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环境病理学,毒理学和肿瘤学期刊

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ISSN 打印: 0731-8898

ISSN 在线: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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Increased TGF-b1* in the Lungs of Asbestos-Exposed Rats and Mice: Reduced Expression in TNF-a Receptor Knockout Mice

卷 20, 册 2, 2001, 12 pages
DOI: 10.1615/JEnvironPatholToxicolOncol.v20.i2.30
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摘要

Inhalation of numerous fibrogenic agents causes interstitial pulmonary fibrosis (IPF) in humans and in a number of animal models. Several of these models provide evidence that certain peptide growth factors (GF) are playing a role in the disease process.Transforming growth factor beta 1 (TGF-b1) is a potent inducer of extracellular matrix production by mesenchymal cells, and we have shown that this peptide is produced in the lung after asbestos exposure. We used in situ hybridization to demonstrate that the mRNA for TGF-b1 is rapidly expressed postexposure at sites of initial asbestos-induced lung injury in both rats and mice. The TGF-b1 is expressed by bronchiolar-alveolar epithelial cells as well as by mesenchymal cells and lung macrophages in exposed animals. Normal rats and mice express little TGF-b1, as we have demonstrated previously for PDGF-A and -B, TGF-a, and TNF-a. TGF-b1 expression is accompanied by collagen and fibronectin production in asbestos-exposed animals. Most interesting, TGF-b1 expression is largely absent in the lungs of TNF-a receptor knockout mice that fail to develop asbestos-induced IPF.We have shown previously that the mRNAs and cognate peptides of PDGF-A and -B and TGF-a, but not TNF-a, are reduced in the fibrosis-resistant knockout mice. In this article, we show that TGF-b1 is included in this group of cytokines, supporting the postulate that TNF-a is necessary for the expression of other, more downstream growth factors, and the consequent development of idiopathic pulmonary fibrosis (IPF).

对本文的引用
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