Professor, Microbiology and Immunology, Jefferson Medical College-Thos Jefferson Univ
Orthopaedic Surgery
Dr. David J. Abraham, MD
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David Abraham is an expert in the field of Orthopaedic Surgery. He went to Jefferson Medical College. David Abraham is a published physician. He has 57 papers published. The most current publication "Modulation of fibrosis in systemic sclerosis by nitric oxide and antioxidants." He is registered with Medicare.
Publications
- Modulation of fibrosis in systemic sclerosis by nitric oxide and antioxidants.
- Loss of PTEN Expression by Dermal Fibroblasts Causes Skin Fibrosis.
- Development of an in vitro model of myotube ischemia.
- Endothelin-1 stimulates colon cancer adjacent fibroblasts.
- Correction: mPGES-1 null mice are resistant to bleomycin-induced skin fibrosis.
- mPGES-1 null mice are resistant to bleomycin-induced skin fibrosis.
- An essential role for resident fibroblasts in experimental lung fibrosis is defined by lineage-specific deletion of high-affinity type II transforming growth factor &I...
- CCN2 is required for bleomycin-induced skin fibrosis in mice.
- Epithelial cells promote fibroblast activation via IL-1alpha in systemic sclerosis.
- Review of the role of erythropoietin in critical leg ischemia.
- Lymphatic and blood vessels in scleroderma skin, a morphometric analysis.
- Angiogenic effects of stromal cell-derived factor-1 (SDF-1/CXCL12) variants in vitro and the in vivo expressions of CXCL12 variants and CXCR4 in human critical leg isc...
- Loss of peroxisome proliferator-activated receptor gamma in mouse fibroblasts results in increased susceptibility to bleomycin-induced skin fibrosis.
- Loss of beta1 integrin in mouse fibroblasts results in resistance to skin scleroderma in a mouse model.
- Pivotal role of connective tissue growth factor in lung fibrosis: MAPK-dependent transcriptional activation of type I collagen.
- Cross-talk between MCP-3 and TGFbeta promotes fibroblast collagen biosynthesis.
- Rac inhibition reverses the phenotype of fibrotic fibroblasts.
- Requirement of transforming growth factor beta-activated kinase 1 for transforming growth factor beta-induced alpha-smooth muscle actin expression and extracellular ma...
- Inducible lineage-specific deletion of TbetaRII in fibroblasts defines a pivotal regulatory role during adult skin wound healing.
- GSK-3beta in mouse fibroblasts controls wound healing and fibrosis through an endothelin-1-dependent mechanism.
- Role of Rac1 in a bleomycin-induced scleroderma model using fibroblast-specific Rac1-knockout mice.
- Fibroblast-specific perturbation of transforming growth factor beta signaling provides insight into potential pathogenic mechanisms of scleroderma-associated lung fibr...
- Heparan sulfate-dependent ERK activation contributes to the overexpression of fibrotic proteins and enhanced contraction by scleroderma fibroblasts.
- Endothelin is a downstream mediator of profibrotic responses to transforming growth factor beta in human lung fibroblasts.
- Possible implication of the effector CD4+ T-cell subpopulation TH17 in the pathogenesis of systemic scleroderma.
- A polymorphism in the CTGF promoter region associated with systemic sclerosis.
- Effect of nitric oxide and peroxynitrite on type I collagen synthesis in normal and scleroderma dermal fibroblasts.
- FAK is required for TGFbeta-induced JNK phosphorylation in fibroblasts: implications for acquisition of a matrix-remodeling phenotype.
- New developments in fibroblast and myofibroblast biology: implications for fibrosis and scleroderma.
- CCN2 is necessary for the function of mouse embryonic fibroblasts.
- Platelet-derived growth factor-beta receptor activation is essential for fibroblast and pericyte recruitment during cutaneous wound healing.
- Constitutive ALK5-independent c-Jun N-terminal kinase activation contributes to endothelin-1 overexpression in pulmonary fibrosis: evidence of an autocrine endothelin ...
- Hammerhead ribozyme-mediated silencing of the mutant fibrillin-1 of tight skin mouse: insight into the functional role of mutant fibrillin-1.
