化学发光免疫分析法检测人巨细胞病毒特异性IgM抗体的研究

目的 评价LIAISON化学发光免疫分析法(CLIA)检测人巨细胞病毒(HCMV)特异性IgM抗体的方法 学特点.方法 采用CLIA法对695例婴儿肝炎综合征和病毒性肺炎患儿的血清进行HCMV-IgM检测,同时用ELISA法进行同一批样本中部分的测定.结果 共检测样本695例,其中阳性151例,阳性率21.7%.CLIA法的灵敏度可达0.82 AU/ml,批内变异系数小于8%,批间变异系数小于10%,相关性系数为0.981～0.999.两种检测方法 的一致性为92.6%,但CLIA测定敏感性显著高于ELISA法(P＜0.05).结论 CLIA法检测HCMV-IgM具有高灵敏度,检测所需时间短,人为影响因素少,结果 准确等优点,适用于临床检测.     

婴儿胆汁淤积性肝病综合征119例人巨细胞病毒检测的意义

目的 探讨人巨细胞病毒感染(CMV)与婴儿胆汁淤积性肝病综合征的关系,以及血清学和分子生物学方法在诊断CMV感染中的作用.方法 婴儿胆汁淤积性肝病综合征住院患儿119例.男71例,女48例;年龄1～7个月,平均2个月.分别在人院时采集急性期和出院时采集恢复期血清进行抗人CMV-IgM抗体和人CMV DNA检测.血清中抗人CMV-IgM抗体检测应用间接ELISA法;应用实时荧光定量PCR检测方法 检测血清中人CMV DNA拷贝数.结果 婴儿胆汁淤积性肝病综合征患儿119例中,人CMV感染63例,阳性率为52.9%(63/119例).CMV感染阳性病例中,血清学方法共诊断52例,其中单份急性期血清抗人CMV-IgM抗体检测阳性47例;双份血清抗人CMV-lgM抗体由阴性转为阳性5例;通过荧光定量PCR检测诊断CMV感染11例(血清抗人CMV-IgM抗体检测阴性,血清CMV DNA检测阳性),占CMV感染病例的17.5%(11/63例).119例患儿中,27例入院时荧光定量PCR检测CMV DNA阳性,其中16例患儿同时抗人CMV-IgM抗体检测阳性、11例血清抗人CMV-IgM抗体检测阴性;出院时15例患儿检测CMV DNA均为阴性.CMV DNA阳性患儿血清中CMV DNA平均拷贝数为1.96×106(6.15×105～8.76×106)拷贝/L.结论 婴儿胆汁淤积性肝病中CMV感染较为常见,病毒感染诊断的确立要充分考虑血清学和分子生物学方法 各自的局限性,二者可互为补充.     

荧光定量聚合酶链式反应法检测婴儿尿液人巨细胞病毒DNA对人巨细胞病毒感染的诊断意义

目的探讨荧光定量聚合酶链式反应（FQ-PCR）方法检测婴儿尿液人巨细胞病毒（HCMV）DNA水平对婴儿HCMV感染的诊断价值。方法采用FQ-PCR检测348例临床疑似HCMV感染婴儿尿液中HCMVDNA水平。同时采用化学发光免疫分析法（CLIA）检测婴儿血清HCMV-IgM抗体。在尿液HCMVDNA检测阳性患儿中比较血清HCMV-IgM抗体检测阳性与阴性患儿尿液中HCMVDNA拷贝数差异。结果FQ-PCR检测尿液HCMVDNA的阳性率为41.74%,CLIA检测婴儿血清HCMV-IgM抗体的阳性率为19.83%。2种方法对HCMV感染诊断的符合率为76.7%。前者诊断阳性率显著高于后者（χ^2=69.44P〈0.01）。在尿液HCMVDNA检测阳性患儿中,IgM抗体阳性组尿液HCMVDNA拷贝数显著高于阴性组（P〈0.01）。结论FQ-PCR检测尿液HCMVDNA是早期诊断婴儿HCMV感染的敏感有效的方法。HCMV感染婴儿尿液中高HCMVDNA拷贝数与活动性HCMV感染密切相关;FQ-PCR方法检测尿液HCMVDNA水平对于判断是否为HCMV活动性感染具有一定意义。     

