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11.
135例海洛因依赖者乙型肝炎病毒标志检测结果分析 总被引:2,自引:0,他引:2
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%.... 相似文献
12.
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。 相似文献
13.
D. R. JASINSKI 《Acta anaesthesiologica Scandinavica》1997,41(1):184-186
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. 相似文献
14.
海洛因成瘾大白鼠中脑腹侧被盖区超微结构变化的研究 总被引:2,自引:0,他引:2
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。 相似文献
15.
Laurie Wermuth PhD Stephen Brummett MSW James L. Sorensen PhD 《Journal of substance abuse treatment》1987,4(3-4):189-196
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. 相似文献
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Debora Steiner Tomer Avidor-Reiss Ester Schallmach Daniella Saya Zvi Vogel 《Journal of molecular neuroscience : MN》1996,27(2):195-203
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 Gi/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. 相似文献
20.
Neuropathology in non-human immunodeficiency virus-infected drug addicts: hypoxic brain damage after chronic intravenous drug abuse 总被引:3,自引:0,他引:3
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 相似文献