Dr. Steven B Abramson, MD - Locations

Internal Medicine New York, NY

About Dr. Steven B Abramson MD

Dr. Steven B Abramson, MD is a doctor primarily located in New York, NY, with other offices in New York, NY and New York, NY. They have 45 years of experience. Their specialties include Internal Medicine and Rheumatology.


Dr. Steven B Abramson has 3 locations

Get Directions NYU Infusion Center Rheumatology 333 E 38th St Fl 4 New York, NY 10016
Get Directions Center For Musculoskeletal & Sports Medicine 333 E 38th St Fl 4 New York, NY 10016
Get Directions NYU Center For Musculoskeletal Care 333 E 38th St Fl 4 New York, NY 10016


Dr. Steven B Abramson has the following 2 SPECIALTIES

Internal Medicine
An internist is a physician who focuses on the diagnosis and treatment of conditions that affect the adult population—both acute and chronic.These doctors are often who adults see as their primary physicians because they treat a broad range of illnesses that do not require surgical or specialist interventions. They also work to help a patient maintain optimal health in order to prevent the onset of disease.In addition to treating the common cold and flu, internists also treat chronic diseases like diabetes and heart disease.

Specialty Expertise

Dr. Steven B Abramson has the following 9 expertise

  • Rheumatic Diseases
  • Knee Osteoarthritis
  • Tendinitis
  • Hip Osteoarthritis
  • Gout
  • Osteoarthritis
  • Arthritis
  • Lupus
  • Inflammation


45 Years Experience

Harvard Medical School

Graduated in 1974

Dr. Steven B Abramson Accepts the Following Insurance

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More about Dr. Steven B Abramson

Our lab is interested in the cytokine, growth factors, extracellular matrix proteins and integrins involved in the chondrocyte signaling pathways and molecular mechanisms that regulate the biology of chondrocytes and bone cells. Basic research is also carried out on the cellular and molecular mechanisms underlying chondrocyte differentiation and maturation. Currently we are employing global gene expression technique such as microarray to study changes in gene expression (Figure 3) in osteoarthritis cartilage as compared to non-arthritic cartilage (Figure 2). We are also currently involved in characterizing the promoters of dysregulated genes in OA with promoter analyses software to characterize and study the influence of transcription factors on these genes. Furthermore, recent evidence suggests that during OA chondrocytes undergo a phenotypic modulation to hypertrophic state which are considered as a??degradativea?? chondrocytes. Hypertrophic chondrocytes synthesize cartilage-degrading proteases and thus probably play a critical role in the progression of the disease. The phenotype of normal chondrocytes is stabilized by the epigenetic status of the cell such as hyper or hypo methylation of target gene promoters. This raises the question as to whether the destabilization of the chondrocytic phenotype in OA is at least, in part, the result of changes in this epigenetic status. Recently, we have undertaken to study epigenetic changes including micro RNA expression, which allows us to study the transcriptional and translational regulation of genes. Furthermore, our laboratory has long standing interest in the functions for nitric oxide (NO) and prostaglandin E2 in the activation of MAP kinase signaling, protease synthesis and cellular death in chondrocyte and synovial fibroblast. Recently, we identified a novel latent tumor growth factor-i??1 (TGF-beta1) activating an extracellular matrix protein F-spondin. F-spondin has not been studied in differentiation of chondrocyte, endochondral ossification, cartilage matrix metabolism and pathological mineralization process. We are planning to develop an F-spondin knock out mouse to explore the functions of F-spondin and TGFb-1 in the development of OA. The fundamental knowledge obtained from these studies is crucial for understanding the pathogenesis and treatment of diseases such as osteoarthritis and rheumatoid arthritis.

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