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514


Drug survival time on anti-TNF agents: Does prior anti-TNF use influence RA outcomes? [Meeting Abstract]

Kishimoto, M; Greenberg, J; Abramson, SB; Harrington, T; Olenginski, TP; Kafka, SP; Reed, G; Hinkle, K; Kremer, J; Cohen, SB
ISI:000232207801403
ISSN: 0004-3591
CID: 59277

Simvastatin and geranyl-geranyl transferase inhibitor exhibit chondroprotective effects [Meeting Abstract]

Attur, M; Al-Mussawir, H; Abeles, AM; Pillinger, MH; Abramson, SB
ISI:000232207800080
ISSN: 0004-3591
CID: 59270

The inflammatory mediator leukotriene B4 (ltb4) exerts catabolic effects on chondrocyte metabolism [Meeting Abstract]

Attur, M; Gomez, PF; Patel, J; Al-Mussawir, H; Pillinger, MH; Abramson, SB
ISI:000232207800079
ISSN: 0004-3591
CID: 59269

Coxib prescribing by rheumatologists in the immediate post-rofecoxib era [Meeting Abstract]

Greenberg, JD; Abramson, SB; Reed, G; Reddy, SM; Hinkle, K; Kremer, J
ISI:000229909102014
ISSN: 0003-4967
CID: 57656

Coxibs and NSAIDs--clearing the air [Editorial]

Moskowitz, R W; Abramson, S B; Berenbaum, F
PMID: 15979006
ISSN: 1063-4584
CID: 522952

The many facets of osteoarthritis: Pathogenesis and markers [Meeting Abstract]

Abramson, SB
ISI:000229909100097
ISSN: 0003-4967
CID: 57652

Comparison of disease activity measures and radiographic features of psoriatic arthritis and a matched rheumatoid arthritis cohort [Meeting Abstract]

Reddy, SM; Greenberg, JD; Abramson, SB; Reed, G; Hinkle, K; Kremer, J
ISI:000229909101455
ISSN: 0003-4967
CID: 57655

The fibroblast-like synovial cell in rheumatoid arthritis: a key player in inflammation and joint destruction

Mor, Adam; Abramson, Steven B; Pillinger, Michael H
Although multiple cell types are present in the rheumatoid joint, the fibroblast-like synovial cell (FLS) is among the most prominent. It is now appreciated that the FLS is not only space-filling, but is directly responsible for cartilage destruction, and also drives both inflammation and autoimmunity. In this article, we consider the normal role of the FLS in healthy joints, and review evidence that implicates the FLS as a central player in the propagation of rheumatoid arthritis
PMID: 15885632
ISSN: 1521-6616
CID: 55952

Matrix metalloproteinase secretion by gastric epithelial cells is regulated by E prostaglandins and mitogen-activated protein kinases

Pillinger, Michael H; Marjanovic, Nada; Kim, Seok-Yong; Scher, Jose U; Izmirly, Peter; Tolani, Sonia; Dinsell, Victoria; Lee, Yong-Chan; Blaser, Martin J; Abramson, Steven B
Since matrix metalloproteinases (MMP) play roles in inflammatory tissue injury, we asked whether MMP secretion by gastric epithelial cells may contribute to gastric injury in response to signals involved in H. pylori-induced inflammation and/or cyclooxygenase inhibition. TNF-alpha, IL-1beta and epidermal growth factor (EGF) stimulated gastric cell MMP-1 secretion, indicating that MMP-1 secretion occurs in inflammatory as well as non-inflammatory situations. MMP-1 secretion required activation of the mitogen-activated protein kinase (MAPK) Erk, and subsequent protein synthesis, but was downregulated by the alternate MAPK, p38. In contrast, secretion of MMP-13 was stimulated by TNF-alpha/IL-1beta but not EGF, was Erk-independent and mediated by p38. MMP-13 secretion was more rapid (peak 6 h) than MMP-1 (peak = 30 h) and only partly depended on protein synthesis, suggesting initial release of a pre-existing MMP-13 pool. Therefore, MMP-1 and MMP-13 secretion are differentially regulated by MAPKs. MMP-1 secretion was regulated by E prostaglandins (PGEs) in an Erk-dependent manner. PGEs enhanced Erk activation and MMP-1 secretion in response to EGF, but inhibited Erk and MMP-1 when TNF-alpha/IL-1beta were the stimuli, indicating that the effects of PGEs on gastric cell responses are context-dependent. These data show that secretion of MMPs is differentially regulated by MAPKs, and suggest mechanisms through which H pylori infection and/or cyclooxygenase inhibition may induce epithelial cell signaling to contribute to gastric ulcerogenesis
PMID: 15640153
ISSN: 0021-9258
CID: 48227

Effect of cardiovascular comorbidities and concomitant aspirin use on selection of cyclooxygenase inhibitor among rheumatologists

Greenberg, Jeffrey D; Bingham, Clifton O 3rd; Abramson, Steven B; Reed, George; Sebaldt, Rolf J; Kremer, Joel
OBJECTIVE: To evaluate the effects of cardiovascular comorbidities and aspirin coprescription on cyclooxygenase (COX)-2 inhibitor (coxib) prescribing patterns among rheumatologists. METHODS: A prospective cohort study was carried out with rheumatoid arthritis and osteoarthritis patients in the Consortium of Rheumatology Researchers of North America registry. Medication and comorbidity data were obtained prospectively from physician and patient questionnaires between March 2002 and September 2003. Multivariate adjusted associations between coxib use and specific cardiovascular variables, including aspirin use, were examined. RESULTS: A total of 3,522 arthritis patients were included. COX inhibitors, including coxibs, nonselective nonsteroidal antiinflammatory drugs (NSAIDs), and meloxicam, were prescribed to a larger proportion of osteoarthritis patients (68.4%) than rheumatoid arthritis patients (47.1%) in our study (P < 0.001). COX inhibitors were prescribed to the majority of aspirin users (51.5%) and a similar proportion of nonusers (49.8%). In multivariate analyses, independent predictors of coxib use versus nonselective NSAID use included diagnoses of osteoarthritis (odds ratio [OR] 2.52, 95% confidence interval [95% CI] 1.81-3.52) and diabetes (OR 1.63, 95% CI 1.06-2.51). Conversely, aspirin use independently predicted selection of a nonselective NSAID rather than a coxib (OR 0.73, 95% CI 0.55-0.98). Neither a history of myocardial infarction nor stroke predicted utilization of a coxib. Similarly, cardiovascular variables did not predict the use of rofecoxib versus celecoxib. CONCLUSION: Our data indicate that COX inhibitor coprescription among aspirin users is frequent. Despite cardiovascular concerns regarding the coxibs, our data suggest that aspirin use, but not cardiovascular comorbidities, predicted the selection of nonselective NSAIDs over coxibs
PMID: 15696570
ISSN: 0004-3591
CID: 50291