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BackgroundTargeting the mitochondria during ischemia/reperfusion (IR) can confer cardioprotection leading to improved clinical outcomes. The cardioprotective potential of (-)-epicatechin (EPI) during IR via modulation of mitochondrial function was evaluated.Methods and resultsIschemia was induced in rats via a 45 min occlusion of the left anterior descending coronary artery followed by 1 h, 48 h, or 3 week reperfusion. EPI (10 mg/kg) was administered IV 15 min prior to reperfusion for the single dose group and again 12 h later for the double dose group. Controls received water. Experiments also utilized cultured neonatal rat ventricular myocytes (NRVM) and myoblasts. A single dose of EPI reduced infarct size by 27% at 48 h and 28% at 3 week. Double dose treatment further decreased infarct size by 80% at 48 h, and 52% by 3 weeks. The protective effect of EPI on mitochondrial function was evident after 1h of reperfusion when mitochondria demonstrated less respiratory inhibition, lower mitochondrial Ca2+ load, and a preserved pool of NADH that correlated with higher tissue ATP levels. Mechanistic studies in NRVM revealed that EPI acutely stimulated maximal rates of respiration, an effect that was blocked by inhibitors of the mitochondrial pyruvate carrier, nitric oxide synthase, or soluble guanylyl cyclase. In myoblasts, knockdown of components of the mitochondrial pyruvate carrier blocked EPI-induced respiratory stimulation.ConclusionsIV EPI confers cardioprotection via preservation of mitochondrial function potentially through enhanced substrate provision. These provocative results document a novel mechanism of a natural product with potential clinical utility.

Motivated by previous authors' work, where Shannon entropy, box covering and information dimension were applied to quantify pulmonary lesions, this paper extends such a contribution in two fashions: (i) Following the approach to quantify pulmonary lesions with Deng entropy and Deng information dimension obtained through box covering method; (ii) exploiting the Shannon and Deng lesion quantification for pulmonary illnesses classification with a bidirectional Long Short Term Memory (bLSTM). The referred pulmonary illnesses are Common Pneumonia (CP) and COVID-19. Shannon entropy and information dimension are performed here and called the Shannon sequence. Then, Deng entropy and Deng information dimension are computed for chest Computed Tomography (CT) images to obtain and combine two data sequences to quantify the pulmonary lesions. The data sequence resulting from the data combination is called the Deng sequence. Both Shannon and Deng sequences are independently used as input for the bLSTM. CT lung scans of 531 healthy subjects, 497 confirmed COVID-19 diagnoses and 516 with CP were analyzed to obtain the Shannon and Deng sequences. The results demonstrate that Deng entropy and Deng information dimension of CT images can differentiate similar lung lesions between COVID-19 and CP. Besides, a statistical analysis shows that: (a) Classification by the bLSTM is better when using the Deng sequence than the Shannon sequence; (b) Deng sequences plus bLSTM significantly outperform DenseNet-201, GoogLeNet and MobileNet-v2 in classifying COVID-19, CP and Normal CT (healthy subjects) in time and accuracy. Hence, the Deng sequence and bLSTM are fast and accurate tools for helping in diagnosing CP and COVID-19. [ABSTRACT FROM AUTHOR]

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Postprandial hyperglycemia, in particular when accompanied by excessive hypertriglyceridemia, is associated with increased cardiovascular risk, mainly in overweight or obese subjects, as it favors oxidative stress, systemic inflammation and endothelial dysfunction. Thus, treatments that favorably modulate metabolism by reducing steep increases in postprandial serum glucose and triglycerides, are of considerable interest. Evidence suggests that (-)-epicatechin (EPI) is responsible for reductions in cardiometabolic risk associated with chocolate consumption; these effects may be associated with favorable effects of EPI on postprandial metabolism. The aims of this study were to assess the effects of EPI on postprandial metabolism in normal-weight and overweight/obese subjects. Twenty adult volunteers (normal and overweight) underwent oral metabolic tolerance tests in the absence and presence of oral EPI (1 mg kg(-1)). Metabolic responses were examined using indirect calorimetry and determining blood glucose and triglycerides at 0, 2 and 4 hours after metabolic load ingestion. Results show that EPI increased postprandial lipid catabolism, as evidenced by a significant decrease in the respiratory quotient, which implies an increase in fat oxidation. The effect was associated with significantly lower postprandial plasma glucose and triglycerides concentrations. The effects were more prominent in overweight subjects. In conclusion, EPI modulates postprandial metabolism by enhancing lipid oxidation accompanied by reductions in glycemia and triglyceridemia.