体外循环中血浆ET-1、TXB2及6-Keto-PGF1α水平变化的探讨

目的:探讨体外循环心内直视手术期间血浆内皮素-1(ET-1)、血栓素B2(TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1α)水平变化及临床意义.方法:采用放射免疫分析分别于8个时点测定20例心内直视手术病人血浆ET-1、TXB2和6-Keto-PGF1α水平.结果:血浆ET-1水平从开放主动脉后即刻(T3)开始明显升高,至CPB停机后6h(T6)达高峰,之后逐渐下降,但仍明显高于手术前(T1)水平(P＜0.01);TXB2水平在阻断主动脉即刻(T2)时逐渐升高,在T3时点达到最高峰,之后水平逐渐下降,至CPB停机后12h(T7)降至正常水平;血浆6-Keto-PGF1α水平从T2时点起急剧升高,T3时点时达最高峰,之后水平逐渐下降,至CPB停机后24h(T8)基本恢复至正常水平.结论:在CPB期间及CPB后动态监测病人血浆ET-1、TXB2及6-Keto-PGF1α可帮助综合判断病人情况,并可根据不同的激素代谢水平变化进行相应处理,如加入内皮素、血栓素A2拮抗剂或前列环素合成剂等,削弱缩血管效应,利于病人早期恢复.     

sCLU蛋白、S100B和NSE在早产儿脑损伤早期诊断中的应用价值

目的:探讨血清分泌型丛生蛋白(sCLU)、S100钙结合蛋白B(S100B)及神经元特异性烯醇化酶(NSE)在早产儿脑损伤(BIPI)早期诊断中的应用价值。方法:选择2018-08—2020-10在泰兴市人民医院住院治疗的98例早产儿作为研究对象,早产儿脑损伤48例作为脑损伤组,早产儿无脑损伤50例为对照组,所有患儿分别于生后1h、12h、3天采集静脉血测定血清sCLU、S-100B蛋白、NSE浓度,通过ROC曲线评价各项指标对早产儿脑损伤的早期诊断效能。结果:脑损伤组患儿出生后1h和12h sCLU、S100B水平均高于对照组,差异有统计学意义(P均0.01)。脑损伤组:与出生后1h比较,出生后12h sCLU水平升高(P0.01),出生后3天sCLU水平降低(P0.01);与出生后12h比较,出生后3天sCLU水平降低(P0.01)。与出生后1h和12h比较,出生后3天S100B水平降低(P0.01)。脑损伤组出生后1h、12h, 3天NSE水平均高于对照组,差异有统计学意义(P均0.01)。脑损伤组与出生后1h比较,出生后12h和3天NSE水平均升高(P0.01)。出生后12h(sCLU+NSE)联合检测对早产儿脑损伤具有较高诊断价值,其敏感度和特异度分别为91.60%、97.10%,AUC值也是最大的为0.926。结论:脑损伤早产儿血清中sCLU、S100B、NSE水平呈动态变化,sCLU、NSE联合检测对BIPI具有较好的的诊断价值。     

金纳多对体外循环脑损伤的保护作用

目的观察金纳多对体外循环脑损伤的保护作用。方法择期行风湿性心脏病二尖瓣置换术患者40例，美国麻醉医师协会分级Ⅱ～Ⅲ级，按随机数字表法随机分为银杏叶提取物组（EGB组）和对照组各20例。银杏叶提取物组（20例）：体外循环管道预充乳酸林格氏液中加入银杏叶提取物注射液1mg／kg；对照组（20例）：体外循环预充乳酸林格氏液。分别于体外循环开始前（T1）、体外循环开始后30min（T2）、体外循环结束时（L）、体外循环结束后2h（T4）、体外循环结束后6h（T5）、体外循环结束后12h（T6）、体外循环结束后24h（T7）7个时间点同步采集桡动脉及颈内静脉血，动脉血进行血气分析，静脉血测定血清S-100β蛋白、神经元特异性烯醇化酶（neuron specific enolase，NSE）浓度。结果CPB开始后即有血清S-100β蛋白和NSE浓度升高，EGB组S-100β蛋白和NSE浓度明显低于对照组，且其达峰时间提前。结论银杏叶提取物能改善脑氧供需平衡，明显减少血清脑损伤标志物S-100β蛋白和NSE的浓度升高，有明确的脑保护作用。     

