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In order to optimize the extracting conditions of colorants from camphor leaves and improve the extraction effect of natural camphor leaf colorants, the effects of three different extraction methods including high-speed wall breaking, ultrasonic wave and hot leaching on colorants extraction were discussed. For high-speed solvent wall breaking, the extraction effects of different times and different concentrations of ethanol/ water were compared. The dyeing process of camphor leaf pigment dyed wool fabric was optimized, and the dyeing performance and the moth-proofing performance of the fabric were studied. The results show that the optimized process for extracting pigments from camphor leaves is: high-speed wall-breaking extraction method, 60% (w/w) ethanol/water mixed solvent, the crude pigment yield can reach 17.37%, and the extracted pigments has a good dyeing effect on wool fabric in the dye bath pH value 5, and the dyed wool fabric has a certain mothproof effect. [ABSTRACT FROM AUTHOR]

The corresponding author explained that 10 mice were used in each group whilst performing liver ischemia/reperfusion experiments, but that two liver samples of the Ago-mir-NC group were damaged during embedding or sectioning, and as a result this group only contained 8 samples. Specifically, the Fig 6D Ago-mir-146a panel appeared similar to the Fig 6G Ago-mir-146a panel despite being used to represent different experimental conditions. They provided an updated Fig 6 with the correct Fig 6D Ago-mir-146a image obtained in the original experiment, as well as the individual level data underlying the published results (S1 File). [Extracted from the article]

Background & Aims A critical role of the Toll-like receptor ( TLR)-4 and its downstream mediators in the pathogenesis of small-for-size liver graft injury has been documented. Recently, the micro RNA-146 (miR-146) was identified as a potent negative regulator of the TLR4 signalling pathway. In this study, the role of miR-146a and miR-146b in the attenuation of TLR-4 signalling and small-for-size liver graft injury was investigated. Methods The expression levels of miR-146a and miR-146b during small-for-size liver graft injury were studied in vivo. In addition, the effects of miR-146a and miR-146b on the expression of IRAK1 and TRAF6 in the rat macrophage cell line NR8383 and rat liver kupffer cells were studied in vitro. The in vivo effect of miR-146a and miR-146b on small-for-size liver graft injury was studied by the tail vein injection of miR-146a mimics and miR-146b mimics. Results The levels of miR-146a and miR-146b decreased with a small-for-size liver graft. MiR-146a and miR-146b inhibited IRAK1 and TRAF6 expression by binding to the 3′ UTR of IRAK1 or TRAF6, respectively, in the rat macrophage cell line NR8383. The administration of miR-146a mimics and miR-146b mimics prevented liver graft injury in small-for-size liver graft injury via the inactivation of IRAK1 and TRAF6 in vivo. Conclusions miR-146a and miR-146b prevent liver injury in small-for-size liver graft injury via the inactivation of IRAK1 and TRAF6. [ABSTRACT FROM AUTHOR]

The prevalent intra- and intertumoral heterogeneity results in undesirable prognosis and therapy failure of pancreatic cancer, potentially resulting from cellular senescence. Herein, integrated analysis of bulk and single-cell RNA-seq profiling was conducted to characterize senescence-based heterogeneity in pancreatic cancer. Publicly available bulk and single-cell RNA sequencing from pancreatic cancer patients were gathered from TCGA-PAAD, PACA-AU, PACA-CA, and GSE154778 datasets. The activity of three senescence-related pathways (cell cycle, DNA repair, and inflammation) was scored utilizing ssGSEA algorithm. A series of functional verifications of crucial genes were accomplished in patient tissue and pancreatic cancer cells. Based upon them, unsupervised clustering analysis was executed to classify pancreatic cancer samples into distinct senescence-based clusters at the bulk and single-cell levels. For single-cell transcriptome profiling, cell clustering and annotation were implemented, and malignant cells were recognized utilizing infercnv algorithm. Two senescence-based clusters were established and highly reproducible at the bulk level, with the heterogeneity in prognosis, clinicopathological features, genomic CNVs, oncogenic pathway activity, immune microenvironment and immune checkpoints. Senescence-relevant gene CHGA, UBE2C and MCM10 were proved to correlate with the migration and prognosis of pancreatic cancer. At the single-cell level, seven cell types were annotated, comprising ductal cells 1, ductal cells 2, fibroblasts, macrophages, T cells, stellate cells, and endothelial cells. The senescence-based classification was also proven at the single-cell level. Ductal cells were classified as malignant cells and non-malignant cells. In the tumor microenvironment of malignant cells, hypoxia and angiogenesis affected senescent phenotype. The heterogeneity in senescence was also observed between and within cell types. Altogether, our findings unveil that cellular senescence contributes to intra- and intertumoral heterogeneity in pancreatic cancer, which might facilitate the development of therapeutics and precision therapy in pancreatic cancer., (© 2025 International Union of Biochemistry and Molecular Biology.)

