二甲双胍干预治疗糖耐量减低30例疗效观察

目的观察二甲双胍干预治疗糖耐量减低（IGT）阻断其向糖尿病转化的疗效。方法将60例超重或肥胖IGT患者随机分成两组各30例．治疗组在节制饮食．增加运动的行为干预基础上加用二甲双胍药物干预．舛照组单行为干预,疗程2年。检测体重、空腹血辘、OGTT2h血糖．并进行对比分析。结果治疗后1年、2年、停止干预治疗后1月空腹血糖、OGTT2h血糖,两组比较差异有统计学意义（P〈0．05）。结论二甲双胍干预治疗1GT患者可使糖尿病发病率降低。     

二甲双胍片治疗糖耐量异常的疗效观察

目的观察二甲双胍片治疗糖耐量异常（IGT）的临床疗效。方法将75例IGT患者随机分为观察组58例和对照组17例。2组均予常规饮食治疗、运动治疗,观察组在此基础上予二甲双胍片口服治疗。观察2组葡萄糖耐量试验2h后（OGTT2h）血糖水平及体质量指数（BMI）变化情况。结果治疗后,观察组OGTT2h血糖水平及BMI均低于治疗前及对照组,差异均有统计学意义（P〈0.05）。结论二甲双胍片可显著降低OGTT2h血糖水平,改善糖耐量,是治疗IGT的有效药物,值得临床推广应用。     

生活方式、二甲双胍及罗格列酮早期干预成人隐匿性自身免疫性糖尿病患者的糖调节受损且胰岛自身抗体阳性同胞的保护效应研究

目的观察生活方式、二甲双胍及罗格列酮早期干预对成人隐匿性自身免疫性糖尿病(LADA)患者的糖调节受损且胰岛自身抗体阳性同胞的保护效应。方法将符合标准的241例患者分为自然转归组、生活方式干预组、二甲双胍干预组、罗格列酮干预组。自然转归组不愿进行生活方式干预及药物治疗;生活方式干预组:提供书面饮食、运动指导方案;二甲双胍干预组:在生活方式干预的基础上,服用二甲双胍0.5 g,3次/d;罗格列酮干预组:在生活方式干预的基础上,服用罗格列酮4 mg,1次/d。干预治疗5年。记录患者的身高、体重、血压、肝肾功能、空腹血糖(FPG)、葡萄糖负荷后2 h血糖(2hPG)、空腹胰岛素(FINS)和C肽、葡萄糖负荷后2 h胰岛素(2hINS)和C肽、谷氨酸脱羧酶抗体(GADA)、胰岛细胞抗体(ICA)、胰岛素抗体(IAA)阳性率及糖尿病发生率。结果生活方式干预、二甲双胍及罗格列酮可显著改善糖尿病前期患者的自然病程,三组分别恢复为正常糖耐量的61.9%、62.7%及66.1%。三组胰岛B细胞功能(空腹、负荷后2 h)中,C肽、胰岛素降低,胰岛素分泌指数增加,进展为LADA的发病率降低。结论生活方式、二甲双胍及罗格列酮干预对胰岛B细胞功能损伤具有保护效应,能有效减少或延缓LADA患者胰岛细胞抗体阳性同胞的空腹血糖受损(IFG)、葡萄糖耐量受损(IGT)、IFG合并IGT患者进展为LADA。     

葡萄糖耐量减低患者二甲双胍干预治疗的临床效果

目的:对葡萄糖耐量减低(impaired glucose tol-erance,IGT)患者予以药物二甲双胍和生活方式干预治疗,前瞻性观察(1年)IGT患者的血糖和颈总动脉内膜-中层厚度(intima-media thickness,IMT)的变化。方法:对葡萄糖耐量减低患者随机分为生活方式治疗组(A组)和二甲双胍药物(250 mg,每日3次)联合生活方式治疗组(B组)治疗1年,1年后复测葡萄糖耐量试验和颈总动脉IMT。结果:在基础状态时,两组的血糖和颈总动脉IMT差异无统计学意义。1年后B组餐后2 h血糖明显低于A组[分别为(7.9±1.2)(、8.7±1.4)mmol/L,P=0.002],B组IMT的增加值明显低于A组[分别为(0.001±0.010)、(0.007±0.014)mm,P=0.042]。结论:二甲双胍治疗明显改善IGT患者的餐后血糖,并能延缓动脉粥样硬化的发展。     