心脏停跳体外循环(CPB)直视术血清肌钙蛋白I的变化

本 文观察对比了 2 3例心脏停跳心内直视术 (CPB)病人术前和术后不同时间段的心肌肌钙蛋白I(cTnI)的动态变化 ,以评价CPB对心肌损伤的程度。1　资料与方法1.1　一般资料2 3例病人均为房间隔缺损 ,其中男性 15例 ,女性 8例 ,年龄在 6岁～ 2 5岁 ,术前经心脏彩超检查确诊 ,肝、肾、肺等功能正常。1.2　方法2 3例患者右房切口行CPB修补术 ,平均CPB时间 5 0min。术前和术后 2h、6h、2 4h、5天、10天和 15天采集静脉血分离血清 ,用微粒子酶免法 (仪器为 :AXSYM全自动免疫分析仪 )测cTnI含量。2　结　果2 3例患者术前cTnI浓度 0 .2 6± …     

浅低温体外循环围术期血清炎症介质的变化

目的 探讨浅低温体外循环围术期炎症介质的释放规律。方法 按入选标准筛选先天性心脏病患者24例，均采用浅低温体外循环心脏直视术，用酶联免疫吸附法测定患者术前（T1）、CPB30min（T2）、CPB结束后2h（T3）、12h（T4）、24h（T5）各时间点血清IL-6、IL-8、IL-10的浓度。结果 所有患者血清IL-6、IL-8、IL-10浓度在CPB开始后均升高（P〈0，01），于术后2h（T3）逐渐达高峰，术后12h（T4）逐渐下降，术后24h（T5）虽仍高于术前（T1）水平，但较高峰时（T3）已明显下降。结论 浅低温CPB术后患者血清IL-6、IL-8、IL-10浓度逐渐升高．术后2h达高峰．并于24h内恢复接近正常水平。     

肺开放策略对体外循环白细胞介素的影响

目的研究肺开放策略(OLC)对体外循环(CPB)手术后白细胞介素的影响。方法选择24例心内直视手术患者,随机分成常规机械通气组(CMV)、早期肺开放组(EOL)、晚期肺开放组(LOL)。EOL组在气管插管后实施OLC,LOL组到达ICU后30min实施OLC;分别于术前、CPB后及到ICU后3、5、24、48h以酶联免疫吸附反应(ELISA)技术测定白细胞介素-6(IL-6)、白细胞介素-8(IL-8)和白细胞介素-10(IL-10)水平。结果各组CPB后IL-8、IL-10、IL-6均较术前显著升高(P<0.01或P<0.05),组间比较差异无显著性(P>0.05)。IL-8水平在两肺开放组呈显著下降趋势,EOL组在到ICU后24h恢复术前水平,LOL组在到ICU后48h后恢复术前水平,但CMV组各时点均显著高于术前(P<0.01或P<0.05)。IL-10水平只在EOL组呈显著下降趋势,EOL组在到ICU后5h即恢复术前水平,而LOL组及CMV组在到ICU后24h仍显著高于术前(P<0.01或P<0.05)。未见OLC对IL-6的显著影响,各时点组间IL-6的差异无显著性(P>0.05)。结论OLC可减轻CPB相关的肺损伤从而减少炎性细胞因子的释放,早期实施OLC优于晚期实施OLC。     

右美托咪定对肝移植患者术后脑损伤的影响

目的：探讨右美托咪定(DEX)对肝移植患者术后脑损伤的影响。方法40例择期行肝移植患者随机分为两组院DEX组和生理盐水组(NS组)。麻醉诱导前DEX组给予DEX负荷量0.5μg/kg,10 min内泵注完毕后以维持量0.5μg/kg/h继续泵注至手术结束;在相同时间内NS组给予等量生理盐水,余同DEX组。分别于术前(T0),切肝前60 min (T1),无肝期10 min(T2)、60 min(T3),新肝期10 min(T4)、60 min (T5)及术毕(T6)时记录血流动力学指标,抽取颈内静脉球部血液,测定血清中星型胶质细胞S-100β蛋白(S-100β蛋白)及神经元特异性烯醇化酶(NSE)水平。结果与NS组比较,DEX组HR于T1~T6时降低(<0.05,<0.01)。与NS组比较,DEX组MAP、CVP和Hb差异无统计学意义(>0.05)。与T0比较,NS组和DEX组S-100β蛋白、NSE水平分别于T1~T6时均升高(<0.05,<0.01);与NS组比较,DEX组S-100β蛋白、NSE水平分别于T1~T6时均降低(<0.05,<0.01)。结论 DEX用于肝移植患者可减轻脑损伤,具有一定的神经保护作用。     

