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Variation in leaf traits is critical for carbon gains and losses during leaf life and drives litter carbon and nutrient losses via decomposition. Accurately quantifying litter decomposition parameters is essential for assessing ecosystem carbon and nutrient dynamics. Leaf litterbags have commonly been employed to measure effects of environmental drivers, decomposers, and plant traits on decomposition rates. There has been much debate regarding the suitability of substituting senesced dead leaves with fresh (green) leaves in litterbags, which has been common practice for mimicking green leaf fall or for practical reasons. Therefore, we tested the null hypothesis that replacement of dead leaves with fresh leaves in litterbag experiments is justified, based on similarities in structural and chemical traits between fresh and dead leaves across plant species and growth forms.We conducted a paired litterbag decomposition experiment with both fresh and dead leaves of 26 common species in subtropical China, in each of five contrasting ecosystems.While fresh leaves generally decomposed faster than dead leaves, this deviation varied among species and growth forms, based on their traits. Overall, there was significant but rather weak correlation between dead leaf decomposition rate k and fresh leaf k, across species and ecosystem types; the deviation between fresh and dead leaf k was larger for fast‐decomposing, mostly herbaceous species. The different decomposition patterns for fresh versus dead leaves were underpinned by key underlying traits integrated in leaf resource economics spectra (LES) for fresh and dead leaves. The dead leaf LES exhibited a greater predictive capability for dead leaf k while the fresh leaf LES had higher explanatory value for the fresh leaf k values.Our findings partly reject the null hypothesis and ask for caution in inferring leaf litter decomposition rates based on green leaf litterbags or traits data. We suggest follow‐up research on substituting senesced roots and stems with fresh ones in decomposition experiments.Synthesis. Human activities and extreme weather events are leading to increasing pulse inputs of fresh plant parts and our study contributes to knowledge on how they contribute to overall decomposition rates besides senesced litter inputs. [ABSTRACT FROM AUTHOR]

Background and Objectives: Periodontitis is an immunoinflammatory disease characterized by irreversible periodontal attachment loss and bone destruction. Ferroptosis is a kind of immunogenic cell death that depends on the participation of iron ions and is involved in various inflammatory and immune processes. However, information regarding the relationship between ferroptosis and immunomodulation processes in periodontitis is extremely limited. The purpose of this study was to investigate the correlation between ferroptosis and immune responses in periodontitis. Methods: Gene expression profiles of gingivae were collected from the Gene Expression Omnibus data portal. After detecting differentially expressed ferroptosis-related genes (FRGs), we used univariate logistic regression analysis followed by logistic least absolute shrinkage and selection operator (LASSO) regression to establish a ferroptosis-related classification model in an attempt to accurately distinguish periodontitis gingival tissues from healthy samples. The infiltration level of immunocytes in periodontitis was then assessed through single-sample gene-set enrichment analysis. Subsequently, we screened out immune-related genes by weighted correlation network analysis and protein–protein interaction (PPI) analysis and constructed an immune-related network based on FRGs and immune-related genes. Results: A total of 24 differentially expressed FRGs were detected, and an 8-FRG combined signature constituted the classification model. The established model showed outstanding discriminating ability according to the results of receiver operating characteristic (ROC) curve analysis. In addition, the periodontitis samples had a higher degree of immunocyte infiltration. Activated B cells had the strongest positive correlation while macrophages had a strong negative correlation with certain FRGs, and we found that XBP1, ALOX5 and their interacting genes might be crucial genes in the immune-related network. Conclusions: The FRG-based classification model had a satisfactory determination ability, which could bring new insights into the pathogenesis of periodontitis. Those genes in the immune-related network, especially hub genes along with XBP1 and ALOX5, would have the potential to serve as promising targets of immunomodulatory treatments for periodontitis. [ABSTRACT FROM AUTHOR]

Abstract: Background: Xenotransplantation is one of the promising strategies for overcoming the shortage of organs available for transplant. However, many immunological obstructions need to be overcome for practical use. Increasing evidence suggests that neutrophils contribute to xenogeneic cellular rejection. Neutrophils are regulated by activation and inhibitory signals to induce appropriate immune reactions and to avoid unnecessary immune reactivity. Therefore, we hypothesized that the development of neutrophil‐targeted therapies may have the potential for increased graft survival in xenotransplantation. Methods: A plasmid containing a cDNA insert encoding the human CD31 gene was transfected into swine endothelial cells (SEC). HL‐60 cells were differentiated into neutrophil‐like cells by culturing them in the presence of 1.3% dimethyl sulfoxide for 48 hours. The cytotoxicity of the differentiated HL‐60 cells (dHL‐60) and peripheral blood‐derived neutrophils was evaluated by WST‐8 assays. To investigate the mechanism responsible for hCD31‐induced immunosuppression, citrullinated histone 3 (cit‐H3) and phosphorylation of SHP‐1 were detected by a cit‐H3 enzyme‐linked immunosorbent assay (ELISA) and Western blotting, respectively. Results: A significant decrease in dHL‐60 and neutrophil‐mediated cytotoxicity in SEC/hCD31 compared with SEC was seen, as evidenced by a cytotoxicity assay. Furthermore, the suppression of NETosis and the induction of SHP‐1 phosphorylation in neutrophils that had been co‐cultured with SEC/CD31 were confirmed by cit‐H3 ELISA and Western blotting with an anti‐phosphorylated SHP‐1. Conclusion: These data suggest that human CD31 suppresses neutrophil‐mediated xenogenic cytotoxicity via the inhibition of NETosis. As CD31 is widely expressed in a variety of inflammatory cells, human CD31‐induced suppression may cover the entire xenogeneic cellular rejection, thus making the generation of human CD31 transgenic pigs very attractive for use in xenografts. [ABSTRACT FROM AUTHOR]