血清抗心磷脂抗体与冠心病相关性研究

为了解血清ＡＣＡ水平恙冠心病相关性，分别用ＥＬＩＳＡ和免疫比浊法对１４８名健康中老年人的ＡＣＡ－ＩｇＧ、ＩｇＭ、ＩｇＡ和ＴＣ、ＨＤＬ含量进行了检测，同时测定了３４例住院冠心病人的ＡＣＡ水平。结果表明：在正常组，３类ＡＣＡ均随年龄递增（Ｐ〈０．０１和Ｐ〈０．０５），且男性高于女性（Ｐ〈０．０１和Ｐ〈０．０５），其中ＡＣＡ－ＩｇＧ的消长与血清ＴＧ呈正相关（Ｐ〈０．０５）；冠心病组的ＡＣＡ－ＩｇＧ阳性检     

血管紧张素原基因M235T分子变异与心肌梗塞的关系

目的为探讨血管紧张素原（ＡＧＴ）基因Ｍ２３５Ｔ分子变异与心肌梗塞（ＭＩ）的关系。方法采用聚合酶链反应、限制性片段长度多态性分析，对５７例ＭＩ患者和７６例无冠心病证据的对照组进行ＡＧＴ基因Ｍ２３５Ｔ等位基因检测。结果ＭＩ患者ＡＧＴ基因２３５ＴＴ型（０．７０）和Ｔ２３５等位基因（０．８２）的频率显著高于对照组（分别为０．４２和０．６３，Ｐ＝０．０１３和Ｐ＜０．０２５）。经校正冠心病的主要危险因素后，ＡＧＴ基因２３５ＴＴ型仍可显著增加心肌梗塞发生的危险性（比数比３．６５，Ｐ＝０．０１６）。结论ＡＧＴ基因２３５ＴＴ型可能是中国人群ＭＩ发病的重要危险因素之一。     

多抗F（ab＇）_2－ELISA测定人血清抗TG－Ab_2及意义

为了克服单抗测定甲状腺球蛋白独特型抗体（抗ＴＧ－Ａｂ＿２）的局限性，便于常规检测，我们建立了兔抗ＴＧ多克隆抗体的Ｆ（ａｂ＇）＿２－ＥＬＩＳＡ测定人血清中的抗ＴＧ－Ａｂ＿２．结果其抗ＴＧ－Ａｂ＿２阳性率：甲亢（Ｇｒａｖｅ＇３）为９．９％（７／７１），桥本氏甲状腺炎为４４．４％（４／９），甲状腺瘤为１６．７％（３／１８），ＳＬＥ为９．５％（４／４２），类风湿性关节炎为０％（０／３２），正常人为０％（０／３５）。     

C-WYCSI用于蒙古族儿童的结构效度分析

目的：用因素分析的方法检验中国韦氏幼儿智力量表（Ｃ－ＷＹＣＳＩ）用于蒙古族儿童的结构效度。方法：比较蒙古族样本与汉族样本和常模样本的因子矩阵模型，并作因子系数的一致性检验。结果：蒙古族样本各分测验的ｇ因素负荷在０．４５至０．７１之间，两因子结构和三因子结构都与汉族样本和常模样本基本相似。蒙古族样本与汉族和常模样本的Ａ因素。Ｂ因素相关系数在０．７５～０．９８之间，Ｃ因素相关为０．７８和０．４１。结论：Ｃ－ＷＹＣＳＩ用于蒙古族儿童有较好的结构效度。     

血管紧张素原基因启动子6G-A突变与先兆子痫关系的研究

为探讨血管紧张素原（ＡＧＴ）基因启动子６Ｇ－Ａ突变与先兆子痫的关系,我们采用等位基因特异性ＰＣＲ法对５８例先兆子痫孕妇和９０例正常孕妇进行了检测,结果,先兆子痫患者中６Ａ等位浪费同于对照组（０．６４）,我们认为ＡＧＴ基因启动子６Ｇ－Ａ突变是先兆子痫发病的因素之一。     

