缺氧对老年肺心病患者甲状腺激素水平的影响

目的　探讨缺氧对老年肺心病患者甲状腺激素的影响。　 方法　使用放免法测定 68例老年肺心病急性期、2 8例缓解期及 2 8例对照组患者体内血清三碘甲状腺原氨酸 (T3)、四碘甲状腺原氨酸 (T4 )、促甲状腺激素(TSH)水平 ,同步测定动脉血中氧分压 (PaO2 )。观察T3、T4 和TSH的变化 ,并分析PaO2 与T3、T4 的相关关系。　 结果　老年肺心病急性期的血清T3、T4 水平分别轻度 :(0 70± 0 15 )、(61 7± 12 1)g·L-1;中度 :(0 48± 0 13)、(32 32± 7 9)g·L-1,重度 :(0 2 3± 0 0 9)、(18 7± 4 7)g·L-1。 3组血清T3、T4 显著低于缓解期 (0 88± 0 17)、(75 7± 15 6)g·L-1和对照组 (0 9± 0 35 )、(83 7± 14 6)g·L-1(P <0 0 1)。动脉血氧分压 (PaO2 )与T3、T4 水平是正相关 (P <0 0 5 ) ,轻、中、重度组和缓解组血清TSH较对照组略高 ,但无统计学意义 ,P >0 0 5。　 结论 　缺氧导致肺心病患者体内的甲状腺激素变化 ,并随着病情加重T3、T4 水平显著降低。监测血清T3、T4 水平有助于判断肺心病危重程度及其预后预测     

不稳定型心绞痛与PAI-1及血小板活性的临床研究

目的　探讨老年不稳定型心绞痛 (UAP)与纤溶酶原激活物抑制剂 1型 (PAI 1)及血小板活化功能的临床意义。　 方法 　测定 87例老年UAP患者发作时的血清PAI 1水平与血小板活化因子CD62p活性 ,并与 89例健康对照组比较。　 结果　UAP组的PAI 1的水平 (99.77± 3 2 .95 ) μg·L-1较对照组 (5 5 .0 0± 2 1.2 3 ) μg·L-1明显升高 (P <0 .0 1) ;而CD62p活性 (12 .5 6± 4.66) %较对照组 (6.3 3± 2 .3 8) %也有显著升高 (P <0 .0 1)。　 结论 　老年不稳定型心绞痛的发作与PAI 1水平和血小板活性增高有密切联系。     

舒林酸抑制人胃腺癌细胞增殖及诱导凋亡

目的在体外对舒林酸抗人胃腺癌细胞增殖和凋亡诱导作用及其机制进行初步研究.方法采用人胃腺癌细胞株MKN45,MKN28作为研究对象.体外药物敏感试验(MTT)检测不同浓度和作用时间的舒林酸对细胞的增殖抑制效应;分别用Hoechst33258细胞核荧光染色、透射电镜和DNA琼脂糖凝胶电泳观察舒林酸诱导的细胞凋亡改变;应用Western斑点免疫印迹法观察经舒林酸2mmol·L-1和4mmol·L-1作用24 h后细胞内环氧化酶-2(COX-2)和凋亡抑制蛋白Bcl-2表达程度的变化.结果舒林酸对人胃腺癌细胞MKN45,MKN28的杀伤率随着剂量的增大和作用时间的延长而增加,舒林酸对不同类型的细胞杀伤率不同.舒林酸能够诱导人胃腺癌细胞MKN45,MKN28产生凋亡,凋亡诱导作用的强弱同样具有时间和剂量依赖性,而且对不同类型胃癌细胞的凋亡诱导效应有显著差异.经舒林酸2 mmol·L-1和4 mmol·L-1作用24 h后,MKN45细胞内COX-2和Bcl-2蛋白比未经舒林酸作用的细胞表达明显减少,而MKN28细胞内COX-2和Bcl-2蛋白的表达未出现明显变化.结论舒林酸在体外对人胃腺癌细胞株MKN45和MKN28有良好的增殖抑制作用,诱导凋亡是其抑制胃癌细胞增殖的重要作用机制.舒林酸对人胃腺癌细胞的抑制和凋亡诱导作用与其抑制细胞内环氧化酶-2,并进而抑制Bcl-2的表达有关,并可能与胃癌细胞的分化状态有关.     

