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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

Fertil Steril. 2003 Feb;79(2):439-41.
Successful pregnancies after combined pentoxifylline-tocopherol treatment in women with premature ovarian failure who are resistant to hormone replacement therapy.

Letur-Konirsch H, Delanian S.

Fertility Center, Department of Obstetrics and Assisted Reproductive Techniques, Institut Mutualiste Montsouris, Paris, France. helene.letumm.fr

OBJECTIVE: To determine whether treatment with combined pentoxifylline (PTX) and tocopherol (Vit.E) can improve uterine parameters in hormonal replacement therapy (HRT)-resistant women with premature ovarian failure (POF), for whom the outcome of assisted reproductive technology is usually negative. We previously reported that uterine radiation-induced fibrosis is reversible by combined PTX-Vit.E treatment. DESIGN: Case report. SETTING: Volunteer participants in an oocyte donation (OD) program in a French public hospital. PATIENT(S): Three women with POF (ages 36 +/- 2 years) using HRT exhibited uterine hormonoresistance, although they had high E(2) plasma levels. Their mean endometrial thickness was 4.9 mm, and they had an echogenic endometrium and thin uterine crosses. INTERVENTION(S): Between May 1998 and April 1999, treatment consisted of 800 mg of PTX combined with 1,000 IU of Vit.E daily for at least 9 months. MAIN OUTCOME MEASURE(S): Endometrial thickness, echogenicity, and pulsatility index of the uterine arteries, assessed by ultrasound and Doppler before and after treatment, and embryo implantation by IVF-OD. RESULT(S): PTX-Vit.E treatment was well tolerated and induced improvements, as mean edematous endometrial thickness increased to 7.4 mm, with nice uterine crosses. Three frozen-thawed ETs resulted in two viable pregnancies. CONCLUSION(S): In women with POF and uterine resistance to HRT, combined PTX-Vit.E reduces fibroatrophic uterine lesions and improves the uterine response to HRT, thus allowing embryo implantation and ongoing pregnancy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12568863&dopt=Abstract

Endocrinology. 1999 Mar;140(3):1423-31.
Autocrine regulation of gonadotropin-releasing hormone secretion in cultured hypothalamic neurons.

Krsmanovic LZ, Martinez-Fuentes AJ, Arora KK, Mores N, Navarro CE, Chen HC, Stojilkovic SS, Catt KJ.

Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

Episodic hormone secretion is a characteristic feature of the hypothalamo-pituitary-gonadal system, in which the profile of gonadotropin release from pituitary gonadotrophs reflects the pulsatile secretory activity of GnRH-producing neurons in the hypothalamus. Pulsatile release of GnRH is also evident in vitro during perifusion of immortalized GnRH neurons (GT1-7 cells) and cultured fetal hypothalamic cells, which continue to produce bioactive GnRH for up to 2 months. Such cultures, as well as hypothalamic tissue from adult rats, express GnRH receptors as evidenced by the presence of high-affinity GnRH binding sites and GnRH receptor transcripts. Furthermore, individual GnRH neurons coexpress GnRH and GnRH receptors as revealed by double immunostaining of hypothalamic cultures. In static cultures of hypothalamic neurons and GT1-7 cells, treatment with the GnRH receptor antagonist, [D-pGlu1, D-Phe2, D-Trp(3,6)]GnRH caused a prominent increase in GnRH release. In perifused hypothalamic cells and GT1-7 cells, treatment with the GnRH receptor agonist, des-Gly10-[D-Ala6]GnRH N-ethylamide, reduced the frequency and increased the amplitude of pulsatile GnRH release, as previously observed in GT1-7 cells. In contrast, exposure to the GnRH antagonist analogs abolished pulsatile secretion and caused a sustained and progressive increase in GnRH release. These findings have demonstrated that GnRH receptors are expressed in hypothalamic GnRH neurons, and that receptor activation is required for pulsatile GnRH release in vitro. The effects of GnRH agonist and antagonist analogs on neuropeptide release are consistent with the operation of an ultrashort-loop autocrine feedback mechanism that exerts both positive and negative actions that are necessary for the integrated control of GnRH secretion from the hypothalamus.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067871&dopt=Abstract

Endocrinology. 1999 Mar;140(3):1183-91.
Possible interactions between gonadotrophs and somatotrophs in the pituitary of tilapia: apparent roles for insulin-like growth factor I and estradiol.

Melamed P, Gur G, Rosenfeld H, Elizur A, Yaron Z.

Department of Zoology, Tel-Aviv University, Ramat Aviv, Israel.

