改良尺骨鹰嘴截骨治疗肱骨髁间骨折

目的:探讨改良尺骨鹰嘴截骨治疗肱骨髁间骨折的手术方法和疗效。方法:2007年5月至2012年12月采取改良尺骨鹰嘴截骨入路治疗肱骨髁间骨折32例,男21例,女11例;年龄18~65岁,平均46.3岁;右侧19例,左侧13例。AO分型,C1型7例,C2型11例,C3型14例;开放性骨折5例(GustiloⅠ型3例,GustiloⅡ型2例)。6例合并其他处骨折,4例合并尺神经损伤,2例合并桡神经损伤。术后定期复查及X线检查,按Cassebaum评分系统评定肘关节功能。结果:32例均获随访,时间9个月~5年,平均1.9年;截骨块愈合时间6~10周,平均7.4周。未发生尺骨鹰嘴关节内骨折,无截骨块不愈合。2例肘后内固定隆起处屈肘轻度疼痛不适,1例骨折块松动,2例出现异位骨化。肘关节功能评定:优19例,良8例,可4例,差1例。结论:改良尺骨鹰嘴截骨治疗肱骨髁间骨折具有不侵袭关节、术中截骨简便、固定简单、截骨块力学稳定性好、截骨并发症发生率低等优点。     

Platelet membrane alterations induced by the local anesthetic dibucaine

Tertiary amine local anesthetics modify a variety of platelet membrane- related functions. The present study explored dibucaine (DB)-induced inhibition of platelet cohesion by examining structural and functional alterations of the human platelet membrane glycoprotein IIb-IIIa complex (GPIIb-IIIa) and platelet Ca2+ homeostasis. Complete inhibition of ADP-induced aggregation was achieved five minutes after platelet exposure to 0.10 to 0.25 mmol/L of DB when fibrinogen binding was reduced by 50%. At higher concentrations of DB (approximately 1 mmol/L), ADP-induced fibrinogen binding was completely blocked. Scatchard analysis revealed loss of high-affinity binding sites in addition to reduction in Bmax. In contrast, chymotrypsin-treated platelets sustained 50% inhibition of fibrinogen binding when incubated with 0.4 to 0.5 mmol/L DB, and kinetic analysis showed that the high- affinity platelet-fibrinogen interactions were reduced but not absent. Fibrinogen binding to chymotrypsin-treated platelets could not be completely inhibited even at high DB concentrations (1 mmol/L). The inhibition of fibrinogen binding to chymotrypsin-treated platelets correlated with changes in binding of a monoclonal antibody (10E5) specific for an epitope on the GPIIb-IIIa complex. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and radioelectroimmunoassay of DB-treated platelets, however, showed no evidence of a reduction or degradation of GP IIb or IIIa. Platelet incubation with DB (five minutes, 0.1 to 1.0 mmol/L) was also accompanied by: increased platelet membrane-associated Ca2+ involving low-affinity binding sites [Kd = 5 X 10(-5) mol/L-]; increased 45Ca2+ uptake which correlated with degradation of actin-binding protein (ABP) and digestion of GPIb as visualized on periodic-acid Schiff (PAS)- stained SDS gels and as inferred from decreased binding of a monoclonal antibody (6D1) directed against this glycoprotein; and enhanced Ca2+ exchange. Thus, exposure of platelets to DB results in membrane-related alterations that may contribute to inhibition of platelet cohesion: Decreased fibrinogen receptor exposure by traditional agonists and diminished accessibility of the GPIIb-IIIa complex to extracellular ligands correlate with DB-induced inhibition of platelet aggregation; and increased calcium uptake and exchange across the platelet membrane likely leads to activation of the calcium-dependent protease(s) which was previously shown to correlate with DB-induced inhibition of ristocetin-induced platelet agglutination.     

艾司洛尔联合胺碘酮治疗心室电风暴160例临床分析

目的：探讨和分析盐酸艾司洛尔与胺碘酮联合使用在治疗心室电风暴患者的效果。方法整群选取该院在2011年9月-2014年6月期间所收治的329例心室电风暴患者,遵照随机与知情自愿原则,分为观察组(160例)和对照组(169例)。给予药物胺碘酮治疗,对观察组患者采用盐酸艾司洛尔与胺碘酮联合治疗方案,疗程结束后,认真观察和对比两组患者所取得治疗的效果。结果观察组患者总有效率为95.0%,明显高于对照组的70.4%,该两组患者总有效率对比,差异有统计学意义(P<0.01);治疗后观察组患者收缩压与心率分别为(104.0±15.0)mmHg、(84.0±13.0)次/min全部低于对照组,该两组患者治疗后的收缩压与心率对比,差异有统计学意义(P<0.05)。结论采用盐酸艾司洛尔联合药物胺碘酮共同治疗心室电风暴患者的临床效果满意,能够提高心室风暴患者的治愈率,具有临床推广价值。     

