Gluteal region morphology: The effect of the weight gain and aging

WOS: 000175778400012PubMed: 12016499The gluteal region is an important secondary sexual character itself and it has its place in the concept of the beauty in all communities, Interestingly, as far as we know, there is not any previous study addressing gluteal region morphology in an objective way in the aesthetic surgery literature. The aim of this study was to define the changes of the gluteal region morphology with aging and weight gain. Beside body weight. a total of five distances between predetermined anatomic points in gluteal region were measured on randomly selected 115 female volunteers, with their age ranging from 17 to 48 years (mean 22.7). All the records were analyzed by a correlation matrix using computer-based SPSS 7.5 program. As women grow older, the width of the gluteal region decreases and the gluteal sulcus elongates laterally and inferiorly. Contrary to aging, with weight gain the gluteal region becomes wider as the gluteal sulcus gets shorter. Although the subject does not sound new, our study is the first, documenting the changes in morphology of the gluteal region in relation to weight gain and aging in an objective way

The immunohistochemical approach to determine the origin and possible function of the juxtaoral organ in dogs

ERDOGAN, DILEK/0000-0002-9981-9475; bahcelioglu, meltem/0000-0001-5279-3450; ERDOGAN, DILEK/0000-0002-1930-3584WOS: 000233312300005PubMed: 16228050Objective: In this study, we applied immunohistochemical techniques on the functionally little known organ of Chievitz (juxtaoral organ [JOO]) in dogs to determine its origin and possible function. Methods: The term abortive materials of 6 Doberman dogs were used for experimental procedures in July 2002 to June 2003 at Gazi University Faculty of Medicine, Ankara, Turkey, after routine light microscopic tissue preparation, the sections were stained with Masson's trichrome stain. In order to elucidate the function -related origin of the organ, we used epidermal growth factor (EGF-r), transforming growth factor (TGF-alpha) and nerve growth factor (NGF-beta) immunohistochemical stains. Results: We observed a very strong and 'widespread immunoreactivity of EGF-r and TGF-a on simple squamous capsular cells. We detected nerve growth factor-beta positivity in granular form both in simple squamous capsular cells and in neighboring connective tissue. However, we did not detect EGF-r reactivity on parenchymal cells except a weak immunoreactivity on central ones. We noticed transforming growth factor-a in most of the parenchymal cells while we observed NGF-beta strongly in all the parenchymal cells. Conclusion: These results may point out that the JOO may be of mesothelial or epithelial origin. Having NGF-alpha. positive granules and close relationship with blood vessels may imply a neurosecretory function. We believe that our study may add new perspectives to the function of the JOO

Distribution, functional role, and signaling mechanism of adrenomedullin receptors in the rat adrenal gland

Adrenomedullin (ADM) is a hypotensive peptide, highly expressed in the mammalian adrenal medulla, which belongs to a peptide superfamily including calcitonin gene-related peptide (CGRP) and amylin. Quantitative autoradiography demonstrated the presence of abundant [125I]ADM binding sites in both zona glomerulosa (ZG) and adrenal medulla. ADM binding was selectively displaced by ADM(22\u201352), a putative ADM-receptor antagonist, and CGRP(8\u201337), a ligand that preferentially antagonizes the CGRP1-receptor subtype. ADM concentration-dependently inhibited K1-induced aldosterone secretion of dispersed rat ZG cells, without affecting basal hormone production. Both ADM(22\u201352) and CGRP(8\u201337) reversed the ADM effect in a concentration-dependent manner. ADM counteracted the aldosterone secretagogue action of the voltage-gated Ca21-channel activator BAYK-8644, and blocked K1- and BAYK-8644-evoked rise in the intracellular Ca21 concentration of dispersed ZG cells. ADM concentration-dependently raised basal catecholamine (epinephrine and norepinephrine) release by rat adrenomedullary fragments, and again the response was blocked by both ADM(22\u201352) and CGRP(8\u201337). ADM increased cyclic-AMP release by adrenal-medulla fragments, but not capsule-ZG preparations, and the catecholamine response to ADM was abolished by the PKA inhibitor H-89. Collectively, the present findings allow us to draw the following conclusions: (1) ADM modulates rat adrenal secretion, acting through ADM(22\u201352)-sensitive CGRP1 receptors, which are coupled with different signaling mechanisms in the cortex and medulla; (2) ADM selectively inhibits agonist-stimulated aldosterone secretion, through a mechanism probably involving the blockade of the Ca21 channel-mediated Ca21 influx; (3) ADM raises catecholamine secretion, through the activation of the adenylate cyclase/PKA signaling pathway