MMP-3和 MMP-7在上皮性卵巢癌中的表达及临床病理意义

目的：探讨基质金属蛋白酶-3（MMP-3）与基质金属蛋白酶-7（MMP-7）在上皮性卵巢癌中的表达及与卵巢癌临床病理特征之间的关系。方法采用免疫组化法对50例上皮性卵巢癌组织、10例正常卵巢组织标本中 MMP-3和 MMP-7的表达情况进行检测。结果MMP-3与 MMP-7在上皮性卵巢癌组织中的表达率明显比正常卵巢组织高,差异有统计学意义（χ^2＝17.29,P ＜0.05;χ^2＝11.26,P ＜0.05）。 MMP-3、MMP-7的阳性表达与卵巢癌的临床分期（χ^2＝11.59,P ＜0.05;χ^2＝4.56,P ＜0.05）、病理分级（χ^2＝16.62,P ＜0.05;χ^2＝4.43, P ＜0.05）显著正相关;有淋巴结转移者 MMP-3和 MMP-7的表达高于无淋巴结转移者,差异有统计学意义（χ^2＝4.9,P ＜0.05;χ^2＝5.4,P ＜0.05）;但二者的表达与组织类型无关。结论 MMP-3与 MMP-7在卵巢癌中表达增高,且与临床分期、病理分级和淋巴结转移有关。 MMP-3、MMP-7高表达在上皮性卵巢癌的发生、发展过程中起重要的作用。     

LATS2基因在上皮性卵巢癌中的表达和临床意义

目的 检测人上皮性卵巢癌组织中大型肿瘤抑制因子2(LATS2)的表达与其发生、发展及临床病理参数之间的相关性.方法 用RT-PCR、SYBR Green实时定量PCR及免疫组化检测LATS2 mRNA和蛋白的表达.结果 LATS2 mRNA在上皮性卵巢癌组织中的表达量低于良性组和正常组(P＜0.01);LATS2的表达水平与组织分化程度(P＜0.05)、FIGO分期(P＜0.01)、有淋巴结转移(P＜0.01)有关.LATS2蛋白主要定位于胞质;上皮性卵巢癌LATS2的阳性表达率均低于良性组和正常组(P＜0.01);LATS2蛋白在临床晚期、组织分化低及有淋巴转移组中的阳性表达率低于临床早期、组织分化高及无淋巴结转移组(P＜0.01).结论 LATS2基因的表达水平可能与上皮性卵巢癌的发生、发展相关,对其早期诊断及预测病情进展具有一定的意义.     

可溶型B7-H3在原发性肝细胞癌患者血清中的表达及临床意义

目的 检测协同刺激分子B7-H3在肝细胞癌患者血清及组织中的表达,并探讨其临床意义.方法 选取原发性肝细胞癌63例患者的癌组织和血清标本;5例肝血管瘤的瘤旁组织作为正常肝组织对照;同期收取50例健康体检人员外周血标本为正常对照.采用ELISA检测肝癌患者和正常人血清中可溶型B7-H3(sB7-H3)的含量,免疫组化检测正常肝组织和肝细胞癌组织中B7-H3的表达.结果 肝细胞癌患者外周血清sB7-H3含量为(4143.47±976,27) pg/mL,显著高于正常对照组(2076.18±605.42)pg/mL(P ＜0.05);且其表达水平与临床分期,是否远处转移及肝癌组织中是否阳性表达B7-H3等参数有关(P＜0.05),与年龄、性别、组织学类型、淋巴结转移及肿瘤大小等临床病理参数无关;与血清学指标CA19-9呈明显正相关(P＜0.05),但与AFP和CEA水平无相关性.结论 肝癌患者血清中sB7-H3表达明显高于正常人,B7-H3表达与疾病临床病理指标相关,表明检测sB7-H3可能对原发性肝癌的诊断有一定价值.     

Trop-2在结直肠癌组织中的表达及其意义

目的 探讨人滋养层细胞表面抗原-2(Trop-2)在结直肠癌中的表达及其意义.方法 用免疫组化法检测84例结直肠癌组织标本及其相对应的癌旁正常组织中的Trop-2表达情况,分析其表达与临床病理特点的关系,进一步采用Westem blot检测34例手术标本的Trop-2表达情况.结果 Trop-2在结直肠癌组织中的表达高于癌旁正常组织(P ＜0.05);Trop-2表达量:直肠癌(RC)组＞左半结肠癌(LSCC)组＞右半结肠癌(RSCC)组(P＜0.05),Dukes'C+D组＞A+B组(P＜0.05),淋巴结转移组＞无淋巴结转移组(P＜0.05),远处转移组＞无远处转移组(P＜0.05);与性别、年龄、分化程度无关.结论 Trop-2在结直肠癌组织中高表达,与Dukes分期、淋巴结转移、远处转移和肿瘤所在部位有关.     