Evaluation of the chronic toxicity and oncogenicity of N,N-diethyl-m- toluamide (DEET)

Chronic toxicity and/or oncogenicity studies were conducted in rats, mice, and dogs with the insect repellent DEET. DEET was mixed in the diet and administered to CD rats for two years at concentrations that corresponded to dosage levels of 10, 30 or 100 mg/kg/day for males and 30, 100, or 400 mg/kg/day for females; to CD-1 mice for 18 months at dosage levels of 250, 500, or 1000 mg/kg/day; and to dogs for one year, via gelatin capsules, at dosage levels of 30, 100, or 400 mg/kg/day. In the rodent studies, each group consisted of 60 animals of each sex, and two concurrent independent control groups, each containing 60 animals/sex were included in each study. Each group in the dog study consisted of four male and four female dogs and one control group was included in the study. Treatment-related effects were observed at the highest dose level in all three studies. For rats, the effects included decreases in body weight and food consumption and an increase in serum cholesterol in females only. In mice, the effects observed were decreases in body weight and food consumption in both sexes. The effects observed in dogs included increased incidences of emesis and ptyalism, and levels of transient reduction in hemoglobin and hematocrit, increased alkaline phosphatase (males only), decreased cholesterol, and increased potassium. One male dog in the high-dose group also exhibited ataxia, tremors, abnormal head movements, and/or convulsions on several occasions during the study. The highest no- observed-effect levels (NO-ELs) for rats, mice and dogs were determined to be 100, 500, and 100 mg/kg/day, respectively. No specific target organ toxicity or oncogenicity was observed in any of the studies.      

Evaluation of the systematic set-up errors using electronic portal image device in the radiotherapy procedures

Objective： The aim of this work was to quantify the extent of set-up errors to conduct a quality assurance （QA） aspect of treatment delivery, verification of the treatment field＇s position on different days using electronic portal. Methods： This study was carried out on 12 patients, treated for pelvis tumor; and total of 240 images obtained by electronic portal image device （EPID） were analyzed. The EPIs acquire using EPID attached to the Siemens linear accelerator. The anatomy match- ing software （Theraview） was used and displacement in two dimensions were noted for each treatment field to study patient setup errors. Results： The percentages of mean deviations less than 5 mm in X direction were 65% ＆ 92%, from 5-10 mm were 31% ＆ 19% and more than 10 mm were 11% ＆ 9% forNP and lateral direction respectively. The percentages of mean deviations less than 5 mm in Y direction were 65% ＆ 63%, from 5-10 mm were 33% ＆ 28% and more than 10 mm were 22% ＆ 29%. The mean deviations in 2D-vector errors were 〈 5 mm in 47% and 46%, 5-10 mm in 36% and 37% and 〉 10 mm in 37% and 37% of images in the NP and lateral direction respectively. Conclusion： The results revealed that the ranges of set up errors are immobilization method to improve reproducibility. The observed variations were not within the limits..     

A murine monoclonal antibody that blocks fibrinogen binding to normal platelets also inhibits fibrinogen interactions with chymotrypsin- treated platelets

We recently described a monoclonal antibody, 10E5 , that completely blocks adenosine diphosphate (ADP) induced fibrinogen binding to platelets and aggregation induced by ADP, epinephrine, and thrombin. Multiple lines of evidence indicate that 10E5 binds to platelet membrane glycoproteins IIb and/or IIIa. Because it has been reported that platelets treated with chymotrypsin aggregate when fibrinogen is added, we tested the effect of 10E5 antibody on chymotrypsin-induced fibrinogen binding and platelet aggregation. Aspirin-treated human platelets were washed in modified Tyrode's buffer (pH 7.5), incubated for 5 minutes at 22 degrees C with 300 micrograms/mL chymotrypsin, and washed again. The amount of 10E5 antibody bound to these platelets (37,232 +/- 2,928 molecules/platelet; mean +/- SEM, N=9) was similar to that bound to unstimulated control platelets (36,910 +/- 2,669) and did not differ significantly from the amount of antibody bound to ADP- treated platelets (P less than .01, N = 5). The amount of 10E5 bound to chymotrypsin-treated platelets correlated directly with the amount of fibrinogen bound to separate aliquots of the same platelet samples (r = .876, P less than .001). The 10E5 antibody caused virtually complete inhibition of both the binding of fibrinogen to chymotrypsin-treated platelets and the aggregation induced by exogenous fibrinogen. Immunoprecipitation studies of 125I-labeled chymotrypsin-treated platelets revealed that the 10E5 antibody bound proteins with molecular weights characteristic of glycoproteins IIb and IIIa. These data suggest that the fibrinogen receptor on chymotrypsin-treated platelets is identical to that on ADP-treated platelets and that this receptor is either near to, or on, the glycoprotein IIb/IIIa complex.