母婴血清胆红素对免疫球蛋白及补体的影响

目的 探讨母婴血清胆红素对免疫球蛋白及补体的影响。方法 同时检测１１８例配对母亲，脐血新生儿和４２例对照组成人的血清免疫球蛋白，补体和总胆红素，结合胆红素含量，并作相关分析。结果 （１）血清Ｂｉｌ－Ｔ，Ｂｉｌ－Ｂ含量高低依次为新生儿〉脐血〉母亲，对照组。（２）母亲和新生儿的血清ＩｇＧ，ＩｇＡ，ＩｇＭ，Ｃ３，Ｃ４均不受母亲Ｂｉｌ－５，Ｂｉｌ－Ｄ的影响。（３）新生儿的血清ＩｇＧ和Ｃ３含量均不受脐血压     

高胆红素血症新生儿蓝光治疗前后脑干听觉诱发电位的改变

目的 为探讨光疗在降低血清胆红素浓度时能否逆转脑干听觉诱发电位的变化。方法 比较１６例高胆红素血症足月新生儿（ＨＢＴＮ）及３６例正常及足月新生儿（ＮＴＮ）的ＢＡＥＰ检测结果，ＨＢＴＮ组经蓝光治疗后的ＢＡＥＰ改变。结果 光疗后胆红素浓度下降，ＢＡＥＰ值相应得到改善，１６例中６例恢复正常，１０例明显好转。结论 光疗不仅能降低血清胆红素浓度而且能逆转胆红素对ＢＡＥＰ的影响，即光疗效能逆转胆红素脑病。     

产前使用缩宫素对新生儿胆红素影响的临床观察

目的:观察产妇在产前使用缩宫素对新生儿胆红素值的影响.方法:对496例正常出生的单胎足月正常新生儿进行分组对照分析.产妇产前应用缩宫素101例,未用缩宫素395例,观察两组病例新生儿经皮胆红素均值及新生儿高胆红素血症的发生率.结果:使用缩宫素组经皮胆红素值与未用药组相近,差异无统计学意义;使用缩宫素组新生儿高胆红素血症的发生率比未用药组稍高,但差异无统计学意义(P>0.05).结论:应用缩宫素组新生儿经皮胆红素值及新生儿高胆红素血症的发生率与未用药组相近,产妇在产前适量应用缩宫素对新生儿胆红素值无影响,不增加新生儿高胆红素血症的发生率.     

新生儿生理性黄疸不同时间胆红素正常值测定研究

【目的】分析西安地区新生儿生理性黄疸不同时间胆红素正常值及相关因素。【方法】对1 452例足月正常新生儿进行12、24、48、72、849、6 h经皮胆红素测定,对204例新生儿黄疸进行经皮胆红素和血清胆红素同步对照研究。【结果】经皮胆红素值与血清胆红素值直线相关,相关系数(r=0.943,P=0.01);直线回归方程:经皮胆红素值=2.286 0.919×血清胆红素值;统计学分析得出12、24、48、72、849、6 h的胆红素值。【结论】本研究得出西安地区足月健康新生儿生理性黄疸不同时间胆红素正常参考值。     

新生儿高胆红素血症诊治中胆红素两种检测方法的价值分析

目的 探讨经皮胆红素检测及血清胆红素检测在新生儿高胆红素血症诊治中的临床价值.方法 选择180例高间接胆红素血症的足月新生儿,采用标准化JH20-1C型经皮胆红素仪进行无创经皮胆红素测定,将其与同步血清胆红素测定值进行比较分析.结果 经皮胆红素测定值51.3～325.6( 169.3±51.2)μmol/L,与血清胆红素测定值68.4～ 338.9(187.5±42.5)μmol/L呈正相关(r=0.91,P＜0.01).结论 经皮胆红素测定无创、操作简便、结果可靠,对检测和诊断新生儿高胆红素血症具有较高的临床应用价值.     

