地方性氟中毒病区中氟对胎儿影响的研究

本文以不同氟水平地区153名怀孕4个月以上的孕妇为对象研究氟对胎儿可能产生的影响。结果表明,随着孕妇尿氟水平的升高其胎儿羊水氟含量也升高,差异显著(p<0.01)。通过对29例胎儿股骨的光镜观察及3例扫描电镜的观察,发现孕妇尿氟、胎儿羊水氟水平高者有明显病理改变,主要表现为骨生成活跃且紊乱。病理改变与尿氟、羊水氟氟水平有关,当尿氟小于2.0mg/L、羊水氟小于0.03mg/L 无病理改变发生。尿氟水平低于3.5mg/L 组,病理改变率为17.39%,(4/23),高于7mg/L 组病理改变率为83.33%(5/6),两者差异显著(P=0.0055);羊水氟水平低于0.05mg/L 组病理改变率为8.3%(1/12),高于0.05mg/L 组为47.06(8/17),差异显著(p=0.0422)。研究结果提示,氟能经过胎盘进入胎儿体内且可用羊水氟水平反应胎儿受氟量的高低及判断能否受到影响,说明氟对人体的作用在胎儿时期即可发生,这为氟中毒的早期防治提供了依据。     

地方性氟中毒病区儿童龋齿调查分析

地方性氟中毒病区儿童龋齿调查分析刘怀中周元庆玄升泽张来福解守兴杨茂伦刘秀荣周天化肖娟滕国兴为了探讨氟病区学龄儿童龋齿发病情况和氟斑牙与龋齿之间关系，我们对林口县古城镇新立村氟病区和非病区以及病区内部饮不同水源的学生儿童进行龋齿调查。现将调查结果分析如...     

地方性氟中毒病区居民寿命的研究

地方性氟中毒病区居民的死亡率、寿命损失率都比非氟病区高;各年龄组的尚存人数、尚存率、平均期望寿命都低于非病区。     

黑龙江省地方性氟中毒重点病区调查报告

目的为了解黑龙江省地氟病重病区的病情现状.方法于2001年9～10月份对地氟病重病区县林甸县、安达市、肇州县进行了抽样调查.结果 3县儿童氟斑牙患病率随病情程度加重,患病率呈上升趋势;儿童尿氟浓度与氟斑牙患病情况及病情程度呈现正相关关系,即随病区程度加重,病情加重,尿氟值升高3县水氟检测结果重病区水氟含量明显高于非病区.结论黑龙江省地氟病病情仍很严重,应加大防治力度.     

地方性氟中毒病区与非病区群体尿氟含量分析

目的分析全国地方性氟中毒病区与非病区人群尿氟含量水平,以便确定地方性氟中毒病区与非病区尿氟含量临界值.方法现场调查与资料分析相结合.结果全国非地方性氟中毒病区以几何均数表示的群体尿氟含量中位数儿童 0.7mg/L、成人0.83mg/L;95%位数儿童为1.43 mg/L、成人为1.59 mg/L99%位数儿童为1.79 mg/L、成人为1.89 mg/L.饮水型和燃煤污染型病区儿童群体尿氟几何均数＞1.43 mg/L,饮水型、燃煤污染型和饮茶型病区成人群体尿氟几何均值均＞1.68 mg/L.结论全国地氟病病区与非病区群体尿氟含量儿童以1.4 mg/L、成人以1.6 mg/L为临界值,饮茶型病区成人尿氟含量更有代表性.     

地方性氟中毒病区与非病区老年性白内障与超氧化物歧化酶

研究证实,地方性氟中毒是老年性白内障的发病原因之一,那么它是如何使其发生与发展的呢?对此笔者进行了相关发病机理的研究,在各种实验对比分析中,发现地方性氟中毒病区的老年性白内障其SOD活性改变显著。考虑可能是导致白内障发生与发展的机理之一。1 材料与方法1.1 材料 以囊内法完整取出晶体计54枚,其中病区白内障晶体28枚,非病区20枚;病区透明晶体3枚,非病区透明晶体3枚。白内障均为老年性白内障,平均年龄59岁,男、女性别无差异;透明晶体取自尸眼或外伤眼。取出之晶体立即置于-20℃冰箱冷冻待     

