听觉-体感觉靶刺激诱发事件相关电位跨模增进效应研究

目的研究听觉-体感觉跨模靶刺激模式下双模增进作用,探讨大脑认知过程不同脑区间相互作用的神经机制。方法选择20例听力正常、躯体感觉功能正常、无任何大脑病史的在读研究生和大学生,其中男性8例,女性12例;年龄20~26岁,平均年龄22.5岁;均为右利手。以受试者的事件相关电位为考察对象,分析听觉-体感觉跨模靶刺激与单一听觉、体感觉靶刺激模式下受试者的行为学数据(反应时间、反应错误率)与事件相关电位(P3、P2幅值和潜伏期)的关系。结果单一听觉、体感觉靶刺激模式下受试者的反应时间[分别为(538±14)ms、(576±18)ms]、P3峰值潜伏期[分别为(455±17)ms、(479±18)ms]均显著大于听觉-体感觉双模靶刺激模式下的值[反应时间(461±20)ms,潜伏期(357±12)ms;P0.001];单一听觉、体感觉靶刺激模式下受试者的反应错误率[分别为(5.1±1.2)%、(19.3±3.1)%]显著小于听觉-体感觉双模靶刺激模式下的值[(2.7±0.6)%;P0.001],说明大脑不仅对听觉-体感觉双模靶刺激有更快的反应速度,而且探测的准确度明显优于单一靶刺激;不同靶刺激模式下,反应时间与P3峰值潜伏期具有显著相关性(r=0.58,P0.001),可以作为跨通道增进效应潜在神经过程的时间指标。结论双模靶刺激模式下存在明显的增进效应,大脑在跨模靶刺激模式下具有更优越的感觉信号神经整合机制。     

视体联合刺激双模增进作用的研究

研究了视体单模靶刺激(V,S)与视体双模联合靶刺激(Sv)条件下大脑认知作用的差异及双模增进作用的神经机制.采用64道脑电(EEG)信号采集系统,记录了14个被试在视觉、体感觉和视体联合靶刺激条件下的脑诱发电位和行为学数据,检测了单模与双模间行为学(反应时间和错误率)和ERPs(P2,P3)数据的差异,并分析了行为学与...     

视、听感觉刺激双模增进作用研究

目的 研究了视(V)、听(A)单模靶刺激与视听双模联合靶刺激(VA)条件下大脑认知作用的差异,进而讨论了双模增进作用的神经机制.方法 采用64道脑电(EEG)信号采集系统,记录了14个被试者在视觉、听觉和视听联合靶刺激条件下的脑诱发电位和行为学数据.检测了单模与双模间行为学[反应时间(RT)与错误率(ER)]和事件相关电位(ERPs)(P2峰值和峰值潜伏期,P3峰值和峰值潜伏期)结果的差异;分析了行为学与ERPs数据间的相关性.结果 结果显示RT、ER和P3峰值潜伏期在单模与双模间的差异具有统计学意义;P3峰值潜伏期与行为学数据特别是反应时间有显著性相关.结论 通过对比视听双模靶刺激和视、听单模靶刺激的行为学和ERPs结果,提示相对视、听单模靶刺激,视听双模靶刺激不仅在早期ERP成份(P1和N1)而且在晚期ERP成分(P2和P3),都表现出优越的感觉信号神经处理机制.     

视体联合刺激双模增进作用的研究

研究了视体单模靶刺激（V,S）与视体双模联合靶刺激（SV）条件下大脑认知作用的差异及双模增进作用的神经机制。采用64道脑电（EEG）信号采集系统,记录了14个被试在视觉、体感觉和视体联合靶刺激条件下的脑诱发电位和行为学数据,检测了单模与双模间行为学（反应时间和错误率）和ERPs（P2,P3）数据的差异,并分析了行为学与ERP数据间的相关性。通过比较视体联合靶刺激和视体单独靶刺激的行为学和ERP结果,提出视体联合刺激双模增进作用可能的神经机制。     

体感电刺激诱发事件相关电位的研究

目的对视觉、听觉、体感3种不同模态下靶刺激诱发的事件相关电位(ERP)进行比较研究,探讨体感电刺激作为脑机接口(BCI)一种新的信号诱发模式的可能性,为基于体感ERP的BCI研究提供理论依据。方法选择17例视力或矫正视力正常、听力正常、躯体感觉正常且无任何大脑病史的被试者,其中男性8例,女性9例;年龄20~26岁,平均年龄22.6岁;均为右利手。分别记录17例健康的被试者在视觉、听觉、体感单通道靶刺激下诱发的脑电图;对3类靶刺激下ERP的时域参数(幅值、潜伏期)、行为学数据(反应时间、错误率)、脑源定位进行比较分析。结果 3类靶刺激模式下的ERP波形具有相似性,体感电刺激诱发的ERP幅值与视觉、听觉靶刺激相比无显著性差异;体感电刺激诱发ERP的峰值潜伏期显著长于视觉靶刺激;体感电刺激的反应时间显著长于视觉靶刺激,错误率也高于视觉、听觉靶刺激;体感电刺激诱发ERP的脑内源与视觉靶刺激相比具有相似性。结论相比于视觉、听觉靶刺激,大脑对于体感电刺激的探测难度高,敏感程度低;但从ERP的波形和幅值上看,体感电刺激可以诱发出稳定的、可被检测到的ERP波形,完全有可能应用于BCI系统作为一种新的ERP诱发模式。     

