贞芪扶正口服液的质量标准

目的制订贞芪扶正口服液质量标准。方法用薄层色谱法鉴别黄芪、女贞子、白术 ;用香草醛 硫酸比色法测定黄芪甲苷的含量。结果平均回收率为 98 95 % ,RSD为 0 81 % (n =5 )。结论建立的方法可控制贞芪扶正口服液的质量     

Implication of brevetoxin B1 and PbTx-3 in neurotoxic shellfish poisoning in New Zealand by isolation and quantitative determination with liquid chromatography-tandem mass spectrometry.

Brevetoxin B1 (BTX-B1) was isolated from Austrovenus stutchburyi following the 1992-1993 outbreak of neurotoxic shellfish poisoning (NSP) in New Zealand. We report here the first isolation of PbTx-3 from the same shellfish and the development of a procedure for quantitative determination of PbTx-3 and BTX-B1. PbTx-3 was isolated by chromatography on columns of SiO2, ODS, and LH-20, followed by reverse-phase HPLCs. In mass spectrometry (MS) with an electrospray ionization (ESI) interface operating in the positive or negative ion mode, the abundant protonated ion [M+H]+ of PbTx-3 (m/z 897) and the de-sodiated ion [M-Na]- of BTX-B1 (m/z 1016) were generated, respectively. These served as precursor ions for collision-induced dissociation, and the product ions of m/z 725 from PbTx-3 and m/z 80 from BTX-B1 were identified, allowing unambiguous confirmation of these toxins by selected reaction monitoring liquid chromatography-tandem mass spectrometry (SRM LC-MS/MS) analysis. The determination limits were 0.4 and 2 ng/g for BTX-B1 and PbTx-3 at a signal-to-noise ratio of five, respectively. This LC-MS/MS method was successfully applied to determine BTX-B1 and PbTx-3 in the NSP-associated toxic shellfish. BTX-B1 was found in both A. stutchburyi and Perna canaliculus, but not in Crassostrea gigas, while PbTx-3 was found in all three.     

抗癌口服液在体内外抗肿瘤作用的实验研究

OBJECTIVETo investigate anti-cancer of the Anti-cancer Oral Liquid (ACOL) for MGC-803 gastric cancer cell line in vivo and vitro. METHODUsing the MTT assay, colonogenic assay and sero-pharmacological experiment by treating with the Chinese traditional med     

Use of N-butyl-2-cyanoacrylate in oral surgery: biological and clinical evaluation

N-butyl-2-cyanoacrylate based tissue adhesive, Tisuacryl, was employed as a nonsuture method for closing wounds in oral surgery. One hundred thirty patients were treated with the adhesive and 30 with suture. The surgical procedures were apicectomy, extraction of molars, and mucogingival grafting. The studied product was well tolerated by the tissue and permitted immediate hemostasis and normal healing of incisions. When Tisuacryl was used as dressing material for donor sites and mucosal ulcerations, pain relief was observed.     

腺病毒介导HSV-TK/GCV系统联合放射治疗口腔鳞癌的研究

目的 探讨单纯疱疹病毒胸苷激酶基因（HSV－TK）／丙氧鸟苷（GCV）自杀基因系统对放射治疗的增敏作用。方法 口腔鳞癌细胞（Tca8113细胞系）经HSV－TK／GCV系统治疗后给予放射治疗，采用LQ和单击多靶（SHMT）模型分析细胞存活曲线参数。结果 细胞存活曲线分析显示：单纯放射治疗组其α为0.1074,β为0.0158,D0为2.2576,Dq为3.5413；与单纯放射治疗组比较，HSV－TK／GCV治疗组α（0.2127)和α：β（9.496)值大，D0（1.4526)和Dq(2.2257)值小，其放射增敏率（SER）为1.55。结论 HSV－TK／GCV系统具有放射增敏作用，可提高放射治疗对口腔鳞癌的治疗疗效。     

192Ir-HDR放疗合并外照射治疗口腔癌报道

目的 探讨早、中期口腔癌应用外照射合并^192Ir—HDR后装放疗的疗效。方法 对16例早、中期口腔癌患者，首先给^60Co或6MV—X加速器外照射，外照总剂量为Dt46～56Gy，23～28次，4～6周。外照结束后1周，给^192Ir—HDR后装组织插植或肿瘤表面贴敷放疗，参考点剂量为Dt18～32Gy,2～5次，3～15天,间隔1～5天。结果 5年生存率为81．3％，无严重的放射后遗症。结论 对早、中期口腔癌，就用外照射合并^192Ir—HDR后装放疗疗效与手术疗效相似，无严重的放射后遗症，且患者能保持外观和正常组织功能，提高了病人生存质量。     

