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Tremendous Advances (tremendous + advance)
Selected AbstractsProteomics: New insights into rheumatic diseasesPROTEOMICS - CLINICAL APPLICATIONS, Issue 2 2009Emilio Camafeita Abstract Tremendous advances undergone in electrophoresis, chromatography, and MS have led proteomic research to unprecedented achievement over the last decade. Proteomics is presently employed for assessing protein expression levels, for monitoring cellular activities and for determination of biochemical pathways, revolutionizing the way we study disease by opening up the possibility to decipher the pathogenesis of clinical manifestations. Over 200 disorders including osteoarthritis (OA), rheumatoid arthritis (RA), and osteoporosis are considered rheumatic diseases (RDs), which affect the musculoskeletal system (joints and other supporting structures of the body such as muscles, tendons, ligaments, and bones) and are a leading cause of disability among older adults. Despite that an autoimmune origin has been proposed for some RDs like RA, the pathogenesis of most of these diseases is still unclear. Therefore, proteomic research on RDs, notably OA and RA, can help clarify underlying disease mechanisms, develop biomarkers to improve early detection, measure response to treatment, and devise new therapies. Achievements in the field of proteomics research on RDs are summarized in this work. [source] The neurobiology and genetics of eating and weight regulationJOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 10 2008J. Hebebrand Over the past 15 years tremendous advances have been made in the elucidation of pathways relevant to eating behaviour and body weight regulation. It has become evident that these pathways are intricately interwoven with those underlying mood and anxiety regulation, motor activity, cognition, sleep, fertility and libido. In addition, advances have been made in determining genetic variation underlying inter-individual differences in body weight. To illustrate these novel findings we will focus on: 1) Monogenic and oligogenic obesity: The underlying genes were initially detected in animal models. Based on mutation screens of the human homologues functionally relevant mutations were detected in the genes coding for leptin, its receptors and the melanocortin-4 receptor (MC4R). The effect of such mutations is large. Leptin gene mutations lead to hyperphagia and subsequently obesity. Hyperphagia, albeit of a substantially reduced magnitude, has also been observed in obese children with mutations in the MC4R. 2) Polygenic obesity: The advent of genome wide association studies has led to the detection of single polygenes, among which FTO features prominently. Typically, a variant predisposing to obesity accounts for a body weight elevated by on average 200 to 1500 grams. Such polygenes act in concert to account for inter-individual differences in body weight. 3) Leptin has been shown to have profound implications for anorexia nervosa. Serum leptin levels in this eating disorders are annormaly low. The hypoleptinemia entails a down-regulation of the hypothalamic-pituitary-gonadal-axis, which underlies the amenorrhea characteristic of anorexia nervosa. Furthermore, the hypoleptinemia induces hyperactivity in a rat model of anorexia nervosa. In patients, leptin levels are inversely correlated with activity levels. [source] Cutaneous sarcoidosis: updates in the pathogenesisJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 7 2010MM Ali Abstract Sarcoidosis is a multiorgan granulomatous disease in which the skin is one of the frequently involved target organs. Cutaneous involvement occurs in a third of patients with sarcoidosis and has protean manifestations. More than a century has passed since the initial description of sarcoidosis, but its cause continues to be an enigma. Recent studies have introduced several new insights into the pathogenesis of this disease. The aim of this literature review was to provide a comprehensive overview on the current updates in the pathogenesis of sarcoidosis. This review has revealed that several genetic polymorphisms are associated with an increased risk of developing sarcoidosis, suggesting that genetic susceptibility to sarcoidosis is probably polygenic. Environmental factors may also modify the susceptibility to sarcoidosis. Evidence favouring an infectious aetiology has been accumulating, but the results of studies are conflicting. The current concept is that the pathogenesis of sarcoidosis involves a T-helper-1-mediated immune response to environmental antigens in a genetically susceptible host. The studies carried out on sarcoidosis have largely focused on the pulmonary aspects and have been mainly conducted by respiratory physicians. In contrast, research conducted on the cutaneous aspects of sarcoidosis is comparatively limited. Although tremendous advances have been made, there is a significant gap between the vast knowledge accumulated on sarcoidosis in recent years and the understanding of this disease. [source] How do membrane proteins sense water stress?MOLECULAR MICROBIOLOGY, Issue 4 2002Bert Poolman Summary Maintenance of cell turgor is a prerequisite for almost any form of life as it provides a mechanical force for the expansion of the cell envelope. As changes in extracellular osmolality will have similar physicochemical effects on cells from all biological kingdoms, the responses to osmotic stress may be alike in all organisms. The primary response of bacteria to osmotic upshifts involves the activation of transporters, to effect the rapid accumulation of osmo-protectants, and sensor kinases, to increase the transport and/or biosynthetic capacity for these solutes. Upon osmotic downshift, the excess of cytoplasmic solutes is released via mechanosensitive channel proteins. A number of breakthroughs in the last one or two years have led to tremendous advances in our understanding of the molecular mechanisms of osmosensing in bacteria. The possible mechanisms of osmosensing, and the actual evidence for a particular mechanism, are presented for well studied, osmoregulated transport systems, sensor kinases and mechanosensitive channel proteins. The emerging picture is that intracellular ionic solutes (or ionic strength) serve as a signal for the activation of the upshift-activated transporters and sensor kinases. For at least one system, there is strong evidence that the signal is transduced to the protein complex via alterations in the protein,lipid interactions rather than direct sensing of ion concentration or ionic strength by the proteins. The osmotic downshift-activated mechanosensitive channels, on the other hand, sense tension in the membrane but other factors such as hydration state of the protein may affect the equilibrium between open and closed states of the proteins. [source] 3222: New developments in dry eye treatmentACTA OPHTHALMOLOGICA, Issue 2010JM BENITEZ-DEL-CASTILLO Purpose This study summarizes the management and therapeutic options for treating dry eye disease. Goals of this review is to identify appropriate therapeutic methods for the management of dry eye disease and recommend a sequence or strategy for their application, based on evidence-based review of the literature. Methods To achieve this a comprehensive review of clinical textbooks and scientific literature was performed and the quality of published evidence graded according to an agreed standard, using objective criteria for clinical and basic research studies. Results There have been tremendous advances in the treatment of dry eye and ocular surface disease in the last decades related to the increase in knowledge regarding the pathophysiology of dry eye. This has led to a paradigm shift in dry eye management from simply lubricating and hydrating the ocular surface with arti,cial tears to strategies that stimulate natural production of tear constituents, maintain ocular surface epithelial barrier function, and inhibit the in,ammatory factors that adversely impact the ability of ocular surface and glandular epithelia to produce tears. Conclusion The authors will present current and future treatment options for dry eye disease. [source] | |||||||||||||