利鲁唑对吗啡镇痛、耐受和依赖作用的影响(英文)

目的　研究利鲁唑对阿片镇痛、耐受及躯体功能的调节。方法　采用冰醋酸扭体 ,5 5℃热板法和热辐射甩尾法观察利鲁唑对小鼠痛阈及吗啡镇痛效应的影响 ;采用小鼠急性和慢性吗啡耐受模型及小鼠吗啡依赖模型 ,观察利鲁唑对吗啡耐受和依赖的作用。结果　单独皮下注射利鲁唑 2 .5～ 10mg·kg- 1在以上 3种模型无镇痛作用 ,然而能剂量依赖性地增强吗啡镇痛效应。利鲁唑 2 .5～ 10mg·kg- 1剂量依赖性地对抗吗啡引起的急性和慢性耐受。在小鼠吗啡依赖模型中 ,利鲁唑 2 .5～ 10mg·kg- 1剂量依赖性地抑制吗啡戒断症状的产生。结论　利鲁唑自身无镇痛作用 ,但能显著增强吗啡镇痛效应 ,并能预防吗啡所引起的耐受和依赖     

Effects of Nicotine on Bone and Calciotropic Hormones in Growing Female Rats

Limited research in young adults and immature animals suggests a detrimental effect of tobacco on bone during growth. This study investigated the effects of nicotine, the major alkaloid component of tobacco, on calciotropic hormone concentrations and bone status in growing female rats. One-month-old animals received either saline (n = 10), nicotine at 3.0 mg/kg/day (n = 10), or nicotine at 4.5 mg/kg/day (n = 10) administered subcutaneously via osmotic minipumps for either 2 or 3 months. Sera, femora, tibiae, and lumbar vertebrae (3–5) were collected at necropsy. The concentrations of serum calcium, phosphorus, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone, calcitonin, and insulin-like growth factor-I were determined. Bone variables evaluated included mineral content and density (vertebrae and femora), cancellous and cortical histomorphometry (tibiae), and bone strength (vertebrae and femora). Statistically significant differences in serum mineral and hormone concentrations were not associated with nicotine dose or exposure time. No significant nicotine treatment effects were detected for bone mineral content and density, bone histomorphometry, or bone strength. We conclude that nicotine treatment for 2 or 3 months at serum concentrations in the upper range of those found in smokers has no detrimental effect on bone mass, volume, or strength in the growing rat. Received: 20 May 1999 / Accepted: 21 January 2000     

电针对吗啡成瘾大鼠戒断-复吸行为影响的初步观察

目的 观察针刺对实验动物戒断及复吸期间操作行为的影响。方法 建立大鼠吗啡自身给药模型，随机分模型对照组、绑缚对照组、针刺治疗组。熄灭期(3d)做相应处理，d4吗啡引燃(2mg／kg体重)，观察动物熄灭踏板数(LPE)、复吸踏板数(LPR)。结果 模型对照组观察到典型熄灭-复吸曲线(ERC)；绑缚对照组该曲线发生变异，主要是缩短了熄灭的过程；针刺治疗组彻底改变了熄灭-复吸曲线的形状，使熄灭反跳现象消失，但复吸值变大。以吗啡平台期平均踏板数(ALPP)为基准值，各组间熄灭平均踏板数(ALPE)和复吸踏板数(LPR)无明显差异。结论 相对于自然戒断，针刺及绑缚在熄灭期间均具有较明显的抑制渴求效果，且针刺比绑缚作用更快．效果更明显；短期(3d)的针刺治疗未达到抗短期复吸(d4)效果。更多结果有待后续观察和进一步验证。     

