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Chronic coronary artery stenosis can lead to regional myocardial dysfunction in the absence of myocardial infarction by repetitive stunning, hibernation or both. The molecular mechanisms underlying repetitive stunning‐associated myocardial dysfunction are not clear. We used non‐targeted metabolomics to elucidate responses to chronically stunned myocardium in a canine model with and without β‐adrenergic blockade treatment. After development of left ventricular systolic dysfunction induced by ameroid constrictors on the coronary arteries, animals were randomized to 3 months of placebo, metoprolol or carvedilol. We compared these two β‐blockers with their different β‐adrenergic selectivities on myocardial function, perfusion and metabolic pathways involved in tissue undergoing chronic stunning. Control animals underwent sham surgery. Dysfunction in stunned myocardium was associated with reduced fatty acid oxidation and enhanced ketogenic amino acid metabolism, together with alterations in mitochondrial membrane phospholipid composition. These changes were consistent with impaired mitochondrial function and were linked to reduced nitric oxide and peroxisome proliferator‐activated receptor signalling, resulting in a decline in adenosine monophosphate‐activated protein kinase. Mitochondrial changes were ameliorated by carvedilol more than metoprolol, and improvement was linked to nitric oxide and possibly hydrogen sulphide signalling. In summary, repetitive myocardial stunning commonly seen in chronic multivessel coronary artery disease is associated with adverse metabolic remodelling linked to mitochondrial dysfunction and specific signalling pathways. These changes are reversed by β‐blockers, with the non‐selective inhibitor having a more favourable impact. This is the first investigation to demonstrate that β‐blockade‐associated improvement of ventricular function in chronic myocardial stunning is associated with restoration of mitochondrial function. Key points: The mechanisms responsible for the metabolic changes associated with repetitive myocardial stunning seen in chronic multivessel coronary artery disease have not been fully investigated.In a canine model of repetitive myocardial stunning, we showed that carvedilol, a non‐selective β‐receptor blocker, ameliorated adverse metabolic remodelling compared to metoprolol, a selective β1‐receptor blocker, by improving nitric oxide synthase and adenosine monophosphate protein kinase function, enhancing calcium/calmodulin‐dependent protein kinase, probably increasing hydrogen sulphide, and suppressing cyclic‐adenosine monophosphate signalling.Mitochondrial fatty acid oxidation alterations were ameliorated by carvedilol to a larger extent than metoprolol; this improvement was linked to nitric oxide and possibly hydrogen sulphide signalling.Both β‐blockers improved the cardiac energy imbalance by reducing metabolites in ketogenic amino acid and nucleotide metabolism.These results elucidated why metabolic remodelling with carvedilol is preferable to metoprolol when treating chronic ischaemic left ventricular systolic dysfunction caused by repetitive myocardial stunning. [ABSTRACT FROM AUTHOR]

It is widely accepted that soil organic carbon cycling depends on the presence and catalytic functionality of extracellular enzymes. Recent reports suggest that combusted and autoclaved soils may have the capacity to degrade organic test substrates to a larger extent than the living, enzyme-bearing soils. In search of the underlying mechanisms, we adsorbed Beta-Glucosidase (BG) and Bovine Serum Albumin (BSA) on the phyllosilicate kaolinite and the manganese oxide birnessite at pH 5 and pH 7. The protein-mineral samples were then subjected to gradual energy inputs of a magnitude equivalent to naturally occurring wildfire events. The abundance and molecular masses of desorbed organic compounds were recorded after ionization with tunable synchrotron vacuum ultraviolet radiation (VUV). The mechanisms controlling the fate of proteins varied with mineralogy. Kaolinite adsorbed protein largely through hydrophobic interactions and, even at large energy inputs, produced negligible amounts of desorption fragments compared to birnessite. Acid birnessite adsorbed protein through coulombic forces at low energy levels, became a hydrolyzing catalyst at low energies and low pH, and eventually turned into a reactant involving disintegration of both mineral and protein at higher energy inputs. Fragmentation of proteins was energy dependent and did not occur below an energy threshold of 0.20 MW cm−2. Neither signal abundance nor signal intensity were a function of protein size. Above the energy threshold value, BG that had been adsorbed to birnessite at pH 7 showed an increase in signal abundance with increasing energy applications. Signal intensities differed with adsorption pH for BSA but only at the highest energy level applied. Our results indicate that proteins adsorbed to kaolinite may remain intact after exposure to such energy inputs as can be expected to occur in natural ecosystems. Protein fragmentation and concomitant loss of functionality must be expected in surface soils replete with pedogenic manganese oxides. We conclude that minerals can do both: protect enzymes at high energy intensities in the case of kaolinite and, in the case of birnessite, substitute for and even exceed the oxidative functionality that may have been lost when unprotected oxidative enzymes were denatured at high energy inputs.

