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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5

Rinsho Byori. 1999 Jan;47(1):70-5.
[Urinary excretion of steroid hormone and 3 beta-hydroxysteroid dehydrogenase activity in normal young adult women]

[Article in Japanese]

Takeyasu M, Kato T.

Research Laboratory of Human Nutrition, Faculty of Home Economics, Kyoritsu Women's University, Tokyo.

The urinary steroid hormone metabolites and the ratio of pregnenetriol (delta 5P3) to pregnanetriol (P3) as indicators of 3 beta HSD activity in the urine of healthy young female were measured by means of capillary gas chromatography. All of the subjects have finished the normal pubertal development, and their adrenal steroid hormone secretion had reached to the stable state. We analyzed the diurnal variation, fluctuation during menstrual cycle and seasonal variation of delta 5P3/P3. We found that the hormone excretion in the urine of the morning during the follicular phase of menstrual cycle was relatively stable, and that the ratio of delta 5P3/P3 correlated highly with that in the total daily urine. In the seasonal variation, the urinary delta 5P3/P3 ratio in the subjects of high urinary DHEA group was relatively high, and that of the low DHEA group was low. Although the difference of delta 5P3/P3 ratio of the both groups was small, but statistically significant. Individual difference in the delta 5P3/P3 ratio was relatively small in comparison with that of the urinary DHEA excretion. About 5% of the all subjects showed marked high value of delta 5P3/P3 ratio. About 80% of the high urinary excretion group showed higher value than the average delta 5P3/P3 ratio. These findings suggest that the normal young female subjects were divided into several groups with regard to the urinary DHEA excretion pattern and delta 5P3/P3 ratio in the urine. Both of them may be a specific individual marker.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067368&dopt=Abstract

Fertil Steril. 2003 Feb;79(2):442-4.
A case of complete hypogonadotropic hypogonadism with a mutation in the gonadotropin-releasing hormone receptor gene.

Wolczynski S, Laudanski P, Jarzabek K, Mittre H, Lagarde JP, Kottler ML.

Department of Gynecological Endocrinology, Medical University, Bialystok, Poland. wolczynskitech.pl

OBJECTIVE: To screen for mutations in the GnRH receptor gene in a case of complete hypogonadotropic hypogonadism (HH) with GnRH resistance. DESIGN: Case report. SETTING: A university hospital. PATIENT(S): A male patient with the complete form of HH without anosmia. INTERVENTION(S): Physical examination and laboratory and genetic studies. MAIN OUTCOME MEASURE(S): Gonadotropins at the basal state and after GnRH administration and GnRH receptor DNA sequencing. RESULT(S): A novel missense mutation, localized in the first amino acid of the extracellular loop found in the heterozygous state, and another mutation, Arg(139)His (R139H), located in the conserved aspartate-arginine-serine motif at the junction of the third transmembrane and second intracellular loop of the GnRH receptor, were identified in the homozygous state. Pedigree studies reveal that both parents were heterozygous for R139H, while the mother carried the missense mutation at codon 1(M1T). CONCLUSION(S): GnRH receptor mutations may account for a larger proportion of cases of HH than previously thought. The phenotypic spectrum of HH seems to vary, and this heterogeneity may be related, at least in part, to the degree of impaired biological activity of the mutated GnRH receptor caused by the allelic type of mutations.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12568864&dopt=Abstract

Anat Embryol (Berl). 1998 Mar;199(3):239-48.
A non-destructive technique for 3-D microstructural phenotypic characterisation of bones in genetically altered mice: preliminary data in growth hormone transgenic animals and normal controls.

Graichen H, Lochmuller EM, Wolf E, Langkabel B, Stammberger T, Haubner M, Renner-Muller I, Englmeier KH, Eckstein F.

Anatomische Anstalt, Ludwig-Maximilians-Universitat, Munchen, Germany.

