孕前及孕期叶酸摄入与小于胎龄儿的关联性分析

目的了解孕前及孕期叶酸摄入与小于胎龄儿的关联性,为小于胎龄儿的防治提供基线数据。方法以2011~2012年在甘肃省妇幼保健院建卡并随访到分娩结局的孕妇为研究对象,用病例对照的研究方法分析孕前及孕期叶酸摄入与小于胎龄儿的关联性。结果在调整了混杂因素后,与未服用叶酸的孕妇相比,在孕前及孕期规律补充叶酸大于20周是小于胎龄儿的保护因素(OR=0.87,95%CI:0.77~0.97),孕期膳食叶酸低于121.02μg/每天是小于胎龄儿的危险因素(OR=1.33,95%CI:1.01~1.76);按是否足月分层后,类似的作用仅在足月小于胎龄儿中体现。结论孕前及孕期叶酸补充不足增加了小于胎龄儿的发生风险,建议育龄期妇女在孕前及孕期适量规律的补充叶酸,同时在孕期增加膳食中叶酸的摄入量。     

胃肠激素检测在小于胎龄儿变化中的临床意义

目的:对68例小于胎龄儿(其中早产36例;足月32例)生后喂奶前及第7d空腹血中生长抑素(somatostatin, SS)、胃动素(motilin, MOT)、胃泌素(gastrin, Gas)浓度进行测定,并以30例足月新生儿作为对照组.方法:应用放射免疫分析测定SS、MOT、Gas浓度.结果:小于胎龄儿组生后喂奶前及第7d空腹血浆MOT、Gas均明显低于对照组,而SS浓度明显高于对照组,并且与胎龄、开始喂养时间及当日进奶等因素相关.结论:小于胎龄儿消化道机能适应胃肠道营养,在严密观察下应用合理的喂养方式早日开始胃肠道营养,将能促进小于胎龄儿胃肠道的发育和成熟.     

104例新生儿生长激素测定及其5年后随访报告

本文采用放射免疫法检测了１０４ 例新生儿（ 其中小于胎龄儿５０ 例和适于胎龄儿５４ 例） 的生长激素。结果显示两组间差异不显著，并在５ 年后对这１０４ 名幼儿进行了生长发育追踪随访调查，结果显示小于胎龄儿其身长体重小于第１０ 百分位数的程度大大高于适龄儿。     

极低出生体重儿临床相关因素及与预后的关系

目的探讨极低出生体重儿的围产期及临床特点,分析其与预后的关系.方法分析110例极低出生体重儿(含12例超低出生体重儿)的一般情况、产科及母孕期情况、新生儿临床特点.结果胎龄小于32w者占79%,小于胎龄儿占17.3%,41%为多胎;32%有胎膜早破史,18%母亲有妊高征;36%有窒息复苏史;产科异常是胎儿早产的主要原因.呼吸暂停、低体温、高胆红素血症及低血糖是常见的并发症;多胎、围产期异常及小于胎龄儿是极低出生体重儿主要死亡原因,生于院内或转运者死亡率明显低于院外出生者(P<0.01).结论加强对高危孕妇及新生儿的监护,普及新生儿窒息复苏知识,将有助于改善极低出生体重儿的预后.     

新生儿血清瘦素水平变化与IGF-Ⅰ、生长激素等相关因素的分析

目的探讨新生儿血清瘦素来源及其与胰岛素样生长因子-Ⅰ(IGF-I)和生长激素的关系.方法采用放射免疫法检测80例新生儿静脉血和脐血瘦素水平,根据不同胎龄新生儿出生体重值分为大于胎龄儿组28例,适于胎龄儿组36例,小于胎龄儿组16例;采用Rohrer's指数=出生体重(g)×10/身长(cm)3估测新生儿营养状态.结果早产儿血清瘦素水平明显低于足月儿(0.66±1.03ng/ml vs 3.59±2.16ng/ml,P＜0.01=;适于胎龄儿血清瘦素水平(3.06±0.96ng/ml明显低于大于胎龄儿(4.03±2.22ng/ml),而高于小于胎龄儿(1.13±1.98ng/ml);足月新生儿血清瘦素水平与Rohrer's指数、新生儿体重、胎龄、血清IGF-Ⅰ、生长激素水平呈显著正相关.结论新生儿体内瘦素主要来源于自身脂肪组织,它反映新生儿的生长营养状态,推测瘦素可能通过IGF-Ⅰ、生长激素共同调节新生儿的生长发育,在胎儿和新生儿生长发育中起重要作用.     