巨细胞病毒UL44,UL32特异性免疫球蛋白M的检测在婴儿巨细胞病毒 …

为探讨巨细胞病毒（ＣＭＶ）ＵＬ４４（Ｐ５２）、ＵＬ３２（Ｐ１５０）特异性免疫球蛋白Ｍ（抗Ｐ５２－（ｇＭ、抗Ｐ１５０－ＩｇＭ）与ＣＭＶ肝炎的临床关系。运用免疫印迹技术（ＩＢ）对２６例为患儿外周血特异性Ｐ５２－ＩｇＭ、抗Ｐ１５０－ＩｇＭ进行检测。结果：２６例患儿中抗Ｐ５２－ＩｇＭ阳经为１００％,抗Ｐ１５０－ＩｇＭ阳性率为６１．５％;在感染抗Ｐ１５０－ＩｇＭ阳性率明显高于围生感染（Ｐ〈０．０１）;围生期     

婴儿巨细胞病毒肝炎检测方法比较

巨细胞病毒(H CM V)肝炎是婴儿时期较常见的一种疾病,严重威胁婴儿的健康发育和生命。婴儿H CM V肝炎的病原诊断常用酶标法检测血清H CM V IgM、IgG,但其灵敏度不高,目前国外以检测外周血多型核白细胞(PM N Ls)中H CM V pp65抗原作为H CM V感染的标准。随着分子生物学技术的发展,荧光定量PCR检测H C M V感染应用也越来越广泛。我们对常用于婴儿H C M V肝炎的诊断方法进行比较,现将结果报告如下。1对象和方法1.1对象2001年11月～2003年2月复旦大学附属儿科医院传染科收治1岁以内各种原因引起的黄疸、肝脾肿大和肝功能异常为…     

人巨细胞病毒肝炎综合征婴儿外周血宿主microRNA表达的变化

目的 观察人巨细胞病毒(HCMV)所致肝炎综合征婴儿治疗前后外周血microRNA(miRNA)水平变化,探讨宿主miRNA与更昔洛韦(GCV)疗效的关系及临床意义.方法 收集HCMV感染所致肝炎综合征婴儿44例为病例组,分为GCV不敏感组(20例)和GCV敏感组(24例);15例同期体检健康婴儿为健康对照组.分别在GCV治疗前2d和停药后(或用药4周末),采集患儿外周静脉血l mL,提取miRNA,采用SYBR Green I实时荧光定量PCR方法检测hsa-miR-92a、hsa-miR-96、hsa-miR-433和hsa-miR-183表达水平,结果 用相对表达量表示.结果病例组has-miR-92a、has-miR-96、has-miR-433和has-miR-183表达水平均高于健康对照组,差异均有统计学意义(P均＜0.05);治疗前GCV不敏感组has-miR-96表达水平(1.24±0.62)低于GCV敏感组患儿(5.43 ±1.11),差异有统计学意义(t=-2.41,P=0.02);治疗后GCV不敏感组has-miR-96(0.70±0.06)和has-miR-183 (2.97±0.14)均明显低于敏感组(6.47±1.01、9.84 ±0.95),差异均有统计学意义(t’=-5.46,P＜0.01;t=-2.52,P=0.019);GCV不敏感组has-miR-183治疗后(2.97±0.14)较治疗前(9.79±1.31)明显下降,has-miR-433治疗后(6.20±0.92)较治疗前(10.90±0.77)表达水平下降,差异均有统计学意义(t=-3.54,P=0.002;t =2.45,P=0.027);GCV敏感组has-miR-183表达水平治疗后(9.84±0.95)较治疗前(9.27±0.96)升高,has-miR-433治疗后(6.57 ±0.71)较治疗前(9.88±1.32)下降,差异均有统计学意义(t=-2.54,P=0.018;t =3.70,P＜0.001).结论 GCV敏感患儿用药前后has-miR-96表达均高于不敏感患儿,用药后敏感患儿has-miR-183表达也高于不敏感患儿,miRNA对临床治疗婴儿肝炎综合征具有指导意义.     

