利他林对注意缺陷多动障碍患儿注意能力影响的ERP研究

目的:探讨注意缺陷多动障碍(ADHD)患儿的视觉空间注意刺激诱发的事件相关电位(ERP)特征,并研究利他林(MPH)对其影响。方法:采用有效提示、无效提示刺激模块对22名ADHD患儿和22名年龄匹配的正常儿童进行ERP检测和记录其行为学表现。ADHD患儿在服MPH前和服MPH后2 h分别接受两次ERP检测。结果:与正常对照组相比,ADHD组在服MPH前,额部N2波潜伏期显著延长(P<0．05),各导联P2、N2波波幅显著降低(P<0．05);服MPH后2 h额部N2波潜伏期显著缩短(P<0．05),各导联波幅显著增高(P<0．05);服MPH后2 h各导联P2、N2波的潜伏期及波幅与正常对照组比较差异无显著意义(P>0．05)。结论:视觉空间注意ERP可以客观检测ADHD患儿注意缺陷的存在及程度,为临床诊断和评价MPH疗效提供了客观依据。     

阿尔茨海默病、血管性痴呆、帕金森病痴呆病人听觉认知电位的比较研究

目的 :探讨听觉事件相关电位 (ERP)在阿尔茨海默病 (AD)、血管性痴呆 (VD)、帕金森病痴呆 (PDD)中的差异及意义。方法 :应用ERP检测方法对 2 4例AD患者、2 2例VD患者、16例PDD患者及 30位正常人进行对照研究。结果 :①ERP的内源成分 :P30 0电位 (即P3波 )三组间异常程度不同 ,呈梯度变化。VD组P3潜伏期最长 ,AD组次之 ,PDD组再次之 (均P <0 .0 5 ) ;②ERP的外源成分 :三组N1波改变各异 ,VD组潜伏期延长 ,波幅降低 ;AD组仅波幅降低 ;PDD组正常 ;③峰间期 :AD、VD两组P2—N2、N2—P3、N1—P3峰间期延长 ,PDD组各波峰间期正常。结论 :AD、VD及PDD三种疾病听觉ERP异常程度及异常成分存在差异 ,上述电生理特征对区分痴呆类型具有一定价值。     

事件相关电位及脑电地形图对睡眠呼吸暂停综合征患者认知功能的评价

目的 :探索睡眠呼吸暂停综合征 (SAS)患者认知功能和临床疗效的评价方法。方法 :利用事件相关电位 (ERP)、脑电地形图 (BEAM)检测和简易智力状态试验 (MMSE)观察SAS患者 (分症状轻的SAS—A和症状重的SAS—B两个亚组 )经鼻持续气道内压通气 (CPAP)治疗前后认知功能的变化 ,并与对照组进行比较。结果 :与对照组比较 ,P30 0潜伏期明显延长 (P <0 0 5 ) ,波辐降低 (P <0 0 5 ) ;SAS—B组MMSE测试得分较低 ,SAS—A组近于正常 ,SAS—A组与SAS—B组之间BEAM总异常率及部分异常频带分布无显著差异 (P >0 0 5 )。结论 :ERP—P30 0、BEAM结合MMSE是观察SAS患者认知功能的有效方法     

癫（疒/间）大鼠听觉事件相关电位P3样波的研究

目的 :研究正常大鼠听觉事件相关电位 (ERP)的P3样波 (下简称听觉P3样电位 )特点及癫大鼠P3样电位变化。方法 :癫组大鼠每日予戊四氮腹腔注射 ,直至达到点燃标准 ;正常组大鼠每日注射生理盐水。记录并分析两组动物听觉ERP特点及其P3样电位的变化。结果 :①在大鼠可发现与人类听觉ERP的P3电位波形、潜伏期及反应特点相似的ERP ;②癫大鼠与正常大鼠相比 ,其P3样电位的听觉ERP的P3电位潜伏期明显延长 (P <0 0 1) ,波幅相对降低 (P >0 0 5 ) ,波形分化不清。结论 :P3样电位的产生具有跨越种属的相似性 ,提示P3样电位在哺乳动物中可能具有共同的神经回路     

