遏制轻型急性胰腺炎向重症转化的非手术 治疗策略

目的 ：探讨遏制急性胰腺炎向重症转化的非手术治疗策略。方法 ：将4年间收治的286例轻型急性胰腺炎分为对照组和治疗观察组。对照组采取常规非手术治疗措施;观察组加用改善胰腺微循环，防治细胞钙超载和抑制胰酶的治疗方法。结果 ：对照组144轻型有20例转化为重症胰腺炎，14例发生全身性并发症;观察组142例轻型有8例转化为重症，2例出现全身性并发症。观察组重症患者血C-反应蛋白和Balthazar CT严重度指数在治疗后各时点较对照组明显降低。结论 ：在常规治疗的基础上加用改善胰腺微循环，防治细胞钙超载和抑制胰酶的治疗措施可能有助于阻止轻型急性胰腺炎向重症化发展。     

腹腔脏器损伤210例诊治分析

目的:探讨腹腔脏器损伤的诊治方法。方法：回顾性分析15年间收治的210例腹腔脏器损伤的临床资料。结果：腹腔穿刺阳性率（88.6%）。术前诊断基本准确125例（59.5%）。210例均行手术治疗，治愈190例（90.5%），死亡20例（9.5%）。结论：腹腔多脏器损伤较为常见。腹腔穿刺是可靠的诊断手段，对有剖腹探查指征的病例应积极手术，探查时既要系统全面，防止遗漏，又要避免重复多余的探查。     

淋巴瘤细胞转染GM-CSF 基因后生物学特性的变化

目的：制备高表达GM－CSF的淋巴瘤细胞系，观察淋巴瘤细胞转染GM－CSF基因后生物学特性的改变。方法：将小鼠GF－CSF真核表达质粒用电穿孔法导入小鼠淋巴瘤细胞系RMA，有限稀释法制备单个细胞克隆，经RT－PCR，骨髓祖细胞增殖实验和集落形成实验筛选相对高表达GM－CSF的RMA克隆，并观察其生物学特性的改变。结果：获得了高表达GM－CS的RMA细胞系,其同基因动物体内致瘤性降低。结论：淋巴瘤细胞系RMA转染GM－CSF基因后致瘤性降低。     

胸大肌肌皮瓣在口腔颌面部缺损修复中的应用

报道２１９例口腔颌面部肿瘤，其中良性肿瘤１８例，恶性肿瘤２０１例，在肿瘤切除后，均采用胸大肌肌皮瓣修复缺损。采用单皮岛肌皮瓣２０１例，双皮岛肌皮瓣１６例，肌皮骨瓣２例。成功２０１例，失败１８例。讨论了胸大肌皮瓣的优点及适用范围。介绍了手术设计、操作方法。分析了成功与失败的影响因素，认为正确，精细的手术技巧是成功的关键因素。     

Responses of CDKs and p53 in Delayed Ischemic Neuronal Death

Stroke is a debilitating disease that affects millions each year.While in many cases cerebral ischemic in jury can be limited by effectivw resuscitation or thrombolytic treatment,the injured neurons wither in a process known as delayed neuronal death(DND).Mounting evidence indicates that DND is not simply necrosis played out in slow motion but apoptosis is triggered.Of particular interest are two groups of signal proteins that participate in apoptosis-cyclin dependent kinases(CDKs) and p53-among a myriad of signaling events after an ischemic insult.Recent investigations have shown that CDKs,a family of enzymes initially known for their role in cell cycle regulation,are activated in injured neurons in DND.As for p53,new reports suggest that its up-regulation may represent a failed attempt to rescue in jured neurons,although its up-regulation was previously considered an indication of apoptosis.These observations thus rekindle an old quest to identify new neuroprotective targets to minimize the stroke damage.In this review,the author will examine the evidence that indicates the participation of CDKs and p53 in DND and then introduce pre-clinical data to explore CDK inhibition as a potential neuroprotective target.Finally,using CDK inhibition as an example,this paper will discuss the pertinent criteria for a viable neuroprotective strategy for ischemic in jury.     

