MMP-9和TIMP-1在实验性肺气肿大鼠肺组织中的表达及其意义

目的研究基质金属蛋白酶(MMP-9)及其组织抑制因子(TIMP-1)在弹性蛋白酶所致肺气肿大鼠肺组织中的表达.方法雄性Wistar大鼠20只,随机分为两组:正常对照组和肺气肿模型组,每组10只.模型组大鼠气管内滴入弹性蛋白酶复制肺气肿模型.25d后,观察各组大鼠肺组织的病理改变,免疫组化方法观察肺组织MMP-9和TIMP-1中的蛋白表达情况.结果肺气肿模型组MMP-9和TIMP-1的表达与正常对照组相比明显增强(P＜0.01),且MMP-9/TIMP-1比值失衡.结论MMP-9/TIMP-1失衡在肺气肿形成中起重要作用.     

Synthesis of 9-Halo Prostaglandin Derivatives and Their Effect on Uterus Contraction

Four 9-halo prostaglandin derivatives were designed and synthesized. Their structures were confirmed by IR, ^1HNMR, MS, etc. The effect on uterus contraction of rats was studied in vitro. It was found that compound β-Br seemed to be the most sensitive and β-Cl somewhat less, while α-Cl and α-Br had almost no action as compared with oxytocin (1 IU/ml).     

Hepatitis C associated with Guillain-Barré syndrome

ABSTRACT— Hepatitis C is frequently associated with immune-mediated diseases, such as cryoglobulinemia. Guillain-Barré syndrome is an acute demyelinating neuropathy of probable immune pathogenesis. We describe two patients with Guillain-Barré syndrome, and associated chronic hepatitis C, the second one previously treated with interferon. The link between both conditions may be hepatitis C being the trigger of this immune polyneuropathy. Guillain-Barré syndrome should be added to the list of conditions associated with hepatitis C.     

HLA-A9 antibodies and epitopes

Fifty pregnancy alloantisera directed towards HLA-A23 and/or A24 antigens were investigated serologically in titration studies against the three sequenced HLA-A9 specificities, A23 (A*2301), A24 (A*2402) and A2403 (A*2403). The reaction patterns of the antisera fell into five categories which allowed the three HLA-A9 specificities to be easily differentiated. Based on the various titre cytotoxicity scores of the antisera five possible antibody specificities were defined: anti-A23; -A24; -A23/24; -A24/2403 and anti-A23/24/2403. One antiserum crossreacted with HLA-A1 and A24. Inspection of the amino acid sequences of 136 HLA-A, B and C molecules allowed the prediction of five unique epitopes corresponding to these antibody specificities, a possible epitope unique to A2403 and confirmation of a likely epitope shared by A1 and A24. These, together with the previously suggested epitopes HLA-A9/ A2/A28 and A1/A23/A24 together with the presence of Bw4 on the three HLA-A9 antigens suggests that the HLA-A9 family of antigens is characterized by a minimum of nine serologically definable epitopes.     

肾病患儿免疫细胞对肾小球上皮细胞合成基质的影响

目的为了明确免疫细胞对肾小球上皮细胞（ｇｌｏｍｅｒｕｌａｒｅｐｉｔｈｅｌｉａｌｃｅｌＧＥＣ）合成功能的直接作用。方法应用肾小球细胞体外培养，同位素掺入及放射免疫技术，以总胶原，层粘连蛋白，Ⅲ型前胶原及Ⅳ型胶原的合成为观察指标，动态研究了不同病理类型原发性肾病综合征（ＩＮＳ）患儿外周血单个核细胞（ｐｅｒｉｐｈｅｒａｌｂｌｏｏｄｍｏｎｏｎｕｃｌｅａｒｃｅｌＰＢＭＣ）对ＧＥＣ生物功能的影响。结果（１）肾病极期未经激素治疗组（未治组）ＰＢＭＣ上清明显促进了ＧＥＣ合成层粘连蛋白；（２）未治ＰＢＭＣ上清抑制了ＧＥＣ合成总胶原；（３）未治组ＰＢＭＣ上清促进了Ⅲ型前胶原的合成，而对Ⅳ型胶原的合成无明显影响；（４）肾病患儿ＰＢＭＣ的上述作用与是否足量激素治疗有关，而与尿蛋白能否阴转、肾组织病理类型、肾病临床类型等无直线相关关系。结论原发性肾病患儿循环免疫细胞可影响ＧＥＣ合成细胞外基质的功能。免疫细胞的这种活性可被激素治疗改变。     

急性病毒性肝炎住院患者血清学分型与流行病学分布研究

本文收集了西安市住院急性病毒性肝炎患者血清标本２９３份，用ＥＬＩＳＡ进行分型检测，并作流行病学调查。结果发现：甲肝占６５．１９％，乙肝占１０．９２％，丙肝占４．７８％，丁肝占３．７５％，戊肝占４．４４％，诊断不明者占１０．９２％。结果表明，在西安市住院的急性病毒性肝炎中，甲肝为主要类型；与以往结果比较，甲肝患者的发病年龄明显后移；除乙肝外，各型肝炎中男性均多于女性，尤以丁肝和戊肝为著；甲肝有明显的     