二甲双胍治疗糖耐量减低伴肥胖患者的临床观察

目的观察二甲双胍对于糖耐量减低伴肥胖患者的疗效。方法将72例患者随机分为对照组和治疗组各36例,对照组采用控制饮食与加强运动的生活方式干预治疗;治疗组在生活方式干预的基础上,口服二甲双胍治疗。将两组治疗后的葡萄糖耐量试验（OGTT）空腹及2h血糖、胰岛素、体重指数（BMI）、总胆固醇、甘油三酯、低密度脂蛋白以及胰岛素抵抗指数（HOMA-IR）的结果差异进行比较。结果治疗组治疗后BMI、BMI、FPG、2hPG、TG、TC、LDL-C、Fins各项指标较对照组改善明显,差异有统计学意义（P〈0.05）。结论二甲双胍可以用于糖耐量减低伴肥胖患者的治疗,能显著改善空腹及餐后血糖、血脂等各项指标。     

二甲双胍治疗糖耐量降低的临床效果和机制

目的探究二甲双胍治疗糖耐量降低的临床效果及其作用机制。方法确诊为糖耐量降低的患者70例,随机分为二甲双胍组与对照组,各35例。指导对照组患者健康宣教、控制饮食及运动干预治疗等干预治疗方法 ,二甲双胍组患者在对照组基础上口服二甲双胍治疗。两组患者接受治疗时间均为12个月。观察两组患者治疗后的体质量指数、空腹血糖及餐后2 h血糖变化情况,并与治疗前比较;同时观察两组患者新发糖尿病情况并进行比较。结果治疗12个月后二甲双胍组患者体质量指数(20.12±2.63)kg/m2、空腹血糖(5.11±0.81)mmol/L、餐后2 h血糖(7.66±1.12)mmol/L均明显优于治疗前水平,差异具有统计学意义(P<0.05);对照组患者治疗前后体质量指数、空腹血糖及餐后2 h血糖对比差异无统计学意义(P>0.05)。治疗后二甲双胍组无新发糖尿病患者,对照组有7例新发糖尿病患者,差异具有统计学意义(P<0.05)。结论二甲双胍应用于糖耐量降低的治疗取得了良好的效果,同时还能够有效的预防或者延缓糖尿病的发生,值得临床推广。     

二甲双胍干预治疗葡萄糖耐量减低的疗效观察

目的:探讨二甲双胍对葡萄糖耐量减低(IGT)患者干预治疗的临床疗效。方法:将48例IGT患者分成两组,治疗组和对照组各24例,两组均予一般治疗,治疗组加用二甲双胍,疗程12个月。结果:12个月后治疗组各项指标(空腹及餐后血糖、血脂、胰岛素敏感指数、体重指数、血压)与对照组比较,差异均有显著性(P<0.01)。结论:二甲双胍对IGT人群的干预治疗,不仅能够有效逆转IGT,降低2型糖尿病(T 2DM)的发生率,而且能够对IGT伴随的代谢紊乱因素进行积极处理。     