新生儿缺氧缺血性脑病发生低血糖15例临床分析

新生儿低血糖是新生儿缺氧缺血性脑病常见并发症。由于新生儿缺氧缺血性脑病临床表现多种 ,故低血糖症状易混淆。近年有报道新生儿低血糖如不及早诊断及治疗 ,反复发作可导致永久性脑损害。因此我院新生儿科自 1999年 1月至 2 0 0 0年 2月对入院的新生儿缺氧缺血性脑病进行微量血糖监测 ,其结果现报告如下。资料与方法一、对象 :1999年 1月以来至 2 0 0 0年 2月入院符合新生儿缺氧缺血性脑病诊断标准。均为足月儿 ,入院时日龄均小于 3天 ,男 89例 ,女 35例 ,其中适于胎龄儿 94例 ,小于胎龄儿 9例 ,大于胎龄儿 2 1例。娩出时均有不同程度的窒…     

106例小于胎龄儿临床分析与随访

１０６例小于胎龄儿临床分析与随访青岛市第二人民医院儿科（２６６０３３）郑青，齐瑛，栾红，李军军北京儿童医院刘红小于胎龄儿系宫内发育迟缓的胎儿，由于其生后合并症多，病死率高，而且关系着以后的生长发育及智力水平，近年来日益受到重视。本文就近五年来收治的１...     

新生儿血清瘦素水平变化与IGF—I、生长激素等相关因素的分析

目的　探讨新生儿血清瘦素来源及其与胰岛素样生长因子 -I(IGF -I)和生长激素的关系。方法　采用放射免疫法检测 80例新生儿静脉血和脐血瘦素水平 ,根据不同胎龄新生儿出生体重值分为大于胎龄儿组 2 8例 ,适于胎龄儿组 36例 ,小于胎龄儿组 16例 ;采用Rohrer’s指数 =出生体重 (g)× 10 /身长 (cm) 3 估测新生儿营养状态。结果　早产儿血清瘦素水平明显低于足月儿 (0 .6 6± 1.0 3ng/mlvs 3.5 9± 2 .16ng/ml,P <0 .0 1=;适于胎龄儿血清瘦素水平 (3.0 6± 0 .96ng/ml明显低于大于胎龄儿 (4.0 3± 2 .2 2ng/ml) ,而高于小于胎龄儿 (1.13± 1.98ng/ml) ;足月新生儿血清瘦素水平与Rohrer’s指数、新生儿体重、胎龄、血清IGF -I、生长激素水平呈显著正相关。结论　新生儿体内瘦素主要来源于自身脂肪组织 ,它反映新生儿的生长营养状态 ,推测瘦素可能通过IGF -I、生长激素共同调节新生儿的生长发育 ,在胎儿和新生儿生长发育中起重要作用     

窒息新生儿缺氧缺血性心肌损害Q-T离散度与血清CK-MB的早期变化及意义

目的探讨窒息新生儿缺氧缺血性心肌损害(HIM)患儿早期Q-T离散度(Q-Td)和血清肌酸激酶同工酶B(CK-MB)的变化,为临床提供早期诊断和治疗依据.方法对66例HIM患儿发病24h内、72h内和治疗7d后的Q-Td和CK-MB值进行检测,并与30例无窒息新生儿对照比较.结果 HIM组与对照组比较:HIM组发病24h内Q-Td与CK-MB即明显升高,72h内达到高峰(P<0.01).经7d治疗后,HIM患儿Q-Td与CK-MB均显著下降,但足月小于胎龄儿(SGA)HIM组下降欠理想,且足月小于胎龄儿HIM组并发症多,多数有循环不良表现,预后差(P<0.05).结论 Q-Td与CK-MB相结合作为HIM的早期特异性敏感指标,对早期诊断及治疗HIM有益.     

高危新生儿血糖早期监测的临床价值

目的了解高危新生儿低血糖发生情况、探讨低血糖病因和降低低血糖发生率及危害性措施，为临床防治提供依据。方法对住院的1026例高危新生儿在生后3d内进行血糖监测。结果高危新生儿低血糖发生率6．53％；早产儿组较之于足月儿组、低出生体重儿和巨大儿组较之于正常出生体重儿组、小于胎龄儿组较之于适于和大于胎龄儿组，低血糖发生率明显增高（P〈0．01）。结论对高危新生儿进行血糖监测很有必要，并尽旱喂养，及时处置。     

Lowering Cortisol enhances growth hormone response to growth hormone releasing hormone in healthy subjects

Cortisol is known to influence growth hormone release probably by modulating somatostatin tone. We examined the effect of metyrapone (the 1 β-hydroxylase inhibitor) treatment on growth hormone response to growth hormone releasing hormone (1 μg kg^-1 body wt). Six healthy male subjects were tested on two occasions 1 wk apart. On one occasion they received metyrapone followed by growth hormone releasing hormone and on the other placebo followed by growth hormone releasing hormone. In all subjects metyrapone produced a significant drop in Cortisol levels. Together with this drop there was a significant enhancement of growth hormone response to growth hormone releasing hormone. The GH response was negatively correlated with the Cortisol level. Growth hormone release in response to growth hormone releasing hormone challenge is thus seen to be heavily influenced by Cortisol levels.     