A chimeric opioid peptide with mixed μ agonist/δ antagonist properties

Abstract: There is evidence to indicate that opioid compounds with mixed μ agonist/δ antagonist properties are analgesics with low propensity to produce tolerance and physical dependence. A chimeric peptide containing the potent and selective μ agonist H‐Dmt‐D‐Arg‐Phe‐Lys‐NH₂ ([Dmt¹]DALDA) (Dmt = 2′,6′‐dimethyltyrosine) and the potent and selective δ antagonist H‐Tyr‐TicΨ[CH₂‐NH]Cha‐Phe‐OH (TICP[Ψ]) (Cha = cyclohexylalanine), connected ‘tail‐to‐tail’ via a short linker, was synthesized using a combination of solid‐phase and solution techniques. The resulting peptide, H‐Dmt→D‐Arg→Phe→Lys‐NH‐CH₂‐CH₂‐NH‐Phe←Cha[NH‐CH₂]ΨTic←Tyr‐H, showed the expected μ agonist/δ antagonist profile in the guinea‐pig ileum and mouse vas deferens assays. Its μ and δ receptor binding affinities were in the low nanomolar range, as determined in rat brain membrane binding assays.     

大黄(庶虫)虫丸对非胰岛素依赖型Ⅳ期糖尿病肾病患者Ⅷ因子相关抗原及纤维蛋白原的影响

目的:探讨大黄(庶虫)虫丸对非胰岛素依赖型Ⅳ期糖尿病肾病(DN)患者Ⅷ因子相关抗原(vWF:Ag)、纤维蛋白原(Fbg)的治疗作用。方法:选择Ⅳ期DN患者60例,用自动凝血机检测vWF:Ag、Fbg的变化,并随机分为治疗组和对照组。治疗组用大黄(庶虫)虫丸,对照组用潘生丁干预治疗,观察大黄(庶虫)虫丸对Ⅳ期DN患者vWF:Ag、Fbg的影响。结果:Ⅳ期DN患者血vWF:Ag、Fbg含量显著增高,与正常对照组比较有极显著差异(P<0.01)。用大黄(庶虫)虫丸治疗后,vWF:Ag、Fbg浓度显著降低(P<0.05或P<0.01),明显优于潘生丁组。结论:大黄(庶虫)虫丸能显著降低Ⅳ期DN患者血vWF:Ag、Fbg含量,改善高凝状态。     

四川省凉山地区静脉吸毒人群药物滥用及其行为特征调查

目的:了解四川省凉山地区静脉吸毒人群药物滥用及行为特征情况,为采取有针对性的戒毒干预措施预防艾滋病病毒的传播提供数据.方法:以社区为基础招募了379名静脉吸毒人员,调查其人口学特征,艾滋病病毒感染情况,药物滥用的种类、吸毒方式和频率,口吸和静脉吸毒时间,共用注射器具情况等.结果:静脉吸毒人群艾滋病病毒感染率为11.3%(43/379).379名被调查者全部为海洛因滥用者,其中247人(65.2%)单独使用过海洛因,297人(78.4%)混合注射过海洛因与安定,滥用过的其他药物有安定(8.2%)和鸦片(1.3%).300人(79.2%)每天静脉注射吸毒一次及以上;曾经共用注射器具静脉吸毒的为247人(65.2%),87人(35.2%)首次静脉注射吸毒即与他人共用注射器具;初次口吸吸毒和静脉注射吸毒的平均年龄分别为22.37岁和25.35岁,口吸吸毒和静脉注射吸毒的平均时间分别为6.41年和3.42年.结论:加强青少年、吸毒人员关于毒品危害和拒绝毒品的健康教育活动,以及开展美沙酮或丁丙诺啡口服治疗海洛因依赖者,降低静脉注射吸毒行为,控制艾滋病病毒的传播.     

吗啡依赖小鼠脑组织cAMP系统的变化及腺苷酸环化酶磷酸化调节

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加味参附汤对吗啡依赖戒断小鼠免疫功能的影响

吗啡依赖小鼠自然戒断后可见脾脏、胸腺萎缩，巨噬细胞Fc受体阳性百分率及吞噬功能、外周血T淋巴细胞总数、T淋巴细胞对PHA的殖反应、脾T淋巴细胞CD4^ 百分率及CD4^ /CD8^ 比值均明显下降；吗啡继续成瘾而未戒断的小鼠的以上指标进一步损伤；加味参附汤（MSFD）治疗小鼠以上指标均有不同程度的恢复；而丁丙诺啡治疗后免疫功能状态仍低于或相当于自然戒断时。提示MSFD能促进吗啡依赖戒断小鼠损伤的免疫功能的恢复，这一作用可能与其对神经内分泌系统的调节有关。     

