tailieunhanh - Báo cáo y học: "Host predisposition by endogenous Transforming Growth Factor-β1 overexpression promotes pulmonary fibrosis following bleomycin injury"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Host predisposition by endogenous Transforming Growth Factor-β1 overexpression promotes pulmonary fibrosis following bleomycin injury. | Journal of Inflammation BioMed Central Research Open Access Host predisposition by endogenous Transforming Growth Factor-p1 overexpression promotes pulmonary fibrosis following bleomycin injury Yussef Haider1 Andrea P Malizia2 Dominic T Keating2 Mary Birch1 Annette Tomlinson1 Gail Martin1 Mark WJ Ferguson1 Peter P Doran3 and Jim J Egan 2 4 Address 1School of Biological Sciences University of Manchester Manchester UK 2National Heart and Lung Transplant Program Mater Misericordiae University Hospital University College Dublin Dublin 3Genome Resource Unit Dublin Molecular Medicine Centre Mater Misericordiae University Hospital University College Dublin Dublin Ireland and 4Advanced Lung Disease Programme Mater Misericordiae University Hospital University College Dublin 44 Eccles Street Dublin 7 Ireland Email Yussef Haider - yhaider@ Andrea P Malizia - amalizia@ Dominic T Keating - dkeating@ Mary Birch - mbirch@ Annette Tomlinson - atomlinson@ Gail Martin - gmartin@ Mark WJ Ferguson - Peter P Doran - pdoran@ Jim J Egan - jegan@ Corresponding author Published 20 September 2007 Received 22 March 2007 Accepted 20 September 2007 Journal of Inflammation 2007 4 18 doi 1476-9255-4-18 This article is available from http content 4 1 18 2007 Haider et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Idiopathic Pulmonary Fibrosis IPF is a progressive diffuse disease involving the lung parenchyma. Despite recent advances the molecular mechanisms of the initiation and progression of this disease remain elusive. Previous studies have demonstrated TGFP1 as a

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