唐山大地震孤儿性格特征与心身健康关系研究

目的调查经历唐山地震的孤儿在地震灾难发生30年后的人格特点及其与心理健康状况的关系。方法共有260例唐山地震的孤儿幸存者和241例经历唐山地震的非孤儿幸存者作为对照参加调查。使用艾森克人格问卷（EPQ）、症状自评量表（SCL-90）、焦虑自评量表、抑郁自评量表、社会支持量表、应对方式问卷对被试进行评估。结果在全部被试中，EPQ-N分与SCL-90总分（r=0.51）、SCL-90总均分（r=0.51）、SCL-90阳性项目数（r=0.52）、SCL-90阳性症状均分（r=0.32）、自评抑郁问卷（r=0.53）、自评焦虑问卷（r=0.51）显著相关，P均〈0.01；地震孤儿组（260例）EPQ-N分高于非孤儿对照组（241例）（47.65±11.41，44.92±9.46，t=2.91，P〈0.01）和EPQ-E分低于对照组（55.7±10.14，58.86±10.13，t=3.41，P〈0.01）；患PTSD的孤儿组（n=32）EPQ-E分低于未患PTSD的孤儿组（n=228）（51.88±11.34，56.32±9.87，t=2.34，P〈0.05），患PTSD的孤儿组EPQ-N分高于未患PTSD的孤儿组（54.84±10.89，46.64±11.14，t=3.910，P〈0.01）。结论唐山地震发生30年后，经历唐山大地震的孤儿幸存者人格特质有明显倾向性，这种人格特征的倾向性与孤儿幸存者的心理健康状况相关。     

车祸事件后创伤后应激障碍的研究

目的 :研究车祸事件后创伤后应激障碍的发生情况及特点。方法 :应用中国精神疾病分类方案与诊断标准第二版修订本中的急性应激障碍 (ASR)和创伤后应激障碍 (PTSD)诊断标准 ,对因车祸住我院治疗的 81例患者进行诊断 ,采用症状自评量表 (SCL -90 ) ,艾森克个性问卷 (EPQ)及症状记录表等进行测评。结果 :车祸后 3个月 ,81例中有 33例 ( 4 0 7%)曾经符合ASR诊断标准 ,31例 ( 38 3%)符合PTSD诊断标准。与非PTSD组比较 ,PTSD组SCL -90总分、总均分、阳性项目数、阴性项目数及躯体化、强迫症状、人际关系敏感、抑郁、焦虑、敌对、恐怖、其它因子分均显著高于非PTSD组 (P <0 0 5～ 0 0 1)。PTSD组情绪稳定度倾向不稳定型 ( 38 71%)的比率高于非PTSD组 (P <0 0 1)。与PTSD发病有关的影响因素为EPQ问卷中神经质、L量表及性别。结论 :车祸事件后PTSD并非罕见 ,与性别及个性心理特征有关。     

应对方式在震后青少年人格特质与PTSD症状间的中介作用

目的:考察人格特质与应对方式对汶川地震幸存青少年出现的创伤后应激障碍(简称PTSD)症状的影响,并检验应对方式在人格特质与PTSD症状间的中介作用。方法:在汶川地震发生半年后,选取四川省绵竹市某乡镇学校4～8年级学生共168人参加此次研究。施测量表包括事件冲击量表儿童版、艾森克人格问卷青少年版以及中学生应对方式量表。结果:神经质、情绪型应对与PTSD症状相关显著,相关系数分别为0.399(P<0.001),0.367(P<0.001);两变量共解释PTSD症状20.1%的变异(Adjusted R2=0.192)。中介效应分析发现情绪型应对部分中介了神经质对PTSD症状的影响。结论:人格影响创伤后应激障碍。情绪型应对部分中介神经质对PTSD症状的影响。     

烟台海难援救军人PTSD发生的影响因素分析

目的：了解影响海难援救军人的创伤后应激障碍（PTSD）发生的相关因素,探讨影响其发生的危险因素及其作用。方法：采用PTSD自评量表,症状自评量表（SCL－90）,生活事件理表（LES）,艾森克问卷（EPQ）和自行编制的涉及应激事件强度和人口学等因素的调查表,在海难事件后1个月对参与善后援救军人进行调查,并分析统计其影响PTSD发生的相关因素。结果：PTSD的得分高低与能否获取经济帮助,对上级领导工作方法和善后处理的满意程度,善后处理中打捞和目睹的尸体量呈显著负相关;与生活事件评分,善后处理中抢救幸存者的数量和EPQ的N得分呈显著正相关;PTSD得分与SCL－90总分,总均分,阳性项目数,阳性症状均分,身体化,强迫症状,人际敏感,抑郁,焦虑,敌对,恐怖,偏执,精神病性和附加因子量表分均呈显著正相关,而与阴性症状项目数呈负相关。结论：该海难事件是一强烈的应激事件,PTSD发生率高,LES量表分和EPQ的N量表得分与PTSD严重程度密切相关,可望通过改善上级领导工作方法和善后处理方法,积极争取支持,以降低其发生或减轻其严重程度。     

