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Using a genetic algorithm together with DFT computations, the stable isomers of Lin+1Fn (n = 2 ~ 17) are obtained. It is found that the Li3F2 is a planar structure, and starting at n = 3, Lin+1Fn adopt three-dimensional configurations with a terminal Li atom or vacancy of F atom. As the cluster sizes increase, the geometries of Lin+1Fn develop, first with cube-like and tubular structures, then forming cage-like arrangements, and eventually favoring rock-salt configurations. The Lin+1Fn (n = 3, 5, 8, 11, 13 and 15) are especially stable and magic number clusters. Low ionization potentials are acquired for Lin+1Fn due to the weakly bonded odd electrons of Li atoms. Particularly, the AIP/VIP for Li14F13 and Li17F16 are only 2.68/2.75 eV and 2.77/2.97 eV, respectively, which indicate that they can be looked as superalkali clusters. Meanwhile, the particularly large hyperpolarizabilities (3237157.14 a.u. and 716489.10 a.u.) for these two isomers are also obtained. According to the electronic structure analysis, Li atoms donate their 2s electrons to the 2p orbitals of F atoms, forming Li–F ionic bonds. Additionally, the spectral properties and the reactivities for the magic number clusters are further investigated. [ABSTRACT FROM AUTHOR]

This study aimed to assess the prognostic value of 18F-fluorodeoxyglucose positron emission tomography/computer tomography (18F-FDG PET/CT) in patients with relapsed multiple myeloma (MM). Fifty-one consecutive patients with relapsed MM were enrolled in this retrospective study. 18F-FDG parameters based on the Italian Myeloma Criteria for PET Use (IMPeTUs) and clinical data were analyzed for overall survival (OS) and progression-free survival (PFS). The Cox proportional risk model was used for univariate and multivariate analysis, and Kaplan-Meier survival curves were used for survival analysis. The median length of follow-up was 20 months (IQR, 5–29 months), the median PFS for the entire cohort was 8 months (IQR, 3–17 months) and the median OS was 21 months (IQR, 8–49 months). Multivariate survival analysis demonstrated that the Deauville score of BM > 3 [HR 2.900, 95% CI (1.011, 8.319), P = 0.048] and the presence of EMD [HR 3.134, 95% CI (1.245, 7.891), P = 0.015] were independent predictors of poor PFS. The presence of EMD [HR 12.777, 95% CI (1.825, 89.461), P = 0.010] and the reduced platelets count [HR 7.948, 95% CI (1.236, 51.099), P = 0.029] were adversely associated with OS. 18F-FDG PET/CT parameters based on IMPeTUs have prognostic significance in patients with relapsed MM. [ABSTRACT FROM AUTHOR]

This experiment was conducted to study the effects of Astragalus polysaccharide (APS) on intestinal antioxidant capacity, immunity, structural integrity, and permeability of hybrid crucian carp (control group, Astragalus polysaccharide stress group (APs), and salt and alkali stress group (SAs)) under saline-alkali environment. The results showed that the CAT activity, MDA activity, and total antioxidant capacity in the APs group was significantly higher than that in the control group (P < 0.05). At 6 h, the activity of intestinal GPX in the SAs group was significantly higher than that in the control group and APs group (P < 0.05). At 48h, the activity of C3 in the APs group was significantly higher than that in the control group (P < 0.05). At 24 h, the content of C4 in the APs group was significantly higher than that in the control group (P < 0.05). At 72 h, the ACP and the AKP activity in the APs group and the SAs group was significantly higher than that in the control group (P < 0.05). Inflammatory cells infiltrated the folds in both the APs and SAs groups. At 72 h, the gene expression levels of claudin 7, claudin 12, claudin c, and ZO-1 in the APs group and SAs group were significantly higher than those in the control group (P < 0.05). At 72 h, the expression of inflammation-related genes in the APs group and SAs group was significantly higher than that in the control group (P < 0.05). In conclusion, APS, as an additive, can alleviate the damage of intestinal physical barrier and immune barrier caused by salt-alkali stress to hybrid crucian carp, including up-regulation of genes for inhibiting inflammation and tight junction and alleviating oxidative stress, thus maintaining the integrity of intestinal structure. [ABSTRACT FROM AUTHOR]

