53 research outputs found
ΣΥΜΒΟΛΗ ΕΙΣ ΤΗΝ ΜΕΛΕΤΗΝ ΤΗΣ ΣΥΣΤΑΣΕΩΣ ΤΩΝ ΛΙΠΟΕΙΔΩΝ ΛΕΥΚΩΝ ΑΙΜΟΣΦΑΙΡΙΩΝ ΦΥΣΙΟΛΟΓΙΚΩΝ ΚΑΙ ΛΕΥΧΑΙΜΙΚΩΝ ΑΤΟΜΩΝ
Extrapituitary Effects of the Growth Hormone-Releasing Hormone
Growth hormone-releasing hormone (GHRH) is a neuropeptide secreted by the hypothalamus that stimulates the synthesis and release of growth hormone (GH) in the pituitary. Accumulating evidence suggests that in addition to GHRH's neuroendocrine action, GHRH is present in several extrahypothalamic tissues and is involved in a variety of cellular processes. Its function is related to the regulation of cell proliferation and differentiation of various nonpituitary cell types. In certain cases, ectopic production of GHRH has also been implicated in carcinogenesis. The mechanisms by which GHRH affects the peripheral extrapituitary tissues remain poorly understood, but it is likely that classic neuroendocrine action as well as paracrine and autocrine pathways are involved. Some headway has been made in the identification of extrapituitary receptors for GHRH and cDNA as splice variants of these GHRH receptors found in various tumors. The fact that the nonpituitary GHRH receptors are not fully identified, however, remains the major obstacle in studying, at a more mechanistic level, the action of local GHRH. This review summarizes the information available regarding the role of GHRH in the extrapituitary tissues with emphasis on its potential therapeutic and diagnostic applications
Depression and social phobia secondary to alcohol dependence
Background: According to the self-medication hypothesis, individuals with depression and anxiety disorders use alcohol to control their symptoms and subsequently become dependent. Conversely, alcohol dependence disorder (ADD) can cause or exacerbate psychiatric disorders. This study analyzed the characteristics of depression and social phobia secondary to ADD. (1) What is their functional impact? (2) Are they independent or associated conditions? (3) Do they completely remit in abstinent individuals? (4) Is the remission of one disorder associated with the remission of the other disorder? Methods: Sixty-four inpatients with ADD were evaluated with depression and anxiety disorder scales upon admission to hospital and after 5 weeks of detoxification. Results: Baseline comparisons differentiated patients with a Hamilton Rating Scale for Depression (HDRS) score >35 (n = 50; 78%) from those with an HDRS score ≤35 by higher levels of generalized anxiety and lower global functioning. Patients with generalized social phobia [Leibowitz Social Anxiety Scale (LSAS) score >60: n = 20; 31.2%] were not distinguishable from those with an LSAS score ≤60 by depressive and anxiety disorder symptoms. In postdetoxification assessment, patients who remitted from depression (HDRS score <7: n = 35; 54.6%) had a lower generalized anxiety and marginally higher levels of hypochondriasis compared to nonremitter subjects (HDRS score ≥7). Patients who remitted from social phobia (LSAS score <30: n = 32; 50%) did not significantly differ from nonremitter subjects in depressive and anxiety disorder symptoms. Generalized anxiety (Hamilton Rating Scale for Anxiety) and hypochondriasis (Whiteley Index) were the significant predictors of global functioning (Global Assessment Scale). Conclusions: Depression and social phobia secondary to ADD are independent conditions that do not completely remit after cessation of drinking. Specific treatments are needed to reduce residual depressive and anxiety symptoms in abstinent alcoholics. Copyright © 2008 S. Karger AG
Inflammatory process in type 2 diabetes - The role of cytokines
Population-based studies have shown strong relationship between inflammatory markers and metabolic disturbances, obesity, and atherosclerosis, whereas inflammation has been considered as a “common soil” between these clinical entities and type 2 diabetes (T2D). The accumulation of macrophages in adipose tissue (AT), the common origin of macrophages and adipocytes, the prevalent presence of peripheral mononuclear cells, and apoptotic beta cells by themselves seem to be the sources of inflammation present in T2D, since they generate the mediators of the inflammatory processes, namely cytokines. The main cvtokines involved in the pathogenesis of T2D are interleukin-1 beta (IL-1 beta), with an action similar to the one present in type 1 diabetes, tumor necrosis factor-alpha (TNF-alpha), and IL-6, considered as the main regulators of inflammation, leptin, more recently introduced, and several others, such as monocyte chemoattractant protein-1, resistin, adiponectin, with either deleterious or beneficial effects in diabetic pathogenesis. The characterization of these molecules targeted diabetes treatment beyond the classical interventions with lifestyle changes and pharmaceutical agents, and toward the determination of specific molecular pathways that lead to low grade chronic inflammatory state mainly due to an immune system’s unbalance
Differences in Expression of Cardiovascular Risk Factors among Type 2 Diabetes Mellitus Patients of Different Age
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Growth hormone-releasing hormone and extra-pituitary tumorigenesis: therapeutic and diagnostic applications of growth hormone-releasing hormone antagonists
Growth hormone-releasing hormone (GHRH) regulates growth hormone release from the pituitary. However, in addition to this neuroendocrine action, much evidence implies an additional role for GHRH in carcinogenesis in non-pituitary tissues. This role of GHRH in cancer development appears to be due to the operation of several mechanisms, which involve the regulation of the growth hormone-dependent hepatic insulin-like growth factor I (IGFI) production, tumoural IGF-I and IGF-II secretion and direct action of GHRH on tumour cells by autocrine and/or paracrine pathways. This review summarises the available information regarding the role of GHRH in tumorigenesis with special emphasis on the direct action of GHRH in primary and experimental cancers
Increased plasma levels of 8-Iso-PGF2α in an elderly Greek population with cognitive impairment
Increased levels of serum advanced glycation end-products in women with polycystic ovary syndrome
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