CHANGES OF PLASMA ENDOTHELIN AND ATRIAL NATRIURETIC PEPTIDE DURING THE ONSET AND AFTER TERMINATION OF PAROXYSMAL SUPRAVENTRIC

ＣＨＡＮＧＥＳＯＦＰＬＡＳＭＡＥＮＤＯＴＨＥＬＩＮＡＮＤＡＴＲＩＡＬＮＡＴＲＩＵＲＥＴＩＣＰＥＰＴＩＤＥＤＵＲＩＮＧＴＨＥＯＮＳＥＴＡＮＤＡＦＴＥＲＴＥＲＭＩＮＡＴＩＯＮＯＦＰＡＲＯＸＹＳＭＡＬＳＵＰＲＡＶＥＮＴＲＩＣＵＬＡＲＴＡＣＨＹＣＡＲＤＩＡＬ...     

EFFECTS OF MTX AND BN_52021 ON PAF－INDUCED CHEMOTAXIS OF PMNs AND I

ＥＦＦＥＣＴＳＯＦＭＴＸＡＮＤＢＮ５２０２１ＯＮＰＡＦ－ＩＮＤＵＣＥＤＣＨＥＭＯＴＡＸＩＳＯＦＰＭＮｓＡＮＤＩＮＴＲＡＥＰＩＤＥＲＭＡＬＡＣＣＵＭＵＬＡＴＩＯＮＯＦＩＮＦＬＡＭＭＡＴＯＲＹＣＥＬＬＳＩＮＧＵＩＮＥＡＰＩＧＳＬｉｕＢａｏｊｕｎ刘宝军，Ｚ...     

EXPRESSION OF TGF－β_1，PDGF AND IGF－1 mRNA IN LUNG OF BLEOMYCIN－A_5－INDUCED PULMONARY FIBROSIS IN RATS

ＥＸＰＲＥＳＳＩＯＮＯＦＴＧＦ－β１，ＰＤＧＦＡＮＤＩＧＦ－１ｍＲＮＡＩＮＬＵＮＧＯＦＢＬＥＯＭＹＣＩＮ－Ａ５－ＩＮＤＵＣＥＤＰＵＬＭＯＮＡＲＹＦＩＢＲＯＳＩＳＩＮＲＡＴＳＬｉＨａｉｃｈａｏ李海潮，ＨｅＢｉｎｇ何冰，ＱｕｅＣｈｅｎｇｌｉ阙呈立ａｎｄＷ...     

EXPRESSION OF P53 GENE IN ORAL SQUAMOUS CELL CARCINOMA AND ITS RELATION WITH CLINICAL AND PATHOLOGICAL PARAMETERS AND PROGNOS

ＥＸＰＲＥＳＳＩＯＮＯＦＰ５３ＧＥＮＥＩＮＯＲＡＬＳＱＵＡＭＯＵＳＣＥＬＬＣＡＲＣＩＮＯＭＡＡＮＤＩＴＳＲＥＬＡＴＩＯＮＷＩＴＨＣＬＩＮＩＣＡＬＡＮＤＰＡＴＨＯＬＯＧＩＣＡＬＰＡＲＡＭＥＴＥＲＳＡＮＤＰＲＯＧＮＯＳＩＳＯＦＰＡＴＩＥＮＴＳＭａｏＣｈｉ...     

SURGICAL TREATMENT OF HALLUX VALGLUS BY RECONSTRUCTION OF METATARSAL ARCH AND MODIFIED MCBRIDE OPERATION （40 CASES REPORT）

ＳＵＲＧＩＣＡＬＴＲＥＡＴＭＥＮＴＯＦＨＡＬＬＵＸＶＡＬＧＬＵＳＢＹＲＥＣＯＮＳＴＲＵＣＴＩＯＮＯＦＭＥＴＡＴＡＲＳＡＬＡＲＣＨＡＮＤＭＯＤＩＦＩＥＤＭＣＢＲＩＤＥＯＰＥＲＡＴＩＯＮ（４０ＣＡＳＥＳＲＥＰＯＲＴ）ＷｅｎｇＸｉｓｈｅｎｇ（翁习生）；Ｈｅ...     

ANGIOTENSIN Ⅱ IMMUNOREACTIVITIES IN CARDIOVASCULAR BRAIN AREAS OF DEVELOPING SPONTANEOUSLY HYPERTENSIVE AND NORMOTENSIVE WIST

ＡＮＧＩＯＴＥＮＳＩＮⅡＩＭＭＵＮＯＲＥＡＣＴＩＶＩＴＩＥＳＩＮＣＡＲＤＩＯＶＡＳＣＵＬＡＲＢＲＡＩＮＡＲＥＡＳＯＦＤＥＶＥＬＯＰＩＮＧ　ＳＰＯＮＴＡＮＥＯＵＳＬＹＨＹＰＥＲＴＥＮＳＩＶＥ　ＡＮＤＮＯＲＭＯＴＥＮＳＩＶＥ　ＷＩＳＴＡＲ　ＫＹＯＴＯＲＡ...     