Carassius auratus gibelio, commonly known as crucian carp, is the main species of freshwater aquaculture in China. Due to high-density aquaculture and environmental pollution, various diseases continue to emerge, especially the diseases caused by pathogenic bacteria have seriously restricted the development of freshwater aquaculture. Among these, Aeromonas hydrophila (AH) is the one of the most serious fish disease causing economic losses among fish farmers. An in-depth understanding of the crucian carp's immune system and its genes involved in the response to bacterial infection is necessary for disease control. In this study, the breeding period was divided into the control group (C group) and the Bacillus licheniformis (B. licheniformis) group (BL group). After 4 weeks of culture, the crucian carp was infected with AH and divided into the control group (Cg group) and the B. licheniformis group (BLg group). After the 72-h challenge, the Illumina-based paired-end sequencing approach to analyze the transcriptome profile of the crucian carp gut following AH infection. A total of 472.05 million valid reads were found from the four intestinal samples and 403.18 million reads were mapped successfully, of which 243.34 million were unique. About GO enrichment analysis, significant differentially expressed genes (DEGs) were more in biological process (406 DEGs), regulation of transcription, DNA-templated (345 DEGs), and signal transduction (304 DEGs). In the cell components, membrane (1913 DEGs) and integral component of membrane (1789 DEGs) had a higher number of significantly different genes. In the molecular function, metal ion binding (780 DEGs), ATP binding (535 DEGs), transferase activity (491 DEGs), and nucleotide binding (482 DEGs) have a large number of significantly different genes. Regarding the KEGG enrich analysis section, this study is arranged in ascending P-value order, andthe most significant signaling paths are lysosome, glucose metabolism, cycline cycline receiver interaction, and phagosome. Among them, the cycline cycline receiver interaction has the highest difference in significant genes. In addition, 5 immune-related genes were selected for real-time fluorescence quantitative PCR analysis to verify the RNA-seq data, and the results showed that the expression of all 5 genes was upregulated, which was consistent with the results of our RNA-seq analysis. After analysis, it was found that B. licheniformis can alleviate the inflammatory response and protect the fish body. Our results provide a reference for further analysis of the antagonism and mitigation mechanism of B. licheniformis against AH. [ABSTRACT FROM AUTHOR]

