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Journal of Cardiothoracic-Renal Research最新文献

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Breaking the barrier of chronic allograft nephropathy (CAN)—Transplant's next major challenge 打破慢性移植物肾病(CAN)的屏障——移植的下一个主要挑战
Pub Date : 2006-03-01 DOI: 10.1016/j.jccr.2005.12.007
Edward S. Kraus
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引用次数: 0
Constructing gene expression-based diagnostic rules for understanding individualized etiology of heart failure 构建基于基因表达的心衰个体化病因诊断规则
Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.002
Zhong Gao, G. Tomaselli, Chiming Wei, R. Winslow
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引用次数: 2
Cyclosporine reduction causes decreasing of angiotensin II and transforming growth factor-beta expression in chronic allograft nephropathy 环孢菌素减少导致慢性移植物肾病血管紧张素II和转化生长因子β表达降低
Pub Date : 2006-03-01 DOI: 10.1016/j.jccr.2005.11.005
Matthew R. Weir , John C. Papadimitriou , Cinthia I. Drachenberg , Hong Song , Stephen T. Bartlett , Chiming Wei

Background

High cyclosporine (CsA) levels might lead to nephrotoxicity due to increasing angiotensin II (AII) and transforming growth factor-beta (TGF-β) production. We hypothesized that a chronic reduction in CsA levels would decrease local renal AII and TGF-β expression and result in improvement of renal function and renal pathological changes in renal transplant recipients.

Methods

We determined the AII and TGF-β expression by immunohistochemical staining (IHCS) in sequential human renal biopsy specimens in patients with chronic allograft nephropathies (time between biopsies: 15.9 ± 0.8 months) after they had their CsA levels reduced by 50%. Pathological evaluation included percentage expression (%) of interstitial fibrosis and tubular atrophy (FIB), vascular sclerosis (VS), transplant glomerulopathy (TG), and vascular hyalinosis (VH). Serum creatinine (CR, mg/dl) and BUN (mg/dl) levels were also investigated.

Results

Renal pathological score significantly improved with chronic reduction in CsA blood levels (FIB: from 52 to 26%, p < 0.05; VS: from 22 to 5%, p < 0.05; TG: from 40 to 13%, p < 0.05; VH: from 17 to 1.8%, p < 0.05, respectively). Renal function also significantly improved with chronic reduction of CsA blood level (BUN: from 84 ± 14 to 40 ± 3 mg/dl, p < 0.05; CR: from 3.4 ± 0.4 to 2.2 ± 0.1 mg/dl, p < 0.05, respectively). AII and TGF-β IHCS score (0–4) and positive staining area (%) were significantly decreased in patients with chronic reduction in CsA levels.

Conclusion

These data indicate that chronic reduction in CsA diminishes production of renal tissue AII and AT1 receptor expression, and results in decreased fibrosis and improvement of renal function in patients with chronic allograft nephropathy.

背景环孢菌素(CsA)水平升高可能导致血管紧张素II(AII)和转化生长因子β(TGF-β)产生增加,从而导致肾毒性。我们假设CsA水平的慢性降低会降低肾移植受者的局部肾AII和TGF-β表达,并导致肾功能和肾脏病理变化的改善。方法采用免疫组化染色法(IHCS)测定慢性移植物肾病患者CsA水平降低50%后(两次活检时间15.9±0.8个月)连续人肾活检标本中AII和TGF-β的表达。病理评估包括间质纤维化和肾小管萎缩(FIB)、血管硬化(VS)、移植性肾小球病变(TG)和血管透明质病(VH)的表达百分比(%)。还调查了血清肌酐(CR,mg/dl)和BUN(mg/dl)水平。结果慢性降低CsA血药浓度可显著改善肾脏病理学评分(FIB:从52%降至26%,p<;0.05;VS:从22%降至5%,p>;0.05;TG:从40%降至13%,p<!0.05;VH:从17%降至1.8%,p<,0.05)。肾功能也随着CsA血液水平的慢性降低而显著改善(BUN:分别从84±14到40±3 mg/dl,p<0.05;CR:从3.4±0.4到2.2±0.1 mg/dl,p<0.05)。CsA水平慢性降低的患者的AII和TGF-βIHCS评分(0-4)以及阳性染色面积(%)显著降低。结论慢性移植物肾病患者CsA的慢性减少减少了肾组织AII和AT1受体的表达,并导致纤维化减少和肾功能改善。
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引用次数: 1
Angiotensin II stimulates a novel angiotensin II type 1 receptor-associated protein, GLP gene expression in rat kidney proximal tubular cells 血管紧张素II刺激大鼠肾近端小管细胞中一种新的血管紧张素II型1受体相关蛋白GLP基因的表达
Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.005
D. Guo, Valérie Tardif, I. Chénier, J. Chan, J. Ingelfinger, X. Chen, T. Inagami
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引用次数: 0
DMNQ S-53 induces apoptosis and inhibits the growth of Lewis lung carcinoma cells in vitro and in vivo DMNQ S-53在体外和体内诱导Lewis肺癌细胞凋亡并抑制其生长
Pub Date : 2006-03-01 DOI: 10.1016/j.jccr.2005.12.004
Jae-Ho Lee , Eun-Ok Lee , Hyo-Jung Lee , Kwan-Hyun Kim , Kyoo-Seok Ahn , Sung-Joon Lee , Ji-Young Kim , Sung-Hoon Kim

