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Biomedical subjects

D R Stewart

Publications and source records attributed to D R Stewart.

72 records · Page 4Linked to original sources
PubMed1976

Malrotation of the bowel in infants and children: a 15 year review.

One hundred and fifty-nine patients with malrotation treated in the Children's Hospital Medical Center between 1951 and 1967 are presented and analyzed with regard to the factors contributing to the success or failure of their management. There were 28 deaths, the majority of which occurred in patients who were less than one month old, had multiple congenital anomalies, or had volvulus of the small bowel with gangrene and perforation. Some of the points we have found most helpful in making the diagnosis are reviewed and the disease as it presents in older children is considered briefly.

Abnormalities, Multiple↗
PubMed1975

Management of acquired tracheal obstructions in infancy.

Endoscopic resection of tracheal subglottic stenosis can be performed safely and effectively. With careful selection, some stenotic rings can be excised without the requirement for prior tracheostomy. Endoscopic resection does not supplant other methods of dilatation, injection, or stenting of subglottic scars, but early resection in appropriate cases may reduce the number of dilatations and obviate the need for a stent and systemic steroids.

Dilatation↗
PubMedDate not supplied

Mechanism of toxic action of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in cultured human luteinized granulosa cells.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) caused a significant decrease in estradiol (E2) production when it was administered to human luteinized granulosa cells (hLGCs) in culture. We investigated the involvement of the epidermal growth factor receptor (EGFR) and protein tyrosine kinase (PTK) in this TCDD-induced toxicity. Upregulation in 125I-EGF binding to EGFR was measured after 24 h of TCDD treatment, while downregulation in EGFR binding was measured after 72 h of TCDD treatment. Upregulation of EGFR binding was associated with a significant decrease in postnuclear (7000 x g supernatant) PTK activity, but this activity was stimulated after 72 h of TCDD treatment. TCDD altered the level of tyrosine phosphorylation in proteins with molecular weights 35, 40, 43, 45, 60, and > 205 kDa. TCDD caused a significant increase in postnuclear cAMP-dependent protein kinase (PKA) after 24 h of treatment. The actions of TCDD on protein kinases were partially blocked by the protein synthesis inhibitor, cycloheximide. On the other hand, TCDD increased nuclear PTK and decreased nuclear PKA activity. E2 inhibited the postnuclear and nuclear activity of both PTK and PKA in control samples, but did not affect TCDD actions on either postnuclear or nuclear PTK activity. However, E2 abolished the stimulatory effect of TCDD on PKA activity in postnuclear protein. In the presence of insulin, TCDD did not induce any additional changes in postnuclear or nuclear PTK. Forskolin (FK) alone inhibited postnuclear PTK activity and stimulated its nuclear activity. The addition of TCDD 20 min after FK resulted in an increase in postnuclear PTK, but there was little change in nuclear PTK as compared to the effect of FK alone. The stimulatory effect of TCDD on postnuclear PKA activity was enhanced by insulin and TCDD reversed the negative effect of FK, but there was no effect of either insulin or FK on the inhibition by TCDD of nuclear PKA activity. TCDD decreased the activity of MAP2 kinase and reduced the binding activity of AP-1 DNA when given alone, and also blocked the E2 stimulation of MAP2K. These findings suggest that TCDD may interrupt the endocrine function of hLGCs through the blockage of the mitotic signal directly or indirectly through the interaction of PTK/MAP2K and PKA signaling.

Cell Cycle↗
PubMedDate not supplied

Classification of adverse reproductive effects can be improved by measurements of multiple biomarkers for ovarian toxicity and early fetal loss.

Hormone assays have been developed and applied for monitoring reproductive function using self-collected urine samples in non-clinical populations of women. Early pregnancy loss, menstrual dysfunction, reduced fertility as well as the site of toxicity can now be assessed using daily early morning urine samples. The understanding of the specific limitations of individual assay systems is important, however, to make the best use of these systems. The use of multiple end-points and computer algorithms is suggested to avoid misclassification of adverse reproductive events.

Algorithms↗