腰椎定点牵压与硬膜外隙注药疗法单独或联合应用治疗腰椎间盘突出症

目的:对比观察硬膜外隙注药与腰椎定点牵压疗法及其联合应用治疗腰椎间盘突出症的疗效。方法:①选择2004-01/2006-01解放军总医院康复医学科门诊诊治的腰椎间盘突出症患者180例,男125例,女55例,年龄20～65岁。患者对治疗方案知情同意。按随机数字表法将患者分为3组:硬膜外隙注药组、腰椎定点牵压疗法组、联合治疗组,每组60例。硬膜外隙注药组:骶管注射利多卡因注射液、胞二磷胆碱、维生素B12、地塞米松混合液,每5d注射1次,共4次。腰椎定点牵压疗法组:采用胸带与下肢固定带牵引,待牵引床启动逐渐使患者腰脊柱拉伸时,术者双手拇指关节突关节连线,由上腰段向腰骶段滑行推压,当拇指推压到病变间隙时,牵引力须达到患者体质量1.5倍左右,迅速向脊柱前方施压。共2次。联合治疗组为两种疗法联合应用。每2次硬膜外隙注药后施行腰椎定点牵压疗法疗法1次,共2次。②于治疗前和治疗后3,6个月采用疼痛强度评分评估疼痛程度(0～10分,0分为无痛,10分为最痛),治疗前和治疗后3个月观察临床体征和评估疗效,疗效评估依据胡有谷的腰椎间盘突出症和国家中医药管理局(1994年)制定的中医病症诊断疗效标准。③计量和计数资料差异比较分别采用t检验和χ2检验。结果:腰椎间盘突出症患者180例均进入结果分析。①疼痛强度变化:治疗后3个月3组疼痛强度评分均较治疗前降低,其中联合治疗组与治疗前比较,差异明显(χ2=2.13,P<0.01)。治疗后6个月,各组病例的疼痛症状大多数获得控制,其中联合治疗组疼痛强度评分与治疗前比较,差异明显(χ2=4.03,P<0.01),联合治疗组和硬膜外隙注药组疼痛强度评分明显低于腰椎定点牵压疗法组(χ2=5.62,6.16,P<0.05)。②临床体征变化:各组治疗后3个月4项体征均较治疗前改善,其中联合治疗组直腿抬高试验阳性患者数明显少于硬膜外隙注药组和腰椎定点牵压疗法组(7,19,14例,χ2=9.24,9.14,P<0.01)。③疗效:联合治疗组治疗有效率明显高于其他硬膜外隙注药组和腰椎定点牵压疗法组[100%(60/60),88%(53/60),92%(55/60),χ2=6.26,6.04,P<0.01],而其他2组间比较,差异不明显(χ2=8.63,P>0.05)。结论:硬脊膜外注药及腰椎定点牵压疗法均是治疗腰椎间盘突出症的有效疗法,联合应用疗效更好。     

猪胸腰段脊髓火器贯通伤后p53基因的早期表达

目的:建立家猪胸腰段脊髓火器贯通伤模型和改良Allen's打击伤后全瘫模型,观察伤后促凋亡基因p53基因的早期表达。方法:实验于2005-05/08在解放军第一七五医院实验室完成。取健康雄性家猪20只,单纯随机分为3组:①火器伤组:9只,在全麻状态下制作胸腰段(L1～L2)脊髓火器伤模型,分为伤后1,3,6h3个时间处死。②打击伤组:9只,L1节段脊髓行改良Allen’s打击,致伤力为500g·cm,处死时间同前。③空白对照组:2只,只麻醉,不造模,伤后6h处死。伤后不同时间点(伤后1,3,6h)和不同节段(伤点、近伤点、中伤点及远伤点)取材,采用SP法进行P53蛋白免疫组化染色,用TJTY-300型全自动图像分析仪测量P53免疫组织化学染色阳性物质吸光度。结果:经补充后20只猪进入结果分析。①脊髓损伤后3h打击伤组伤点,火器伤组近伤段脊髓P53蛋白的表达高于空白对照组(P<0.001),随着时间推移,打击伤组和火器伤组P53蛋白的表达呈升高趋势(P<0.001),且火器伤组要高于打击伤组(P<0.0001)。②在脊髓损伤后6h,打击伤组仅在伤点和近伤段P53蛋白的表达高于空白对照组(5.57±0.82,3.21±0.43,P<0.05),而火器伤组近伤段、中伤段及远段伤均高于空白对照组(6.46±0.66,4.27±0.39,1.16±0.17,P<0.05)。结论:①细胞凋亡基因p53在脊髓损伤中的表达有一定的时空性,在脊髓损伤后3h出现P53蛋白表达量的增加。②脊髓火器伤的波及范围较打击伤更为广泛。     

