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Hall K.C.,The Hospital for Special Surgery | Hall K.C.,Cornell University | Blobel C.P.,The Hospital for Special Surgery | Blobel C.P.,Cornell University
PLoS ONE | Year: 2012

ADAM17 (a disintegrin and metalloproteinase) is a membrane-anchored metalloproteinase that regulates the release of EGFR-ligands, TNFα and other membrane proteins from cells. ADAM17 can be rapidly activated by a variety of signaling pathways, yet little is known about the underlying mechanism. Several studies have demonstrated that the cytoplasmic domain of ADAM17 is not required for its rapid activation by a variety of stimuli, including phorbol esters, tyrosine kinases and some G-protein coupled receptors. However, phosphorylation of cytoplasmic residue T735 was recently reported as a crucial step for activation of ADAM17 by IL-1β and by the p38 MAP-kinase pathway. One possible mechanism to reconcile these results would be that T735 has an inhibitory role and that it must be phosphorylated as a pre-requisite for the activation of ADAM17, which would then proceed via a mechanism that is independent of its cytoplasmic domain. To test this hypothesis, we performed rescue experiments of Adam17-/- cells with wild type and mutant forms of ADAM17. However, these experiments showed that an inactivating mutation (T735A) or an activating mutation (T735D) of cytoplasmic residue T735 or the removal of the cytoplasmic domain of ADAM17 did not significantly affect the stimulation of ADAM17 by IL-1β or by activation of MAP-kinase with anisomycin. Moreover, we found that the MAP-kinase inhibitor SB203580 blocked activation of cytoplasmic tail-deficient ADAM17 and of the T735A mutant by IL-1β or by anisomycin, providing further support for a model in which the activation mechanism of ADAM17 does not rely on its cytoplasmic domain or phosphorylation of T735. © 2012 Hall, Blobel.

The International Association of HealthCare Professionals is pleased to welcome David Lefkowitz, MD, FACC, Cardiologist, to their prestigious organization with his upcoming publication in The Leading Physicians of the World. He is a highly trained and qualified cardiologist with a vast expertise in all facets of his work, especially nuclear cardiology and internal medicine. Dr. Lefkowitz has been in practice for 21 years and is currently serving patients at his own private practice located in New York City, New York. Additionally he is on staff at NewYork-Presbyterian Hospital and The Hospital for Special Surgery, and is a Clinical Assistant Professor at Weill Cornell Medical College. In 1987, Dr. Lefkowitz received his Medical Degree cum laude from SUNY Downstate College of Medicine in New York City, New York. He then went on to complete his residency at Yeshiva University’s Albert Einstein College of Medicine, where he was Chief Resident. Dr. Lefkowitz has earned the coveted title of  Fellow of the American College of Cardiology, and maintains a professional membership with the American Society of Echocardiography, the American Medical Association, and the American Society of Nuclear Cardiology. Dr. Lefkowitz attributes his successful career to his love of medicine; he can’t imagine doing anything else. Learn more about Dr. Lefkowitz by reading his upcoming publication in The Leading Physicians of the World. is a hub for all things medicine, featuring detailed descriptions of medical professionals across all areas of expertise, and information on thousands of healthcare topics.  Each month, millions of patients use FindaTopDoc to find a doctor nearby and instantly book an appointment online or create a review. features each doctor’s full professional biography highlighting their achievements, experience, patient reviews and areas of expertise.  A leading provider of valuable health information that helps empower patient and doctor alike, FindaTopDoc enables readers to live a happier and healthier life.  For more information about FindaTopDoc, visit:

Bedi A.,University of Michigan | Maak T.,The Hospital for Special Surgery | Walsh C.,University of Michigan | Rodeo S.A.,The Hospital for Special Surgery | And 5 more authors.
Journal of Shoulder and Elbow Surgery | Year: 2012