尘肺血脂、肝胆B超检查

测定了尘肺患者血清ＴＣ、ＴＧ值,并进行了肝胆Ｂ超检查。结果尘肺组血清ＴＧ、ＴＣ均值均低于对照组,Ｂ超检查结果与对照组比较差异无显著意义。     

经皮黄疸仪在新生儿黄疸中的临床价值探讨

目的:通过新生儿经皮胆红素的动态监测,早期发现新生儿高胆红素血症,早期进行干预。方法:应用经皮胆红素检测仪和血清同时对165例新生儿进行胆红素检测结果进行线性相关分析。结果:经皮胆红素检测仪和血清胆红素测定值有线性正相关关系,相关系数(r=0.478,P<0.000)。结论:新生儿胆红素经皮测试与血清胆红素测定相比,操作简便,安全、有效、无创、易接受、利于重复进行及动态监测,可及时预测黄疸的发生与转归。     

经皮胆红素仪在新生儿病理性黄疸筛查中的应用

目的:探讨经皮胆红素仪在新生儿病理性黄疸筛查中的实用价值。方法:采用国产JD-2型经皮胆红素仪对1 076例足月新生儿进行胆红素测定,并将筛出的35例病理性黄疸新生儿的经皮检测值与静脉血清胆红素值进行比较。结果:正常新生儿与病理性黄疸新生儿从出生第2天开始,经皮胆红素值有明显差异,病理性黄疸新生儿经皮检测值与血清检测值差异无统计学意义。结论:经皮胆红素仪具有方便、安全的特点,对早期新生儿黄疸的筛查及动态监测有良好的临床应用价值。     

新生儿胆红素经皮动态测试与早期干预

目的:通过新生儿经皮胆红素动态测试,早期发现新生儿高胆红素血症,早期干预。方法:将1554例新生儿在生后3、5、7天进行测试,用JD-1经皮黄疸仪进行测试,同时目测。阳性者均经血清胆红素测试,对测试值超过异常的给予干预。结果:皮测阳性率大于目测。结论:新生儿胆红素经皮测试,与传统目测方法相比更科学、更准确,利于早期发现新生儿高胆红素血症、早期干预。     

经皮胆红素测定在新生儿黄疸中的应用

目的评价经皮胆红素测定（TCB）在新生儿黄疸中的应用价值。方法测定26例新生儿的前额处的TcB读数及血清胆红素（SRB），并对二者做直线相关分析。结果新生儿前额处的TcB读数平均值与血清胆红素值（包括血清总胆红素、血清未结合胆红素及血清结合胆红素）均存在显著直线相关，且得出3个直线回归方程。结论经皮胆红素测定仪以其简便、安全的特点，可作为临床监测胆红素的一种手段，且可由经皮检测值推算出血清总胆红素、血清未结合胆红素、血清结合胆红素值。     

阿克苏市和宜宾市汉族新生儿高胆红素血症相关因素对比研究

目的 通过绘制四川宜宾市翠屏区汉族新生儿和新疆阿克苏市汉族新生儿生后120 h内经皮小时胆红素测定曲线图,分析不同地区相同民族之间新生儿高胆红素血症的发生率、发生时间以及峰值期,为两地区的汉族新生儿高胆红素血症的预防、评估及处理提供理论参考依据。方法 选择2018年1月—2019年12月在宜宾市第三人民医院产科出生的汉族和新疆兵团第一师医院产科出生的健康新生儿为研究对象,详细记录可能与新生儿黄疸有关的相关研究指标,监测其出生后5天经皮胆红素值(TCB),分别计算每一时段的TCB P₂₅、P₅₀和P₇₅值,并绘制成曲线图,分析新生儿高胆红素血症的围生期影响因素。结果 本研究共纳入新生儿1 605例,在同一时龄,宜宾市汉族新生儿经皮胆红素P₂₅、P₅₀、P₇₅值均高于阿克苏市汉族新生儿;宜宾市汉族新生儿高胆红素血症发生率高于阿克苏市汉族新生儿(χ²=118.5,P<0.001)。早产、开奶时间>24 h、头颅血肿、孕母应用催产素是发生新生儿高胆红素血症的独立危险因素(OR=8.331、19.640、2.982、4.019)。结论 出生后5日内,新生儿胆红素水平随着日龄的增长逐渐升高,其中宜宾市汉族新生儿出生后小时胆红素水平上升速率较阿克苏汉族新生儿高,高胆红素血症的发生率亦高于阿克苏市汉族新生儿。     