A non-destructive, three-dimensional technique for microstructural phenotypic characterisation of skeletal elements in genetically altered mice is presented. Preliminary data in bovine growth-hormone transgenic animals and control littermates are shown. The technique is based on microcomputed tomography (microCT) and digital postprocessing and allows for a differential quantitative analysis of the cortical and trabecular bone compartments in the axial and peripheral skeleton. The distal femora and the first lumbar vertebral bodies of six animals were CT scanned in the axial plane with an isotropic resolution of 20 microm. The periostal surface and the marrow spaces were segmented fully automatically, and the trabecular and cortical compartments were separated interactively. After 3-D reconstruction, various regions of interest (diaphyseal, metaphyseal and epiphyseal) were selected for the analysis. The femora and vertebrae of the transgenic animals showed obvious differences in size, shape, and trabecular arrangement compared with the control animals. The total bone mass was increased by a factor of two to three, but the trabecular bone was increased much more (up to 12 times) than the cortical bone. The transgenic animals showed an increased ratio of trabecular vs cortical bone (0.90 to 1.27 vs 0.14 to 0.36 in the femoral diaphysis) and an elevated trabecular bone volume fraction (49% to 73% vs 18% to 43% in the femoral metaphysis). The mean 3-D cortical thickness was similar in the normal and transgenic animals (values between 93 microm and 232 microm in the dia- and metaphyses), but the minimal cortical thickness was lower in the transgenic animals (22 to 31 microm vs 54 microm to 110 microm in the diaphysis). The technique presented is suitable for phenotypic characterisation of bone structure in genetically altered mice.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068090&dopt=Abstract

Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999 Feb;87(2):233-7.
Sex hormone receptor status of the dental pulp and lesions of pulpal origin.

Whitaker SB, Singh BB, Weller RN, Bath KR, Loushine RJ.

Department of Endodontics, School of Dentistry, Medical College of Georgia, Augusta 30912-1244, USA.

OBJECTIVE: The purpose of this study was to determine whether the dental pulp and lesions of pulpal origin (eg, pulp polyps, periapical granulomas, and periapical cysts) exhibit receptors for the sex steroid hormones estrogen, progesterone, and androgen. STUDY DESIGN: Staining for the receptors of the hormones estrogen, progesterone, and androgen was accomplished through use of available immunohistochemical detection techniques. Pulpal tissues were obtained from freshly extracted human third molars; the other tissues were obtained from the Oral and Maxillofacial Pathology Laboratory archives. Ten samples of each tissue were processed and immunostained for these specific receptors. RESULTS: Staining for estrogen and androgen receptors was essentially negative for all cell populations examined. However, positive progesterone receptor staining of varying degrees was noted in 8 of 10 pulpal specimens. Primarily, pulpal fibroblasts and odontoblasts exhibited positive immunoreactivity. CONCLUSIONS: The results of this study suggest that although the dental pulp may be a potential target tissue for progesterone, evidence is lacking with respect to the other sex steroid hormones.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10052381&dopt=Abstract

J Physiol. 1999 Mar 1;515 ( Pt 2):463-73.
Influence of nitric oxide modulators on cholinergically stimulated hormone release from mouse islets.

Aring;kesson B, Lundquist I.

Department of Pharmacology, University of Lund, Lund, Sweden.

1. We have investigated, with a combined in vitro and in vivo approach, the influence on insulin and glucagon release stimulated by the cholinergic, muscarinic agonist carbachol of different NO modulators, i.e. the nitric oxide synthase (NOS) inhibitors NG-nitro-L-arginine methyl ester (L-NAME), NG-monomethyl-L-arginine (L-NMMA) and 7-nitroindazole as well as the intracellular NO donor hydroxylamine. 2. At basal glucose (7 mM) carbachol dose-dependently stimulated insulin release from isolated islets with a half-maximal response at approximately 1 microM of the agonist. In the presence of 5 mM L-NAME (a concentration that did not influence basal insulin release) the insulin response was markedly increased along the whole dose-response curve and the threshold for carbachol stimulation was significantly lowered. 3. Carbachol-stimulated islets displayed an increased insulin release and a suppressed glucagon release in the presence of L-NAME, L-NMMA or 7-nitroindazole. Significant suppression of glucagon release (except for L-NAME) was achieved at lower concentrations (approximately 0.1-0.5 mM) of the NOS inhibitors than the potentiation of insulin release (1.0-5.0 mM). The intracellular NO donor hydroxylamine dose-dependently inhibited carbachol-induced insulin release but stimulated glucagon release only at a low concentration (3 microM). 4. In islets depolarized with 30 mM K+ in the presence of the KATP channel opener diazoxide, NOS inhibition by 5 mM L-NAME still markedly potentiated carbachol-induced insulin release (although less so than in normal islets) and suppressed glucagon release. 5. In vivo pretreatment of mice with L-NAME was followed by a markedly increased insulin release and a reduced glucagon release in response to an i.v. injection of carbachol. 6. The data suggest that NO is a negative modulator of insulin release but a positive modulator of glucagon release induced by cholinergic muscarinic stimulation. These effects were also evident in K+ depolarized islets and thus NO might exert a major influence on islet hormone secretion independently of membrane depolarization events.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10050013&dopt=Abstract

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