The pathogenesis of rotator cuff degeneration remains poorly defined, and the incidence of degenerative tears is increasing in the aging population. Rates of recurrent tear and incomplete tendon-to-bone healing after repair remain significant for large and massive tears. Previous studies have documented a disorganized, fibrous junction at the tendon-to-bone interface after rotator cuff healing that does not recapitulate the organization of the native enthesis. Many biologic factors have been implicated in coordinating tendon-to-bone healing and maintenance of the enthesis after rotator cuff repair, including the expression and activation of transforming growth factor-β, basic fibroblast growth factor, platelet-derived growth factor-β, matrix metalloproteinases, and tissue inhibitors of metalloproteinases. Future techniques to treat tendinopathy and enhance tendon-to-bone healing will be driven by our understanding of the biology of this healing process after rotator cuff repair surgery. The use of cytokines to provide important signals for tissue formation and differentiation, the use of gene therapy techniques to provide sustained cytokine delivery, the use of stem cells, and the use of transcription factors to modulate endogenous gene expression represent some of these possibilities. © 2012 Journal of Shoulder and Elbow Surgery Board of Trustees.

Grenier S.,The Hospital for Special Surgery | Donnelly P.E.,The Hospital for Special Surgery | Gittens J.,The Hospital for Special Surgery | Torzilli P.A.,The Hospital for Special Surgery
Journal of Biomechanics | Year: 2015

Surface damage to articular cartilage is recognized as the initial underlying process causing the loss of mechanical function in early-stage osteoarthritis. In this study, we developed structure-modifying treatments to potentially prevent, stabilize or reverse the loss in mechanical function. Various polymers (chondroitin sulfate, carboxymethylcellulose, sodium hyaluronate) and photoinitiators (riboflavin, irgacure 2959) were applied to the surface of collagenase-degraded cartilage and crosslinked in situ using UV light irradiation. While matrix permeability and deformation significantly increased following collagenase-induced degradation of the superficial zone, resurfacing using tyramine-substituted sodium hyaluronate and riboflavin decreased both values to a level comparable to that of intact cartilage. Repetitive loading of resurfaced cartilage showed minimal variation in the mechanical response over a 7 day period. Cartilage resurfaced using a low concentration of riboflavin had viable cells in all zones while a higher concentration resulted in a thin layer of cell death in the uppermost superficial zone. Our approach to repair surface damage initiates a new therapeutic advance in the treatment of injured articular cartilage with potential benefits that include enhanced mechanical properties, reduced susceptibility to enzymatic degradation and reduced adhesion of macrophages. © 2014 Elsevier Ltd.

Voos J.E.,The Hospital for Special Surgery | Mauro C.S.,The Hospital for Special Surgery | Kelly B.T.,The Hospital for Special Surgery
Operative Techniques in Orthopaedics | Year: 2010

Femoroacetabular impingement is an increasingly recognized cause of hip and groin pain in the athlete. Loss of hip motion from femoroacetabular impingement may result in compensatory injury patterns involving the hemipelvis, including osteitis pubis, sports hernia, sacroiliac joint pain, muscle strains, low back pain, and posterior hip subluxations. Failure to recognize and address intra-articular hip pathology, in addition to treating compensatory injury patterns, can result in continued disability in a subset of athletes. © 2010 Elsevier Inc.

Goldring S.R.,The Hospital for Special Surgery
Therapeutic Advances in Musculoskeletal Disease | Year: 2012

The articular cartilage and the subchondral bone form a biocomposite that is uniquely adapted to the transfer of loads across the diarthrodial joint. During the evolution of the osteoarthritic process biomechanical and biological processes result in alterations in the composition, structure and functional properties of these tissues. Given the intimate contact between the cartilage and bone, alterations of either tissue will modulate the properties and function of the other joint component. The changes in periarticular bone tend to occur very early in the development of OA. Although chondrocytes also have the capacity to modulate their functional state in response to loading, the capacity of these cells to repair and modify their surrounding extracellular matrix is relatively limited in comparison to the adjacent subchondral bone. This differential adaptive capacity likely underlies the more rapid appearance of detectable skeletal changes in OA in comparison to the articular cartilage. The OA changes in periarticular bone include increases in subchondral cortical bone thickness, gradual decreases in subchondral trabeular bone mass, formation of marginal joint osteophytes, development of bone cysts and advancement of the zone of calcified cartilage between the articular cartilage and subchondral bone. The expansion of the zone of calcified cartilage contributes to overall thinning of the articular cartilage. The mechanisms involved in this process include the release of soluble mediators from chondrocytes in the deep zones of the articular cartilage and/or the influences of microcracks that have initiated focal remodeling in the calcified cartilage and subchondral bone in an attempt to repair the microdamage. There is the need for further studies to define the pathophysiological mechanisms involved in the interaction between subchondral bone and articular cartilage and for applying this information to the development of therapeutic interventions to improve the outcomes in patients with OA. © The Author(s), 2012.