吸液态氧对高原移居青年肺通气功能的影响

目的　探讨在高原地区吸入液态氧对移居青年肺通气功能的影响。　方法　将进驻海拔 370 0m半年的 4 0名健康青年随机分为两组 ,每组 2 0人。一组为对照组 ,受试者用EGM型踏车功量计做坐位踏车运动 ,初始负荷功率 2 5W ,每 3min递增 5 0W ,以 6 0rpm/min连续踏车直至力竭。另一组为实验组 ,在运动前10min开始用面罩吸液态氧 ,每min吸入量为 4L ,在踏车运动中全程吸氧 ,踏车方式同对照组。计算每位受试者运动功率 2 2 5W时的每分钟肺通气量 (VE)。　结果　吸氧组和对照组VE 分别为 32 16± 3 6 2与 38 78± 2 2 3;血氧饱和度 (SaO2 )分别为 84 10± 4 2 2与 73 70± 2 34。VE 明显降低 ,SaO2 明显增高 ,差异非常显著(P <0 0 1)。　结论　吸液态氧能明显改善高原移居青年的肺通气量并提高做功效率。     

Insulin resistance is associated with decreased clinical status in cystic fibrosis

Patients with cystic fibrosis (CF) frequently have impaired glucose tolerance and progression to diabetes (DM) with clinical features of both insulin-dependent and non-insulin-dependent diabetes. One feature of non-insulin-dependent DM is decreased insulin sensitivity, also known as insulin resistance. The goal of this study was to determine whether patients with CF exhibit insulin resistance and to determine the potential effect of insulin resistance on clinical status. We also sought to determine whether insulin resistance is associated with a specific CF genotype. We studied 18 patients with CF (8 with normal glucose tolerance, 5 with impaired glucose tolerance, 5 with DM), and 20 lean control subjects matched for age, weight, and sex. All control subjects had normal glucose tolerance. The clinical status for each CF patient was determined according to a modified National Institutes of Health scoring system. Each subject underwent a three-step hyperinsulinemic euglycemic clamp (insulin doses of 10, 40, 120 mU/m ² per minute). Results from the 120 mU/m ² per minute infusion defined maximal glucose disposal rate (defined in milligrams per kilogram body weight per minute) at steady state with peripheral insulin levels 195 ± 20 mU/ml. Subjects with CF demonstrated insulin resistance (control subjects = 13.6 ± 1.1, patients with CF = 10.2 ± 1.6 mg/kg per minute; p = 0.003). When each subgroup was compared separately with control subjects, all subgroups were statistically insulin resistant (glucose disposal rate, patients with CF and normal glucose tolerance = 10.8; those with impaired glucose tolerance = 8.4; those with DM = 10.1 mg/kg per minute), and the patients with CF with impaired glucose tolerance were the most insulin resistant. When plotted versus glucose disposal rate, a striking positive correlation between worsened clinical status and insulin resistance ( r = 0.85) is demonstrated. Furthermore, there is no correlation between insulin resistance and fasting blood glucose, subject age, or percent ideal body weight (all r values not significant). In conclusion, patients with CF exhibit insulin resistance that is associated with worsened clinical status. We believe it is the combination of insulin resistance and decreased insulin secretion that is responsible for the high incidence of CF-related diabetes. (J Pediatr 1997;130:948-56)     

Pharmacokinetics of trofosfamide and its dechloroethylated metabolites

 To contribute to effective and safe outpatient treatment, we investigated the metabolism of trofosfamide (Trofo) after oral administration. We analyzed Trofo metabolism in 15 patients aged from 3 to 73 years who were treated with 150 or 250 mg/m² Trofo in combination with etoposide. Serum samples were collected with 13 patients after oral administration, and Trofo and its dechloroethylated metabolites were quantified by gas chromatography. Urine samples were collected from five patients and analyzed by same method. Ifosfamide (Ifo) was the main metabolite in serum and urine (AUC_Trofo:AUC_Ifo 1:13), whereas cyclophosphamide (Cyclo) was formed in smaller amounts (AUC_Ifo:AUC_Cyclo 18:1). Ifo and Cyclo were further oxidized in the chloroethyl side chains to form 2- and 3-dechloroethylifosfamide in varying quantities. The urinary excretion of Trofo and its dechloroethylated metabolites amounted to about 10% of the total dose. Our results confirm former in vitro observations about the metabolism of Trofo. The main side-chain metabolites Ifo and Cyclo can be further activated by oxidation and formation of their respective phosphoramide mustards. Hence, Trofo is an interesting agent for oral chemotherapy. Received 21 July 1996 / Accepted: 11 November 1996     

长期口服VP-16联合顺铂治疗肺癌38例疗效分析

长期低剂量口服ＶＰ－１６（５０ｍｇ／ｍ２／ｄ×２１天）联合静滴ＤＤＰ（２０ｍｇ／ｍ２／ｄ×５天）治疗肺癌病人３８例，其中ＳＣＬＣ２４例，ＣＲ４例，ＰＲ１６例，有效率８３．３％；ＮＳＣＬＣ１４例，ＰＲ５例，有效率３５．７％。平均缓解时间ＳＣＬＣ６个月，ＮＳＣＬＣ６．５个月。毒副作用主要表现为骨髓抑制、脱发和胃肠道反应，其它毒性少见。