健胎液对胎儿宫内发育迟缓孕鼠血浆、胎盘NO含量的影响

为从孕鼠血浆和胎盘一氧化氮（ＮＯ）水平探讨中药“健胎液”治疗胎儿宫内发育迟缓（ＩＵＧＲ）的机理，采用被动吸烟法建立ＩＵＧＲ动物模型，应用镀铜镉还原和内标比色法（Ｇｒｅｉｓ法），测定ＩＵＧＲ组、ＩＵＧＲ加健胎液组（用药组）孕鼠血浆及胎盘组织中ＮＯ的稳定代射终产物亚硝酸基／硝酸基（ＮＯ－２／ＮＯ－３）含量，并以正常孕鼠作对照。结果：与正常对照组和用药组相比，ＩＵＧＲ组胎鼠平均出生体重显著降低（Ｐ＜００１），ＩＵＧＲ组血浆及胎盘组织中ＮＯ－２／ＮＯ－３含量均显著降低（Ｐ＜００５～００１），而用药组和正常组相比，胎鼠平均出生体重、血浆及胎盘组织中ＮＯ－２／ＮＯ－３含量均无显著性差异（Ｐ＞００５）。结论：胎儿宫内发育迟缓的发生与ＮＯ的合成和释放显著降低，因而影响胎盘微循环，限制了母儿宫内发育迟缓。     

孕妇和葡萄胎患者血清中IgD含量观察

应用单向免疫琼脂扩散法测定了３５名正常人，１２７名孕妇，３１名葡萄胎患者血清中ＩｇＤ含量（单位）。结果分别为正常人２２．５±１２．６，孕＜３个月２３．８±１３．８，孕３～６个月３０．５±２６．２，孕＞６个月以上５５．６±１０．８，葡萄胎患者６１．８±１３．２。孕＞６个月及葡萄胎患者血清中ＩｇＤ含量与正常人比较有极显著差异（Ｐ＜０．０１），葡萄胎患者与孕＞６个月血清中ＩｇＤ含量比较，有显著差异（Ｐ＜０．０５），其原因与血清中的β－ＨＣＧ含量增加有关。血清中ＩｇＤ含量与β－ＨＣＧ回归分析表明呈明显正相关（ｒ＝０．６６３７Ｐ＜０．０１）。测定孕妇和葡萄胎患者血清中ＩｇＤ含量，对其免疫病理研究具有十分重要的临床参考价值。     

前置胎盘致胎儿宫内发育迟缓的超声观察

本文对１９８例各型前置胎盘进行了观察，同时设３０６例正常胎儿做对照。用直接计算法计算出孕２８周以后各孕周、各型前置胎盘孕妇之胎儿ＨＣ、ＡＣ、ＦＬ的平均值，与本地区相应孕周正常胎儿ＨＣ、ＡＣ、ＦＬ的平均值，对各配对均数进行ｔ检验，求出Ｐ值。其结果，中央型前置胎盘孕妇之胎儿ＨＣ、ＡＣ、ＦＬ明显小于正常组，Ｐ≤０．０１，统计学上具有非常显著性差异；部分性者，Ｐ≤０．０１，有显著性差异，边缘性者，Ｐ＞０．０５，无显著性差异。前置胎盘之孕妇胎儿出生后体重与对照组相比，８０％低于第５０百分位数，其中３８％低于第１０百分位数。观察证实前置胎盘致孕妇孕期出血，确可影响胎儿正常发育，导致胎儿宫内发育迟缓（ＩＵＧＲ）。本文对各型前置胎盘对胎儿ＨＣ、ＡＣ、ＦＬ的影响进行了探讨。认为Ｂ超可做为判定前置胎盘是否导致ＩＵＧＲ的首选检查方法。     

