Optimal substation capacity planning method in high-density load areas considering renewable energy

With the increasing penetration of renewable energy, the adaptability of the existing substation planning model in terms of capacity and quantity of transformer needs to be further studied when preferring large-capacity substations. Considering the variations of renewable energy penetration rate and load, this paper proposes a method to optimize the total capacity of substations in distribution networks. This paper introduces the influence of renewable energy access on power supply reliability and introduces the idea of partitioning for economic analysis of reliability. An economic analysis model for simultaneously optimizing the capacity and quantity of substation transformer in the distribution network is constructed, taking into account the effects of reducing net load and enhancing the reliability of the distribution feeders resulting from renewable energy access to the medium and low voltage side of the substation. Various wiring means of the distribution network are retained and the impact of renewable energy access on the reliability of the network power supply is quantified. The optimization model is solved by the multivariate universe optimizer(MVO) algorithm with stronger optimality finding capability and short solving time. Finally, the case study results of a regional distribution network are employed to demonstrate and verify the validity and rationality of the method

Investigating the bearing performance of the foundation under the combined effects of flood scouring and soaking

Abstract Bearing capacity degradation of foundations under the impact of the flood is one of the major reasons responsible for the collapse and damage to the rural buildings, posing a serious threat to the local village societies. Based on a case study of a rural building foundation had been destroyed by flooding. This paper investigated the deterioration process of rural building foundations under the combined effect of dynamic scouring and static soaking caused by flooding. Using the two-dimensional shallow water equation, erosion depth was calculated for different flood velocities. Then, the bearing capacity degradation under the combined scouring-soaking effect was analyzed using the finite element method. Finally, investigating the influence of inflow direction and building group masking on the foundation's bearing capacity. The results indicate that under the combined effect, the bearing capacity of village building foundations decreases by 47.88%, with scouring slightly more impactful than soaking. Inflow angle has minimal effect on bearing performance, while the masking effect of the building group provides better protection for the foundation of rear buildings

An Integrated Approach for Simulating Debris-Flow Dynamic Process Embedded with Physically Based Initiation and Entrainment Models

Recent studies have indicated that the accurate simulation of debris flows depends not only on the selection of numerical models but also on the availability of precise data on the initial source location and depth. Unfortunately, it is currently difficult to obtain quantitative data on source locations and depths during field investigations or model experiments of debris flow disasters. Therefore, in this study, we propose an integrated approach for simulating the debris-flow dynamic process that includes the physically based slope initiation source estimation and the entrainment-incorporated process simulation. We treat the potential slip surfaces’ locations and depths as random variables to search for the critical surface corresponding to the minimum stability factor by Monte Carlo simulation. Using the spatial variation interval of the soil parameters, we estimate the range of possible critical slip surfaces and the interval of the initiation source volume. Moreover, we propose a wet/dry front treatment method applied to the finite difference scheme and integrate it into our entrainment-incorporated model to improve the stability and accuracy of the numerical solution over complex topography. The effectiveness of the method is demonstrated through a case study of the 2010 Hongchun debris flow event in Yingxiu town. The result indicates that our method is effective in simulating debris flow dynamics, including slope initiation source estimation and dynamic process simulation

Dynamic Perturbations of CD4 and CD8 T Cell Receptor Repertoires in Chronic Hepatitis B Patients upon Oral Antiviral Therapy

Long-term treatment with nucleos(t)ide analogs (NUCs) can improve the antiviral T cell response in chronic hepatitis B (CHB) patients. Whether and to what extent the T cell response is improved by NUCs in the early stage leading to hepatitis B e antigen (HBeAg) seroconversion remain to be clarified. A total of 22 CHB patients undergoing 2-year telbivudine-based therapy were enrolled, including 10 exhibiting a complete response (CR) and 12 exhibiting a non-complete response (NCR) according to HBeAg seroconversion at week 52. Peripheral CD4+ and CD8+ T cells were sorted at baseline, weeks 12, and 24. The T cell receptor β chain (TCRβ) complementarity-determining region 3 was analyzed by unbiased high-throughput sequencing. Compared with NCR group, patients in CR group had a much lower percentage of persistent clonotypes (P < 0.001) but remarkably higher percentages of new and expanded clonotypes (P < 0.05) between any two time points for both CD4 and CD8 subsets. The CD4 T cells exhibited a stronger response than CD8 population in the patients. The number of new and expanded clonotypes was inversely associated with the decline of viral antigen. In conclusion, NUC-based therapy induces a broad and vigorous T cell response with rapid decline of antigenemia during the early stage of treatment. A broad T cell expansion is crucial for HBeAg seroconversion. Our findings suggest that the potent suppression of hepatitis B virus replication by NUC monotherapy complemented with additional immunomodulatory strategies may increase the likelihood of a functional cure for CHB in the future

Dynamic Perturbations of CD4 and CD8 T Cell Receptor Repertoires in Chronic Hepatitis B Patients upon Oral Antiviral Therapy

Effective Protection of Fundamental Rights in a pluralist worl

Additional file 1 of Pregabalin mitigates microglial activation and neuronal injury by inhibiting HMGB1 signaling pathway in radiation-induced brain injury