“泳疗”对新生儿血胆红素水平的影响

目的:探讨"泳疗"对新生儿体内胆红素水平的影响。方法:随机抽取236例足月阴道分娩新生儿,分为两组:研究组(游泳)127例,对照组(沐浴)109例,利用经皮胆红素测定仪测定两组新生儿生后1～5天经皮胆红素值(Trarscutaneons billirubin,TCB)变化。结果:研究组TCB明显低于对照组(P<0.01);研究组胎便初排时间及粪便转黄时间均短于对照组(P<0.05,P<0.01)。结论:通过"泳疗"可促进胎便的尽早排出,较快地降低新生儿血胆红素水平、减少高胆红素血症的发生。     

分娩方式对足月新生儿小时胆红素值的影响

目的：创建足月新生儿生后小时胆红素均值曲线图,分析不同分娩方式对小时胆红素值的影响。方法选择胎龄≥37周且出生体重≥2500 g的新生儿1796例,生后开始每6小时监测经皮胆红素值,直至生后96 h。将所测得胆红素数据绘制生后小时胆红素均值曲线图;并分析分娩方式对生后小时胆红素的影响。结果小时胆红素生后的变化随着生后时龄的延长逐渐增高;不同分娩方式新生儿生后小时胆红素值差异有统计学意义;母亲合并高危因素的新生儿同一时龄的小时胆红素值剖宫产分娩亦高于自然分娩。结论足月新生儿小时胆红素正常值对指导新生儿高胆红素血症的防治起着重要作用,剖宫产分娩新生儿小时胆红素值高于同时龄自然分娩新生儿。     

4875例新生儿高胆红素血症发病的危险因素及其影响

目的 分析新生儿高胆红素血症发病的危险因素及其影响.方法 选择2009年1月至2012年12月本院普通新生儿病区12 975例住院治疗患儿中的4 875例高胆红素血症患儿为研究对象（本研究遵循的程序符合南方医科大学附属深圳妇幼保健院人体试验委员会所制定的伦理学标准,得到该委员会批准,分组征得受试对象监护人的知情同意,并与之签署临床研究知情同意书）,并按照出生情况将其分为早产儿组（n=414）和足月儿组（n=4 461）.监测两组患儿经皮胆红素值（TCB）和血清总胆红素值（TSB）.结果 本研究高胆红素血症发病率为37.6％（4 875/12 975）.新生儿高胆红素血症危险因素分别为围生期因素（48.5％）、感染因素（19.4％）、母乳性黄疸（17.2％）、ABO溶血病（10.2％）及其他因素（4.7％）.早产儿组和足月儿组上述各高胆红素血症发病危险因素比较,差异均有统计学意义（χ^2 =23.11,5.49,28.64,2.67,212.07;P＜0.05）.结论 早产儿相对足月儿易罹患高胆红素血症.对具有新生儿高胆红素血症危险因素的新生儿,尤其是早产儿,加强胆红素水平监测,并对TSB水平较高者及时实施干预措施,可有效降低胆红素脑部的发生率,改善其预后.     

Effects of 1,2,4-trichlorobenzene on estuarine macrobenthic communities exposed via water and sediment