肝症口服液含药血清对TGFα诱导SMMC-7721细胞增殖和ERK蛋白的影响

目的观察肝症口服液含药血清对TGFα诱导人肝癌细胞增殖和信号传导因子ERK影响.方法采用血清药理学方法,以病理鼠血清作对照,应用MTT比色法观察中药鼠血清对TGFα诱导人肝癌细胞SMMC-7721增殖的抑制作用.用免疫组化方法检测中药血清对信号传导因子ERK蛋白表达影响.结果中药血清作用24 h对SMMC-7721细胞抑制率达25%,P＜0.05;作用48 h抑制率达30%,P＜0.001;中药血清作用24 h对1μg·L-1 TGFα诱导的SMMC-7721细胞增殖抑制率为12.3%,P＞0.05;作用48 h抑制率为16%,P＜0.05;中药血清作用24 h对5μg·L-1TGFα诱导的SMMC-7721细胞增殖抑制率为8.9%,P＞0.05,作用48 h抑制率为17.2%,P＜0.001.中药血清对TGFα诱导的肝癌细胞SMMC-7721增殖有明显的抑制作用,抑制效应呈时间依赖性.中药血清能抑制ERK蛋白在细胞核中的表达.结论肝症口服液含药血清能够抑制TGFα诱导的人肝癌细胞增殖,阻断TGFα在细胞内的信号传导.     

卡维地洛对外源性羟自由基诱导心肌细胞凋亡的影响

目的 :观察卡维地洛 (Carvedilol)对外源性羟自由基诱导心肌细胞凋亡的影响。方法 :采用培养的第 2代心肌细胞 ,随机分成 4组 :1.正常对照组 :仅用DMEM培养 ;2 .羟自由基组 :FeSO410 0 μmol·L- 1 +H2 O2 10 0 μmol·L- 1 ;3.卡维地洛组 :卡维地洛终浓度为 1μmol·L- 1 ;4 .卡维地洛 +羟自由基组 :卡维地洛 1μmol·L- 1 +FeSO4 10 0 μmol·L- 1 +H2 O2 10 0 μmol·L- 1 。观察心肌细胞存活率和形态学 ,流式细胞仪检测细胞凋亡率。结果 :1.羟自由基组心肌细胞存活率降低 ,和对照组比较有显著性差异(P <0 0 5 ) ;卡维地洛 +羟自由基组细胞存活率较羟自由基组高 (P <0 0 5 )。 2 .羟自由基组凋亡率较高 ,明显高于对照组 (P <0 0 5 ) ;卡维地洛 +羟自由基组的细胞凋亡率显著低于羟自由基组 (P <0 0 5 )。3.羟自由基组凋亡心肌细胞呈特征性超微结构及AnnexinV+ PI- 荧光染色。结论 :卡维地洛能减轻外源性羟自由基诱导的心肌细胞凋亡。     

肝硬化合并血行播散型肺结核1例

1　病史摘要　患者王某 ,男 ,37岁。因黄疸 1月伴发热 2周。入院前一年“右侧腓神经”曾受伤 (工伤 )。初步拟诊右腓总神经损伤 ,酒精性合并胆汁性肝硬化。追询病史有长期酗酒史。体检 :体温 38.5℃ ,脉搏 80次 /min,呼吸 2 2次 /min,血压 90 /6 0mm Hg。皮肤巩膜轻度黄染。心肺 (- )。肝脏右肋下 6 cm,剑突下 8cm,质韧 ,边钝 ,无叩痛。脾脏肋下 6 cm。红细胞 3.6 3× 10 1 2· L- 1 ,白细胞 4 6× 10 9· L- 1 ,血红蛋白 10 g· L- 1 白球蛋白比4 2 /2 6 g· L- 1 ,谷丙转氨酶 ,谷草转氨酶正常 ,总胆红素 5 7Umol· L- 1 ,直接胆红素 4 …     