Introduction: Currently, the cause of psoriatic arthritis (PsA) is unknown, and the effectiveness of current drug treatments is unsatisfactory. In March 2019, the US Food and Drug Administration (FDA) approved risankizumab, a humanized immunoglobulin G1 (IgG1) monoclonal antibody targeting the p19 subunit of interleukin (IL)-23, for the treatment of PsA in adults. This study aimed to conduct a meta-analysis of double-blind, randomized, placebo-controlled trials to evaluate the effectiveness and safety of risankizumab in moderate-to-severe PsA. Methods: We conducted a thorough search of relevant databases from the establishment of the databases to October 1, 2023. We conducted a meta-analysis using Stata 12.0 and utilized I2 and Egger tests to assess heterogeneity and publication bias among the studies. Bias assessment was performed using the risk bias map and bias risk summary diagram generated by Revman5.4 software. The review protocols were registered on PROSPERO (CRD42023451894) and adhered to the preferred reporting item of system evaluation (PRISMA) guideline. Results: Six randomized controlled trials (RCTs) involving 5038 patients with PsA treated with either risankizumab or placebo were included in the analysis. At 24 weeks, the risankizumab group demonstrated a significantly higher American College of Rheumatology-20 (ACR20) response rate compared to the placebo group (RR 1.760, 95% CI 1.568–1.977, P < 0.001). Additionally, the risankizumab group showed a significantly higher Minimal Disease Activity (MDA) response rate compared to the placebo group (RR 1.827, 95% CI 1.048–3.184, P < 0.05). The risankizumab group also exhibited improvement in Short Form 36 Questionnaire (SF-36) score (SMD 0.51, 95% CI 0.33–0.69, P < 0.001), with significantly lower Health Assessment Questionnaire Disability Index (HAQ-DI) score (SMD − 0.27, 95% CI − 0.37 to − 0.17, P < 0.001) and higher Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F) score (SMD 0.27, 95% CI 0.20–0.35, P < 0.001) compared to the placebo group. Moreover, the risankizumab group had a significantly lower Psoriasis Area and Severity Index (PASI) score (SMD − 6.12, 95% CI − 10.02 to 2.23, P < 0.001). A study by Mease et al. indicated that patients receiving risankizumab generally demonstrated numerical improvements in the Leeds Enthesitis Index (LEI), although the small sample size limits the evidence. Further research is necessary to provide evidence-based guidelines. There were no significant differences in the incidence of serious adverse events (SAE) and serious treatment-emergent adverse events (STEAE) between the risankizumab and placebo groups (RR 0.76, 95% CI 0.45–1.28, P = 0.31; RR 0.99, 95% CI 0.49–1.99, P = 0.97, respectively), and the overall incidence of adverse events (AE) was not comparable (RR 1.10, 95% CI 0.63–1.94, P = 0.73). Conclusion: Risankizumab showed superior efficacy across multiple outcome measures compared to placebo, with no significant increase in adverse events. Our findings endorse risankizumab as an excellent treatment option for PsA, offering valuable insights for clinicians and patients when choosing appropriate therapeutic interventions. Trial Registration: Retrospectively registered (CRD42023451894, 16 August 2023). [ABSTRACT FROM AUTHOR]

The patterns and biological functions of copper homeostasis-related genes (CHRGs) in acute myeloid leukemia (AML) remain unclear. We explored the patterns and biological functions of CHRGs in AML. Using independent cohorts, including TCGA-GTEx, GSE114868, GSE37642, and clinical samples, we identified 826 common differentially expressed genes. Specifically, 12 cuproptosis-related genes (e.g., ATP7A, ATP7B) were upregulated, while 17 cuproplasia-associated genes (e.g., ATOX1, ATP7A) were downregulated in AML. We used LASSO-Cox, Kaplan-Meier, and Nomogram analyses to establish prognostic risk models, effectively stratifying patients with AML into high- and low-risk groups. Subgroup analysis revealed that high-risk patients exhibited poorer overall survival and involvement in fatty acid metabolism, apoptosis, and glycolysis. Immune infiltration analysis indicated differences in immune cell composition, with notable increases in B cells, cytotoxic T cells, and memory T cells in the low-risk group, and increased monocytes and neutrophils in the high-risk group. Single-cell sequencing analysis corroborated the expression characteristics of critical CHRGs, such as MAPK1 and ATOX1, associated with the function of T, B, and NK cells. Drug sensitivity analysis suggested potential therapeutic agents targeting copper homeostasis, including Bicalutamide and Sorafenib. PCR validation confirmed the differential expression of 4 cuproptosis-related genes (LIPT1, SLC31A1, GCSH, and PDHA1) and 9 cuproplasia-associated genes (ATOX1, CCS, CP, MAPK1, SOD1, COA6, PDK1, DBH, and PDE3B) in AML cell line. Importantly, these genes serve as potential biomarkers for patient stratification and treatment. In conclusion, we shed light on the expression patterns and biological functions of CHRGs in AML. The developed risk models provided prognostic implications for patient survival, offering valuable information on the regulatory characteristics of CHRGs and potential avenues for personalized treatment in AML. [ABSTRACT FROM AUTHOR]