对人的全面的辩证的认识

医学科学研究的主要对象是人,医务工作者的崇高职责是“治病救人”。因此如何认识人,在医疗实践和医学科学研究中具有重要的意义。一、人是自然的生物,人体是部分和整体的统一体。人不是上帝创造的,也不是超自然的、非物质的、神秘的、抽象的东西,人是有血     

论合道德的人性的安乐死与不道德的非人性的安乐死

安乐死问题的争论，关键是准确把握安乐死的实质以及对最基本人权——生命权的尊重。对濒临死亡或者逼近死亡的病人．能否实施安乐死，是否任何形式的安乐死都可以实施。反对主动安乐死，提倡实施被动安乐死，反对安乐死问题上的无痛苦致死术，实施无痛苦死亡。     

妊娠期妇女的生理的局部性的变化分析

妊娠是胚胎和胎儿在母体内发育成长的过程.这是一个非常复杂、变化极其协调的生理过程.妊娠时,因胎儿成长的需要,母体所有的器官、系统均会产生连续性的变化.这种生理性的变化,是正常生物功能的延续,以渐进的方法 发生,来调整其功能,以供给胎儿生长过程中所需之氧气和养分.     

前列腺癌的MRS的研究

近年来前列腺恶性肿瘤呈明显上升趋势,自20世纪70年代以来,超声、CT、MRI、核医学等医学影像学检测方法发展迅速,但对早期肿瘤诊断的敏感性及特异性不强.因此,有待新的检查技术的开展.三维磁共振波谱成像(MRS)能动态地监测细胞内的代谢变化,助于诊断早期前列腺肿瘤,特别对中央带前列腺癌(PCa)的检出有重要价值.就MRS对前列腺癌的特异性和敏感性做一综述.     

深静脉栓塞的的临床研究

目的 对42例深静脉拴塞(DVT)的诊断和溶拴治疗进行初步临床研究。方法 从DVT患者的远端静脉慢滴入尿激酶(UK)和中药三七总甙(血塞通)，并在拴塞部位上方用皮条阻滞浅静脉，以减少静脉的回流，治疗前后均作深静脉造影对照。结果 本组深静脉造影的再通率为82％。结论 从患肢远端静脉滴入溶栓剂进行溶栓治疗优于全身用药。本方法简单易行，易于推广应用，再通率与时限、病因有关。     

绿化的杀菌作用的观察

<正> 绿化有良好的环境效应为人所共知,如对于调节微小气候、防尘降尘、吸收有害气体、减弱噪声等已有不少报导。除此之外,树木还有杀菌作用,也有过少量报导。为了观察亚热带地区城镇绿化的杀菌作用,我们对百色城绿化进行综合考察之后,于一九八二年四月又对百色城不同绿化地区的空气含菌量进行了监测,初步发现了定的效应。     

语言的任意性的思考

自从索绪尔在其普通语言学课程讲义中提出“语言符号是任意的”以来,语言学家对这一提法的“是与否”的论证就从没停息过。在这一过程中,人们加深了对语言本质的认识,促进了与之相关的其他学科的发展。本文试图对语言符号的任意性提出自己的一些看法。并非索绪尔最先指出语言中的音义关系带有约定性,不过,却是索绪尔首先为音义关系的任意性确定了在理论体系中头等重要的地位。他认为语言不是分类命名集,不是给已经存在的概念范畴命名,相反是在语言系统中创造出概念范畴,这就从根本上否定了孤立的符号单位具有外在于系统的价值。     

新发现的传染病的特点

20世纪70年代以来,全球新发现的传染病有40多种,其特点是:①病毒是主要病原体;②相当部分是动物源性传染病;③人群对新传染病缺乏免疫力;④缺乏特效治疗和免疫预防;⑤新传染病给社会做成一定恐慌.     

紫丁香的化学成分的研究

紫丁香(Syringa oblata Lindl)别名丁香、紫花丁香为木犀科(Oleaceae)丁香属(Syringa) 植物,该植物约19种,我国有15种.地域分布广泛,多分布于辽宁、北京、河北、陕西、河南等地.     