Growth and growth hormone in Turner syndrome: Looking back,looking ahead

Short stature is the most ubiquitous feature of Turner syndrome (TS). Today, many girls with TS are treated with recombinant human growth hormone (GH) to accelerate growth in childhood and to improve adult height. Here, we will review the history of our understanding of growth in TS, reflect on the path of clinical trials ultimately leading to regulatory approval for clinical use of GH, discuss factors associated with growth outcomes and survey the current unanswered questions about growth and GH in TS.     

The past,present, and future of child growth monitoring: A review and primer for clinical genetics

Child growth measurements are critical vital signs to track, with every individual child growth curve potentially revealing a story about a child's health and well-being. Simply put, every baby born requires basic building blocks to grow and thrive: proper nutrition, love and care, and medical health. To ensure that every child who is missing one of these vital aspects is identified, growth is traditionally measured at birth and each well-child visit. While the blue and pink growth curves appear omnipresent in pediatric clinics, it is surprising to realize that their use only became standard of care in 1977 when the National Center for Health Statistics (NCHS) adopted the growth curve as a clinical tool for health. Behind this practice lies a socioeconomically, culturally, and politically complex interplay of individuals and institutions around the world. In this review, we highlight the often forgotten past, current state of practice, and future potential of this powerful clinical tool: the growth reference chart, with a particular focus on clinical genetics practice. The goal of this article is to understand ongoing work in the field of anthropometry (the scientific study of human measurements) and its direct impact on modern pediatric and genetic patient care.     

Relationship between practice organization and cardiovascular risk factor recording in general practice.

BACKGROUND: Research findings suggest that the level of cardiovascular risk factor recording in general practice is not yet optimal. Several studies indicate a relation between the organization of cardiovascular disease prevention at practice level and cardiovascular risk factor recording. AIM: To explore the relation between the organization of cardiovascular disease prevention and risk factor recording in general practice. METHOD: A cross-sectional study was conducted using data on adherence to selected practice guidelines and on cardiovascular risk factor recording from 95 general practices. Practice guidelines were developed beforehand in a consensus procedure. Adherence was assessed by means of a questionnaire and practice observations. Risk factor recording was assessed by an audit of 50 medical records per practice. RESULTS: Factor analysis of risk factor recording revealed three dimensions explaining 76% of the variance: recording of health-related behaviour, recording of clinical parameters, and recording of medical background parameters. Adherence to the guideline 'proactively invite patients to attend for assessment of cardiovascular risk' was related to a higher recording level in all three dimensions. Practice characteristics did not show a consistent relationship to the level of risk factor recording. CONCLUSION: This study indicates that the presence of a system of proactive invitation was related to the recording of cardiovascular risk factors in medical records in general practice.     

IGF-1 regulate the expression of uncoupling protein 2 via FOXO1

Abstract

Mitochondria uncoupling protein2 (UCP2) expressed ubiquitously is a key molecule of energy metabolism. Insulin-like growth factor-1 (IGF-1) is a hormone, a target molecule of growth hormone (GH) signal pathway, which is also known as the drug “mecasermin” for clinical usages. IGF-1 is seemed to be closely related to metabolic diseases, such as adult GH deficiency. However, there has not been reports depicted possible relationship with each other. So, we sought to elucidate the mechanisms by which expression of UCP2 is regulated by IGF-1 via FOXO1. The findings suggested that three sequences in the consensus UCP2 promoter play complementary functional roles in the functional expression of FOXO1. So, we found that FOXO1 is involved in IGF-1-mediated energy metabolism greater than that of direct action of GH via STAT5. Our findings suggested that IGF-1 was involved in energy metabolism by regulating the expression of UCP2 via the PI3K/Akt/FOXO1 pathway.     

