高血压病人β-内啡肽、肾素-血管紧张素、醛固酮的意义

有关高血压病人与血浆β -内啡肽 (β -ＥＰ)的致病关系已有过报道 ,但与血管紧张素Ⅰ、Ⅱ(Ａ -Ⅰ、Ａ -Ⅱ)、醛固酮系统联检还甚少 ,我们收集了部分样本进行比较分析 ,现作如下报道。材料和方法一、病人组 :3 0例 (男 13 ,女 17) ,年龄 3 0～ 83岁 ,平均5 6 8岁 ,均为按ＷＨＯ规定的高血压标准确诊的住院病人。二、正常人组 :3 0例 (男 2 0 ,女 10 ) ,年龄 2 9～ 75岁 ,平均5 2 6岁 ,经体检排除心血管系统等内科疾患。三、β-ＥＰＲＩＡｋｉｔ购自Ｐｅｎｉｎｓｕｉａ产品 ,肾素 -血管紧张素 -醛固酮ＲＩＡｋｉｔ购自中国原子能研究院北方…     

急性胰腺炎患者血浆肾素活性、血管紧张素-Ⅱ变化的动态研究

目的本文旨在通过观察急性胰腺炎(AP)时肾素活性、血管紧张素Ⅱ改变,指导AP的治疗及严重程度的判断.方法采用放射免疫分析法(RIA),分别测定重症急性胰腺炎(SAP)、轻型急性胰腺炎(MAP)、急性胆囊炎(AC)、急性阑尾炎(AA)、消化性溃疡急性期(PU)病人及健康对照组(HC)的血浆肾素活性(PRA)、血管紧张素Ⅱ(AT-Ⅱ)水平(PU组仅测定AT-Ⅱ).SAP组发病后24h内(SAP.A)及恢复期(SAP.R)与MAP组发病后24h(MAP.A)及恢复期(MAP.R)分别采血检测两项指标.结果PRA、AT-Ⅱ发病后24小时的测定值,SPA.A组分别为3.84±1.92ng/ml@h、386.68±178.53pg/ml.MAP.A组分别为1.88±0.93ng/ml@h、142.68±83.57pg/ml;HC组分别为0.68±0.45ng/ml@h、43.51±31.04pg/ml.SAP.A与MAP.A组三项指标显著升高.SAP.R分别为1.34±0.76ng/ml@h、44.71±27.93pg/ml.MAP.R分别为1.18±0.69ng/ml@h、41.82±17.88pg/ml.SAP.A与MAP.A比较及SAP.A、MAP.A分别与HC组比较,两项指标的统计结果为p＜0.05,具有显著性差异.SAP.R与SAP.A比较,两项指标的统计结果为p＜0.05,具有显著性差异.MAP.R与MAP.A比较,两项指标的统计结果为p＜0.05,具有显著性差异.SAP.A与MAP.A组两项指标(或单项指标)分别与AC、AA及PU组比较,前两组均显著高于后者,统计学处理p＜0.05.结论1.AP时多种原因引起的循环血容量降低导致AP早期RAAS的激活,且激活程度与AP早期血容量丢失的严重程度有关.2.AP时血浆AT-Ⅱ的升高是机体的一种代偿机制,但加剧了AP时的胰腺微循环障碍.     

1测定醛固酮浓度/肾素活性(SAC/PRA)值在原发性醛固酮增多症中的临床意义

目的:探讨测定SAC/PRA值对原发性醛固酮增多症的诊断价值.方法:采用放射免疫分析法测定48例原发性醛固酮增多症患者和30例正常人的血浆肾素(PRA),血管紧张素Ⅱ(AT-Ⅱ)以及血清醛固酮(Aldo),并计算醛固酮浓度/肾素活性(SAC/PRA)比值.结果:正常组PRA、AT-Ⅱ、Aldo测定值分别为0.57±0.08ng/ml/h,36.03±6.11ng/L,0.33±0.04nmol/L;原醛患者PRA、AT-Ⅱ、Aldo测定值分别为0.14±0.08ng/ml/h,21.21±7.55ng/L,1.07±0.34nmol/L.与正常对照组比较,均有极显著性差异(p＜0.001).SAC/PRA(ng/dl/ng*ml-1*h-1)913±409.结论:合理使用SAC/PRA比值有助于原发性醛固酮增多症的诊断.     

