幼儿胸腺的应用解剖学

目的:对童尸胸腺进行应用解剖学研究,为胸腺手术和经皮胸腺穿刺术提供解剖学依据.方法:30例福尔马林固定童尸标本,解剖观测胸腺的形态、大小、位置与毗邻以及血液供应.结果:30例胸腺均为2叶型,左叶长、宽、厚度为59.41、23.74、8.02 mm,右叶长、宽、厚度为60.20、22.49、8.39 mm;左叶上极80.0%高出颈静脉切迹,最高1例高出至甲状腺下缘,而右叶上极63.3%高于颈静脉切迹而无高出至甲状腺下缘者;两侧叶下极48.3%平对第3肋软骨或其上、下缘处;两侧缘76.7%超出胸骨两侧缘;胸腺两侧叶动脉的来源72.0%来自于同侧的胸廓内动脉或甲状腺下动脉,静脉93.2%汇入头臂静脉或甲状腺下静脉.结论:幼儿胸腺的形态、位置变异较大,血供呈多源性.掌握其形态学特点对于胸腺疾病的诊断和治疗具有重要的应用价值.     

经皮穿刺胸腺的应用解剖

目的通过穿刺胸腺组织诊断胸腺肿瘤,注入抗肿瘤药物治疗重症肌无力等。方法解剖观察成尸标本37具,观测胸腺的位置、形态,经皮穿刺进针点及深距。结果胸腺位于胸骨后方长(88.3±21.8)mm,宽(32.3±10.5)mm,厚(5.1±2.3)mm。经皮从胸骨柄上缘颈静脉切迹穿刺点穿刺至胸骨角后方深距(62.8±14.1)mm。从胸锁乳突肌内侧下段穿刺点至胸骨柄后方深距(45.0±9.2)mm,向前内进针角度为17.7°±7.9°。结论可经皮穿刺胸腺组织诊断胸腺增生或肿瘤,介入注射抗肿瘤药物治疗重症肌无力等。     

伴行静脉动脉化腓肠神经移植的应用解剖

目的:为吻合伴行静脉腓肠神经移植提供解剖学基础。方法:观察12例成人下肢固定标本腓肠神经伴行静脉的起止、行程、长度、外径和静脉瓣。摹拟伴行静脉腓肠神经移植体切除术。结果:腓肠神经的伴行静脉起自小隐静脉,注入静脉;长度为(19.4±2.1)cm(17.6～21.8cm),起始处外径为(1.2±0.1)mm(1.0～1.4mm),注入处外径为(1.8±0.2)mm(1.6～2.2)mm。在起始和注入处各有1对静脉瓣。结论:可行吻合伴行静脉腓肠神经移植。     

小儿门静脉及其主要属支的形态观察

用从初生至身长150cm的童尸180具(分为6组),观察了小儿门静脉的汇合状况.测量了小儿门静脉及其主要属支的长度和外径等,并藉此探讨了小儿门静脉形态结构的年龄特征.主要结果为:(1)门静脉合成有三种类型,“π”型占56.1%、“F”型占 28.g%“K”型占15.0%,门脾角变动于76～128°之间,平均为103.618.7°(2)门静脉长度分别为16.0±3.2 22.5±6.0、29.6±6.9、35.1±10.7、39.1±8.2和412±7.7mm,直线回归方程为y((mm)=3.4056X(cm)～11.2466:门静脉外径分别为4.6±1、0、6.1±1.5、6.8±1.0、7.8±2.2、9.0±1.7和10.5±2.2mm,直线回归方程为y(mm)=15.967IX(cm)～27.2044.( 3)脾静脉和肠系膜上、下静脉的长度和外径的测量值与成人资料相衔接.     

第1-4对肋间静脉的应用解剖

在32具成人尸体上解剖观察了第14对肋间静脉间的组合型式、交通支、上、下端的汇入处及瓣膜发现第一肋间静脉经肋骨小头下向上可汇入椎静脉、头臂静脉、锁骨下静脉,其中以椎静脉为主(右侧40.63%左侧37.5%),汇入处外径右侧2.03±0.76mm,左侧2.13±0.91mm。第1-4对肋间静脉间的组合型式也相当复杂。右侧以第二与第三肋间静脉共干江入夺静脉弓较多,占28.13%,汇入处外径4.36±2.12mm。左侧以第二,第三和第四肋间静脉共干汇入奇静脉或副半奇静脉较多,占37.5%,汇入处外径2.56±1.71mm。同侧第1-4肋间静脉之间的纵行交通支左侧有19支(占59.4%),右侧有10支(占31.3%),主要是第一与第二肋间静脉之间的交通支。静脉内瓣膜较少(右侧19处,左侧11处)。     