脑血管病患者中无肌阵挛症状的巨大SEP探讨

目的 :观察脑血管病患者中无肌阵挛症状者的巨大SEP。方法 :对 2 16例急性脑血管病患者进行正中神经体感诱发电位 (SEP)检测 ,并以 4 3例 4 0岁以上健康人作为对照组。巨大SEP标准为 :①N2 0成分振幅 >5 μV ;②P2 5或N35成分振幅 >10 μV。 结果 :2 16例中巨大SEP者 2 7例 (12 5 % ) ,其中P2 5或N35及N2 0成分均增高者 18例 (6 6 7% ) ,P2 5或N35成分增高而N2 0成分正常 9例 (33 3% )。与对照组比较N2 0、P2 5、N35成分差异均有显著意义 (P <0 0 0 1、P <0 0 0 1、P <0 0 1)。结论 :脑血管病患者所呈现的无肌阵挛症状的巨大SEP的表现主要是N2 0及P2 5或N35成分波幅均增高 ,仅少数N2 0成分正常 ,这与皮质反射性肌阵挛的特征性P2 5或N35成分增高、而N2 0成分均正常的巨大SEP类型有一定差别     

帕金森病患者诱发电位研究

目的 :研究帕金森病 (PD)患者脑干听觉诱发电位 (BAEP)和视觉诱发电位 (VEP)的变化及其与临床症状的关系。方法 :检测 70例PD患者BAEP和VEP ,并设正常对照组 6 0例作对照。结果 :PD组BAEP异常 31例 (44 % ) ,正常对照组异常 11例 (18% ) ,P <0 0 1。VEPN75、P10 0、N135的潜伏期分别为 93 2± 15 1ms、12 5 2± 12 .4ms和 15 7 2± 19 5ms ,均较正常对照组 83 1± 14 8ms、10 4 2± 7 3ms和139 4± 14 4ms明显延长 ,P <0 0 1;PD患者VEP的P10 0潜伏期与UPDRS评分呈正相关 ,r =0 6 1,P <0 0 1。结论 :BAEP和VEP可客观地反映PD患者听觉和视觉通路电生理的变化。     

视觉事件相关电位

一、概况 事件相关电位(event-related potential,ERP)1965年由Sutton提出。一般认为有广义和狭义之说,广义指ERP的全部成分,包括P1、N1、P2、N2、P3,MMN、N400、CNV,而狭义仅指P1、N1、P2、N2、N3。关于刺激模式,国内外大多采用听觉刺激。目前国内使用的仪器     

鼻咽癌患者放射治疗后认知功能的变化分析

目的 :观察鼻咽癌患者治疗前后认知功能的变化 ,探讨用听觉事件相关电位 (ERP)的P30 0成分作为放射治疗中早期发现中枢神经系统损害的指标的可能性。方法 :对 32例首发并且只接受60 CO放射治疗的鼻咽癌患者在治疗前后分别进行听觉ERP的P30 0成分和认知能力量表测定 ,并将结果进行了比较。结果 :32例病人放射治疗后听觉ERP中N2 (即N2 0 0、P3波 (即P30 0 )潜伏期较治疗前明显延长 ,P3波幅明显降低 ,差异有显著意义 (P <0 .0 1) ,治疗后认知能力量表测定得分较治疗前明显下降 ,差异有显著意义 (P <0 .0 1或P <0 .0 5 )。结论 :鼻咽癌患者在接受放射治疗后认知功能明显下降 ,听觉ERP的P30 0成分可作为鼻咽癌放射治疗中中枢神经系统受损害的一个观察指标应用于临床。     

军人心理创伤后应激障碍患者与健康军人事件相关电位的对照研究

目的　探讨军人心理创伤后应激障碍 ( PTSD)患者 3种事件相关电位 ( ERP)的变异。方法　应用美国 Nicolet Bravo脑诱发电位仪 ,采用光和声成对刺激、反应时间以及听觉靶 -非靶刺激序列技术 ,检测 66例 PTSD和 3 6名正常人 ( NC)的关联性负变 ( CNV)、P30 0 、以及失配性负波 ( MMN)。结果　 1 CNV:M1 潜伏期 PTSD组 [( 5 0 3 .4± 1 3 9.2 ) ms]长于 NC组[( 4 2 0 .1± 1 2 3 .6) ms;P<0 .0 1 ],M2 波幅 PTSD组 [( 1 8.9± 7.9) μv]高于 NC组 [( 1 1 .7± 5 .8) μv;P<0 .0 1 ],指令信号后负变化 ( PINV)的出现率 PTSD组 ( 3 9% )高于 NC组 ( 3 % ;P<0 .0 1 )。 2 P30 0 :在靶刺激中 ,Cz脑区的 P3潜伏期 PTSD组[( 3 1 5 .4± 1 7.8) ms]短于 NC组 [( 3 3 6.7± 1 5 .5 ) ms;P<0 .0 1 ],Pz脑区的 N2 潜伏期 PTSD组 [( 2 78.5± 2 1 .8) ms]长于 NC组 [( 2 63 .4± 1 4.2 ) ms;P<0 .0 1 ],Pz脑区的 P3波幅 PTSD组 [( 3 .4± 1 .8) μv]低于 NC组 [( 5 .9± 2 .4) μv;P<0 .0 1 ]。在非靶刺激中 ,Cz脑区的 P2 波幅 PTSD组 [( 2 .5± 1 .4) μv]低于 NC组 [( 3 .4± 0 .1 ) μv;P<0 .0 1 ]。 3 MMN:潜伏期 PTSD组[( 2 1 4.2± 2 5 .7) ms]长于 NC组 [( 1 93 .7± 2 2 .6) ms;P<0 .0 1 ],波幅 PTSD组 [( 8.5     

