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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

J Pain Symptom Manage. 2002 Jun;23(6):501-9.
Prevalence and treatment of menopausal symptoms among breast cancer survivors.

Harris PF, Remington PL, Trentham-Dietz A, Allen CI, Newcomb PA.

Department of Medicine, University of Wisconsin, Madison, WI, USA.

Women diagnosed with breast cancer often experience early menopause secondary to treatment effects, yet physicians may be reluctant to prescribe hormone replacement therapy (HRT) because of the potential increased risk of recurrence. To assess the burden of menopausal symptoms, HRT use, and alternative treatments in recent breast cancer survivors, a population-based, case-control study was conducted among breast cancer survivors and age-matched controls. Wisconsin women 18-69 years old with a new diagnosis of breast cancer 8-11 months prior to interview (n = 110) and control subjects randomly selected from population lists (n = 73) responded to a standardized telephone questionnaire that elicited information on menopausal symptoms, estrogen and alternative therapies (prescription medications, vitamins, herbal preparations, soy products, acupuncture, chiropractic) used to alleviate symptoms. We used multivariate logistic regression to obtain odds ratios and 95% confidence intervals (CI) for symptoms of menopause, use of estrogen, and use of alternative therapies. Breast cancer survivors were 5.3 (95% CI 2.7-10.2) times more likely to experience symptoms, 25 (95% CI 8.3-100) times less likely to use estrogen, and 7.4 (95% CI 2.5-21.9) times more likely to use alternatives than controls. Soy, vitamin E, and herbal remedies were the most common alternative therapies reported by participants; use was greater in cases compared to controls. Most soy users reported increasing soy products specifically to reduce the chances of a diagnosis of recurrent breast cancer. Among cases, tamoxifen users (n = 62) reported a higher prevalence of symptoms and a higher prevalence of alternative treatments. This is the first population-based survey of menopausal symptoms and treatments that compares breast cancer cases with disease-free controls. Cases are both more likely to experience menopausal symptoms and less likely to use HRT than controls. Instead, cases treat menopausal symptoms with vitamin E and soy products, even though the safety and efficacy of these therapies are unproven. The increased use of soy products in this population has not been previously documented.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12067774&dopt=Abstract

Horm Behav. 2002 Dec;42(4):424-36.
Salivary hormone concentrations in mothers and fathers becoming parents are not correlated.

Berg SJ, Wynne-Edwards KE.

Department of Biology, Queen's University, Kingston, K7L 3N6, Canada.

A time- and date-matched set of saliva samples (N = 229) from nine couples first expecting, and then caring for, their first child were used to test whether hormone changes in the father could be predicted by the hormonal status of the mother. Testosterone, cortisol, and estradiol were quantified from saliva. Neither testosterone nor estradiol concentration was correlated within couples before or after the birth, although there was a positive correlation for cortisol concentration in the mother and father before the birth. As the hormone that might be influenced by chemical signals, that already played a similar role in men and women, and that had been empirically linked to paternal behavior, cortisol concentration was also compared with sex steroid concentrations. The mother's cortisol concentration was positively correlated to the father's testosterone concentration, and the mother's testosterone concentration was positively correlated with the father's cortisol concentration. However, both effects were similar in magnitude to the cortisol to cortisol correlation, and all could parsimoniously be explained by similar responses to a shared environment. Thus, this analysis rejects parallels in peripheral hormone concentrations of estradiol, testosterone, and cortisol in mothers and fathers. However, the available data were not able to test or reject hypotheses about local neuroendocrine homology, nor to control for masking effects of other hormonal demands on men and women, nor to determine the relative importance of shared environment versus mother-father signaling.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12488109&dopt=Abstract

Eur J Intern Med. 2002 Jun;13(4):276-279.
Citrate infusion test in the diagnosis of hypocalcemia due to a mutation in the calcium-sensing receptor gene.

Poppe K, Karmali R, Lissens W, Vanhaelst L, Liebaers I, Fuss M, Velkeniers B.

