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本文引用的文献

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Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT).肺动脉高压诊断和治疗指南:欧洲心脏病学会(ESC)和欧洲呼吸学会(ERS)肺动脉高压诊断和治疗工作组,得到国际心肺移植学会(ISHLT)认可。
Eur Heart J. 2009 Oct;30(20):2493-537. doi: 10.1093/eurheartj/ehp297. Epub 2009 Aug 27.
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Updated clinical classification of pulmonary hypertension.肺动脉高压的更新临床分类。
J Am Coll Cardiol. 2009 Jun 30;54(1 Suppl):S43-S54. doi: 10.1016/j.jacc.2009.04.012.
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Biomarkers in pulmonary hypertension.肺动脉高压中的生物标志物
Eur Respir J. 2008 Aug;32(2):503-12. doi: 10.1183/09031936.00160307.
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The cancer paradigm of severe pulmonary arterial hypertension.重度肺动脉高压的癌症模式
Am J Respir Crit Care Med. 2008 Sep 15;178(6):558-64. doi: 10.1164/rccm.200709-1369PP. Epub 2008 Jun 12.
5
4,5-Dihydro-1H-imidazol-2-yl)-[4-(4-isopropoxy-benzyl)-phenyl]-amine (RO1138452) is a selective, pseudo-irreversible orthosteric antagonist at the prostacyclin (IP)-receptor expressed by human airway epithelial cells: IP-receptor-mediated inhibition of CXCL9 and CXCL10 release.4,5-二氢-1H-咪唑-2-基)-[4-(4-异丙氧基苄基)-苯基]-胺(RO1138452)是一种对人呼吸道上皮细胞表达的前列环素(IP)受体具有选择性、拟不可逆性的正构拮抗剂:IP受体介导对CXCL9和CXCL10释放的抑制作用。
J Pharmacol Exp Ther. 2008 Feb;324(2):815-26. doi: 10.1124/jpet.107.129312. Epub 2007 Oct 25.
6
Role of endothelium-derived CC chemokine ligand 2 in idiopathic pulmonary arterial hypertension.内皮细胞源性CC趋化因子配体2在特发性肺动脉高压中的作用
Am J Respir Crit Care Med. 2007 Nov 15;176(10):1041-7. doi: 10.1164/rccm.200610-1559OC. Epub 2007 Sep 6.
7
Absence of T cells confers increased pulmonary arterial hypertension and vascular remodeling.T细胞缺失会导致肺动脉高压加重和血管重塑。
Am J Respir Crit Care Med. 2007 Jun 15;175(12):1280-9. doi: 10.1164/rccm.200608-1189OC. Epub 2007 Apr 5.
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Angiogenesis in chronic lung disease.慢性肺病中的血管生成
Chest. 2007 Mar;131(3):874-879. doi: 10.1378/chest.06-2453.
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Chemokine: receptor structure, interactions, and antagonism.趋化因子:受体结构、相互作用及拮抗作用
Annu Rev Immunol. 2007;25:787-820. doi: 10.1146/annurev.immunol.24.021605.090529.
10
Chemokine CXCL10 promotes atherogenesis by modulating the local balance of effector and regulatory T cells.趋化因子CXCL10通过调节效应T细胞和调节性T细胞的局部平衡促进动脉粥样硬化的发生。
Circulation. 2006 May 16;113(19):2301-12. doi: 10.1161/CIRCULATIONAHA.105.605121. Epub 2006 May 8.

CXC-趋化因子配体 10 在特发性肺动脉高压中的作用:生存改善的标志物。

CXC-chemokine ligand 10 in idiopathic pulmonary arterial hypertension: marker of improved survival.

机构信息

Pulmonary and Critical Care Medicine, Respiratory Institute, Cleveland Clinic, 9500 Euclid Avenue A90, Cleveland, OH 44195, USA.

出版信息

Lung. 2010 Jun;188(3):191-7. doi: 10.1007/s00408-010-9232-9. Epub 2010 Feb 26.

DOI:10.1007/s00408-010-9232-9
PMID:20186422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2886668/
Abstract

CXC-chemokine ligand 10 (CXCL10) inhibits angiogenesis and attracts activated T lymphocytes. Abnormal angiogenesis and lymphocytic infiltration participate in the pathobiology of pulmonary arterial hypertension (PAH). We hypothesized that serum CXCL10 is elevated in idiopathic PAH and that it is associated with clinical outcomes. This was a cohort study that included 40 idiopathic PAH patients (age = 44 +/- 14 years, 37 females) and 22 healthy controls (age = 35 +/- 6 years, 18 females). It took place at the Pulmonary Vascular Program at the Cleveland Clinic. Serum CXCL10 levels were measured by an enzyme-linked immunosorbent assay. A cutoff value of CXCL10 for best distinguishing alive and dead patients was obtained from a receiver operating characteristic curve (ROC). Survival and time to clinical worsening curves according to the appropriate CXCL10 level were derived by the Kaplan-Meier method and compared by means of the log-rank test. The prognostic value of CXCL10 and of other variables of interest was tested by Cox proportional hazards regression analysis. Serum CXCL10 levels were elevated in PAH subjects compared to controls [CXCL10 pg/ml (mean +/- SEM) for PAH: 306 +/- 73, and for controls: 92 +/- 10; p < 0.0001]. CXCL10 levels higher than 111 pg/ml discriminated survivors from nonsurvivors with a sensitivity of 81% and a specificity of 75% (area under the ROC curve = 0.74). After a mean follow-up of 23.5 +/- 13.5 months since the day of venous sampling, higher CXCL10 levels were associated with improved survival (hazard ratio for mortality = 0.10, 95% confidence interval = 0.01-0.97; p = 0.01). Serum CXCL10 is elevated in PAH and this is associated with improved survival.

摘要

CXC-趋化因子配体 10(CXCL10)抑制血管生成并吸引激活的 T 淋巴细胞。异常的血管生成和淋巴细胞浸润参与了肺动脉高压(PAH)的病理生理学过程。我们假设特发性 PAH 患者的血清 CXCL10 升高,并且与临床结果相关。这是一项队列研究,包括 40 名特发性 PAH 患者(年龄=44±14 岁,37 名女性)和 22 名健康对照者(年龄=35±6 岁,18 名女性)。该研究在克利夫兰诊所的肺血管计划中进行。通过酶联免疫吸附试验测量血清 CXCL10 水平。通过接受者操作特征曲线(ROC)获得用于最佳区分存活和死亡患者的 CXCL10 截断值。根据适当的 CXCL10 水平得出生存和临床恶化时间曲线,并通过对数秩检验进行比较。通过 Cox 比例风险回归分析测试 CXCL10 及其他感兴趣变量的预后价值。与对照组相比,PAH 患者的血清 CXCL10 水平升高[PAH:306±73 pg/ml(平均值±SEM),对照组:92±10 pg/ml;p<0.0001]。CXCL10 水平高于 111 pg/ml 可区分存活者和非存活者,其敏感性为 81%,特异性为 75%(ROC 曲线下面积=0.74)。在静脉取样后平均 23.5±13.5 个月的随访期间,较高的 CXCL10 水平与生存率提高相关(死亡率的风险比=0.10,95%置信区间=0.01-0.97;p=0.01)。PAH 患者的血清 CXCL10 升高,并且与生存率提高相关。