麻辣的还是牛肉的

寝室老大一次大姨妈来了．正巧赶在中午．我们几个都去食堂吃饭了，所以老大就去楼下的小卖店去买，我们寝室楼下的小卖店有一个微波炉，好多不愿意去食堂吃饭的MM们就到那用微波炉煮方便面（我想每个大学都应该有吧），所以一到中午的时候本来就不大的小卖店就人满为患．老板娘更是忙得不可开交。     

尾加压素Ⅱ对培养的心脏成纤维细胞增殖和胶原基因表达的影响

目的 观察尾加压素Ⅱ(urotensinⅡ,UⅡ)在体外对乳鼠心脏成纤维细胞(CFs)增殖和Ⅰ型胶原(CoL-Ⅰ)基因表达的直接影响,以探讨UⅡ在心力衰竭心肌重塑中的作用。方法 以胰酶消化和差速贴壁法分离和纯化SD乳鼠的CFs,采用四氮唑盐(MTT)比色法测定细胞增殖,RT-PCR测定CoL-ⅠmRNA表达水平。结果 UⅡ对CFs增殖呈浓度依赖性,随着UⅡ作用浓度的增加,MTT光吸收值呈先升高后降低的趋势,其中1×10^-8 mol/L和1×10^-9 mol/L的UⅡ作用显著(P<0.05);1×10-7 mol/L、1×10^-8 mol/L和1×10^-9 mol/L浓度的UⅡ能促进CFs的CoL-ⅠmRNA表达(P<0.01)。结论 UⅡ可直接促进CFs的增殖及CoL-ⅠmRNA表达,作用大小与UⅡ浓度有关,提示UⅡ在心力衰竭心肌重塑的病理生理过程中可能发挥重要作用。     

Effect of angiotensin Ⅱ and angiotensin Ⅱ type 1 receptor antagonist on the proliferation,contraction and collagen synthesis in rat hepatic stellate cells

Background Angiotensin Ⅱ （Ang Ⅱ） is a very important vasoactive peptide that acts upon hepatic stellate cells （HSCs）, which are major effector cells in hepatic cirrhosis and portal hypertension. The present study was aimed to investigate the effects of Ang Ⅱ and angiotensin Ⅱ type 1 receptor antagonist （AT1RA） on the proliferation, contraction and collagen synthesis in HSCs.
Methods HSC-T6 rat hepatic stellate cell line was studied. The proliferation of the HSC cells was evaluated by MTT colorimetric assay while HSC DNA synthesis was measured by ^3H-thymidine incorporation. The effects of angiotensin Ⅱ and AT1RA on HSCs contraction were studied by analysis of the contraction of the collagen lattice. Cell culture media were analyzed by RT-PCR to detect secretion of collagen Ⅰ （Col Ⅰ）, collagen Ⅲ （Col Ⅲ） and transforming growth factor β1 （TGF-β1） by enzyme linked immunosorbent assay. HSC was harvested to measure collagen Ⅰ, collagen Ⅲ and tissue inhibitor of metalloproteinase-1 （TIMP-1） mRNA expression.
Results Ang Ⅱ （（1×10^-10-1×10^-4）mol/L）stimulated DNA synthesis and proliferation in HSCs compared with untreated control cells. AT1RA inhibited angiotensin Ⅱ induced proliferation of HSCs. A linear increase in the contractive area of collagen lattice correlated with the concentration of angiotensin Ⅱ （1×10^-9-1×10^-5 mol/L） and with time over 48 hours. AT1RA blocks angiotensin Ⅱ induced contraction of collagen lattice. Col Ⅰ, Col Ⅲ and TGF-β1 levels of the Ang Ⅱ group were higher than those of control group and this increase was downregulated by AT1RA. The mRNA expressions of Col Ⅰ, Col Ⅲ and TIMP-1 were higher in HSCs from the Ang Ⅱ group than the control group and downregulated by AT1RA.
Conclusions Angiotensin Ⅱ increased DNA synthesis and proliferation of HSCs in a dose-dependent manner, stimulated the contraction of HSCs dose- and time-dependently. Angiotensin also promoted excretion of Col I, Col Ⅲ and TGF-β1 lev     

