卵巢支持—间质细胞瘤1例

患者,女,１８岁,未婚,因全身多毛２年、闭经、声音低沉１１月,于１９９８年８月６日入院。月经４～４／２８～３０ｄ,已正规月红３ａ。以往健康,无特殊疾病,查体：身高１－５６ｍ,体重５１ｋｇ,皮肤粗糙,上、下嘴唇长有胡须、四肢、下腹部及肛周有浓密体毛,声音低沉,喉结不明显,双侧乳房微微隆起,心肺听诊无异常。腹股沟未扪及肿块。阴毛呈男性分布,阴蒂肥大,长１ｃｍ,大小阴唇发育差。肛查：子宫小,活动,右附件区可触及６ｃｍ×６ｃｍ×５ｃｍ大小活动的实性肿块,左附件正常。化验：１７羟类固醇（１７—ＯＨ）２２－…     

白细胞介素-13对成年人支气管哮喘的影响

目的 通过检测白细胞介素(IL)-13浓度及其变化,探讨它在成人支气管哮喘(哮喘)发病机制中的意义,同时检测IL-10、肿瘤坏死因子(TNF)-α浓度,探讨它们与IL-13的相互关系.方法 以31例哮喘患者(哮喘组)及9例健康者(对照组)作为研究对象.采集诱导痰及外周血标本,制作成涂片进行细胞学分析;用酶联免疫吸附法测定IL-13、TNF-α及IL-10浓度.结果 哮喘组血清IL-13浓度高于对照组[分别为(89.88±36.75)ng/L和(27.03±12.19)ng/L,P＜0.01],诱导痰中浓度也高于对照组[分别为(69.14±24.48)ng/L和(18.74±8.87)ng/L,P＜0.01],且血清中的浓度高于诱导痰中的浓度(P＜0.05);激素使用患者诱导痰中浓度比非激素使用患者低(P＜0.05),诱导痰中IL-13浓度与嗜酸粒细胞百分比呈显著正相关(r=0.54,P＜0.05).哮喘组诱导痰中TNF-α及IL-10浓度均较对照组高[TNF-α分别为(66.32±18.74)ng/L和(5.36±6.86)ng/L,P＜0.01;IL-10分别为(118.08±55.17)ng/L和(5.66±8.03)ng/L,P＜0.05].哮喘组中,发作期诱导痰中IL-10浓度高于稳定期浓度(P＜0.05).轻度哮喘患者诱导痰中TNF-α浓度与重度哮喘患者比较差异有统计学意义(P＜0.05).结论 IL-13是与哮喘发病病理过程相关的细胞因子,与嗜酸粒细胞的活动关系密切,参与哮喘气道炎性反应及气道高反应性的发生,哮喘患者在激素治疗后其浓度降低.     

基于双向转诊服务模式的社区心脑血管疾病康复治疗管理信息化

本文分析了社区卫生服务中心心脑血管康复治疗的业务服务现状及问题，给出了一种基于社区卫生服务中心与区域中心医院之间通过双向转诊及双向卫生服务新型模式建立的社区卫生服务心脑血管疾病康复治疗的服务体系、业务流程，阐明了建立社区卫生服务心脑血管疾病康复治疗信息系统的意义及需求，并给出该系统的结构及功能，以及该系统的应用效果分析。     

实验性肺动脉高压大鼠模型血清Zn、Cu、Mn、Fe、Na、K、Ca、Mg的变化

本实验研究选用实验性肺动脉高压(Pulmonary hapertension PHT)大鼠模型。观察了该动物模型的血清Zn、K、Cu、Mg、Mn、Ca、Fe、Na的变化。实验结果表明:在常压低氧状态下,血清Zn、Mn、K、Ca、Mg降低,Cu、Fe升高。提示对肺动脉高压患者予以适当的元素调治,是有客观依据的。     

柏银汤配合米非司酮对异位妊娠患者输卵管功能的影响分析

目的观察中医药结合治疗异位妊娠的临床疗效。方法将96例患者随机分为2组,治疗组（48例）采用米非司酮配合中药柏银汤口服,对照组（48例）采用单纯米非司酮治疗。结果治疗组成功率及输卵管通畅率明显高于对照组,差异有显著性。结论柏银汤配合米非司酮治疗异位妊娠可显著提高疗效。     

雌激素受体在口腔扁平苔藓中的表达变化及意义

雌激素受体 (ＥｓｔｒｏｇｅｎＲｅｃｅｐｔｏｒ,ＥＲ)可将雌激素信息传递至细胞内引起生物学效应 ,在机体的生长发育、机能维持和生理代谢方面发挥重要作用[1] 。研究受体对了解某些疾病的发病机制有重要意义 ,对临床治疗也有应用价值[2 ] 。口腔扁平苔藓 (Ｏｒａｌｌｉｃｈｅｎｐｌａｎｕｓ,ＯＬＰ)是一种口腔粘膜较常见疾病 ,其致病原因和机制尚不明确。本研究采用免疫组织化学方法研究ＥＲ在ＯＬＰ上皮细胞中的表达变化及其与ＯＬＰ发病的关系。1　材料和方法1.1　标本制备选取 40例ＯＬＰ的活检标本 (男 14例 ,女 2 6例 ;平均年龄 44 .…     