The metabolic syndrome: Validity and utility of clinical definitions for cardiovascular disease and diabetes risk prediction

The purpose of clinical definitions of the metabolic syndrome is frequently misunderstood. While the metabolic syndrome as a physiological process describes a clustering of numerous age-related metabolic abnormalities that together increase the risk for cardiovascular disease and type 2 diabetes, clinical definitions include obesity which is thought to be a cause rather than a consequence of metabolic disturbance, and several elements that are routinely measured in clinical practice, including high blood pressure, high blood glucose and dyslipidaemia. Obesity is frequently a central player in the development of the metabolic syndrome and should be considered a key component of clinical definitions. Previous clinical definitions have differed in the priority given to obesity. Perhaps more importantly than its role in a clinical definition, however, is obesity in isolation before the hallmarks of metabolic dysfunction that typify the syndrome have developed. This should be treated seriously as an opportunity to prevent the consequences of the global diabetes epidemic now apparent. Clinical definitions were designed to identify a population at high lifetime CVD and type 2 diabetes risk, but in the absence of several major risk factors for each condition, are not optimal risk prediction devices for either. Despite this, the metabolic syndrome has several properties that make it a useful construct, in conjunction with short-term risk prediction algorithms and sound clinical judgement, for the identification of those at high lifetime risk of CVD and diabetes. A recently published consensus definition provides some much needed clarity about what a clinical definition entails. Even this, however, remains a work in progress until more evidence becomes available, particularly in the area of ethnicity-specific waist cut-points.     

铁、锌、铅对学龄儿童生长激素分泌的影响

目的研究7～17岁儿童生长激素分泌水平,并探讨血清铁、血清锌和血铅含量对生长激素分泌的影响。方法采取分层整群抽样对济宁市744名7～17岁青少年儿童,空腹采集静脉血5ml,运用放射免疫法测定血清生长激素含量,分光光度法测定血清铁含量,电位溶出法测定血清锌和全血中铅的含量。结果男、女童生长激素分泌的突增年龄分别为11岁和9岁;9～10岁年龄段女童分泌量显著高于男童,12岁以后男童分泌水平反超女童;随着血清铁含量的增加,生长激素分泌量呈逐渐增大趋势,低、中、高3个血清铁含量组生长激素分泌量差异有统计学意义（F=18.78,P〈0.05）;锌充足组生长激素分泌量高于缺乏组,差异有统计学意义（t=9.338,P〈0.01）;随着血铅含量增加,生长激素分泌水平逐渐降低,经方差分析显示：相对安全组、超标组和高铅组生长激素分泌量差异有统计学意义（F=6.68,P〈0.05）。结论女童生长激素分泌的突增期早于男童;血清中铁、锌含量的增加能促进生长激素的分泌,血铅的增加则抑制生长激素的分泌。     

Evidence for a Local Action of Growth Hormone in Embryonic Tooth Development in the Rat

Abstract

Studies in non-dental embryonic tissues have suggested that an interaction between growth hormone and its receptor may play a role in growth and development before the foetal pituitary gland is competent. This study reports the distribution of growth hormone, its rezceptor and binding protein in developing rat tooth germs from embryonic day 17 to 21 and postnatal day 0 using antibodies specific for each of these proteins. Four foetal rats were processed at each time point (E17, EM, E20/21 and postnatal day 0). Following routine fixation and paraffin embedding, sections were treated with antisera to rat growth hormone, rat growth hormone binding protein and growth hormone receptor. Localization of antibody/antigen complexes was subsequently visualized by addition of biotinylated IgG and reaction with streptavidin peroxidase and diaminobenzidine. Assessment of the level of staining was qualitative and based on a subjective rankings ranging from equivocal to very strong staining. Overall, growth hormone and its binding protein were located both in the cellular elements and throughout the extracellular matrix, whereas the growth hormone receptor showed an exclusively intra-cellular location. All three proteins were detectable in cells of the dental epithelium and mesenchyme at the primordial bud stage (E17) which occurs prior to expression of pituitary growth hormone. At the cap stage of odontogenesis (E18-19), numerous cells in both the dental epithelium and mesenchyme were intensely immunoreactive for growth hormone, its binding protein and receptor. In the succeeding early bell stage (E20-21), most of the mesenchymal cells in the dental pulp were mildly positive for these proteins, while the dental epithelium and adjacent mesenchyme were more immunoreactive. At the late bell stage (postnatal day 0), all three proteins were localized in dental epithelium, differentiating mesenchymal cells the cuspal surface facing the epithelial-mesenchymal interface, preodontoblasts, and odontoblasts forming dentine. From these observations, immunoreactive growth hormone, its receptor and binding protein appear to be expressed in odontogenic cells undergoing histodiierentiation, morphodifferentiation and dentinogenesis in a cell-type and stage-specific pattern throughout embryonic tooth development. This suggests the possibility that growth hormone, or a growth hormone-like protein, plays a paracrindautocrine role in tooth development in utero.