前列地尔治疗糖尿病性周围神经病变的临床研究

目的:研究前列地尔(商品名:凯时,Lipo PGE1)治疗糖尿病周围神经病变(DPN)的临床疗效及观察其不良反应.方法:100例糖尿病周围神经病变患者随机分为治疗组46例,给予Lipo PGE110μg/d,共4周.对照组54例,应用维生素B1100mg 维生素B12500μg/d,共4周.结果:治疗组痛觉过敏、痛觉减退、肢体麻木、肢体疼痛、腱反射减弱治疗后有效率达79%、64%、95%、87%、78%,明显高于对照组的52%、43%、60%、50%和33%(P均＜0.05).运动神经传导速度(MVC)、感觉神经传导速度(SCV)治疗后均有一定提高,与对照组比较有显著差异(P均＜0.05).结论:Lipo PGE1是治疗DPN较为理想且安全的药物.     

注射用前列地尔与前列地尔注射液治疗早期慢性重型肝炎的比较

目的 :观察注射用前列地尔 (PGE1 CD)与前列地尔注射液 (Lipo PEG1)治疗早期慢性重型肝炎的疗效与安全性。方法 :14 3例早期慢性重型肝炎的病人分 3组 ,3组病人均予相同的基础治疗。Lipo PGE1组 5 0例 ,加用Lipo PGE12 0 μg +5 %葡萄糖注射液 4 0mL ,微泵静脉注射 ,qd×2 8d。PGE1 CD组 5 3例 ,加用PGE1 CD 0 .1mg +5 %葡萄糖注射液 5 0 0mL ,iv ,gtt ,qd× 2 8d。对照组 4 0例 ,仅予基础治疗。结果 :治疗总有效率Lipo PGE1组为 6 6 % ,PGE1 CD组为 5 6 % ,对照组为 35 %。Lipo PGE1组与对照组比较差异有非常显著意义(P <0 .0 1)。不良反应率Lipo PGE1组为 18% ,PGE1 CD组为 5 7% ,对照组为 0。 3组间比较差异有显著意义 (P <0 .0 5 )。结论 :PGE1 CD与Lipo PGE1治疗早期慢性重型肝炎安全而有效 ,而Lipo PGE1的不良反应发生率低     

前列地尔联合甲钴胺治疗糖尿病神经病变的疗效观察

目的:观察前列地尔注射液联合甲钴胺治疗糖尿病周围神经病(DPN)的临床疗效。方法:将糖尿病并发神经病变的患者随机分为对照组38例和治疗组39例,两组均以降糖、降压、降脂等常规治疗,同时给予甲钴胺500μg静脉滴注,1次/d;治疗组加用前列地尔10μg加入氯化钠注射液10 ml静脉入小壶,1次/d。两组疗程均为2周。比较两组治疗前后症状、神经传导速度变化及临床疗效。结果:两组在治疗前后症状均有明显改善,治疗组有效率89.2%,对照组有效率63.2%,治疗组优于对照组(P<0.01),治疗过程中无明显不良反应。结论:前列地尔联合甲钴胺治疗糖尿病神经病变疗效肯定,安全性好。     

前列地尔联合α 硫辛酸治疗糖尿病周围神经病变50例

目的观察前列地尔联合α 硫辛酸治疗糖尿病周围神经病变的疗效与安全性。方法将96例糖尿病周围神经病变患者随机分为治疗组50例和对照组46例。两组均接受糖尿病常规治疗,并禁用任何改善血液循环和影响神经传导的药物。治疗组给予前列地尔10 μg加入0.9%氯化钠注射液50 mL微泵持续静脉注射,qd;同时给予α 硫辛酸450 mg加0.9%氯化钠注射液100 mL静脉滴注,qd。对照组给予前列地尔10 μg加0.9%氯化钠注射液50 mL微泵持续静脉注射,qd。疗程均为20 d。记录两组疗效与不良反应。结果治疗组总有效率（84.0%）显著高于对照组（60.9%,χ2＝6.491,P＜0.05）,治疗组神经传导速度明显提高（P＜0.05）。两组均未见明显不良反应。结论前列地尔联合α 硫辛酸可明显提高糖尿病周围神经病变的疗效。     