自然流产妇女T淋巴细胞亚群的研究

本文对有自然流产史的未孕及已孕妇女进行了外周血Ｔ淋巴细胞亚群（Ｔｌｙｍｐｈｏｃｙｔｅｓｕｂｐｏｐｕｌａｔｉｏｎ，ＴＬＳ）的检测并对其中８例做了免疫治疗，结果表明：有自然流产史的未孕组较正常未孕组细胞减少（Ｐ＜０．０５）；细胞增多（Ｐ＜０．０２），故比值明显降低（Ｐ＜０．０１）。有自然流产史早孕组较正常早孕组间细胞元明显差异，而细胞有明显差异（Ｐ＜０．０５），因此有自然流产史早孕组比值较正常早孕组明显下降（Ｐ＜０．０５）。正常早孕妇女细胞较未孕组减少（Ｐ＜０．０５），细胞无明显变化（Ｐ＞０．０５），因此早孕组比未孕组明显降低（Ｐ＜０．０５）。有自然流产史的未孕组及早孕组细胞无明显差异（Ｐ＞０．０５）。经免疫治疗受孕成功妇女，比值上升，接近于正常早孕组。从实验结果表明，细胞免疫功能失调，是引起流产的原因之一，免疫治疗可以改善自然流产妇女的细胞免疫功能，从而获得成功妊娠。     

绞股蓝总皂甙抗大鼠海马结构缺血再灌注损伤的实验研究

探讨大鼠海马结构缺轿再灌注损伤机理及绞股蓝总皂甙抗缺血再灌注损伤的作用，结果：ＩＲ组海马组织中ＭＤＡ含量高于组（Ｐ〈０．０１），而ＳＯＤ含量低于ＳＯＣ组（Ｐ〈０．０１），差异非常显著：ＩＲ＋ＧＰ组海马组织中ＭＤＡ含量明显低于ＩＲ组（Ｐ〈０．０１），而ＳＯＣ含量明显高于ＩＲ组（Ｐ〈０．０１），ＩＲ组海马组织Ｎａ＾＋－Ｋ＾＋－ＡＴＰａｓｅ，Ｃａ＾２＋－ＡＴＰａｓｅ的活性明显低于ＳＯＣ组（Ｐ〈０．０１）     

正常与自发性高血压大鼠血浆,组织内皮素分布变化的观察

本文采用放射免疫分析法测定了自发性高血压大鼠（ＳＨＲ）与正常血压大鼠（ＷＫＹ）血浆、脑和主动脉知管中内皮素量的变化。结果发现，ＳＨＲ血浆、脑和主动脉中ＥＴ含量均显著增高（Ｐ分别〈０．０１、〈０．００２和〈０．０１）；ＷＫＹ脑较血管组织含量低（Ｐ〈０．０１），ＳＨＲ两者则无显著性差异（Ｐ〉０．０５）。提示，ＳＨＲ血浆和组织中内皮素分布的变化与自发性高血压的发生、发展可能有密切的。     

脑血管疾病患者体液中SOD,MDA含量测定

本文对６７例脑卒中（脑梗塞４２例、脑出血２５）病人血清、红细胞、脑脊液、尿进行了超氧化歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）的含量测定。以３４名正常人相同样品作对照。结果：脑卒中患者各标本中ＳＯＤ的含量显著低于对照组（Ｐ〈０．０５￣０．０１），ＭＤＡ含量显著高于对照组（Ｐ〈０．０５）￣０．０１）；脑卒中急性期ＳＯＤ含量低于恢复期，ＭＤＡ含量高于恢复期，具有显著差异（Ｐ〈０．０５）；且脑出血患者血清、红     

被动吸烟孕妇血中儿茶酚胺的含量及其与低体重新生儿发生率的关系

用荧光分光光度法测定了不同孕期的２７５例被动吸烟孕妇和１３０例正常妊娠妇女血中儿茶酚胺（ＣＡ）含量，并对其与低出生体重儿（ＬＢＷ）发生率之间的关系进行了探讨。结果表明：被动吸烟Ａ组（平均每日被动吸烟５～１４支）和Ｂ组（平均每日≥１５支）孕妇孕中期和孕早期血中去甲肾上腺素（ＮＥ）含量，均显著高于同孕期正常妊娠组（Ｐ＜０．０５），且Ｂ组孕中期含量升高尤为显著（Ｐ＜０．０１）；多巴胺（ＤＡ）含量与正常妊娠组比，仅Ｂ组临产前含量显著降低（Ｐ＜０．０５）；被动吸烟Ａ、８两组ＬＢＷ发生率分别是正常妊娠组的２．２７倍和３．２１倍，其中小于胎龄儿（ＳＧＡ）的发生率分别是正常妊娠组的２．９１和３．５０倍。提示被动吸烟所致孕妇血中ＮＥ明显升高与ＬＢＷ的发生可能有关系。因此，社会和家庭对孕妇被动吸烟可能给胎儿发育所带来的危害应给予足够的重视。     

