IL-1、hs-CRP和亚临床甲减与妊娠期糖尿病的相关性研究

目的 探讨亚临床甲减、IL-1及hsCRP对妊娠期糖尿病的影响及其相关性.方法 选取2014年5月至2016年3月在唐山市协和医院妇产科检查的SCH合并GDM孕中期孕妇138例为观察组,根据促甲状腺素(TSH)的值,将其分为轻度亚临床甲减A组82例(TSH 2.5~4.22 mIU/L),重度亚临床甲减B组56例(TSH≥4.22 mIU/L).另选同期甲状腺功能正常的GDM孕妇50例为对照组.采用罗氏Cobas e601化学发光分析仪检测促甲状腺素(TSH)、甲状腺过氧化物酶抗体(TPOAb)、空腹胰岛素(FINS);ELISA法检测血清白细胞介素1(IL-1);运用贝克曼DXC800全自动生化分析仪检测超敏C反应蛋白(hs-CRP),空腹血糖(FBS),糖化血红蛋白(HbA1c),计算胰岛素抵抗指数(HoMA-IRII),对结果进行分析比较.结果 研究B、A组TPOAb 、HoMA-IRI、IL-1、hsCRP水平高于对照组,研究B组IL-1、hsCRP高于研究A组,差异有统计学意义(P< 0.05);研究B组IRI高于研究A组和对照组,差异有统计学意义(P<0.05).研究A、B组TSH、IL-1、hsCRP与HoMA-IRI呈正相关,IL-1、hsCRP与TSH呈正相关,差异有统计学意义(P<0.05).结论 IL-1、hsCRP可能在SCH合并GDM的发生发展过程中起重要作用,SCH与GDM发生有一定相关性.     

甲状腺功能减退合并妊娠期糖尿病孕妇IGF-1、IL-6、TNF-α检测的临床意义

目的 探讨甲状腺功能减退合并妊娠期糖尿病孕妇血清IGF-1、IL-6、TNF-α的变化及临床意义.方法 选取2016年3月至2017年3月在唐山市协和医院妇产科检查的甲状腺功能减退或亚临床甲状腺功能减退合并GDM孕妇70例.根据甲状腺功能分为甲减合并GDM组(A组)32例;亚临床甲减合并GDM组(B组)38例;另选同期健康体检孕妇40例为对照组.采用罗氏Cobas e601化学发光分析仪检测促甲状腺素(TSH),血清游离甲状腺素(FT4);ELISA法检测血清胰岛素样生长因子(IGF-1),白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α),并对结果进行分析比较.结果 A组和B组IL-6和TNF-α水平高于对照组,IGF-1低于对照组;A组IL-6和TNF-α水平高于B组,IGF-1低于B组,差异有统计学意义(t=4.681～10.784,P＜0.05).A组和B组患者血清IL-6、TNF-α与TSH均呈正相关,IGF-1与TSH呈负相关;A组IL-6、TNF-α与FT4呈负相关,IGF-1与FT4呈正相关(γ=0.287 ～0.438,P＜0.05).结论 IGF-1、IL-6和TNF-α在甲减、亚临床甲减合并GDM的发病中起重要作用,这三种细胞因子水平的检测有助于探讨其在共病中的原因,从而指导疾病的诊断和治疗,具有一定的临床意义.     

亚临床甲状腺功能减退症孕妇左旋甲状腺素治疗剂量及影响因素探讨

目的 探讨亚临床甲状腺功能减退症孕妇患者行L-T4替代治疗的剂量以及影响因素.方法 选取我院收治的62例亚临床甲状腺功能减退症孕妇患者进行L-T4替代治疗,根据TSH值分为A组(TSH＞ 5.0mIU/L)和B组(2.5 mIU/L≤TSH≤5.0mIU/L),治疗过程中根据患者的TSH水平对L-T4的治疗剂量进行调整直至治疗达标,其中妊娠中晚期(0.3mIU/L＜ TSH＜ 3.0mIU/L),妊娠早期(0.3mIU/L＜ TSH＜ 2.5mIU/L).结果 亚临床甲状腺功能减退症患者TSH基线水平与L-T4替代治疗达标剂量呈正相关性(r=0.543,P＜0.01);TSH治疗达标时,A组L-T4替代治疗的剂量显著高于B组(P＜0.01);甲状腺自身抗体阳性组L-T4替代治疗的剂量显著高于阴性组(P＜0.05).结论 TSH基线水平以及甲状腺自身抗体状况可能会对亚临床甲状腺功能减退症孕妇行L-T4治疗的达标剂量产生影响.     

