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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

Endocrinology. 2002 Nov;143(11):4483-6.
The gene locus encoding iodothyronine deiodinase type 3 (Dio3) is imprinted in the fetus and expresses antisense transcripts.

Hernandez A, Fiering S, Martinez E, Galton VA, St Germain D.

Department of Medicine, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA.

The mouse Dio3 gene codes for the type 3 iodothyronine deiodinase (D3), a conserved selenocysteine-containing enzyme that inactivates thyroid hormones and is highly expressed during early development. The mouse Dio3 gene and its human homolog map to chromosomal regions that are known to contain imprinted genes. We assessed the allelic expression of the Dio3 using a mouse model in which the gene had been inactivated by the introduction of a critical mutation in the selenocysteine codon. We compared Dio3 gene expression in fetuses that were either wild type or heterozygous (+/-Dio3) for the mutation. D3 enzymatic activities in the head, limbs, liver and body of heterozygous fetuses (E14 to E18) that inherited the mutation from the mother were no different from those found in their wild type littermates. However, D3 activities in heterozygous animals that inherited the mutation from the father were only 18 to 28% of the activities of their wild type littermates in these same tissues. No detectable activity was found in fetuses homozygous for the mutation indicating full inactivation of the enzyme. Northern analysis of mRNA from E15 fetuses showed that the Dio3 mRNA transcripts generated from the paternal allele were at least 5 times more abundant than the transcripts originated from the maternal allele. We conclude that the Dio3 gene is subject to genomic imprinting and preferentially expressed from the paternal allele in the mouse fetus. We also identified a gene that is transcribed antisense from the Dio3 locus. The Dio3 gene likely belongs to the same cluster of imprinted genes detected in mouse chromosome 12 and human chromosome 14 and should be considered as a candidate gene that might play a role in the phenotypic abnormalities associated with uniparental disomy of those chromosomes, a condition in which gene expression is altered due to abnormal genomic imprinting.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399446&dopt=Abstract

J Androl. 2002 Nov-Dec;23(6):825-9.
Possible relationship between seminal plasma inhibin B and spermatogenesis in patients with azoospermia.

Garem YF, Arini AF, Beheiry AH, Zeid SA, Comhaire FH.

Department of Andrology and Dermatology, Faculty of Medicine, Alexandria University, Egypt.

Inhibin B is bidirectionally secreted by Sertoli cells, basal secretion into the circulation exerts negative feedback on follicle-stimulating hormone secretion, and serum inhibin B is considered a marker of spermatogenesis. The precise role of apical secretion is unknown. The objective of our work was to study the relationship between seminal inhibin B and spermatogenesis. Dimeric inhibin B was measured by immunoassay in seminal plasma of volunteers with normozoospermia (n = 10, group 1), in men after vasectomy (n = 10, group 2), and in men with azoospermia (n = 50, group 3). Testicular biopsy and testicular sperm extraction were performed in men with azoospermia. Seminal inhibin B levels were higher in men in group 1 than in men in groups 2 and 3 (P <.0001). In seminal plasma, inhibin B presents a positive correlation with alpha glucosidase activity (r =.37, P =.002). Seminal inhibin B is inversely related with serum FSH (r = -.58, P <.001), and presents a weak positive correlation with serum testosterone concentration (r =.29, P =.03). No difference was found between inhibin B levels in seminal plasma of patients with nonobstructive or obstructive azoospermia, and between positive or negative outcome of TESE. We conclude that inhibin B secretion by Sertoli cells is differentially regulated. The contribution of accessory sex glands limits the use of seminal plasma inhibin B as a marker of spermatogenesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399529&dopt=Abstract

J Androl. 2002 Nov-Dec;23(6):845-53.
Inhibin B regulating follicle-stimulating hormone secretion during testicular recrudescence in the male golden hamster.

Jin W, Herath CB, Yoshida M, Arai KY, Saita E, Zhanquan S, Ren L, Watanabe G, Groome NP, Taya K.

Department of Basic Veterinary Sciences, The United Graduate School of Veterinary Sciences, Gifu University, Japan.

