Jewish Hospital

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.

Influence of cerebral hemodynamics on stroke risk: One‐year follow‐up of 30 medically treated patients

Abstract: The importance of hemodynamic factors in the pathogenesis and treatment of ischemic cerebrovascular disease is not clear. We have investigated the relationship between cerebral hemodynamics and the subsequent risk of stroke in 30 medically treated patients with symptomatic occlusion or greater than 75% intracranial stenosis of the carotid arterial system. Positron emission tomography (PET) was used to evaluate the regional hemodynamic status of the cerebral circulation. Clinical follow-up to 1 year post-PET was available for all patients. The incidence at 1 year of all strokes was 1/9 for patients with normal hemodynamics and 1/21 for patients with abnormal hemodynamics. The 1-year incidence of ipsilateral ischemic stroke was 1/9 for hemodynamically normal patients and 0/21 in the abnormal group. The 21 patients in the abnormal group fulfilled entry criteria for the Extracranial-Intracranial Bypass Trial. The 0/21 incidence of ipsilateral ischemic stroke at 1 year was compared with the 1-year rate of 0.109 for the 714 medically treated patients from the Bypass Trial. We were able to reject with better than 90% certainty (p = 0.089) the hypothesis that our sample of patients came from a population with an ipsilateral ischemic stroke rate of 0.109 or greater. Thus, in this small sample, we found no evidence that PET evidence of abnormal cerebral hemodynamics identifies a subgroup of patients at higher risk for early stroke if treated medically with antithrombotic drugs.

The plasminogen activator inhibitor-1 gene, hypofibrinolysis, and osteonecrosis.

Abstract: In 59 patients with osteonecrosis of the hip, four genes associated with thrombophilia or hypofibrinolysis along with coagulation tests were studied to determine the pathoetiologic associations of heritable coagulation disorders with osteonecrosis. Patients did not differ from healthy control subjects for the thrombophilic Factor V Leiden, prothrombin, or methylenetetrahydrofolate reductase mutations. The plasminogen activator inhibitor-1 gene was shifted toward homozygosity for the 4G polymorphism; 41% of patients with osteonecrosis were homozygous for the 4G/4G polymorphism versus 20% of 40 healthy control subjects. The gene product of the 4G polymorphism, hypofibrinolytic plasminogen activator inhibitor activity, was higher in patients than in control subjects (median 19.2 versus 6.3 U/mL); 61% of patients had high plasminogen activator inhibitor activity (> or = 16.4 U/mL) versus 5% of control subjects. Stimulated tissue plasminogen activator activity (inhibited by plasminogen activator inhibitor activity) was lower in patients than in control subjects (3.10 versus 5.98 IU/mL); 31% of patients had low stimulated tissue plasminogen activator activity (< 2.28 IU/mL) versus 3% of control subjects. Heritable hypofibrinolysis conferred by the 4G/4G mutation of the plasminogen activator inhibitor-1 gene seems to be a major pathoetiology of primary osteonecrosis.

Effects of prednisone and deflazacort on mineral metabolism and parathyroid hormone activity in humans

Abstract: The effects of two different glucocorticoids, prednisone and deflazacort, (an oxazoline derivative of prednisolone) on bone metabolism were analyzed in 10 patients with disorders that required glucocorticoid therapy. Significant elevations in blood immunoreactive parathyroid hormone, alkaline phosphatase and urinary calcium, phosphate, hydroxyproline and nephrogenous cyclic AMP were observed during prednisone therapy in addition to an increase in the exchangeable calcium pool as estimated by 47Ca-kinetic analyses. In contrast to these changes, deflazacort therapy induced minimal, and in some instances, no changes in these indices. In fact, in studies wherein prednisone therapy was followed by deflazacort alterations in bone metabolism, iPTH, and nephrogenous cAMP observed during prednisone were reversed. The data are consistent with the fact that the skeletal effects of prednisone therapy are mediated, at least in part, by increased parathyroid hormone activity, and that deflazacort is less potent in this regard.