二甲双胍对糖尿病前期患者血清C反应蛋白及胰岛素敏感指数的影响

目的:观察糖尿病前期患者应用二甲双胍降糖治疗或强化生活方式干预前后血清、高敏C反应蛋白(hs-CRP)及胰岛素敏感指数水平变化情况。方法:筛选糖尿病前期患者176例,随机分成二甲双胍治疗组、强化生活方式干预组和对照组,二甲双胍治疗组52例,在一般生活方式干预基础上给予二甲双胍片口服;强化生活方式干预组60例,根据个人饮食习惯为基础,制定热能。给予低脂饮食,控制饮食,配合适当的体育锻炼。对照组64例,仅给予一般生活方式干预。测定干预治疗前后的空腹血糖、餐后2 h血糖、糖化血红蛋白、体重指数、血脂、hs-CRP、胰岛素敏感指数变化。结果:经干预治疗2年后,对照组糖耐量转为正常21例(32.81%),转为糖尿病12例(18.75%);二甲双胍组糖耐量转为正常41例(78.85%),转为糖尿病3例(5.77%),强化生活方式干预组转为正常32例(53.33%),转为糖尿病4例(6.67%)。与对照组相比,二甲双胍组及强化生活方式干预组的糖尿病发生率差异有统计学意义(P<0.05)。干预治疗2年后,二甲双胍治疗组及强化生活方式干预组各项指标均有明显变化,且二甲双胍治疗组效果优于强化生活方式干预组(P<0.01)。结论:糖尿病前期时,血清hs-CRP水平已经开始升高,且胰岛素敏感性下降,二甲双胍降糖治疗或强化生活方式干预均能明显减低血糖,并降低血清C反应蛋白(CRP)水平,改善胰岛素敏感性,二甲双胍作用更明显。     

二甲双胍联合运动疗法对糖耐量减低患者的干预效果

目的 观察二甲双胍联合运动疗法对糖耐量减低（IGT）患者的干预效果. 方法 86例IGT患者采用二甲双胍联合运动疗法治疗,观察治疗前后空腹血糖及口服75 g葡萄糖2 h后血糖水平、体重指数变化及IGT的转归情况. 结果 经干预后,患者的空腹血糖水平、口服75 g葡萄糖2 b后血糖水平、体重指数均明显下降（均P＜0.01）,72例（83.7%）患者糖耐量恢复正常,14例（16.3%）患者仍维持IGT阶段（均述未能坚持运动,且未加以饮食控制）,无一例转为糖尿病. 结论 二甲双胍联合运动疗法干预IGT效果良好.     

二甲双胍干预治疗糖耐量低减患者的临床观察

目的为观察二甲双胍对糖耐量低减患者糖代谢,胰岛素敏感性及其转规的影响。对68例糖耐量低减患者进行了为期6个月的二甲双胍治疗研究。方法干预治疗组在饮食控制加运动治疗的基础上予二甲双胍片0.5g,3次/d,疗程三个月。观察空腹血糖、餐后2h血糖、血浆空腹胰岛素(FINS)、餐后2h胰岛素(INS2h)、糖化血红蛋白等项变化。结果二甲双胍干预治疗三个月后与对照组相比BMI、WHR、FPG、PG2h、FINS明显下降P<0.05;INS2h、UNER显著下降P<0.01。结论二甲双胍片干预治疗糖耐量低减患者可使其糖耐量恢复正常。     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

In vitro studies on sterically stabilized liposomes (SL) as enzyme carriers in organophosphorus (OP) antagonism

This study describes a new approach for organophosphorous (OP) antidotal treatment by encapsulating an OP hydrolyzing enzyme, OPA anhydrolase (OPAA), within sterically stabilized liposomes. The recombinant OPAA enzyme was derived from Alteromonas strain JD6. It has broad substrate specificity to a wide range of OP compounds: DFP and the nerve agents, soman and sarin. Liposomes encapsulating OPAA (SL)* were made by mechanical dispersion method. Hydrolysis of DFP by (SL)* was measured by following an increase of fluoride ion concentration using a fluoride ion selective electrode. OPAA entrapped in the carrier liposomes rapidly hydrolyze DFP, with the rate of DFP hydrolysis directly proportional to the amount of (SL)* added to the solution. Liposomal carriers containing no enzyme did not hydrolyze DFP. The reaction was linear and the rate of hydrolysis was first order in the substrate. This enzyme carrier system serves as a biodegradable protective environment for the recombinant OP-metabolizing enzyme, OPAA, resulting in prolongation of enzymatic concentration in the body. These studies suggest that the protection of OP intoxication can be strikingly enhanced by adding OPAA encapsulated within (SL)* to pralidoxime and atropine.     

