β-连环蛋白和细胞周期蛋白D1在宫颈癌组织中的表达及意义

目的：探讨宫颈癌组织中β-连环生白（β-cat）和细胞周期蛋白DI（cyclin D1）的表达及其意义。方法：应用免疫组织化学卵法．检测68例宫颈癌（UCC）、22例宫颈上皮内瘤变（CIN）和10例正常宫颈（NCE）组织中β-cat与cyclin DI的表达,分析两者表达与宫颈癌临床病理特征的关系。结果：正常宫颈组织、宫颈上皮内瘤变组织和宫颈癌（Ⅰ～Ⅱa期）组织中,β-cat异常表达率分别为0％、45．5％、69．1％（P〈0．01）,cyclinD1阳性表达率分别为10．O％、40．9％和60．3％（P〈0．01）;两者异常表达与宫颈癌的临床分期、病理分级和淋巴结转移均有关（P〈0．05）,与患者的年龄、原发灶大小及病理组织类型均无关（P〉0．05）;两者表达有显著的正相关性（P〈0．01）。结论：β-cat异常表达可能通过激活靶基因cyclinD1过度表达,参与了宫颈癌的发生与发展。     

p16、Rb和cyclin D1蛋白在横纹肌肉瘤中的表达及其意义

目的：探讨细胞周期相关蛋白表达异常与横纹肌肉瘤（RMS）的关系。方法：应用S－P免疫组化方法观察p16,Rb和cyclinD1蛋白在RMS中的表达状态。结果：p16,Rb和cyclinD1蛋白表达阳性率分别为55．3％,61．7％和51．1％,在胚胎性横纹肌肉瘤（ERMS）,p16和Rb蛋白表达阳性率为75．0％（21／28）和67．9％（19／28）,明显高于在腺泡状横纹肌肉瘤（ARMS）中的表达（P＜0．05）,p16蛋白阳性率在I,Ⅱ级横纹肌肉瘤分别为75．0％和73．3％,高于Ⅲ级横纹肌肉瘤（45．0％）;p16蛋白阴性及cyclinD1蛋白过表达组,局部浸润,复发或转移发生率高于p16蛋白阳性及cyclinD1蛋白阴性组;11／47例（23．4％）出现两种以上蛋白表达异常。结论：P16,Rb和cyclinD1蛋白异常可能与部分横纹肌肉瘤发生发展有关,且横纹肌肉瘤的发生可能涉及两种以上基因异常。     

PTEN/MMAC1蛋白在42例原发性肺癌中的表达研究

目的 研究抑癌基因PTEN／MMAC1在原发性肺癌中的表达状况及其临床意义。方法 应用SP免疫组织化学方法检测42例手术切除肺癌标本PTEN的表达。结果 （1）肺癌组PTEN蛋白表达总缺失率为40．48％，小细胞癌表达缺失率75．00％，鳞癌31．58％，腺癌33．33％。肺癌细胞的分化程度不同，其PTEN表达缺失存在明显差别，高分化和低分化肺癌PTEN表达缺失率分别为13．33％，72．73％（P＜0．01）；鳞癌高分化组缺失率为12．50％，低分化组缺失率为66．67％（P＜0．05）；腺癌高分化组缺失率为14．29％，低分化组缺失率为80．00％（P＜0．05）；本组有淋巴结转移组与无淋巴结转移组缺失率分别为66．67％，25．93％，两者之间有显著差异（P＜0．01），不同的临床分期间PTEN缺失率亦有显著的差别，Ⅲa期缺失率较高。生存时间≤12月，＜60月，＞12月，≥60月，PTEN蛋白缺失率分别为71．43％，25．00％，14．29％，三者之间差异显著（P＜0．05）。结论 肺癌PTEN／MMAC1在蛋白质水平的表达缺失可能有助于其预后的判断。     

β-链接素和基质金属蛋白酶-7在结直肠腺瘤一腺癌组织表达的意义

目的 探讨β-链接素(β-cat)和基质金属蛋白酶7(MMP-7)表达与结直肠癌发牛发展和浸润转移的关系。方法制作结直肠腺瘤-腺癌组织芯片，免疫组织化学检测β-cat和MMP-7在结直肠腺瘤-腺癌组织的表达。结果(1)β-cat胞核异常表达率在腺瘤癌变组织(35．9％)显著高于腺瘤(16．7％)及腺癌组织(19．7％，P＜0．05)：(2)腺瘤伴重度异度增生者β-cat胞质、胞核异常表达率显著高于轻度者(P＜0．05)。(3)溃疡型、淋巴结转移阳件及C-D期腺癌组β-cat胞核异常表达率均显著高于降起型、淋巴结阴性及A-B期组(P＜0．05或P＜0．01)。(4)MMP-7阳性表达率在腺癌组织(69．2％)显著高于正常黏膜(15．0％)、腺瘤(35．0％)及癌变组织(46．2％，P＜0．05或P＜0．01)。(5)溃疡型、淋巴结转移阳性及C-D期腺癌组MMP-7阳性表达率均显著高于隆起型、淋巴结阴性及A-B期腺癌组(P＜0．05)。(6)β-cat胞质、胞核异常表达与MMP-7阳性表达显著正相关(P＜0．01)。结论 β-cat胞质及胞核异常表达与结直肠癌的发生密切相关，可能是结直肠癌发生的早期事件；同时β-cat还可能通过胞核易位增强其下游靶基因MMP-7的降解作用促进结直肠癌浸润转移。     

