川崎病患儿血清可溶性血管细胞黏附分子-1、肿瘤坏死因子-α水平变化的意义

目的探讨可溶性血管细胞黏附分子-1（sVCAM-1）与肿瘤坏死因子-α（TNF-α）在川崎病（KD）发病中的意义。方法采用双抗体夹心酶联免疫法（ELISA）分别测定确诊为KD34例患儿急性期血清sVCAM-1、TNF-α水平,测定其中32例恢复期患儿血清sVCAM-1、TNF-α水平,26例健康儿童为健康对照组。结果KD组血清急性期sVCAM-1、TNF-α[（97.8±35.6）、（73.9±21.7）μg/L]均高于健康对照组[（41.2±8.9）、（2.7±1.8）μg/L],差异有显著性（Pa〈0.01）;KD患儿恢复期血清sVCAM-1、TNF-α水平[（46.9±16.8）、（4.3±2.9）μg/L]下降显著与急性期比较差异有显著性（Pa〈0.01）;而KD恢复期患儿与健康对照组无显著差异（P〉0.05）,且sVCAM-1与TNF-α呈正相关（r=0.798P〈0.001）。结论sVCAM-1、TNF-α可能参与KD发病的病理过程,血清sVCAM-1、TNF-α检测有助于对KD病情发展作出判断。     

流行性乙型脑炎患儿脑脊液和血清S100β蛋白水平的变化及其意义

目的探讨流行性乙型脑炎（乙脑）患儿脑脊液和血清S100β蛋白水平的变化及其意义。方法乙脑患儿45例,分别在极期和恢复期空腹采静脉血2mL,极期采脑脊液1mL,ELISA法测定其脑脊液和血清S100β蛋白水平。20例拟行非心脏外科手术治疗的行腰麻的患儿采取肘静脉血2mL和脑脊液1mL作为对照。采用ELISA法检测S100β蛋白水平。结果轻型、普通型、重型乙脑患儿极期脑脊液S100β蛋白分别为（0.35±0.12）、（0.76±0.15）、（1.29±0.22）μg/L,血清S100β蛋白分别为（0.08±0.04）、（0.14±0.07）、（0.22±0.12）μg/L;对照组脑脊液S100β蛋白为（0.05±0.03）μg/L,血清S100β蛋白为（0.03±0.02）μg/L。乙脑患儿极期脑脊液和血清S100β蛋白水平均显著高于对照组（Pa〈0.01）,且随临床分型加重而增高。乙脑患儿恢复期血清S100β蛋白为（0.08±0.03）μg/L,较极期[（0.24±0.13）μg/L]显著下降（P〈0.01）。结论乙脑患儿脑脊液和血清S100β蛋白水平与临床分型相关,检测乙脑患儿脑脊液和血清S100β蛋白水平的变化,有助于判定脑组织受损的严重程度及评估患儿的预后。     

孕酮对缺氧缺血性脑病新生大鼠皮层和海马神经元凋亡及一氧化氮水平的影响

目的探讨孕酮对HIE新生大鼠皮层和海马组织神经元凋亡率及一氧化氮（NO）水平的影响。方法7日龄新生Wistar大鼠30只随机分为3组：假手术组、缺氧缺血（HI）组和药物预防组。HI组和药物预防组动物先行左侧颈总动脉结扎术,置37℃恒温的密闭容器中,以1.5L/min的速度吸入80mL/L氧气和920mL/L氮气混合气体2.5h,建立HIE动物模型。假手术组仅分离左侧颈总动脉,不结扎,亦不做缺氧处理。药物预防组大鼠于建立模型前30min按8mg/kg腹腔注射0.5g/L孕酮溶液,假手术组和HI组注射同等量的9g/L盐水,24h后处死动物,采用流式细胞仪检测其皮层和海马神经元凋亡情况,硝酸还原酶法检测其NO水平的变化。结果HI组大鼠皮层和海马组织神经元凋亡率分别为（10.09±0.36）%、（12.32±0.28）%,明显高于假手术组[（2.49±0.23）%、（2.58±0.26）%]（Pa〈0.01）,药物预防组大鼠皮层和海马组织神经元凋亡率为（3.47±0.32）%、（4.56±0.30）%,明显低于HI组（Pa〈0.05）。HI组大鼠皮层和海马组织NO水平分别为（51.36±9.71）μmol/L、（52.34±4.26）μmol/L,明显高于假手术组水平[（18.16±6.24）μmol/L、（19.28±3.58）μmol/L）]（Pa〈0.01）,药物预防组大鼠皮层和海马组织NO水平为（33.47±8.02）μmol/L、（32.57±4.27）μmol/L,明显低于HI组（Pa〈0.05）。结论孕酮通过降低新生大鼠HI时皮层和海马组织神经元凋亡率和NO水平,拮抗神经元凋亡发挥对缺氧缺血性脑损伤的保护作用。     