四川灾区教师创伤后应激障碍与其气质特征的关系研究

目的考察创伤后应激障碍(PTSD)与气质特征的关系。方法采用方便取样。本研究通过采用外部行为特征—气质调查表(FCB-TI)以及创伤后应激障碍检查量表平民版(PCL-C)对380名四川某地教师进行了研究。结果①气质特征中敏捷性、坚持性、情绪反应性、耐受性及活动性均与PTSD的状况存在相关。PTSD阳性检出率为24.2%,在阳性检出者中敏捷性与情绪反应性与PCL-C的总分存在相关;②在PCL-C量表的回避反应、创伤经历反复重现反应、社会功能缺失反应因素及总分上男性组得分与女性组得分的差异有统计学意义(t=2.028,3.645,2.616,2.860;P<0.01);③在PCL-C量表的警觉增高反应、创伤经历反复重现反应、社会功能缺失反应因素及总分在各年龄组之间的差异有统计学意义(F=5.760,3.890,4.525,5.113;P<0.01);④回归分析显示,情绪反应性、年龄、敏捷性、性别、坚持性及活动性6个变量对PTSD的状况存在预测作用。结论气质差异是解释创伤性应激障碍状况的一个变量。     

精神创伤后应激障碍与述情障碍的相关性分析

目的:研究旨在了解经历精神创伤后,创伤后应激障碍(PTSD)患者的症状特征与述情障碍的关系。方法:试验组为35名经历过精神创伤发生PTSD的患者,对照组为35名经历过精神创伤未发生PTSD的创伤暴露者,在不影响测验症状的情况下分别完成创伤后应激障碍临床筛查表平民版量表(PCL-C)及述情障碍20个条目量表(TAS-20)中文版。结果:PTSD患者述情障碍的发生率(57.14%)高于未发生PTSD的创伤幸存者(11.42%),PTSD患者的TAS-20总分(t=-5.271,P0.001)、因子1(F1:情感辩别不能)(t=-6.113,P0.001)及因子2(F2:情感描述不能)(t=-4.660,P0.001)得分高于对照组,差异有统计学意义。总分及因子分与PTSD症状的相关分析表明,PTSD患者的症状特征与TAS-20总分及F1、F2因子显著相关。结论:精神创伤暴露者中PTSD患者与未发生PTSD的创伤幸存者的述情障碍表现明显不同,TAS-20量表在临床具有较好的辅助诊断价值。     

汶川地震极重灾区社区居民创伤后应激障碍发生率及影响因素

目的:调查汶川地震后,极重灾区社区居民创伤后应激障碍发生率及影响因素,为进一步开展灾后心理卫生服务提供依据.方法:采用整群随机抽样的方法,从安县京安小区、什邡红白镇两个临时安置点社区居民2685人中,随机抽取820名社区居民登记人口学背景、受灾状况,并使用PTSD检查量表平民版(PTSD Checklist-Civilian Version,PCL-C)和领悟社会支持量表(Perceived Social Support Scale,PSSS)进行评估,依据DSM-Ⅳ中PTSD的诊断标准确诊PTSD患者.结果:在完成的820份调查评估资料中,785份PCL-C和PSSS问卷有效.男女比例为1:1.41;平均年龄(43±18)岁;26.0%患有躯体疾病,28.4%有地震前饮酒习惯,23.6%有震后饮酒行为.不同年龄居民PSSS总分及2因子分差异均无统计学意义(P>0.05).PTSD的临床检出率为12.4%(97/785),女性PTSD发生率高于男性(15.3%vs.8.3%,P=0.003),地震中有曾被掩埋经历者PTSD发生率高于无被掩埋经历者(26.3%vs.11.6%,P=0.018),有丧亲者的PTSD发生率高于无丧亲者(18.7%vs.11.1%,P=0.015).以PTSD诊断是否成立为因变量,一般资料为自变量进行Logistic回归分析显示:女性(OR=2.070,95%CI:1.274～3.365)、有曾被掩埋经历者(OR=2.806,95%CI:1.249～6.306)、亲人丧失(OR=1.537,95%CI:1.087～2.173)及PSSS评分偏低(OR=0.960,95%CI:0.941～0.979)是PTSD发生的危险因素.结论:在灾后社区重建过程中,临时安置点社区居民存在较高的创伤后应激障碍的发生率,女性、有曾被掩埋经历、亲人丧失及个人感受到的社会支持偏低是PTSD发生的危险因素.     

