Dr. Victor J Thannickal MD
Pulmonologist | Pulmonary Disease
1530 3rd Avenue South FOT 1105 Birmingham AL, 35294About
Dr. Victor Thannickal practices Pulmonology in Birmingham, AL. A pulmonologist is a physician who possesses specialized knowledge and skill in the diagnosis and treatment of pulmonary conditions and diseases. Dr. Thannickal manages patients who need life support and mechanical ventilation, and is specially trained in diseases and conditions of the chest, particularly pneumonia, asthma, tuberculosis, emphysema, and complicated chest infections.
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Oxidative protein cross-linking reactions involving L-tyrosine in transforming growth factor-beta1-stimulated fibroblasts.
- The paradox of reactive oxygen species: injury, signaling, or both?
- Activation of the pro-survival phosphatidylinositol 3-kinase/AKT pathway by transforming growth factor-beta1 in mesenchymal cells is mediated by p38 MAPK-dependent induction of an autocrine growth factor.
- Pathogenetic mechanisms in usual interstitial pneumonia/idiopathic pulmonary fibrosis.
- Mechanisms of pulmonary fibrosis.
- Modulation of prosurvival signaling in fibroblasts by a protein kinase inhibitor protects against fibrotic tissue injury.
- CCR2-mediated recruitment of fibrocytes to the alveolar space after fibrotic injury.
- Hydrogen peroxide is a diffusible paracrine signal for the induction of epithelial cell death by activated myofibroblasts.
- Constitutive activation of prosurvival signaling in alveolar mesenchymal cells isolated from patients with nonresolving acute respiratory distress syndrome.
- Classification of interstitial pneumonias: what do gene expression profiles tell us?
- Idiopathic pulmonary fibrosis : new concepts in pathogenesis and implications for drug therapy.
- Combinatorial activation of FAK and AKT by transforming growth factor-beta1 confers an anoikis-resistant phenotype to myofibroblasts.
- Idiopathic interstitial pneumonia: a clinicopathological perspective.
- Epithelial-mesenchymal interactions in pulmonary fibrosis.
- Effects of the protein kinase inhibitor, imatinib mesylate, on epithelial/mesenchymal phenotypes: implications for treatment of fibrotic diseases.
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