Raf激酶抑制蛋白在宫颈癌中的表达及其临床意义

目的 探讨Raf激酶抑制蛋白(Raf kinase inhibitor protein,RKIP)在宫颈癌中的表达及其临床意义.方法 应用免疫组织化学方法检测RKIP在正常官颈组织、官颈上皮内瘤变组织、官颈癌及其转移淋巴结组织的表达,并在体外应用RT- PCR及Western印迹方法检测RKIP mRNA及蛋白在4种不同来源的宫颈癌细胞系中的表达情况,探讨其与官颈癌临床病理学特征的关系.结果 RKIP在宫颈癌转移淋巴结中的阳性表达率低于宫颈癌组织;RKIP在宫颈癌组织的表达低于正常宫颈组织及宫颈上皮内瘤变组织,差异有统计学意义(x2 =9.211,P＜0.05);而RKIP在正常官颈组织及官颈上皮内瘤变组织的表达差异无统计学意义(x2=0.805,P＞ 0.05);RKIP在宫颈癌组织中的表达与淋巴结转移有关(x2=10.341,P＜0.05),与肿瘤的病理类型、分化程度及临床分期无关(x2分别为0.190、4.101、1.402,P＞0.05).RT- PCR及Western印迹结果显示RKIP在高侵袭性宫颈癌细胞系Caski中的表达低于其他各组(x2=4.08,P＜0.05).结论 RKIP基因在宫颈上皮内瘤变向官颈癌转变中可能起重要作用,是官颈癌发生淋巴结转移的重要标记.     

Ezrin在浆液性卵巢癌中的表达及临床意义

目的通过检测Ezrin在正常卵巢上皮和浆液性卵巢癌组织中的差异表达,探讨其对浆液性卵巢癌发生发展的影响。方法收取浆液性卵巢癌冷冻组织40例,正常卵巢上皮27例,提取总RNA,采用Real-time PCR技术检测Ezrin mRNA在两组样本中的表达差异;选取有完整临床病理资料的浆液性卵巢癌石蜡包埋组织134例,以及27例非卵巢癌病例的卵巢上皮组织,通过免疫组织化学染色检测两组样本中Ezrin蛋白质的表达差异,并应用SPSS 20.0软件分析其与临床病理的相关性。结果 Ezrin mRNA在新鲜卵巢癌组织中的表达显著低于正常卵巢上皮组织(P0.05)。Ezrin蛋白在石蜡包埋卵巢癌组织中也相应降低(P0.05)。Ezrin蛋白质表达水平与年龄、手术满意程度及化疗敏感程度无相关性,与细胞分化、病理分期及大网膜转移显著相关,(P0.05)。Ezrin表达水平高的浆液性卵巢癌病例的无进展生存期(PFS)值和总生存期(OS)值都明显高于表达水平低的病例(P0.05)。但Ezrin并不能作为浆液性卵巢癌的独立预后因素。结论 Ezrin的表达下调与浆液性卵巢癌的发生发展、转移等病理过程相关,其可以作为临床预后的潜在指标。     

IL-17A在卵巢癌组织中的表达及临床意义

目的探讨炎症因子IL-17A在卵巢癌组织中的表达及其与卵巢癌患者临床病理特征间的关系。方法免疫组织化学法(immunohistochemistry,IHC)检测上皮性卵巢癌(34例)、卵巢交界性肿瘤(23例)、卵巢良性肿瘤(24例)石蜡组织切片中IL-17A的分布及表达情况,分析IL-17A表达与卵巢癌患者年龄、肿瘤大小、病理分型、临床分期、淋巴结转移等临床病理特征间的关系。结果免疫组化染色发现IL-17A主要表达在淋巴细胞胞浆,肿瘤细胞几乎不表达。卵巢癌患者组织中IL-17A阳性率为64.7%,卵巢交界性肿瘤和卵巢良性肿瘤患者组织中IL-17A阳性率分别为21.7%、8.3%。卵巢癌患者组织中IL-17A阳性表达水平明显高于卵巢交界性肿瘤、卵巢良性肿瘤患者,差异具有统计学意义(P0.001;P0.000 1)。IL-17A表达与卵巢癌患者病理分化水平、淋巴结转移相关(P0.05),而与年龄、肿瘤大小、病理类型、临床分期无关。结论卵巢癌患者组织中高表达IL-17A可能参与卵巢癌患者疾病的进程,有望作为卵巢癌临床预后辅助预测指标。     