常规与微创冠脉搭桥术围手术期血浆S100-B蛋白水平的相关研究

目的: 通过测定体外循环和非体外循环条件下冠脉搭桥术患者血浆S100-B蛋白水平的变化，比较2种手术方式对脑损伤程度有无不同，探讨术中影响血浆S100-B蛋白水平变化的相关因素。方法: 30例择期行冠脉搭桥术的患者，分为体外循环组（CPB group，A组）和微创非体外循环组（non-CPB group，B组）,每组均为15例。于术前、麻醉后、主动脉侧壁钳开放时、术毕时、术后2 h、6 h、12 h和24 h采血测血浆S100-B蛋白浓度。结果： （1） 两组患者血浆S100-B蛋白浓度均在升主动脉侧壁钳开放时显著高于术前，且A组患者血浆S100-B蛋白浓度峰值是B组的3倍多（2.32±0.26 μg/L和0.71±0.14 μg/L）,之后逐渐降低，到术后24 h基本接近正常。（2） 术中患者血浆S100-B蛋白升高水平与体外循环转机时间或心表手术操作时间呈正相关（A组：r＝0.659，P＜0.05;B组：r＝0.584, P＜0.05）。结论： 血浆S100-B蛋白水平可以用来评价2种冠脉搭桥术对脑的损伤程度，术后连续检测对于诊断脑损伤并及时采取相应预防措施具有重要价值;非体外循环微创冠脉搭桥术较常规体外循环下手术更能够有效降低对脑损伤的程度和术后出现神经功能障碍的风险。     

体外循环瓣膜置换术时IL-6、IL-8、IL-10水平的变化

目的:观察体外循环心内直视手术中及术后促炎因子白细胞介素-6(IL-6)、白细胞介素-8(IL-8)和抗炎因子白细胞介素-10(IL-10)水平的变化。方法:随机选择12例择期行瓣膜置换术、心功能II~IV级的风湿性心脏病患者,分别于下列9个时点采取混合静脉血7mL:麻醉诱导前、诱导后30min、主A阻断后30min、主A开放后10min、主A开放后30min、体外循环(CPB)后30min、CPB后8h、术后24h、术后72h。以3000r／min转速离心10min后留取上清液,酶联免疫吸附反应(ELISA)技术测定细胞因子IL-6、IL-8及IL-10水平。术中输入晶胶体液及血管活性药物维持血流动力学稳定。结果:自主A开放后30min-术后72hIL-6、IL-8水平显著升高,抗炎因子IL-10水平自主A阻断后30min-术后72h也升高。各参数的峰值都位于CPB结束后30min。结论:体外循环瓣膜置换术可使血中IL-6、IL-8和IL-10水平产生明显变化,这些变化于CPB后30min达到高峰,并持续至术后数日。     

高迁移率族蛋白B1在脂多糖致幼年大鼠脑损伤中的表达

目的 探讨高迁移率族蛋白B1(high mobility gnmp box 1,HMGB1)在脂多糖(LPS)致幼年大鼠脑损伤中的表达变化.方法 SD大鼠随机分为对照组(NS组,n=80),颈外动脉注射生理盐水;脂多糖组(LPS组,n=80),颈外动脉注射LPS,于注射药物后6、12、24、48、72 h处死,甲酰胺法测脑组织伊文思蓝(EB)含量;免疫组织化学技术检测脑组织HMGBI、神经元特异性烯醇化酶(NSE)、胶质纤维酸性蛋白(GFAP)的表达;RT-PCR技术检测HMGB1 mRNA的表达变化.结果 LPS组脑组织的EB含量、NSE、GFAP蛋白表达均为6 h开始增加,24 h达高峰;HMGB1蛋白及HMGB1 mRNA于6 h开始增加,24 h达高峰,与EB含量、NSE、GFAP蛋白含量呈正相关.各时间点与NS组比较,差异显著.结论 HMGB1可能作为晚期炎症因子参与LPS致脑损伤的发生发展过程.     

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。