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[Objective] Sustainable Development Goal 15.3.1 (SDG 15.3.1) is one of the important indicators to characterize land degradation.Exploring the impact of land use change and ecosystem service values (ESVs) on SDG 15.3.1 is a key factor to improve land degradation. [Methods] Based on land use and carbon stock changes, a new evaluation rule was established for SDG15.3.1 index, and the completion of SDG 15.3.1 was evaluated. The equivalent factor method was used to calculate the value of ecosystem services to quantitatively analyse the impact of land use change on ESV. [Results] (1) The land use type change was frequent in the study area, which mainly showed that high forest land, water body and construction land increased, cultivated land, grassland and shrub decreased, and unused land remained basically unchanged; (2) The spatial distribution pattern of ESV was high in the middle, low arround, high in the west and low in the east; From 2000 to 2020, the total ESV loss was 7.32×108 yuan. From 2000 to 2010, the ESV loss of land degradation area was 3.03×109 yuan. From 2010 to 2020, the ESV loss in land degradation areas was 2.28×109 yuan. (3) According to the evaluation results of SDG15.3.1, the indicators of SDG15.3.1 for 2000—2010 and 2010—2020 are 5.22 percent and 4.77 percent, respectively, while the net land restoration area was -1.62×105 hm2 and -2.4×105 hm2. The SDG15.3.1 target had improved, but the zero land degradation growed target is still not achieved. [Conclusion] The research results provided a reference for the impact of land use change on ecosystem services in the process of achieving SDG 15.3.1 in plateau urban agglomerations.

Cell-free (CF) networks can reduce cell boundaries by densely deploying base stations (BSs) with additional hardware costs and power sources. Integrating a reconfigurable intelligent surface (RIS) into CF networks can cost-effectively increase the capacity and coverage of future wireless systems. This paper considers an RIS-aided CF system where each user is supported by a devoted RIS and can establish connections with multiple BSs for coherent transmission. Specifically, each RIS can enhance signal transmission between users and their selected BSs through passive beam-forming, but also randomly scattered signals from other non-selected BSs to users, causing additional signals and interference in the network. To gain insights into the system performance, we first derive the average signal-to-interference-plus-noise ratio (SINR) received by each user in a closed-form expression. Subsequently, we formulate an optimization problem aimed at maximizing the weighted sum-SINR of all users in the RIS-CF network. This optimization considers both BS transmit power allocation and BS selections as variables to be jointly optimized. To tackle the complexity of this nonconvex optimization problem, we develop an innovative two-layer iterative approach that offers both efficiency and efficacy. This algorithm iteratively updates the transmit power allocation and BS selections to converge to a locally optimal solution. Numerical results demonstrate significant performance improvement for the RIS-CF network using our proposed scheme. These results also highlight the effectiveness of jointly optimizing BS transmit power allocation and BS selections in the RIS-CF network. [ABSTRACT FROM AUTHOR]

(−)‐Epigallocatechin‐3‐gallate (EGCG) has been shown antibacterial activity against Campylobacter jejuni; however, the relevant antibacterial mechanism is unknown. In this study, phenotypic experiments and RNA sequencing were used to explore the antibacterial mechanism. The minimum inhibitory concentration of EGCG on C. jejuni was 32 µg/mL. EGCG‐treated was able to increase intracellular reactive oxygen species levels and decline bacterial motility. The morphology and cell membrane of C. jejuni after EGCG treatment were observed collapsed, broken, and agglomerated by field emission scanning electron microscopy and fluorescent microscopy. The RNA‐seq analysis presents that there are 36 and 72 differential expressed genes after C. jejuni was treated by EGCG with the concentration of 16 and 32 µg/mL, respectively. EGCG‐treated increased the thioredoxin expression, which was a critical protein to resist oxidative stress. Moreover, downregulation of the flgH and flgM gene in flagellin biosynthesis of C. jejuni was able to impair the flagella, reducing cell motility and virulence. The primary antibacterial mechanism revealed by RNA‐seq is that EGCG with iron‐chelating activity competes with C. jejuni for iron, causing iron deficiency in C. jejuni, which potentially impacts the survival and virulence of C. jejuni. The results suggested a new direction for exploring the activity of EGCG against C. jejuni in the food industry. Practical Application: A deeper understanding of the antibacterial mechanism of EGCG against C. jejuni was more beneficial in improving the food safety, eliminating concerns about human health caused by C. jejuni in future food, and promoting the natural antibacterial agent EGCG application in the food industry. [ABSTRACT FROM AUTHOR]

