自我效能感在大学生主观社会支持与抑郁间的中介作用

目的:探讨自我效能感在大学生主观社会支持与抑郁间的作用机制.方法:采用贝克抑郁自评量表(BDI-13)、一般自我效能感量表(GSES)、社会支持问卷(SRRS)对451名大学生进行问卷调查.结果:抑郁与自我效能感(r=-0.421)和主观社会支持(r=-0.329)呈负相关关系(P＜0.001);自我效能感在主观支持与抑郁间起着部分中介作用,其中中介效应占总效应的比例为23.87％.结论:提高大学生对社会支持的主观感知能力,并提高其自我效能感水平,将有利于减少大学生抑郁情绪的发生.     

自我效能在2型糖尿病患者社会支持与病耻感间的中介效应

目的:分析2型糖尿病自我效能、社会支持、病耻感三者间关系,并探讨自我效能在社会支持与病耻感间的中介作用,为降低糖尿病患者病耻感提供理论依据。方法:采用便利抽样法,使用一般资料调查表、糖尿病管理自我效能量表(DMSES)、感知社会支持量表(PSSS)、2型糖尿病病耻感评估表(DSAS-2)对2019年1-6月郑州市某三甲医院内分泌科住院的202例2型糖尿病患者进行问卷调查。结果:2型糖尿病患者自我效能量表总分为(135.67±38.13)分,感知社会支持量表总分为(62.82±11.61)分,病耻感量表总分为(52.15±10.77)分。相关分析显示,自我效能、感知社会支持和病耻感三者间存在相关性(r=0.295,-0.432,-0.371;P0.01)。中介效应分析结果显示,自我效能作为中介变量对病耻感产生影响,其中介效应占总效应比例的28.1%。结论:2型糖尿病患者病耻感接近中等水平,社会支持和自我效能处于中等水平,自我效能在社会支持与病耻感间存在部分中介效应。     

女性心理障碍与中介变量之间关系

目的探讨女性心理障碍与中介变量之间的相互关系。方法采用症状自评量表(SCL-90)、领悟社会支持量表(PSSS)、特质应对方式问卷(TCSQ)、自我接纳问卷(SAQ)、一般自我效能感量表(GSES)、被他人所容纳量表(ATOS)对女性进行调查,女性心理障碍与中介变量之间相互作用关系采用多元回归分析。结果家庭支持对女性心理障碍严重程度有正向预测作用(Beta=0.297,P<0.01),家庭支持主要影响抑郁情绪(Beta=0.307,P<0.01)和精神病性症状(Beta=0.302,P<0.01)。SCL-90总分对中介变量无显著的预测作用,人际关系敏感对社会支持(Beta=0.170,P<0.05)有正向预测作用,精神病性症状对社会支持(Beta=0.226,P<0.01)和积极应对(Beta=0.209,P<0.01)有正向预测作用。结论中介变量丧失心理健康的保护作用是女性心理障碍的重要因素之一。心理障碍对中介变量无显著影响,人际关系敏感和精神病性症状能增加社会支持,精神病性症状还能增加积极应对。     

硕士新生的自我效能感对应对方式和抑郁的中介效应

目的:探讨硕士新生的自我效能感在应对方式和抑郁之间的中介效应。方法:采用一般自我效能感量表(GSES)、流调用抑郁自评量表(CES-D)、特质应对方式问卷(TCSQ)对硕士新生进行调查,用SPSS的层次回归分析得出三者之间的关系。结果:自我效能感与抑郁呈显著负相关、与积极应对呈显著正相关、与消极应对呈显著负相关,积极应对方式与抑郁和消极应对方式呈显著负相关,消极应对方式与抑郁呈显著正相关。应对方式对抑郁具有显著地预测效果(P0.001);自我效能感在应对方式与抑郁关系间起部分中介作用。结论:硕士新生的抑郁可能与其应对方式有关,而自我效能感起到部分中介作用。     

应对方式在医学院校硕士新生自我效能感与抑郁间的多重中介作用

目的:探讨特质应对方式在医学院校硕士新生自我效能感与抑郁之间的多重中介效应。方法:采用一般自我效能感量表(GSES)、特质应对方式问卷(TCSQ)、流调用抑郁自评量表(CES-D)对某医科大学884名新入学硕士研究生进行调查,运用结构方程模型分析变量之间的关系。结果:抑郁与积极应对、自我效能感呈显著负相关(r=-0.41～-0.36,p0.01),与消极应对呈显著正相关(r=0.54,p0.01);自我效能感与积极应对呈显著正相关(r=0.39,p0.01),与消极应对呈显著负相关(r=-0.34,p0.01)。回归分析显示自我效能感、积极和消极应对能显著预测抑郁,可解释其34%的变异。结构方程模型分析和Bootstrap检验显示积极应对和消极应对在自我效能感和抑郁之间的中介作用显著,并且是完全中介作用(95%CI=-0.19～-0.08/-0.30～-0.20);消极应对的中介作用更比积极应对更强(95%CI=0.05～0.22)。结论:应对方式在自我效能感与抑郁之间起多重中介作用。     

