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Biomedical subjects

E Reiter

Publications and source records attributed to E Reiter.

14 recordsLinked to original sources

P-element homologous sequences are tandemly repeated in the genome of Drosophila guanche.

In Drosophila guanche, P-homologous sequences were found to be located in a tandem repetitive array (copy number: 20-50) at a single genomic site. The cytological position on the polytene chromosomes was determined by in situ hybridization (chromosome O: 85C). Sequencing of one complete repeat unit (3.25 kilobases) revealed high sequence similarity between the central coding region comprising exons 0 to 2 and the corresponding section of the Drosophila melanogaster P element. The rest of the sequence has diverged considerably. Exon 3 has no coding function and the inverted repeats have disappeared. The P homologues of D. guanche apparently have lost their mobility but have retained the coding capacity for a protein similar to the 66-kDa P-element repressor of D. melanogaster. Divergence between different repeat units indicates early amplification of the sequence at this particular genomic site. The presence of a common P-element site at 85C in Drosophila subobscura, Drosophila madeirensis, and D. guanche suggests that clustering of the sequence at this location took place before the phylogenetic radiation of the three species.

Amino Acid Sequence

Growth hormone and prolactin stimulate androgen receptor, insulin-like growth factor-I (IGF-I) and IGF-I receptor levels in the prostate of immature rats.

In this study we investigated the involvement of several different pituitary hormones on rat prostate development. 22-day-old Wistar rats, hypophysectomized (hypox) at 19 days of age were supplemented with highly purified human prolactin (hPRL), human luteinizing hormone (hLH), porcine follicle-stimulating hormone (pFSH), and bovine growth hormone (bGH) or with saline. Quantitative analysis of RNAs shows that treatment with either PRL or GH increases significantly steady-state mRNAs levels of the following genes in the prostate: androgen receptor (AR) (respectively 3.5- and 4.8-fold above hypox controls), IGF-I (5- and 2.7-fold), and IGF-I receptor (2.9- and 2.3-fold). LH and FSH, by contrast, have negative effects on these parameters. To test whether the enhancing effect of PRL and GH on AR-mRNA abundance was followed by increased content in the protein itself, binding assays were performed with the androgen agonist [3H]R1881 (131 and 153 fmol/mg protein while hypox controls contained 110 fmol/mg protein). In addition to the well-documented presence of prolactin receptors in prostatic tissues, we have further demonstrated, by means of nuclease S1 protection assays plus dot- and Northern-blot analyses, that a GH receptor mRNA is produced in the immature rat prostate. Moreover, we observed not only strong lactogenic but also purely somatogenic binding to be occurring in the immature prostates. Finally, we have studied IGF-I mRNA content in separated epithelial/stromal cell fractions and have concluded that IGF-I expression is principally located in the prostatic stroma. Taken together, these results suggest that PRL and GH are involved in regulating AR synthesis, at least partially by direct action on the organ. In this context IGF-I appears as a paracrine factor playing a role in epithelium/stroma interactions during prostatic development.

Age Factors

Normative data for the steroidogenic response of mineralocorticoids and their precursors to adrenocorticotropin in a healthy pediatric population.

The responses of mineralocorticoids and their precursors 1 h after a 0.25-mg bolus of ACTH has not previously been established in infancy or childhood. We report the steroidogenic responses of pregnenolone, progesterone (Prog), deoxycorticosterone (DOC), corticosterone (B), 18-hydroxycorticosterone (18OHB), and aldosterone (A) measured 1 h after a 0.25-mg bolus of ACTH in 102 healthy children who were divided into 5 age groups: group 1 (< 1 yr; n = 22), group 2 (1-5 yr; n = 22), group 3 (6-12 yr; n = 15), group 4 (early to midpuberty; n = 21), and group 5 (late puberty; n = 22). Baseline pregnenolone levels were constant throughout childhood; however, there was a significant fall in the stimulated level after the first year of life (group 1 vs. 2, P < 0.0125). Baseline Prog levels rose significantly with the onset of puberty (group 3 vs. 4, P < 0.0125), but levels did not increase after ACTH stimulation during puberty. Both baseline and stimulated levels of Prog, DOC, and 18OHB were significantly higher in group 3 males than in group 3 females (P < 0.05). Stimulated levels of DOC and corticosterone were constant during childhood, the only exception being the fall in the stimulated level of both steroids with the onset of puberty in males (group 3 vs. 4, P < 0.0125). The baseline level of 18OHB also fell with the onset of puberty in males (P < 0.0125), but a similar fall was not seen in females or in the stimulated level of 18OHB in either sex. The stimulated aldosterone level was higher in group 1 males than in group 2 males (P < 0.0125); a similar difference was not observed in females. The differences that we observed confirm the importance of specific age- and sex-related reference data when patients with possible abnormalities of mineralocorticoid synthesis are evaluated.

