持续静脉滴注安定治疗频繁发作的小儿癫痫

目的探讨持续静脉滴注安定法治疗频繁发作小儿癫痫的疗效.方法对28例频繁发作癫痫的患儿,采用安定持续静脉滴注,按发作情况调整滴注速度,比较治疗前后的发作频率;应用荧光偏振免疫法测定血安定浓度.结果持续静脉滴注安定治疗后每日发作次数较治疗前明显减少(P<0.01).血安定浓度的安全有效范围为574.50±291.57μg/ml.安定静脉滴注速度与血药浓度呈正相关(γ=0.941,P<0.01).结论持续静脉滴注安定是一种安全有效的控制小儿频繁发作癫痫的辅助治疗方法.     

大肠肿瘤组织中EB病毒的原位杂交检测

目的：探讨EB病毒感染与人大肠癌发生的关系。方法：用原位分子杂交法对130例人大肠癌标本中EB病毒小分子RNA片段进行检测。结果：130例标本中有6例（4.48％）癌组织呈阳性反应，其中4例为男性，4例有明显淋巴细胞浸润。结论：EB病毒感染可能与我国部分大肠腺癌的发生有关，肿瘤细胞间质中大量淋巴细胞浸润可能是EB病毒感染的重要病理学特征。     

一种简单、稳定、可靠的屏氧酶1基因多态性分析法

目的：建立一种简单、稳定、可靠的PON1基因多态性分析法。方法：取外周静脉血100μl，用ROSE法提取基因组DNA，用两对引物：P192F 5′-TAT TGT TGC TGT GGG ACC TGA G-3′,P192R 5′-CAC GCT AAA CCC AAA TAC ATC TC-3′；P55F 5′-GAA GAG TGA TGT ATA GCC CCA G-3′,P55R 5′-TTT AAT CCA GAG CTA ATG AAA GCC-3分别进行PCR扩增，用限制性内切酶AlwI,NlaⅢ对两种PCR产物分别进行酶切，3％琼脂糖凝胶电泳。结果：扩增的两个PCR产物在192、55多态性位点大小分别为99bp、170bp。Alw I酶切后，凝胶电脉得到完全酶切（66bp,33bp)，部分酶切（99bp、66bp、33bp)，未被酶切（99bp)三种类型DNA片段（RR，QR，QQ基因型）；NlaⅢ酶切后，凝胶电脉得到部分酶切（170bp,126bp,44bp)，未被酶切（170bp)两种类型DNA片段（LM，LL基因型）。经双盲重复检测，结果一致。应用此方法对胃癌患者血样标本检测，发现其PON1基因多态性在192位点频率较高。结论：采用一步PCR－RFLP技术可以建立简单、稳定、可靠的PON1基因多态性分析法。     

大鼠脑组织单胺类递质及其代谢产物的检测方法研究

目的 :研究大鼠脑组织中单胺类递质及其代谢产物的高效液相反相离子对色谱测定法。方法 :采用LiChrosorbC18,10 μm色谱柱 ,流动相为甲醇 :水 (4 0 :60 ) ,含 0 .0 2 8g LEDTANa2 ,0 .15g LSDS ,0 .2ml LH2 SO4(pH 2 .5～ 3 ) ,荧光检测波长 :λEX=2 85 ,λEM=3 3 3。结果 :对 87只大鼠脑组织中 4种单胺类递质及其代谢产物的含量进行了同时测定 ,高香草酸 (HVA) 2 .5 0～ 40 .0 μg ml、去甲肾上腺素 (NE) 0 .0 1～ 0 .5 0 μg ml、多巴胺 (DA)0 .0 5～ 1.0 0 μg ml、5 羟色胺 (5 HT) 0 .0 2 5～ 0 .5 0 μg ml,峰面积与其含量呈良好的线性关系。 结论 :该法操作简便、快速、准确 ,为组织中单胺类递质及其代谢产物检测的一种理想方法 ,并适用于临床相关研究。     

