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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

Eur J Pharmacol. 1999 Mar 19;369(2):195-203.
Acute hemodynamic and renal effects of adrenomedullin in rats with aortocaval shunt.

Willenbrock R, Pagel I, Krause EG, Scheuermann M, Dietz R.

Franz Volhard Clinic at the Max Delbruck Center for Molecular Medicine, University Hospital Charite, Humboldt University of Berlin, Germany. willenbrocvk-berlin.de

Heart failure is characterized by increased vascular resistance and water retention. Adrenomedullin is a peptide hormone with vasodilating and diuretic properties whose efficacy in heart failure has not been well established. We used an aortocaval shunt model of moderate heart failure in rats and infused increasing doses of adrenomedullin, both as bolus injections and 20-min infusions. In controls, a clear dose-dependent 4.8+/-1.0 to 13.6+/-2.3 mm Hg decrease in arterial blood pressure was observed after injection of 1 microg to 30 microg of adrenomedullin. In rats with aortocaval shunt, the hypotensive responses were significantly diminished. The urine flow rate, which was diminished at baseline in rats with aortocaval shunt, was increased and normalized by adrenomedullin administration. The glomerular filtration rate increased after infusion of adrenomedullin (0.5 microg/kg min(-1)) from 2.37+/-0.25 to 3.47+/-0.43 ml/min (P<0.01) in controls and from 1.79+/-0.33 to 2.58+/-0.49 (P<0.05) in rats with aortocaval shunt. Similarly, renal blood flow was significantly increased by adrenomedullin in both groups. Our results indicate a beneficial effect of adrenomedullin on renal function in rats with aortocaval shunt. These data suggest that adrenomedullin might be of potential therapeutic value in heart failure, without inordinately decreasing blood pressure.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10206179&dopt=Abstract

zc5.so-net.ne.jp

PURPOSE: To identify characteristic features of growth hormone (GH)-producing pituitary adenomas. MATERIALS AND METHODS: A total of 174 pathologically proven pituitary adenomas were evaluated retrospectively on magnetic resonance (MR) images to determine the signal intensity (on T2-weighted images), maximum diameter, and amount of suprasellar and infrasellar extension. For microadenomas, sellar depth was also measured. GH-producing adenomas were classified at histologic evaluation as densely or sparsely granulated. Specimens from 38 adenomas were stained to assess the amounts of fibrous tissue, iron, and amyloid they contained. Results were correlated with the size and hormonal activity of adenomas by using the chi2, unpaired t, and Mann-Whitney U tests. RESULTS: Among 174 pituitary adenomas, 42 were GH-producing adenomas. Of these, 16 were densely granulated, and 24 were sparsely granulated (two histologic specimens were lost). Signal intensity was evaluated among 153 adenomas. On T2-weighted MR images, hypointensity was seen more commonly in adenomas that produced GH (16 of 40 cases [40%]; P <.001) than in those that did not; hypointensity was nearly exclusive to densely granulated GH-producing adenomas. The amounts of amyloid, fibrous tissue, and iron contained in adenomas demonstrated little relationship with signal intensity. Average suprasellar extension was significantly smaller in adenomas that produced GH (-0.8 mm) than in those that did not (5.3 mm) (P <.001). GH-producing adenomas tended to demonstrate infrasellar extension rather than suprasellar extension. Average sellar depth associated with GH-producing microadenomas (13.3 mm) was significantly greater than for non-GH-producing microadenomas (9.7 mm; P <.001). CONCLUSION: Characteristic features regarding growth direction and T2 signal intensity can be identified for GH-producing adenomas. RSNA, 2003.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819334&dopt=Abstract

Curr Opin Rheumatol. 2003 Jul;15(4):464-8.
Hormone therapy: evolving concepts.

Hendrix SL.

Women's Health Initiative, Wayne State University School of Medicine, Hutzel Women's Hospital, Detroit, Michigan 48201, USA. shendried.wayne.edu

OBJECTIVE: To review the medical literature published in 2002 regarding menopausal hormone therapy and its impact on clinical practice. METHODS: A literature search was performed using MEDLINE with the keywords of menopause, sex steroids, and hormone replacement therapy. Randomized clinical trials were reviewed. An evidence-based review is presented. RESULTS: Menopausal hormone therapy has undergone radical change since the publication of the Women's Health Initiative randomized prospective trial of combined estrogen plus progestin therapy for disease prevention. After a mean of 5.2 years of follow-up, the E + P versus placebo trial of 16,608 women was stopped because the health risks of taking E + P exceeded the benefits. An increase in breast cancer risk, coupled with an adverse trend in overall risk-benefit ratio, reached the preset stopping boundaries. In addition, there was an increased risk of nonfatal myocardial infarction, stroke, and pulmonary embolism. The decreased risks seen for osteoporotic fracture and colorectal cancer were outweighed by the above risks. The FDA has required mandatory label changes for all hormone products based on these findings. The Women's Health Initiative found that treatment with estrogen plus progestin for up to 5 years is not beneficial overall. There is early harm for coronary heart disease, continuing harm for stroke and venous thromboembolism, and increasing harm for breast cancer. This risk-benefit profile is not consistent with a viable intervention for primary prevention of chronic diseases in postmenopausal women. Menopausal hormone therapy should be reserved for women with moderate to severe vasomotor symptoms. CONCLUSIONS: In the past 20 years, menopause has become a household word, with much better understanding of its consequences. The growing numbers of menopausal women and clinical trials have coincided to draw increasing attention to the perimenopausal and menopausal years. Better studies of older therapies and the expanded number of new choices today, with more in development and evaluation, have complicated provider and patient choices but greatly improved the potential for effective intervention.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819476&dopt=Abstract [PubMed - in process]