应对方式在医学院校硕士新生自我效能感与抑郁间的多重中介作用

目的:探讨特质应对方式在医学院校硕士新生自我效能感与抑郁之间的多重中介效应。方法:采用一般自我效能感量表(GSES)、特质应对方式问卷(TCSQ)、流调用抑郁自评量表(CES-D)对某医科大学884名新入学硕士研究生进行调查,运用结构方程模型分析变量之间的关系。结果:抑郁与积极应对、自我效能感呈显著负相关(r=-0.41～-0.36,p0.01),与消极应对呈显著正相关(r=0.54,p0.01);自我效能感与积极应对呈显著正相关(r=0.39,p0.01),与消极应对呈显著负相关(r=-0.34,p0.01)。回归分析显示自我效能感、积极和消极应对能显著预测抑郁,可解释其34%的变异。结构方程模型分析和Bootstrap检验显示积极应对和消极应对在自我效能感和抑郁之间的中介作用显著,并且是完全中介作用(95%CI=-0.19～-0.08/-0.30～-0.20);消极应对的中介作用更比积极应对更强(95%CI=0.05～0.22)。结论:应对方式在自我效能感与抑郁之间起多重中介作用。     

应对方式在医学院校硕士新生自我效能感与抑郁间的多重中介作用

目的:探讨特质应对方式在医学院校硕士新生自我效能感与抑郁之间的多重中介效应。方法:采用一般自我效能感量表(GSES)、特质应对方式问卷(TCSQ)、流调用抑郁自评量表(CES-D)对某医科大学884名新入学硕士研究生进行调查,运用结构方程模型分析变量之间的关系。结果:抑郁与积极应对、自我效能感呈显著负相关(r=-0.41～-0.36,P0.01),与消极应对呈显著正相关(r=0.54,P0.01);自我效能感与积极应对呈显著正相关(r=0.39,P0.01),与消极应对呈显著负相关(r=-0.34,P0.01)。回归分析显示,自我效能感、积极和消极应对能显著预测抑郁,可解释其34%的变异。结构方程模型分析和Bootstrap检验显示,积极应对和消极应对在自我效能感和抑郁之间的中介作用显著,并且是完全中介作用(95%CI=-0.19～-0.08/-0.30～-0.20);消极应对的中介作用比积极应对更强(95%CI=0.05～0.22)。结论:应对方式在自我效能感与抑郁之间起多重中介作用。     

抑郁认知易感性在应激-抑郁中的中介效应

目的:探讨抑郁认知易感性在应激-抑郁关系中是起中介效应还是调节效应.方法:1201名大学生完成了认知方式问卷、学生日常生活和学业应激量表等系列自评量表.使用层次回归法分析抑郁认知易感性的调节效应与中介效应.结果:认知易感性影响个体抑郁症状的出现,在应激-抑郁中,认知易感性是中介变量.抑郁认知易感者比非抑郁认知易感者感受到更高水平的应激,表现出更明显的抑郁和焦虑症状.结论:认知易感性在应激-抑郁中起着中介效应.     

大学生社会支持、毕生发展模型与一般自我效能感的关系

目的了解大学生社会支持、SOC策略与其一般自我效能感的关系。方法采用社会支持评定量表(SSRS)、SOC问卷、一般自我效能感量表(GSES),随机抽取河海大学、南京师范大学不同年级被试857人。结果①相关分析表明,社会支持与SOC策略存在显著正相关(r=0.32,P=0.01);社会支持与一般自我效能感存在显著正相关(r=0.69,P=0.001);SOC策略与一般自我效能感存在显著正相关(r=0.49,P=0.001);②回归分析进一步表明,社会支持对一般自我效能感(F=9.275,P<0.01)和SOC策略回归效应显著(F=82.452,P<0.001);③SOC策略在社会支持的基础上对一般自我效能感回归效应显著(F=73.614,P<0.001),对社会支持和一般自我效能感起到中介作用。结论大学生社会支持的获得、SOC策略的使用影响其一般自我效能感;SOC策略在社会支持与一般自我效能感之间起中介作用。     

大学生情绪调节自我效能感在虐待与抑郁间的中介作用

目的:探讨大学生情绪调节自我效能感与儿童期虐待经历的关系,以及情绪调节自我效能感在虐待与抑郁间的中介作用。方法:从哈尔滨市4所高校选取475名大学生,采用情绪调节自我效能感量表(RES)的中文版、儿童期虐待问卷(CTQ)、流调中心用抑郁量表(CES-D)进行测查,其中CTQ采用回顾性调查。结果:躯体忽视和躯体虐待负向预测调节积极情绪效能感(POS)(β=-0.38、-0.52);情感忽视和性虐待负向预测调节沮丧/痛苦情绪效能感(DES)(β=-0.35、-0.31);躯体忽视负向预测调节生气/愤怒情绪效能感(ANG)(β=-0.23);躯体忽视和躯体虐待正向预测抑郁(β=0.78、3.20)。POS在情感忽视、躯体忽视、性虐待与抑郁之间具有中介作用(中介效应介于0.021~0.029);DES在情感忽视、躯体忽视、躯体虐待、性虐待与抑郁之间起着中介作用(中介效应介于0.017~0.040);ANG在情感忽视、躯体忽视与抑郁之间存在中介作用(中介效应介于0.016~0.019)。结论:低情绪调节自我效能感可能与儿童期虐待经历有关,情绪调节自我效能感在虐待与抑郁之间具有中介作用。     

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。