Macrobenthic animal communities that colonized sand-filled aquaria were exposed to 1,2,4-trichlorobenzene (TCB), a recent replacement for polycholorinated biphenyls in the electrical industry. In one test, communities established by planktonic larvae entrained in continuously supplied unfiltered seawater for 50 days were exposed to waterborne TCB for 6 days; in the second test, the toxicant was added to the sediment before 8 weeks of colonization. Concentrations that affected community structure were usually two orders of magnitude lower for waterborne TCB than for sediment-bound TCB, but the same types of organisms were affected by each route of exposure. The lowest TCB concentrations (measured) that affected average numbers of individuals exposed via the water were 0.04 mg/liter for mollusks, 0.4 mg/liter for arthropods, and 4 mg/liter for annelids. Average number of species was significantly lower than the control at 4 mg/liter. For TCB exposures via the sediment, the lowest concentrations (nominal) that affected average numbers of individuals were 100 micrograms/g for mollusks and echinoderms, and 1000 micrograms/g for arthropods and annelids. Average number of species in experimental aquaria was significantly lower than the control at greater than or equal to 100 micrograms/g. TCB persisted in sediments, but some leached into water throughout the 8-week exposure via sediment.     

Responses of rats and nonhuman primates to 2,5,2′,5′-tetrachlorobiphenyl

In a series of experiments that were conducted on rats it was shown that a single oral dose of 2,5,2′,5′-tetrachlorobiphenyl (TCB) in excess of 1,5 g/kg body weight produced heavy mortality within 2 to 3 days. The rats receiving doses below 1.0 g/kg were essentially free of gross abnormalities. Animals pretreated with phenobarbital were able to survive without obvious ill effects when given 1.25 g/kg of TCB while those given SKF 525A were all dead within 4 days, thus relating metabolism with toxicity of the compound. Rats given 100 ppm TCB in the diet for 3 weeks showed less liver hypertrophy and fewer biochemical changes than rats given a similar dose of Aroclor 1248. When monkeys were administered a single dose of 18 mg/kg of TCB/kg body weight, 12% of the unmetabolized compound was excreted in the feces within 14 days. Since only small amounts of TCB were detected in the tissues, it was postulated that a majority of the compound had been metabolized and excreted. At the dose employed, TCB caused only a slight proliferation in the hepatic endoplasmic reticulum and minimal changes in the activities of hepatic microsomal enzymes.     

Maternal hepatic and embryonic effects of 1,2,4-trichlorobenzene in the rat

The possible maternal hepatic and reproductive effects of 1,2,4-trichlorobenzene (TCB) were assessed in rats given 0, 36, 120, 360, and 1200 mg/kg/day of TCB on Days 9-13 of gestation. The animals were sacrificed on Day 14 of pregnancy. Maternal deaths (2/9 rats, 6/6 rats) were recorded in the 360 and 1200 mg/kg/day treatment groups and body weight gain was significantly decreased in the 360 mg/kg/day TCB group. Maternal liver weight, liver/body weight ratio, and hepatic microsomal protein content were unaffected by TCB treatment. Although Day 14 NADPH-cytochrome c reductase activity was affected only at 360 mg/kg/day TCB, the maternal hepatic microsomal cytochrome P-450 content was significantly increased by administration of both 120 and 360 mg/kg/day of TCB. Hepatic microsomal aminopyrine N-demethylase, ethoxyresorufin O-deethylase, and UDP-glucuronyl transferase activity towards p-nitrophenol were also increased at 120 and 360 mg/kg TCB. Glutathione S-transferase activity to 1-chloro-2,4-dinitrobenzene and 1,2 dichloro-4-nitrobenzene were both increased by pretreatment with TCB. Although pretreatment with 360 mg/kg/day TCB did not increase resorptions, embryolethality, or teratogenicity, embryonic development was significantly retarded by all four growth criteria used (head length, crown-rump length, somite number, and protein content).     

