1,721,541 research outputs found
Letter regarding the article 'Heart failure with preserved ejection fraction. Frommechanisms to therapies' by Lamand colleagues
No full textNo abstract availabl
Evaluation of the hair cell regeneration and claudin b and phoenix gene expression during exposure to low concentrations of cadmium and zinc in early developing zebrafish larvae
No full textZebrafish possess hair cells on the body surface similar to that of mammals inner hear, in particular in the neuromasts, and due to its ability in regenerating damaged hair cells, is regularly used as a powerful animal model to study in vivo cytotoxicity. Among the factors leading to hair cell disruption, metal ions are of particular concern since they are important environmental pollutants. To date, several studies on zebrafish hair cell regeneration after metal exposure exist, while no data on regeneration during continuous metal exposure are available. In the present study, neuromast hair cell disruption and regeneration were assessed in zebrafish larvae for the first time during zinc (Zn) and cadmium (Cd) continuous exposure and a visual and molecular approach was adopted. Fluorescent vital dye DASPEI was used to assess hair cell regeneration and the gene expression of claudin b (cldnb) and phoenix (pho), was analyzed. Metallotionein-2 (mt2) gene expression was used as standard molecular marker of metal toxicity and confirmed the higher toxicity of Cd compared to Zn. In addition, Cd caused a delay in hair cell regeneration compared to Zn. Molecular analysis showed cldnb gene expression increased in relation to the metal concentrations used, confirming the involvement of this gene in hair cell regeneration. On the contrary, a dramatic decrease of pho gene expression was observed in Cd exposed groups, suggesting a negative impact of Cd on pho expression, thus negatively interfering with hair cell regeneration in zebrafish larvae exposed to this metal
New onset of electrocardiographic abnormalities heralding hypertrophic cardiomyopathy in an adult athlete.
No full textA 41-year-old male asymptomatic athlete with unremarkable personal and family history of heart disease underwent annual preparticipation screening. No abnormalities were noted on prior testing. On this occasion, a 12-lead electrocardiogram showed diffused and marked repolarization abnormalities. He was therefore referred for echocardiography, which showed moderate asymmetric hypertrophy localized at the mid-apical portions of the left ventricular anterolateral wall. Cardiac magnetic resonance confirmed the diagnosis of hypertrophic cardiomyopathy. Re-evaluation of the electrocardiogram performed the previous year revealed a completely normal tracin
Pharmacological treatment options for hypertrophic cardiomyopathy: high time for evidence.
No full textEffect of dietary probiotic on clownfish: a molecular approach to define how lactic acid bacteria modulate development in a marine fish
No full textThe spectrum of myocarditis: from pathology to the clinics
No full textMyocarditis is an inflammatory disease of the myocardium, which may occur in isolation or as part of systemic infectious/immune/autoimmune conditions, characterized by vast aetiologic, clinical and histopathologic heterogeneity. The broad spectrum of myocarditis can be categorized according to the prevalent histopathologic pattern including lymphocytic, lympho-histiocytic, eosinophilic and neutrophilic forms, giant cell myocarditis and myocarditis with granulomata. Diverse histopathologic substrates generally reflect different aetiologies and pathogenetic mechanisms and may be critical to clinical decision-making. Active vasculitis, when present, completes the inflammatory spectrum. Unfortunately, the correlation of histopathologic patterns, clinical presentation and disease course in myocarditis is still largely unresolved, due to limited availability of bioptic samples at specific stages of disease and impracticality of serial sampling. We here review the elements supporting an aetiology-driven diagnostic work-up in myocarditis, emphasizing the importance of integrating pathologic studies with clinical features and information derived from multimodality imaging. Furthermore, we explore myocardial inflammation in genetic cardiomyopathies, its role in driving clinical variability and the potential of transcriptomic and proteomic analysis in our understanding of these complex interrelations
Ventricular arterial coupling alteration and long term prognosis in patients with hypertrophic cardiomyopathy
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