血管内皮功能障碍对肥胖伴高血糖患者胰岛分泌功能的影响

目的　探讨血管内皮功能障碍对胰岛 β细胞分泌功能的影响。 　方法　正常体重(NW )组 81例 ,单纯肥胖 (Ob)组 14 0例 ,肥胖伴高血糖 (Ob HG)组 97例。测定体质指数 (BMI)、腰臀围比 (WHR)、血压、血脂、空腹血糖和胰岛素 (FBG和FIns)及餐后血糖和胰岛素 (2hBG和 2hIns)。采用稳态模式法评价胰岛素抵抗 (HOMA IR)和 β细胞功能 (HOMA β)。用高分辨率血管外超声测定肱动脉对血流介导的内皮依赖性血管扩张 (EDD)及硝酸甘油的扩张反应。　结果　与Ob组比较 ,Ob HG组WHR、血压、甘油三酯 (TG)、FIns、2hIns和HOMA IR等显著升高 ,HOMA β明显降低 ,并伴有EDD所标志的血管内皮功能显著下降。相关分析显示 ,β细胞功能与EDD在Ob HG组呈显著正相关 (r=0 2 5 9,P <0 0 5 ) ,在Ob组和NW组无显著相关。在对Ob HG组影响EDD的因素进行控制后 ,EDD仍与 β细胞功能显著相关 (r =0 4 5 8,P <0 0 1)。多元逐步回归分析表明影响 β细胞功能的主要因素在Ob HG组为FBG、FIns和EDD ,在Ob组为FBG和HOMA IR。　结论　内皮依赖性舒张功能障碍可能是导致肥胖者 β细胞功能衰退 ,引发 2型糖尿病 (T2DM )的重要危险因素。     

Reconstitution of chemokine-induced actin polymerization in undifferentiated human leukemia cells (HL-60) by heterologous expression of interleukin-8 receptors

The chemokines interleukin-8 (IL-8) and GRO bind in neutrophils to the interleukin-8 receptor and (IL-8R and ) triggering reorganization of the actin cytoskeleton and activation of phospholipase C (PLC). Reconstitution of chemokine-induced activation of PLC indicated coupling of IL-8R and to pertussis toxin-insensitive or . To identify the signal transduction mechanisms of chemokine-induced actin response, undifferentiated human leukemia cells (HL-60 cells) constitutively expressing , and were chosen for reconstitution studies. Expression of recombinant receptors after transfection of the cells with the cDNA of IL-8R and was confirmed by binding studies with radiolabeled ligands. IL-8R bound IL-8 with high affinity (Kd1 nM) and GRO with low affinity (Kd 1 M), whereas IL-8R bound both IL-8 and GRO with high affinity (Kd1 nM). Flow cytometric actin measurements indicated that high affinity ligand-receptor interactions in both receptor transfectants displayed inducible responses. Pretreatment of transfectants with pertussis toxin caused ADP-ribosylation of G-proteins and blocked chemokine-induced polymerization, indicating involvement of or , but not in this response.accepted by M.J. Parnham     

异甘草酸镁联合降脂治疗非酒精性脂肪型肝炎及对肝功能的影响

目的：探析异甘草酸镁联合降脂治疗非酒精性脂肪型肝炎疗效及对肝功能影响。方法以该院2011年5月-2014年10月期间所收治92例非酒精性脂肪型肝炎患者展开研究,对照组给予以调脂为主综合治疗,观察组加用异甘草酸镁,比较两组治疗前后PCⅢ、C-ⅠV、HA及ALT、AST、TBIL、γ-GT等肝纤维化指标。结果两组治疗前各肝纤维化指标的比较无统计学意义(P>0.05);治疗后,观察组PCⅢ、C-ⅠV、HA等指标均显著降低,与治疗前比较差异有统计学意义(P<0.05),与对照组治疗后的组间比较差异有统计学意义(P<0.05)。组间比较上,两组治疗前ALT、AST、TBIL、γ-GT等肝功能指标的比较无统计学意义(P>0.05),治疗后两组各指标的比较差异有统计学意义(P<0.05);组内比较上,两组治疗前后各指标的比较差异有统计学意义(P<0.05)。结论异甘草酸镁可保护肝细胞,与降脂治疗联合应用于NASH患者可有效抑制肝细胞纤维化,促进肝功能的恢复,应用价值高。     

孟鲁司特钠联合硫酸镁治疗老年支气管哮喘的疗效观察

目的：探讨孟鲁司特钠联合硫酸镁治疗老年支气管哮喘的临床疗效。方法选取2012年6月至2013年6月玉林市第二人民医院收治的老年支气管哮喘患者80例,按照随机数字表法分为观察组与对照组各40例。对照组给予吸氧、抗感染、祛痰、β2受体激动剂、糖皮质激素等常规治疗,观察组在对照组的基础上加用孟鲁司特钠片和硫酸镁注射液治疗。观察并比较两组的临床疗效。结果观察组总有效率为97．1％明显高于对照组的77．1％,复发率为5．7％明显低于对照组的28．6％,差异均有统计学意义（ P＜0．05）;观察组喘息、咳嗽及胸闷等症状缓解时间均明显早于对照组,差异有统计学意义（P＜0．05）。两组患者治疗前肺功能指标比较,差异无统计学意义（P＞0．05）;治疗后肺功能指标较治疗前均明显改善,观察组改善程度优于对照组,差异有统计学意义（P＜0．05）。两组均未见呼吸抑制、血压下降等严重不良反应。结论孟鲁司特钠片联合硫酸镁注射液治疗老年支气管哮喘临床疗效显著,症状缓解快,复发率低,安全可靠,值得临床推广。     

