bcl—2,p53蛋白及PCNA表达与横纹肌肉瘤临床病…

目的：研究横纹肌肉瘤（ＲＭＳ）中ｂｃｌ－２、ｐ５３、ＰＣＮＡ表达与其临床病理的相关性。方法：对５０例横纹肌肉瘤进行免疫组化ＡＢＣ法标记。结果：ｂｃｌ－２、ｐ５３基因蛋白和ＰＣＮＡ，发现ｂｃｌ－２、ｐ５３、ＰＣＮＡ阳性表达率分别为２８％、７２％、７０％，其阳性表达与年龄、性别及不同组织类型的ＲＭＳ无关。但民分化程度有关，Ｐ５３、ＰＣＮ在低分化ＲＭＳ阳性率分别为８５％、９５％，显著高于 化ＲＭＳ４２．     

p53、p21、p185蛋白表达与横纹肌肉瘤分化及预后的关系

目的研究ｐ５３、ｒａｓ和ｃ－ｅｒｂＢ－２癌基因蛋白产物ｐ２１、ｐ１８５在横纹肌肉瘤（ＲＭＳ）中的表达及其与ＲＭＳ的分型、分级和预后的关系。方法对确诊的５０例中的４１例有随访的ＲＭＳ用免疫组化ＡＢＣ法标记ｐ５３、ｐ２１、ｐ１８５蛋白，结果发现ｐ５３、ｐ２１、ｐ１８５在ＲＭＳ的阳性率分别为７２％、６８％、６０％，其阳性表达与年龄、性别和ＲＭＳ的组织类型差异无显著性（Ｐ＞０．０５）；但与分化程度有关，其中ｐ５３、ｐ２１在低分化ＲＭＳ的阳性率分别为８５％和８０％，显著高于高分化ＲＭＳ的４２．９％和２８．６％（Ｐ＜０．０５）；ｐ５３蛋白在有转移组ＲＭＳ的阳性率为８６．４％，显著高于无转移组６０．７％（Ｐ＜０．０５）；有随访的４１例病例中。存活１年的ｐ５３蛋白阳性率为８６．７％，显著高于３年的４１．７％（Ｐ＜０．０５）。结论ｐ５３、ｐ２１蛋白表达可作为肿瘤分化及恶性程度的评价指标，而ｐ５３更能反映肿瘤预后，是肿瘤预后差的重要指标之一。     

bcl-2、p53表达与乳腺癌预后的关系

目的：探讨ｂｃｌ２ 、ｐ５３ 表达与乳腺癌预后的关系。方法：应用免疫组化ＬＳＡＢ法检测６４ 例乳腺癌及３０ 例乳腺良性病变的表达。分析ｂｃｌ２、ｐ５３ 与乳腺癌组织学分级、腋淋巴结转移、复发和预后的关系。结果：ｂｃｌ２ 与ｐ５３ 表达之间差异有显著性,呈负相关（ Ｐ＜ ０－０５） 。ｂｃｌ２ 和ｐ５３ 表达与组织学分级有关（ Ｐ＜ ０－０５） ,ｂｃｌ２ 表达随分级增加阳性率降低,ｐ５３ 则相反。ｐ５３ 表达与腋淋巴结转移有关（ Ｐ＜ ０－０５） 。ｂｃｌ２ 表达与腋淋巴结转移无关（ Ｐ＞ ０－０５） 。ｐ５３ 表达复发组明显高于无复发组（ Ｐ＜０－０５）;ｂｃｌ２ 表达与有无复发无关（Ｐ＞０－０５）。ｐ５３ 表达阳性率≤５ 年生存组明显高于＞ ５ 年生存组,呈负相关（ Ｐ＜ ０－０５）;ｂｃｌ２ 表达与生存期无关（Ｐ＞ ０－０５） 。结论：ｂｃｌ２ 表达与预后无关,其阳性表达可反映肿瘤属分化较好或属早期阶段。ｐ５３ 可单独作为预后指标;ｐ５３ 表达与预后呈负相关。     