人巨细胞病毒肝炎综合征婴儿外周血宿主microRNA表达的变化北大核心CSCD

目的观察人巨细胞病毒（HCMV）所致肝炎综合征婴儿治疗前后外周血microRNA（miRNA）水平变化,探讨宿主miRNA与更昔洛韦（GCV）疗效的关系及临床意义。方法收集HCMV感染所致肝炎综合征婴儿44例为病例组,分为GCV不敏感组（20例）和GCV敏感组（24例）;15例同期体检健康婴儿为健康对照组。分别在GCV治疗前2d和停药后（或用药4周末）,采集患儿外周静脉血1mL,提取miRNA,采用SYBRGreenI实时荧光定量PCR方法检测hsa—miR一92a、hsa—miR一96、hsa—miR-433和hsa—miR一183表达水平,结果用相对表达量表示。结果病例组hsa—miR-92a、hsa—miR一96、bsa—miR-433和hsa—miR一183表达水平均高于健康对照组,差异均有统计学意义（P均〈0．05）;治疗前GCV不敏感组hsa—miR-96表达水平（1．24±0．62）低于GCV敏感组患儿（5．43±1,11）,差异有统计学意义（t：一2．41,P=0．02）;治疗后GCV不敏感组hsa—miR-96（0．70±0．06）和hsa—miR一183（2．97±0．14）均明显低于敏感组（6．47±1．01、9．84±0．95）,差异均有统计学意义（t’=一5．46,P〈0．01;t=一2．52,P=0．019）;GCV不敏感组hsa—miR一183治疗后（2．974-0．14）较治疗前（9．79±1．31）明显下降,hsa—miR-433治疗后（6．20±0．92）较治疗前（10．90±0．77）表达水平下降,差异均有统计学意义（t=一3．54,P=0．002;t：2．45,P=0．027）;GCV敏感组hsa—miR-183表达水平治疗后（9．84±0．95）较治疗前（9．27±0．96）升高,hsa—miR-433治疗后（6．57±0．71）较治疗前（9．88±1．32）下降,差异均有统计学意义（t=-2．54,P=0．018;t=3．70,P〈0．001）。结论GCV敏感患儿用药前后hsa—miR-96表达均高于不敏感患儿,用药后敏感患儿hsa-miR一-83表达也高于不敏感患儿,miRNA对临床治疗婴儿肝炎综合征具有指导意义。     

聚合酶链反应诊断婴儿肝炎综合征巨细胞病毒感染

我们应用PCR检测肝炎综合征尿中巨细胞病毒DNA特异片段,以了解本地区巨细胞病毒感染现状。对象及方法一、一般资料住院肝炎综合征患者64人。新生儿7例,<3mo45例,＞3mo12例。出生体重＜2500g23例。母乳喂养31例、人工喂养23例．混合喂养10例。二、诊断标准按全国小儿巨细胞病毒感染学术会议拟定的巨细胞病毒感染诊断试行标准[1]。实验室检查检出巨细胞病毒DNA特异片段。三、方法入院后用清洁试管取患儿及母亲尿。经两次离心标本,弃上清液．加入引物（430bp）,再加人TapDNA多聚酶。经处理后开始循环。循环参数：90Clmin．65C0．5mi…     

人巨细胞感染的检测和新生儿肝炎综合征关系的探讨

本文应用ＰＣＲ及ＥＣＬ技术检测新生儿肝炎综合征患儿尿液中的ＨＣＭＶ－ＤＮＡ，阳性率分别为６６．７％及５３．３％，对照组为１４．３％，与ＨＣＭＶ病毒分离基本一致，甚致更为敏感，文章指出，凡肝炎综合症患儿均应进行病毒学检测。     

Sudden infant death syndrome and infant mortality in Aboriginal and non-Aboriginal infants

The aim of this study was to investigate sudden infant death syndrome (SIDS) in the context of total infant mortality for Aboriginal and non-Aboriginal infants. Deaths for infants born in Western Australia from 1980 to 1988 inclusive were ascertained from a total population data base. Infant mortality rates and rates by period and cause of death were calculated for both populations. Aboriginal infants had a mortality rate three times that for non-Aboriginal infants (23.6 cf. 7.9 per 1000 live births) and both populations showed a similar rate of decline in mortality over the study period. There were differences in the proportion of deaths occurring neonatally and postneonatally in the two populations. In terms of SIDS, 21% of the deaths in Aboriginal infants occurred neonatally compared with 7% for non-Aboriginal infants. The overall cause of infant death distribution differed significantly between the two populations ( P < 0.001). During the study period, Aboriginal infants showed a significant increase in deaths due to SIDS and a significant decrease in those due to birth defects and low birthweight. These results suggest it would be useful to review the pathology and diagnosis of sudden unexplained death in infancy.     

Chediak-Higashi syndrome in a Chinese infant

ABSTRACT. Chediak-Higashi syndrome in Chinese has not been previously reported in the English literature. A 14-month Chinese girl who presented with partial oculocutaneous albinism and Pseudomonas infection was found to have the classical intracytoplasmic inclusion bodies in the leucocytes by light and electron microscopy. Other characteristic features typical of this syndrome included hepatosplenomegaly, defective chemotaxis, and coarse but sparse melanin granules in hair shaft. She was also found to have hypertriglyceridaemia, a rare lipid abnormality occasionally reported in children suffering from this syndrome.
Despite vigorous therapy with high dose ascorbate, corticosteroid and intravenous antibiotics, she died in the accelerated phase of Pseudomonas septicaemia.     

