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Accurate solar power generation forecasting is paramount for optimizing renewable energy systems and ensuring sustainability in our evolving energy landscape. This study introduces a pioneering approach that synergistically integrates Boosting Cascade Forest and multi-class-grained scanning techniques to enhance the precision of solar farm power output predictions significantly. While Boosting Cascade Forest excels in capturing intricate, nonlinear variable interactions through ensemble decision tree learning, multi-class-grained scanning reveals fine-grained patterns within time-series data. Evaluation with real-world solar farm data demonstrates exceptional performance, reflected in low error metrics (mean absolute error, 0.0016; root mean square error 0.0036) and an impressive R-squared score of 99.6% on testing data. This research represents the inaugural application of these advanced techniques to solar generation forecasting, highlighting their potential to revolutionize renewable energy integration, streamline maintenance, and reduce costs. Opportunities for further refinement of ensemble models and exploration of probabilistic forecasting methods are also discussed, underscoring the significance of this work in advancing solar forecasting techniques for a sustainable energy future. [ABSTRACT FROM AUTHOR]

Hepatic encephalopathy depicts the cluster of neurological alterations that occur during acute or chronic hepatic injury. Hyperammonemia, inflammatory injury, and oxidative stress are the main predisposing factors for the direct and indirect changes in cerebral metabolism causing encephalopathy. The aim of this study was to evaluate the possible synergistic effect between aminoguanidine (AG; 100 mg/kg, p.o.) and L-carnosine (CAR; 200 mg/kg, p.o.) on hepatic encephalopathy that was induced by thioacetamide (TAAI 3/4 100 mg/kg, i.p.) administered three times weekly for six weeks. Behavioral changes, biochemical parameters, histopathological analysis, and immunohistochemical and ultrastructural studies were conducted 24 h after the last treatment. Combining AG with CAR improved TAA- induced locomotor impairment and motor incoordination evidenced by reduced locomotor activity and decline in motor skill performance, as well as ameliorated cognitive deficits. Moreover, both drugs restored the levels of serum hepatic enzymes and serum and brain levels of ammonia. In addition, the combination significantly modulated hepatic and brain oxidative stress biomarkers, inflammatory cytokines, and cleaved caspase-3 expression. Furthermore, they succeeded in activating nuclear erythroid 2-related factor 2 (Nrf2) expression and heme oxygenase-1 (HO-1) activity and ameliorating markers of hepatic encephalopathy, including hepatic necrosis and brain astrocyte swelling. This study shows that combining AG with CAR exerted a new intervention for hepatic and brain damage in hepatic encephalopathy due to their complementary antioxidant, anti-inflammatory effects and hypoammonemic effects via Nrf2/HO-1 activation and NO inhibition. Key words: hepatic encephalopathy, aminoguanidine, carnosine, Nrf2 activator, heme oxygenase-1. L'encephalopathie hepatique rassemble sous un meme terme la constellation d'alterations neurologiques qui surviennent en presence de lesions hepatiques aigues et chroniques. L'hyperammoniemie, les lesions inflammatoires et le stress oxydatif constituent les principaux facteurs predisposant aux modifications directes et indirectes du metabolisme cerebral qui entrainent l'encephalopathie. Cette etude portait sur l'effet synergique eventuel entre l'aminoguanidine (AG; 100 mg/kg, p.o.) et la L-carnosine (CAR; 200 mg/kg, p.o.) sur une encephalopathie hepatique engendree par l'administration de thioacetamide (TAAI 3/4 100 mg/kg, i.p.) trois fois par semaine pendant six semaines. Nous avons etudie les modifications du comportement ainsi que des parametres biochimiques, et mene des etudes histopathologiques, immunohistochimiques et ultrastructurelles 24 h apres la derniere administration. L'association de l'AG avec la CAR permettait d'attenuer le trouble locomoteur et le manque de coordination motrice engendres par le TAA, mis en evidence par une diminution de l'activite locomotrice et des performances sur le plan des habiletes motrices, ainsi que d'attenuer les deficits cognitifs. En outre, les deux medicaments permettaient de retablir les taux seriques d'enzymes hepatiques ainsi que les taux seriques et cerebraux d'ammoniaque. De plus, l'association medicamenteuse permettait de moduler de maniere appreciable les biomarqueurs du stress oxydatif et les cytokines inflammatoires hepatiques et cerebrales, ainsi que l'expression de la caspase-3 clivee. Enfin, l'administration des medicaments parvenait d'activer l'expression de Nrf2 (pour << nuclear erythroid 2-related factor 2 >>) et l'activite de l'heme oxygenase-1 (HO-1), avec des ameliorations en matiere de marqueurs de l'encephalopathie hepatique, y compris la necrose hepatique et le gonflement des astrocytes cerebraux. Cette etude expose que l'association de l'AG avec la CAR constituerait un nouveau mode d'intervention contre les dommages hepatiques et cerebraux dans l'encephalopathie hepatique en raison de leurs effets antioxydants et anti-inflammatoires complementaires, ainsi que d'effets anti-ammoniemiques par l'intermediaire de l'activation de la voie de signalisation Nrf2/HO-1 et de l'inhibition de celle du NO. Mots-cles : encephalopathie hepatique, aminoguanidine, carnosine, activateur de Nrf2, heme oxygenase-1., 1. Introduction Hepatic encephalopathy (HE) is a common neuropsychiatrie disorder that is considered to be one of the most debilitating signs of hepatic cirrhosis resulting in severe hepatocellular dysfunction (Elwir [...]