肝细胞癌及癌旁肝组织中bcl—2和p53蛋白表达与？…

目的：探讨ｂｃｌ－２和ｐ５３蛋白的表达与端粒酶活性的相关性及其与ＨＣＣ发生的关系。方法：利用端粒酶原位标记法显示端粒酶活性,采用Ｓ－Ｐ法免疫组化技术的检测ｂｃｌ－２和ｐ５３蛋白。结果：端粒酶在ＨＣＣ中的阳性率（９１．７％）显著高于癌旁肝组织（５８．３％）（Ｐ〈０．０５）,端粒酶活性强度与ＨＣＣ分化程度无关（Ｐ〉０．０５）;癌组织中ｂｃｌ－２和ｐ５３蛋白的阳性率均高于癌旁组织（Ｐ〈０．０１）;ＨＣＣ     

乳腺导管原位癌病理形态及c-erbB-2、p53和PCNA表达

目的：对乳腺导管原位癌进行病理形态分析，并行ｃ－ｅｒｂＢ－２、ｐ５３癌基因蛋白、增殖细胞核抗原（ＰＣＮＡ）表达以及相关性的研究，以期为临床判断潜在恶性程度及预后提供参考指标。方法：运用病理形态分析以及枸橼酸－微波－ＡＢＣ免疫组化法对２５例常规福尔马林固定、石蜡包埋乳腺导管原位癌组织进行回顾性研究。结果：（１）２５例乳腺原位导管癌ｃ－ｅｒｂＢ－２、ｐ５３、ＰＣＮＡ表达的阳性率分别为３６．０％，４０．０％和４０．０％；（２）粉刺型ｃ－ｅｒｂＢ－２、ｐ５３、ＰＣＮＡ表达的阳性率均高于非粉刺型，而且ｃ－ｅｒｂＢ－２阳性率相差有显著性（Ｐ＜０．０５）；（３）坏死、核异型性、核分裂数与ｃ－ｅｒｂＢ－２、ｐ５３、ＰＣＮＡ的表达有关，其中，坏死与ＰＣＮＡ阳性表达显著相关（Ｐ＜０．０５），核异型性与ｃ－ｅｒｂＢ－２蛋白表达显著相关（Ｐ＜０．０５）。结论：乳腺导管原位癌无论病理形态还是生物学行为都是异质性的，除了组织学亚型，某些形态指标以及ｃ－ｅｒｂＢ－２癌基因蛋白的表达也可作为恶性度指标。     

免疫组化和PCR—SSCP检测p53基因异常的一致性探讨

目的：探讨免疫组化检测ｐ５３蛋白表达和ＰＣＲ－ＳＳＣＰ检测ｐ５３基因突变的一致性。方法：单克隆抗体ＤＯ－７检测８５例非小细胞肺癌（ＮＳＣＬＣ）的ｐ５３蛋白表达，ＰＣＲ－ＳＳＣＰ检测其中３１例腺癌的ｐ５３基因突变。结果：８５例ＮＳＣＬＣ中ｐ５３蛋白表达阳性率为６８％（５８／８５），３１例腺癌中ｐ５３蛋白表达阳性率为６１％（１９／３１），１４例（４６％）出现ｐ５３基因５～８外显子突变，ｐ５３蛋白免疫组化和ＰＣＲ－ＳＳＣＰ检测ｐ５３基因突变无显著相关（χ２＝０．１，Ｐ＝０．７６），其一致率为５２％。结论：ｐ５３蛋白表达并不能很好地反映ｐ５３基因突变。     

乳腺癌和癌前病变中细胞凋亡及其与bcl-2、PCNA表达的关系

目的：探讨细胞凋乳腺癌变过程中的作用及其与细胞增殖以及ｂｃｌ－２、ＰＣＮＡ表达的关系。方法：利用ＴＵＮＥＬ法及免疫组化Ｓ－Ｐ法检测５４例乳腺癌及２７例非癌病变中细胞凋亡指数（ＡＩ）以及ｂｃｌ－２、ＰＣＮＡ的表达,同时计算核分裂指数（ＭＩ）。结果：“正常”乳腺上皮、增生性导管、原位主浸润性癌的Ａ少ＭＩ分别为：０．１０％±０．１２％、０．３１％±０．４３％、０．４１％±０．２１％、０．７４％±０．５６     

