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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 Biol Chem. 2003 Aug 29;278(35):32899-904. Epub 2003 Jun 18.
Regulation of proglucagon transcription by activated transcription factor (ATF) 3 and a novel isoform, ATF3b, through the cAMP-response element/ATF site of the proglucagon gene promoter.

Wang J, Cao Y, Steiner DF.

Department of Biochemistry and Molecular Biology, University of Chicago, Illinois 60637, USA.

Glucagon, the second major glucose-regulated hormone in the control of glucose homeostasis, functions as a counter-regulator to insulin and is specifically produced by the pancreatic alpha cells. Its excessive biosynthesis and secretion is associated with diabetes mellitus. The expression of the proglucagon gene has been demonstrated to be regulated by a cAMP-dependent pathway through cAMP-response element-binding protein (CREB) and possibly other transcription factors bound to its cAMP-response element (CRE)/activated transcription factor (ATF) site. Elsewhere we have shown that ATF3, a member of the ATF/CREB subfamily of the basic leucine zipper domain proteins, is expressed predominantly in the alpha cells of the pancreatic islets. In our attempts to further dissect the role of ATF3 proteins in alpha cells, we have identified and characterized a novel alternatively spliced form, ATF3b, and have compared the specific binding ability of ATF3 and ATF3b on the CRE/ATF motif of the proglucagon promoter. Our findings indicate the existence of a novel mechanism by which the transcription of the proglucagon gene is regulated in response to cAMP signals, in addition to CREB and in relation to glucose fluctuations in pancreatic alpha cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12815047&dopt=Abstract [PubMed - in process]

J Physiol. 2003 Sep 1;551(Pt 2):721-8. Epub 2003 Jun 18.
Acute and chronic effects of oestrogen on endothelial tissue-type plasminogen activator release in postmenopausal women.

Hoetzer GL, Stauffer BL, Irmiger HM, Ng M, Smith DT, DeSouza CA.

Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, CO 80309 and Divisions of Cardiology.

The capacity of vascular endothelium to locally release tissue-type plasminogen activator (t-PA) represents an important endogenous defence mechanism against intravascular fibrin deposition and thrombosis. We determined the influence of chronic and acute oestrogen administration on endothelial t-PA release in postmenopausal women. Sixty-three healthy postmenopausal women were studied: 31 non-users (age 58 +/- 1 years) and 32 users of hormone replacement therapy, including oestrogen alone (ORT: 62 +/- 2 years; n = 15) and in combination with progesterone (HRT: 57 +/- 1 years; n = 17). Net endothelial t-PA release was determined in vivo, in response to intrabrachial infusions of bradykinin and sodium nitroprusside. To examine the acute effects of oestrogen on endothelial t-PA release, bradykinin and sodium nitroprusside dose-response curves were repeated in the presence of 17 beta-oestradiol in 20 of the 31 non-users. Net endothelial release of t-PA was ~30 % higher (P < 0.01) in women taking ORT (from 2.0 +/- 1.0 to 83.6 +/- 9.2 ng (100 ml tissue)-1 min-1) compared with those taking HRT (from 1.4 +/- 0.4 to 63.5 +/- 5.6 ng (100 ml tissue)-1 min-1) and those not taking supplementation (1.0 +/- 0.7 to 63.0 +/- 4.7 ng (100 ml tissue)-1 min-1). Intra-arterial infusion of 17 beta-oestradiol significantly potentiated bradykinin-induced t-PA release. Net endothelial release of t-PA was ~45 % higher (P < 0.01) after (from 1.0 +/- 0.8 to 87.4 +/- 9.9 ng (100 ml tissue)-1 min-1) versus before (1.2 +/- 0.6 to 60.8 +/- 5.6 ng (100 ml tissue)-1 min-1) acute 17 beta-oestradiol administration. Our results suggest that oestrogen has a direct modulatory effect on the capacity of the endothelium to release t-PA in healthy postmenopausal women. However, progesterone appears to oppose the favourable influence of oestrogen on endothelial fibrinolytic capacity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12815179&dopt=Abstract [PubMed - in process]

Methods Cell Sci. 2002;24(1-3):61-4.
Androgen receptor expression in archival human breast tumors.

Arya P, Andritsch IH, Krishan A.