The unique organization of the teleost pituitary, in which cells are grouped according to their characteristic hormone, makes this a suitable model for studying pituitary paracrine interactions. In a number of fish, including tilapia, there are variations in the circulating levels of the gonadotropins and GH, which are elevated during the reproductive season, suggesting interactions between the reproductive and growth axes. The aim of this study was to investigate paracrine interactions between the gonadotrophs and somatotrophs in the tilapia pituitary. Initially, dispersed pituitary cells were separated on a density gradient in which the gonadotrophs were found in the least dense fractions, and the somatotrophs were concentrated in the densest fraction. After 4 days in culture, cells in the least dense fractions showed characteristic cytoplasmic extensions not seen in the somatotrophs, which appeared small and failed to form aggregates; somatotrophs were found, however, attached to other non-GH cells. Staining of the nuclei with 4,6-diaminidino-2-phenyl-dihydrochloride revealed that the isolated somatotrophs had undergone nuclear condensation and fragmentation typical of apoptosis. Addition of either estradiol or human recombinant insulin-like growth factor I (IGF-I; 10 nM) to the somatotroph cultures increased the number of cell aggregates and reduced the number of condensed or fragmented nuclei. Immunocytochemical studies on pituitary sections revealed IGF-I immunoreactivity in regions of the proximal pars distalis that stain with gonadotropin IIbeta antisera and also in regions of the rostral pars distalis characteristic of corticotrophs; immunoreactive IGF-I was never seen in the region of the somatotrophs. Incubation of cells from the different fractions with testosterone (10 nM; 24 h) revealed that cells of the least dense fractions, which were rich in gonadotrophs, possessed aromatizing ability, which was absent in the somatotroph-enriched fraction. These results suggest that estradiol and IGF-I, both generated from cells other than the somatotrophs, may exert antiapoptotic effects and thus possibly control the size of this population of cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067842&dopt=Abstract

Endocrinology. 1999 Mar;140(3):1054-9.
Cloning of thyrotropin-releasing hormone precursor and receptor in rat thymus, adrenal gland, and testis.

Montagne JJ, Ladram A, Nicolas P, Bulant M.

Laboratoire de Bioactivation des Peptides, Institut J. Monod, Paris, France.

TRH is a hypophysiotropic peptide that acts mainly via the hypothalamic-pituitary-thyroid axis, but TRH immunoreactivity is also detected in several peripheral tissues. PCR with two pairs of primers enabling amplification of three fragments of TRH complementary DNA (cDNA) was used to demonstrate local production of TRH. Products of the expected size were detected in the testis, adrenal gland, lymphoid organs, thymus, and spleen. The amplified cDNA fragments were cloned and sequenced to show that the TRH gene is expressed in the thymus, spleen, and adrenal gland. Competitive RT-PCR showed that the TRH messenger RNA content of the testis was about one third that of the hypothalamus, whereas the adrenal gland contained 2% and the thymus 6%. HPLC analysis of thymus and spleen extracts showed small amounts of TRH, with a particular processing pattern of pro-TRH in lymphoid organs. The expression of the TRH receptor gene in peripheral organs was investigated to determine whether TRH had an autocrine or a paracrine action. cDNA fragments that encompassed the coding region of the receptor were identified in the testis, adrenal gland and thymus. No signal was detected in the spleen. These findings indicate that TRH may have a biological activity in extrapituitary organs and may act locally in the testis, adrenal gland, and thymus.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067825&dopt=Abstract

Clin Nephrol. 1999 Feb;51(2):83-91.
Differential kinetics of circulating angiotensin IV and II after treatment with angiotensin II type 1 receptor antagonist and their plasma levels in patients with chronic renal failure.

Shibasaki Y, Mori Y, Tsutumi Y, Masaki H, Sakamoto K, Murasawa S, Maruyama K, Moriguchi Y, Tanaka Y, Iwasaka T, Inada M, Matsubara H.

Department of Medicine II, Kansai Medical University, Moriguchi, Osaka, Japan.

BACKGROUND: Angiotensin II (Ang II) C-terminal hexapeptide (referred to as Ang IV) possesses the characteristics of a real hormone with specific receptors and biological effects. Clinical application of Ang II type 1 receptor (AT1-R) antagonists cause an increase in plasma Ang II level, which may result in enhanced production of Ang IV. PATIENTS AND METHODS: In this study, we measured plasma Ang IV and Ang II levels in patients with chronic renal failure (CRF), and also examined the changes in Ang IV and Ang II levels after administration of an ATI-R antagonist. RESULTS: Ang II and Ang IV levels in CRF patients untreated with hemodialysis (n = 16) were 15.8+/-3.6 and 6.0+/-1.1 pg/ml, respectively, which did not differ significantly from Ang II (20.6+/-2.4) and Ang IV levels (8.6+/-1.1) in normal controls (n = 23). The ratio of Ang IV to Ang II was 38%, similar to that in the controls (41%). Ang II or Ang IV levels in CRF patients treated with hemodialysis (n = 12) were also similar to the control values. Ang IV levels had a significant correlation with Ang II levels (r = 0.59). When hypertensive patients were treated with an AT1-R antagonist candesartan for 7 days, Ang II and Ang IV levels were increased 5.5- and 4.1-fold relative to the control levels, respectively. Ang II levels 28 and 56 days after treatment were significantly lower than those 7 days after treatment, whereas Ang IV levels did not differ significantly from those 7 days after treatment. Similar differential kinetics in Ang II and Ang IV levels after long-term (90 days) treatment with an AT1-R antagonist was also confirmed in experiments using rats. Significant decrease in blood pressure continued during long-term treatment with an AT1-R antagonist. CONCLUSION: These findings demonstrated that plasma Ang IV levels in patients with CRF did not differ significantly from those in normal subjects, and that treatment with an AT1-R antagonist caused marked increases in both Ang II and Ang IV levels. In contrast, during long-term treatment plasma Ang II levels were more rapidly decreased than Ang IV levels, suggesting longer-lasting enhancement of the action of Ang IV rather than that of Ang II after treatment with an AT1-R antagonist.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10069643&dopt=Abstract

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