Biomedical subjects

I Oliver

Publications and source records attributed to I Oliver.

At least 37 records · Page 2Linked to original sources

PubMed1994

Hairy function as a DNA-binding helix-loop-helix repressor of Drosophila sensory organ formation.

Sensory organ formation in Drosophila is activated by proneural genes that encode basic-helix-loop-helix (bHLH) transcription factors. These genes are antagonized by hairy and other proline-bHLH proteins. hairy has not been shown to bind to DNA and has been proposed to form inactive heterodimers with proneural activator proteins. Here, we show that hairy does bind to DNA and has novel DNA-binding activity: hairy prefers a noncanonical site, CACGCG, although it also binds to related sites. Mutation of a single CACGCG site in the achaete (ac) proneural gene blocks hairy-mediated repression of ac transcription in cultured Drosophila cells. Moreover, the same CACGCG mutation in an ac minigene transformed into Drosophila creates ectopic sensory hair organs like those seen in hairy mutants. Together these results indicate that hairy represses sensory organ formation by directly repressing transcription of the ac proneural gene.

Amino Acid Sequence↗

PubMed1993

Inhibition of angiotensin converting enzyme with enalapril maleate in infants with congestive heart failure.

We studied the inhibition of angiotensin converting enzyme (ACE) in eight infants with congestive heart failure (CHF) poorly controlled with digoxin and diuretics, treated orally with 0.25 mg kg-1 enalapril maleate once a day. Baseline ACE activities were compared between these infants and control children without CHF or ACE inhibitor. Except for one infant who vomited, inhibition of ACE activity was 75.5 +/- 12.2%, 75.5 +/- 10.5% and 51.7 +/- 12.2%, at 4, 12 and 24 h after drug intake respectively. There was no correlation between postnatal age and inhibition of ACE activity. In infants with CHF, mean baseline ACE activity was significantly higher than in control infants (36.4 +/- 7.2 mu ml-1 vs 26.9 +/- 6.9 mu ml-1, P < 0.05). These results were very similar to those seen in adults.

Aging↗

PubMed1993

[Statistic study of 5,473 somatotropin secretion stimulation pharmacologic tests (n=9). Proposed weighting coefficient].

A total of 5,473 pharmacological provocative growth hormone release tests were carried out in 3,143 children. Mean age was 9 years 9 months (range 3-16 years) and mean bone age was 7 years 6 months (range 2-14 years). Tests were of 9 different types: 1) arginine (n = 625); 2) clonidine (n = 339); 3) insulin (n = 198); 4) ornithine (n = 162); 5) insulin + arginine (n = 203); 6) clonidine + betaxolol (n = 2,003); 7) L-dopa (n = 685); 8) glucagon = propranolol (n = 443); 9) glucagon + betaxolol (n = 815). All growth hormone determinations were performed using the same radioimmunoassay. Distribution of values obtained with each test was gausso-logarithmic. Mean peak levels with their 95% confidence limit were as follows: 1) 10.2 and 0.45; 2) 11.5 and 0.7; 3) 11.8 and 0.8; 4) 14.2 and 1.2; 5) 14.3 and 0.9; 6) 15.7 and 1.1; 7) 19.8 and 2.1; 8) 20.8 and 2.3; 9) 21.0 and 2.5. These data indicate low specificity, with up to two-fold differences in mean peak levels from one test to another; proportions of peaks under 10 ng/ml ranged from 29% to 69%. Thus, the rate of patients diagnosed with growth hormone deficiency may vary substantially according to the test used. To reduce these discrepancies, we suggest adjustment of test results using a weighting coefficient of 1) 1.9; 2) 1.48; 3) 1.4; 4) 1.16; 5) 1.06; 6) 1.01; 7) 0.73; 8) 0.69; 9) 0.66.

Adolescent↗

PubMed1988

Cytotoxicity of 4-hydroxyanisole and tyrosinase activity in variant cell lines of B16 melanoma.

The melanocytotoxic effects of 4-hydroxyanisole (4-OHA) are thought to depend upon its conversion to toxic oxidation products by the enzyme tyrosinase. In this study, the cytotoxicity of 4-OHA was examined in different B16 melanoma cell lines that show varying levels of tyrosinase and after stimulation by melanocyte-stimulating hormone (MSH) and all-trans-retinoic acid (RA). 4-OHA decreased cell survival of three melanotic and one amelanotic cell line in culture, but the effect was unrelated to their tyrosinase activity or the subcellular localization of the enzyme. Although stimulation of tyrosinase activity with RA enhanced the cytotoxicity of 4-OHA, no similar enhancement occurred with alpha-MSH. It appears that there is no relationship between the cytotoxic effects of 4-OHA and intracellular tyrosinase and the enhancement of its cytotoxicity by RA may well be related to the antiproliferative effects of the retinoid.

Animals↗

PubMed1987

Effect of PUVA on plasma and skin immunoreactive alpha-melanocyte stimulating hormone concentrations.

Plasma alpha-melanocyte stimulating hormone (alpha-MSH) concentrations were measured in patients receiving PUVA therapy as treatment for mycosis fungoides, and PUVA or UVB as treatment for psoriasis. Skin immunoreactive alpha-MSH was also measured in those patients who received PUVA. The mean plasma and skin alpha-MSH concentrations after 2-3 weeks of PUVA were not significantly different from pre-treatment values and showed no relationship either to skin type or to the degree of tanning that occurred in response to PUVA. Plasma alpha-MSH concentrations were also unchanged after UVB. There was also no short term change in plasma alpha-MSH concentrations in patients after receiving their first treatment with PUVA. It would appear that circulating and skin alpha-MSH levels are unaffected by UV and show no causal relationship to PUVA induced pigmentation.

Adult↗

PubMed1982