This paper proposes a novel methodology to improve stability in a transmission system under critical conditions of operation when additional loads that take the system to the verge of stability are placed in weak bus bars according to the fast voltage stability index (FVSI). This paper employs the Newton–Raphson method to calculate power flows accurately and, based on that information, correctly calculate the FVSI for every transmission line. First, the weakest transmission line is identified by considering N − 1 contingencies for the disconnection of transmission lines, and then all weak nodes associated with this transmission line are identified. Following this, critical scenarios generated by stochastically placed loads that will take the system to the verge of instability will be placed on the identified weak nodes. Then, the methodology will optimally size and place a single static VAR compensator SVC in the system to take the transmission system to the conditions before the additional loads are connected. Finally, the methodology will be validated by testing the system for critical contingencies when any transmission line associated with the weak nodes is disconnected. As a result, this paper's methodology found a single SVC that will improve the system's stability and voltage profiles to similar values when the additional loads are not connected and even before contingencies occur. The methodology is validated on three transmission systems: IEEE 14, 30, and 118 bus bars. [ABSTRACT FROM AUTHOR]

This paper attempts to elucidate the transformative integration of computational techniques within power systems, underscoring their critical role in enhancing system modeling, control, and the efficient integration of renewable energy. It breaks down the two-sided nature of technological progress, highlighting both gains in operational efficiency and new challenges such as real-time processing, data management, and cybersecurity. Through meticulous analysis of query-based research patterns and mathematical frameworks, this study delves into the balancing act between specificity and breadth in scholarly inquiries while evaluating the impact and evolution of research trends through citation analysis. The convergence of interests and transient research trends is evident, particularly in Artificial Intelligence and optimization. This comprehensive narrative anticipates a sophisticated trajectory for power systems, advocating for continuous innovation and strategic research to foster sustainable, resilient, and intelligent energy networks. [ABSTRACT FROM AUTHOR]

This paper addresses the challenges in forecasting electrical energy in the current era of renewable energy integration. It reviews advanced adaptive forecasting methodologies while also analyzing the evolution of research in this field through bibliometric analysis. The review highlights the key contributions and limitations of current models with an emphasis on the challenges of traditional methods. The analysis reveals that Long Short-Term Memory (LSTM) networks, optimization techniques, and deep learning have the potential to model the dynamic nature of energy consumption, but they also have higher computational demands and data requirements. This review aims to offer a balanced view of current advancements and challenges in forecasting methods, guiding researchers, policymakers, and industry experts. It advocates for collaborative innovation in adaptive methodologies to enhance forecasting accuracy and support the development of resilient, sustainable energy systems. [ABSTRACT FROM AUTHOR]

Background: Nonalcoholic fatty liver disease (NAFLD) is a global health problem. Identification of factors contributing to the onset and progression of NAFLD have the potential to direct novel strategies to combat NAFLD. Methods: We examined the time course of western diet (WD)-induced NAFLD and its progression to nonalcoholic steatohepatitis (NASH) in age-matched female and male Ldlr-/- mice, with time-points at 1, 4, 8, 20 and 40 weeks on the WD. Controls included Ldlr-/- mice maintained on a purified low-fat diet (LFD) for 1 and 40 weeks. The approach included quantitation of anthropometric, plasma and liver markers of disease, plus hepatic histology, lipids, oxylipins, gene expression and selected metabolites. Results: One week of feeding the WD caused a significant reduction in hepatic essential fatty acids (EFAs: 18:2, ω6, 18:3, ω3) which preceded the decline in many C20-22 ω3 and ω6 polyunsaturated fatty acids (PUFA) and PUFA-derived oxylipins after 4 weeks on the WD. In addition, expression of hepatic inflammation markers (CD40, CD44, Mcp1, Nlrp3, TLR2, TLR4, Trem2) increased significantly in both female & male mice after one week on the WD. These markers continued to increase over the 40-week WD feeding study. WD effects on hepatic EFA and inflammation preceded all significant WD-induced changes in body weight, insulin resistance (HOMA-IR), oxidative stress status (GSH/GSSG ratio) and histological and gene expression markers of macrosteatosis, extracellular matrix remodeling and fibrosis. Conclusions: Our findings establish that feeding Ldlr-/- mice the WD rapidly lowered hepatic EFAs and induced key inflammatory markers linked to NASH. Since EFAs have an established role in inflammation and hepatic inflammation plays a major role in NASH, we suggest that early clinical assessment of EFA status and correcting EFA deficiencies may be useful in reducing NASH severity. [ABSTRACT FROM AUTHOR]

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