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Institution

Jewish Hospital

HealthcareCincinnati, Ohio, United States
About: Jewish Hospital is a healthcare organization based out in Cincinnati, Ohio, United States. It is known for research contribution in the topics: Antigen & Population. The organization has 3881 authors who have published 3414 publications receiving 123044 citations.


Papers
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Journal ArticleDOI
TL;DR: It is speculated that primary, heritable thrombophilia or hypofibrinolysis causesThrombotic venous occlusion in the head of the femur, leading to venous hypertension and hypoxic death of bone (osteonecrosis).
Abstract: In 31 patients with osteonecrosis (primarily of the hip), 74% had 1 or more primary coagulation disorders. In 18 patients, 15 (83%) who had coagulation disorders, the osteonecrosis was initially identified as idiopathic and was not associated with known underlying drugs (glucocorticoids) or diseases (alcoholism, sickle cell disease, Gaucher's disease). In 13 patients, 8 (62 %) who had coagulation disorders, the osteonecrosis was initially identified as secondary, and was associated with glucocorticoids in 12 patients, and with alcoholism in 1. The coagulation disorders included thrombhophilia (increased tendency to intravascular thrombosis) and hypofibrinolysis (reduced ability to lyse thrombi). Of the 18 patients initially thought to have idiopathic osteonecrosis, thrombophilia alone was found in 12% (resistance to activated protein C in 6%, low protein C in 6%), hypofibrinolysis alone was found in 50% (high lipoprotein(a) in 44%, low stimulated tissue plasminogen activator activity was found in 6%), and mixed thrombophilia hypofibrinolysis was found in 22%. Resistance to activated protein C was more common in these 18 patients than in healthy controls (11% versus 0%), as was high lipoprotein(a) (67% versus 20%). Of the 13 patients with secondary osteonecrosis, thrombophilia alone was found in 8% (low protein C), hypofibrinolysis alone was found in 30% (high Lp(a) in 15%, low tissue plasminogen activator activity in 15%), and mixed thrombophilia hypofibrinolysis was found in 23%. Low tissue plasminogen activator activity was more common in the 13 patients with secondary osteonecrosis than in controls (27% versus 7%), as was low protein C (23% versus 0%). In aggregate, these findings lead us to the speculation that primary, heritable thrombophilia or hypofibrinolysis causes thrombotic venous occlusion in the head of the femur, leading to venous hypertension and hypoxic death of bone (osteonecrosis).

185 citations

Journal Article
TL;DR: Maximal prednisone doses, changes in body habitus in response to corticosteroid therapy, IgG aCL levels, and clinical evidence of venous thrombosis and vasculitis were associated with osteonecrosis in patients with SLE.
Abstract: Objective. To study clinical and laboratory factors in patients with systemic lupus erythematosus (SLE) to identify subgroups at extraordinary risk for developing osteonecrosis. Methods. 31 of 103 (30%) patients with SLE had developed osteonecrosis. Patients were studied to identify clinical characteristics that differentiated patients with and without osteonecrosis. Subjects were studied to determine whether and to what degree factors leading to thrombophilia (anticardiolipin antibodies, aCL) or hypofibrinolysis [lipoprotein(a)] are associated with osteonecrosis. Results. Clinically, the patients with osteonecrosis had significant increases in Cushingoid body habitus, thrombophlebitis, vasculitis, cigarette smoking, and preeclampsia. Highest prednisone dose was positively associated with osteonecrosis. Although IgG aCL were also found to be associated with osteonecrosis, particularly in the white patients with SLE, lipoprotein(a) levels were not increased in either the white or black patients. Conclusion. Maximal prednisone doses, changes in body habitus in response to corticosteroid therapy, IgG aCL levels, and clinical evidence of venous thrombosis and vasculitis were associated with osteonecrosis in patients with SLE.

185 citations

Journal ArticleDOI
TL;DR: An autoradiographic binding assay employing 125I-labeled heat-aggregated mouse IgG2b myeloma protein was used to demonstrate receptors for IgG on 20–45% of Balb/c thymocytes and on 70–80% of splenocytes, dependent upon aggregate size.
Abstract: An autoradiographic binding assay employing 125I-labeled heat-aggregated mouse IgG2b myeloma protein (MOPC 141) was used to demonstrate receptors for IgG on 20–45% of Balb/c thymocytes and on 70–80% of splenocytes. Binding could also be shown with heat or BDB aggregates of another IgG2b (MOPC 195), with IgG1 and with human γ-globulin, but not with aggregated chicken γ-globulin, IgA, BSA, nor with aggregated Fab fragments of IgG2b. Optimum binding was obtained at 37°C. Detection of binding was dependent upon aggregate size with complexes of more than 100 IgG molecules being optimal, aggregates of 6–25 detecting splenocytes but not thymocytes, and aggregates of less than 6 binding to a negligible extent. Comparison of grain counts on various cell types showed mastocytoma cells (P815) and macrophages averaging 40–50 grains/cell/day, allogeneically activated thymocytes 20–30, splenocytes 2–3, L5178 lymphoma cells 1, and positive thymocytes 0.6 grains/cell/day. Double labeling experiments for surface Ig, θ-antigen, and agg IgG receptor on mouse spleen cells indicated that a relatively high density of receptor was present on about 80% of B cells, 30% of T cells, and 60% of SIg-, θ-, null cells.

184 citations

Journal ArticleDOI
TL;DR: Treatment of a murine model of nonalcoholic fatty liver disease with a dual FXR/TGR5 agonist decreased intrahepatic inflammation and altered the immune phenotype of monocytes and macrophages, indicating potential targeting strategies for treatment of NAFLD.

183 citations

Journal ArticleDOI
TL;DR: It is speculated that symptomatic myalgia in statin-treated patients with concurrent vitamin D deficiency may reflect a reversible interaction betweenitamin D deficiency and statins on skeletal muscle.

182 citations


Authors

Showing all 3894 results

NameH-indexPapersCitations
John C. Morris1831441168413
David L. Kaplan1771944146082
Robert H. Purcell13966670366
Nancy J. Cox135778109195
Jennifer S. Haas12884071315
David A. Cheresh12533762252
John W. Kappler12246457541
Philippa Marrack12041654345
Arthur Weiss11738045703
Thomas J. Kipps11474863240
Michael Pollak11466357793
Peter M. Henson11236954246
Roberto Bolli11152844010
William D. Foulkes10868245013
David A. Lynch10871459678
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20232
202217
202148
202038
201944
201828