败血症休克大鼠心肌Intermedin及其受体基因表达

目的:探讨败血症休克大鼠心肌组织中Intermedin(IMD)及其受体系统mRNA表达及机制。方法:盲肠结扎穿孔法复制大鼠败血症性休克模型,测量其血流动力学;半定量RT-PCR检测心肌组织中IMD、CRLR、RAMP1、RAMP2和RAMP3mRNA水平。结果:败血症性休克大鼠出现严重低血糖和高乳酸血症,晚期出现严重心力衰竭;休克早期心肌IMD、RAMP1和RAMP3mRNA水平分别较假手术组增高128%、143.2%和133.4%(P<0.01);休克晚期则无增加。结论:IMD及其受体系统参与感染性休克过程,可能与心力衰竭发生有关。     

血浆同型半胱氨酸含量在皮质下动脉硬化性脑病患者中的变化

目的 研究皮质下动脉硬化性脑病(subcortical Arteriosclerotic Encephalopathy, SAE)患者脑MRI分型与血浆同型半胱氨酸(homocyteine,Hcy)含量的关系.方法 对93例诊断为SAE患者行常规脑MRI检查,并进行Kinkel分型,同时应用酶联免疫吸附双抗夹心法测定血浆Hcy含量,与对照组进行对比分析.结果 SAE组平均血浆Hcy水平(14.60±4.23 )μmmol/L,与对照组(10.04±2.09 )μmmol/L比较差异有统计学意义(P<0.05),并随Kinkel分型的增高、血浆Hcy水平有增高趋势.结论 血浆Hcy浓度增高,可能是SAE的危险因素之一,且与病情轻重有关.     

Effects of PI3K inhibitor NVP-BKM120 on acquired resistance to gefitinib of human lung adenocarcinoma H1975 cells

The effects of class I PI3K inhibitor NVP-BKM120 on cell proliferation, cell cycle distri- bution, cellular apoptosis, phosphorylation of several proteins of the PI3K/AKT signaling pathway and the mRNA expression levels of HIFl-ct, VEGF and MMP9 in the acquired gefitinib resistant cell line H1975 were investigated, and whether NVP-BKM120 can overcome the acquired resistance caused by the EGFR T790M mutation and the underlying mechanism were explored. MTT assay was performed to detect the effect of gefitinib, NVP-BKM120, NVP-BKM120 plus 1 ~unol/L gefitinib on growth of H1975 cells. The distribution of cell cycle and apoptosis rate of H1975 cells were examined by using flow cytometry. The mRNA expression levels of tumor-related genes such as HIFI-a, VEGF and MMP9 were detected by using real-time quantitative PCR. Western blotting was used to detect the ex- pression level of phosphorylated proteins in the PI3K/AKT signaling pathway, such as Ser473-p-AKT, Ser235/236-p-S6 and Thr70-p-4E-BP1, as well as total AKT, $6 and 4E-BP1. The results showed that the NVP-BKM120 could inhibit the growth of H1975 cells in a concentration-dependent manner, and H1975 cells were more sensitive to NVP-BKM120 than gefitinib （IC50：1.385 vs. 15.09 ~mol/L respec- tively）, whereas combination of NVP-BKM120 and gefitinib （1 ~trnol/L） did not show more obvious ef- fect than NVP-BKM120 used alone on inhibition of cell growth （P〉0.05）. NVP-BKM120 （1 ~unol/L） increased the proportion ofH1975 cells in G0~G1 phase and the effect was concentration-dependent, and 2 ~maol/L NVP-BKM120 promoted apoptosis ofH1975 cells. There was no significant difference in the proportion of H1975 cells in G0-G1 phase and apoptosis rate between NVP-BKM120-treated alone group and NVP-BKM120 plus genfitinib （1 ~unol/L）-treated group or between DMSO-treated control group and gefitinib （1 Ixmol/L）-treated alone group （P〉0.05 for all）. It was also found that the mRNA expression levels of these genes were down-regulated by NVP-BKM120 （1 ~unol/L）, and NVP-BKM120 （1 ~tmol/L） or NVP-BKM120 （1 pmol/L） plus gefitinib （1 ~tmol/L） obviously inhibited the activation of Akt, $6 and 4E-BP1 as compared with control group, but single use of gefitinib （1 pmol/L） exerted no significant effect. These data suggested that NVP-BKM120 can overcome gefitinib resistance in H1975 cells, and the combination of NVP-BKM120 and gefitinib did not have additive or synergistic effects. It was also concluded that NVP-BKM120 could overcome the acquired resistance to gefitinib by down-regulating the phosphorylated protein in PI3K/AKT signal pathways in H1975 cells, but it could not enhance the sensitivity of H 1975 cells to gefitinib.