53 research outputs found
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Fathers of special needs infants and toddlers enrolled in early intervention programs : patterns of involvement.
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Unsuspected vasculitis and intracranial hemorrhage following thrombolysis
Treatment with thrombolytic agents such as streptokinase or tissue plasminogen activator (TPA) is an accepted standard for the treatment of patients with acute myocardial infarction (MI)
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A devastating sequel of thrombolytic therapy may be the development of a hemorrhagic complication, particularly intracranial bleeding, which, although rare, is usually associated with significant neurologic sequelae or death.
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While various risk factors have been correlated with the development of intracranial hemorrhage following thrombolysis, a possible relationship between bleeding and a clinically unsuspected underlying vasculitis has not been previously reported. This report deals with the case of a 49‐year‐old man who died of multiple intracranial hemorrhages after thrombolytic therapy for acute MI and who was found at autopsy to have had polyarteritis nodosa of the coronary arteries and vasculitis of the meningeal vessels
Mitochondrial DNA mutations in oxyphilic and chief cell parathyroid adenomas
Abstract Background The potential pathogenetic significance of mitochondrial DNA (mtDNA) mutations in tumorigenesis is controversial. We hypothesized that benign tumorigenesis of a slowly replicating tissue like the human parathyroid might constitute an especially fertile ground on which a selective advantage conferred by mtDNA mutation could be manifested and might contribute to the oxyphilic phenotype observed in a subset of parathyroid tumors. Methods We sought acquired mitochondrial DNA mutations by sequencing the entire 16.6 kb mitochondrial genome of each of thirty sporadic parathyroid adenomas (18 chief cell and 12 oxyphil cell), eight independent, polyclonal, parathyroid primary chief cell hyperplasias plus corresponding normal control samples, five normal parathyroid glands, and one normal thyroid gland. Results Twenty-seven somatic mutations were identified in 15 of 30 (9 of 12 oxyphil adenomas, 6 of 18 chief cell) parathyroid adenomas studied. No somatic mutations were observed in the hyperplastic parathyroid glands. Conclusion Features of the somatic mutations suggest that they may confer a selective advantage and contribute to the molecular pathogenesis of parathyroid adenomas. Importantly, the statistically significant differences in mutation prevalence in oxyphil vs. chief cell adenomas also suggest that mtDNA mutations may contribute to the oxyphil phenotype.</p
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