Sudden infant death syndrome in Aboriginal and non-Aboriginal infants

This study, based on routinely recorded data, was designed to compare the epidemiology of sudden infant death syndrome (SIDS) in Aboriginal and non-Aboriginal infants in Western Australia (WA). All cases of SIDS occurring in infants born in WA from 1980 to 1988 were included in the study. There were 66 Aboriginal (6.1 per 1000 live births) and 337 non-Aboriginal (1.7 per 1000 live births) infants who died from SIDS. It was found that there was a significant linear increase in the Aboriginal SIDS rate over the study period while the non-Aboriginal rate remained relatively constant. For non-Aboriginal infants, there was an elevated risk of SIDS for young maternal age, single marital status and male gender but this was not found for Aboriginal infants. There was a significant difference in the age at death distribution for the two populations. Low birthweight and preterm birth were risk factors for both Aboriginal and non-Aboriginal infants. There may be differences in the aetiology and/or classification of SIDS between the two populations.     

Near miss sudden death in an infant with Wolff-Parkinson-White syndrome

A 6 month old infant with known Wolff-Parkinson-White syndrome presented with an out of hospital cardiac arrest. An electrocardiogram in the emergency department demonstrated atrial fibrillation with rapid ventricular response. The child subsequently was resuscitated and underwent successful interruption of an accessory connection after failing medical therapy. This case underlines the need to reassess the indications for invasive electrophysiologic testing in young children.     

Growth and the sudden infant death syndrome

Objective : To compare the growth curves based on measurements of body weight for male and female infants dying of sudden infant death syndrome (SIDS) with those of male and female controls. Methods : The data were drawn from a large case control study of SIDS carried out in New Zealand between 1987 and 1990. Results : The mean birthweight for the cases was 3049 g and for the controls 3526 g. The mean growth curves for the male and female controls were close to the 50th centile of growth charts used in New Zealand. The growth curve for the male cases diverged from that of the controls, being closer to the 25th percentile. The differences between the female cases and controls were less pronounced. The differences in weekly weight increments derived from the curves for the cases and controls for nine 4-week periods were not statistically significant after taking into account race, manner of feeding and maternal smoking for any 4-week period. Conclusions : SIDS cases were lighter at birth, but their growth velocity was normal postnatally.     

Cholinergic and oxidative stress mechanisms in sudden infant death syndrome

Aim:  To determine whether biochemical parameters of cholinergic and oxidative stress function including red cell acetylcholinesterase (AChE), serum/plasma thyroglobulin, selenium, iron, ferritin, vitamins C, E, and A affect risk in apparent life-threatening event (ALTE), sudden infant death syndrome (SIDS), and sudden unexpected death in infancy (SUDI). To assess these biochemical parameters as a function of age; and for influence of pharmacology and epidemiology, including infant health, care, and feeding practices.
Methods:  A multicentre, case–control study with blood samples from 34 ALTE and 67 non-ALTE (control) infants matched for age, and 30 SIDS/SUDI and four non-SIDS/non-SUDI (post-mortem control) infants.
Results:  Levels/activity of the biochemical parameters were not significantly different in ALTE vs. control infants, with the exception of higher vitamin C levels in the ALTE group (p = 0.009). In ALTE and control groups, AChE and thyroglobulin levels increased and decreased respectively from birth to attain normal adult levels from 6 months. Levels of iron and ferritin were higher in the first 6 month period for all infant groups studied, intersecting with vitamin C levels peaking around 4 months of age.
Conclusion:  Lower AChE levels and higher combined levels of iron and vitamin C in the first 6 months of life may augment cholinergic and oxidative stress effect, particularly at the age when SIDS is most prevalent. This may contribute to risk of ALTE and SIDS/SUDI events during infancy.     

Metal content of the liver in sudden infant death syndrome

Abstract The metals zinc, iron, copper, manganese, calcium, magnesium, potassium and sodium were analysed in the livers of 67 Australian infants who had died from Sudden Infant Death Syndrome (SIDS) and 29 infants who had died from other causes (non-SIDS). The results were evaluated in relation to medical data and fatty acid composition of the livers. In infants less than 6 months old the liver potassium levels were significantly lower in SIDS than in non-SIDS infants. No other significant differences in metals between the SIDS and non-SIDS livers were found. Zinc, iron and copper levels in infant liver fell with age during the first year.