大学生社会支持与幸福感的关系:自尊的中介作用

目的探讨大学生社会支持、自尊与幸福感的关系。方法以217名大学生为被试,用领悟社会支持量表、自尊调查表和幸福感指数量表进行问卷调查。结果①幸福感与社会支持(r=0.44,P<0.001)和自尊(r=0.60,P<0.001)均呈显著正相关;社会支持与自尊也呈显著正相关,(r=0.40,P<0.001);②自尊在社会支持与幸福感之间起部分中介作用,其中介效应为(β=0.31,P<0.01)。结论社会支持既能直接影响幸福感,也能通过自尊的中介作用间接影响幸福感。     

大学生自尊与幸福感的关系:社会支持的中介作用

目的探讨大学生自尊水平对其幸福感的直接效应,以及通过社会支持的中介作用所起产生的间接效应。方法以202名大学生为被试,用社会支持评定量表、缺陷感量表和牛津幸福感量表修订版进行问卷调查。结果①幸福感与自尊(r=0.57,P<0.001)和社会支持(r=0.56,P<0.001)均呈显著正相关;自尊与社会支持也呈显著正相关(r=0.35,P<0.001);②社会支持在自尊与幸福感之间的关系中起部分中介作用,其中介效应为β=0.28,P<0.01。结论自尊既能直接影响幸福感,也能通过社会支持的中介作用间接影响幸福感。     

高师生害羞与孤独感的关系:社会支持的中介作用

目的探讨社会支持在高师生害羞与孤独感之间的中介作用。方法采用害羞量表、领悟社会支持量表及感情与社会孤独量表对525名高师生进行调查。结果①相关分析表明,孤独感与害羞有显著正相关(r=0.414,P<0.01),与社会支持有显著负相关(r=-0.558,P<0.01);害羞与社会支持有显著负相关(r=-0.29,P<0.01);②路径分析表明,害羞不仅可以直接预测孤独感,还可以通过社会支持间接预测孤独感。结构模型拟合指数GF I=0.99,CF I=1.00,NF I=0.99,拟合良好。结论社会支持是害羞与孤独感关系的中介变量。     

大学生宿舍人际关系预测抑郁：家庭环境调节的心理韧性中介模型

目的 探讨大学生宿舍人际关系与抑郁的关系,以及心理韧性的中介作用和家庭环境的调节作用。方法 采用宿舍人际关系诊断量表、青少年心理韧性量表、家庭环境量表中文版（FES-CV）、流调中心用抑郁量表（CES-D）对山西省1 874名大学生进行问卷调查。结果 (1)大学生宿舍人际关系与心理韧性呈负相关（r=-0.50,P<0.01）,与家庭环境呈负相关（r=-0.23,P<0.01）,与抑郁呈正相关（r=0.73,P<0.01）;心理韧性与家庭环境呈正相关（r=0.18,P<0.01）,与抑郁呈负相关（r=-0.53,P<0.01）;家庭环境与抑郁呈负相关（r=-0.27,P<0.01）。(2)宿舍人际关系能显著正向预测抑郁（β=0.72,P<0.01）,宿舍人际关系能显著负向预测心理韧性（β=-0.47,P<0.01）,当宿舍人际关系与心理韧性一起预测抑郁时,心理韧性对抑郁的负向预测作用显著（β=-0.22,P<0.01）,宿舍人际关系对抑郁的正向预测作用依然显著（β=0.61,P<0.01）。宿舍人际关系和抑郁的直接效应为0.61...     

大学生幸福感与物质主义的关系及社会支持的中介作用

目的:探讨大学生幸福感与物质主义的关系,以及社会支持在这两者之间的中介作用。方法:选取418名在校大学生,采用生活满意度量表(SWLS)测量被试的生活满意度水平,情感平衡量表(PANAS)测量其积极情感和消极情感水平,物质主义量表(MVS)测量其物质主义水平,社会支持量表(SSRS)测量其社会支持水平。结果:物质主义负向预测幸福感总分(β=-0.18),负向预测生活满意度(β=-0.15),正向预测负性情感(β=0.03),对正性情感没有预测作用。Bootstrap检验结果显示,社会支持在幸福感与物质主义之间起部分中介作用,中介作用大小为-0.01(95%CI:-0.03~-0.01)。结论:物质主义水平负向预测幸福感,社会支持在幸福感与物质主义关系中起部分中介作用。     