肝硬变患者TIPS术后血浆内皮素、肾素活性、血管紧张素II水平的变化

目的 :探讨肝硬变患者TIPS术前后血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素II(ATII)水平的变化。方法 :选择临床确诊肝硬变患者 5 4例 ,随机将其分成TIPS组 2 4例和对照组 30例。应用放射性免疫分析法测定了 2 4例肝硬变患者TIPS术前后和 30例对照组治疗前后及 30例正常组血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素II(ATII)的含量。结果 :5 4例肝硬变患者血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素II(ATII)治疗前后均高于正常组 (P <0 0 0 1)。TIPS组术前与对照组治疗前血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素II(ATII)浓度相比差异无显著性 (P >0 0 5 ) ,TIPS组术后与对照组保肝治疗二月后再次测定血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素II(ATII)。TIPS组术后血浆内皮素 (ET)、肾素活性(PRA)、血管紧张素II(ATII)浓度显著低于治疗前 ,治疗前后相比差异有显著性 (P >0 0 1)。对照组治疗后血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素II(ATII)浓度下降不显著 ,治疗前后相比差异无显著性 (P >0 0 5 )。结论 :TIPS术有降低血浆内皮素 (ET)、肾素活性 (PRA)、血管紧张素II(ATII)的作用     

糖尿病患者肾素-血管紧张素-醛固酮系统变化的临床意义

糖尿病（DM）高血压是其微血管病变所致的一种并发症,而糖尿病病患者血管内皮损伤可能是其重要原因之一[1]。其发病机制目前尚不十分明确,国内关于TXB2和6－keto-PGF1a,ET和CGRP等激素与糖尿病血管病变^[1-3],以及肾素－血管紧张素0－醛固酮系统（RAAS）变化与高血压之间关系的报道较多。有关肾素活性,血管紧张素II及醛固酮含量变化与糖尿病合并高血压之间的关系报道甚少,为此,本地31例正常人,63例2型糖尿病患者（其中29例合并高血压）血浆肾素活性,血管紧张素II及醛固酮的含量进行了观察,现报道如下。     

低氧诱导因子-1α和内皮素-1基因在大鼠低氧性肺动脉高压中的表达

目的　探讨低氧诱导因子 1(HIF 1α)和内皮素 1(ET 1)基因表达在低氧性肺动脉高压发病过程中的变化和作用。方法　复制低氧性肺动脉高压大鼠模型 ,测定平均肺动脉压 ,弹力纤维染色显示腺泡内肺动脉 ,用放射免疫法测ET含量 ,原位杂交方法进行检测HIF 1αmRNA。结果　HIF 1αmRNA在低氧各组腺泡内肺动脉有表达 ,低氧 14d组 (0 2 5 6 9± 0 0 46 8)和低氧 2 8d组 (0 2 2 5 8±0 0 45 3)染色强于低氧 5d组 (0 145 5± 0 0 2 72 )和正常组 (0 110 9± 0 0 2 2 4) ;ET 1mRNA在低氧各组腺泡内肺动脉有表达 ,低氧 14d组 (0 412 2± 0 0 783)和低氧 2 8d组 (0 36 84± 0 0 72 9)染色强于低氧5d组 (0 2 0 17± 0 0 34 9)和正常组 (0 185 5± 0 0 36 1) ,HIF 1α和ET 1基因表达在H14d组和H2 8d组明显增加 (P <0 0 5 )。肺动脉血中ET 1含量在H14d组 [(15 8 78± 2 5 14)pg/ml]和H2 8d组 [(142 93± 2 3 38)pg/ml]明显高于H5d组 [(79 6 8± 12 5 4)pg/ml]和正常组 [(6 5 37± 10 82 )pg/ml](P <0 0 5 ) ;H14d组 [(34 0± 5 8)mmHg]和H2 8d组 [(2 9 0± 4 7)mmHg]的mPAP也明显高于H5d组[(19 0± 3 5 )mmHg]和正常组 [(17 0± 2 8)mmHg](P <0 .0 5 ) ,并且与肺动脉血中ET 1含量呈正比(rs=0     

