交往焦虑量表的信效度及其在中国大学生中的适用性

目的:分析交往焦虑量表的信效度,评估其在中国大学生中的适用性.方法:1439名大学生、58名精神科神经症住院病人以及24名社交焦虑的大学生分别接受交往焦虑量表、社交苦恼与回避量表以及焦虑自评量表的自评,其中30名大学生2周后重测.结果:交往焦虑量表的Cronbach α系数为0.81,重测系数为0.78,信度指标良好;与社交苦恼及回避量表的相关为0.66,与焦虑自评量表的相关为0.29,正常大学生与住院病人量表得分差异不显著,但两者与社交焦虑大学生的得分差异显著,说明其聚合效度与区分效度良好.结论:该量表具有良好的测量学指标,可以作为我国大学生社交焦虑研究的有效工具.     

人际关系团体训练课程对提高大学生人际交往能力的效果

目的:将团体训练课程引入到大学生选修课程,探讨人际关系团体训练课程对提高大学生人际交往能力的作用。方法:将136名大学生分为实验组、安慰剂组和控制组3组进行干预研究,采用交往焦虑量表、羞怯量表、社交回避与苦恼量表进行评估。结果:实验组训练后的交往焦虑(F=23.40,P0.01),羞怯(F=23.38,P0.01)、社交回避与苦恼(F=15.63,P0.01)的得分均显著低于训练前,而安慰剂组和控制组训练前后没有显著变化(P0.05)。结论:人际关系团体训练课程效果显著,能够有效地减少大学生的交往焦虑,改善大学生人际交往的社交回避与苦恼、羞怯的程度。     

团体认知治疗对大学生社交焦虑的影响

目的探讨团体认知治疗对大学生社交焦虑的影响。方法选取1000名大学生,采用《人际关系综合诊断量表》进行测试,筛取量表分≥9分(人际交往存在一般困扰者)223人。根据自愿原则,选取人际困扰的大学生30名,随机分为2组,每组15人:实验组采用团体认知治疗进行干预,每周1次,共8周;对照组不给予任何干预。两组在干预前后分别进行交往焦虑量表、社交回避及苦恼量表测定,比较实验组、对照组在干预前后量表得分的差异。结果心理辅导组:交往焦虑得分干预前后有显著性差异(t=2.97,P<0.05)。社交回避及苦恼量表总分在干预前后有显著性差异(t=3.09,P<0.05),其因子分:回避因子分干预前后有显著性差异(t=2.61,P<0.05),苦恼因子分在干预前后有显著性差异(t=2.56,P<0.05)。对照组:交往焦虑得分前后测验比较无显著性差异(t=-1.13,P>0.05)。社交回避及苦恼量表总分前后测验无显著性差异(t=0.85,P>0.05),其回避因子分前后测验无显著性差异(t=1.09,P>0.05),苦恼因子分前后测验无显著性差异(t=0.45,P>0.05)。结论团体认知治疗能有效改善被试的社交焦虑情绪,减少社交回避行为,改善社交苦恼症状,提高社会交往能力。     

大一新生社交回避与苦恼的现状及其与人格的相关性研究

目的了解大学新生社交回避及苦恼状况,探讨社交回避及苦恼与人格的关系。方法采用艾森克人格问卷简式量表(EPQ-RSC)、社交回避及苦恼量表(SADS)为调查工具,对随机抽取的某医学院2008级临床、护理专业280名本科生进行调查,数据进行t检验、Pearson相关分析、多元逐步回归分析。结果 1大一新生社交回避及苦恼、社交回避、社交苦恼均处于中等水平;2社交回避及苦恼、社交回避、社交苦恼与内外倾(E)、神经质(N)、掩饰性(L)相关显著;3逐步多元回归结果发现,E、N、L为新生社交回避及苦恼的有效预测因素。结论新生社交回避及苦恼状况处于中等水平;人格是影响社交回避及苦恼的重要因素。     

自尊对自尊需要与社交焦虑的调节与中介作用

目的考察自尊对自尊需要与社交焦虑、社交回避之间关系的调节和中介作用。方法采用自编的自尊需要问卷、M.Rosenberg自尊量表、社交回避及苦恼量表对534名福州市高校大学生进行问卷调查。结果用逐步多元分析,当回归方程纳入自控后,自尊对社交焦虑、社交回避的影响下降,说明自尊对自尊需要与社交焦虑、社交回避之间的关系具有中介作用,而自尊对自尊需要与社交焦虑、社交回避之间的关系不具有调节作用。结论提高大学生自尊水平来降低其社交焦虑体验、社交回避行为是有效途径。     

团体治疗职业中专学生社交焦虑和自尊的干预研究

目的研究团体治疗对中专学生社交焦虑和自尊的干预效果,以寻求改善中专学生社交焦虑和自尊的途径。方法采用社交回避与苦恼量表(SAD)对温州市职工中等卫生学校的学生共进行问卷调查。结果团体治疗8周后,社交回避与苦恼量表(SAD)总分为(11.82±4.64),低于治疗前(18.45±5.01,P<0.01);焦虑分量表分为(4.31±2.32),低于治疗前(9.22±3.42,P<0.01);回避分量表分(6.86±2.61),低于治疗前(6.86±2.61),低于治疗前(9.97±3.27,P<0.01);自尊量表(SES)评分在团体治疗后为量表分(34.89±4.78),高于治疗前(28.62±4.36,P<0.01)。结论团体治疗对社交焦虑和自尊水平均有改善作用。     