软骨形态发生蛋白1诱导真皮成纤维细胞表达软骨细胞表型的实验研究

目的应用软骨形态发生蛋白(CDMP)生长因子,体外诱导真皮成纤维细胞向成软骨细胞表型分化,探讨其作为组织工程化软骨种子细胞的可行性.方法取包皮环切术后丢弃真皮组织共3例,成纤维细胞体外培养扩增至第二代,以1×104/cm2密度接种,12 h后加入细胞诱导液(10%胎牛血清F-12培养液,CDMP1终浓度为100 ng/ml)单层培养,未加的成纤维细胞培养用CDMP1为对照.诱导7 d后观察细胞形态变化,Image Plus图像分析软件计算细胞长宽比例.激光共聚焦显微镜分别观察诱导前后细胞内Ⅰ、Ⅱ、Ⅲ型胶原表达及分布,Western印迹检测诱导前后细胞Ⅱ型胶原蛋白表达.反转录聚合酶链式反应(RT-PCR)检测诱导后成软骨相关的Sox9、聚集蛋白聚糖与Ⅱ、Ⅸ型胶原mRNA表达;同时检测与成骨相关的X型胶原、碱性磷酸酶(AKP)mRNA表达.培养第二代细胞以2×107个细胞/ml细胞密度进行离心管法培养,诱导14 d后行阿辛蓝与Ⅱ型胶原免疫组化染色.结果诱导后可见单层培养的成纤维细胞形态由长梭形向软骨细胞样多角形转变,Image Plus图像分析软件计算细胞诱导后的长宽比例为(1.40±0.15),较诱导前(7.40±1.30)差异有显著意义(P＜0.05);与正常软骨细胞(1.29±0.24)差异无显著意义.免疫荧光激光共聚焦观察发现诱导后细胞内出现Ⅱ型胶原表达,Ⅰ、Ⅲ型胶原表达呈阳性.RT-PCR检测成软骨相关的Sox9,聚集蛋白聚糖,Ⅱ、Ⅸ型胶原mRNA表达阳性;X型胶原、AKP未检测到mRNA阳性表达.Western印迹检测细胞诱导后Ⅱ型胶原蛋白表达阳性.离心管培养诱导7 d后阿辛蓝染色示糖胺聚糖(GAG)均匀分布于基质中,免疫组化染色示基质中Ⅱ型胶原表达阳性.结论第二代成人真皮成纤维细胞在CDMP1生长因子诱导下可向成软骨细胞表型分化,并能分泌软骨细胞特异性基质,有望成为软骨组织工程新的种子细胞来源.     

NAD对AngⅡ诱导的心肌成纤维细胞Ⅰ型胶原mRNA表达的影响

目的   探讨烟酰胺腺嘌呤二核苷酸(NAD) 对血管紧张素II（AngII)诱导的大鼠心肌成纤维细胞I型胶原mRNA表达的作用。方法   提取新生Wistar大乳鼠原代心肌成纤维细胞,传代培养,采用2~4代细胞。实验分为空白对照组,AngII (0.01、 0.1、 1μmol／L)组,NAD(250μmol／L)组, AngII(1μmol／L)+ NAD (250μmol／L )组,FAM组,Sirt1-siRNA+AngII(1μmol／L)组,Sirt1-siRNA 组,Sirt1-siRNA+ NAD（250μmol／L）组,Sirt1-siRNA+Ang II(1mol／L)+NAD（250μmol／L）组。刺激24h后,提取总RNA, Real time RT-PCR法分别检测SIRT1和I型胶原mRNA的表达。结果   心肌成纤维细胞I型胶原mRNA的表达随着AngⅡ浓度升高明显增加(P＜0.05),呈浓度依赖性。与空白对照组比较,NAD（250μmol／L）组SIRT1 mRNA表达增高(P＜0.05)。与AngⅡ（1μmol／L）组比较,AngII (1μmol／L)+ NAD(250μmol／L )组I型胶原mRNA的表达明显减少(P＜0.01)。相对于FAM组,Sirt1-siRNA转染后各组SIRT1 mRNA的表达减少(P＜0.05),而心肌成纤维细胞I型胶原mRNA表达增多(P＜0.05)。结论   NAD可以抑制心肌成纤维细胞 I型胶原mRNA的表达,SIRT1影响I型胶原mRNA的表达,它们对Ang II诱导的心肌纤维化有保护作用。     