精神分裂症患者的脑功能显像与神经心理测验的相关研究

本研究应用单光子发射断层摄影术（ＳＰＥＣＴ）、ＨＲ成套神经心理测验（成人）修订本［ＨＲＢ（Ａ）－ＲＣ］和修订韦氏记忆测验（ＷＭＳ－ＲＣ）对３２例住院精神分裂症患者的脑功能改变及脑功能显像与神经心理测验之关系进行探讨。结果显示，精神分裂症患者存在额叶、颞叶和基底节的脑血灌流量降低，同时表现程度不同的神经心理功能损害，此改变在阴性症状和阳性症状的病人间无差异。脑血灌流量降低与损伤指数（ＤＱ）和记忆商数（ＭＱ）未见明显关系。相关分析表明，ＤＱ与ＴＥＳＳ评分呈显著正相关（ｒ＝０．３６，Ｐ＜０．０５）；ＭＱ与住院次数（ｒ＝－０．４２，Ｐ＜０．０５）、ＢＰＲＳ评分（ｒ＝－０．５６，Ｐ＜０．０１）、ＳＡＰＳ评分（ｒ＝－０．３９，Ｐ＜０．０５）和ＳＡＮ评分（ｒ＝－０．３７，Ｐ＜０．０５）呈显著负相关，与ＧＡＳ评分（ｒ＝０．５３，Ｐ＜０．０１）呈显著正相关     

多发性硬化患者者血清TGF—β的检测及其临床意义

目的：探讨转化生长因子－β１（ＴＧＦ－β１）在多发性硬化（ＭＳ）发生、发展中的作用。方法：采用酶联免疫吸附ＥＬＩＳＡ方法,对４５例ＭＳ患者血清ＴＧＦ－β１的含量进行了测定。结果：与对照组和ＮＩＮＤ组相比,ＭＳ患者血清ＴＧＦ－β１含量明显下降（Ｐ〈０．０１）;与ＳｔａｂｌｅＭＳ组相比,ＲＲＭＳ组和ＣＰＭＳ组ＴＧＦ－β１含量亦明显下降（Ｐ〈０．０５）;动态观察显示,随着病性的好转,ＴＧＦ－β１含量亦逐     

老年脑血管病患者脂蛋白（α）检测及其临床意义

用放免的方法测定了５０例脑血管病（ＣＶＤ）患者血清脂蛋白（α）［Ｌｐ（α）］浓度，对比分析了患者Ｌｐ（α）、甘油三脂（ＴＧ）、总胆固醇（ＴＣ）、高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）、低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）、脱脂蛋白Ａ－Ｉ（ａｐｏＡ－Ｉ）、ａｐｏＢ１００的浓度及变化，分析了Ｌｐ（α）浓度及ＴＧ、ＴＣ和胶脂蛋白的相关性。结果：ＣＶＤ患者血清Ｌｐ（α）浓度（０．２２４±０．０４ｇ／Ｌ），显著高于对     

抗纤复方及TGF-β对胶原基因启动子活性的影响

目的：研究ＴＧＦ－β及中药抗纤复方对小鼠前胶原α２（Ｉ）基因上游启动子活性的影响。方法：以含小鼠胶原α２（Ｉ）上游０．４、０．８、２．０ｋｂ启动片段为研究靶序列,以氯毒素乙酰枯转移酶（ＣＡＴ）作报告基因,应用基因技术研究小鼠胶原启动子活性。结果：ＴＧＦ－β可促进小鼠前胶原α２（Ｉ）基因妄动序列的启动活性,而中药抗纤复方可抑制其启动活性。结论：ＴＧＦ－β和中药抗纤复方都可作用于胶原α２（Ｉ）基因调控     

认知功能筛选测验在老年期痴呆中的应用

认知功能筛选测验（ＣＡＳＩ）是用于评估痴呆患者认知功能的工具。本文收集各种老年期痴呆１７３例，测试结果：评定员之间的一致性为０．８６２，２０个项目与总分之间的相关系数为０．３４８－０．８３３，９个因子与ＣＡＳＩ总分之间的相关系数为０．７１３－０．８８６，Ｃｒｏｎｂａｃｈａ＝０．９０１，说明该测验内部一致性极好，ＣＡＳＩ总分与ＧＡＳ的相关系数为０．６１３，与ＣＧＩ－ＳＩ的相关系数为－０．７４９，以Ｓ     

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.