Adolescent

Normative data for adrenal steroidogenesis in a healthy pediatric population: age- and sex-related changes after adrenocorticotropin stimulation.

The normal response to a single 0.25-mg dose of ACTH-(1-24) is not well established in infancy or childhood. We report the adrenal steroidogenic responses of 17-hydroxypregnenolone (17OH Preg), 17-hydroxyprogesterone (17OH Prog), 11-deoxycortisol, cortisol, deoxycorticosterone, dehydroepiandrosterone (DHEA), DHEA sulfate, androstenedione (A'dione), and testosterone in 102 healthy children who were divided into 5 groups: group 1 (less than 1 yr old; n = 22), group 2 (1-5 yr old; n = 22), group 3 (6-12 yr old; n = 15), group 4 (early-midpuberty; n = 21), and group 5 (late puberty; n = 22). Baseline and stimulated levels of 17OH Preg were significantly higher in group 1 infants than in group 2 children (P less than 0.01). Baseline levels of 17OH Prog increased in late puberty (P less than 0.01). Baseline and stimulated levels of DHEA rose in late puberty (group 5 vs. group 3, P less than 0.01). DHEA levels in late pubertal females were higher than those in their male counterparts (P less than 0.01). DHEA sulfate levels did not change after ACTH administration in any age group. Baseline and stimulated levels of A'dione rose significantly before the onset of puberty in female children (group 2 vs. group 3, P less than 0.01). The calculated ratio of 17OH Preg/17OH Prog in group 1 was significantly higher than that in other groups of children (P less than 0.01). The calculated, baseline DHEA/A'dione ratio was higher in group 1 than in older children (P less than 0.01). Stimulated ratios were higher in late pubertal females than in males (P less than 0.01). In both sexes baseline and stimulated ratios of 17OH Prog/deoxycorticosterone increased in puberty, such that late pubertal children had higher levels than prepubertal children (P less than 0.01). These data confirm the need for interpretation ACTH stimulation test data to be based upon age- and sex-specific norms.

17-alpha-Hydroxypregnenolone

[Contact eczema and "standard test"--do "International Standard Test Series" coincide with Austrian local characteristics?].

Testing with a "standard" group of substances has proved of great value when allergic contact dermatitis is suspected and the offending agent cannot be pinpointed by careful history-taking. But internationally standardized series do not take into account locally important and individual factors, changing consumer habits or economic aspects. We have, thus, compared the suitability of two standard series, the ICDRG-European and the DKG-German standard, for Austrian purposes. 1,478 patients with a clinical diagnosis of contact dermatitis were patch tested between 11/88 and 4/90 with the ICDRG allergens; the second collective of 505 patients was tested between 5/90 and 1/91 with the DKG series. Only 12 out of the 27 substances of the ICDRG series exceeded the critical incidence of 1%; 6 were below this limit but positive in more than 0.5% and 9 hardly ever aroused positive reactions. In the DKG series, 17 out of 23 substances surpassed the limit, 2 were positive in more than 0.5%, and 4 caused virtually no reactions. However, 4 allergens with frequent sensitization rates were included neither in the ICDRG nor in the DKG series and 2 others were missing in the over-dimensioned ICDRG standard. Our results demonstrate that internationally established standard series have to adapted for the local situation in Austria, and that a constant review is essential with replacement of allergens as necessary according to changing production techniques and consumer habits. Suggestions for an "Austrian standard patch test series" are proposed on the basis of our results but in spite of being helpful in general terms interpretation of such a test in the individual patient with eczema remains problematic.

Allergens

[Contact eczema and epicutaneous tests--distribution of allergens and changes in the spectrum in Vienna].

Thousands of contact antigens have been defined. It is, however, remarkable that only a small group of substances (15 to 20) have proved to be frequent or otherwise important causes of allergic contact dermatitis. In agreement with reports from comparable centres, metals are high up on the "hitlist" of frequent allergens (nickel 24%, cobalt 9%, chromates 6%), followed by ingredients of cosmetics and toiletries (fragrances 16%, balsam of Peru 10%, Kathon 5%), whilst already way back are topical medicines (neomycin 4%, parabens 3%, lanolin 2%, benzocaine 1%) and rubber additives (thiuram-mix 2% and carba-mix 1%). Almost all other substances lie below the 1% limit. There was only one remarkable exception in comparison with the results of most other European studies, namely thiomersal, which is widely distributed as a preservative in vaccines in Austria and climbed to second place, with a sensitization rate of 18%. Although the phenylborate mercurials (historic sensitizations due to topical antiseptics) still reached a surprisingly high incidence of 6%, there were hardly any cases of cross-sensitization with thiomersal. A comparison with the international literature illustrates Austria-specific trends and a change in the spectrum over the past years. Interpretation of patch testing requires great specialist knowledge and experience.