IMPROVEMENT OF A DIRECT DTNB ASSAY OF GLUTATHIONE PEROXIDASE AND EFFECT OF SELENIUM RICH YEAST IN MICE BLOOD GLUTATHIONE PERO

ＩＭＰＲＯＶＥＭＥＮＴＯＦＡＤＩＲＥＣＴＤＴＮＢＡＳＳＡＹＯＦＧＬＵＴＡＴＨＩＯＮＥＰＥＲＯＸＩＤＡＳＥＡＮＤＥＦＦＥＣＴＯＦＳＥＬＥＮＩＵＭＲＩＣＨ　ＹＥＡＳＴＩＮＭＩＣＥＢＬＯＯＤＧＬＵＴＡＴＨＩＯＮＥＰＥＲＯＸＩＤＡＳＥＡＣＴＩＶＩＴＹＢａｏＪ...     

EFFECTS OF LOSARTAN AND PD123319 ON ANTIGENSIN Ⅱ- INDUCED PROTO-ONCOGENE EXPRESSION AND PROTEINSYN-TEHSIS IN CULTURED NEONATAL RAT CARDIAC MYOCYTES

ＥＦＦＥＣＴＳＯＦＬＯＳＡＲＴＡＮＡＮＤＰＤ１２３３１９ＯＮＡＮＴＩＧＥＮＳＩＮⅡ┐ＩＮＤＵＣＥＤＰＲＯＴＯ┐ＯＮＣＯＧＥＮＥＥＸＰＲＥＳＳＩＯＮＡＮＤＰＲＯＴＥＩＮＳＹＮ┐ＴＥＨＳＩＳＩＮＣＵＬＴＵＲＥＤＮＥＯＮＡＴＡＬＲＡＴＣＡＲＤＩＡＣＭＹＯＣ...     

ROLE OF COLLAGEN METABOLISM CHANGES IN THE PATHOGENESIS OF PULMONARY HYPERTENSION IN RATS AND ITS REVERSIBILITY

ＲＯＬＥＯＦＣＯＬＬＡＧＥＮＭＥＴＡＢＯＬＩＳＭＣＨＡＮＧＥＳＩＮＴＨＥＰＡＴＨＯＧＥＮＥＳＩＳＯＦＰＵＬＭＯＮＡＲＹＨＹＰＥＲＴＥＮＳＩＯＮＩＮＲＡＴＳＡＮＤＩＴＳＲＥＶＥＲＳＩＢＩＬＩＴＹＳｕｎＲｅｎｙｕ（孙仁宇）；ＹａｎＹｉｚｈａｏ（严仪昭）；...     

EFFECT OF HYPOXIA ON DNA SYNTHESIS AND C－MYC GENE EXPRESSION OF PULMONARY ARTERY SMOOTH MUSCLE CELLS

ＥＦＦＥＣＴＯＦＨＹＰＯＸＩＡＯＮＤＮＡＳＹＮＴＨＥＳＩＳＡＮＤＣ－ＭＹＣＧＥＮＥＥＸＰＲＥＳＳＩＯＮＯＦＰＵＬＭＯＮＡＲＹＡＲＴＥＲＹＳＭＯＯＴＨＭＵＳＣＬＥＣＥＬＬＳＬｕｏＬａｎ（罗兰）；ＬｉＳｈｉｑｉａｎｇ（李世强）ａｎｄＣａｉＹｉｎｇｎｉａｎ...     

Hypoxia-inducible factor-1 alpha regulates the role of vascular endothelial growth factor on pulmonary arteries of rats with hypoxia-induced pulmonary hypertension

