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Least squares support vector machine (LSSVM) and variational mode decomposition are common research methods for wind speed time series prediction. Addressing the challenge of selecting relevant parameters of LSSVM and VMD, a fractional‐order Beetle swarm optimization algorithm is proposed to optimize the relevant parameters. To weaken the negative impact of wind speed volatility on the accuracy of the prediction model, a two‐stage modal decomposition strategy based on extreme‐point symmetric mode decomposition, FO‐BSO algorithm, and VMD is proposed. ESMD is used to decompose the original wind speed time series. The diversity entropy is introduced as the criterion, and the FO‐BSO‐VMD secondary decomposition is applied for the high‐entropy modal components to further weaken the volatility of wind speed. Simulation results show that compared with the original LSSVM model, the ESMD‐FO‐BSO‐VMD‐LSSVM model presented in this study exhibits an average 44.10% increase in the fitting degree of wind speed prediction over three steps, which verifies the superior performance of the model in short‐term multistep wind speed prediction. [ABSTRACT FROM AUTHOR]

Septic encephalopathy (SE) represents a severe inflammatory syndrome linked to elevated septic mortality rates, lacking specific therapeutic interventions, and often resulting in enduring neurological sequelae. The present investigation endeavors to elucidate the involvement of C-X-C Motif Chemokine Receptor 2 (CXCR2) in the pathogenesis of SE and to explore the potential of CXCR2 modulation as a therapeutic avenue for SE. Employing a murine SE model induced by lipopolysaccharide (LPS) administration, CXCR2 knockout mice and the CXCR2 inhibitor SB225002 were utilized to assess neutrophil recruitment, endothelial integrity, and transendothelial migration. Our findings substantiate that either CXCR2 deficiency or its inhibition curtails neutrophil recruitment without impacting their adhesion to cerebral endothelial cells. This phenomenon is contingent upon endothelial CXCR2 expression rather than CXCR2's presence on neutrophils. Furthermore, the CXCR2 blockade preserves the integrity of tight junction protein ZO-1 and mitigates F-actin stress fiber formation in cerebral endothelial cells following septic challenge. Mechanistically, CXCL1-mediated CXCR2 activation triggers cerebral endothelial actin contraction via Rho signaling, thereby facilitating neutrophil transmigration in SE. These observations advocate for the potential therapeutic efficacy of CXCR2 inhibition in managing SE. [ABSTRACT FROM AUTHOR]

Introduction: This study aimed to determine whether bone morphogenetic protein-4 (BMP-4), which increases in response to intimal hyperplasia, promotes phenotype transition in vascular smooth muscle cells (VSMCs). Methods: Balloon injury was used to induce intimal hyperplasia in rats. Hematoxylin-eosin staining was used to detect the alteration of vascular structure. Serum levels of BMP-4 and lactate were detected by ELISA. Human aortic smooth muscle cells (HA-SMCs) were cultured. Protein and mRNA expression levels were detected through Western blot and real-time PCR. Cell migration was measured by transwell assay. Results: Our data showed that serum concentration of BMP-4 was upregulated after balloon injury. Treatment with BMP-4 inhibitor DMH1 (4-(6-(4-isopropoxyphenyl)pyrazolo(1,5-a)pyrimidin-3-yl)quinoline) suppressed the abnormal expression of BMP-4 and inhibited the intimal hyperplasia induced by balloon injury. Compared to BMP-4-negative medium, BMP-4-positive medium was associated with higher synthetic VSMC marker expression levels and lower in contractile gene markers in cultured HA-SMCs. Transfection of monocarboxylic acid transporters-4 (MCT-4) siRNA inhibited the excretion of lactate induced by BMP-4. Conclusion: Our analyses provided evidence that BMP-4 and its regulator Smad-4 are key regulators in MCT-4-mediated lactate excretion. This indicates that BMP-4 stimulates the phenotypic transition of VSMCs via SMAD-4/MCT-4 signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Programmed death ligand-1 (PD-L1) is involved in the negative regulation of immune responses in a variety of diseases. We evaluated the contribution of PD-L1 to the activation of immune cells that promote atherosclerotic lesion formation and inflammation. Methods and results: Compared to ApoE−/− mice that were provided a high-cholesterol diet in combination with anti-PD-L1 antibody developed a larger lipid burden with more abundant CD8+ T cells. The anti-PD-L1 antibody increased the abundance of CD3+PD-1+, CD8 + PD-1+,CD3+IFN-γ+ and CD8+IFN-γ+ T cell under high-cholesterol diet, as well as the serum tumor necrosis factor-α (TNF-a), IFN-γ, PF, GNLY, Gzms B and LTA. Interestingly, the anti-PD-L1 antibody increased the serum level of sPD-L1. In vitro, blocking of PD-L1 on the surface of mouse aortic endothelial cells with anti-PD-L1 antibody stimulated the activation and secretion of cytokines, including IFN-γ, PF, GNLY, Gzms B and LTA, from cytolytic CD8+IFN-γ+ T cell. However, the concentration of sPD-L1 was lower after treatment of the MAECs with anti-PD-L1 antibody. Conclusions: Our findings highlighted that blocking of PD-L1 promoted up-regulation of CD8 + IFN-γ + T cell-mediated immune responses, leading to the secretion of inflammatory cytokine that exacerbated the atherosclerotic burden and promoted inflammation. However, further studies are needed to gain insight into whether PD-L1 activation could be a novel immunotherapy strategy for atherosclerosis. [ABSTRACT FROM AUTHOR]

High external quantum efficiency (EQE) up to 25% has recently been reported from tetra(t‐butyl)rubrene (TBRb)‐based organic light‐emitting diodes (OLEDs), but its physical origin is still vague. Herein, using the featured responses of the evolution processes of electron‐hole pairs to an external magnetic field, an unreported high‐level reverse intersystem‐crossing (HL‐RISC) from upper‐level triplet to lowest singlet excitons (T2→S1) is observed when T2 is well confined in the active layer of pure TBRb. This HL‐RISC channel becomes stronger with lowering operational temperatures because it is not an endothermic process. Due to the larger separation distance of TBRb molecules with four tert‐butyl groups, the intersystem‐crossing (ISC) process of polaron pairs is stronger than the singlet fission (SF) process existing in pure TBRb, which is markedly different from the behaviors of excited states in pure rubrene (Rb) with negligible ISC and strong SF. More importantly, HL‐RISC is stronger in TBRb than in Rb‐doped systems, which is consistent with the higher EQE frequently reported from TBRb‐doped OLEDs. Thus, this work deepens the physical understanding of microscopic processes in typical organic multi‐functional semiconductors of TBRb or Rb and paves the way for fabricating further high‐efficiency yellow OLEDs. [ABSTRACT FROM AUTHOR]