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Biomedical subjects

W Driscoll

Publications and source records attributed to W Driscoll.

5 recordsLinked to original sources
PubMed1996

Effect of methylene blue on refractory neonatal hypotension.

Excess nitric oxide is a mediator of the hypotension in septic shock. Nitric oxide dilates vascular smooth muscle through activation of soluble guanylate cyclase. We report the increase in blood pressure caused by methylene blue (MB), a soluble guanylate cyclase inhibitor, in five neonates with presumed septic shock unresponsive to colloids, inotropic agents, and corticosteroids. MB was given intravenously at a dose of 1 mg/kg during a 1-hour period. MB increased blood pressure in each patient (average, 33% +/- 20%). Blood pressure subsequently decreased to near baseline values in three patients, who then received a second infusion of MB. Blood pressure again increased in these patients. Three of five patients were weaned from inotropic support within 72 hours. Three of five patients survived and were discharged home. We suggest that MB increased blood pressure in these neonates with refractory hypotension.

Blood Pressure↗
PubMed1994

A comparison of information recorded using the Thylstrup Fejerskov index, Tooth Surface Index of Fluorosis and Developmental Defects of Enamel index.

This study considers information recorded using three different indices of enamel defects/fluorosis. The comparisons were based on photographs of subjects taken in two areas with < 0.1 and with 0.7 ppm fluoride in their drinking water. The three indices used were the Thylstrup Fejerskov index, the Tooth Surface Index of Fluorosis (TSIF) and the Developmental Defects of Enamel (DDE) index. Each was scored by a different examiner. All three indices were able to detect significant differences in opacity/fluorosis prevalence between the two areas. However, it was clear from the results that information collected using these different enamel opacity/fluorosis indices was not directly comparable for individual teeth even though prevalences of defects were similar for two of the indices, the TSIF and the DDE index.

Dental Enamel↗
PubMed1990

Modulation of the biological activity of thyrotrophin by anti-human thyrotrophin monoclonal antibodies.

The mechanism by which monoclonal antibodies enhance the biological activity of a number of hormones is poorly understood. One such antibody (GC73), which binds to human but not bovine TSH, enhances the bioactivity of human TSH in vivo. We have investigated whether GC73 enhancement of TSH bioactivity involves potentiation of hormone-receptor activation assessed by the cyclic AMP (cAMP) responses of both primary human thyrocyte cultures and a TSH-responsive human thyrocyte cell line (SGHTL-45). GC73 had no effect on basal cAMP production. In contrast to its enhancement of the bioactivity of human TSH in vivo, it markedly inhibited the cAMP response to 1 and 10 mU human TSH/ml in primary thyrocytes. This effect was dose-dependent with neutralization of the bioactivity of TSH occurring at 2 mg GC73/ml. GC73 had no effect on the bioactivity of bovine TSH. In contrast, a second anti-TSH monoclonal antibody (TC12), which binds to both human and bovine TSH, inhibited the bioactivity of both species of TSH. Similar results were obtained using SGHTL-45 cells, although the peak concentrations of cAMP were lower. We conclude that binding of GC73 to human TSH resulted in inhibition rather than enhancement of the in-vitro biological activity of human TSH. We suggest that GC73 enhancement of human TSH bioactivity seen in vivo does not result from a mechanism involving potentiation of receptor activation by human TSH.

Antibodies, Monoclonal↗