Aquatic Insects and Trace Metals: Bioavailability,Bioaccumulation, and Toxicity

Abstract

The uptake of metals from food and water sources by insects is thought to be additive. For a given metal, the proportions taken up from water and food will depend both on the bioavailable concentration of the metal associated with each source and the mechanism and rate by which the metal enters the insect. Attempts to correlate insect trace metal concentrations with the trophic level of insects should be made with a knowledge of the feeding relationships of the individual taxa concerned. Pathways for the uptake of essential metals, such as copper and zinc, exist at the cellular level, and other nonessential metals, such as cadmium, also appear to enter via these routes. Within cells, trace metals can be bound to proteins or stored in granules. The internal distribution of metals among body tissues is very heterogeneous, and distribution patterns tend to be both metal and taxon specific. Trace metals associated with insects can be both bound on the surface of their chitinous exoskeleton and incorporated into body tissues. The quantities of trace meals accumulated by an individual reflect the net balance between the rate of metal influx from both dissolved and particulate sources and the rate of metal efflux from the organism. The toxicity of metals has been demonstrated at all levels of biological organization: cell, tissue, individual, population, and community. Much of the literature pertaining to the toxic effects of metals on aquatic insects is based on laboratory observations and, as such, it is difficult to extrapolate the data to insects in nature. The few experimental studies in nature suggest that trace metal contaminants can affect both the distribution and the abundance of aquatic insects. Insects have a largely unexploited potential as biomonitors of metal contamination in nature. A better understanding of the physico-chemical and biological mechanisms mediating trace metal bioavailability and exchange will facilitate the development of general predictive models relating trace metal concentrations in insects to those in their environment. Such models will facilitate the use of insects as contaminant biomonitors.     

Steroidal sapogenin contents in some domestic plants

In order to find out the values of the steroid resources for the future use. the compositions and contents of steroidal sapogenins from 13 domestic plants have been investigated. As a result,Dioscorea nipponica, D. quinqueloba andSmilax china were found to have large amount of diosgenin. And pennogenin inTrillium kamtschaticum andParis verticillata, yuccagenin inAllium fistulosum, hecogenin inAgave americana and neochlorogenin inSolanum nigum were appeared to be major steroidal sapogenins.     

Alzheimer’s disease – current trends in basic and clinical research. Highlights from the 16th ECNP

Advances in the molecular biological knowledge of neuronal nicotinic acetylcholine receptors (nAChRs) have led to a growing interest by the pharmaceutical industry in the development of novel compounds that selectively modulate nAChR function. The ability of (-)-nicotine, an activator of nAChRs, to enhance attentional aspects of cognition in animals and humans, to exert neuroprotective and anxiolytic-like effects, and presumably to mediate the negative correlation between smoking and Alzheimer's (and Parkinson's) Disease, has focused interest on the potential therapeutic utility of modulators of nAChR function for treatment of some of the deficits associated with these progressive, neurodegenerative conditions. Numerous compounds are known which activate nAChRs and which might serve as lead compounds toward the development of such agents. The pharmacologic diversity of neuronal nAChR subtypes suggests the possibility of developing selective compounds which would have more favourable side-effect profiles than existing agents. This broader class of agents, collectively called cholinergic channel modulators (ChCMs), is anticipated to encompass compounds which would have more favourable side-effect profiles than existing agents, which generally exhibit low selectivity. This selectivity may be achieved by preferentially activating some subtypes of nAChRs (i.e., Cholinergic Channel Activators, ChCAs) or inhibiting the function of other subtypes (Cholinergic Channel Inhibitors, ChCIs). An overview of the biology of nAChRs and the rationale for the use of ChCMs for the treatment of dementia related to neurodegenerative diseases are presented, followed by a discussion of lead compounds and compounds under consideration for clinical evaluation.