Adolescent

Serum concentrations of 25-hydroxyvitamin D in Florida children: effect of anticonvulsant drugs.

The mean serum concentration of 25-hydroxyvitamin D (25OHD), determined by nonchromatographic radioassay, was significantly lower (P less than .02) in Florida children with epilepsy treated with anticonvulsant drugs (34.4 +/- 11.3 [SD] ng/ml) than in normal subjects (40.9 +/- 14.3), despite exposure of both groups to sunlight throughout the year. In 12% of children treated with anticonvulsant drugs, the 25OHD level was below the lowest value recorded in the control group. The mean serum concentration of 25OHD in normal Philadelphia children (27.5 +/- 9.1 ng/ml) was significantly less than in either group of Florida subjects. Annual monitoring of calcium homeostasis and vitamin D status is indicated in Southern children receiving anticonvulsant drugs, but routine vitamin D supplementation of such patients is unnecessary.

Anticonvulsants

Concentrations of 24,25-dihydroxyvitamin D and 25-hydroxyvitamin D in paired maternal-cord sera.

Mean serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)2D) and 25-hydroxyvitamin D (25OHD), measured by competitive radioassays, were significantly higher in maternal serum than in cord serum of term infants in both black and white subjects. There were positive correlations between maternal and cord levels of both metabolites of vitamin D. Serum concentrations of 24,25(OH)2D and 25OHD were significantly lower in white pregnant subjects than in nonpregnant women. In utero levels of 24,25(OH)2D and 25OHD probably reflect maternal stores of these metabolites.

Dihydroxycholecalciferols

Synthesis of 1,25-dihydroxyvitamin D in the nephrectomized pregnant rat.

Pregnant rats were maintained on diets either adequate or deficient in vitamin D. On the 20th day of gestation, animals were either nephrectomized bilaterally or sham operated. Immediately therafter, four groups of nephrectomized or sham-operated pregnant rats received iv [26,27-3H]25-hydroxyvitamin D3 ([26,27-3H]25OHD3), while two groups received [1,2-3H,4-14C]D3. The animals were sacrificed 10-24 h later. The distribution of the radiolabeled metabolites of vitamin D3 was determined in extracts of maternal plasma, maternal intestinal tract, placentae, and fetuses after Sephadex LH-20 column chromatography. Both vitamin D3 and 25OHD3 crossed the placenta and entered the fetus. In anephric animals receiving [26,27-3H]-25OHD3, 24,25-dihydroxyvitamin D and a polar peak eluting in the position of 1,25-dihydroxyvitamin D [1,25(OH)2D] and 25,26-dihydroxyvitamin D were identified in extracts of maternal plasma and intestinal tracts and of placentae and fetuses. The identities of 24,25-dihydroxyvitamin D and 1,25 (OH)2D were confirmed by high pressure liquid chromatography. In rats receiving [1,2-3H,4-14C]D3, approximately 50% of the polar metabolite consisted of 1,25(OH)2D. We conclude that the anephric pregnant rat is able to synthesize 1,25(OH)2D, that the fetal portion of the feto-placental unit is the most likely site of production of this hormone, and that this metabolite of vitamin D is able to cross the placenta from the fetus to the mother.

Animals

Measurement of 24,25 dihydroxyvitamin D in sera of neonates and children.

Serum concentration of 25OHD and 24,25(OH)2D were measured in lipid extracts of serum by competitive radioassay following separation of the metabolits by Sephadex LH-20 column chromatography. The concentration of 24,25(OH)2D in children and adolescents (3.3 +/- 1.3 SD ng/ml) was significantly greater (P less than 0.01) than the levels recorded in neonates (1.8 +/- 0.6 ng/ml), and was approximately one-tenth the concentration of 25OHD in the two populations (children 35.2 +/- 9.2 ng/ml; neonates 14.4 +/- 3.4 ng/ml, P less than 0.01). Although 24,25(OH)2D is present in significant quantities in the sera of children and adolescents, its metabolic function remains unknown at present.

Adolescent