支气管哮喘患儿急性发作期血清白细胞介素-25、12的变化及其意义

目的探讨哮喘患儿急性发作期血清IL-25、12水平变化及其在哮喘发病中的作用。方法随机选取于本院就诊的哮喘急性发作期患儿30例作为观察组。男20例,女10例;年龄4～13岁;发作程度：轻度8例,中度17例,重度5例。随机选取同期同年龄组健康体检儿童27例作为健康对照组。男18例,女9例;年龄4～14岁。二组年龄及性别均无统计学差异（Pa〉0.05）。分别抽取各组儿童静脉血4mL,离心后留取血清标本置-70℃冰箱保存,采用ELISA法测定二组儿童血清IL-25、12水平。结果哮喘急性发作期患儿血清IL-25水平[（56.75±11.68）ng/L]显著高于健康对照组[（45.77±10.43）ng/L],差异有统计学意义（t=3.726P〈0.05）;哮喘急性发作期患儿血清IL-12水平[（42.12±12.96）ng/L]显著低于健康对照组[（57.12±14.42）ng/L],差异有统计学意义（t=-4.136P〈0.05）;血清IL-25水平与IL-12水平呈显著负相关（r=-0.420P〈0.01）。结论哮喘患儿急性发作期血清IL-25水平升高和IL-12水平降低与哮喘的发作关系密切。增强IL-2的活性,可为哮喘的治疗提供新的靶点与理论依据。     

左旋精氨酸对模拟缺血再灌注乳兔培养窦房结细胞损伤的保护作用（英文）

目的观察模拟缺血再灌注（IR）培养乳兔窦房结细胞（SANC）损伤及左旋精氨酸（L-Arg）的保护作用。方法对SANC模拟低糖缺氧培养,添加L-Arg和L-Arg加L-NAME（L-Arg抑制剂）与培养细胞共同孵育,吖啶橙（AO）标记细胞凋亡,检测细胞内过氧化物歧化酶（SOD）活性、丙二醛（MDA）、总一氧化氮合酶（NOS）、氧化亚氮（NO）水平。细胞分为正常对照组、I120R120组、I120R120加L-Arg组、I120R120加L-Arg加L-NAME组4组。结果凋亡细胞体积明显缩小,核呈黄绿色,断裂为多个碎块状,由膜包裹着凸起于细胞表面呈黄绿色凋亡小体。与I120R120组凋亡率[（5.21±1.59）%]比较,I120R120加L-Arg组凋亡率[（8.70±3.10）%]显著降低（P〈0.01）;I120R120加L-Arg组细胞SOD活性[（46 820±14 450）U/g]较I120R120组[（25 030±8 440）U/g]显著上升,而I120R120加L-Arg组MDA[（5.55±3.71）mmol/g]、NO[（3.65±1.02）U/g]和NOS[（3.73±0.24）μmol/L]较I120R120组MDA[（8.42±4.21）mmol/g]、NO[（4.62±1.20）U/g]和NOS[（4.96±0.52）μmol/L]显著下降（Pa〈0.05）;而I120R120加L-Arg加L-NAME组各指标较I120R120组无显著性差异（Pa〉0.05）。结论补充NO合成底物L-Arg能清除自由基,增加SOD活性,增强细胞抗氧化损伤能力,可能是阻断氧自由基所介导的细胞凋亡机制之一。     

出生后长期缺锌对大鼠生长发育及生长激素的影响

目的 研究出生后长期缺锌对大鼠生长发育的影响及其机制。方法 选取刚出生的SD大鼠3窝,每窝1只母鼠、10只仔鼠,3窝母鼠与仔鼠体重相近,仔鼠雌雄各半。随机分为3组,缺锌组（ZD）、配饲组（PF）、对照组（ZA）。实验期60 d。测定大鼠身长、股骨长度、直径、重量,血清生长激素（GH）含量。结果 ZD组身长[（16.15±0.67）cm]明显低于PF组[（20.94±0.98）cm]及ZA组[（23.08±0.11）cm]（P〈0.01）;ZD组股骨长度[（2.61±0.22）cm]明显低于PF组[（3.38±0.10）cm]及ZA组[（3.54±0.08）cm]（P〈0.01）;ZD组股骨直径[（0.30±0.03）cm]明显低于PF组[（0.37±0.33）cm]及ZA组[（0.42±0.01）cm]（P〈0.01）;ZD组股骨重量[（0.65±0.10）g]明显低于PF组[（1.07±0.07）g]及ZA组[（1.28±0.08）g]（P〈0.01）;ZD组血清生长激素水平[（0.47±0.04）ng/ml]明显低于PF组[（0.66±0.11）ng/ml]及ZA组[（0.75±0.07）ng/ml]（P〈0.01）。结论 出生后长期缺锌可导致动物体内生长激素水平下降,是导致生长迟缓的原因之一。     