- CCN2 is necessary for adhesive responses to transforming growth factor-beta1 in embryonic fibroblasts.
- Contribution of activin receptor-like kinase 5 (transforming growth factor beta receptor type I) signaling to the fibrotic phenotype of scleroderma fibroblasts.
- Mechanisms and consequences of fibrosis in systemic sclerosis.
- Signaling pathways regulating intercellular adhesion molecule 1 expression by endothelin 1: comparison with interleukin-1beta in normal and scleroderma dermal fibrobla...
- Increased endogenous angiogenic response and hypoxia-inducible factor-1alpha in human critical limb ischemia.
- Chemokine receptor CCR2 expression by systemic sclerosis fibroblasts: evidence for autocrine regulation of myofibroblast differentiation.
- Matrix contraction by dermal fibroblasts requires transforming growth factor-beta/activin-linked kinase 5, heparan sulfate-containing proteoglycans, and MEK/ERK: insig...
- Activation of key profibrotic mechanisms in transgenic fibroblasts expressing kinase-deficient type II Transforming growth factor-{beta} receptor (T{beta}RII{delta}k).
- CCN2 (connective tissue growth factor) promotes fibroblast adhesion to fibronectin.
- Regulation of collagen type I in vascular smooth muscle cells by competition between Nkx2.5 and deltaEF1/ZEB1.
- Endothelin-1 promotes myofibroblast induction through the ETA receptor via a rac/phosphoinositide 3-kinase/Akt-dependent pathway and is essential for the enhanced cont...
- Endothelin-1 induces expression of matrix-associated genes in lung fibroblasts through MEK/ERK.
- TGF-beta signaling and the fibrotic response.
- Insights into the molecular mechanism of Chronic fibrosis: the role of connective tissue growth factor in scleroderma.
- Constitutive connective tissue growth factor expression in scleroderma fibroblasts is dependent on Sp1.
- Identification of PLOD2 as telopeptide lysyl hydroxylase, an important enzyme in fibrosis.
- Fibroblast-specific expression of a kinase-deficient type II transforming growth factor beta (TGFbeta) receptor leads to paradoxical activation of TGFbeta signaling pa...
- Monocyte chemoattractant protein 3 as a mediator of fibrosis: Overexpression in systemic sclerosis and the type 1 tight-skin mouse.
- Connective tissue growth factor gene regulation. Requirements for its induction by transforming growth factor-beta 2 in fibroblasts.
- Prostacyclin derivatives prevent the fibrotic response to TGF-beta by inhibiting the Ras/MEK/ERK pathway.
- CTGF expression in mesangial cells: involvement of SMADs, MAP kinase, and PKC.
- Myogenic cell proliferation and generation of a reversible tumorigenic phenotype are triggered by preirradiation of the recipient site.
- Connective tissue growth factor: a new and important player in the pathogenesis of fibrosis.
Schools
Jefferson Med CollThos Jefferson Univ
Procedures Preformed
- Disc Replacement
- Dressing and-or Debridement of Wound, Infection, or Burn (incl. Negative Pressure Wound Therapy)
- Dural Repair or Other Spinal Spinal Cord Repair
- Herniated Disc Surgery
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Conditions Treated
- Arm Fracture (incl. Elbow and Shoulder)
- Ataxia
- Back Pain
- Bursitis
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Doctors Specialties
- Orthopedic Surgery
- Orthopaedic Surgery
Accepted Insurances
Education
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William Beaumont Hospital -
Thomas Jefferson University -
Jefferson Medical College
Drug Facts
| NPI NUMBER | 1205897964 | |
| NPPES Provider LastName | ABRAHAM | |
| NPPES Provider FirstName | DAVID | |
| NPPES Provider ZIPCode | 196103203 | |
| NPPES Provider State | PA | |
| Specialty Description | Orthopedic Surgery | |
| Total Claim Count | 295.0 | |
| Distinct Opioid Count | 3.0 | |
| Opioid Claim Count | 156.0 | |
| Percent Opioid Claims | 52.88 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1205897964 |
| Last Name Of The Provider | ABRAHAM |
| First Name Of The Provider | DAVID |
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