胎儿胸腺细胞悬液腹腔移植防治内源性哮喘临床及免疫学研究

报告用胎儿胸腺细胞悬液移植注射防治内源性哮喘患儿３４例。结果：治愈６７．６５％，显效２６．４７％，有效２．９４％，与胸腺素组（治愈６０％，显效２２．８６％，有效１１．４３％）比较无显著性差异（Ｐ＞０．０５），与常规治疗组（治愈０％，显效２５％，有效４０．６３％）比较总有效率和治愈率均有非常显著性差异（Ｐ＜０．０１）。患儿ＣＤ＿３、ＣＤ＿８明显低于正常对照组（Ｐ＜０．０１），ＣＤ＿４轻微升高（但Ｐ＞０．０５）．ＣＤ＿４／ＣＤ＿８明显高于正常对照组（Ｐ＜０．０１），提示患儿存在细胞免疫功能不全和免疫调节紊乱。经胎儿胸腺治疗后３个月患儿细胞免疫功能恢复正常，与正常对照组比较Ｐ＞０．０５。这些结果提示：胎儿胸腺具有调节机体细胞免疫功能，防治内源性哮喘反复发作的作用，且方法简单、安全，可作临床上一种防治手段。     

精氨酸加压素在内毒素热限形成中的作用

本文观察了家兔静脉注射不同剂量ＥＴ后中隔区，下丘脑组织及血浆中ＡＶＰ含量的变化。结果显示：在ＥＴ发热过程中，中隔区，下丘脑及血浆ＡＶＰ含量均显著增多（Ｐ＜０．０１）；ＥＴ发热达热限时，体温不再升高，中隔区与血浆ＡＶＰ含量也不再增多，且中隔区及血浆ＡＶＰ含量变化与体温变化呈明显正相关（ｒ＝０．９８４，０．０５＜Ｐ＜０．０１；ｒ＝０．９９４，Ｐ＜０．０１）；此时，下丘脑升高的ＡＶＰ含量开始下降（Ｐ０。     

2010年广州某医疗中心儿童夏季细菌性腹泻的病原学调查

目的研究广州地区小儿夏季细菌性腹泻的病原菌分布。方法采集2010年5～7月广州市妇女儿童医疗中心珠江新城院区腹泻患儿的大便标本进行常规病原菌的分离培养,通过生化反应和血清凝集试验进行鉴定和分型,并使用金标法对空肠弯曲菌抗原进行检测。结果从110份标本中检出44株病原菌,检出率为40.0%。其中致病性大肠埃希菌17株,2岁以下患儿检出15株;空肠弯曲菌12株,2岁以下患儿检出10株;沙门菌6株;念珠菌纯生长6株;产气荚膜杆菌3株。结论广州地区夏季儿童细菌性腹泻的主要病原菌是致病性大肠埃希菌及空肠弯曲菌,两者的易感人群以2岁以下婴幼儿为主。     

Changes in activity of neutral proteases in tissues of ground squirrels in the dynamics of hibernation

Total activities of neutral proteases in the cerebral, hepatic, and myocardial tissues of ground squirrel vary during hibernation: in autumn (before hibernation) activities of the enzymes in the brain and myocardium start increasing, while in the liver they do not change. A common feature for all tissues is minimum activity of active neutral proteases in the middle of hibernation month 1 bout, while the maximum activity is recorded before awakening. Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 146, No. 9, pp. 278–280, September, 2008     

MiRNA调控肿瘤细胞中P-gP表达的研究进展

微小RNA（miRNA）是一类高度保守的非编码单链RNA分子,与靶基因mRNA3’端非编码区结合,抑制mRNA的翻译,促进靶基因降解。而这种调控机制与很多肿瘤细胞中P型糖蛋白（P,glycoprotein,p-gp）的表达有着密切的联系。p-gp是与耐药相关的跨膜蛋白,过表达可导致肿瘤细胞产生多药耐药（multidrugresistance,MDR）。就miRNA的生物学特性、p-gP的功能进行综述,关系。肿瘤MDR是临床化学治疗失败的主要原因,本文并重点介绍其调控肿瘤细胞中P-gP表达和MDR的     