新生儿佝偻病骨代谢转换生化标志物检测的意义

目的探讨骨代谢转换生化标志物血清β胶原分解片断（β-CTx）、骨碱性磷酸酶（BALP）和骨钙素（BGP）测定在新生儿佝偻病诊断中的意义。方法选取30例佝偻病新生儿（病例组）和30例健康新生儿（健康对照组）,每例儿童均采集空腹静脉血2mL,电化学发光免疫分析法检测血清β-CTx,ELISA法测定BALP和BGP水平,并对这三项测定指标的灵敏度、特异度、漏诊率、误诊率、诊断符合率、Youden指数、阳性预测值和阴性预测值进行计算和分析,同时测定其血清钙、磷和AKP水平,并进行左手腕关节X线摄片。结果病例组血清β-CTx、BALP和BGP水平分别为（1.58±0.49）μg/L、（291.5±78.4）U/L和（15.2±5.9）μg/L,健康对照组分别为（1.16±0.38）μg/L、（137.1±64.7）U/L和（10.1±4.3）μg/L,病例组明显高于对照组,二组比较均有极显著性差异（Pa〈0.001）。病例组血清β-CTx、BALP和BGP水平异常者分别为28例（93.3%）、26例（86.7%）和24例（80.0%）,明显高于对照组[2例（6.7%）、2例（6.7%）和3例（10.0%）]（Pa〈0.001）。血清β-CTx的灵敏度、特异度、诊断符合率、Youden指数、阳性预测值和阴性预测值均高于血清BALP和BGP,但无统计学意义,其漏诊率和误诊率显著低于血清BALP和BGP（χ^2=9.7124,11.2913,16.9212,18.3671Pa〈0.01）。结论血清BALP和BGP水平测定是准确反映骨代谢转换的生化标志物,也是诊断新生儿佝偻病特异而敏感的指标;血清β-CTx水平测定是诊断新生儿佝偻病、反映骨吸收活动特异性很高的敏感指标。     

肺炎患儿血清一氧化氮、肿瘤坏死因子检测及其临床意义

为阐明支原体肺炎和腺病毒肺炎时一氧化氮(NO)和肿瘤环死因子(TNF)的变化,采用比色法、双抗体夹心ELISA法对32例支原体肺炎患儿、19例腺病毒肺炎患儿和20例健康儿进行血清NO、TNF测定。结果:支原体肺炎患儿血清NO、TNF为47.7±14.4μmol/L、37.1±9.8μg/L,和腺病毒肺炎患儿为68.2±13.9μmol/L、54.7±10.1μg/L,均较对照组(25.1±5.5μmol/L、8.2±2.9μg/L)明显升高,(P<0.01);而且NO、TNF呈显著正相关(r=0.816,P<0.01),两种病原之间比较,腺病毒肺炎患儿血清NO、TNF水平均高于支原体肺炎。提示:NO和TNF在腺病毒肺炎和支原体肺炎的发病机理中起一定作用。     

急性一氧化碳中毒患儿血清S-100β蛋白检测的意义

目的探讨急性一氧化碳中毒（CO）患儿血清S-100β蛋白水平的变化及其临床意义。方法采用酶联免疫吸附试验双抗体夹心法检测28例急性CO中毒患儿（病例组）及20例健康儿童（健康对照组）血清S-100β蛋白水平,并比较不同程度中毒患儿及迟发性脑病发生组与未发生组患儿血清S-100β的差异。结果健康对照与病例组儿童血清S-100β蛋白水平分别为（0.037±0.014）和（0.517±0.346）μg/L,二组比较有显著差异（t=6.197P〈0.001）;重度组与中度组、中度组与轻度组患儿S-100β相比,均有显著差异（t=5.381P〈0.001;t=3.067P〈0.01）;迟发性脑病发生组与未发生组血清S-100β蛋白水平分别为（0.943±0.155）和（0.347±0.233）μg/L,二组比较差异显著（t=6.761P〈0.001）。结论检测急性CO中毒患儿血清S-100β蛋白水平,有助于评估急性期脑组织受损的严重程度及预测迟发性脑病的发生。     

