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Biomedical subjects

J J Saad

Publications and source records attributed to J J Saad.

3 recordsLinked to original sources

Pars superioris in endolymphatic hydrops.

A volumetric study was made of the endolymphatic compartments of the pars superioris (utricle and semicircular canals). Selected for this comparative study were 15 ears from subjects with unilateral endolymphatic hydrops, 15 contralateral ears, and 15 normal ears. There was an increase in the total volume as well as in the utricular volume. This increase was also correlated with vestibular and auditory symptoms, disclosing a substantial increase in volumes with increasing hearing loss. The magnitude of volume increase correlated inversely with the frequency of vertiginous attacks; no correlation was found with the duration of the disease.

Aged↗

Otologic manifestations of the hydantoin syndrome.

The temporal bones of a newborn infant with hydantoin syndrome showed multiple middle ear and inner ear anomalies. There was a constellation of bony and membranous defects involving the oval and round windows, cochlear ducts, cochlear aqueducts, endolymphatic ducts and sacs, and vestibular labyrinths. To the authors' knowledge, supernumerary vestibular sensory epithelial structures and an inner ear epidermoid cyst have not been previously reported. Wide communications between the subarachnoid space and inner ear were of surgical relevance.

Abnormalities, Drug-Induced↗

Upper airway epithelial cells support eosinophil survival in vitro through production of GM-CSF and prostaglandin E2: regulation by glucocorticoids and TNF-alpha.

Production of GM-CSF by epithelial cells has been implicated in eosinophil survival within the airways, although GM-CSF promotes neutrophil and monocyte survival as well. Using primary cultures of human airway epithelial cells, we undertook a comprehensive examination of factors that enhance eosinophil survival or apoptosis. Unstimulated epithelial cells were compared to epithelial cells stimulated with TNF-alpha in the presence or absence of dexamethasone. A striking increase in survival was observed when peripheral blood eosinophils were cultured with supernatants derived from unstimulated and TNF-alpha-stimulated epithelial cells. Cultured epithelial cells were examined for transcripts of cytokines shown to enhance eosinophil survival (GM-CSF, IL-3, IL-5, IL-13, and IFN-gamma), and transcripts for cytokines promoting apoptosis (IL-10 and TGF-beta). GM-CSF transcripts, but not the other cytokines, were present in unstimulated epithelial cells, and levels were increased with TNF-alpha stimulation. TNF-alpha stimulation increased the levels of GM-CSF and PGE2 in epithelial cell supernatants and dexamethasone suppressed the TNF-alpha induced increases. The survival effects of the TNF-alpha-stimulated supernatants were effectively blocked by neutralizing antibodies to GM-CSF or by dexamethasone treatment of epithelial cells. Selectivity of GM-CSF for eosinophil versus neutrophil survival was demonstrated and suggests that epithelial cell regulation of GM-CSF and PGE2 contribute to eosinophil survival in vitro and may contribute to eosinophil accumulation in allergic disease.

Apoptosis↗