In the present study, to clarify whether inhibin affects follicle-stimulating hormone (FSH) secretion in the recrudescence of the male golden hamster, we used a recently developed specific enzyme-linked immunosorbent assay (ELISA) in order to measure 2 forms of inhibin molecules: inhibin B and inhibin pro-alphaC. In addition, we used the radioimmunoassay (RIA) to measure immunoreactive (ir-)inhibin, FSH, luteinizing hormone (LH), and testosterone. And finally, we used the proliferating cell nuclear antigen (PCNA) and computer-assisted sperm motion analysis (CASA) methods to ascertain how well spermatogenesis and sperm motility recover from the photoinhibition caused by exposure to a short-day (SD; 10-hour light: 14-hour dark) photoperiod. Animals were exposed to SD for 15 weeks, and then their testes were checked carefully and found to be completely regressed. Thereafter, those animals were transported to a long-day (LD; 14-hour light: 10-hour dark) photoperiod. Sampling was carried out at weeks 0 (exposed SD 15 weeks), 1, 2, 4, 6, 8, and 10. Plasma FSH rapidly increased and reached peak levels 2 weeks after transferral to the LD photoperiod and then declined to normal LD levels at week 6. Circulating ir-inhibin, inhibin B, and inhibin pro-alphaC rose to normal LD levels by week 4. A highly significant inverse correlation was observed between plasma FSH and inhibin B but not between FSH and either ir-inhibin or inhibin pro-alphaC. Plasma testosterone recovered to normal LD levels within 1 week. Sperm motility parameters were low until week 2 and recovered to normal LD levels from weeks 4 to 10. PCNA-labeled cells were confined to the spermatogenic cells of the seminiferous tubules, though Leydig and Sertoli cell nuclei were never stained for PCNA during the period studied. The number of pachytene spermatocytes and the diameter of seminiferous tubules increased in a time-dependent manner after transferral from SD to LD. In conclusion, these results suggest that 1) secretion of inhibin B may be stimulated by an early rise in FSH; 2) inhibin B suppresses FSH secretion from weeks 2 to 10, after transferral to the LD photoperiod; and 3) testes recrudescence is based on the increase in the number of sperm cells instead of the increase in the number of Sertoli and Leydig cells of the male golden hamster.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399532&dopt=Abstract

J Androl. 2002 Nov-Dec;23(6):919-21.
Serum androgen bioactivity during 5alpha-dihydrotestosterone treatment in elderly men.

Raivio T, Tapanainen JS, Kunelius P, Janne OA.

Biomedicum Helsinki, Institute of Biomedicine, University of Helsinki, Finland. taneli.raivielsinki.fi

The androgens used in the treatment of age-related androgen decline have different bioactivities that cannot be evaluated with conventional detection methods for serum steroids. We have recently developed a recombinant cell bioassay for the determination of androgen bioactivity in human serum that is based on androgen-specific interaction between the ligand-binding domain (LBD) and the N-terminal region of the androgen receptor (AR). In this work, we examined the effect of topically applied 5alpha-dihydrotestosterone (DHT; 7.5-10 g of 2.5% DHT gel daily for 6 months) on circulating androgen bioactivity in 14 men (age range, 51-63 years) with symptoms of andropause and pretreatment serum testosterone less than 15 nM, or serum sex hormone-binding globulin concentration greater than 30 nM, or both. The mean (+/-SEM) pretreatment androgen bioactivity was 3.3 +/- 0.3 nM testosterone equivalents, and the levels correlated with serum testosterone concentration (r =.55, P <.05). DHT gel treatment induced a sixfold increase (from 1.5 +/- 0.1 nM to 9.0 +/- 0.7 nM) in mean serum DHT level, whereas endogenous testosterone and estradiol levels measured with radioimmunoassays were suppressed by approximately 70% and approximately 50%, respectively (P <.0001). Concomitantly, serum androgen bioactivity increased by sevenfold (from 3.3 +/- 0.3 to 23.6 +/- 2.8 nM testosterone equivalents; P <.0001). We conclude that DHT gel therapy in elderly men significantly increases their circulating androgen bioactivity as measured with a mammalian cell bioassay. An androgen-specific bioassay such as ours may enable investigation of other androgens with different bioactivities, such as selective AR modulators.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399539&dopt=Abstract

maroon.tc.umn.edu

The present report examines the in vitro genotoxicity (micronucleus assay) of herbicides and adjuvants and reports on an in vivo human study on potential endocrine effects of pesticides, including herbicides. Adjuvants are used in conjunction with 2,4-dichlorophenoxy acetic acid (2,4-D) and other herbicides. Earlier pesticide applier survey results (n = 709) show that 59% of the applicators used adjuvants, and the majority of this group used paraffinic oils and/or surfactant mixtures. As a beginning effort to explore the role of adjuvants and herbicides in hormonally based reproductive effects, a prospective, controlled study was performed to analyze blood specimens from three different exposure groups (applicators using herbicides only; applicators using both herbicides and insecticides; and applicators using fumigants in addition to herbicides and insecticides; and a control group composed of other agricultural workers including organic farmers). The applicators and controls were age- and smoking-matched. Study subjects (n = 78) were tested before, during, and after completion of pesticide application season for the effects of pesticide products on hormone levels in the bloodstream. Of the applicator exposure groups examined, only the herbicide group showed significant endocrinologic differences from controls. Free testosterone levels were significantly elevated in post-season measurements (p = 0.032), and follicle-stimulating hormone (FSH) was significantly decreased at the height of the season (p = 0.016) and in the post-season (p = 0.010) as compared to controls. These endocrinologic findings are discussed in terms of their possible relationship to potential endocrine effects of herbicides, herbicide contaminants, and adjuvants. In vitro genotoxicity examination compared four different commercially available surfactant mixtures with 12 different commercial herbicide products, including six different chlorophenoxy herbicides. Only one herbicide yielded a significant dose-response curve. All four adjuvants showed positive dose-response effects. These preliminary data suggest that adjuvants are not inert but are toxicologically active components added to herbicide mixtures. Whether adjuvant toxicant effects are additive or are independent of herbicide effects is poorly understood.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10188198&dopt=Abstract

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