协同刺激分子B7-H6在卵巢癌中的表达及其临床意义

探讨协同刺激分子B7-H6在卵巢癌组织中的表达及其临床意义。采用免疫组织化学法检测112例卵巢癌组织芯点中B7-H6的表达情况,同时选取10例卵巢良性肿瘤组织作为对照,采用χ2检验分析B7-H6表达水平与患者临床病理参数的相关性,Log-rank检验比较B7-H6不同表达水平与患者预后的关系。结果显示:B7-H6主要表达于卵巢恶性肿瘤细胞的胞膜及胞质,染色呈弥漫性棕黄色颗粒状。B7-H6在卵巢癌组织中的阳性表达率为69.1%(76/110),远处转移的肿瘤患者B7-H6高表达率显著高于未转移的肿瘤患者(χ2=4.807,P=0.028),FIGO III-IV期患者B7-H6表达水平显著高于I-II期患者(χ2=4.671,P=0.031),且B7-H6高表达的患者术后总生存率显著低于B7-H6低表达的患者(χ2=3.995,P=0.0456),但B7-H6表达水平与患者年龄、肿瘤大小、肿瘤部位、病理分级以及淋巴结转移比较,差异无统计学意义(P>0.05)。研究结果表明协同刺激分子B7-H6在卵巢癌组织中高表达,其表达水平与患者肿瘤远处转移、FIGO分期及预后密切相关,提示B7-H6可能参与了卵巢恶性肿瘤的发生和发展,其对卵巢癌的临床诊断及预后判断具有潜在价值。     

胃癌组织中CD26的表达与临床病理特征及预后的相关性

目的探讨CD26的表达与胃癌临床病理学特征及预后的相关性。方法采用免疫组化EliVision Super法检测90例胃癌组织及相应90例癌旁正常胃黏膜组织、12例低级别上皮内瘤变和6例高级别上皮内瘤变组织中CD26蛋白的表达,分析其表达与临床病理学特征及预后的关系。结果 CD26在胃癌肿瘤细胞中的阳性率为67.8%(61/90),在高级别上皮内瘤变组织中的阳性率为50%(3/6),两者差异无统计学意义(P0.05);在低级别上皮内瘤变及癌旁正常胃黏膜腺上皮中均不表达;CD26表达与胃癌浸润深度(r=0.248,P=0.015)和pTNM分期(r=0.255,P=0.012)呈正相关。CD26在胃癌肿瘤浸润性淋巴细胞(tumor infiltrating lymphocytes, TILs)及间质细胞中均无表达。Kaplan-Meier及Log-rank单因素生存分析显示,CD26表达、肿瘤大小、浸润深度、远处转移和pTNM分期为胃癌预后的不良因素(P0.05)。多因素Cox回归模型分析显示,肿瘤大小、远处转移和pTNM分期均为影响胃癌预后的独立危险因素(P0.05),而肿瘤细胞中CD26表达、浸润深度并非预后的独立危险因素(P0.05)。结论 CD26的表达在胃癌的发生、进展中扮演重要角色,其可作为胃癌侵袭能力、远处转移、临床病理分期、早期诊断及负性预后因子的重要参考指标。     

PTP1B蛋白高表达在卵巢癌临床预后评价中的意义

目的探讨PTP1B在上皮性卵巢癌中的表达及与临床病理特征和预后的关系。方法应用Oncomine数据库和免疫组化法检测卵巢癌组织中PTP1B的表达情况,进一步分析PTP1B表达与卵巢癌临床病理特征及预后的关系。结果通过Oncomine数据库分析发现PTP1B在卵巢浆液性囊腺癌组织中的表达高于正常组织(P 0. 001)。免疫组化结果显示PTP1B表达与卵巢癌FIGO分期(P 0. 001)和大网膜转移相关(P=0. 002)。Kaplan-Meier生存分析显示,与PTP1B低表达组相比,PTP1B高表达组患者的总生存期更短(P 0. 001)。多因素分析显示FIGO分期和PTP1B表达是影响卵巢癌患者总生存期的独立预后因素。结论卵巢癌中PTP1B表达与肿瘤进展和患者不良预后密切相关。PTP1B可能是影响卵巢癌患者不良预后的有价值评估指标之一。     

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.     

Platelet-activating factor receptor and respiratory and metabolic responses to hypoxia and hypercapnia

Activation of the platelet-activating factor receptor (PAFR) regulates neural transmission. A PAFR blocker reduced the peak hypoxic (pHVR) but not hypercapnic ventilatory (HCVR) responses in rats [Am. J. Physiol. 275 (1998) R604]. To further examine the role of PAFR in respiratory control, genotype-verified PAFR -/- and PAFR +/+ adult male mice underwent hypoxic and hypercapnic challenges. HCVR was similar in the two groups (p-NS). However, pHVR was significantly reduced in PAFR -/- mice (38 +/- 13% baseline [S.D.]) compared to PAFR +/+ mice (78 +/- 16% baseline; P < 0.001, ANOVA), with reduced tidal volume recruitments during pHVR. In addition, hypoxic ventilatory depression was attenuated in PAFR -/- mice (P < 0.01), and was primarily due to attenuation of the time-dependent decreases in oxygen consumption during sustained hypoxia (P < 0.01). Thus, PAFR expression/function modulates components of the acute ventilatory and metabolic adaptations to hypoxia but not to hypercapnia. Imbalances in PAFR activity may lead to maladaptive regulation of the tightly controlled metabolic-ventilatory relationships during hypoxia.