907 resultados para Endocrine


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One of the hallmarks of cancer is its unlimited replicative potential that needs a compensatory mechanism for the consequential telomere erosion. Telomerase promoter (TERTp) mutations were recently reported as a novel mechanism for telomerase re-activation/expression in order to maintain telomere length. Pancreatic endocrine tumors (PETs) were so far recognized to rely mainly on the alternative lengthening of telomeres (ALT) mechanism. It was our objective to study if TERTp mutations were present in pancreatic endocrine tumors (PET) and could represent an alternative mechanism to ALT. TERTp mutations were detected in 7% of the cases studied and were mainly associated to patients harbouring hereditary syndromes. In vitro, using PET-derived cell lines and by luciferase reporter assay, these mutations confer a 2 to 4-fold increase in telomerase transcription activity. These novel alterations are able to recruit ETS transcription factor members, in particular GABP-α and ETV1, to the newly generated binding sites. We report for the first time TERTp mutations in PETs and PET-derived cell lines. Additionally, our data indicate that these mutations serve as an alternative mechanism and in an exclusive manner to ALT, in particular in patients with hereditary syndromes.

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Mode of access: Internet.

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Mode of access: Internet.

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"Founded upon a course of lectures (Lane Medical Lectures) delivered at Stanford University, California, in the summer of 1913."

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"Published in response to requests for the printing of a series f lectures given before a variety of medical organizations during the last two years."--Pref.

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"References for further reading" at end of some of the chapters."

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Includes bibliographical references and index.

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"References for further reading" at end of some of the chapters."

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Prepared for the ICRDB Program by the Current Cancer Research Project Analysis Center.

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Mode of access: Internet.

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Since the landmark contributions of Homer Smith and co-workers in the 1930s there has been a considerable advance in our knowledge regarding the osmoregulatory strategy of elasmobranch fish. Smith recognised that urea was retained in the body fluids as part of the 'osmoregulatory ballast' of elasmobranch fish so that body fluid osmolality is raised to a level that is iso- or slightly hyper-osmotic to that of the surrounding medium. From studies at that time he also postulated that many marine dwelling elasmobranchs were not capable of adaptation to dilute environments. However, more recent investigations have demonstrated that, at least in some species, this may not be the case. Gradual acclimation of marine dwelling elasmobranchs to varying environmental salinities under laboratory conditions has demonstrated that these fish do have the capacity to acclimate to changes in salinity through independent regulation of Na+, Cl- and urea levels. This suggests that many of the presumed stenohaline marine elasmobranchs could in fact be described as partially euryhaline. The contributions of Thomas Thorson in the 1970s demonstrated the osmoregulatory strategy of a fully euryhaline elasmobranch, the bull shark, Carcharhinus leucas, and more recent investigations have examined the mechanisms behind this strategy in the euryhaline elasmobranch, Dasyatis sabina. Both partially euryhaline and fully euryhaline species utilise the same physiological processes to control urea, Na+ and Cl- levels within the body fluids. The role of the gills, kidney, liver, rectal gland and drinking process is discussed in relation to the endocrine control of urea, Na+ and Cl- levels as elasmobranchs acclimate to different environmental salinities. (C) 2003 Elsevier Inc. All rights reserved.

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One of the great challenges in biology is to understand how particular complex morphological and physiological characters originated in specific evolutionary lineages. In this article, we address the origin of the vertebrate hypothalamic-pituitary-peripheral gland (H-P-PG) endocrine system, a complex network of specialized tissues, ligands and receptors. Analysis of metazoan nucleotide and protein sequences reveals a patchwork pattern of H-P-PG gene conservation between vertebrates and closely related invertebrates (ascidians). This is consistent with a model of how the vertebrate H-P-PG endocrine system could have emerged in relatively few steps by gene family expansion and by regulatory and structural modifications to genes that are present in a chordate ancestor. Some of these changes might have resulted in new connections between metabolic or signaling pathways, such as the bridging of 'synthesis islands' to form an efficient system for steroid hormone synthesis.

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The growth performance and endocrine responses of male weaner pigs (3 to 8 weeks of age) was evaluated in two different environments (clean and dirty) and housing (single or groups of 10 pigs/pen) conditions. The dirty environment contained significantly elevated ammonia, carbon dioxide and dust levels compared with the clean environment. Pigs grew faster and consumed more feed in the clean environment and this was associated with reduced plasma cortisol concentrations compared with pigs in the dirty environment. Pigs housed in groups in the dirty environment had increased β-endorphin and decreased IGF-I concentrations compared to group housed pigs in the clean environment. Feed conversion efficiency did not differ due to environment or group housing. Plasma concentration of cortisol, p-endorphin, IGF-I and IGF-II did not differ between single and group housed pigs. Activity of the hypothalamic-pituitary-adrenal (HPA) axis was greater in response to environmental conditions than group housing, and this was associated with reduced growth in weaner pigs. © 2004 Elsevier B.V. All rights reserved.

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Obesity and the metabolic syndrome have both reached pandemic proportions. Together they have the potential to impact on the incidence and severity of cardiovascular pathologies, with grave implications for worldwide health care systems. The metabolic syndrome is characterized by visceral obesity, insulin resistance, hypertension, chronic inflammation, and thrombotic disorders contributing to endothelial dysfunction and, subsequently, to accelerated atherosclerosis. Obesity is a key component in development of the metabolic syndrome and it is becoming increasingly clear that a central factor in this is the production by adipose cells of bioactive substances that directly influence insulin sensitivity and vascular injury. In this paper, we review advances in the understanding of biologically active molecules collectively referred to as adipokines and how dysregulated production of these factors in obese states mediates the pathogenesis of obesity associated metabolic syndrome.