多柔比星肾病肾损伤早期核因子-κB和血管紧张素ⅠⅡ的表达及关系探讨

目的　探讨在多柔比星 (阿霉素 )肾病综合征 (NS)幼年大鼠肾损伤过程中核因子 (NF) κB和血管紧张素ATⅠ、ATⅡ的表达及其相关性。方法　 4周龄雄性Wistar大鼠单侧肾切除加腹腔注射阿霉素造成NS模型 ,分别以免疫组织化学和原位杂交检测ATⅠ、ATⅡ和NF κB。结果　肾病组随着病变时间的延长 ,NF κB和ATⅠ、ATⅡ表达的强度和部位均呈增强趋势 ,治疗组在相同时间点则两者都有不同程度下调 (P <0 .0 5 )。结论　在阿霉素肾病损伤过程中NF κB和ATⅠ、ATⅡ起着介导作用。     

Adrenergic signalling between rat taste receptor cells

In taste buds, synaptic transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the β agonist isoproterenol and blocked by the β antagonist propranolol. The α agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple α (α1a, α1b, α1c, α1d, α2a, α2b, α2c) and β (β1, β2) subtypes of adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that adrenergic transmission within the taste bud may play a paracrine role in taste physiology.     

Human osteoblasts' proliferative responses to strain and 17beta-estradiol are mediated by the estrogen receptor and the receptor for insulin-like growth factor I.

The mechanism by which mechanical strain and estrogen stimulate bone cell proliferation was investigated using monolayer cultures of human osteoblastic TE85 cells and female human primary (first-passage) osteoblasts (fHOBs). Both cell types showed small but statistically significant dose-dependent increases in [3H]thymidine incorporation in response to 17beta-estradiol and to a single 10-minute period of uniaxial cyclic strain (1 Hz). In both cell types, the peak response to 17beta-estradiol occurred at 10(-8) - 10(-7) M and the peak response to strain occurred at 3500 microstrain ((mu)epsilon). Both strain-related and 17beta-estradiol-related increases in [3H]thymidine incorporation were abolished by the estrogen receptor (ER) modulator ICI 182,780 (10-8 M). Tamoxifen (10(-9) - 10(-8) M) increased [3H]thymidine incorporation in both cell types but had no effect on their response to strain. In TE85 cells, tamoxifen reduced the increase in [3H]thymidine incorporation associated with 17beta-estradiol to that of tamoxifen alone but had no such effect in fHOBs. In TE85 cells, strain increased medium concentrations of insulin-like growth factor (IGF) II but not IGF-I, whereas 17beta-estradiol increased medium concentrations of IGF-I but not IGF-II. Neutralizing monoclonal antibody (MNAb) to IGF-I (3 microg/ml) blocked the effects of 17beta-estradiol and exogenous truncated IGF-I (tIGF-I; 50 ng/ml) but not those of strain or tIGF-II (50 ng/ml). Neutralizing antibody to IGF-II (3 microg/ml) blocked the effects of strain and tIGF-II but not those of 17beta-estradiol or tIGF-I. MAb aIR-3 (100 ng/ml) to the IGF-I receptor blocked the effects on [3H]thymidine incorporation of strain, tIGF-II, 17beta-estradiol, and tIGF-I. HOBs and TE85 cells, act similarly to rat primary osteoblasts and ROS 17/2.8 cells in their dose-related proliferative responses to strain and 17beta-estradiol, both of which can be blocked by the ER modulator ICI 182,780. In TE85 cells (as in rat primaries and ROS 17/2.8 cells), the response to 17beta-estradiol is mediated by IGF-I, and the response to strain is mediated by IGF-II. Human cells differ from rat cells in that tamoxifen does not block their response to strain and reduces the response to 17beta-estradiol in TE85s but not primaries. In both human cell types (unlike rat cells) the effects of strain and IGF-II as well as estradiol and IGF-I can be blocked at the IGF-I receptor.     

