Forecasting a Short-Term Photovoltaic Power Model Based on Improved Snake Optimization, Convolutional Neural Network, and Bidirectional Long Short-Term Memory Network.

The precision of short-term photovoltaic power forecasts is of utmost importance for the planning and operation of the electrical grid system. To enhance the precision of short-term output power prediction in photovoltaic systems, this paper proposes a method integrating K-means clustering: an improved snake optimization algorithm with a convolutional neural network-bidirectional long short-term memory network to predict short-term photovoltaic power. Firstly, K-means clustering is utilized to categorize weather scenarios into three categories: sunny, cloudy, and rainy. The Pearson correlation coefficient method is then utilized to determine the inputs of the model. Secondly, the snake optimization algorithm is improved by introducing Tent chaotic mapping, lens imaging backward learning, and an optimal individual adaptive perturbation strategy to enhance its optimization ability. Then, the multi-strategy improved snake optimization algorithm is employed to optimize the parameters of the convolutional neural network-bidirectional long short-term memory network model, thereby augmenting the predictive precision of the model. Finally, the model established in this paper is utilized to forecast photovoltaic power in diverse weather scenarios. The simulation findings indicate that the regression coefficients of this method can reach 0.99216, 0.95772, and 0.93163 on sunny, cloudy, and rainy days, which has better prediction precision and adaptability under various weather conditions.

LDHA mediated degradation of extracellular matrix is a potential target for the treatment of aortic dissection.

Aortic dissection (AD) is a disease with high mortality and lacks effective drug treatment. Recent studies have shown that the development of AD is closely related to glucose metabolism. Lactate dehydrogenase A (LDHA) is a key glycolytic enzyme and plays an important role in cardiovascular disease. However, the role of LDHA in the progression of AD remains to be elucidated. Here, we found that the level of LDHA was significantly elevated in AD patients and the mouse model established by BAPN combined with Ang II. In vitro, the knockdown of LDHA reduced the growth of human aortic vascular smooth muscle cells (HAVSMCs), glucose consumption, and lactate production induced by PDGF-BB. The overexpression of LDHA in HAVSMCs promoted the transformation of HAVSMCs from contractile phenotype to synthetic phenotype, and increased the expression of MMP2/9. Mechanistically, LDHA promoted MMP2/9 expression through the LDHA-NDRG3-ERK1/2-MMP2/9 pathway. In vivo, Oxamate, LDH and lactate inhibitor, reduced the degradation of elastic fibers and collagen deposition, inhibited the phenotypic transformation of HAVSMCs from contractile phenotype to synthetic phenotype, reduced the expression of NDRG3, p-ERK1/2, and MMP2/9, and delayed the progression of AD. To sum up, the increase of LDHA promotes the production of MMP2/9, stimulates the degradation of extracellular matrix (ECM), and promoted the transformation of HAVSMCs from contractile phenotype to synthetic phenotype. Oxamate reduced the progression of AD in mice. LDHA may be a therapeutic target for AD.

Transketolase drives the development of aortic dissection by impairing mitochondrial bioenergetics.

AIM: Aortic dissection (AD) is a disease with rapid onset but with no effective therapeutic drugs yet. Previous studies have suggested that glucose metabolism plays a critical role in the progression of AD. Transketolase (TKT) is an essential bridge between glycolysis and the pentose phosphate pathway. However, its role in the development of AD has not yet been elucidated. In this study, we aimed to explore the role of TKT in AD. METHODS: We collected AD patients' aortic tissues and used high-throughput proteome sequencing to analyze the main factors influencing AD development. We generated an AD model using BAPN in combination with angiotensin II (Ang II) and pharmacological inhibitors to reduce TKT expression. The effects of TKT and its downstream mediators on AD were elucidated using human aortic vascular smooth muscle cells (HAVSMCs). RESULTS: We found that glucose metabolism plays an important role in the development of AD and that TKT is upregulated in patients with AD. Western blot and immunohistochemistry confirmed that TKT expression was upregulated in mice with AD. Reduced TKT expression attenuated AD incidence and mortality, maintained the structural integrity of the aorta, aligned elastic fibers, and reduced collagen deposition. Mechanistically, TKT was positively associated with impaired mitochondrial bioenergetics by upregulating AKT/MDM2 expression, ultimately contributing to NDUFS1 downregulation. CONCLUSION: Our results provide new insights into the role of TKT in mitochondrial bioenergetics and AD progression. These findings provide new intervention options for the treatment of AD.