唐山地区2012～2014年孕早期亚临床甲状腺功能减退的调查分析

目的 了解唐山地区2012 ～2014年孕早期亚临床甲减(SCH)发病情况,以减低SCH对孕妇及胎儿造成的不良后果.方法 对首次产检的孕妇建卡并进行游离甲状腺素(FT4)、促甲状腺激素(TSH)、甲状腺过氧化物酶抗体(TPO-Ab)、甲状腺球蛋白抗体(Tg-Ab)的检测,选取TSH＞ 2.5 mIU/L,F-T4浓度正常的孕妇,设计专用表格,记录孕妇的体能检查指征及相关病史.结果 孕妇的SCH发病率逐年升高,年龄＞30岁孕妇的SCH发病率较高,SCH孕妇复发性流产的发病风险较对照组升高,SCH孕妇的甲状腺自身抗体阳性比例较高.结论 唐山地区的孕妇孕早期SCH的发病率逐年上升,且有较高的复发流产比率,应该加大对于亚甲减的早期检测、干预,降低对孕妇及胎儿造成不良后果.     

亚临床甲减并发妊娠期糖尿病的临床分析

目的 探讨孕中期亚临床甲减孕妇并发妊娠糖尿病的发生率及糖代谢的变化,并分析其临床特点.方法 选取2010年1月至2013年1 1月在唐山市妇幼保健院诊断为亚临床甲减(SCH)的孕妇635例.对SCH孕妇给予左旋甲状腺激素(L-T4)治疗,治疗目标为TSH 0.3-2.5 mlU/L,按治疗效果分为治疗达标组401例,治疗未达标组234例.另选择同期正常孕妇300例作为对照组.在孕中期(24～ 28周)进行甲状腺功能(TSH、FT4、FT3)检测及75g葡萄糖耐量试验(OGTT),比较各组妊娠期糖尿病(GDM)的发病率及OGTT结果.结果 治疗未达标组GDM的发生率明显高于治疗达标组和对照组,差异有统计学意义(x2=17.22,15.04,P ＜0.05);治疗未达标组OGTT空腹和1h血糖值明显低于治疗达标组和对照组,差异有统计学意义(P值均＜0.05).结论 未积极治疗或治疗未达标的SCH孕妇较正常孕妇更容易发生GDM,甲状腺激素的补充治疗有助于降低SCH孕妇的GDM发病率.     

妊娠亚临床甲减患者血清TSH、TPO-AB水平与妊娠结局的相关性研究

目的探讨妊娠期合并亚临床甲状腺功能减退(亚甲减)患者血清促进甲状腺素(TSH),甲状腺过氧化物酶抗体(TPOAb)水平与妊娠结局的关系。方法选取2016年1月至2017年2月在我院定期接受产前检查、定期围产保健且住院分娩的亚甲减患者300例,根据有无接受治疗分为亚甲减治疗组(n=189)和亚甲减未治疗组(n=111);根据血清TSH中位数水平分为高TSH水平组(n=95)和低TSH水平组(n=205);并根据血清TPOAb检测是否为阳性分为TPOAb阳性组(n=182)与TPOAb阴性组(n=118)。另选取同期300例健康孕妇为对照组。对各组妊娠结局进行统计分析。结果亚甲减未治疗组流产、早产、GDM、妊娠期高血压疾病、胎儿生长受限、低出生体重儿发生率均明显高于亚甲减治疗组及对照组(P<0.05)。亚甲减孕妇中,高TSH水平组流产、早产、GDM、妊娠期高血压疾病、胎儿生长受限、低出生体重儿发生率均明显高于低TSH水平组(P<0.05);TPOAb阳性组流产、早产、GDM、妊娠期高血压疾病、低出生体重儿发生率均明显高于TPOAb阴性组(P<0.05)。结论妊娠合并亚甲减可增加流产、早产、GDM、妊娠期高血压疾病、胎儿生长受限、低出生体重儿发生率,且血清TSH水平越高及TPOAb阳性,不良妊娠结局风险越高。     