前列地尔联合刺五加治疗糖尿病周围神经病变的临床观察

目的 探讨前列地尔(Lipo PGE1,凯时)联合刺五加治疗糖尿病周围神经病变的作用及其不良反应.方法 选取80例糖尿病周围神经病变患者,随机分为观察组(前列地尔 刺五加)40例,对照组(刺五加)40例.两组控制血糖方法相同,对照组给予刺五加注射液(每支20 ml含总黄酮100 mg)40～60 ml加入生理盐水250 ml中静脉滴注,每天1次;观察组给予刺五加注射液(每支20 ml含总黄酮100 mg)40～60 ml加入生理盐水250 ml中静脉滴注 前列地尔10 ug静脉滴注,每天1次,两组疗程均为4周,观察其对神经传导速度(SNCV、MNCV)的影响.结果 治疗4周后,患者主观症状和体征有较明显改善,前列地尔联合刺五加治疗糖尿病周围神经病变总有效率为82.5%,对照组总有效率为55.0%,两组疗效比较,有显著差异性(P＜0.01).同时改善神经传导速度,两组疗效比较,有显著差异性(P＜0.01).药物治疗过程中未见明显不良反应.结论 前列地尔联合刺五加是治疗糖尿病周围神经病变安全且有效的药物.     

甲钴胺联合前列地尔治疗糖尿病周围神经病变的疗效观察

目的:观察甲钴胺联合前列地尔治疗糖尿病周围神经病变的疗效。方法:将96例糖尿病周围神经病变患者随机均分为2组。所有患者均给予糖尿病饮食、运动治疗及胰岛素强化治疗,血糖稳定后,2组均肌肉注射甲钴胺500μg·d-1,qd,观察组同时静脉滴注前列地尔100μg·d-1,qd,2组疗程均为30d。疗程结束后评定疗效。结果:观察组的有效率为97.92%,对照组的有效率为79.17%,2组比较差异有统计学意义(P<0.01)。2组治疗后的感觉神经传导速度较治疗前比较,差异有统计学意义(P<0.01),且观察组感觉神经传导速度变化较对照组显著(P<0.01)。结论:甲钴胺联合前列地尔治疗糖尿病周围神经病变可有效改善患者的症状,提高临床疗效,且不良反应轻微。     

前列地尔联合甲钴胺辅治糖尿病周围神经病变的疗效观察

目的 观察前列地尔联合甲钴胺辅治糖尿病周围神经病变(DPN)的临床疗效.方法 将DPN患者80例随机分成治疗组42例和对照组38例.在控制血糖基础上,对照组给予甲钴胺500μg肌内注射,每天1次,连续14d;治疗组在对照组治疗基础上加用前列地尔10μg+生理盐水100ml静脉滴注,每天1次,连续14d.观察2组临床疗效及治疗前后神经传导速度.结果 治疗组总有效率为97.6%高于对照组的65.8%,差异有统计学意义(P＜0.05).2组治疗后正中神经和腓总神经运动传导速度(MCV)及感觉传导速度(SCV)均快于治疗前(P＜0.05);且治疗组治疗后正中神经和腓总神经MCV及SCV均快于对照组(P＜0.05).结论 前列地尔联合甲钴铵辅治DPN,对神经传导速度及症状、体征的改善均有良好作用,且无明显不良反应,值得推广应用.     