Division of Experimental Therapeutics, University of Miami Medical School, Miami, FL 33101, USA. poonam_aryotmail.com

Hormone receptors play a major role in growth and hormonal therapy of breast and prostate tumors. Quantitative results from the ligand binding assays cannot determine heterogeneity in receptor expression nor can they discriminate between expression of the stromal and the tumor cells. Availability of antibodies to hormone receptors has led to the development of immunohistochemistry as a standard method for monitoring of hormone receptor expression under a microscope. However, this method is based on examination of a small number of cells. Laser flow cytometry has been extensively used for monitoring of receptor expression in human liquid tumors. As most of the hormone receptor expression is nuclear, we have developed methods for flow cytometric analysis of receptor expression in nuclei isolated from enzyme treated paraffin sections. The present report based on gated analysis of androgen receptor expression in nuclei isolated from archival formalin fixed/paraffin embedded breast tumors shows that receptor expression in aneuploid sub-populations is greater than that of the diploid cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12815292&dopt=Abstract [PubMed - in process]

Curr Opin Nephrol Hypertens. 2003 Jul;12(4):349-55.
Extracellular calcium-sensing receptors in the parathyroid gland, kidney, and other tissues.

Quarles LD.

PURPOSE OF REVIEW The discovery of the extracellular calcium-sensing receptor, CasR has broadened our understanding of calcium homeostasis and led to the development of new pharmacological agents, calcimimetics, for treating hyperparathyroidism. In the present review, I discuss the function of CasR as well as provide evidence for the presence of additional calcium-sensing mechanisms in the skeleton and possibly other tissues.RECENT FINDINGS Inactivating and activating mutations of the CasR respectively cause hereditary hyperparathyroidism, and demonstrate the predominant role of the CasR in controlling parathyroid gland function. Calcimimetics, which increase the sensitivity of CasR to extracellular calcium have been developed to treat secondary and primary hyperparathyroidism. In recent clinical trials in patients with end stage kidney disease, the calcimimetic cinacalcet suppressed parathyroid hormone to a greater degree than conventional therapy with vitamin D analogues without causing hypercalcemia or hyperphosphatemia. CasR receptor also has functions in other tissues, including regulation of renal calcium excretion and calcitonin secretion by thyroidal C-cells, but the presence of redundant sensing mechanisms for extracellular calcium in other tissues, including bone, confounds the assessment of the receptor's function at these sites. Mouse genetic approaches have so far failed to identify any essential, non-redundant role for the calcium-sensing receptor in regulating chondrogenesis or osteogenesis, and have failed to establish a function for the protein outside of the parathyroid gland, kidney, and thyroidal C-cells. Rather, there is evidence for other putative calcium sensing receptor-like mechanisms in osteoblasts that remain to be identified.SUMMARY Sensing of extracellular calcium by CasR is important in regulating calcium homeostasis, but CasR may have vestigial function in various tissues where it is expressed in low abundance. The relative importance of CasR and the novel calcium-sensing mechanisms in mediating response to extracellular calcium in many of these tissues remain to be determined.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12815330&dopt=Abstract [PubMed - in process]

Curr Opin Nephrol Hypertens. 2003 Jul;12(4):363-71.
Involution of the parathyroid glands after renal transplantation.

Lewin E.

PURPOSE OF REVIEW The aim of this article is to review the most recent development on the reversibility of secondary hyperparathyroidism after kidney transplantation. A successful kidney transplantation is expected to correct the abnormalities of mineral metabolism that during uremia lead to secondary hyperparathyroidism. Kidney transplanted patients might, however, still present persistent hyperparathyroidism and hypercalcemia. In order to improve the understanding of the fate of secondary hyperparathyroidism after kidney transplantation an experimental model on reversal of uremia by an experimental isogenic kidney transplantation was established.RECENT FINDINGS In recent years clinical and experimental studies have suggested an important role of the calcium sensing receptor and vitamin D receptor in the parathyroid glands for the abnormal regulation of parathyroid hormone secretion and parathyroid cell proliferation in uremia. The expression of these receptors is diminished in the parathyroid glands of uremic patients with severe secondary hyperparathyroidism and in experimental models of uremic rats on a high phosphorus diet. Secondary hyperparathyroidism is reversed rapidly by reversal of uremia by an experimental kidney transplantation in the rat. Despite normalization of the circulating parathyroid hormone levels, diminished expression of parathyroid calcium sensing and vitamin D receptor messenger RNA persist. Implantation of several isogenic parathyroid glands into a single rat results in a transient, short lasting period of hypercalcemia followed by normalization of parathyroid hormone and plasma calcium levels, despite persistent increased parathyroid mass.SUMMARY Advances are clearly being made in the understanding of the molecular mechanisms of disturbed parathyroid function in uremia. How the hyperplastic uremic parathyroid glands are regulated after reversal of uremia by kidney transplantation remains, however, to be elucidated.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12815332&dopt=Abstract [PubMed - in process]

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as hair loss. The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

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