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Accurate solar radiation forecasting is essential to operate power systems safely under high shares of photovoltaic generation. This paper compares the performance of several machine learning algorithms for solar radiation forecasting using endogenous and exogenous inputs and proposes an ensemble feature selection method to choose not only the most related input parameters but also their past observations values. The machine learning algorithms used are: Support Vector Regression (SVR), Extreme Gradient Boosting (XGBT), Categorical Boosting (CatBoost) and Voting-Average (VOA), which integrates SVR, XGBT and CatBoost. The proposed ensemble feature selection is based on Pearson coefficient, random forest, mutual information and relief. Prediction accuracy is evaluated based on several metrics using a real database from Salvador, Brazil. Different prediction time-horizons are considered: 1 h, 2 h and 3 h ahead. Numerical results demonstrate that the proposed ensemble feature selection approach improves forecasting accuracy and that VOA performs better than the other algorithms in all prediction time horizons.

This paper proposes an ensemble voting model for solar radiation forecasting based on machine learning algorithms. Several ensemble models are assessed using a simple average and a weighted average, combining the following algorithms: random forest, extreme gradient boosting, categorical boosting, and adaptive boosting. A clustering algorithm is used to group data according to the weather, and feature selection is applied to choose the most-related inputs and their past observation values. Prediction performance is evaluated by several metrics using a real-world Brazilian database, considering different prediction time horizons of up to 12 h ahead. Numerical results show the weighted average voting approach based on random forest and categorical boosting has superior performance, with an average reduction of 6% for MAE, 3% for RMSE, 16% for MAPE, and 1% for R2 when predicting one hour in advance, outperforming individual machine learning algorithms and other ensemble models.

An experimental model of acute pulmonary damage was developed based on the intravenous injection of the phospholipase A2 (PLA2)-rich venom of Pseudechis papuanus (Papuan black snake) in mice. Venom caused pulmonary edema, with the accumulation of a protein-rich exudate, as observed histologically and by analysis of bronchoalveolar lavage fluid (BALF). In parallel, venom induced an increase in all of the pulmonary mechanical parameters evaluated, without causing major effects in terms of tracheal and bronchial reactivity. These effects were abrogated by incubating the venom with the PLA2 inhibitor varespladib, indicating that this hydrolytic enzyme is responsible for these alterations. The venom was cytotoxic to endothelial cells in culture, hydrolyzed phospholipids of a pulmonary surfactant, and reduced the activity of angiotensin-converting enzyme in the lungs. The pretreatment of mice with the nitric oxide synthase inhibitor L-NAME reduced the protein concentration in the BALF, whereas no effect was observed when mice were pretreated with inhibitors of cyclooxygenase (COX), tumor necrosis factor-α (TNF-α), bradykinin, or neutrophils. Based on these findings, it is proposed that the rapid pathological effect of this venom in the lungs is mediated by (a) the direct cytotoxicity of venom PLA2 on cells of the capillary–alveolar barrier, (b) the degradation of surfactant factor by PLA2, (c) the deleterious action of nitric oxide in pulmonary tissue, and (d) the cytotoxic action of free hemoglobin that accumulates in the lungs as a consequence of venom-induced intravascular hemolysis. Our findings offer clues on the mechanisms of pathophysiological alterations induced by PLA2s in a variety of pulmonary diseases, including acute respiratory distress syndrome (ARDS).

An experimental model of acute pulmonary damage was developed based on the intravenous injection of the phospholipase A[sub.2] (PLA[sub.2] )-rich venom of Pseudechis papuanus (Papuan black snake) in mice. Venom caused pulmonary edema, with the accumulation of a protein-rich exudate, as observed histologically and by analysis of bronchoalveolar lavage fluid (BALF). In parallel, venom induced an increase in all of the pulmonary mechanical parameters evaluated, without causing major effects in terms of tracheal and bronchial reactivity. These effects were abrogated by incubating the venom with the PLA[sub.2] inhibitor varespladib, indicating that this hydrolytic enzyme is responsible for these alterations. The venom was cytotoxic to endothelial cells in culture, hydrolyzed phospholipids of a pulmonary surfactant, and reduced the activity of angiotensin-converting enzyme in the lungs. The pretreatment of mice with the nitric oxide synthase inhibitor L-NAME reduced the protein concentration in the BALF, whereas no effect was observed when mice were pretreated with inhibitors of cyclooxygenase (COX), tumor necrosis factor-α (TNF-α), bradykinin, or neutrophils. Based on these findings, it is proposed that the rapid pathological effect of this venom in the lungs is mediated by (a) the direct cytotoxicity of venom PLA[sub.2] on cells of the capillary–alveolar barrier, (b) the degradation of surfactant factor by PLA[sub.2] , (c) the deleterious action of nitric oxide in pulmonary tissue, and (d) the cytotoxic action of free hemoglobin that accumulates in the lungs as a consequence of venom-induced intravascular hemolysis. Our findings offer clues on the mechanisms of pathophysiological alterations induced by PLA[sub.2] s in a variety of pulmonary diseases, including acute respiratory distress syndrome (ARDS).

An experimental model of acute pulmonary damage was developed based on the intravenous injection of the phospholipase A (PLA )-rich venom of (Papuan black snake) in mice. Venom caused pulmonary edema, with the accumulation of a protein-rich exudate, as observed histologically and by analysis of bronchoalveolar lavage fluid (BALF). In parallel, venom induced an increase in all of the pulmonary mechanical parameters evaluated, without causing major effects in terms of tracheal and bronchial reactivity. These effects were abrogated by incubating the venom with the PLA inhibitor varespladib, indicating that this hydrolytic enzyme is responsible for these alterations. The venom was cytotoxic to endothelial cells in culture, hydrolyzed phospholipids of a pulmonary surfactant, and reduced the activity of angiotensin-converting enzyme in the lungs. The pretreatment of mice with the nitric oxide synthase inhibitor L-NAME reduced the protein concentration in the BALF, whereas no effect was observed when mice were pretreated with inhibitors of cyclooxygenase (COX), tumor necrosis factor-α (TNF-α), bradykinin, or neutrophils. Based on these findings, it is proposed that the rapid pathological effect of this venom in the lungs is mediated by (a) the direct cytotoxicity of venom PLA on cells of the capillary-alveolar barrier, (b) the degradation of surfactant factor by PLA , (c) the deleterious action of nitric oxide in pulmonary tissue, and (d) the cytotoxic action of free hemoglobin that accumulates in the lungs as a consequence of venom-induced intravascular hemolysis. Our findings offer clues on the mechanisms of pathophysiological alterations induced by PLA s in a variety of pulmonary diseases, including acute respiratory distress syndrome (ARDS).

Abstract Mucopolysaccharidoses (MPS) constitute a heterogeneous group of rare genetic disorders caused by enzymatic deficiencies that lead to the accumulation of glycosaminoglycans (GAGs). Clinical observations suggest a health-related impairment in quality of life in patients with MPS. Professionals with extensive experience in the care of patients with inborn errors of metabolism, such as MPS, held a meeting in April 2017 to discuss and propose recommendations for the evaluation and management of quality of life in MPS patients in Latin America. In the light of this scenario, the present work summarizes the content of the discussions and presents the recommendations produced at the meeting. The panel had suggested the use of the following tools for the assessment of health-related quality of life (HRQoL): Children's Health Assessment Questionnaire (CHAQ) for children and patients unable to express their feelings, Health Assessments Questionnaire (HAQ) and EuroQol 5 Domains (EQ-5D) scales for adult patients. Based on the scores verified in these scales, the panel proposes interventions that aim reducing the impairment of the quality of life in patients with MPS disorders.