钠对高血压大鼠血浆及组织血管紧张素Ⅱ的影响

目的 :观察钠对自发性高血压大鼠 (SHR)血浆及组织中血管紧张素Ⅱ (AngⅡ )的影响。方法 :2 0只雄性 8周龄SHR随机分为高钠组和对照组 (每组 10只 ) ,分别给予 2 %NaCl溶液和自来水喂养 6周 ,放射免疫法测定血浆肾素活性 (PRA)、血浆和组织AngⅡ。结果 :高钠组SHRPRA较对照组下降 [(1.13± 0 .72 )∶(1.94±0 .96 ) μg·L-1·h-1,P <0 .0 5 ) ],血浆AngⅡ水平略有下降 [(89.4± 1.4 )∶(111.6± 1.3)ng·L-1·h-1],但差异无显著性意义 (P >0 .0 5 ) ,高钠组SHR的心脏、血管AngⅡ水平较对照组升高分别为 [(2 2 7.1± 1.1)∶(15 1.4±1.1) pg/ g ,P <0 .0 1;(5 7.1± 1.5 )∶(30 .7± 2 .0 ) pg/ g ,P <0 .0 5 ]肾脏AngⅡ水平两组间差异无显著性意义。 结论 :钠负荷对血浆及组织AngⅡ的影响是不同的。     

地尔硫治疗急性冠状动脉综合征的剂量及疗效观察

目的 :观察地尔硫治疗急性冠状动脉综合征的剂量及临床疗效。方法 :2 5例急性冠状动脉综合征患者静脉滴注地尔硫 1～ 5 μg·kg-1·min-1,持续用药 4 8h。结果 :ST段抬高型心绞痛及非ST段抬高型心绞痛用药前后心绞痛发作次数明显减少 (P <0 .0 5 ) ;地尔硫治疗ST段抬高型心绞痛较非ST段抬高型心绞痛更为有效 (P <0 .0 5 )。地尔硫可不同程度地降低心率、血压及心肌氧耗量 ,其中用药后 2h及 12h心肌氧耗量明显下降 (P <0 .0 5 )。结论 :静脉滴注地尔硫 1～ 3μg·kg-1·min-1可有效改善各种类型心绞痛的发作 ,且其不良反应小、安全性高     

皮肌炎致急性呼吸衰竭1例

1　病史摘要患者男性 ,5 0岁 ,因面部皮诊 1个月 ,发热 ,咳嗽 2周。既往体健。入院查体 :T37.9℃ ,R2 0次 /min,BP110 /70 mm Hg,神清 ,浅表淋巴结无肿大 ,前额 ,鼻部 ,颞部皮肤有对称性暗红色斑丘疹 ,双肘部伸侧皮肤有对称性暗红色斑疹 ,有少许鳞屑 ,无破溃及结痂 ,HR 90次 /min,两肺底部可闻中量爆裂音及细小水泡音 ,肝脾触及 ,无杵状指 (趾 ) ,肌力 5级。白细胞 4 .9× 10 9· L- 1 ,血色素 13g· L- 1 ,尿蛋白 (+)～ (+++) ,天门冬酸氨基转移酶 (AST) 348U· L- 1 ,乳酸脱氢酶 (L DH ) 12 6 3～ 15 6 6 U· L- 1 ,肌酸激酶 (CK…     

多巴酚丁胺负荷超声心动图试验在心肌梗死冠脉重建术前后判定存活心肌的对比研究

目的:采用多巴酚丁胺负荷超声心动图(DSE)试验评价心肌梗死(MI)病人冠脉重建术(CRV)后心室运动功能恢复的临床意义.方法:选择30例急性心肌梗死病人,在冠脉重建术前、术后6个月,以不同剂量多巴酚丁胺(5、10、15、20、25、30μg·kg-1·min-1)连续静注5min后,用二维超声心动图观察患者室壁运动异常(WMA)节段的变化.结果:在不同剂量多巴酚丁胺下,CRV前后患者的心率、收缩压均呈升高反应(P＜0.05),WMA均有不同程度上的改变(P＜0.05).结论:DSE试验是识别MI区域存活心肌有价值的方法之一.多巴酚丁胺从5μg·kg-1·min-1开始有效,10～15μg·kg-1·min-1达高峰,≥20μg·kg-1·min-1则在术前对部分病人有诱发心肌缺血,使收缩功能恶化及频发室早出现.     

Drugs inhibiting the hepatic fibrogenesis

The treatment of chronic liver disease represents still now an open problem in medicine. The first objective of therapy has to be the causal agent removal; however, there are many cases (viral infections, autoimmunity, genetic disease) in which it is not possible to reach this issue; in these situations the secondary objective of the therapy is to inhibit the hepatic fibrogenesis, in attempt of easing or blocking the transformation of chronic liver disease in cirrhosis. The aim of this work is to review the various compounds which showed an antifibrotic activity, using a simple classification model, allowing a fast setting of different compounds. These last, on the basis of their main action, can be divided into two main groups: drugs with direct action, which interfere with collagen metabolism (for instance interferons, glucocorticoids, prolyl 4-hydroxylase inhibitors, cyclosporin A, colchicine, D-penicillamine, phosphatidylcholine and so on) and drugs with indirect action, that decrease the inflammatory stimuli, capable of stirring up the fibrogenetic hepatic process (S-adenosylmethionine, malotilate, ursodeoxycholic acid, ribavirin and so on). There are drugs that have both mechanisms of action, without the prevalence of one or other mechanism (prostaglandins).     

