转化生长因子β1抗体复合缓释载体生物蛋白胶应用于鞘管区预防屈肌腱粘连的生物力学分析

目的:单纯生物蛋白胶是一种良好的缓释载体,拟通过与转化生长因子β1抗体复合应用于肌腱损伤局部,观察其对鞘管区屈肌腱粘连的预防作用和对肌腱愈合的影响。方法:实验于2003-01/04在解放军第四军医大学西京医院骨科研究所完成。①实验动物:将72只来亨鸡(leghorn)按随机化原则分为单纯转化生长因子β1抗体组、单纯生物蛋白胶组、转化生长因子β1抗体复合生物蛋白胶组及生理盐水组,每组18只。实验过程中对动物处置符合动物伦理学要求。②实验方法:分别将鸡左足第三、四趾趾深屈肌腱横断,作The 4-strand Cruciate repair缝合,然后按照分组,用1 mL无菌注射器,向鞘管区分别注入0.2 mL转化生长因子β1抗体(8 mg/L)和生理盐水,用生物蛋白胶专用注射器向鞘管区分别注入0.2 mL生物蛋白胶和转化生长因子β1抗体生物蛋白胶复合液。③实验评估:术后5 d行早期功能锻炼,在第1,3,8周麻醉后处死取材,第四趾标本分别行大体观察、组织学检查和缝合处粘连评分。第三趾在SHIMADZU SPL-10kN型材料实验机上进行生物力学测试。结果:转化生长因子β1抗体复合生物蛋白胶组术后3,8周,缝合处粘连程度评分、肌腱滑动距离、模拟主动屈曲度及屈曲功均优于其余3组,且差异有显著性意义(P<0.05)。4个处理组的最大抗断裂载荷差异无显著性意义(P>0.05)。结论:转化生长因子β1抗体复合缓释载体生物蛋白胶可以有效预防术后肌腱粘连,并且不影响肌腱的正常愈合进程。     

甲醛存在下阿米卡星的单扫描示波极谱法测定

研究了在Britton-Robinson(pH8.0)介质中,阿米卡星(AMK)甲醛衍生物的单扫描示波极谱行为,并对其电极反应机理作了研究。在选定条件下,AMK浓度在6.0×10^-7～5.0×10^-5mol·L^-1范围内与峰电流呈线性,相关系数为0.9998,检测限为2.4×10^-7mol·L^-1。方法无需前处理即可用于针剂、尿及血清样品中痕量AMK测定,回收率90%～110%,相对标准偏差小于4.1%。     

棉酚衍生物和酚醛类化合物的合成及抗生育作用

合成了一批三羟基萘醛、多羟基联苯醛、多羟基联萘醛和一些棉酚衍生物,提供抗生育研究。     

亚甲基二膦酸的合成

目的：改进工艺，合成药用原料亚甲基二膦酸。方法：以亚膦酸三异丙酯为原料，经取代、缩合、水解等反应而合成目标产物。结果：产物结构经红外光谱、核磁共振等分析确证；制成药盒符合中国药典2000年版标准。结论：此合成工艺实用可行。     

天然有机化合物质谱研究——Ⅺ.苯丙型苷快原子轰击质谱MNa~+的MIKES谱

研究了六种苯丙型苷与Na~+加合离子的快原子轰击质谱(FAB—MS)和质量分离离子动能谱(MIKES)。结果表明:在FAB谱中[M+Na]~+加合离子的丰度要比[M+H]~+离子高得多。由此可给出糖苷的分子量信息,[M+Na]~+离子的MIKES谱可给出糖基序列信息。     

抗心肌缺血药2,6-二甲基-4-双取代苯基-1,4-二氢吡啶-3,5-二羧酸酯的合成

本文报道了9个新的2,6-二甲基-4-双取代苯基-1,4-二氢吡淀-3,5-二羧酸酯的合成。初步药理试验表明:化合物I_6具有较强的抑制KCl诱发兔主动脉条的收缩作用,增加冠脉血流量和心输出量,降低心肌耗氧量;增强小鼠抗缺氧能力;对大鼠心肌缺血有保护作用;能缩小兔缺血心肌再灌流引起的心肌梗塞范围。     

巯基化合物对离体大鼠心脏缺血再灌所致心律失常的保护作用

本文研究了半胱氨酸(Cys)及其结构类似物半胱胺(MEA),N-乙酰半胱氨酸(NAC)、胱胺(CSSC),γ-氨丙基甲基异硫脲(APMT),对离体大鼠Langendortff心脏缺血再灌所致心律失常的保护作用.给药(0.1,0.6,3,6μmol/min)10min,结扎LAD 10 min再灌5 min。结果表明含游离巯基的Cys,NAC,MEA在0.6和3.6 μmol/min时,与生理盐水对照组相比可显著降低室颤发生率(P<0.01～0.001),缩短室颤时程(P<0.01～0.001).CSSC和APMT未见明显保护作用。此外,Cys,NAC和MEA还可明显增加冠脉流量(P<0.01),CSSC和APMT则反而使冠脉流量降低。     

双边栝楼中栝楼酯碱的结构研究

自双边栝楼(TrichosanthesrosthorniiHarms)干燥果皮的脂溶性部分分离到一个新生物碱,经核磁共振谱、质谱和红外光谱等数据分析,确定结构为α-(苯甲酰胺)-苯丙酸-3-[(1-苯基)亚乙基]氨-2-羟基丙酯(Ⅰ),命名为栝楼酯碱(trichosanatine)。     

Comparison of high resolution cytogenetics, fluorescence in situ hybridisation, and DNA studies to validate the diagnosis of Prader-Willi and Angelman's syndromes

Eighty seven referrals with Prader-Willi syndrome and 49 with Angelman's syndrome were studied. High resolution cytogenetics was performed on all probands. Molecular studies, performed on the proband and both parents in each case, utilised multiple probes from within and distal to the 15(q11-13) region in order to establish the presence of DNA deletion or uniparental disomy. In addition, FISH, with probes at D15S11 and GABR beta 3 from the Prader-Willi syndrome/Angelman's syndrome region, was performed on a subset of 25 of these patients. In the referral group with Prader-Willi syndrome, 62 patients had a normal karyotype and 25 were deleted on high resolution cytogenetics. Twenty nine were found to be deleted with DNA techniques. In the Angelman's syndrome group, 37 had a normal karyotype and 12 were deleted on high resolution cytogenetics while 26 were deleted on molecular studies. The diagnosis was reassessed in 35 referrals with Prader-Willi syndrome and 11 with Angelman's syndrome following a non-deleted, non-disomic result. Of individuals who were neither deleted nor disomic on DNA studies, a false positive rate of 11.4% (4/35) for Prader-Willi syndrome and 16.7% (2/12) for Angelman's syndrome was found for a cytogenetically detected deletion. The false negative rate for deletion detected on high resolution cytogenetics was 19.5% (12/62) for Prader-Willi syndrome and 35% (13/37) for Angelman's syndrome. Thus high resolution cytogenetics was shown to be unreliable for deletion detection and should not be used alone to diagnose either syndrome. There were no discrepancies with FISH in 25 cases when FISH was compared with the DNA results, indicating that FISH can be used reliably for deletion detection in both syndromes.