细胞分化帮助剂提高低浓度As2O3对肝癌细胞凋亡作用的体外实验

目的 研究细胞分化帮助剂（CDA-Ⅱ）促进低浓度三氧化二砷（As2O3）对肝癌细胞株HepG-2，BEL-7402凋亡的协同效应。方法 用四甲基偶氮唑蓝（MTT）法检测单用CDA-Ⅱ或As2O3和联用对肝癌细胞株HepG-2，BEL-7402生长及抑制率的影响；用乳酸脱氢酶（LDH）法检测药物对细胞膜的毒性反应；流式细胞仪（FCM）分析细胞周期和凋亡率变化。结果 单用CDA-Ⅱ和As2O3分别为3．0mg／ml和50μmol／L时，肝癌细胞株BEL-7402，HepG-2发生凋亡达到最大值，而联用5μmol／LAs2O3＋1mg／mlCDA-Ⅱ可达到同样效果；结果显示：该浓度下HepG2的抑制率可达88％；BEL-7402的抑制率在100％；LDH检测表明联用比单用As2O310μmol／L更安全。流式细胞仪结果显示凋亡率联合组为40．2％，明显高于单用组As2O3（11．3％）或CDA-Ⅱ（8．7％）。结论 细胞分化帮助剂1mg／mlCDA-Ⅱ联用5μmol／LAs2O3可促进肝癌细胞株HepG-2，BEL-7402凋亡，可以明显降低As2O3的使用浓度，减少对正常细胞的毒副作用。二者联用具有协同作用。     

"化浊养胃汤"治疗慢性萎缩性胃炎90例临床观察

近年来,笔者采用自拟化浊养胃汤治疗慢性萎缩性胃炎(CAG)90例,疗效满意,现报告如下。1临床资料1.1一般资料共150例均为本院消化科门诊及住     

人胃癌特异性DNA结合蛋白质

作者用不同的方法都发现转化的Rat3-3细胞核中有一种能与Ha-ras癌基因上游区2.5kb特异结合的蛋白质,分子量大约为35kD。此蛋白质不能与6.6kb基因本身结合。在未转化的细胞中无此蛋白质。作者还做了20个胃癌病人手术切下的胃癌组织和周边组织,结果是胃癌组织细胞核内有与2.5kb结合的蛋白质,而周边组织没有。     

稀土暴露与儿童生长发育的相关性研究

目的　探讨稀土暴露对儿童生长发育的影响。方法　在江西省某稀土矿区和对照区对 4 72名 7～ 10岁的儿童进行生长发育有关指标测量 ,并使用ICP -HS对 112名儿童血样进行稀土水平的测定 ;采用简单相关和多元回归等方法分析稀土负荷水平与儿童生长发育指标的关系。结果　稀土矿区儿童血稀土总量为 (2 18± 1 0 8)ng/ g ,是对照区 (1 2 6± 0 35 )ng/g的 1 73倍 ,有显著性差异。相关分析结果提示 ,血中稀土负荷水平与儿童的肺活量和血压 2指标均呈负相关 ;多因素分析显示 ,血中总稀土含量及母亲从事稀土作业情况被引入肺活量和血压 2指标的回归方程。结论　矿区稀土暴露对儿童的生长发育可能有不利影响     

KSHV-GPCR and CXCR2 transforming capacity and angiogenic responses are mediated through a JAK2-STAT3-dependent pathway

The Kaposi's sarcoma herpesvirus encodes a G-protein-coupled chemokine receptor termed KSHV-GPCR. Expression of this constitutively active GPCR leads to cell transformation and vascular overgrowth characteristic of Kaposi's sarcoma. Previously, we have shown that CXCR2, the closest human homolog, is similarly able to transform cells if continuously stimulated or constitutively activated by amino-acid exchange D138V of the DRY sequence. Here, we demonstrate that STAT3 activation is a prerequisite for transformation in KSHV-GPCR and CXCR2 transfected NIH 3T3 cells. In KSHV-GPCR and D138V transfected cells, STAT-3 is constitutively phosphorylated on Tyr705. In CXCR2 transfected NIH 3T3 cells and human microvascular endothelial cells (HMEC), which express the CXCR2 constitutively, STAT3 is phosphorylated upon stimulation with IL-8 (CXCL8). Focus formation in NIH 3T3 cells transfected with the KSHV-GPCR, CXCR2, or the D138V mutant, was blocked by the specific JAK2 inhibitor AG490. Typical functions of the CXCR2 including actin stress fiber formation, haptotaxis, and the angiogenic response in HMEC shown by tube formation in Matrigel were blocked by AG490. These data suggest that the transforming capacity and migratory responses that are involved in tumor development, metastasis, and angiogenesis in KSHV or CXCR2-expressing cells is at least partially mediated through a JAK2-STAT3 dependent pathway.