Polyethylene glycol versus low-ionic-strength solution in pretransfusion testing: a blinded comparison study

BACKGROUND: Polyethylene glycol (PEG) has been shown to potentiate antigen-antibody reactions. STUDY DESIGN AND METHODS: To investigate the utility of PEG in pretransfusion testing, a blinded comparison study of PEG and a low-ionic-strength additive solution (LISS) was conducted. A total of 500 patient samples were tested in parallel with reagent antibody-detection cells using blind-coded PEG and LISS potentiators. RESULTS: In 34 (34%) of 100 samples with known antibodies in the Rh, Kell, Duffy, Kidd, and MNS systems, PEG antiglobulin reactions were stronger (total score, 382) than LISS antiglobulin reactions (total score, 216), and in 66 cases (66%), they were equal to those of LISS. Of 400 samples without detectable antibodies, 384 were negative with PEG and LISS, and 16 were positive in PEG tests and negative in LISS. Seven of the 16 were clinically important antibodies (D, 1; E, 3; Fya, 1; Jka; 1; Jkb, 1), and four were clinically benign antibodies (Le(a), 2; McCc, 1; Sda, 1). Five of the 16 demonstrated inconclusive PEG reactions, for a false-positive rate of 5 in 400 (1.3%). Of the 500 samples, none was negative in PEG tests and positive in LISS (0% false-negative rate). CONCLUSION: Although PEG demonstrates a relatively high false-positive rate, PEG is more sensitive than LISS in detecting clinically significant antibodies.     

Biliary lithotripsy: early observations in 106 patients. Work in progress

One hundred six patients underwent extracorporeal shock wave lithotripsy for cholelithiasis. Of these, 28 patients underwent cholangiographically guided lithotripsy for bile duct stones to assist nonoperative stone removal by endoscopic or radiologic intervention. Fragmentation occurred in 20 of 28 cases (71%) with an average of two lithotripsy sessions. Hemobilia was observed in four patients (14%) for a 24-hour period. Seventy-eight of the 106 were outpatients with symptomatic cholecystolithiasis with one to five calculi who underwent cholecystographic or ultrasound-(US) guided shock wave lithotripsy as definitive therapy. US examination showed stone fragmentation in 86% of cases. With an average of 1.6 treatment sessions and 4,750 shocks, fragments were 4 mm or smaller in 46% of patients. Nine percent of patients had no fragments after an average of 10 weeks, but long-term follow-up is not yet available. Two patients developed acute pancreatitis attributable to fragment passage and one patient acute cholecystitis, likely due to cystic duct obstruction by a fragment.     

Antibody to virion structural proteins in mammals bearing avian sarcoma virus-induced tumors.

The production of antibody to virion structural proteins was examined in rabbits and hamsters bearing tumors induced by avian sarcoma virus (ASV). Antibody activity was analyzed by the immunoprecipitation of polypeptides from preparations of radiolabeled ASV virions. Antipolymerase and antiglycoprotein activities were monitored by inhibition of the enzyme activity of virion polymerase and by neutralization of focus formation by group D ASV, respectively. All sera from hamsters bearing primary ASV-induced tumors had antibody against the viral gs antigens, but no antipolymerase or antiglycoprotein activity was detectable. Most sera from hamsters bearing tumors induced by injection of cloned hamster tumor cells displayed anti-gs activity, and in addition, some sera exhibited anti-polymerase activity as well. All sera from rabbits bearing primary tumors contained antibody against the gs antigens and the virion polymerase, and some of these sera were shown to have antibody against the virion glycoprotein, gp85, as well.