HIF-1α和VEGF在宫颈癌中的表达及相关性研究

目的：探讨缺氧诱导因子-1α（HIF-1α）及血管内皮生长因子（VEGF）在宫颈癌发生发展过程中蛋白表达情况及两者的相关性。方法：应用免疫组织化学S-P方法检测10例正常宫颈（NCE）、18例宫颈上皮内瘤变（CIN）、77例宫颈癌（ICC）组织中HIF-1α和VEGF蛋白的表达情况。结果：在正常宫颈上皮、宫颈上皮内瘤变组织、宫颈癌（Ⅰ—ⅡA期）组织中，HIF．1d蛋白的阳性表达率分别是0．00％、33．33％、70．13％（P〈0．05），VEGF蛋白的阳性表达率分别为10．00％、44．44％、74．00％（P〈0．05）；且随HIF—1α表达增强，VEGF阳性表达率递增，两者呈正相关（P〈0．05）。结论：HIF-1α及VEGF的表达与宫颈癌的发生发展密切相关且两者呈正相关，HIF-1α蛋白可能以转录激活的形式上调VEGF基因的表达，诱导血管生成，促进了宫颈癌的发生发展。     

卵巢上皮性肿瘤中Skp2、p27kipl、E-cad的表达

目的检测Skp2、p27kipl和E-cad在卵巢上皮性肿瘤中的表达情况及其相互关系。方法采用免疫组化SP法，检测99例卵巢上皮性肿瘤组织中Skp2、p27kipl及E-cad的表达。结果p27kipl在卵巢良性肿瘤、交界性肿瘤的表达率分别为76．5％、70．6％高于卵巢癌29．2％（P〈0．05），在早期癌中的表达高于晚期癌（P〈0．05）。Skp2在卵巢良性肿瘤、交界性肿瘤的表达率分别为0、23．5％，均低于卵巢癌50．8％（P〈0．05），在早期癌的表达低于晚期癌（P〈0．05）。卵巢癌中skp2表达与组织分化有关，在低分化癌的阳性表达率高于高分化癌（P〈0．05），在组织学类型方面，浆液性癌中skp2的阳性表达率高于非浆液性癌（P〈0．05）。E—cad在良性肿瘤、交界性肿瘤和卵巢癌表达率分别为88．2％、82．4％、55．4％，恶性组低于良性组（P〈0．05）。E—cad在早期癌的表达率高于晚期癌（P〈0．05）。Skp2表达与p27kipl表达呈负相关（P〈0．05），E-cad表达与p27kipl表达呈正相关（P〈0．05），而E-cad表达与Skp2表达则呈负相关（P〈0．05）。结论skp2过度表达与p27kipl表达减少可能与卵巢上皮性肿瘤的发生发展密切相关，而E-cad在晚期卵巢癌中表达降低可能反映了卵巢癌分化程度的降低。     

热休克蛋白在子宫颈鳞癌的表达及其意义

目的：探讨热休克蛋白（heat shock proteins,HSPs)家族中HSP27、HSP70、HSP90α在子宫颈鳞癌中的表达及其意义。方法：应用免疫组化S－P法观察41例子宫颈鳞癌和10例慢性子宫颈炎组织中HSP27、HSP70、HSP90α的表达。结果：HSP27、HSP70、HSP90α在子宫颈鳞癌中的阳性表达率分别为46．3％、70．7％、80．4％，在慢性子宫颈炎组织中的阳性表达率分别为10．0％、30．0％、20．0％，子宫颈鳞癌与慢性子宫颈炎之间差异有显著性（P＜0．05）。随着子宫颈鳞癌病理分级和临床分期的升高，HSP27表达逐渐降低，而HSP70、HSP90α表达逐渐增加（P＜0．05）。结论：HSP27、HSP70、HSP90α在子宫颈鳞癌的发生发展过程中可能扮演着重要的角色，HSP27主要参与子宫颈鳞癌的早期发生。     