Curcumin Reduces Cardiac Fibrosis by Inhibiting Myofibroblast Differentiation and Decreasing Transforming Growth Factor β1 and Matrix Metalloproteinase 9 / Tissue Inhibitor of Metalloproteinase 1

Objective: To study the effect of curcumin on fibroblasts in rats with cardiac fibrosis. Methods: The rats were randomly divided into 4 groups(n=12 in each group): the normal control, isoproterenol(ISO), ISO combined with low-dose curcumin(ISO+Cur-L), and ISO combined with high-dose curcumin(ISO+Cur-H) groups. ISO+Cur-L and ISO+Cur-H groups were treated with curcumin(150 or 300 mg·kg-1·day-1) for 28 days. The primary culture of rat cardiac fibroblast was processed by trypsin digestion method in vitro. The 3rd to 5th generation were used for experiment. Western blot method was used to test the expression of collagen type Ⅰ/Ⅲ, α-smooth muscle actin(α-SMA), transforming growth factor(TGF)-β1, matrix metalloproteinase(MMP)-9 and tissue inhibitor of metalloproteinase(TIMP)-1. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetr-azolium bromide(MTT) assay was applied to test the proliferation of fibroblast. Result: Curcumin significantly decreased interstitial and perivascular myocardial collagen deposition and cardiac weight index with reducing protein expression of collagen type Ⅰ/Ⅲ in hearts(P0.05). In addition, curcumin directly inhibited angiotensin(Ang) Ⅱ-induced fibroblast proliferation and collagen type Ⅰ/Ⅲ expression in cardiac fibroblasts(P0.05). Curcumin also inhibited fibrosis by inhibiting myofibroblast differentiation, decreased TGF-β1, MMP-9 and TIMP-1 expression(P0.05) but had no effects on Smad3 in Ang Ⅱ incubated cardiac fibroblasts. Conclusions: Curcumin reduces cardiac fibrosis in rats and Ang Ⅱ-induced fibroblast proliferation by inhibiting myofibroblast differentiation, decreasing collagen synthesis and accelerating collagen degradation through reduction of TGF-β1, MMPs/TIMPs. The present findings also provided novel insights into the role of curcumin as an anti-fibrotic agent for the treatment of cardiac fibrosis.     

罗布麻提取物对Ang Ⅱ诱导的心肌成纤维细胞的影响

目的探讨罗布麻提取物对血管紧张素II（Angiotensin Ⅱ,Ang Ⅱ）诱导的大鼠心肌纤维化细胞的影响及其可能作用机制。方法采用Ang Ⅱ诱导心肌成纤维细胞复制心肌纤维化模型,细胞分组为空白对照组（C组）、模型组（Ang Ⅱ组）、罗布麻提取物高剂量组（0.8mg.L-1,Ang Ⅱ＋AVE1）、罗布麻提取物中剂量组（0.4mg.L-1,Ang Ⅱ＋AVE1）、罗布麻提取物低剂量组（0.2mg.L-1,Ang Ⅱ＋AVE1）及阳性药对照缬沙坦组（10-6mg.L-1,Ang Ⅱ＋VL）,给药48h后,通过MTT检测心肌成纤维细胞增殖情况,ELISA法及RT-PCR法检细胞上清及细胞中Ⅰ、Ⅲ型胶原、TGF-β（Transforming growthfactor-β）蛋白及mRNA的表达。结果在Ang Ⅱ诱导的心肌纤维化模型中,罗布麻提取物可抑制ECM（Extracellularmatrix）胶原成分（Col Ⅰ和Col Ⅲ）的积聚;TGF-β在心肌纤维化大鼠心肌中表达显著增加,罗布麻提取物可降低TGF-βmRNA及蛋白的表达。结论罗布麻提取物可通过对降低TGF-β的表达延缓心肌纤维化的发生发展。     

Atorvastatin reduces myocardial fibrosis in a rat model with post-myocardial infarction heart failure by increasing the matrix metalloproteinase-2/tissue matrix metalloproteinase inhibitor-2 ratio