精神分裂症患者n-back工作记忆神经机制异常的ERP研究

目的:比较精神分裂症患者与正常人在参量变化的工作记忆负荷水平下所诱发的ERP成分及其脑区分布差异,探讨精神分裂症患者工作记忆功能损害的神经机制。方法:精神分裂症患者以及正常对照各20名参加了n-back(n=0,1,2)工作记忆任务的ERP实验,同时记录行为数据及EEG,离线处理数据。结果:精神分裂症患者在1-back及2-back任务中行为表现明显较正常人差(P0.01)。正常人P3波幅随记忆负荷增长而成比例下降(0-back1-back2-back),而精神分裂症患者仅0-back的P3波幅显著高于1-back及2-back,(0-back1-back=2-back)。三种负荷条件下,精神分裂症组中央区的P3峰值均显著高于正常组,而2-back条件下的顶区P3峰值显著高于正常组。高记忆负荷与低记忆负荷的任务相减均得到一差异波N450成分。在顶区,精神分裂症患者的1-0差异波N450成分的波幅显著高于正常组,而2-1差异波N450成分的波幅显著低于正常组(P0.05)。结论:精神分裂症患者存在显著的工作记忆损害,其中短时贮存功能损害可能与患者顶叶的生理低效能及工作记忆容量下降有关。     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Muscle strength and serum testosterone,cortisol and SHBG concentrations in middle-aged and elderly men and women

Forty healthy males (M) and females (F) divided into two different age groups i.e. M50 years (range 44–57; n= 9), F50 years (range 43–54; n= 9), M70 years (range 64–73; n= 11) and F70 years (range 63–73; n= 11) volunteered as subjects for examination of muscle cross-sectional area (CSA) and maximal voluntary isometric force production characteristics of the leg extensor muscles and serum androgen and sex hormone binding globulin (SHBG) concentrations. The CSA in the male groups was greatly larger (P < 0.01) than in the female groups and both elderly groups demonstrated slightly (n.s.) smaller values in the CSA than the two middle-aged groups. Maximal force of 2854 ± 452 N in M50 was greater (P < 0.05) than that of 2627 ± 752 N recorded for F50 as well as the force of 2787 ± 843 in M70 was greater (P < 0.001) than that of 1849 ± 295 recorded for F70. The force between F50 and F70 differed significantly (P < 0.05) from each other. The maximal rate of force production in M50 was greater (P < 0.01) than in F50 as well as in M70 greater (P < 0.001) than in F70. Both middle-aged groups demonstrated greater (P < 0.05) values than the respective elderly groups of the same sex. The individual values in the CSA correlated with the values in maximal force both in the middle-aged subjects (r= 0.66; P < 0.01) and in the elderly subjects (r= 0.69; P < 0.01). The mean concentration of serum testosterone in M50 was slightly (n.s.) greater than in M70 and in F50 significantly (P < 0.05) greater than in F70. Serum SHBG levels were lower in the males (P < 0.01) than in the females and serum testosterone/SHBG ratio in M70 and in F70 were lower (P < 0.05) than in M50 and in F50, respectively. In the females significant positive correlations were observed between the individual values in serum testosterone concentration and the values both in the CSA (r= 0.46; P < 0.05) and in maximal force (r= 0.62; P < 0.01) as well as between serum testosterone/SHBG ratio and both the CSA (r= 0.55; P < 0.05) and maximal force (r= 0.68; P < 0.01). The present results imply that the decreasing basal level of blood testosterone over the years in aging people, especially in females, may lead to decreasing anabolic effects on muscles thus having an association with age-related declines in the maximal voluntary neuromuscular performance capacity in aging people.     

海洛因成瘾与学习记忆

海洛因成瘾是我国发病最高,危害最大的一种成瘾性疾病,而其中枢机制则是解决临床预防和治疗的关键,至今仍不清楚。既往工作表明,学习记忆功能在海洛因成瘾的中枢机制中居于重要的中心环节。本文在总结既往海洛因成瘾研究工作基础上联系学习记忆功能,试图从系统整合层次分析相关领域研究工作的不足和今后工作的发展方向。