伯基特淋巴瘤与EB病毒的关系及其p53和bcl-2蛋白的表达

目的 了解柏基特淋巴瘤和ＥＢ病毒的关系及ｐ５３和ｂｃｌ－２蛋白的表达。方法 采用ＰＣＲ、原位ＰＣＲ及免疫组化ＬＳＡＢ方法,检测了２８例伯基特淋巴瘤石蜡包埋的组织块。结果 发现８例ＥＢ病毒ＤＮＡ阳性,阳性率为２８．５％,８例阳性病例做了原位杂交,其中３例为阳性。２７例做了ｐ５３和ｂｃｌ－２免疫组化检测,生病例各为１２例（４４．４％）和１３例（４８．１％）。Ⅰ￣Ⅱ期和Ⅲ￣Ⅳ期ｐ５３和ｂｃｌ－２阳性病例     

肝细胞癌及癌旁肝组织中bcl-2和p53蛋白表达与端粒酶活性的相关性研究

目的：探讨ｂｃｌ２ 和ｐ５３ 蛋白的表达与端粒酶活性的相关性及其与 Ｈ Ｃ Ｃ 发生的关系。方法：利用端粒酶原位标记法显示端粒酶活性,采用 Ｓ Ｐ 法免疫组化技术检测ｂｃｌ２ 和ｐ５３ 蛋白。结果：端粒酶在 Ｈ Ｃ Ｃ 中的阳性率（９１７ ％ ） 显著高于癌旁肝组织（５８３ ％ ）（ Ｐ＜ ００５） ,端粒酶活性强度与 Ｈ Ｃ Ｃ 分化程度无关（ Ｐ＞ ００５） ;癌组织中ｂｃｌ２ 和ｐ５３ 蛋白的阳性率均高于癌旁组织（ Ｐ＜ ００１） ; Ｈ Ｃ Ｃ 和癌旁组织中端粒酶活性程度随ｂｃｌ２ 蛋白表达增强而升高,并呈明显正相关,但与ｐ５３ 蛋白表达强度无明显相关性。结论：ｂｃｌ２ 蛋白的过度表达可能是端粒酶激活的重要途径之一,ｂｃｌ２ 蛋白过度表达可能通过激活端粒酶使肝细胞恶性转化导致 Ｈ Ｃ Ｃ 发生,而ｐ５３ 基因突变可能对端粒酶的激活无直接影响。     

c-erbB-2、p53、bcl-2和nm23-H1在肺癌中的表达

目的：探讨ｃｅｒｂＢ２、ｐ５３、ｂｃｌ２和ｎｍ２３Ｈ１基因在肺癌发生发展过程中的作用。方法：用免疫组化ＡＢＣ法对原发性肺癌组织中４种基因的表达和突变进行检测。结果：５８例肺癌中,３１例（５３４５％）ｐ５３过度表达,１８例（３１０３％）ｂｃｌ２过度表达。ｃｅｒｂＢ２与ｎｍ２３Ｈ１在１０例小细胞肺癌（ＳＣＬＣ）中未见表达。而在４８例非小细胞肺癌（ＮＳＣＬＣｓ）中两者过度表达率均为５０％。ｃｅｒｂＢ２与ｎｍ２３Ｈ１表达呈正相关（Ｐ＜００５）。腺癌ｎｍ２３Ｈ１的表达明显高于鳞癌（Ｐ＜００５）。ｐ５３、ｂｃｌ２蛋白表达在肺癌分化程度中呈负相关（Ｐ＜００５）。ｎｍ２３Ｈ１、ｐ５３和ｂｃｌ２的表达与患者的生存率有关（Ｐ＜００５）。结论：ｃｅｒｂＢ２、ｐ５３、ｂｃｌ２和ｎｍ２３Ｈ１基因蛋白产物的检测对肺癌患者的诊治和预后评估有积极意义。     

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.     

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.     

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.