University Texas Health Scien Center 11937 Us Highway 271, Tyler, TX 75708 (903)8773451 (Phone)
Certifications:
Critical Care Medicine, 1987 Internal Medicine, 1980 Pulmonary Disease, 1982
Awards:
Healthgrades Honor Roll
Languages:
English
Hospitals:
University Texas Health Scien Center 11937 Us Highway 271, Tyler, TX 75708
University of Texas Health Center at Tyler 11937 Us Highway 271, Tyler, TX 75708
Education:
Medical School Temple University School Of Medicine Graduated: 1977 Medical School Temple Hospital Graduated: 1978 Medical School Temple Hospital Graduated: 1980 Medical School Temple Hospital Graduated: 1983
Dr. Idell graduated from the Temple University School of Medicine in 1977. He works in Tyler, TX and specializes in Pulmonary Disease. Dr. Idell is affiliated with UT Health Northeast.
Temple University - Doctor of Philosophy Temple University, School of Medicine - Doctor of Medicine Temple University Hospital - Fellowship - Pulmonary Disease (Internal Medicine) Temple University Hospital - Residency - Internal Medicine
Board certifications:
American Board of Internal Medicine Certification in Internal Medicine American Board of Internal Medicine Sub-certificate in Pulmonary Disease (Internal Medicine)
License Records
Steven Idell
Address:
Tyler, TX 75703
License #:
MD021887E - Expired
Category:
Medicine
Type:
Medical Physician and Surgeon
Steven Idell
License #:
MT003274T - Expired
Category:
Medicine
Type:
Graduate Medical Trainee
Us Patents
Intrapleural Single-Chain Urokinase Alone Or Complexed To Its Soluble Receptor Protects Against Pleural Adhesions
The present invention relates to methods of preventing or decreasing the severity of scarring in a subject comprising: obtaining a pharmaceutical composition comprising a single chain urokinase plasminogen activator molecule (scuPA) or a scuPA mimetic; and administering the pharmaceutical composition to a subject; wherein scarring in the subject is either prevented or decreased relative to an amount of scarring that would be expected if the pharmaceutical composition were not administered to the subject. The invention also relates to methods of screening for compounds that prevent or decrease the severity of scarring in a subject.
Mirella Ezban - Kobenhavn K, DK Claude Piantadosi - Durham NC, US Steven Idell - Tyler TX, US
International Classification:
A61K038/39 A61L009/04
US Classification:
424/045000, 514/012000
Abstract:
The present invention relates to the use of modified factor VI[ for manufacture of medicaments for treatment of Acute Lung Injury (ALI) or Acute Respiratory Distress Syndrome (ARDS) in humans.
Regulation Of Urokinase Receptor Expression By Phosphoglycerate Kinase
Sreerama Shetty - Tyler TX, US Steven Idell - Tyler TX, US
International Classification:
A61K038/48
US Classification:
424094500
Abstract:
The present invention provides methods for treating inflammatory diseases, neoplastic diseases, wound healing and preventing scarring by administering a therapeutically effective amount of phosphoglycerate phosphokinase (PGK) peptide, polypeptide, protein, mutant or mimetic to a subject. The invention also relates to methods of screening for compounds for modulation of uPAR expression or activity. The present invention further provides coding sequences of phosphoglycerate kinase peptides, polypeptides, or proteins, or mutants, or mimetics thereof as a gene therapy for inflammatory diseases, cancer, wound healing, or tissue scarring.
Peptide Inhibition Of Lung Epithelial Apoptosis And Pulmonary Fibrosis
Sreerama Shetty - Tyler TX, US Steven Idell - Tyler TX, US
Assignee:
Board of Regents, The University of Texas System - Austin TX
International Classification:
A61K 38/00 C07K 7/00 A61K 38/10
US Classification:
514 13, 530326, 530300, 514 2
Abstract:
During lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). In the bleomycin lung injury model, p53 and PAI-1 are induced while uPA and uPAR are inhibited. A 20 residue peptide DGIWKASFTTFTVTKYWFYR termed PP-1 (the Cav-1 scaffolding domain) or peptide NYHYLESSMTALYTLGH, termed PP-2, protected LECs from bleomycin-induced apoptosis in vitro and in vivo and prevented subsequent pulmonary fibrosis by attenuating lung epitheilial damage. Pharmaceutical compositions, peptide multimers and deliverable polypeptides comprising the above peptides are dislcosed. The peptides and functional variants, peptide multimers, cell-targeted polyepeptides and pharmaceutical compositions are used in methods for inhibiting apoptosis of injured or damaged lung epithelial cells and for treating acute lung injury and consequent pulmonary fibrosis.
Inhibition Of Pulmonary Fibrosis With Nutlin-3A And Peptides
In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, as they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.
Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).
Treatment Of Idiopathic Pulmonary Fibrosis With Glycogen Synthase Kinase 3 Form Beta Inhibitors
Pharmaceutical compositions and methods are described which rely upon glycogen synthase kinase 3 (form β; GSK 3β) inhibitors, most preferably 9-ING-41, to inhibit fibrotic pulmonary remodeling in vivo including proliferation and differentiation of myofibroblasts to fibrotic fibroblasts in several mouse models. Therapeutic targeting of GSK-3β with the clinically useful specific inhibitor, 9-ING-41, mitigates fibrotic pulmonary remodeling in vivo and provides a mode of therapy of human IPF by specific GSK-3β inhibition with 9-ING-41.
Methods and composition for delivery of enzymes to a subject's airway. In some aspects, nebulized composition of enzymes, such as plasminogen activators are provided. In further aspects perfluorocarbon compositions comprising enzymes, such as plasminogen activators are provided. Compositions may, in some aspects, be used for the treatment of lung infections or acute lung injury, such as inhalational smoke induced acute lung injury (ISALI).