STAT5、cyclinD1和c-myc蛋白在非小细胞肺癌中的表达及临床意义

目的：探讨信号转导和转录激活因子-5（STATS）、细胞周期素D1（cyclinD1）和c-myc蛋白在非小细胞肺癌（NSCLC）中的表达及意义。方法：用免疫组化SP法检测38例手术切除的NSCLC和20例正常肺组织中STATS、cyclinD1和c-myc的表达。结果：STATS、cyclinD1和c-myc在NSCLC中的表达明显高于正常肺组织（P〈0．01），且它们的表达与患者的年龄、肿瘤大小、组织分化程度、淋巴结转移及TNM分期等病理因素无关（P〉0．05）。在NSCLC中，STATS和cyclinD1的表达呈正相关（P〈0．05），而STATS与c-myc的表达、cyclinD1和c-myc的表达无相关性。结论：在NSCLC中存在STATS、cyclinD1和c-myc的过度表达，但与临床病理因素无关。在肿瘤的发生中，STATS可能是通过上调cyclinD1表达，促进细胞周期进展和细胞转化，诱导肿瘤的形成。     

血浆sIL-2R对急性期川崎病调节性T 细胞的影响

目的探讨sIL-2R血浓度对急性期川崎病（ KD）患儿调节性T细胞（ Treg）的影响。方法急性期KD患儿33例,正常同龄对照儿童14例。流式细胞术检测外周血CD4＋CD25＋Foxp3＋Treg细胞的比例和CD4＋CD25＋T细胞磷酸化STAT5（pSTAT5）蛋白平均荧光强度（MFI）;流式微球阵列术（CBA）检测血浆sIL-2R、IL-2、IL-7、IL-15的浓度;荧光定量PCR（real-time PCR）检测CD4＋CD25＋T细胞Foxp3、GITR、CTLA-4、IL-2Rα、IL-2Rβ、IL-2Rγ和CD 4＋CD25-T 细胞 IL-17A、RoR-γt 等基因mRNA表达。结果（1）急性期KD患儿CD4＋CD25＋Foxp3＋Treg细胞比例及相关分子Foxp3、GITR、CTLA-4 mRNA表达明显低于同龄对照组（P＜0．05）,Th17细胞相关因子IL-17A、ROR-γt mRNA表达明显增高（P＜0．05）,IVIG治疗后呈不同程度的恢复（P＜0．05）。（2）急性期KD患儿CD4＋CD25＋T细胞pSTAT5蛋白水平显著下调（P＜0．05）,IVIG治疗后明显上调（P＜0．05）。（3）急性期KD患儿血浆sIL-2R浓度显著增高（P＜0．05）,IVIG治疗后下降（P＜0．05）;其中KD合并冠脉损伤组（KD-CAL＋）明显高于无冠脉损伤组（KD-CAL-）（P＜0．05）;IL-2、IL-7、IL1-5浓度无明显改变（P＞0．05）。（4）急性期KD患儿CD4＋CD25＋T细胞IL-2Rα、IL-2Rβ基因mRNA表达明显低于同龄对照组（P＜0．05）,IVIG治疗后呈不同程度的升高（ P＜0．05）;IL-2Rγ基因mRNA表达无明显改变;sIL-2R血浓度与IL-2RβmRNA、pSTAT5及Foxp3 mRNA表达呈负相关（ P＜0．05）;pSTAT5与Foxp3 mRNA表达呈正相关（ P＜0．05）。结论血浆sIL-2R明显增高可致IL-2/STAT5信号途径传导异常,这可能是导致急性期KD Treg细胞下调的因素之一。     

石蜡包埋人胰腺癌组织中Smad4蛋白和转化生长因子β1及其Ⅱ型受体的表达

目的：探讨转化生长因子（TGF）－β通路中Smad4蛋白,TGFβ1和转化生长因子βⅡ型受体（TβRⅡ）的关系及它们在胰腺癌中的可能作用机制。方法：用EnVision免疫组织化学技术检测56份石蜡包埋人胰腺癌标本Smad4蛋白,TGFβ1和TβRⅡ蛋白表达的情况。结果：56份胰腺癌组织Smad4,TGFβ1和TβRII阳性率分别为58．93％（33）,66．07％（37）和60．71（34）,对应正常胰腺组织阳性率分别为89．29％（50）,25．00％（14）和25．00％（14）,TGFβ1的表达与临床分期,肿瘤的有无转移相关（P＜0．05）,TGFβ1和TβRII之间也有相关关系（P＜0．05）,结论：胰腺癌组织中Smad4表达降低,TGFβ1与TβRII则呈过表达,TGFβ1和TβRII对胰腺癌的发生可能有协同作用。Smad在TGF－β诱导基因表达调控和随后的生长抑制中是关键的转录因子,但TGFβ有时也可能以与Smad4无关的形式起作用。     

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。