视觉工作记忆多通道脑电θ分量因果流的研究

目的 工作记忆是一种在认知活动中对信息进行瞬时加工和贮存的记忆系统.笔者通过研究健康受试者在视觉工作记忆模式多通道脑电(multi-channel EEGs)的因果流(CF)分布模式,从信息传递特征角度为研究工作记忆机制提供支持.方法 记录8例健康受试者共80次Sternberg视觉工作记忆实验中的16通道EEGs.对原始EEGs进行预处理后,应用快速傅里叶变换(FFT)分别计算每个通道EEG的能量,选取能量值最大的通道为特征通道,对这个特征通道EEG进行时频分析,确定工作记忆特征频段.计算EEGs特征频段分量的定向传递函数(DTF)以及因果流.结果 工作记忆EEG能量集中在Fz通道的θ频段(4～8 Hz).EEG θ频段因果流的特征模式:Fz通道因果流为最大的正值,C3、C4、C5、C6通道因果流为前4个绝对值最大的负值.结论 θ频段为工作记忆EEG的特征频段.额叶(Fz)是工作记忆信息流出的关键脑区(因果源),C3、C4、C5、C6为信息流入的主要脑区(因果汇).     

视、听感知下模拟驾驶行为的脑电实验比较研究

目的 研究基于视觉、听觉以及视听融合感知的刺激源对脑电(EEG)识别率的影响。方法试验分别从视觉、听觉和视听融合3种情况提供与交通环境相关的刺激源,在不同刺激源的提示下,受试者利用左右手想象运动对车辆进行启动和制动控制,并对采集的脑电数据进行特征提取和分类处理,得到与想象运动相关的C3、C4导联上的特征信号和分类结果。...     

基于小波变换的听觉脑机接口技术研究

基于听觉的脑机接口系统为视力减退或者无法控制眼球运动的闭锁综合症患者提供了一种新的交流通道,使其可以与外界环境进行简单的交流.为了实现在线二分类听觉脑机接口系统,采用包含两种靶刺激、一种非靶刺激的三音oddball范式作为听觉刺激,通过一维离散小波变换对所得脑电数据进行单次样本特征提取,选取低频的特征向量,并采用支持向量机(SVM)进行目标与非目标的识别.结果表明,利用小波变换可以有效地单次提取特征向量P300,相当于20次靶刺激响应的叠加结果,最终目标识别正确率可高达80％以上,达到与视觉诱发的BCI模式可比的效果,可以用于二分类的脑机接口系统.     

颞叶癫痫工作记忆障碍theta振荡缺失的研究

目的 颞叶癫痫(TLE)是一类重要的成人癫痫综合征,工作记忆障碍是TLE常见的认知障碍,研究TLE工作记忆障碍的神经机制具有重要的科学价值和临床意义.theta振荡是频率范围在4～8 Hz的大脑神经同步电活动,与工作记忆行为有密切的关系,因此本研究以TLE患者的工作记忆障碍为研究对象,研究其工作记忆行为学障碍时theta振荡的改变,为进一步研究TLE工作记忆障碍的神经机制提供参考.方法 实验数据来自TLE组(18例TLE患者)和正常对照组(18名健康志愿者),在受试者执行延迟样本匹配范式视觉工作记忆任务的同时,记录34通道头皮脑电数据,选取长度为3s的延迟时间脑电为工作记忆实验数据.应用傅里叶变换计算两组每个通道脑电的能量密度,选取对照组能量密度最大的通道为工作记忆特征通道;应用短时傅里叶变换方法计算两组特征通道脑电时频分布,选取对照组能量密度大的频段为工作记忆特征频段;计算两组每个通道脑电特征频率分量的能量密度空间分布.结果 TLE组比正常对照组存在显著的工作记忆行为学低下:TLE组正确率较对照组显著减小(P＜0.05),反应时间较对照组显著加长(P＜0.001);工作记忆的特征通道为额中线(Fz),特征频段为theta;TLE组比正常对照组Fz通道在特征频段的脑电能量密度明显减小(P＜0.05);TLE组比正常对照组额区(7个通道)在特征频段的脑电能量密度明显减小(P＜0.01),以上差异均有统计学意义.结论 Theta振荡的减弱与缺失是TLE工作记忆行为学低下可能的神经机制.     

基于共空域频谱模式的少通道运动想象分类

针对少通道脑电数据采集如2～3通道的情况下,利用每个通道信号的2～ 10个延时来扩展EEG信号的通道数,然后再利用共空域模式CSP算法进行特征抽取.针对每个通道信号的延时选取问题,提出利用非参数化估计互信息熵的方法来选择最佳个数的延时因子.应用多个时延的共空域频谱模式(C SSP)算法,对2008年BCI竞赛数据集Ⅱb中的9个受试者以及实验室采集的13个受试者的想象运动数据集分析,结果表明可以使两个数据集的平均Kappa系数分别达到0.6与0.34.该方法可以依据8～ 30 Hz内频段的区分度自动优化权重系数,从而提高少通道数目下想象运动的分类正确率.     

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。