Background The cholesterol-lowering statin drugs have some non-lipid-lowering effects,such as inhibiting myocardial remodeling.However,the underlying mechanism is still unclear.Methods The left anterior descending coronary artery was ligated to establish a rat model of heart failure,and the rats were divided into a sham operation (SO) group,myocardial infarction model (MI) group,and MI-atorvastatin group.Changes in hemodynamic parameters were recorded after the final drug administration.Histological diagnosis was made by reviewing hematoxylin and eosin (HE) stained tissue.Real-time quantitative polymerase chain reaction (PCR)was performed to determine the expressions of type Ⅰ and type Ⅲ collagen,matrix metalloproteinase-2 (MMP-2),and tissue matrix metalloproteinase inhibitor-2 (TIMP-2).Further,primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of atorvastatin on cardiac fibroblast proliferation.Results The model of heart failure was established and the results of HE staining and Masson's trichrome staining revealed that the rats in the heart failure group showed obvious hyperplasia of fibrotic tissue,which was significantly reduced in the atorvastatin group.Real-time quantitative PCR showed that the MI group showed a significantly increased expression of type Ⅰ and type Ⅲ collagen,MMP-2,and TIMP-2,but a significantly reduced MMP-2/TIMP-2 ratio.Compared with the MI group,the atorvastatin group showed significantly reduced expression of type Ⅰ and Ⅲcollagen,unchanged expression of MMP-2,significantly reduced expression of TIMP-2,and an increased MMP-2/TIMP-2 ratio.We further found that atorvastatin significantly inhibited the Ang Ⅱ-induced flbroblast proliferation and the expression of type Ⅰ and type Ⅲ collagen in cardiac flbroblasts while increasing the MMP-2/TIMP-2 ratio.Conclusions These data suggest that atorvastatin can inhibit cardiac fibroblast proliferation and enhance collagen degradation by increasing the MMP-2/TIMP-2 ratio,thereby inhibiting the formation of myocardial fibrosis in rats with heart failure after myocardial infarction.     

强心饮对肿瘤坏死因子α诱导的大鼠心肌成纤维细胞增殖和胶原合成以及激活蛋白1mRNA表达的影响

目的：研究激活蛋白1（activator protein—1．AP-1）在肿瘤坏死因子严世芸：（turnor necrosis factor—α，TNFα）诱导新生大鼠心肌成纤维细胞（cardiac fibroblasts，CFs）增殖、胶原合成中的作用，探讨强心饮抑制心肌纤维化的作用机制。方法：胰酶消化法分离培养乳鼠CFs．建立TNFα诱导新生大鼠CFs纤维化模型。将CFs按培养方式不同分为正常对照组、模型组和强心饮5％含药血清组、10％含药血清组和20％含药血清组。治疗24h后，采用荧光实时定量聚和酶链式方法检测不同浓度强心坎对CFs AP-1mRNA表达的影响，甲基噻唑基四唑法检测强心欣对CFs增殖的影响；羟脯氧酸法检测对CFs胶原合成量的影响。结果：TNF—α作用CFs24h舌．与空白对照组相比。AP-1mRNA表达明显增加（P〈0．05），细胞增殖和胶原合成增加（P〈0．05）；强心饮干预后，CFs增殖和胶原合成减少（P〈0．05），AP1mRNA表达下调（P〈0．05）。结论：强心饮能够抑制TNF-α诱导的CFs增殖和胶原合成增加，具有抗心肌纤维化作用，其机制可能与下调AP-1 mRNA表达有关。     

TNF-α对培养乳鼠心肌成纤维细胞的作用

目的:探讨不同浓度TNF-α对培养乳鼠心肌成纤维细胞增殖、分泌AngⅡ、胶原及AT1受体表达的影响。方法:原代培养SD乳鼠心肌成纤维细胞,采用MTT法检测心肌成纤维细胞增殖,羟脯氨酸测定法观察成纤维细胞培养上清胶原含量,酶免法检测心肌成纤维细胞培养液AngⅡ含量,免疫细胞化学法观察心肌成纤维细胞膜AT1受体的表达变化。结果:TNF-α呈浓度依赖性的促进培养的乳鼠心肌成纤维细胞分泌AngⅡ和胶原,促进心肌成纤维细胞增殖及AT1受体的表达。结论:TNF-α促进心肌成纤维细胞分泌AngⅡ介导了心肌纤维化而参与心肌改建。