凯时注射液治疗糖尿病周围神经病变及皮肤溃疡的临床评价

目的：观察凯时（前列腺素E1脂微球制剂, Lipo PGE1）在治疗糖尿病末梢神经病变及足溃疡中的疗效和安全性。方法糖尿病末梢神经病变及足溃疡92例,随机分两组,治疗组：凯时10~20μg＋生理盐水20 ml,缓慢静推,1次/d,疗程2~4周。同时应用弥可保500μg,1次/d肌内注射,连用4周；对照组：弥可保500μg,1次/d肌内注射,两组同时均行全面代谢控制,局部生理盐水＋胰岛素＋庆大霉素换药。结果2~4周治疗后,治疗组痛觉过敏治疗后有效率达78.9%,明显高于对照组的61.9%,神经传导速度改善的有效率也有明显的提高（P〈0.05）。结论凯时在治疗糖尿病周围神经病变及皮肤溃疡中可加强疗效而且安全。     

前列地尔联合甲钴胺辅治糖尿病周围神经病变的疗效观察

目的观察前列地尔联合甲钴胺辅治糖尿病周围神经病变(DPN)的临床疗效。方法将DPN患者80例随机分成治疗组42例和对照组38例。在控制血糖基础上,对照组给予甲钴胺500μg肌内注射,每天1次,连续14d;治疗组在对照组治疗基础上加用前列地尔10μg+生理盐水100ml静脉滴注,每天1次,连续14d。观察2组临床疗效及治疗前后神经传导速度。结果治疗组总有效率为97.6%高于对照组的65.8%,差异有统计学意义(P<0.05)。2组治疗后正中神经和腓总神经运动传导速度(MCV)及感觉传导速度(SCV)均快于治疗前(P<0.05);且治疗组治疗后正中神经和腓总神经MCV及SCV均快于对照组(P<0.05)。结论前列地尔联合甲钴铵辅治DPN,对神经传导速度及症状、体征的改善均有良好作用,且无明显不良反应,值得推广应用。     

高压氧联合前列地尔治疗糖尿病周围神经病变

目的评价高压氧联合前列地尔对糖尿病周围神经病变的疗效,探讨治疗糖尿病周围神经病变的有效方法。方法 88例糖尿病周围神经病变患者分为两组。治疗组44例,予高压氧联合前列地尔治疗,高压氧疗法采用大型空气加压舱,治疗压力为0.2MPa,每日1次;前列地尔10μg,静脉注射,每日1次;对照组44例,单独使用前列地尔10μg,静脉注射,每日1次。两组患者疗程均为4周。结果治疗组显效率、总有效率分别为42%、100%,明显高于对照组的21%、61%,两组间差异有统计学意义(P<0.05),治疗组神经传导速度及血流动力学改善均明显高于对照组(P<0.01)。结论高压氧联合前列地尔对糖尿病周围神经病变的治疗效果显著,可作为糖尿病周围神经病变的常规治疗方法。     

The aminomethylation of 1-cyano-isochromane and 1-cyano-isothiochromane

The Aminomethylation of 1-Cyano-isochromane and 1-Cyano-isothiochromane Aminomethylation of 1-cyano-isochromane (1a) and 1-cyano-isothiochromane (1i) can be achieved via reaction of carbanions 2 with α-haloamines 3 . Dialkylaminomethyl and dialkylaminobenzyl compounds 4 are formed.     

Preferential induction of CYP1A1 and CYP1B1 in CCSP-positive cells.

Both benzo[a]pyrene (BaP) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are potent ligands of aryl hydrocarbon receptors (AhR). Although animal studies indicate that both compounds induce pathological changes in the peripheral lung, the specific cell type involved remains unclear. Clara cells, expressing Clara cell specific protein (CCSP) and abundant in cytochrome P450, are nonciliated bronchiolar epithelial cells in the peripheral lung. Here we explore the hypothesis that CCSP-positive Clara cells are highly responsive to AhR ligands and are the primary cell type involved in BaP- and TCDD-induced toxicities. The responsiveness to AhR ligands was evaluated by measuring the respective mRNA and protein levels of cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) using real-time RT-PCR and immunocytochemistry assays. Two in vitro models were used: primary cultures of human small airway epithelial (SAE) cells and rat lung slice cultures. In the presence of calcium, human SAE cells differentiated into CCSP-positive cells. BaP- and TCDD-induced mRNA and protein levels of CYP1A1 and CYP1B1 levels were significantly elevated in CCSP-positive cell cultures. Similarly, AhR mRNA and protein levels were increased in CCSP-positive cell cultures, as determined by real-time RT-PCR and Western blot analysis. When rat lung slice cultures were treated with BaP or TCDD for 24 h, CYP1A1 and CYP1B1 proteins were strongly induced in Clara cells. These results indicate that, in the peripheral lung of both rats and humans, CCSP-positive cells (Clara cells) may be more sensitive to AhR ligands than other cell types.     