Additional file 1: Fig. S1. Body weight changes in mice receiving radiation or pregabalin. Body weight changes in mice after 14 days of continuous injection of pregabalin (PGB) or saline solution (Con) in RIBI mice. For days 1–4 post-treatment, n = 14–23 mice per group. For days 5–8 post-treatment, n = 10–15 mice per group. For days 9–14 post-treatment, n = 4–9 mice per group. Fig. S2. Microglial body size and CD68 expression changes after radiation in vivo. A Representative confocal images of IBA1 and CD68 co-labeling in the cortex of mice 3, 7, or 14 days after radiation. Red: IBA1, green: CD68. B-C Quantification of the body size of IBA1+ cells and the proportion of CD68+ area / IBA1+ area in the cortex. Data were analyzed by one-way ANOVA followed by the Student’s t-test analysis. All other groups were compared with the control group. n = 4 mice per group and 2–3 slices per mouse for immunofluorescence staining. Data were presented as mean ± SEM, *p < 0.05, **p < 0.01, and ***p < 0.001. Fig. S3. Pregabalin inhibited microglia activation in the cortex of RIBI mice. A Representative images of IBA1 and CD68 co-labeling in the cortex of mice 3 days after radiation. Red: IBA1, green: CD68. B Quantification of the proportion of CD68+ area / IBA1+ area in the cortex of mice 3 days after radiation. C Representative images of IBA1 and CD68 co-labeling in the cortex of mice 7 days after radiation. D Quantification of the proportion of CD68+ area / IBA1+ area in the cortex of mice 7 days after radiation. Data were analyzed by one-way ANOVA followed by the Student’s t-test analysis. All other groups were compared with the indicated group. n = 4 mice per group and 2–3 slices per mouse for immunofluorescence staining. Data were presented as mean ± SEM, *p < 0.05, **p < 0.01, and ***p < 0.001. Fig. S4. Pregabalin inhibited microglia activation in the hippocampus of RIBI mice. A-B Representative confocal images of IBA1 and CD68 co-labeling in the hippocampal CA1 (A) and DG (B) regions of RIBI mice 14 days after pregabalin treatment. Red: IBA1, green: CD68, and blue: DAPI. n = 4 mice per group and 2–3 slices per mouse for immunofluorescence staining. See Fig. 1I-J for statistical data in the main text. Fig. S5. Effect of pregabalin on microglial inflammatory response induced by radiation in vitro. A-D Q-PCR analysis the effects of pregabalin, with different concentration (1 µM, 6.25 µM, 12.5 µM, 25 µM, and 50 µM), on the mRNA levels of inflammatory factors Il-1β, Tnf-α, Cox-2, and iNos in BV2 cells after a single dose of 10 Gy radiation. Data were analyzed by one-way ANOVA followed by the Student’s t-test analysis. All other groups were compared with the indicated group. n = 3 per group for Q-PCR analysis in vitro. Data were presented as mean ± SEM, ns = not significant, **p < 0.01, and ***p < 0.001. Fig. S6. Effect of pregabalin on IL-6 and TNF-α expressions in microglia after radiation. A Representative immunofluorescent images of IL-6 and β-tubulin in BV2 cells among the different groups. Staining with β-tubulin to visualize cytoskeleton and staining with DAPI to visualize nucleus. B The fluorescence intensity data of IL-6 were recorded by confocal microscopy. C Representative immunofluorescent images of TNF-α and β-tubulin in BV2 cells among the different groups. D The fluorescence intensity data of TNF-α were recorded by confocal microscopy. Data were analyzed by one-way ANOVA followed by the Student’s t-test analysis. All other groups were compared with the indicated group. n = 3 per group for immunofluorescence staining in vitro. Data were presented as mean ± SEM, ns = not significant and **p < 0.01. Fig. S7. Pregabalin inhibited microglial inflammatory response not by acting on astrocyte in vitro. A Schematic diagram of BV2 cells incubated with the culture supernatant from astrocyte after different treatment. B-E Q-PCR analysis of Il-1β, Tnf-α, iNos, and Icam-1 mRNA levels in BV2 cells after incubated with the supernatant from pregabalin-treated astrocyte. Data were analyzed by one-way ANOVA followed by the Student’s t-test analysis. All other groups were compared with the indicated group. n = 4 per group for Q-PCR analysis in vitro. Data were presented as mean ± SEM, ns = not significant and *p < 0.05. Fig. S8. Effect of pregabalin on potential chemokines in injured neurons. A-G Q-PCR analysis of Mmp9, Cgrp, Tac1, Cx3cl1, Ccl21, Mmp2, and Ccl2 mRNA levels in neurons after treatment with the different supernatant from BV2 cells. Data were analyzed by one-way ANOVA followed by the Student’s t-test analysis. All other groups were compared with the indicated group. n = 3 per group for Q-PCR analysis in vitro. Data were presented as mean ± SEM, ns = not significant, *p < 0.05, and ***p < 0.001. Fig. S9. Knocking out TLR2/TLR4/RAGE mitigated microglia activation. A-C Schematic diagram of CRISPR/Cas9-mediated TLR2/TLR4/RAGE knockout in BV2 cells and Q-PCR analysis was used to detect the knockout efficiency. D-F Q-PCR analysis of Il-6, Tnf-α, and Cox-2 mRNA levels in activated BV2 cells which were treated with culture supernatant from radiation-injured (activated) or normal (control) neurons for 24 h. Data were analyzed by one-way ANOVA followed by the Student’s t-test analysis. All other groups were compared with the indicated group. n = 3–4 per group for Q-PCR analysis in vitro. Data were presented as mean ± SEM, *p < 0.05, **p < 0.01, and ***p < 0.001. Table S1. List of primers used for RNA analyses. Table S2. List of antibodies used in this study. Table S3. List of gRNA sequences used for CRISPR/Cas9-mediated gene knockout. Table S4. List of oligonucleotide sequences used for plasmid construction. Table S5. List of primers used for the verification of CRISPR/Cas9-mediated gene knockout