人际交往训练对大学生人际交往能力及心理健康水平的影响

目的探讨人际交往团体训练对提高大学生人际交往能力和心理健康水平的影响。方法选取15名大学生进行人际交往干预训练,采用羞怯量表、社交回避与苦恼量表(SAD)、交流恐惧自陈量表(PRCA-24)、症状自评量表(SCL-90)进行评估。结果实验组在SCL-90总分及强迫、人际关系敏感、恐怖3个因子分上,训练后比训练前有显著下降(P<0.05),而对照组没有显著差异;实验组训练后社交回避与苦恼量表(P<0.05)、交流恐惧量表、羞怯量表得分显著低于训练前(P<0.01),对照组没有显著变化;训练后实验组在社交回避与苦恼、交流恐惧(P<0.01)、羞怯量表得分显著低于对照组(P<0.05);而训练前没有显著差异。结论通过人际交往团体心理训练,能够改善大学生强迫、人际关系敏感、恐怖等因子,提高其心理健康水平;对大学生人际交往的社交回避与苦恼、交流恐惧、羞怯等能够产生积极的改善作用;人际交往训练有助于改善被训练者的主观感受,对人际交往产生积极的期待。     

社交回避与苦恼对手机成瘾的影响:孤独感、安全感和沉浸的多重中介效应

目的:以孤独感、安全感和沉浸为中介考察社交回避与苦恼对手机成瘾的预测作用。方法:采用社交回避与苦恼量表、孤独感量表、安全感量表、沉浸量表和手机成瘾指数量表对487名大学生进行测量。结果:(1)社交回避与苦恼、孤独感、沉浸、手机成瘾之间呈显著两两正相关,且分别与安全感呈负相关;(2)孤独感、安全感、沉浸在社交回避与苦恼和手机成瘾的关系中起到完全中介作用。结论:个体社交回避与苦恼水平越高,孤独感越强,越容易缺乏安全感并体验到更强的沉浸感,导致个体更容易手机成瘾。     

哈萨克族大学生自我接纳、社交焦虑与自尊三者间的相关性

目的:了解哈萨克族大学生社交焦虑、自我接纳与自尊间的关系,为哈萨克族大学生心理健康干预、身心健康发展提供支持。方法:在新疆4所高校随机抽取1006名哈萨克族大学生采用自我接纳问卷、自尊量表和社交回避与苦恼量表进行问卷调查,并对结果进行统计分析。结果:哈萨克族大学男生的自我接纳和自尊得分高于女生,并且存在统计学差异(t=3.569,4.267;P0.01)。社交苦恼、社交回避和社交焦虑总分男生均低于女生,并且也存在统计学差异(t=-2.162,-2.258,-2.417;P0.01)。城市哈萨克族大学生自尊得分低于农村学生,社交回避和社交焦虑总分农村学生高于城市学生得分,并且均存在统计学差异(t=-8.49,-2.58;P0.05)。年级方面除了自尊不同年级学生得分存在统计学差异外(t=10.99,P0.01),其他方面得分差异均无统计学意义(P0.05)。哈萨克族大学生自我接纳与自尊存在正相关关系(r=0.593,P0.01);社交苦恼和社交焦虑总分与社交回避呈现正相关关系(r=0.692,0.918;P0.01)。回归方程显示,自尊在自我接纳与社交焦虑总分及各维度间存在中介作用。结论:哈萨克族大学生社交焦虑、自我接纳、自尊间存在密切联系,并且自尊在社交焦虑和自我接纳之间起到中介作用。     

大中学生社交焦虑特征初探

摘要目的比较大中学生社交焦虑水平的差异,探析社交焦虑者的心理特征。方法抽取大学生365人,高中生259人,采用团体施测的方法分别进行社交焦虑量表和其他相关量表的自我评估：社交回避与苦恼量表、人际交往量表、抑郁自评量表、孤独量表、状态一特质焦虑量表、惧怕否定评价量表、艾森克人格问卷。结果男生的社交焦虑水平显著高于女生,大学生的社交焦虑水平显著高于高中生,社交焦虑者在人格问卷的N分以及孤独、抑郁、害怕否定评价等分高于非社交焦虑者,而E分显著低于非社交焦虑者。结论在大中学生中,男生社交焦虑水平显著高于女生,大学生的社交焦虑水平显著高于高中生;社交焦虑者一般具有内向、不稳定、孤独、抑郁、害怕否定评价等特征。     

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.     

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.     

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.     

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.     

类赖氨酰氧化酶2与肿瘤转移和发生

类赖氨酰氧化酶2(lysyl oxidase-like 2,LOXL2)是赖氨酰氧化酶(lysyl oxidase,LOX)基因家族的成员之一,其表达产物能促进胶原沉积.LOXL2的过表达能促进纤维化,并与肿瘤侵袭、转移及不良预后有关.目前大部分学者认为LOXL2是一种转移促进基因,也有实验支持其是一种肿瘤抑制基因.研究发现LOXL2可以通过激活Snail/Ecadherin通路或Src/FAK通路促进转移.LOXL2有望作为肿瘤生物标志物,用于预后判断,成为一个新的治疗靶点.