Phenyllactic acid (PLA) generally recognized as a natural organic acid shows against Vibrio parahaemolyticus activity. In this study, V. parahaemolyticus ATCC17802 (Vp17802) was cultured under the stress of 1/2MIC PLA, and then the antibacterial mechanisms were explored via transcriptomics. The minimum inhibitory concentration (MIC) of PLA against Vp17802 was 3.2 mg/mL, and the time-kill analysis resulted that Vp17802 was inhibited. PLA was able to destroy the bacterial membrane, leading to the leakage of intracellular substances and decline of ATP levels. The RNA-sequencing analysis results indicated that 1616 significantly differentially expressed genes were identified, among which 190 were up-regulated and 1426 were down-regulated. Down-regulation of the icd2 gene in the TCA cycle mediates blockage of tyrosine metabolic, arginine biosynthesis, and oxidative phosphorylation, causing insufficient energy supply of Vp17802. Moreover, PLA could cause amino acids, metal ions, and phosphate transporters to be blocked, affecting the acquisition of nutrients. The treatment by PLA altered the expression of genes encoding functions involved in quorum sensing, flagellar assembly, and cell chemotaxis pathway, which may be interfering with the biofilm formation in Vp17802, reducing cell motility. Overall, 1.6 mg/mL PLA inhibited the growth of Vp17802 by disrupting to uptake of nutrients, cell metabolism, and the formation of biofilms. The results suggested a new direction for exploring the activity of PLA against Vp17802 and provided a theoretical basis for bacterial pathogen control in the food industry. Key points: •RNA sequencing was carried out to indicate the antibacterial mechanism of Vp17802. •The icd2 gene in the TCA cycle mediates blockage of metabolic of Vp17802. •The biofilm formation has interfered with 1.6 mg/mL PLA, which could reduce cell motility and virulence. [ABSTRACT FROM AUTHOR]

Introduction: Glioblastoma patients have a highly immunosuppressive tumor microenvironment and systemic immunosuppression that comprise a major barrier to immune checkpoint therapy. Based on the production of endocannabinoids by glioblastomas, we explored involvement of endocannabinoid receptor 2 (CB2R), encoded by the CNR2 gene, which is predominantly expressed by immune cells, in glioblastoma-related immunosuppression. Materials & Methods: Bioinformatics of human glioblastoma databases was used to correlate enzymes involved in the synthesis and degradation of endocannabinoids, as well as CB2Rs, with patient overall survival. Intrastriatal administration of luciferase-expressing, murine GL261 glioblastoma cells was used to establish in in vivo glioblastoma model for characterization of tumor growth and intratumoral immune cell infiltration, as well as provide immune cells for in vitro co-culture experiments. Involvement of CB2Rs was determined by treatment with CB2R agonist (GW405833) or CB2R antagonist (AM630). ELISA, FACS, and immunocytochemistry were used to determine perforin, granzyme B, and surface marker levels. Results: Bioinformatics of human glioblastoma databases showed high expression of CB2R and elevated endocannabinoid production correlated with poorer prognosis, and involved immune-associated pathways. AM630treatment of GL261 glioblastoma-bearing mice induced a potent antitumor response, with survival plateauing at 50% on Day 40, when all control mice (median survival 28 days) and mice treated with GW405833 (median survival 21 days) had died. Luciferase tumor imaging revealed accelerated tumor growth by GW405833 treatment, but stable or regressing tumors in AM630-treated mice. Notably, in spleens, AM630 treatment caused an 83% decrease in monocytes/macrophages, and 1.8- and 1.6-fold increases in CD8+ and CD4+ cells, respectively. Within tumors, there was a corresponding decrease in tumor-associated macrophages (TAMs) and increase in CD8+ T cells. In vitro, lymphocytes from AM630-treated mice showed greater cytotoxic function (increased percentage of perforin- and granzyme B-positive CD8+ T cells). Discussion: These results suggest that inhibition of CB2R enhances both immunosuppressive TAM infiltration and systemic T-cell suppression through CB2R activation, and that inhibition of CB2Rs can potently counter both the immunosuppressive tumor microenvironment, as well as systemic immunosuppression in glioblastoma.