妊娠早期孕妇发生亚临床甲减的影响因素分析

目的调查本地区妊娠早期孕妇发生亚临床甲减(SCH)的患病情况及分析其影响因素。方法采用横断面流行病学调查方法,纳入妊娠早期孕妇2036例,按照TSH、FT4水平分为亚甲减组、正常对照组,描述两组孕妇一般情况,比较两组间实验室检测指标等因素的差异。结果2036例孕妇中亚甲减组116例(5.7%)。亚甲减组年龄、孕次、BMI的均值高于正常组,差异具有统计学意义(P<0.05)。实验室检测指标分析,亚甲减组血清TSH、TG-Ab、CHO水平高于正常组,FT4水平低于正常组,差异均有统计学意义(P<0.05)。多因素Logistic回归分析显示BMI[OR=2.187(1.593~3.003)]、孕次[OR=2.584(1.184~5.638)]是妊娠早期发生亚临床甲减的危险因素(P<0.05);而FT4[OR=0.630(0.496~0.800)]则是其保护因素(P<0.05)。结论BMI、孕次是妊娠早期亚临床甲状腺功能减退发生的独立危险因素,低水平FT4也是以后发生SCH的危险因素,应积极检测并预防,以降低不良妊娠结局的发生。     

促甲状腺激素和甲状腺自身抗体在甲状腺疾病中的诊断价值分析

目的分析促甲状腺激素和甲状腺自身抗体在甲状腺疾病中的诊断价值。方法选取本院2018年6月至2019年3月收治的82例甲状腺疾病患者作为研究组,其中甲状腺机能减退症患者(甲减)29例、毒性弥漫性甲状腺病患者(GD)32例、桥本甲状腺炎患者(HT)21例。另外选择同期本院体检的30例健康者作为对照组。对所有研究对象的TSH、TRAb、TGAb以及TPOAb指标进行检测,汇总并观察不同疾病4种指标变化情况。结果 GD组、甲减组、HT组患者的TGAb、TPOAb血清水平明显高于对照组,差异具有统计学意义(P0.05);GD组患者TSH血清水平明显低于对照组,TRAb血清水平显著高于对照组(P0.05);甲减组患者TSH血清水平明显高于对照组,差异具有统计学意义(P0.05)。结论促甲状腺激素和甲状腺自身抗体可以一定程度反映患者甲状腺疾病情况,可为临床上提供诊断甲状腺疾病的原始资料,值得推广应用。     

甲状腺功能减退与妊娠期血栓前状态的相关分析

目的 探讨甲状腺功能减退对凝血功能的影响,分析甲状腺功能减退与妊娠期血栓前状态的相关性.方法 选取2012年1月至2017年2月我院临床甲状腺功能减退孕妇46例为甲减组,亚临床甲状腺功能减退孕妇39例为亚临床甲减组,随机抽取50例甲状腺功能正常且无合并其他疾病的健康孕妇为对照组,比较3组受试者的甲状腺功能与凝血功能相关指标.结果 与对照组比较,甲减组的促甲状腺激素(TSH)、纤维蛋白(FIB)较高,游离甲状腺素(FT4)、凝血酶原时间(PT)较低,亚临床甲减组TSH较高,PT较低,差异均有统计学意义(P＜0.05).甲减组与亚临床甲减组比较,甲减组FIB较高,差异有统计学意义(P＜0.05).结论 甲状腺功能减退会导致妊娠期血栓前状态,增加患者体内血栓形成的风险,临床上应予重视并给予积极治疗.     

中老年女性亚甲减症与骨密度的相关性分析

目的 探讨中老年女性亚临床甲状腺减退症与骨密度(bone mineral density,BMD)的相关性.方法 收集中老年女性亚临床甲状腺减退症(亚甲减)及健康体检者的骨密度及部分生化指标的检测结果,并进行对比分析.结果 中老年女性亚甲减组与正常对照组相比,亚临床甲减组的骨密度测定中T值下降(P＜0.05);生化指标中25羟基维生素D3水平低于对照组(P＜0.05),ALP和PTH无统计学意义(P＞0.05);甲状腺功能检测FT4和T4在正常范围内有一定程度的下降(P＜0.05).结论 亚甲状腺功能减退症可能引起骨量丢失,骨密度降低,亚临床甲状腺功能减退患者的骨密度受血清促甲状腺激素(TSH)的影响.     

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。