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The randomness of power grid has been greatly increased as the new energy power proportion increases due to the uncertainty of wind turbine (WT) and photovoltaic (PV) power, posing significant challenges to grid security and economic efficiency. In this paper, the typical‐day WT and PV power outputs were obtained by the Latin hypercube sampling method. A multiobjective dual‐layer optimization model has the goal of reducing network loss and voltage deviation. The Whale Optimization Algorithm (WOA) was employed to solve the model. Based on the optimization results, the dispatch schemes for reactive power compensation devices, energy storage systems, and on‐load voltage regulation devices are formulated to improve system stability and smooth the output fluctuations of new energy sources. Finally, the proposed method is verified in the improved AC/DC hybrid grid based on IEEE 39‐notes system. The results indicated that the method can effectively reduce the network loss and smooth voltage fluctuations. It provides a theoretical basis for the stable and economical of grids with a high proportion of new energy power.

Lung cancer is a major malignant tumor with high morbidity and fatality rates. For many years, traditional treatments for lung cancer have struggled to achieve a favorable outlook and prognosis. It is crucial to identify and innovate novel clinical therapeutic strategies and techniques to prevent tumor progression and prolong the survival time of patients with lung cancer. Cellular immunotherapies have revolutionized the treatment of malignant tumors and have been gradually applied in clinical practice. CAR-T therapy is the best-known cellular therapy and has achieved remarkable clinical outcomes in patients with hematological malignancies, but its effect on patients with lung cancer and other solid tumors is not satisfactory, partly because of the heterogeneity and complexity of lung cancers and the sterile TMEs. To further improve the clinical effect, multiple approaches and strategies have been adopted, including discovering new tumor antigen targets, improving safety, enhancing cytotoxicity, and increasing durability. Moreover, other cell-based immunotherapies have also showed great potential for the treatment of lung cancer, including TCR-T cells, TILs, CIK cells, NK cells, macrophages, and dendritic cells, which enriched the number of treatment choices for patients with lung cancer. In summary, the present article summarizes and highlights recent advances and challenges in the use of cellular immunotherapies for the treatment of lung cancer, which might stimulate new ideas for the further development of cellular immunotherapies.

Acute kidney injury (AKI) is an extremely dangerous clinical syndrome with high morbidity and mortality. Stem cell-based therapies have shown great promise for AKI treatment. Urine-derived stem cells (USCs) are a novel cell source in tissue engineering and cell therapy which provide advantages of simple, noninvasive, and low-cost harvest methods, efficient proliferation, and multi-differentiation potential. Here, we described the therapeutic effects of USCs in a rat model of cisplatin-induced AKI as a novel therapy. In vivo, the intravenous administration of USCs alleviated the renal functional damage in AKI rats, for the levels of blood urea nitrogen (BUN) and serum creatinine (SCr) were significantly decreased. The USCs-treated group also exhibited improved histological and ultrastructural changes, promoted proliferation, and inhibited apoptosis in renal tissues. After the USC therapy, the expression levels of proinflammatory cytokines (TNF-α and IL-6) and apoptosis-related proteins (BAX and cleaved caspase-3) were downregulated. In addition, the presence of a few GFP-labeled USCs was confirmed in rat renal tissues. In vitro, rat tubular epithelial (NRK-52E) cells were incubated with cisplatin to induce cell damage and then cocultured with USCs. After coculture with USCs, the cisplatin-induced NRK-52E cells showed higher cell viability and a lower apoptosis ratio than those of the control group, and cell cycle arrest was improved. In conclusion, our results demonstrated that USC therapy significantly improved the renal function and histological damage, inhibited the inflammation and apoptosis processes in the kidney, and promoted tubular epithelial proliferation. Our study exhibited the potential of USCs in the treatment of AKI, representing a new clinical therapeutic strategy.