Background: The association between dietary zinc intake and epilepsy remains unclear. This study aimed to investigate the relationship between zinc intake from the diet and epilepsy, employing Mendelian randomization (MR) to explore potential causal links between zinc and epilepsy., Methods: The cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2013 and 2018. Among the 4,434 participants included, 1.5% (67/4,434) reported having epilepsy. Restricted cubic spline models and logistic regression models were employed to examine the relationships between dietary zinc intakes and epilepsy. Subsequently, a 2-sample Mendelian randomization (MR) analysis was conducted using the inverse variance weighted (IVW) approach as the primary analysis., Results: In the restricted cubic spline (RCS) analysis, the relationship between dietary zinc consumption and epilepsy displayed an L-shaped curve (nonlinear, p  = 0.049). After multivariate adjustments, the adjusted odds ratios for epilepsy in T2 (5.0-11.0 mg/day) and T3 (≥11.0 mg/day) were 0.49 (95% confidence interval [CI]: 0.26-0.92, p  = 0.026) and 0.60 (95% CI: 0.31-1.17, p  = 0.132), respectively, compared to the lowest dietary zinc consumption tertile (T1, ≤5.0 mg/day). The IVW method indicated that genetically predicted zinc intake per standard-deviation increase was inversely associated with three types of epilepsy, including all types of epilepsy (OR = 1.06, 95% CI: 1.02-1.11, p  = 0.008), generalized epilepsy (OR = 1.13, 95% CI: 1.01-1.25, p  = 0.030), and focal epilepsy (documented hippocampal sclerosis) (OR = 1.01, 95% CI: 1.00-1.02, p  = 0.025)., Conclusion: Our findings suggest that a daily zinc intake ranging from 5.0 to 11.0 mg is associated with the lowest risk of epilepsy. Furthermore, Mendelian randomization (MR) studies provide additional support for the existence of a causal relationship between zinc and epilepsy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Huang, Gao, Chen, Wang, Lu, Gao, Hu and Fang.)

Background: Previous studies suggest a link between diet-derived circulating antioxidants and epilepsy, but the causal relationship is unclear. This study aims to investigate the causal effect of these antioxidants on epilepsy., Methods: To assess the causal link between dietary antioxidants and epilepsy risk, we conducted a two-sample Mendelian randomization (MR) analysis. This involved examining antioxidants such as zinc, selenium, α- and γ-tocopherol, vitamin A (retinol), vitamin C (ascorbate), and vitamin E (α-tocopherol). We utilized instrumental variables (IVs) which were genetic variations highly associated with these commonly used antioxidants. Exposure data were sourced from a comprehensive genome-wide association study (GWAS). We aggregated data from the International League Against Epilepsy (ILAE) Consortium sample, which included various types of epilepsy, as an outcome variable. Finally, we applied the inverse variance weighting method and conducted sensitivity analyses for further validation., Results: Based on the primary MR estimates and subsequent sensitivity analyses, the inverse variance weighting (IVW) method revealed that a genetically predicted increase in zinc per standard deviation was positively associated with three types of epilepsy. This includes all types of epilepsy (OR = 1.06, 95% CI: 1.02-1.11, p  = 0.008), generalized epilepsy (OR = 1.13, 95% CI: 1.01-1.25, p  = 0.030), and focal epilepsy (documented hippocampal sclerosis) (OR = 1.01, 95% CI: 1.00-1.02, p  = 0.025). However, there is no evidence indicating that other antioxidants obtained from the diet affect the increase of epilepsy either positively or negatively., Conclusion: Our research indicates that the risk of developing epilepsy may be directly linked to the genetic prediction of zinc, whereas no such association was found for other antioxidants., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Huang, Chen, Wang, Pan, Lu, Gao, Hu and Fang.)