Influence of genetic polymorphisms of CYP1A1 and GSTM1 on the urinary levels of 1-hydroxypyrene

The aim of the present study is to evaluate the influence of the genetic polymorphism of two enzymes involved in the biotransformation of xenobiotics, cytochrome P450 1A1 (CYP1A1) and glutathione-S-transferase M1 (GSTM1), on the urinary levels of 1-hydroxypyrene (1-OH-P) in workers exposed to polycyclic aromatic hydrocarbons (PAHs) and in unexposed workers (controls). The study group consisted of 30 controls recruited among employees of a service company and 171 PAHs-exposed workers from two electric steel plants and an iron foundry (all males, ranging between 18 and 60 years of age). Determination of airborne PAHs and urinary 1-OH-P was performed by high-performance liquid chromatography (HPLC) with fluorimetric detection. Polymerase chain reaction (PCR)-based restriction fragment length polymorphism (RFLP) was used to determine the genetic polymorphisms of CYP1A1 (CYP1A1*2A and CYP1A1*2B) and GSTM1. No influence of the genetic polymorphism of CYP1A1 and GSTM1 on the urinary levels of 1-OH-P was observed in this study.     

Toxicokinetics and Bioavailability of Oral and Intravenous 1, 1 -Dichloroethylene

Toxicokinetics and Bioavailability of Oral and Intravenous 1,1-Dichloroethylene.PUTCHA, L., BRUCKNER, J. V., D'SOUZA, R., DESAI, F., AND FELDMAN,S. (1986). Fundam. Appl. Toxicol. 6, 240–250. Althoughaliphatic halocarbons have been identified as contaminants ofdrinking water supplies, little definitive information is availableon their gastrointestinal (G.1) absorption and toxicokinetics.Therefore, a study of a representative halocarbon, 1,1-dichloroethylene(1,1-DCE), was undertaken to contrast the kinetics of the chemicalfollowing iv injection with that following oral administration.Four dosage-levels of 1,1-DCE (10, 25, 50, and 100 mg/kg BW)in 50% aqueous polyethylene glycol 400 were given iv and poto fasted and nonfasted male Sprague—Dawley rats. Serialblood samples were taken from the tail artery of the lightlyetherized animals for up to 490 min after dosing. 1,1-DCE concentrationsin the whole blood were determined by gas chromatographic head-spaceanalysis. Evaluation of the iv data revealed that disappearanceof 1,1-DCE from the systemic circulation followed a triexponentialpattern. Light ether anesthesia did not appear to alter thepharmacokinetics of iv-injected 1,1-DCE. There was no differencebetween nonfasted and fasted iv rats in biological half-life(t) or in any other pharmacokinetic parameter. Total body clearance,t apparent volume of distribution and volume of distributionin the central compartment did show increases with increasingdose in these animals. Oral dosing experiments revealed that1,1-DCE was absorbed very rapidly and completely from the G.I.tract. Peak blood levels were reached 2 to 8 min following oraladministration of 1,1-DCE as an aqueous suspension. The t of1,1-DCE in orally dosed rats was somewhat longer than in theiriv counterparts The t values for nonfasted, orally dosed ratswere longer than for their fasted counterparts, suggesting delayedabsorption due to the presence of food in the G.I. tract. Bioavailabilityof 1,1-DCE, as determined by comparing areas under blood concentrationversus time curves (AUCs), was equivalent in animals given thesame dose of 1,1-DCE iv and po. AUCs increased with increasingdose in iv and po groups, but the increases were not proportionalto dose.