胚胎胸腺的替代治疗

目的 探索小鼠同种异体胚胎胸腺移植可否作为T淋巴细胞缺陷的治疗方法.方法 选择切除C57小鼠的胸腺作为制作细胞免疫缺陷的模型.30只小鼠被分为三组,每组10只.第一组为正常小鼠作为对照组;第二组行胸腺切除术,作为模型对照组;第三组是胚胎胸腺移植为实验组.检测脾脏总T细胞计数及其平均体重所含T细胞数;流式细胞术检测Th(helper T cell)细胞,Tc(cytotoxic T cell)细胞以及调节性T细胞(regulatory T cells,Tregs)的含量,并用简化的RT-PCR方法检测T细胞DNA删除环(TRECs).结果 三组小鼠分别剩余9只、8只,8只.T淋巴细胞总数三组分别为(16.24±2.98)×107、(4.58±1.29)×107、(9.92±2.24)×107.平均体重T淋巴细胞含量分别为(7.53±1.35)×106、(2.38±0.66)×106、(5.23±1.10)×106.两组都有统计学意义(P<0.05).对照组含量最高,胸腺切除组含量最少,胚胎胸腺移植组位于两者之间.T淋巴细胞亚群分析中,三组Th细胞分别为(7.19±0.38)%、(1.51±0.37)%、(3.33±0.40)%;Tc细胞为(7.21±0.41)%、(1.31±0.32)%、(3.41±0.48)%;Tregs为(2.17±0.21)%、(0.48±0.12)%、(1.12±0.12)%.Th,Tc以及Tregs含量在三组间有统计学意义(P<0.05),A组含量最高,B组含量最少,C组位于两者之间.RT-PCR分析中,ΔΔCT值进行统计分析及进行三组ΔΔCT值的总体趋势的比较.ΔΔCT值对照组为17.04±1.69,胸腺切除组为9.53±0.84;胚胎胸腺移植组为12.45±1.51,三组的差异有统计学意义(P<0.05).结论 胚胎胸腺移植可以提高细胞免疫功能的恢复,但无法使其恢复到正常水平.     

小儿颈外静脉穿刺的解剖学研究

目的 :为临床儿科静脉穿刺抽血提供解剖学依据。方法 :在 30例 (6 0侧 )甲醛固定的小儿尸体上解剖并观测了颈外静脉的深度、外径、长度及毗邻关系 ,并与大隐静脉、肘正中静脉进行了对比。结果 :双侧颈外静脉上段的平均深度为 3.6 1± 0 .46 m m,左侧外径为 3.34± 0 .78m m,右侧外径为 3.86± 0 .6 4mm,左侧长度为 35 .6 7± 3.30 mm,右侧长度为 41.6 2± 4.19mm。结论 :小儿浅静脉穿刺抽血应当首选颈外静脉上段 ,次选大隐静脉 ,肘正中静脉基本上不适用于穿刺。     

下颌后静脉的形态学特点及其临床意义

目的:明确下颌后静脉的解剖学特点及其与下颌角之间的解剖关系,为下颌角截骨术中避免损伤下颌后静脉提供解剖学依据。方法:22侧福尔马林固定成人尸体头颈部标本,解剖观测下颌后静脉的走行、构成、长度、外径及其与周围结构的关系。结果:下颌后静脉位于下颌骨后缘,由颞浅静脉和上颌静脉合成。起始处外径为(5.6±2.6)mm,长度为(4.46±2.08)cm。围绕下颌支后缘静脉长度为(4.27±0.80)cm,围绕下颌体下缘静脉长度为(2.02±0.42)cm。结论:在改脸形手术中预切除下颌角的后缘和下缘均有静脉围绕,尤其在下颌支后缘的中段,静脉口径粗大,与下颌支之间仅隔以菲薄骨膜,在下颌角截骨术中要注意避免损伤此静脉。     

胸腺上皮性肿瘤52例的临床病理分析

目的 探讨胸腺上皮性肿瘤的临床病理学特点,评价2004年WHO胸腺肿瘤分类的可重复性及其临床意义.方法 收集2001年1月至2009年6月间52例胸腺七皮性肿瘤的资料,对其形态学特征和免疫表型进行回顾性复习,按照2004年WHO胸腺肿瘤分类进行组织学分型,并对临床资料加以分析和总结.结果 胸腺瘤45例,胸腺癌7例.胸腺瘤中以AB型最多见,占33.3%(15/45),其次为B2型和B3型,均为20.0%(9/45).A型和B1型相对少见,分别占13.4%(6/45)和8.9%(4/45).另有2例化生性胸腺瘤(4.4%).7例胸腺癌中6例为鳞状细胞癌分化,1例为神经内分泌癌.临床上,多数患者因咳嗽或胸痛就诊,部分病例为体检中偶然发现.胸腺瘤中13例伴有重症肌无力(25.0%).影像学上,49例(94.2%)位于前纵隔,其中A、AB、B1和多数B2型胸腺瘤表现为边缘光整、密度均匀的肿块,少数B2型、多数B3型胸腺瘤和胸腺癌表现为边界欠清、外形不规则和密度不均的肿块.48例手术Masaoka分期为:Ⅰ期20例(41.7%),Ⅱ期15例(31.3%),Ⅲ期11例(22.9%),Ⅳ期2例(4.1%).分析显示,组织学分型与临床分期有显著相关性(χ~2=32.5,P＜0.01).结论 基于细胞形态、功能和遗传学的2004年WHO胸腺肿瘤分类具有较高的可重复性,并在一定程度上反映胸腺瘤各亚型的生物学行为,对临床治疗和预后判断有指导意义.     

以足底内侧动脉深支内侧支为蒂游离足内侧皮瓣的应用解剖

目的 :为以足底内侧动脉深支的内侧支为蒂足内侧皮瓣设计的改进提供解剖学基础。方法 :在 32侧成人下肢标本及 2只灌注红色乳胶成人新鲜足标本 ,解剖观测了足底内侧动脉深支的内侧支分支分布、吻合、外径及长度 ,皮瓣的静脉和神经分布。结果 :内侧支长 (2 .6± 0 .2 )cm ,外径 (1.0± 0 .1)mm ;伴行静脉 1条占 75 % ,外径 (1.3± 0 .3)mm ,伴行静脉 2条者占 2 5 % ,外径 (0 .9± 0 .2 )mm ;皮瓣供区有隐神经终支和足背内侧皮神经内侧支分布。结论 :①足内侧皮瓣可以是足底内侧动脉深皮内侧支或由跗内侧动脉供血 ;②静脉为动脉伴行静脉和大隐静脉深、浅两套 ;③皮瓣有隐神经终支和足背内侧皮神经内侧支 ;④游离足内侧皮瓣适用于手部创面修复的特殊要求。     

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.