293细胞检测致癌物的应用研究

目的 探讨应用293细胞对致癌物进行细胞转化及致瘤性等研究,为检测可疑致癌物提供实验依据.方法 应用微囊藻毒素LR(Microcystin LR,MC-La)对293细胞进行转化培养,取转化后的细胞进行软琼脂克隆实验、血清依赖性实验以及免疫缺陷小鼠体内致瘤实验来验证MC-LR转化的293细胞的致癌性.结果 293细胞在MC-LR的作用下,逐渐表现出转化细胞的特性:血清依赖程度显著降低,在软琼脂培养基中锚着独立生长并形成细胞集落,在SCID小鼠体内形成浸润性肿瘤组织.结论 293细胞易于培养并对环境致癌物敏感,可用于可疑致癌物的检测.     

贵州黔东南地区育龄人群地中海贫血基因类型分析

目的了解贵州黔东南州育龄人群地中海贫血基因类型及其分布。方法 2017年1月~2019年3月对930例疑似地中海贫血的育龄人群采用PCR结合导流杂交进行α、β地中海贫血基因检测。结果 930例病例中检出地中海贫血422例,检出率45.38%,α地中海贫血193例(20.75%),β地中海贫血212例(22.80%),α复合β地中海贫血23例(1.83%)。12种α地中海贫血基因类型主要为--SEA/αα(67.87%)、-α3.7/αα(9.84%)和-α4.2/αα(7.25%),8种β地中海贫血基因类型以CD41-42/N(61.79%)、CD17/N(26.89%)和IVS-Ⅱ-654/N(6.13%)常见,8种α合并β地中海贫血基因类型主要为-α3.7/CD41-42(41.19%)和--SEA/CD41-42(23.53%)。结论贵州黔东南州β地中海贫血检出率高于α地中海贫血,主要基因类型为CD4142/N和--SEA/αα。     

Factor of selectivity in organization of complex behavior in primates

Selectivity in the activity of the mammalian brain is examined on the basis of an analysis of a substantial experimental material obtained in our laboratory during the investigation of the conditioned reflex and delayed behavior in lower and higher primates.Translated from Fiziologicheskii Zhurnal SSSR imeni I. M. Sechenova, Vol. 73, No. 2, pp. 269– 276, February, 1987.     

Induction of high frequency activity in the somatosensory thalamus of rats in vivo results in long-term potentiation of responses in SI cortex

Summary Extracellular single-unit techniques were employed to record unitary activity simultaneously from the thalamic ventral posterior medial (VPM) nucleus and the ipsilateral primary somatosensory cortex of adult rats. Cross-correlation analysis triggered by the spontaneous firing of thalamocortical relay neurons in VPM and the discharge of layer IV neurons in the corresponding ipsilateral cortical barrel indicated that the paired-units included in this study were strongly correlated in their activity. The baseline responses of highly correlated cortical/thalamic pairs to a 10 ms deflection of a vibrissa on the contralateral side were measured using poststimulus time histograms. After establishing the baseline response, high frequency activity in VPM was induced in one of two ways: i) direct electrical stimulation of thalamic neurons or ii) whisker stimulation in the presence of bicuculline methiodide (BIC) released near the thalamic neurons. Both methods resulted in a conditioning stimulus (CS) paradigm consisting of bursts of high-frequency activity (50–100 Hz) with an inter-burst interval of 150 ms (7 Hz). Almost immediately following the presentation of the CS, the response of layer IV cortical neurons to vibrissa stimulation increased by 37–62% over baseline values, which was maintained after the effects of BIC had worn off in VPM. This enhancement in the response of the cortical neurons was not accompanied by a concomitant increase in the thalamic responses. Thus, these results strongly suggest that the potentiation first occurred at the thalamocortical synapse.     