地方性氟中毒病区人群摄氟量与尿氟的关系

饮水氟与尿氟之间关系及意义已有很多资料报道,但燃煤污染型氟中毒地区人群摄氟量与尿氟的关系及意义如何?报道很少,现将本文结果报道如下。1 材料和方法1.1 调查点选择 燃煤污染型氟中毒病区选7个摄氟量不同的观察点;饮水型氟中毒病区选7个水氟含量不同的观察点。1.2 尿样采集及检测 每个观察点随机抽取若干儿童、成人晨尿用离子选择电极法测定尿氟。1.3 摄氟量调查方法     

大安市地方性氟中毒病区病情监测结果

大安市是饮水型地方性氟中毒病区，病因是居民饮用含氟量高的浅层地水导致氟化物在体内蓄积所致氟中毒。近十几年来随着农村经济的快速发展，很多病区部分居民自家打了深井，降低了饮水氟含量，这样原来所订、中、重病区地方性氟中毒的发病率和病情严重程度就会发生一定变化，同时近5年来大安市氟病区新建改水工程总量累计超过氟病区总数的一半以上，为掌握这些氟病区病情现状，     

地方性氟中毒病区人群血清酶学研究

近年来,对地方性氟中毒非骨相损伤与血液生化学改变的研究日益深入,并取得大量资料。许多资料证明,长期生活在病区人群血液生化学方面,有许多指标有所改变,而有些人经X线检查尚未出现氟骨症样改变时,其血液生化指标已有明显改变,可能对地方性氟中毒早期诊断和发病机理的研究具有实际意义,但目前看来还不能反映出明确的普遍规律性,观点不能统一。为此,本文在不同类型病区人群中随机选出部分人群采血样,应用生化自动分析仪同时进行多种分析,以探讨氟中毒病区人群早期生化改变特点,在早期诊断、发病机理的研究中的意义。     

慢性氟中毒对人胎心肌的影响

对５例氟病区５～７个月胎龄的胎儿心肌进行电镜及体视学检查，发现病区胎儿心肌线粒体肿胀，体积增大及嵴减少或消失，病区胎儿线粒体体积和密度显著大于非病区组，表明过量的氟化物对人胎心肌细胞有明显影响。     

实验性氟中毒大鼠关节滑膜细胞的体视学研究

为探讨氟中毒对关节滑膜的损伤，用１２只Ｗｉｓｔａｒ大鼠随机分为对照组和实验组。实验大鼠饲以５０ｍｇ／Ｌ含氟水１２０ｄ后，取关节滑膜进行超微结构体视学检查。结果显示：氟中毒大鼠关节滑膜细胞体积缩小，线粒体肿胀、增生，与对照组比较，差异有显著性（Ｐ＜０．０５）。表明过量氟对滑膜细胞有损伤作用。     

改饮低氟水4年后氟中毒孕妇胎儿骨骼发育研究

目的探讨氟中毒孕妇脱离氟中毒环境后机体对胎儿骨骼发育影响。方法选择德州市德城区作为研究地区,筛选出该地区2017年1月至2019年6期间20名氟中毒孕产妇为观察组,选择该地区同一时期的健康孕产妇20例为对照组,收集两组孕妇新生儿的头围、双顶径、股骨长度及骨密度等指标,比较两组结果,以判断氟中毒对胎儿骨骼发育有无影响。结果观察组头围、双顶径及股骨长度及其骨密度值均低于对照组,差异有统计学意义(P<0.01)。结论脱离氟中毒环境后,氟中毒孕妇机体对胎儿骨骼发育仍有一定影响,导致胎儿骨骼发育缓慢。     

Circadian clock signals in the adrenal cortex

Circadian secretion of steroid hormones by the adrenal cortex is required to maintain whole body homeostasis and to adequately respond to or anticipate environmental changes. The richly vascularized zona glomerulosa (ZG) cells in the pericapsular region regulate osmotic balance of body fluid by secreting mineralocorticoids responding to circulating bioactive substances, and more medially located zona fasciculata (ZF) cells regulate energy supply and consumption by secreting glucocorticoids under neuronal and hormonal regulation. The circadian clock regulates both steroidogenic pathways: the clock within the ZG regulates mineralocorticoid production via controlling rate-limiting synthetic enzymes, and the ZF secretes glucocorticoid hormones into the systemic circulation under the control of central clock in the suprachiasmatic nucleus. A functional biological clock at the systemic and cellular levels is therefore necessary for steroid synthesis and secretion.     