Grenier S.,The Hospital for Special Surgery | Bhargava M.M.,The Hospital for Special Surgery | Torzilli P.A.,The Hospital for Special Surgery
Journal of Biomechanics | Year: 2014

The objective of this study was to develop an in vitro cartilage degradation model that emulates the damage seen in early-stage osteoarthritis. To this end, cartilage explants were collagenase-treated to induce enzymatic degradation of collagen fibers and proteoglycans at the articular surface. To assess changes in mechanical properties, intact and degraded cartilage explants were subjected to a series of confined compression creep tests. Changes in extracellular matrix structure and composition were determined using biochemical and histological approaches. Our results show that collagenase-induced degradation increased the amount of deformation experienced by the cartilage explants under compression. An increase in apparent permeability as well as a decrease in instantaneous and aggregate moduli was measured following collagenase treatment. Histological analysis of degraded explants revealed the presence of surface fibrillation, proteoglycan depletion in the superficial and intermediate zones and loss of the lamina splendens. Collagen cleavage was confirmed by the Col II-3/4Cshort antibody. Degraded specimens experienced a significant decrease in proteoglycan content but maintained total collagen content. Repetitive testing of degraded samples resulted in the gradual collapse of the articular surface and the compaction of the superficial zone. Taken together, our data demonstrates that enzymatic degradation with collagenase can be used to emulate changes seen in early-stage osteoarthritis. Further, our in vitro model provides information on cartilage mechanics and insights on how matrix changes can affect cartilage's functional properties. More importantly, our model can be applied to develop and test treatment options for tissue repair. © 2013 Elsevier Ltd.

Ellis S.,The Hospital for Special Surgery | DeOrio J.K.,Duke University
Operative Techniques in Orthopaedics | Year: 2010

Total ankle replacement represents an alternative to arthrodesis in the setting of advanced ankle arthrosis. The INBONE total ankle system is a Food and Drug Administration-approved, nonmobile-bearing implant with intramedullary modular stems that afford additional fixation in both the tibia and talus. Although approved for use only with cement, it is used universally without cement. A sophisticated leg assembly and intramedullary guidance system greatly increase the accuracy of implant position. Increased polyethylene thickness with a saddle geometry spreads out stresses across the ankle joint while maintaining stability. Although formal clinical data have not been published, the implant shows promise and may be well suited not only for standard primary total ankle replacement, but also in the setting of instability, moderate deformity, or failure of previous arthroplasty. As always, patients should be alerted to the potential complications with total ankle replacement. The purpose of this article is to describe the surgical technique for implanting the INBONE total ankle. © 2010 Elsevier Inc.

The Hospital For Special Surgery | Date: 2010-02-24

Expanding cannula and retractor devices and methods of use are provided. An expanding cannula and retractor device includes a first tube, a second tube positioned within the first tube, and an expandable continuous membrane connecting distal portions of the first and second tubes. The membrane can expand into an annulus based on the movement of the second tube relative to the first tube in order to contact tissue and maintain the position of the device.

The Hospital For Special Surgery | Date: 2010-02-24

External fixation devices and methods of use are provided. A device for external fixation of a joint includes a first pin block for connection to a first skeletal element and a second pin block for connection to a second skeletal element. The device includes a connection assembly that is releasably attached to at least one of the pin blocks. The device is locked in an original position when the connection assembly is attached to both of the pin blocks, and is unlocked when the connection assembly is detached from at least one of the pin blocks.

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