James J Filiano

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The sudden infant death syndrome (SIDS) is the leading cause of postneonatal infant mortality in the United States today, despite a dramatic 38% decrease in incidence due to a national risk reduction campaign advocating the supine sleep position. Our research in SIDS brainstems, beginning in 1985 and involving a single, large dataset, has become(More)
Neuropathologic studies in SIDS victims support the concept that they are not entirely 'normal' prior to death, but rather possess underlying vulnerabilities which put them at risk for sudden death. This concept forms a key link in a triple-risk model for the pathogenesis of SIDS proposed by us. According to this model, sudden death in SIDS results from the(More)
The sudden infant death syndrome (SIDS) is postulated to result from a failure of homeostatic responses to life-threatening challenges (e.g. asphyxia, hypercapnia) during sleep. The ventral medulla participates in sleep-related homeostatic responses, including chemoreception, arousal, airway reflex control, thermoregulation, respiratory drive, and blood(More)
Abnormalities in specific mitochondrial respiratory enzymes and DNA (mtDNA) have been reported in cardiomyopathy. In this study, we report 4 cases of severe hypertrophic cardiomyopathy (HCM) in which specific cardiac mitochondrial enzyme activity defects were found, including complex I (n = 2), complex III (n = 2), complex IV (n = 2) and complex V (n = 1).(More)
Microdeletions of 1q43q44 result in a recognizable clinical disorder characterized by moderate to severe intellectual disability (ID) with limited or no expressive speech, characteristic facial features, hand and foot anomalies, microcephaly (MIC), abnormalities (agenesis/hypogenesis) of the corpus callosum (ACC), and seizures (SZR). Critical regions have(More)
Abnormalities in central respiratory control during sleep, arousal and/or cardiac activity have been reported in some infants who subsequently die of the sudden infant death syndrome (SIDS). We postulate that these abnormalities may result from dysfunction of the ventral and ventrolateral medulla, which, based on animal data, is an integrative site for(More)
We evaluated the hypothesis that a 'central oxygen detector' in the brainstem is necessary for depressions of ventilatory activity to be manifested in the newborn. Decerebrate piglets, ventilated with 100 % O(2), were studied following neuromuscular blockade. The vagi and carotid sinus nerves were sectioned bilaterally in order to remove the influence of(More)
Muscarinic cholinergic activity in the human arcuate nucleus at the ventral medullary surface is postulated to be involved in cardiopulmonary control. A significant decrease in [3H]quinuclidinyl benzilate binding to muscarinic receptors in the arcuate nucleus is now shown to occur in sudden infant death syndrome (SIDS) infants, compared to infants dying(More)
The histology and location of human respiratory chemosensitive fields are not known. In contrast, the physiology of respiratory chemosensory areas in the ventral medulla of cats has been studied extensively, and their anatomy has been partially described. Using basic principles of comparative cytoarchitecture and computer-aided reconstructions of(More)
The human arcuate nucleus is postulated to be homologous to ventral medullary surface cells in animals that participate in ventilatory and blood pressure responses to hypercarbia and asphyxia. Recently, we reported a significant decrease in muscarinic cholinergic receptor binding in the arcuate nucleus in victims of the sudden infant death syndrome compared(More)