SR-BI-mediated HDL cholesteryl ester delivery in the adrenal gland

In adrenocortical cells, scavenger receptor class B, type I (SR-BI) is localized in specialized plasma membrane compartments, called microvillar channels, that retain high density lipoprotein particles (HDL) and are sites for the selective uptake of cholesteryl esters (CE). Formation of microvillar channels is regulated by adrenocorticotropic hormone (ACTH) and requires SR-BI expression. Subsequent to SR-BI-mediated delivery to the plasma membrane, HDL-CE is metabolized to free cholesterol by hormone sensitive lipase and transported to the mitochondria for steroid synthesis via START domain proteins. The relevance of SR-BI to adrenal steroidogenesis is evident by the impairment of glucocorticoid-mediated stress response in the absence of SR-BI-mediated HDL-CE uptake in mice. On the molecular level, SR-BI mediates HDL-CE selective uptake by forming a hydrophobic channel. In addition, SR-BI facilitates bi-directional flux of cholesterol by modifying the phospholipid content of the plasma membrane. SR-BI most likely accomplishes these functions by forming homo-oligomers in the plasma membrane. Examination of SR-BI oligomerization using fluorescence resonance energy transfer spectroscopy revealed that SR-BI multimerizes via its C-terminal region. Overall, SR-BI is the cell surface receptor responsible for selective uptake of lipoprotein cholesterol and its ultimate delivery to sites of hormone synthesis in steroidogenic tissues.     

氟中毒大鼠服硒对体内氟及抗氧化酶和脂类影响的实验研究

目的研究硒对氟中毒大鼠体内氟、抗氧化酶和脂类代谢的影响作用。方法Ｗｉｓｔａｒ大鼠饮２．６３ｍｍｏｌ／Ｌ高氟水１０个月后分为氟、氟加２．０ｍｇ／ｋｇ硒、改饮正常水、改正常水加硒４组,再喂养１０个月。观察尿氟动态变化,测定骨、组织、血清氟和硒,同时测血ＧＳＨ－ｐｘ、ＳＯＤ、ＬＰＯ及血ＴＣ、ＴＧ、ＨＤＬ－Ｃ、ＬＤＬ－Ｃ等。结果氟加硒组较氟中毒组尿氟排泄增高,骨、组织氟降低,酶和脂代谢改善;改正常水加硒组,排尿氟和降体氟作用优于单纯改水组,酶和脂类指标水平更趋正常。结论一定浓度范围内的硒对氟中毒大鼠具有排高氟和调整自由基、脂类代谢紊乱作用。改正常水加硒则有促进氟中毒恢复的作用。     

硒锌制剂拮抗慢性氟中毒的实验研究

目的：探讨硒锌制剂对慢性氟中毒的影响及其机理。方法：Wistar大鼠在饮含50mg/L高氟水的同时通过灌胃方式给予不同剂量的硒锌制剂,2个月后,测量大鼠尿液氟浓度和r-GT活性,血液GSH－Px活性及肾组织中LPO水平,GSH含量和SOD活性,结果：发现硒锌制剂通过促进尿氟排泄,增强全血GSH－PX的肾SOD活性,增加肾GSH含量而抑制氟中毒引起的脂质过氧化作用,从面降低尿r-GT活性和肾LPO含量,结论：提示一定剂量的硒锌制剂对慢性氟中 明显的拮抗作用,其机理可能与通过促进尿氟排泄和抗脂质过氧化作用有关。     

The adrenal cortex and sexual differentiation during early human development

Human sexual differentiation is a critical process whereby a strict dimorphism is established that enables future reproductive success as phenotypic males and females. Significant components of this differentiation pathway unfold during the first three months of gestation when they are sensitive to disruption by abnormal hormonal influences. Excessive exposure of female development to androgens in conditions such as congenital adrenal hyperplasia causes virilization. However, recently we have suggested that female development normally takes place in the presence of low, yet significant, levels of androgen, implying a need for strict regulation to avoid virilization and the potential for a biological role of androgens in females that has not been fully elucidated. Here, we review androgen-dependent male differentiation of the external genitalia in humans, and link this to current understanding of female development and steroidogenesis in the developing adrenal cortex.