Diabetic peripheral neuropathy (DPN) poses a significant threat, affecting half of the global diabetic population and leading to severe complications, including pain, impaired mobility, and potential amputation. The delayed manifestation of diabetic neuropathy (DN) makes early diagnosis challenging, contributing to its debilitating impact on individuals with diabetes mellitus (DM). This review examines the multifaceted nature of DPN, focusing on the intricate interplay between oxidative stress, metabolic pathways, and the resulting neuronal damage. It delves into the challenges of diagnosing DN, emphasizing the critical role played by hyperglycemia in triggering these cascading effects. Furthermore, the study explores the limitations of current neuropathic pain drugs, prompting an investigation into a myriad of pharmaceutical agents tested in both human and animal trials over the past decade. The methodology scrutinizes these agents for their potential to provide symptomatic relief for DPN. The investigation reveals promising results from various pharmaceutical agents tested for DPN relief, showcasing their efficacy in ameliorating symptoms. However, a notable gap persists in addressing the underlying problem of DPN. The results underscore the complexity of DPN and the challenges in developing therapies that go beyond symptomatic relief. Despite advancements in treating DPN symptoms, there remains a scarcity of options addressing the underlying problem. This review consolidates the state-of-the-art drugs designed to combat DPN, highlighting their efficacy in alleviating symptoms. Additionally, it emphasizes the need for a deeper understanding of the diverse processes and pathways involved in DPN pathogenesis. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) has emerged as a major chronic liver illness characterized by increase of lipid content in the liver. This study investigated the role of lauric acid to treat NAFLD in male adult Sprague Dawley rats. In this study, to induce NAFLD in the rats, a high-fat diet (HFD) was administered for eight consecutive weeks. Lauric acid groups received lauric acid (250 and 500 mg/kg; orally), concurrently with HFD for eight consecutive weeks. Lauric acid could ameliorate the serum levels of TG, TC, ALT, AST, blood glucose, and insulin. Moreover, lauric acid significantly elevated the levels of SOD, GSH, catalase, and IL-10. Additionally, it lowered the hepatic levels of MDA, ROS, MPO, 4-HNE, interleukin (IL)-1β, and tumor necrosis factor (TNF-α). Furthermore, lauric acid significantly up-regulated the hepatic expression of IRS1, AMPK, PI3K, and SIRT1 genes. In parallel, lauric acid could improve the histopathological picture of the liver and reduce the liver apoptosis via decreasing the expression of annexin V (Anx V). Finally, our data proposed that lauric acid could be an effective candidate for the NAFLD treatment. [ABSTRACT FROM AUTHOR]

Objective(s): Our study was conducted to evaluate the synergistic effect of arginine (ARG) and Lactobacillus plantarum against potassium dichromate (K2Cr2O7) induced-acute hepatic and kidney injury. Materials and Methods: Fifty male Wistar rats were divided into five groups. The control group received distilled water. The potassium dichromate group (PDC) received a single dose of PDC (20 mg/kg; SC). The arginine group (ARG) and Lactobacillus plantarum group received either daily doses of ARG (100 mg/kg, PO) or L. plantarum (109 CFU/ml, PO) for 14 days. The combination group (ARG+L. plantarum) received daily doses of ARG (100 mg/kg) with L. plantarum (109 CFU/ml), orally for 14 days, before induction of acute liver and kidney injury. Forty eight hours after the last dose of PDC, serum biochemical indices, oxidative stress biomarkers, pro-inflammatory cytokines, histopathological and immunohistochemical analysis were evaluated. Results: Combining ARG with L. plantarum restored the levels of serum hepatic & kidney enzymes, hepatic & renal oxidative stress biomarkers, and TLR 4/ NF-κB signaling pathway. Furthermore, they succeeded in decreasing the expression of iNOS and ameliorate the hepatic and renal markers of apoptosis: Caspase-3, Bax, and Bcl2. Conclusion: This study depicts that combining ARG with L. plantarum exerted a new bacteriotherapy against hepatic and renal injury caused by PDC. [ABSTRACT FROM AUTHOR]