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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

Arch Biochem Biophys. 1999 Mar 15;363(2):219-26.
Vitamin D receptor interacts with DnaK/heat shock protein 70: identification of DnaK interaction site on vitamin D receptor.

Swamy N, Mohr SC, Xu W, Ray R.

Vitamin D Laboratory, Boston University School of Medicine, Boston, Massachusetts, 02118, USA.

Vitamin D receptor (VDR) regulates the expression of vitamin D-dependent genes upon binding to its cognate ligand, 1alpha, 25-dihydroxyvitamin D3 (1,25(OH)2D3). This process represents a complex interaction of ligand-bound VDR with nuclear proteins like retinoid X receptor, nuclear accessory factors, and regulatory elements of the target gene. Expression of full-length VDR in Escherichia coli revealed that VDR binds DnaK, a member of heat-shock protein (Hsp) family, with high affinity. By systematic N-terminal truncation of VDR, the interaction site of DnaK on VDR was localized within a 17-amino-acid segment (105-122) representing the "hinge region" between the DNA-binding and hormone-binding domains of VDR. The putative DnaK-binding site was further localized between residues 105 to 109 of VDR by using binding-energy-minimization studies. The interaction of DnaK with VDR did not influence the binding of 1,25(OH)2D3 or nuclear accessory factor(s) to VDR. Furthermore, bovine brain Hsp 70, similar to DnaK, interacted with VDR-ligand-binding domain (105-427). These results suggest that DnaK/Hsp 70 may interact with VDR prior to the activation of the latter by 1,25(OH)2D3-binding. 1999 Academic Press.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068443&dopt=Abstract

Lik Sprava. 1998 Oct-Nov;(7):61-3.
[The level of sex steroid hormones in the blood of women with duodenal peptic ulcer]

[Article in Russian]

Petrov EE.

The content was studied of estriol, estradiol, progesterone, and testosterone in the blood of 30 women suffering from duodenal ulcer (DU). Of these, 15 female subjects were at reproductive age (with their menstrual function unimpaired), other 15 were in menopause. The results were compared with those obtained in essentially healthy women at similar ages. It is ascertained that in DU there take place changes in the ovarian hormonal function, that are especially pronounced in those female persons in the menopause (the progesterone level is decreased, that of testosterone strikingly increased). In women at reproductive age the relation of the revealed changes to DU is less convincing and is recordable in but a small proportion of the patients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10050461&dopt=Abstract

Eur J Histochem. 1998;42(4):259-70.
Subcellular localization of estradiol receptor in MCF7 cells studied with nanogold-labelled antibody fragments.

Kessels MM, Qualmann B, Thole HH, Sierralta WD.

Max-Planck-Institut fur experimentelle Endokrinologie, Hannover, Germany.

Ultrastructural localization studies of estradiol receptor in hormone-deprived and hormone-stimulated MCF7 cells were done using F(ab') fragments of three different antibodies (#402, 13H2, HT277) covalently linked to nanogold. These ultra-small, non-charged immunoreagents, combined with a size-enlargement by silver enhancement, localized estradiol receptor in both nuclear and cytoplasmic areas of non-stimulated target cells; stimulation with the steroid induced a predominantly nuclear labelling. In the cytoplasm of resting cells, tagging was often observed at or in the proximity of stress fibers. In the nucleus a large proportion of receptor was found inside the nucleolus, specially with the reagent derived from antibody 13H2. We postulate that different accessibilities of receptor epitopes account for the different labelling densities observed at cytoskeletal elements and the nucleoli.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068898&dopt=Abstract

Exp Cell Res. 1999 Mar 15;247(2):399-409.
Adipocyte-epithelial interactions regulate the in vitro development of normal mammary epithelial cells.

Zangani D, Darcy KM, Shoemaker S, Ip MM.

Grace Cancer Drug Center, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, New York, 14263, USA.

Mammary epithelial organoids (MEO), isolated from pubescent rats, were cultured within a reconstituted basement membrane in transwell inserts, in the presence or absence of mature mammary adipocytes in the lower well. This system allowed for free medium exchange between the two compartments, without direct cell-to-cell contact. When cultured in serum-free medium supplemented with insulin, prolactin, hydrocortisone, progesterone, and various epidermal growth factor (EGF) concentrations, mammary adipocytes did not affect epithelial cell growth, but enhanced epithelial differentiation. Casein and lipid accumulations were monitored as indicators of functional differentiation of MEO. Mammary adipocytes significantly enhanced casein and lipid accumulation within the MEO, independently of EGF concentration. Furthermore, adipocytes induced MEO to preferentially undergo alveolar morphogenesis, inhibited squamous outgrowth, and increased lumen size. These findings demonstrate that morphological and functional differentiation of mammary epithelial cells is profoundly enhanced by the adipose stroma and that these effects are mediated by diffusible paracrine factors. This new model can be exploited in future studies to define the mechanisms whereby hormones and growth factors regulate mammary gland development and carcinogenesis. Moreover, it could complement in vivo reconstitution/transplantation studies, which are currently employed to evaluate the role of specific gene deletions in the regulation of mammary development. 1999 Academic Press.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066368&dopt=Abstract

Eur J Med Res. 1999 Feb 25;4(2):78-84.
Investigations of bone turnover in renal osteopathy.

Muller A, Stein G, Lehmann G, Hein G.

Rheumatologie und Osteologie, Klinik fur Innere Medizin IV, Rheumalabor, Erlanger Allee 101, 07740 JENA, Germany. i5admolkim.med.uni-jena.de.

The renal bone disease which develops in chronic renal failure (CRF) is not an uniform disorder. Histomorphometry is accepted to be the best method for characterising the state of disease. The purpose of this study was to evaluate the suitability of pyridinium crosslinks in serum and urine as indicators of bone degradation processes. Patients with CRF had significantly higher Pyridinoline (Pyd) and Deoxypyridinoline (Dpyd) levels in serum and urine compared to normal controls except the urinary excretion in the subgroup of glomerulonephritis. A correlation was found between the serum levels of crosslinks and those of both creatinine and parathormone. The Pyd and Dpyd serum levels in patients under dialysis treatment were significantly higher than those of normal controls. With regard to bone turnover urinary crosslink measurements are of minor importance in CRF. In contrast, serum measurements could be helpful in revealing bone resorption both in patients with CRF and those under dialysis treatment.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066644&dopt=Abstract

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DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.

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