Smoking practices in New York City: The use of a population-based survey to guide policy-making and programming

To inform New York City’s (NYC’s) tobacco control program, we identified the neighborhoods with the highest smoking rates, estimated the burden of second-band smoke exposure, assessed the early response to state taxation, and examined cessation practices. We used a stratified random design to conduct a digit-dialed telephone survey in 2002 among 9,674 New York City adults. Our main outcome measures included prevalence of cigarette smoking, exposure to second-hand smoke, the response of smokers to state tax increases, and cessation practices. Even after controlling for sociodemographic factors (age, racelethnicity, income, education, marital status, employment status, and foreign-born status) smoking rates were highest in Central Harlem and in the South Bronx. Sixteen percent of nonsmokers reported frequent exposure to second-hand smoke at home or in a workplace. Among smokers with a child with asthma, only 33% reported having a no-smoking policy in their homes. More than one fifth of smokers reported reducing the number of cigarettes they smoked in response to the state tax increase. Of current smokers who tried to quit, 65% used no cessation aid. These data were used to inform New York City’s smoke-free legislation, taxation, public education, and a free nicotine patch give-away program. In conclusion, large, local surveys can provide essential data to effectively advocate for, plan, implement, and evaluate a comprehensive tobacco control program. Dr. Mostashari (the guarantor) made substantial contributions to the conception, design, and supervision of this paper, the analysis and interpretation of data, the drafting of the paper, critical revisions of the paper for important intellectual content, and the acquisition of data and funding for this research. Dr. Kerker made substantial contributions to the analysis and interpretation of data, the drafting of the paper and critical revisions of the paper for important intellectual content. Ms. Hajat made substantial contributions to the acquisition of data and critical revisions of the paper for important intellectual content. Dr. Miller made substantial contributions to the conception of this paper and critical revisions of the paper for important intellectual content. Dr. Frieden made substantial contributions to the conception, design, and supervision of this paper and critical revisions of the paper for important intellectual content.     

Prevention of precipitated withdrawal symptoms by activating central cholinergic systems during a dependence-producing schedule of morphine in rats

Previous studies in this and other laboratories have suggested an important role for central cholinergic neurons in the expression of morphine withdrawal symptoms. This study was designed to determine whether the symptoms of withdrawal could be mitigated by normalization of the effect of morphine on cholinergic neurons. Since this effect is generally inhibitory, we used centrally acting cholinergic agonists to augment central cholinergic tone during chronic morphine infusion. Rats were made dependent following the intra-arterial (i.a.) infusion of increasing concentrations (35-100 mg kg(-1) day(-1)) of morphine over 5 days. I.a. injection of 0.5 mg/kg of naloxone precipitated a profound withdrawal response that included a dramatic increase in mean arterial pressure (MAP) which was maintained over the 60-min observation period, a short duration increase in heart rate (HR), and characteristic opiate withdrawal symptoms. In separate groups of rats, non-toxic doses (50 and 250 microg/kg) of the acetylcholinesterase (AChE) inhibitor, diisopropylflurophosphate (DFP) were administered as single daily injections concomitant with the morphine infusion. DFP treated rats, exhibited significantly reduced expression of the naloxone-evoked pressor response. The apparent anti-withdrawal effect of DFP was not reproduced by the selective peripherally acting AChE inhibitor, echothiophate, although both compounds effectively reduced the expression of certain other withdrawal symptoms. The centrally acting muscarinic cholinergic receptor agonist, arecoline, resulted in an even more impressive suppression of withdrawal symptoms. While not all symptoms associated with morphine withdrawal are mediated via central cholinergic pathways, these results suggest that physical dependence on morphine can be suppressed to a significant degree by the augmentation of central cholinergic activity during morphine administration.