Background Hypoxia-inducible factor-1α (HIF-1α) is one of the pivotal mediators in the response of lungs to decreased oxygen availability, and increasingly has been implicated in the pathogenesis of pulmonary hypertension. Vascular endothelial growth factor (VEGF), a downstream target gene of HIF-1α, plays an important role in the pathogenesis of hypoxic pulmonary hypertension and hypoxic pulmonary artery remodelling. In this study, we investigated the dynamic expression of HIF-1α and VEGF in pulmonary artery of rats with hypoxia-induced pulmonary hypertension. Methods Forty male Wistar rats were exposed to hypoxia for 0, 3, 7, 14 or 21 days. Mean pulmonary arterial pressure (mPAP), vessel morphometry and right ventricle hypertrophy index (RVHI) were estimated. Lungs were inflated and fixed for in situ hybridisation and immunohistochemistry. Results mPAP values were significantly higher than the control values after 7days of hypoxia ［(18.4±0.4) mmHg, P<0.05］. RVHI developed significantly after 14 days of hypoxia. Expression of HIF-1α protein increased in pulmonary arterial tunica intima of all hypoxic rats. In pulmonary arterial tunica media, HIF-1α protein was markedly increased by day 3 (0.20±0.02, P<0.05), reached the peak by day 7, then declined after day 14 of hypoxia. HIF-1α mRNA increased significantly after day 14 of hypoxia （0.20±0.02, P<0.05）. VEGF protein began to increase markedly after day 7 of hypoxia, reaching its peak around day 14 of hypoxia (0.15±0.02, P<0.05). VEGF mRNA began to increase after day 7 of hypoxia, then remained more or less stable from day 7 onwards. VEGF mRNA is located mainly in tunica intima and tunica media, whereas VEGF protein is located predominantly in tunica intima. Linear analysis showed that HIF-1α mRNA, VEGF and mPAP were correlated with hypoxic pulmonary artery remodelling. HIF-1α mRNA was positively correlated with VEGF mRNA and protein (P<0.01). Conclusion HIF-1α and VEGF are both involved in the pathogenesis of hypoxia-induced pulmonary hypertension in rats.     

THE ROLES OF bcl-2 GENE FAMILY IN THE PULMONARY ARTERY REMODELING OF HYPOXIA PULMONARY HYPERTENSION IN RATS

Objective. To investigate the roles of apeptosis in the pulmonary artery remodeling of pulmonary hypertension secondary to hypoxia and illustrate the relative genes expression. Methods. Thirty rats were divided into hypoxia group(10%O2, 8h/d) and normal control group. On the 15th day of hypoxia, pulmonary artery pressure and fight ventricular hypertrophy index were measured and pulmonary artery vessels were studied by light microscope. Then terminal deoxynucleotidyl transferase-mediateddUTP nick-end labeling(TUNEL)technique was used to detect nucleosomal DNA fragmentation of apeptotic cells.In situ hybridization and RT-PCR were used to detect the expression level of bel-2 and bax. Results. The pulmonary artery pressure and right ventricular hypertrophy index of hypoxia group were increased significantly, the pulmonary artery wall of hypoxic group become incrassate than control group. Apeptotic cells can be found in lung with hypoxia or without hypexia. Compared with control group, apeptotic index of hypoxic group decreased significantly. Through the methods of in situ hybridization and RT-PCR, we found the expression of bel-2 increased whereas bax decreased significantly in the hypoxic group. Conclusion. The alternation in bel-2 and bax expression induced by hypoxia play an important role in the pulmonary artery remodeling which is the main pathologic change of p~monary hypertension secondary to hypoxia.     

低氧大鼠肺血管中血小板衍化生长因子α，β受体基因表达的变化

肺血管构形重建是慢性低氧性肺动脉高压的重要发病学环节。肺血管壁细胞增生、肥大，细胞外间质成分堆积及部分非肌性化小动脉肌性化致肺血管壁增厚、管腔狭窄、弹性下降，使肺动脉高压得以维持。在调控间质细胞增殖中，血小板衍化生长因子（PDGF）的作用尤引人注目。动脉粥样硬化、高血压、血管成形术后再狭窄等体动脉增生性病理过程中，有关PDGF及其受体的作用有较多报道。基于Northern分子杂交结果显示出低氧大鼠肺组织PDGF受体基因表达增强［”，本研究进一步用原位杂交技术动态观察了低氧性肺动脉高压形成过程中肺组织PDGF－a，…     

慢性低氧性肺动脉高压大鼠肺内血管内皮生长因子表达的变化

为了解低氧对肺内血管内皮生长因子（ＶＥＧＦ）基因表达的影响及ＶＥＧＦ在肺动脉闹压发生中的作用，以常压低氧建立大鼠肺动脉高压模型，采用Ｅｌｉｓａ检测大鼠肺动脉血血清ＶＥＧＦ的含量改变，以体外转录并用ＤＩＧ－ＵＴＰ标记的ＶＥＧＦ ｃＲＮＡ探针进行肺组织原位杂交，检测大鼠肺内ＶＥＧＦ ｍＲＮＡ表达的变化。结果发现：低氧３周后，大鼠形成明显的肺动脉高压；大鼠肺动脉血血清中ＶＥＧＦ含量在低氧３周组为４２０．     

