错误潜伏期有延长趋势，但无统计学意义。结论：口服银杏竹鼠肌肉成分可增强小鼠学习记忆能力，增强小鼠体质，提高小鼠生活质量。这一结果也提示银杏竹鼠肌肉成分很有可能成为极有应用前景和开发前景的保健食品。     

去势后大鼠海马结构一氧化氮合酶阳性神经元的变化

目的：观察去势后大鼠海马结构一氧化氮合酶（NOS）阳性神经元的变化。方法：用黄递酶组织化学染色方法观察切除双侧卵巢后雌后SD大鼠海马结构NOS阳性神经元的形态，分布的变化，并进行计算机图像分析。结果：去势后海马结构NOS阳性神经元分布变化有区域差异性；NOS阳性神经元在下托、海马（CA）一区邻近下托的部分、CA三区、CA四区（CA4）和齿状回（DG）数目明显减少，而在CA二区数目明显明显增多，CA4和DG的NOS阳性神经元平均密度降低，胞体的平均周长和平均截面积都明显减少。结论：雌激素可能通过影响海马结构NOS的表达来影响学习和记忆。     

Human osteoblasts' proliferative responses to strain and 17beta-estradiol are mediated by the estrogen receptor and the receptor for insulin-like growth factor I.

The mechanism by which mechanical strain and estrogen stimulate bone cell proliferation was investigated using monolayer cultures of human osteoblastic TE85 cells and female human primary (first-passage) osteoblasts (fHOBs). Both cell types showed small but statistically significant dose-dependent increases in [3H]thymidine incorporation in response to 17beta-estradiol and to a single 10-minute period of uniaxial cyclic strain (1 Hz). In both cell types, the peak response to 17beta-estradiol occurred at 10(-8) - 10(-7) M and the peak response to strain occurred at 3500 microstrain ((mu)epsilon). Both strain-related and 17beta-estradiol-related increases in [3H]thymidine incorporation were abolished by the estrogen receptor (ER) modulator ICI 182,780 (10-8 M). Tamoxifen (10(-9) - 10(-8) M) increased [3H]thymidine incorporation in both cell types but had no effect on their response to strain. In TE85 cells, tamoxifen reduced the increase in [3H]thymidine incorporation associated with 17beta-estradiol to that of tamoxifen alone but had no such effect in fHOBs. In TE85 cells, strain increased medium concentrations of insulin-like growth factor (IGF) II but not IGF-I, whereas 17beta-estradiol increased medium concentrations of IGF-I but not IGF-II. Neutralizing monoclonal antibody (MNAb) to IGF-I (3 microg/ml) blocked the effects of 17beta-estradiol and exogenous truncated IGF-I (tIGF-I; 50 ng/ml) but not those of strain or tIGF-II (50 ng/ml). Neutralizing antibody to IGF-II (3 microg/ml) blocked the effects of strain and tIGF-II but not those of 17beta-estradiol or tIGF-I. MAb aIR-3 (100 ng/ml) to the IGF-I receptor blocked the effects on [3H]thymidine incorporation of strain, tIGF-II, 17beta-estradiol, and tIGF-I. HOBs and TE85 cells, act similarly to rat primary osteoblasts and ROS 17/2.8 cells in their dose-related proliferative responses to strain and 17beta-estradiol, both of which can be blocked by the ER modulator ICI 182,780. In TE85 cells (as in rat primaries and ROS 17/2.8 cells), the response to 17beta-estradiol is mediated by IGF-I, and the response to strain is mediated by IGF-II. Human cells differ from rat cells in that tamoxifen does not block their response to strain and reduces the response to 17beta-estradiol in TE85s but not primaries. In both human cell types (unlike rat cells) the effects of strain and IGF-II as well as estradiol and IGF-I can be blocked at the IGF-I receptor.     

肝细胞癌的相关血清标志物

HCC的早期诊断是其治疗的关键，HCC血清标志物的检测又为其诊断提供了有利的途径，并且操作简单，敏感性高和特异性强。目前常用的血清标志物为AFP、AFP变异体、AFP mRNA、AFU、GGT、DCP、AIF、GPC3等。这些标志物的联合使用有助于HCC的诊断及预后。     

手术治疗125例分化性甲状腺癌的5年随访结果分析

目的：探讨甲状腺全切除术在治疗分化性甲状腺癌中的临床应用价值。方法：采用我院1988年1月～2001年5月甲状腺全切除术或甲状腺侧叶切除加峡部切除术治疗分化性甲状腺癌125例,对其手术并发症发生、局部复发、转移情况及术后5年生存率进行回顾性对比分析。结果：甲状腺全切除术术后并发症发生率高于甲状腺侧叶切除加峡部切除术组;局部复发、转移率低于侧叶切除加峡部切除术组;5年生存率两组无显著性差异。结论：甲状腺全切除术是治疗甲状腺癌有效的手术方式,但应掌握手术指征,改进、提高手术技术,减少并发症。     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.