急性病毒性心肌炎患儿血清肿瘤坏死因子-α、白细胞介素-6水平变化的意义

目的探讨急性病毒性心肌炎（AVM）患儿血清肿瘤坏死因子-α（TNF-α）及白细胞介素-6（IL-6）水平变化的意义。方法应用放射免疫法（RIA）和酶联免疫吸附法（ELISA）检测53例AVM患儿及20例健康儿童血清TNF-α及IL-6水平,分析TNF-α及IL-6血清水平与儿童AVM发生的关系。结果AVM组急性期血清TNF-α和IL-6水平分别为（526.7±32.9）和（3.23±0.53）mg/L,健康对照组分别为（383.1±27.5）和（1.63±0.22）mg/L,二组比较均有显著性差异（Pa〈0.05）;临床治愈后,AVM组TNF-α及IL-6分别降至（407.3±34.4）和（1.97±0.29）mg/L,与健康对照组比较均无显著性差异（Pa〉0.05）。结论AVM患儿急性期血清TNF-α和IL-6明显增高,心肌炎治愈后降至正常,检测TNF-α及IL-6血清水平及变化有助于判断AVM患儿病情及心肌损害程度。     

Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene

OBJECTIVES: Polychlorinated biphenyls (PCBs) and dichlorodiphenyl dichloroethene (DDE) are ubiquitous toxic environmental contaminants. Prenatal and early life exposures affect pubertal events in experimental animals. We studied whether prenatal or lactational exposures to background levels of PCBs or DDE were associated with altered pubertal growth and development in humans.Study design: Follow-up of 594 children from an existing North Carolina cohort whose prenatal and lactational exposures had previously been measured. Height, weight, and stage of pubertal development were assessed through annual mail questionnaires. RESULTS: Height of boys at puberty increased with transplacental exposure to DDE, as did weight adjusted for height; adjusted means for those with the highest exposures (maternal concentration 4+ ppm fat) were 6.3 cm taller and 6.9 kg larger than those with the lowest (0 to 1 ppm). There was no effect on the ages at which pubertal stages were attained. Lactational exposures to DDE had no apparent effects; neither did transplacental or lactational exposure to PCBs. Girls with the highest transplacental PCB exposures were heavier for their heights than other girls by 5.4 kg, but differences were significant only if the analysis was restricted to white girls. CONCLUSIONS: Prenatal exposures at background levels may affect body size at puberty.     

Prevention and treatment of overweight and obesity in children and adolescents

Increasing numbers of obese children and adolescents all over the world demand an investment in the primary and secondary prevention of obesity and overweight in this age group. The goal of preventive measures in children is to avoid the negative short- and long-term health problems associated with obesity. Primary prevention aims at establishing a healthy, active lifestyle and keeping children and adolescents within a range of body weight which is considered to be healthy. Constant availability and affordability of palatable and energy-dense food in the affluent society of the western world demands preventive strategies. Universal or public health prevention seems to be the most suitable form because several other cofactors of morbidity and mortality of affluent societies can also be prevented. However, in most European countries there is a lack of awareness of the necessity of prevention programmes, not only among the general population but also among the medical society. More awareness and consciousness to the problem of obesity must be generated in order to lead to effective therapeutic programmes. For those children and adolescents who are already obese, secondary prevention is mandatory. Therapeutic intervention programmes for the obese aim at long-term weight maintenance and normalisation of body weight and body fat. They have to modify eating and exercise behaviour of the obese child and establish new, healthier behaviour and lifestyle. Treatments programmes must include behavioural components in order to permanently change nutrition and physical exercise of the obese children and adolescents. However, long-term results of treatment programmes in European countries are scarce and the reported results, even of multidisciplinary regimens, are not impressive. Conclusion In most European countries there is an urgent need not only for a growing awareness of the problem of obesity in children and adolescents but also for development of new comprehensive approaches in treating this group.     

Hypokalemia and Hyperkalemia in Infants and Children: Pathophysiology and Treatment

Potassium is the second most abundant cation in the body. About 98% of potassium is intracellular and that is particularly in the skeletal muscle. Electrical disturbances associated with disorders of potassium homeostasis are a function of both the extracellular and intracellular potassium concentrations. Clinical disorders of potassium homeostasis occur with some regularity, especially in hospitalized patients receiving many medications. This article will review the pathophysiology of potassium homeostasis, symptoms, causes, and treatment of hypo- and hyperkalemia.