低氧影响大鼠肺内碱性成纤维细胞生长因子及其受体的表达

目的:观察慢性低氧对肺内成纤维细胞生长因子及其受体表达的影响。方法:置SD大鼠于含10％O2低氧箱内1周、2周或3周,用RT—PCR法测定不同低氧时间大鼠肺动脉和肺组织bFGF mRNA,SP免疫组织化学染色法检测肺组织bFGF及其受体蛋白表达水平。结果:低氧1周时,肺动脉、肺组织内bFGF表达水平(分别为5303±756;4876±674),较对照组(分别为2578±384;1462±231)明显升高(P<0.05),持续至低氧第2周,低氧3周时,bFGF回复到低氧前水平。低氧1周、2周大鼠肺组织内bFGF受体表达增加,3周时与正常对照无差异。结论:慢性低氧能刺激大鼠肺内bFGF的表达,bFGF可能参与低氧性肺动脉高压发病的病理和病理生理学过程。     

胰岛素降低STZ诱导的短期糖尿病大鼠心肌原癌基因c-myc的表达

目的观察原癌基因c-myc在糖尿病大鼠心肌肥大中的表达及胰岛素对其干预作用.方法腹腔注射链脲菌素60 mg·kg-1诱导大鼠糖尿病模型,1、3及7天时分别测定其血糖及体重情况.第3天时提取左心室总RNA,采用PT-PCR法测定原癌基因c-myc的表达.结果正常组大鼠的平均血糖水平为5.55±1.23 mmol·L-1,糖尿病组大鼠在腹腔注射链脲菌素后1、3、7天其血糖水平分别为21.92±6.94 mmol·L-1、26.42±1.82 mmol·L-1、28.98±7.27 mmol·L-1,胰岛素预处理组大鼠在腹腔注射链脲菌素后1、3、7天其血糖水平分别为16.59±1.13 mmol·L-1、18.34±1.82 mmol·L-1、17.77±1.22 mmol·L-1.3天时糖尿病组大鼠原癌基因c-myc的表达量是对照组的4倍,胰岛素预处理可以显著抑制c-myc原癌基因的表达.结论糖尿病大鼠的心肌肥大与c-myc原癌基因的过多表达有关,胰岛素预处理可抑制c-myc原癌基因的表达.     

DDPH对缺氧内皮细胞条件培养液致肺动脉平滑肌细胞PDGF mRNA表达的影响

利用地高辛标记的ｃＤＮＡ探针，原位检测ＤＤＰＨ［１－（２，６－二甲基苯氧基）－２－（３，４－二甲氧基苯乙胺基）丙烷酸盐］对缺氧内皮细胞条件培养液致猪ＰＡＳＭＣＰＤＧＦ基因表达的影响。实验分６组：常氧、低氧无血清培养液组（Ｎ、Ｈ组），常氧、低氧内皮细胞条件培养液组（ＮＥＣＣＭ、ＨＥＣＣＭ组），ＮＥＣＣＭ＋ＤＤＰＨ、ＨＥＣＣＭ＋ＤＤＰＨ组。用自动图像分析仪检测各组细胞ＰＤＧＦ－Ａ和－Ｂ链杂交产物的平均光密度（ＯＤ）值。结果：ＨＥＣＣＭ组ＰＤＧＦ－Ａ和－Ｂ链ｍＲＮＡ表达量分别是ＮＥＣＣＭ组的１．４０、１．４９倍（Ｐ＜０．０１），分别是Ｎ组的１．８倍、１．７倍（Ｐ＜０．０１），ＨＥＣＣＭ＋ＤＤＰＨ组ＰＤＧＦ－Ａ、－Ｂ链ｍＲＮＡ表达量分别为ＨＥＣＣＭ的０．７３倍、０．６５倍（Ｐ＜０．０１），与ＮＥＣＣＭ组相比，均无显著差异。提示ＤＤＰＨ在ＰＤＧＦ基因转录水平抑制ＨＥＣＣＭ诱导的ＰＡＳＭＣ的增殖。     

Role of Na~+/H~+ antiporter in pulmonary artery smooth muscle of hypoxic pulmonary hypertension in the rat

Hypoxicpuirno-naryhypertensionischaracterizedbyelevatedpulmonaryarterypressureandpulmonaryvascularremodeling.Thearchitecturalchangesinthepulmonaryvasculatureincludeextensionofsmoothmuscleintomoredistalvesselswhicharenormallynonmuscularandanincreaseinmuscularityofmusculararteries.Thestimulusforpulmonaryarterysmoothmuscleproliferationisnotfullyunderstood,butitappearstoinvolvereleaseofgrowthfactorsandothervasoactivesubstancesthatareactivatorsofNa+/H+exchange.TheNa+/H+antiporter(NHE)isacellmemb…