活动性肺结核患者血清Fad D9重组蛋白、sCD14-ST及单核细胞P糖蛋白水平及其临床意义

目的探讨活动性肺结核(APTB)患者血清Fad D9重组蛋白、可溶性白细胞分化抗原14亚型(sCD14-ST)、单核细胞P糖蛋白(Pgp)表达及其临床意义。 方法选取96例APTB患者(APTB组),按照肺部病灶有无空洞和病灶肺叶数分亚组。同期选择体检健康且经γ干扰素释放试验检测阴性者(健康对照组,HC组)及阳性者(结核潜伏感染组,LTBI组)各48例。比较各组血清Fad D9重组蛋白、sCD14-ST、Pgp水平。评估Fad D9重组蛋白、sCD14-ST、Pgp诊断APTB和鉴别APTB、LTBI的价值。 结果Fad D9重组蛋白、sCD14-ST、Pgp水平APTB组＞LTBI组＞HC组,且有空洞者高于无空洞者,病灶肺叶≥3个者高于＜3个者(P＜0.05)。Fad D9重组蛋白、sCD14-ST、Pgp对APTB诊断和APTB、LTBI鉴别有良好效能(P＜0.05)。 结论APTB患者血清Fad D9重组蛋白、sCD14-ST及Pgp明显升高,且与肺部病灶的严重程度有关。     

Bcl-2和Caspase-9对儿童癫痫持续状态近期预后的预测价值

目的探讨血清B细胞淋巴瘤相关蛋白-2(Bcl-2)和半胱氨酸天冬氨酸蛋白酶-9(Caspase-9)对儿童癫痫持续状态(SE)近期预后的预测价值。 方法选择SE患儿62例为SE组,选择同期体检健康儿童62例为对照组;按照预后将SE患儿分为预后不良组和预后良好组。癫痫持续状态严重程度量表(STESS)评估SE患儿SE严重程度。ELISA检测各组血清Bcl-2和Caspase-9水平。结果SE组Bcl-2和Caspase-9水平高于对照组(P＜0.05)。预后不良组和预后良好组STESS评分、Bcl-2和Caspase-9水平比较,差异有显著性(P＜0.05)。STESS评分、Bcl-2和Caspase-9是影响SE患儿近期预后的独立影响因素(P＜0.05);入院血清Bcl-2和Caspase-9联合检测对SE患者近期预后具有较好的预测效能(P＜0.05)。 结论血清Bcl-2和Caspase-9是SE患儿近期预后的有效预测指标。     

SNHG6靶向miR-101/TGFBR1促进AMI小鼠左心室心肌纤维化

目的探讨SNHG6对急性心肌梗死(AMI)小鼠左心室心肌的影响。 方法将30只雄性C57/BL6小鼠构建成AMI小鼠后随机均分为AMI组、AMI+SNHG6组、AMI+miR-101-3p组、AMI+SNHG6+miR-101-3p组、AMI+miR-101-3p+TGFBR1组,另设正常小鼠6只为假手术组。qRT-PCR检测AMI小鼠SNHG6、miR-101-3p表达水平。心脏彩超检测各组小鼠左室射血分数(LVEF);马松和天狼星红染色法以及免疫组化分析各组小鼠左心室心肌纤维化变化。将H9C2细胞株分为阴性对照组(转染空质粒)、SNHG6组(转染质粒SNHG6)、miR-101-3p组(转染质粒miR-101-3p)。Western blotting检测各组TGFBR1蛋白表达;采用双荧光素酶报告基因法预测并验证SNHG6/miR-101-3p/TGFBR1荧光素酶活性及调控机制。 结果AMI小鼠较假手术组SNHG6表达显著增加,miR-101-3p降低(P＜0.05)。与AMI组比较,AMI+SNHG6组小鼠LVEF降低,心肌纤维化程度加重(P＜0.05);AMI+miR-101-3p组LVEF升高,心肌纤维化程度减轻(P＜0.05)。AMI+SNHG6+miR-101-3p组较AMI+SNHG6组LVEF升高、心肌纤维化程度减轻(P＜0.05),而AMI+miR-101-3p+TGFBR1组较AMI+miR-101-3p组LVEF降低、心肌纤维化程度加重(P＜0.05)。双荧光素酶报告基因法验证显示,miR-101-3p组SNHG6、TGFBR1野生型质粒的荧光素酶活性较阴性对照组明显降低(P＜0.05)。 结论SNHG6抑制miR-101-3p上调TGFBR1加重AMI小鼠左心室心肌纤维化。