血清NSE,TNF-α,LSA联检对肺癌诊断的意义

目的 :探讨神经元特异性烯醇化酶 (NSE)、肿瘤坏死因子 -α(TNF -α)及脂质唾液酸 (LSA)在肺癌中的表达及其诊断价值。方法 :收集肺癌病人血清 78份 ,良性肺病患者血清 32份 ,正常对照血清 10 9份。采用酶联免疫吸附试验 (ELISA)和化学发光免疫分析法分别测定血清中的NSE、TNF -α及LSA。结果 :肺癌患者血清中的NSE、TNF -α、LSA分别为 19 78± 12 10ng/ml、135 6 4± 4 9 0 1pg/ml、1 0 6± 0 31mg/ml,明显高于良性肺病组 7 5 6± 3 4 1ng/ml、84 70± 2 4 89pg/ml、0 78± 0 18mg/ml及正常对照组 8 0 1± 2 81ng/ml、71 2 5± 13 5 0pg/ml、0 70± 0 13mg/ml(p <0 0 1)。对肺癌诊断的阳性率分别为 6 2 82 %、84 6 2 %、75 6 4 。联合检测阳性率达92 31%。结论 :血清NSE、TNF -α、LSA在肺癌病人中有较高的阳性率 ,联检阳性率更高 ,故NSE、TNF -α、LSA的联检是肺癌的非常有用的辅助诊断指标。 阳性标准为NSE >16 0ng/ml,TNF -α >10 0pg/ml,LSA >0 5 8mg/ml。     

心脏病患者心包内皮素的研究

内皮素 (ｅｎｄｏｔｈｅｌｉｎ,ＥＴ)具有强烈的血管收缩效应。 1990年以来我们发现和证明人心包存在具有内分泌功能 ,存在局部肾素血管紧张素Ⅱ等[1] 。本实验通过人间皮细胞培养 ,高效液相结合放免分析 (ＨＰＬＣ ＲＩＡ)方法 ,进一步研究人类心脏病心包组织中是否存在内皮素 ,探讨人心包间皮细胞的内分泌功能及其作用。1　材料和方法1 1　材料 :选择 45例心脏直视手术病人 (男性 2 3例 ,平均年龄 47 5± 15 5岁 ;女性 2 2例 ,平均年龄 45 5± 17 6岁 ) ,其中冠心病病人 10例 ,风心病病人 2 5例 ,先心病病人 10例 (房间隔缺损 6例 ,室间…     

冠心病人血浆AT-Ⅰ、AT-Ⅱ、ALD RIA联检结果分析

本文就148例冠心病病人血浆血管紧张素Ⅰ（AT-Ⅰ）、血管紧张素Ⅱ（AT-Ⅱ）及醛固酮（ALD）射免疫分析（RLA）测定结果进行分析，发现冠心病与肾素-血管紧张素-醛固酮系统（RAS）功能状态有关。     

肾素-血管紧张素-醛固酮系统检测研究进展

肾素-血管紧张素-醛固酮系统(RAAS)由一系列激素及相应的酶组成,通过对血容量和外周阻力的控制,调节人体血压、水和电解质平衡,维持机体内环境恒定。目前检测血清或血浆肾素活性(PRA)、血管紧张素Ⅱ(AⅡ)和醛固酮(ALD)水平已成为原发性和继发性高血压分型诊断、治疗及研究的重要指标。本文从RAAS的临床意义及其检测方法进行了     

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.     

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.     

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.     

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.