135例海洛因依赖者乙型肝炎病毒标志检测结果分析

１３５例海洛因依赖者乙型肝炎病毒标志检测结果分析张立学，郑纳新，赖倩（解放军３０７医院．北京．１０００３９）摘要＊＊本文对１３５例海洛因依赖者做乙型肝炎病毒（ＨＢＶ）标志物栓测，结果显示：ＨＢＶ感染阳性率为６５．９％，ＨＢｓＡｇ阳性携带率为７．４％．...     

医学生"网络成瘾症"产生的原因和对策

文章针对目前医学生“网络成瘾症”的现状进行了分析,并指出了产生的原因和解决问题的办法,以求达到标本兼治。最后提出三点预防医学生“网络成瘾症”的对策：一是高校及其附属医院要为医学生营造宽松愉快的学习、生活环境;二是呼吁家长关注医学生身心发展的特殊规律,建立良好的家庭环境;三是建立和完善与网络社会相应的法律法规,规范医学生的网上行为。     

Tolerance and dependence to opiates

In the 19th century, investigators recognized that addiction to opiates involves tolerance and dependence. In the United States, the National Academy of Sciences and the Public Health Service initiated systematic investigations into opiate addiction in 1929. Tolerance and dependence to morphine, the prototype for opiate drugs, were the emphasis of human studies for the next fifty years. This presentation highlights salient features of tolerance and dependence learned in these studies and relates these findings to clinical use in treating pain.     

海洛因成瘾大白鼠中脑腹侧被盖区超微结构变化的研究

目的　模仿人类吸毒成瘾方式建立海洛因成瘾动物模型 ,研究其中脑腹侧被盖区超微结构改变 ,为深入研究海洛因成瘾神经生物学、行为学、神经药理学、成瘾戒断治疗等奠定基础。方法　采用递增法人为建立海洛因成瘾动物模型 ,设立对照组和模型组 ,取两组动物中脑腹侧被盖区于电镜下观察超微结构改变。结果　海洛因成瘾大白鼠中脑腹侧被盖区神经元胞体、轴突、树突都出现变性、坏死、调亡等超微病理结构改变。正常对照组电镜超微影像正常。结论　海洛因成瘾大鼠脑组织出现广泛性、多发性损害 ,且以变性为主 ,神经元凋亡是海洛因成瘾致脑神经元死亡的主要形式。     

Bridges and barriers to recovery: Clinical observations from an opiate recovery project

Clinical issues are described in opiate addicts attempting to taper off methadone maintenance, and techniques are suggested to help this patient population. The observations were generated in an experimental “Tapering Network” project, in which opiate addicts on methadone maintenance had the opportunity to receive individual and group counseling, relapse prevention training, self-help groups, and other services. Vignettes illustrate clinical problems with intimacy and social isolation, identity as a former addict, and a “post methadone syndrome” characterized by vulnerability, dramatic swings in mood, and disordered thinking for a period of up to six months after detoxification. To counteract these barriers to recovery, a program model is suggested that uses curricula available in the emerging literature on treatment of substance abuse. These techniques can provide bridges to recovery.     

海洛因依赖80例临床资料分析

本文对首次住院的８０例海洛因依赖者的临床资料进行分析。男性７２例，女性８例，无职业者４０％。个体户占３５％，工人占２４％，初中文化者占８５％。入院前滥用毒麻药品现象较严重。停止使用海洛因后均出现典型的戒断症状，精神依赖很强。使用丁丙诺啡替代递减疗法近期效果满意。住院期间偷吸毒品现象严重，复吸率极高。     

针刺对海洛因依赖的脱毒疗效及其防复吸潜力的临床研究

目的 比较针刺、针刺加阿片、阿片加丁丙诺啡及阿片加韩氏戒毒仪4种方法的脱毒疗效及其对脱毒末期稽延性戒断症状和心理渴求的影响。方法 应用戒断症状量表观察脱毒疗效，应用视觉类比量表(VAS)研究心理渴求程度。结果 针刺改善海洛困依赖者戒断症状的优势主要表现在治疗的第6天以后，改善渴求心理的优势表现在第8天以后，且无明显副作用。结论 针刺具有防复吸潜力。可作为解决稽延性戒断症状和消除心理依赖的治疗方法。     

Inhibition and superactivation of the calcium-stimulated isoforms of adenylyl cyclase

It was shown previously that chronic exposure to opiate agonists increases adenylyl cyclase (AC) activity, a phenomenon termed AC superactivation (or supersensitization). More recently, we showed that acute G_i/o-coupled receptor activation inhibits the activity of several AC isozymes, including Ca²⁺/calmodulin-stimulated AC-I and -VIII, whereas chronic receptor activation induces their superactivation. Here, we report that both acute μ-opioid receptor-induced inhibition and chronic induced superactivation of AC-I and -VIII are pertussis toxin sensitive. In addition, we show that proteins that interfere with the activity of {ie195-2} subunits ({ie195-3} scavengers) strongly attenuate the acute inhibition of AC-I and -VIII and the superactivation of AC-I, and abolish the superactivation of AC-VIII. Based on these results, we suggest that {ie195-4} is involved in the acute inhibition and chronic agonist-induced superactivation of AC types I and VIII.     

Neuropathology in non-human immunodeficiency virus-infected drug addicts: hypoxic brain damage after chronic intravenous drug abuse

Neuropathological studies were carried out on 180 human immunodeficiency virus-seronegative intravenous drug addicts. The findings in victims of acute heroin intoxication (n = 116) were congestion (99.1%), capillary engorgement (68.1%), and/or perivascular bleeding (68.1%) – hemodynamic processes attributable to toxic primary respiratory failure. In a high percentage of these cases (88%), cerebral edema was also present. In 18 cases of acute heroin intoxication who survived for periods of hours or days, the sole postmortem finding was ischemic nerve cell damage, resembling that typically seen in systemic hypoxia. Semiquantitative analysis revealed nerve cell loss in the hippocampal formation and/ or Purkinje cell layer in 26% of the 162 chronic drug abusers. By contrast, in nearly 80% of these cases, the hippocampus showed enhanced expression of glial fibrillary acid protein by astrocytes and/or a proliferation of microglia, demonstrated by CD68 expression. Since such reactive processes are produced by primary neuronal damage, it can be assumed that chronic intravenous drug abuse results in obviously ischemic nerve cell loss. This could be demonstrated in the hippocampus, but it must also occur throughout the whole brain. The demonstration of ischemic nerve cell damage and neuronal loss or secondary reactive alterations has not been described previously. Received: 31 March 1995 / Revised, accepted: 27 November 1995