铁路系统医院136篇口腔修复、正畸学论文的统计分析

通过对铁路系统医院１３６篇口腔修复、正畸学论文的统计分析，来评价医院口腔修复、正畸的科研水平，同时也揭示了科研工作中存在的问题。指出只有加强科研协作、扩大学术交流、增加科研投入，提高科研水平，使科研成果更趋完善。     

偏瘫病人下肢功能康复阻碍因素初探

观察了10项因素对偏瘫病人下肢功能康复的影响,其结果表明:①下肢功能水平;②平衡功能障碍;③足下垂内翻;④髋关节屈曲外旋挛缩;⑤深感觉障碍;⑥疼痛等几项因素对偏瘫病人下肢功能康复有显著的影响。     

Discovery of methoxyacetylcarbamide in the urine of normal adults and phenylketonuric children

In order to study metabolic distinctions in phenylketonuria, urinary metabolites in the form of trimethylsilyl derivatives have been characterized by high resolution gas chromatography and mass spectrometry. A previously unknown metabolite has been found in the urine of some untreated phenylketonuric infants between 2 and 5 yr of age. The metabolite was absent in healthy children of the same age. The metabolite appeared to be present in the urine of apparently healthy adults (25-32 yr old). The metabolite was identified as methoxyacetylcarbamide on the basis of mass fragmentation analysis and compared with synthetic methoxyacetylcarbamide. Their retention times and mass spectra coincided.     

Prevention of Bone Loss by Clodronate in Early Postmenopausal Women with Vertebral Osteopenia: A Dose-Finding Study

This double-masked, placebo-controlled study was undertaken to determine the efficacy and safety of oral clodronate in the prevention of bone loss in early postmenopausal women with vertebral osteopenia. Altogether 610 women with a mean age of 53 years were recruited for the study. They were 1–5 years postmenopausal and their lumbar spine bone mineral density (BMD) was at least 1 standard deviation below the mean of premenopausal women (T-score ≤−1). The subjects were randomized into five study groups to receive either placebo, clodronate 65 mg, 400 mg or 800 mg daily, or intermittent clodronate in 3 month cycles with 400 mg daily for 15 days followed with no treatment for 75 days for 3 years. One hundred and eighty-seven of 509 women who completed the primary study continued in the extension study of 2 years in which previous placebo users were switched to clodronate 800 mg daily, while previous users of 400 mg or 800 mg of clodronate used either placebo or 800 mg of clodronate daily. In the primary study clodronate was administered in the evening, and in the extension 1 h before breakfast on an empty stomach. In the primary study mean changes in lumbar spine BMD were −3.4% in the placebo group and +0.4% in 800 mg clodronate group [difference between groups at 3 years 3.8% (95% CI 2.7% to 4.9%, p<0.0001)], and in the trochanter area BMD −1.1% in the placebo group, and + 0.4% in the 800 mg clodronate group [difference between groups at 3 years 1.5% (95% CI 0.05% to 2.9%)]. During the extension study mean changes in lumbar spine BMD were +1.5% in the clodronate group and −0.2 % in the placebo group [difference between groups 1.7% (CI 0.4% to 3.0%, p = 0.010)] and in trochanter BMD were +2.5% in the clodronate group and no change in the placebo group [difference between groups 2.1% (CI 0.3% to 3.9%, p = 0.007)]. No statistically significant differences between the placebo and 800 mg clodronate groups were found in the femoral neck BMD. In the primary study the urinary excretion of type I collagen aminoterminal telopeptide (NTX) decreased by 44% (p<0.0001 compared with placebo) and that of deoxypyridinoline by 18% (p<0.0001) in the clodronate 800 mg group. In the extension study urinary NTX decreased by 51% (p<0.0001) in those who were switched to 800 mg of clodronate and increased by 67% (p<0.0001) in those who stopped using that dose. There was no difference in the frequency of gastrointestinal complaints between clodronate- and placebo-treated patients in the primary study, but they were more common among women who received clodronate in the extension phase. Clodronate in daily doses of 400–800 mg caused a slight elevation of aminotransferase levels, usually within the reference range. In bone biopsies no defect in mineralization was found. In conclusion, clodronate in a daily dose of 800 mg prevents early postmenopausal bone loss at the sites of the skeleton in which cancellous bone predominates. It effectively reduces bone resorption and bone turnover rate. Antifracture efficacy of clodronate remains to be established by prospective, placebo-controlled trials. Received: 4 March 2002 / Accepted: 9 July 2002