Serum transforming growth factor-β1 level reflects disease status in patients with esophageal carcinoma after radiotherapy

AIM: To evaluate the relationship between changes in serum transforming growth factor β1 (TGFβ1) level and curative effect of radiotherapy (RT) in patients with esophageal carcinoma.METHODS: Ninety patients with histologically confirmed esophageal carcinoma were enrolled. Serum samples for TGFβ1 analysis were obtained before and at the end of RT. An enzyme-linked immunosorbent assay was used to measure serum TGFβ1 level. Multivariate analysis was performed to investigate the relationship between disease status and changes in serum TGFβ1 level.RESULTS: Serum TGFβ1 level in patients with esophageal carcinoma before RT was significantly higher than that in healthy controls (P ＜ 0.001). At the end of RT, serum TGFβ1 level was decreased in 67.82% (59/87) of the patients. The overall survival rate at 1,3 and 5 years was 48.28% (42/87), 19.54% (17/87)and 12.64% (11/87), respectively. Main causes of death were local failure and regional lymph node metastasis.In patients whose serum TGFβ1 level decreased after RT,the survival rate at 1, 3 and 5 years was 61.02% (36/59),28.81% (17/59) and 18.64% (11/59), respectively. The survival rate at 1 year was 17.86% (5/28) in patients whose serum TGFβ1 level increased after RT, and all died within 18 mo (P ＜ 0.01).CONCLUSION: Serum TGFβ1 level may be a useful marker for monitoring disease status after RT in patients with esophageal carcinoma.     

初诊T2DM短期胰岛素强化治疗40例分析

目的观察初诊T2DM短期胰岛素强化治疗的疗效。方法对40例初诊T2DM患者采用三餐前皮下注射短效胰岛素和睡前注射中效胰岛素2wk，并检测治疗2wk前后FPG、PPG、GHbA1C及血脂等值进行比较。结果两组治疗后FPG、PPG、GHbA1C及血脂各值均显著低于治疗前p〈0．05（x^2=4．940—11．544）。结论胰岛13细胞功能异常和（或）胰岛素抵抗是T2DM发病的基本环节，早期强化胰岛素治疗能获得血糖的有效控制，减少或延缓并发症的发生。     

Inhibition of the expression of lysyl oxidase and its substrates in cadmium-resistant rat fetal lung fibroblasts.

Copper (Cu)-dependent lysyl oxidase (LO) catalyzes crosslinking of collagen and elastin stabilizing the extracellular matrix (ECM). Chronic inhalation of cadmium (Cd), a toxic metal, induces emphysema. To probe mechanisms of Cd injury to the lung, we developed Cd-resistant (CdR) cells from rat fetal lung fibroblasts (RFL6) by chronic exposure to CdCl(2) from 1 to 40 microM and further examined their expressions of LO, LO substrates, and Cu-scavenging thiols. Levels of cellular thiols, metallothionein, and glutathione in CdR cells were elevated to 13.0- and 3.2-fold of parental controls, respectively, whereas LO mRNA and protein levels were markedly reduced in these cells, with catalytic activity declining to only 16% of the parental control. A conspicuous 52 kDa species rather then the normal 50 kDa proenzyme appeared in the CdR cell extract but not in the conditioned medium, which was codistributed with the endoplasmic reticulum marker [DiOC5(3)] within the cell, implying the Cd-induced 52 kDa species as a product of an abnormal LO-processing defect in secretion. Addition of Cu into CdR cell cultures enhanced the expression of LO mRNA, protein and catalytic activities reflecting limitation of Cu bioavailability for LO in these cells. With inhibition of LO, CdR cells also displayed downregulation of collagen and elastin, substrates of LO. Restoration of collagen synthesis by exposure of CdR cells to purified LO or Cu suggests that inhibition of LO and limitation of Cu cofactor by Cd, as key phenotype changes, accelerated collagen and elastin damage, a critical event pertinent to emphysema pathogenesis.