Maternal hepatic effects of 1,2,4,5-tetrachlorobenzene in the rat

1,2,4,5-Tetrachlorobenzene (TCB) is an industrial intermediate used in the production of 2,4,5-trichlorophenoxyacetic acid. This herbicide contains trace quantities of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Because of possible maternal hepatic or reproductive effects of this uncharged, low-molecular weight, lipophilic chlorinated benzene 0, 30, 100, 300, and 1000 mg/kg/day of TCB was orally administered to rats on Days 9, 10, 11, 12, and 13 of gestation and the animals were sacrified on Day 14 of pregnancy. No maternal deaths were recorded and body weight gain was significantly decreased only in the 1000 mg/kg/day group. Maternal liver weight, liver to body weight ratio, and hepatic microsomal protein content were unaffected by TCB treatment. Although Day 14 NADPH-cytochrome c reductase activity was not affected, the maternal hepatic microsomal cytochrome P-450 content was significantly increased by administration of 1000 mg/kg/day of TCB. Microsomal N-demethylation of aminopyrine was slightly increased from 2.4 to 3.4 and 3.5 nmole/mg protein/min at doses of 300 and 1000 mg/kg TCB. However, maternal hepatic microsomal ethoxyresorufin O-deethylase activity was greatly increased from 14 to 30, 40, 50, and 49 pmole/mg protein/min in pregnant rats administered 0, 30, 100, 300, and 1000 mg/kg/day TCB. The microsomal rates of p-nitrophenol and phenolphthalein glucuronidation in vitro were not increased by TCB administration. The maternal hepatic microsomal enzyme induction observed after TCB administration to pregnant rats suggests the presence both cytochrome P-450 and P-448 inducers in the sample of 1,2,4,5-tetrachlorobenzene used.     

Estrogenic activity of styrene oligomers after metabolic activation by rat liver microsomes

In this study we examined estrogenic activity of styrene oligomers after metabolic activation by rat liver microsomes. Trans-1,2-diphenylcyclobutane (TCB), cis-1,2-diphenylcyclobutane (CCB), 1,3-diphenylpropane, 2,4-diphenyl-1-butene, 2,4,6-triphenyl-1-hexene, and 1-alpha-phenyl-4ss-(1 -phenylethyl)tetralin were negative in the yeast estrogen screening assay and estrogen reporter assay using estrogen-responsive human breast cancer cell line MCF-7. However, TCB exhibited estrogenic activity after incubation with liver microsomes of phenobarbital-treated rats in the presence of reduced nicotinamide adenine dinucleotide phosphate (NADPH). Minor activity was observed when liver microsomes of untreated or 3-methylcholanthrene-treated rats were used instead of those from phenobarbital-treated rats. CCB, 1,3-diphenylpropane, and 2,4-diphenyl-1-butene also exhibited estrogenic activity after metabolic activation by liver microsomes, but the activity was lower than that of TCB. 2,4,6-Triphenyl-1-hexene and 1-alpha-phenyl-4ss-(1 -phenylethyl)tetralin did not show estrogenic activity after such incubation. When TCB was incubated with liver microsomes of phenobarbital-treated rats in the presence of NADPH, three metabolites were detected by high-performance liquid chromatography (HPLC). One metabolite isolated by HPLC exhibited a significant estrogenic activity. The active metabolite was identified as trans-1-(4-hydroxyphenyl)-2-phenylcyclobutane by mass and nuclear magnetic resonance spectral analysis. These results suggest that the estrogenic activity of TCB was caused by the formation of the 4-hydroxylated metabolite.     

The effects of polychlorinated biphenyls given prenatally on the neurobehavioral development of mice.

When tested at adulthood, albino mice exposed in utero to 3,4,3′,4′-tetrachlorobiphenyl (TCB) demonstrated signs of neurotoxicity. The most severely affected subjects (TCB-spinners) displayed a neurobehavioral syndrome consisting of intermittent stereotypic circling, head bobbing, and hyperactivity. TCB-spinners were found to be markedly hyperactive during the dark phase of the diurnal phase and showed impaired forelimb grip strength, ability to traverse a wire rod, visual placement responding, and acquisition of one-way avoidance. Some mice did not display the spinning syndrome (TCB-nonspinners), but were found to be deficient in traversing a wire rod and avoidance acquisition. None of the TCB-exposed mice were found to have depressed neuromuscular reflexes in response to a variety of stimuli. Tissue distribution studies demonstrated that TCB levels were not detectable in adult mice following prenatal exposures. The results of these experiments demonstrate that prenatal exposure to TCB can influence neurobehavioral functioning of mice during adulthood and, in some cases, such effects can be observed in the absence of clinical signs of toxicity.