Müllerian inhibiting substance blocks autophosphorylation of the EGF receptor by inhibiting tyrosine kinase

The fetal regressor Müllerian inhibiting substance (MIS), in concentrations as low as picomolar, inhibited the growth of A-431 cells and the autophosphorylation of its epidermal growth factor (EGF) receptor. The inhibition of membrane phosphorylation was due neither to the reduction of the total number of EGF receptor binding sites, nor to stimulation of intrinsic phosphates, but rather to inhibition of tyrosine kinase activity. MIS control of EGF receptor autophosphorylation by tyrosine kinase may be one mechanism by which Müllerian duct regression in the embryo and the inhibition of A-431 proliferation is initiated. In addition, MIS as an inhibitor of phosphorylation may furnish a tool to probe the role of membrane phosphorylation in growth control.     

地塞米松纳米粒子的制备及体内抑制血管再狭窄的研究

目的　制备地塞米松纳米粒子并应用于动物模型验证其效果。方法　采用 PL GA为载体 ,制备了地塞米松纳米粒子 ,对其进行了表征。结果　纳米粒子粒径在 2 5 0 nm左右 ,载药量高达 17%以上 ,包封率为 97% ,可维持长时间稳定的体外释放 ,应用于兔球囊损伤模型 ,明显抑制了血管内膜增生 ,取得了较好的效果。结论　纳米粒子是一种良好的药物载运体系     

Sex-specific fetal lung development and müllerian inhibiting substance

Male neonates develop respiratory distress syndrome (RDS) with a greater incidence and mortality than do female neonates; the cause of this male disadvantage remains obscure. Male fetuses are exposed to higher levels of androgens and Müllerian inhibiting substance (MIS). Androgens have been shown to inhibit fetal lung maturation, and recent evidence in vitro indicates that MIS, a Sertoli cell-derived glycoprotein made early in ontogeny of the testis, may also inhibit lung development. To study whether this fetal regressor might inhibit maturation of the fetal lung in vivo, we injected human recombinant MIS (rMIS) into fetal rats, measured serum levels of rMIS using an enzyme-linked immunosorbent assay, and analyzed fetal lung tissue histologically and for protein, glycogen, DNA, and disaturated phosphatidylcholine content. Peak serum levels of recombinant MIS were measured at 6 h, with an apparent elimination half-life of 3 h, and without leakage into adjacent littermates injected with vehicle alone. Female fetal rat lung tissue exposed to recombinant MIS (10(-9) M, 10(-8) M) revealed depressed disaturated phosphatidylcholine content both 48 and 72 h after injection compared with female vehicle-injected littermates. Male lungs of the same gestational age appeared inhibited at a higher (10(-8) M) rMIS dose. These inhibitory effects observed in vivo confirm those previously seen in vitro and suggest that MIS, as well as androgens, may play a causative or important ancillary role in the sexual dimorphism that characterizes the neonatal respiratory distress syndrome.     

Akt suppresses androgen-induced apoptosis by phosphorylating and inhibiting androgen receptor

Whereas several apoptosis-related proteins have been linked to the antiapoptotic effects of Akt serine-threonine kinase, the search continues to explain the Akt signaling role in promoting cell survival via antiapoptotic effects. Here, we demonstrate that Akt phosphorylates the androgen receptor (AR) at Ser-210 and Ser-790. A mutation at AR Ser-210 results in the reversal of Akt-mediated suppression of AR transactivation. Activation of the phosphatidylinositol-3-OH kinase/Akt pathway results in the suppression of AR target genes, such as p21, and the decrease of androgen/AR-mediated apoptosis, which may involve the inhibition of interaction between AR and AR coregulators. Together, these findings provide a molecular basis for cross-talk between two signaling pathways at the level of Akt and AR-AR coregulators that may help us to better understand the roles of Akt in the androgen/AR-mediated apoptosis.