Role of Thrombin in Activation of Neurons in Rat Hippocampus

The effect of thrombin, an agonist of proteinase-activated receptor (PAR) family, was studied on cultured rat hippocampal neurons. Thrombin in a concentration range of 1 pM - 10 nM induced a transitory dose-dependent increase in intracellular free calcium concentration. Involvement of PAR1 in neural response to thrombin was corroborated in experiments with TFLLRN, a selective synthetic peptide agonist of these receptors. In a calcium-free medium and after treatment with cyclopiazonic acid (inhibitor of Ca(2+)-ATPase in the endoplasmic reticulum) activation of PAR not only mobilized Ca(2+) from intracellular stores, but also induced Ca(2+) entry into the cells. Thrombin decreased Ca(2+) signal triggered by activation of NMDA-subtype glutamate receptors.     

Neuroprotective potential of ceftriaxone in in vitro models of stroke

Astrocytic glutamate transporters are considered an important target for neuroprotective therapies as the function of these transporters is abnormal in stroke and other neurological disorders associated with excitotoxicity. Recently, Rothstein et al., [Rothstein JD, Patel S, Regan MR, Haenggeli C, Huang YH, Bergles DE, Jin L, Dykes Hoberg M, Vidensky S, Chung DS, Toan SV, Bruijn LI, Su ZZ, Gupta P, Fisher PB (2005) Beta-lactam antibiotics offer neuroprotection by increasing glutamate transporter expression. Nature 433:73-77] reported that beta-lactam antibiotics (including ceftriaxone, which easily crosses the blood-brain barrier) increase glutamate transporter 1 (GLT-1) expression and reduce cell death resulting from oxygen-glucose deprivation (OGD) in dissociated embryonic cortical cultures. To determine whether a similar neuroprotective mechanism operates in more mature neurons, which show a different pattern of response to ischemia than primary cultures, we exposed acute hippocampal slices obtained from rats treated with ceftriaxone for 5 days (200 mg/kg; i.p.) to OGD. Whole-cell patch clamp recording of glutamate-induced N-methyl-d-aspartate (NMDA) currents from CA1 pyramidal neurons showed a larger potentiation of these currents after application of 15 microM dl-threo-beta-benzyloxyaspartic acid (TBOA; a potent blocker of glutamate transporters) in ceftriaxone-injected animals than in untreated animals, indicating increased glutamate transporter activity. Western blot analysis did not reveal GLT-1 upregulation in the hippocampus. Delay to OGD-induced hypoxic spreading depression (HSD) recorded in slices obtained from ceftriaxone-treated rats was longer (6.3+/-0.2 vs. 5.2+/-0.2 min; P<0.001) than that in the control group, demonstrating a neuroprotective action of the antibiotic in this model. The effect of ceftriaxone was also tested in organotypic hippocampal slices obtained from P7-9 rats (>14 days in vitro). OGD or glutamate (3.5-5.0 mM) damaged CA1 pyramidal neurons as assessed by propidium iodide (PI) fluorescence. Similar damage was observed after pre-treatment with ceftriaxone (10-200 microM; 5 days) and ceftriaxone exposure did not result in GLT-1 upregulation as assayed by Western blot. Treatment of slice cultures with dibutyryl cAMP (100-250 microM; 5 days) increased GLT-1 expression but did not reduce cell damage induced by OGD or glutamate. Thus we confirm the neuroprotective effect of antibiotic exposure on OGD-induced injury, but suggest that this action is related to independent modulation of transporter activity rather than to the level of GLT-1 protein expression. In addition, our results indicate that the protective effects of beta-lactam antibiotics are highly dependent on the experimental model.     

内毒素血症在肝癌发生发展中的作用

目的:探讨内毒素血症在肝癌发生发展中作用。方法:利用饮水中加入0.03%TAA,4个月形成肝硬化,6个月形成肝癌动物的模型。TAA+LPS组从第5个月开始皮下注射内毒素,至实验结束。在肝癌发生发展过程中进行血浆内毒素水平、γ-GT活性、DNA指数、增殖指数,并对N-ras、p53基因点突变进行分析。结果:内毒素可增加bcl-2与p53蛋白过度表达与增加N-ras、p53基因的点突变,增加自由基生成与降低抗氧化酶活性,加重DNA损伤。结论:内毒素能够促进TAA诱发肝癌变的过程。