Blood Press Monit. 2003 Apr;8(2):57-61.
Hormone replacement therapy does not affect 24-h ambulatory blood pressure in healthy non-smoking postmenopausal women.

Mills PJ, Farag NH, Matthews S, Nelesen RA, Berry CC, Dimsdale JE.

aDepartments of Psychiatry.

OBJECTIVEControversies surrounding the physiological effects of hormone replacement therapy (HRT) currently lie at the forefront of medicine. Important interindividual factors that affect blood pressure, such as smoking, body mass and sodium intake, may account for the conflicting findings seen in studies examining the effects of HRT on blood pressure.DESIGNThe study was a randomized, double-blind, placebo-controlled trial.METHODSThe effect of combination HRT and estrogen-only replacement therapy (ERT) on ambulatory blood pressure was examined in a sample of 46 healthy, normotensive, non-smoking, non-obese postmenopausal women between 45 and 65 years of age. Twenty-four hour urinary sodium excretion was examined prior to and following treatment. The women were randomized to 3 months' treatment with HRT, ERT or placebo.RESULTSAfter treatment, there were no significant effects of either HRT or ERT on daytime or night-time systolic or diastolic blood pressure. Sodium excretion was similar across the groups. There were no effects of treatment on night-time blood pressure dipping.CONCLUSIONSThe findings from this prospective treatment study support the conclusion that HRT has no significant effect on daytime or night-time blood pressure in a sample of healthy, non-smoking postmenopausal women.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819556&dopt=Abstract [PubMed - in process]

Diabetologia. 2003 Jul;46(7):917-25. Epub 2003 Jun 18.
Direct and indirect effects of amino acids on hepatic glucose metabolism in humans.

Krebs M, Brehm A, Krssak M, Anderwald C, Bernroider E, Nowotny P, Roth E, Chandramouli V, Landau BR, Waldhausl W, Roden M.

Division of Endocrinology and Metabolism, Department of Internal Medicine III, University of Vienna Medical School, Wahringer Gurtel 18-20, 1090 Vienna, Austria.

AIM/HYPOTHESIS: The study was designed to examine the contribution of direct (substrate-mediated) and indirect (hormone-mediated) effects of amino acids on hepatic glucose metabolism in healthy men. METHODS: The protocols were: (i) CON+S (n=7): control conditions with somatostatin to inhibit endogenous hormone release resulting in fasting plasma concentrations of amino acids, insulin (approximately 28 pmol/l) and glucagon (approximately 65 ng/l), (ii) AA+S ( n=7): amino acid infusion-fasting insulinaemia-fasting glucagonaemia, (iii) GLUC+S ( n=6): fasting amino acids-fasting insulinaemia-hyperglucagonaemia (approximately 99 ng/l) and (iv) AA-S (n=5): amino acid infusion without somatostatin resulting in amino acid-induced hyperinsulinaemia (approximately 61 pmol/l)-hyperglucagonaemia (approximately 147 ng/l). Net glycogenolysis was calculated from liver glycogen concentrations using (13)C nuclear magnetic resonance spectroscopy. Total gluconeogenesis (GNG) was calculated by subtracting net glycogenolysis from endogenous glucose production (EGP) which was measured with [6,6-(2)H(2)]glucose. Net GNG was assessed with the (2)H(2)O method. RESULTS: During AA+S and GLUC+S, plasma glucose increased by about 50% (p<0.01) due to a comparable rise in EGP. This was associated with a 53-% (p<0.05) and a 65% increase (p<0.01) of total and net GNG during AA+S, whereas net glycogenolysis rose by 70% (p<0.001) during GLUC+S. During AA-S, plasma glucose remained unchanged despite nearly-doubled (p<0.01) total GNG. CONCLUSION/INTERPRETATION: Conditions of postprandial amino acid elevation stimulate secretion of insulin and glucagon without affecting glycaemia despite markedly increased gluconeogenesis. Impaired insulin secretion unmasks the direct gluconeogenic effect of amino acids and increases plasma glucose.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12819901&dopt=Abstract [PubMed - in process]

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