社交网站自我呈现对社会幸福感的影响:社会支持与孤独感的链式中介作用

目的:探讨社交网站自我呈现、社会支持、孤独感和社会幸福感的关系,了解社会幸福感形成的内在机制。方法:采用社交网站自我呈现问卷、社会支持量表、孤独感量表、社会幸福感量表对505名大学生进行调查。结果:①社交网站积极自我呈现、社会支持和社会幸福感两两之间均呈显著正相关(r=0.108,0.391,0.433;P0.05),社交网站真实自我呈现、社会支持和社会幸福感两两之间也呈显著正相关(r=0.226,0.371,0.433;P0.05),而社会支持、社会幸福感和孤独感显著负相关(r=-0.407,-0.381;P0.01);②社交网站积极自我呈现和真实自我呈现均可以直接影响社会幸福感(β=0.92,1.18;P0.001),还可以通过社会支持的中介作用以及社会支持和孤独感的链式中介作用两条间接路径对社会幸福感产生影响,且社交网站真实自我呈现还可通过第三条间接路径即孤独感的独立中介作用对社会幸福感产生影响(β=0.17;P0.05)。结论:社交网站自我呈现对社会幸福感有重要影响,社会支持和孤独感在两者之间起独立中介作用和链式中介作用。     

独生子女大学生森田质性格与总体幸福感、自尊水平关系研究

目的了解独生子女大学生中森田质性格分布情况,探讨森田质性格、总体幸福感及自尊水平关系。方法采用一般情况调查问卷、总体幸福感量表(GWB)、自尊量表(SES)和森田质性格调查表对大学生中独生子女进行测查。结果①独生子女大学生中森田质性格所占比例为26.3%;②森田质性格大学生的总体幸福感显著低于非森田质性格大学生(t=-7.68,P<0.05);森田质性格大学生的自尊水平显著高于非森田质性格大学生(t=7.43,P<0.01);③自尊水平与总体幸福感显著相关(r=0.362,P<0.05),森田质性格与总体幸福感显著相关(r=-0.588,P<0.05);回归分析显示森田质性格、高自尊水平对总体幸福感有负向预测作用(β=0.38,F=14.56,P<0.01)。结论森田质性格、高自尊水平对独生子女大学生总体幸福感水平有负向预测作用。     

宿舍人际关系与睡眠质量及高校新生主观幸福感的关系

目的 考察宿舍人际关系对高校新生主观幸福感的影响及睡眠质量的中介作用。方法 基于方便取样,采用大学生宿舍人际关系调查问卷、匹兹堡睡眠质量指数量表和大学生主观幸福感量表对遵义市687名高校新生进行调查。结果 城镇学生主观幸福感总分(157±22)高于农村学生得分(151±24),(t=2.85,P<0.01)。相关分析显示,宿舍人际关系总分与主观幸福感总分呈显著正相关(r=0.51,P<0.01),与睡眠质量总分呈显著负相关(r=-0.26,P<0.01),睡眠质量总分与主观幸福感总分呈显著负相关(r=-0.36,P<0.01)。宿舍关系对主观幸福感的直接效应显著(β=0.45,P<0.01)。利用Mplus 8.3检验睡眠质量的中介作用,结果表明睡眠质量在宿舍人际关系对高校新生主观幸福感的影响中起部分中介作用,中介效应占总效应的19.18%。结论 宿舍人际关系对高校新生主观幸福感产生直接影响,并通过睡眠质量间接影响高校新生主观幸福感。     

自我和谐影响大学生主观幸福感的多重中介比较

目的探讨自我和谐影响大学生主观幸福感的内在心理机制。方法采用自我和谐、社交焦虑、主观幸福感以及安全感问卷对466名大学生进行调查研究。结果①自我和谐、安全感与大学生主观幸福感显著正相关(P<0.05),社交焦虑与大学生主观幸福感显著负相关(r=-0.352,P<0.05);②社交焦虑、安全感在自我和谐对主观幸福感的影响中发挥着并行多重中介作用,当它们进入回归方程时,自我和谐对主观幸福感的影响减少(β=-0.305,t=4.49,P<0.05);③安全感对社交焦虑有明显的负向预测作用(β=-0.43,t=2.54,P<0.05)。结论自我和谐通过社交焦虑、安全感的并行多重中介作用对大学生主观幸福感产生影响。     

大学生网络受欺负、领悟社会支持与孤独感的关系

目的:探讨大学生网络受欺负、领悟社会支持与孤独感的关系。方法:采用UCLA孤独感量表、领悟社会支持量表和网络受欺负量表对815名大学生进行调查。结果:1在网络受欺负的经历上,男生显著多于女生(t=6.82,P<0.01),低年级生显著多于高年级生(t=3.82,P<0.01),理工类学生显著多于文史类学生(t=3.84,P<0.01);2女生的领悟社会支持要显著高于男生(t=2.99,P<0.01);3上网时间较少的学生的孤独感显著低于上网时间较长的学生(F=3.13,P<0.05);4网络受欺负与领悟社会支持呈显著负相关(r=-0.17,P<0.01),和孤独感呈显著正相关(r=0.20,P<0.01)。孤独感和领悟社会支持呈显著负相关(r=-0.45,P<0.01);5领悟社会支持在大学生网络受欺负和孤独感之间具有部分中介效应,中介效应量为0.07。结论:网络受欺负既能直接影响大学生的孤独感,又能通过领悟社会支持间接影响孤独感。     

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.     

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.     

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.