1,006 research outputs found

    Precision medicine in heart failure no longer a visual theory but a realistic opportunity

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    Over the last decades, major advances in the understanding of pathophysiology in a wide spectrum of cardiovascular diseases provided several effective pharmacological and non-pharmacological therapies [1]. Along with novel rehabilitation and follow up strategies, these advances have improved the survival rate of cardiac diseases, globally, and contributed generally to a significant increase in life expectancy [2]. As a consequence, there is a parallel increase of patients suffering from challenging and multifaceted syndromes such as heart failure (HF). HF is a recognised pandemic disease, with a progressively increasing prevalence in the aging population [3]. It is a major public health issue, considering both its social and economic implications. HF patients are characterised by a high level of complexity because of the advanced age and the presence of multiple relevant comorbidities requiring dedicated polytherapy [1]. Therefore, overall mortality of HF patients is still unacceptably high, exceeding that of several neoplasms, carrying a risk of approximately 10% at 12 months from clinical onset [4]

    Heart failure and anti tumor necrosis factor-alpha in systemic chronic inflammatory diseases.

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    Tumor necrosis factor alpha (TNF-alpha) antagonists have emerged as an effective therapy for patients with diseases as Crohn's disease, rheumatoid arthritis, and other chronic systemic inflammatory diseases. In the last years, there has been a growing interest in the role that inflammatory cytokines, which sustain the pathogenesis of these diseases, plays in regulating cardiac structure and function, particularly in the progression of chronic heart failure. In fact there is an increase of anti-TNF alpha levels in advanced heart failure but the treatment with anti-TNF alpha has been shown to worsen the prognosis of heart failure in randomized controlled trials. Patients with rheumatoid arthritis have an increased risk for cardiovascular disease and anti-TNF alpha therapy seems to be beneficial on the risk of cardiovascular disease. In Crohn's disease the increased risk of cardiovascular disease is controversial and therefore it is impossible to demonstrate an effect in reduction of the risk; however, heart failure in patients treated with anti-TNF alpha, despite in a small proportion, has been observed. On the basis of this observation, anti-TNF alpha therapy is contraindicated in patients with Crohn's disease and III-IV New York Heart Association heart failure class

    HEAT SHOCK PROTEINS AND ULCERATIVE COLITIS: THE START OF A NEW ERA?

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    We read with great interest the article written by Abou El Azm and coworkers, published in the last issue of the Arab Journal of Gastroenterology [1]. In this article, the authors investigated the molecular expression of heat shock proteins (HSP) 70 and 90 in relation to the grades of inflammation and dysplasia in patients with ulcerative colitis (UC) before and after treatment. In this study, in agreement with other published studies [2–4], the authors not only found a potential role for HSP 70 and HSP 90 for assessment of the activity and prognosis of UC, but also such markers predicted the presence of dysplasia and differentiated it from reactive atypia [1]. HSP had been found not only a marker of active disease, thus considering UC as a ‘‘chaperonopathy by mistake’’, but also show a key role in the psychosocial setting in which inflammatory bowel diseases manifest themselves [5]. Furthermore, they could represent a new diagnostic tool to differentiate the different phenotypes of UC, thus allowing to tailor a targeted approach to better manage UC patients [6]. However, some unresolved issues still remain about the potential roles of HSP in both the acute and the longstanding disease. First, it should be interesting to assess the role of HSP in the infections associated to UC flares, like Clostridium difficile and Cytomegalovirus (CMV) infections. In fact, HSP could be investigated as a further marker of inflammation in case of severe and steroid-refractory disease; with regard to CMV infection, mucosal levels of HSP could differentiate when CMV plays a role of direct pathogen or when it represents merely a ‘‘silent bystander’’. Second, in longstanding UC, an integrated approach of colorectal cancer surveillance, by using the advanced endoscopic imaging together with mucosal markers, like HSP, could result in being markedly helpful, both to clinicians and pathologist. In fact, current guidelines recommend that image-enhanced endoscopy (IEE) may increase the yield of detection of dysplasia, thus representing a reasonable alternative to the random sampling of colon using standard white light [7]. The use of both IEE and new biomarkers, like HSP, predicting future occurrence of colonic neoplasia, could lead to a more centralised approach of UC patients, in which a ‘‘biomarker-based surveillance’’ might play a pivotal rol

    Costruzione e sperimentazione di una turbina cross-flow per acquedotti

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    La memoria descrive una nuova micro turbina idraulica con capacità di regolazione della portata, per installazioni in piccoli corsi d’acqua, su acquedotti esistenti o a valle di impianti di depurazione delle acque. Viene inoltre descritta l’installazione del prototipo della turbina nella rete idropotabile di un comune siciliano

    Myocarditis evolving in cardiomyopathy: When genetics and offending causes work together

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    Myocarditis is an infectious-inflammatory disease often superimposed to individual genetic background which could favour or inhibit its progression into a chronic heart muscle disorder (most often dilated cardiomyopathy, rarely arrhythmogenic, or right-sided cardiomyopathy). Post-myocarditis cardiomyopathy is likely caused by a complex interaction between the viral infection and an individual predisposition. Some viruses are able to highlight a clinical phenotype replicating a model similar to the genetically determined conditions, while other can affect the resolution or the progressive remodelling of the left ventricle after the infectious process. The identification of specific individual genetic backgrounds, or genes favouring the progression of the disease, are important future research goals for precision medicine aiming at a specific and individualized treatment for patients affected with myocarditis
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