Background Research has suggested significant correlations among ageing, immune microenvironment, inflammation and tumours. However, the relationships among ageing, immune microenvironment, cystitis and bladder urothelial carcinoma (BLCA) in the bladder have rarely been reported. Methods Bladder single-cell and transcriptomic data from young and old mice were used for immune landscape analysis. Transcriptome, single-cell and The Cancer Genome Atlas Program datasets of BLCA and interstitial cystitis/bladder pain syndrome (IC/BPS) were used to analyse immune cell infiltration and molecular expression. Bladder tissues from mice, IC/BPS and BLCA were collected to validate the results. Results Eight types of immune cells (macrophages, B-cells, dendritic cells, T-cells, monocytes, natural killer cells, γδ T-cells and ILC2) were identified in the bladder of mice. Aged mice bladder tissues had a significantly higher number of T-cells, γδ T-cells, ILC2 and B-cells than those in the young group ( P  < 0.05). Three types of T-cells (NK T-cells, γδ T-cells and naïve T-cells) and three types of B-cells (follicular B-cells, plasma and memory B-cells) were identified in aged mice bladder. Chemokine receptor 7 (CCR7) is highly expressed in aged bladder, IC/BPS and BLCA ( P  < 0.05). CCR7 is likely to be involved in T- and B-cell infiltration in aged bladder, IC/BPS and BLCA. Interestingly, the high CCR7 expression on BLCA cell membranes was a prognostic protective factor. Conclusions In this study, we characterised the expression profiles of immune cells in bladder tissues of aged and young mice and demonstrated that CCR7-mediated T- and B-cell filtration contributes to the development of bladder ageing, IC/BPS and BLCA.

Background Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory disease of the bladder for which no effective therapy is currently available. Understanding the pathogenesis of IC/BPS and identifying effective intervention targets are of great clinical importance for its effective treatment. Our work focuses on elucidating the key targets and underlying mechanisms of IC/BPS. Methods We established an experimental autoimmune cystitis (EAC) mouse model and generated gene knockout mice to elucidate key mediators triggering chronic inflammatory damage in IC/BPS through using single-cell RNA sequencing, proteomic sequencing, and molecular biology experiments. Results Our study revealed that the infiltration and activation of macrophages, T cells, and mast cells exacerbated inflammatory bladder damage in both IC/BPS and EAC mice. Notably, cell-cell communication among bladder immune cells was significantly enhanced in EAC mice. Macrophages, as the main cell types altered in EAC mice, received and transmitted the most intensity signalling. Mechanistically, macrophages synthesized and secreted S100A9, which in turn facilitated macrophage polarization and promoted the production of pro-inflammatory cytokines. S100A9 emerged as an important pro-inflammatory and pathogenic molecule in IC/BPS and EAC. Further analysis demonstrated that S100A9 activation enhanced the inflammatory response and exacerbated bladder tissue damage in IC/BPS patients and EAC mice via TLR4/NF-κB and TLR4/p38 signalling pathways. Importantly, inhibition of S100A9 with paquinimod, as well as genetic knockout of S100A9, significantly attenuated the pathological process. Conclusions S100A9 is an important pro-inflammatory and pathogenic molecule in IC/BPS and EAC. Targeting S100A9-initiated signalling pathways may offer a novel therapeutic strategy for IC/BPS.

[This corrects the article DOI: 10.1155/2019/8035076.].

A comprehensive understanding of the distribution and water movement of the substrate in root areas is crucial to the design and management of drip irrigation systems, which is a significant step to maximizing crop water use efficiency by understanding the hydrodynamics in soilless substrates. In this study, an improved HYDRUS-2D model by the dynamic root growth model was used to simulate water movement under the condition of drip irrigation and the water uptake process of the root, and then, compared with the observed data. Substrate water content under drip irrigation was also measured with the calibrated ECH20-EC5 sensors. The situation of substrate water movement was analyzed under the conditions of different depths, different initial water content, and different irrigation amount. The substrate water movement under different drip irrigation conditions was explored. The results showed that incorporating the defined initial and boundary conditions and the hydraulic characteristics of the substrate into the model enabled HYDRUS model to predict the movement and position of water in unsaturated porous media by solving Richards equation. Under drip irrigation, the substrate wetting body was approximately a quarter ellipse, and the water would continue to move to the area where the wetting front did not reach within 1 h after irrigation. The simulation results of the improved HYDRUS-2D model agreed well with those observed by the ECH2O-EC5 sensors, and the model could provide a basis for precision irrigation of soilless substrate culture under drip irrigation.