创伤后应激障碍患者免疫水平的相关性

目的探讨创伤后应激障碍(PTSD)患者免疫功能的变化及其与PTSD患者病情严重程度的相关性。方法入组15例无躯体损伤的精神创伤后应激障碍患者[PCL-C量表得分52~79分,平均(62±8)分]为实验组,15例经历精神创伤事件未发生创伤后应激障碍且PCL-C量表得分12分[(得分0~11分,平均(4±4)分]的预恢复人群(预恢复至常态/基本无症状)为对照组,两组均用酶联免疫吸附方法测定血清细胞因子(IL-2、IL-6、IL-10、肿瘤坏死因子)水平,并分析其与PCL-C量表得分的相关性。结果实验组与对照组间非参数检验除白介素IL-2有显著性差异外(Z=-2.780,P=0.005),其余3项生物学指标差异均无显著性。实验组血清IL-2、IL-6、IL-10、肿瘤坏死因子水平与PCL-C量表得分无显著相关性。结论创伤后应激障碍患者白介素IL-2水平异常,其免疫学水平及相关性有待进一步研究。     

精神创伤后应激障碍的神经递质水平相关性

目的探讨精神创伤后应激障碍(PISD)患者单胺类神经递质水平变化及其与PTSD的相关性,为理解临床的症状特点和治疗提供理论依据。方法入组15例无躯体损伤的精神创伤后应激障碍患者(PCL-C量表得分>50分),15例经历精神创伤事件未发生PTSD且PCL-C量表得分<12分的预恢复人群,两组均用酶联免疫吸附方法对其进行血浆单胺类神经递质(去甲肾上腺素、5-羟色胺、多巴胺)上述3项生物学指标检测。结果对两组间去甲肾上腺素水平行t检验(t=0.518,P=0.608)和5-羟色胺水平行t检验(t=0.199,P=0.844)及多巴胺水平行非参数检验(Z=-0.249,P=0.803(双侧)),上述单胺类神经递质水平PTSD组与对照组间差异无统计学意义。同时对PTSD组的上述3项生物学指标与PCL-C量表得分做相关性研究,均显示无显著相关。结论创伤后应激障碍患者神经递质水平及相关性有待进一步研究。     

舟曲泥石流灾区居民创伤后应激障碍症状调查

目的调查舟曲泥石流灾区居民创伤后应激障碍症状(PTSD)的发生率,为灾区居民进行心理干预和心理健康教育提供科学依据。方法按随机抽样的原则,采用创伤后应激障碍检查量表平民版(PCL-C),对293名灾区居民进行自填式调查问卷调查,按照有无PTSD分为PTSD组和正常组,比较两组在社会人口学资料和受灾程度方面的心理健康状况。用logistic回归分析筛选PTSD的危险因素。结果 1灾区居民PTSD症状群筛查总阳性率为34.47%,创伤经历反复重现组阳性率最高(86.35%);2两组在性别、婚姻状况、受教育程度、职业、有无亲人死亡、房屋是否倒塌、有无伤残等方面存在显著性差异(P=0.000,0.016,0.000,0.000,0.000,0.017,0.026);3Logistic回归分析筛选出5个PTSD的预测因素,分别为女性、未婚、亲人死亡、受教育程度相对低和有房屋倒塌者(OR=2.34,0.34,0.45,0.77,0.71)。结论舟曲泥石流灾区居民PTSD症状发生率较高,不同特征的受灾居民创伤后应激障碍症状表现及严重程度不同,应采取有针对性的心理干预措施。     

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.     

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.     

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 myoelectric activity in prepubertal and adult males and females

The purpose of this investigation was to compare children and adults of both genders with respect to torque-velocity, electromyogram (EMG)-velocity and torque-EMG relationships during maximal voluntary knee extensor muscle actions. Four groups of ten subjects each were studied comprising 11-year-old girls and boys and female and male physical education students (22–35 years). Maximal voluntary eccentric (lengthening) and concentric (shortening) actions of the knee extensors were performed at the constant velocities of 45, 90 and 180° · s^–1. Average values for torque and EMG activity, recorded by surface electrodes from the quadriceps muscle, were taken for the mid 40° of the 80° range of motion. The overall shapes of the torque- and EMG-velocity relationships were similar for all four groups, showing effects of velocity under concentric (torque decrease and EMG increase) but not under eccentric conditions. Eccentric torques were always greater than velocity-matched concentric ones, whereas the eccentric EMG values were lower than the concentric ones at corresponding velocities. Torque output per unit EMG activity was clearly higher for eccentric than for concentric conditions and the difference was of similar magnitude for all groups. Thus, the torque-EMG-velocity relationships would appear to have been largely independent of gender and to be fully developed at a prepubertal age.