Background: 6-(1-Proproxyiminomethyl)-5,8-dimethoxy-1,4-naphthoquinone S-53 (DMNQ S-53) was synthesized to develop a novel anti-tumor agent against lung cancer. Methods: Cytotoxicity assay, DNA fragmentation assay, cell cycle analysis, mitochondrial potential measurement and Western blotting were employed in vitro and also Lewis lung carcinoma (LLC) animal model was used for evaluating the anti-tumor of DMNQ S53 in vivo. Results and conclusions: DMNQ S-53 exerted cytotoxicity against LLC cells with IC50 of ∼5 μM. DMNQ S-53 also increased the sub G1 cell population stained by propidium iodide (PI) as well as ladder-like DNA fragmentation in a concentration dependent manner. Western blot analysis revealed that DMNQ S-53 induced apoptosis was associated with the activation of caspase-9 and -3, cleavage of poly (ADP-ribose) polymerase (PARP) and the increased ratio of Bax to Bcl-2 expression in LLC cells in a concentration dependent manner. In addition, DMNQ S-53 reduced mitochondrial potential suggesting the involvement of the mitochondrial intrinsic pathway. Furthermore, intraperitoneally injection of DMNQ S-53 resulted in the inhibition of the tumor volume/weight of LLC cells inoculated on the flank of C57BL6 mice up to ∼50%. Taken together, these results strongly indicate that DMNQ S-53 may inhibit LLC tumor growth in vitro and in vivo via apoptosis induction through the mitochondria-mediated caspase activation pathway.

背景:合成了6-(1-丙氧基氨基甲基)-5,8-二甲氧基-1,4-萘醌S-53(DMNQ S-53),开发了一种新型的抗癌症抗肿瘤药物。方法:采用细胞毒性试验、DNA片段分析、细胞周期分析、线粒体电位测定和蛋白质印迹法,建立Lewis肺癌(LLC)动物模型,评价DMNQ S53的体内抗肿瘤作用。结果和结论:DMNQ S-53对LLC细胞具有细胞毒性,IC50为~5μM。DMNQ S-53还以浓度依赖的方式增加了由碘化丙啶(PI)染色的亚G1细胞群以及梯状DNA片段。Western印迹分析显示,DMNQ S-53诱导的LLC细胞凋亡与胱天蛋白酶-9和-3的激活、聚ADP核糖聚合酶(PARP)的切割以及Bax与Bcl-2表达比例的增加有关,且呈浓度依赖性。此外,DMNQ S-53降低了线粒体电位,表明参与了线粒体内在途径。此外,腹膜内注射DMNQ S-53导致接种在C57BL6小鼠侧翼的LLC细胞的肿瘤体积/重量抑制高达~50%。总之,这些结果有力地表明,DMNQ S-53可以通过线粒体介导的胱天蛋白酶激活途径诱导细胞凋亡,在体外和体内抑制LLC肿瘤生长。
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引用次数: 1
New sniper assignment for a celebrity—role of endothelin-1 in diabetic cardiomyopathy 内皮素-1在糖尿病性心肌病中的作用
Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.11.006
Jun Ren, Chiming Wei
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引用次数: 2
Outcomes of surgical ventricular restoration following recent myocardial infarction 近期心肌梗死后手术心室修复的结果
Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.001
J. Williams, N. Patel, Lois U. Nwakanma, J. Conte
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引用次数: 2
Outcomes of surgical ventricular restoration following recent myocardial infarction 近期心肌梗死后手术心室修复的结果
Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.12.006
I. Kron
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引用次数: 0
Oxidative DNA damage and DNA mismatch repair pathway play an important role in failing human myocardium DNA氧化损伤和DNA错配修复途径在心肌衰竭中起重要作用
Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.11.004
R. Lin, Daqing Gao, Yesong Gu, P. Bonde, Torin P. Fitton, J. Hare, J. Conte, G. Williams, Chiming Wei
{"title":"Oxidative DNA damage and DNA mismatch repair pathway play an important role in failing human myocardium","authors":"R. Lin, Daqing Gao, Yesong Gu, P. Bonde, Torin P. Fitton, J. Hare, J. Conte, G. Williams, Chiming Wei","doi":"10.1016/J.JCCR.2005.11.004","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.11.004","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"61 2 1","pages":"41-49"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78078184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Hope or hype: The obsession for tetrahydrobiopterin and GTP cyclohydrolase I (GTPCH I) in cardiovascular medicine 希望还是炒作:心血管医学对四氢生物蝶呤和GTP环水解酶I (GTPCH I)的痴迷
Pub Date : 2006-03-01 DOI: 10.1016/J.JCCR.2005.11.002
Jun Ren
{"title":"Hope or hype: The obsession for tetrahydrobiopterin and GTP cyclohydrolase I (GTPCH I) in cardiovascular medicine","authors":"Jun Ren","doi":"10.1016/J.JCCR.2005.11.002","DOIUrl":"https://doi.org/10.1016/J.JCCR.2005.11.002","url":null,"abstract":"","PeriodicalId":100759,"journal":{"name":"Journal of Cardiothoracic-Renal Research","volume":"102 1","pages":"15-21"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80527272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
期刊
Journal of Cardiothoracic-Renal Research
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