Introduction and hypothesis Genome-wide association studies suggest that autophagy plays an important regulatory role in inflammatory and autoimmune diseases. Inflammation and immune regulation disorders are involved in the occurrence and development of interstitial cystitis/bladder pain syndrome (IC/BPS). However, the changes and roles of autophagy in IC/BPS have not been reported. Therefore, this study aimed to investigate bladder autophagy and inflammation changes in patients with IC/BPS. Methods Bladder specimens ( n = 5) from patients with cystectomy due to end-stage IC/BPS were collected. The bladder samples of the control group ( n = 5) were derived from the normal area bladder tissue after radical cystectomy. H&E and toluidine blue staining were used for histological evaluation. The co-location of LC3, alpha-smooth muscle actin (α-SMA), and autophagosome was investigated with double-labeled immunofluorescence and transmission electron microscopy (TEM). The expression of IL-6, TNF-α, Bax, caspase-3, and BCL-2 in the detrusor layer was analyzed using immunohistochemistry (IHC) and Western blot (WB). Results Compared with the control group, bladder tissue from IC/BPS patients revealed thinner and edematous epithelium with many mast cells ( P < 0.05) infiltrating into the muscle layer. By using TEM ( P < 0.05), double-labeled immunofluorescence ( P < 0.05), and Western blot ( P < 0.05) in IC/BPS patients, autophagy was also found and was significantly increased in detrusor myocytes. IHC and WB indicate the expression of BCL-2 ( P < 0.05) was decreased, while IL-6, TNF-α, Bax, and caspase-3 expression was elevated ( P < 0.05). Conclusions The number of autophagosomes in detrusor cells was increased in IC/BPS. However, autophagy of detrusor muscle cells may not have sufficient phagocytic activity to effectively remove damaged proteins and mitochondria, which may lead to the continued deterioration of IC/BPS inflammation and apoptosis.

This paper introduces the whole construction of the control standardization simulation system based on the HCM5000G DC control and protection platform, which can meet the requirements of engineering design and various control performance indexes by adopting the standardization design of the self-control and localization platform. In this paper, the construction principle of the standardized control system and the optimization strategy of the control structure are discussed in detail, and the engineering simulation model is realized by using the real-time digital simulation system with the layered and distributed standardized interface design, which provides an important reference for the future large-scale application of the control and protection of DC Engineering.

Clarifying the locations, molecular markers, functions and roles of bladder interstitial cells is crucial for comprehending the pathophysiology of the bladder. This research utilized human, rat and mouse bladder single‐cell sequencing, bioinformatics analysis and experimental validation. The main cell types found in human, rat and mouse bladder tissues include epithelial cells, smooth muscle cells, endothelial cells, fibroblasts, myofibroblasts, neurons and various immune cells. Our study identified two significant types of interstitial cells (PTN+IGFBP6+PI16 (CD364)+ CD34+) and myofibroblasts (STC1+PLAT+TNC+). These two types of interstitial cells are mainly located in the subepithelial lamina propria, between muscles and between muscle bundles. In the CYP (cyclophosphamide)‐induced bladder injury mouse model, the interaction types and signals (MK, MIF, GDF and CXCL) of fibroblasts and myofibroblasts significantly increased compared with the normal group. However, in the aging mouse model, the signals CD34, LAMININ, GALECTIN, MK, SELPLG, ncWNT, HSPG, ICAM and ITGAL‐ITGB2 of fibroblasts and myofibroblasts disappeared, but the signals PTN and SEMA3 significantly increased. Our findings identified two crucial types of interstitial cells in bladder tissue, fibroblasts and myofibroblasts, which play a significant role in normal bladder physiology, CYP‐induced bladder injury and aging bladder development. Clarifying the locations, molecular markers, functions and roles of bladder interstitial cells is important for understanding the pathophysiology of the bladder. In this paper, the location, molecular markers and functions of bladder interstitial cells were elucidated by sequencing of human, mouse and rat bladder single cells, bioinformatics analysis and experimental verification. In this study, two important types of interstitial cells, fibroblasts (PTN+IGFBP6+PI16 (CD364)+ CD34+) and myofibroblasts (STC1+PLAT+TNC+), were identified. At the same time, we found that two important types of interstitial cells fibroblasts and myofibroblasts could play an important role in normal bladder physiology, CYP‐induced bladder injury and aging bladder development.