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D O'Halloran

Publications and source records attributed to D O'Halloran.

4 recordsLinked to original sources
PubMed1989

Evidence for neuropeptide Y synthesis in the rat anterior pituitary and the influence of thyroid hormone status: comparison with vasoactive intestinal peptide, substance P, and neurotensin.

Neuropeptide Y (NPY), a 36-amino acid member of the pancreatic polypeptide family, was found to be present by RIA and immunocytochemistry in the rat anterior pituitary gland. NPY prohormone messenger RNA (mRNA) was identified in the pituitary by Northern blot analysis. The possible regulation of NPY was examined by determining the effects of thyroid hormone manipulation on peptide synthesis. Three other anterior pituitary neuropeptides, neurotensin (NT), substance P (SP), and vasoactive intestinal peptide (VIP), were studied for comparison. Hypothyroidism was found to significantly increase the pituitary content of NPY, SP, and VIP and their respective mRNAs but to decrease the quantity of NT. Immunocytochemistry revealed very weak NPY immunoreactivity in scattered cells in control rat anterior pituitaries, but in hypothyroid rats a greater number of positive cells were seen, and the staining was relatively intense. These positive cells were identified as a subset of thyrotropes. In T4-induced hyperthyroidism NPY, NT, and VIP levels were unaffected whereas SP concentrations fell considerably. TRH treatment produced a decrease in NT and had no effect on NPY, SP, or VIP. These changes were found only in the pituitary; no net change occurred in hypothalamic peptide and mRNA levels. Since the changes in pituitary peptide and mRNA levels occurred coordinately it appears that regulation by thyroid hormone status occurs, at least in part, directly at the level of gene transcription. The changes in these 4 regulatory peptides in hypothyroidism and their known powerful effects on pituitary function suggest that they may have a significant paracrine or autocrine influence in controlling the alterations in pituitary secretion.

Animals↗
PubMed1988

Investigation of aminoglycoside nephrotoxicity in cystic fibrosis patients.

Cystic fibrosis patients are a special risk group for nephrotoxic effects of amino-glycosides (AG). The traditional methods of assessing renal damage are very insensitive, and toxicity is not detected until serious functional damage is evident. The aims of the present study were to monitor early markers of nephrotoxicity in cystic fibrosis patients treated with gentamicin. Urinary excretion of beta-N-acetylglucosaminase (beta-NAG, a lysosomal enzyme) and low molecular weight proteins as identified on sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) were prospectively studied in cystic fibrosis outpatients and inpatients. Urinary excretions of beta-NAG and low molecular weight proteins were normal in cystic fibrosis patients not being treated with gentamicin. All patients being treated with intravenous gentamicin (average dose, 2.5 g over 9 days) showed markedly elevated urinary excretion of beta-NAG. SDS-PAGE of serial urine samples from CF patients during intravenous AG therapy showed increasing excretion of low molecular weight proteins. Protein excretion profiles from control subjects showed no change over equivalent time periods. CF patients receiving nebulized AG did not show altered protein excretion. beta-NAG excretion patterns were similar to changes detected in the SDS-PAGE system. No gross nephrotoxicity developed in these patients. Blood urea nitrogen, plasma creatinine, and plasma magnesium concentrations remained within normal limits. The pattern of protein excretion on SDS-PAGE was consistent with renal tubular rather than glomerular damage. The SDS-PAGE system provides an additional means of monitoring early subclinical nephrotoxicity of AG in CF patients.

Acetylglucosaminidase↗