Department of Endocrinology, Vrije Universiteit Brussel (AZ-VUB), Laarbeeklaan 101, 1090, Brussels, Belgium

The calcium-sensing receptor (Ca-R) is a G-protein-coupled surface receptor that plays a crucial role in calcium homeostasis via parathyroid hormone secretion. Mutations of this receptor can cause a gain in, or loss of, function, leading to hypo- or hypercalcemia, respectively. We report here a family with hypocalcemia in whom a heterozygous missense mutation in exon 4 was demonstrated, predicting a proline to leucine substitution (P221L) in the extracellular part of the Ca-R. Clinical symptoms were limited to fatigue. When serum calcium was further lowered via a citrate infusion, a significant increase in circulating iPTH was observed, although with lower peak values than in normal controls, suggesting a gain in function of the Ca-R. Treatment with calcium supplements and calcitriol led to prohibitive hypercalciuria without normalizing serum calcium. The aims of this case report are: (1) to present a mutation in the Ca-R with a gain in function at a codon where previously loss of function was described, and (2) to suggest that measuring circulating iPTH during a citrate infusion in the presence of familial hypocalcemia is an additional test to diagnose this particular form of hypoparathyroidism.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12067826&dopt=Abstract [PubMed - as supplied by publisher]

Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E50-7.
Regulation of the human brain natriuretic peptide gene by GATA-4.

He Q, Mendez M, LaPointe MC.

Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan 48202, USA.

Brain natriuretic peptide (BNP) is a cardiac hormone constitutively expressed in the adult heart. We previously showed that the human BNP (hBNP) proximal promoter region from -127 to -40 confers myocyte-specific expression. The proximal hBNP promoter contains several putative cis elements. Here we tested whether the proximal GATA element plays a role in basal and inducible regulation of the hBNP promoter. The hBNP promoter was coupled to a luciferase reporter gene (1818hBNPLuc) and transferred into neonatal ventricular myocytes (NVM), and luciferase activity was measured as an index of hBNP promoter activity. Mutation of the putative GATA element at -85 of the hBNP promoter [1818(mGATA)hBNPLuc] reduced activity by 97%. To study transactivation of the hBNP promoter, we co-transfected 1818hBNPLuc with the GATA-4 expression vector. GATA-4 activated 1818hBNPLuc, and this effect was eliminated by mutation of the proximal GATA element. Electrophoretic mobility shift assay showed that an oligonucleotide containing the hBNP GATA motif bound to cardiomyocyte nuclear protein, which was competed for by a consensus GATA oligonucleotide but not a mutated hBNP GATA element. The beta-adrenergic agonist isoproterenol and its second messenger cAMP stimulated hBNP promoter activity and binding of nuclear protein to the proximal GATA element. Thus the GATA element in the proximal hBNP promoter is involved in both basal and inducible transcriptional regulation in cardiac myocytes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12067842&dopt=Abstract

Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E85-93.
Hypothalamic thyrotropin-releasing hormone mRNA responses to hypothyroxinemia induced by sleep deprivation.

Everson CA, Nowak TS Jr.

Department of Neurology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. ceversocw.edu

Sleep deprivation in rats results in progressive declines in circulating concentrations of both total and free thyroxine (T(4)) and triiodothyronine (T(3)) without an expected increase in plasma thyroid-stimulating hormone (TSH). Administration of thyrotropin-releasing hormone (TRH) results in appropriate increases in plasma TSH, free T(4), and free T(3) across experimental days, suggesting deficient endogenous TRH production and/or release. This study examined transcriptional responses related to TRH regulation following sleep deprivation. In situ hybridization was used to detect and quantitate expression of mRNAs encoding prepro-TRH and 5'-deiodinase type II (5'-DII) in brain sections of six rats sleep deprived for 16-21 days, when there was marked hypothyroxinemia, and in sections from animals yoked to the experimental protocol as well as from sham controls. TRH transcript levels in the paraventricular nucleus (PVN) were essentially unchanged at 15-16 days but increased to about threefold control levels in three of four rats sleep deprived for 20-21 days, a change comparable to that typically found in prolonged experimental hypothyroidism. There was no evidence for suppression of 5'-DII mRNA levels, which would be a sign of T(3) feedback downregulation of neurons in the PVN. A failure to increase serum TSH in response to hypothyroxinemia and to increased prepro-TRH mRNA expression indicates that alterations in posttranscriptional stages of TRH synthesis, processing, or release likely mediate the central hypothyroidism induced by sleep deprivation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12067847&dopt=Abstract

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