Multiple abiotic and biotic drivers of long-term wood decomposition within and among species in the semi-arid inland dunes:A dual role for stem diameter

Litter decomposition in sunny, semi-arid and arid ecosystems is controlled by both biotic factors including litter traits and abiotic factors including UV light, but for wood decomposition it still remains uncertain which of these environmental factors are the predominant controls among different woody species. In these dry ecosystems, it is likely that the stem diameter and spatial position of the dead wood are of particular importance especially where wood can be buried versus exposed due to substrate displacement by wind. Here we focus on the fact that stem diameter can affect decomposition rates both via the relative surface exposure to sunlight or soil and via higher resource quality of narrower stems to decomposers. In a field manipulation experiment, we investigated the relative importance of litter position (sand burial vs. surface vs. suspended above the surface), UV radiation (block versus pass) and stem diameter class (<2, 2–4, 4–8, 8–13 and 13–20 mm) on the mass loss of woody litters of four shrub species in an inland dune ecosystem in northern China. We found that after 34 months of in situ incubation, the mass loss of buried woody litters was three times faster than those of suspended and surface woody litters (53.5 ± 2.7%, 17.0 ± 1.0% and 14.4 ± 1.2%, respectively). In surface and suspended positions, litter decomposition rates were almost equally low and most mass loss was during the first 2 years, when bark was still attached and UV radiation had no significant effect on woody litter mass loss. These findings suggest that sand burial is the main environmental driver of wood decomposition via its control on microbial activity. Moreover, wood N and diameter class were the predominant factors driving woody litter decomposition. A key finding was that wider stems had slower litter decomposition rates not only directly (presumably via greater relative surface exposure) but also indirectly via their higher wood dry matter content or lower wood N; these effects were modulated by litter position. Our findings highlight a dual role of stem diameter on wood decomposition, that is, via relative surface exposure and via wood traits. The accuracy and confidence of global carbon cycling models would be improved by incorporating the different effects of stem diameter on woody litter decomposition and below-ground wood decomposition processes in drylands

Effect progress of complement system in neural repair after spinal cord injury

Spinal cord injury has the characteristics of high mortality and disability rates, and the treatment of spinal cord injury has been a worldwide problem. With the deepening of spinal cord injury research and the advancement of treatment methods, the survival rate of patients has improved, but the clinical efficacy is still not ideal. New research has found that the immune response is involved in the entire process of pathological changes and regeneration and repair after spinal cord injury. Among them, the complement system plays an important role in the occurrence and development of spinal cord injury. This article mainly reviews the role of the complement system in secondary spinal cord injury and regeneration and repair after spinal cord injury, including the doubleedged sword effect of the complement system, the impact of the complement system on axonal regeneration and synaptic maintenance, and possible signaling pathways, with a view to improving the treatment of spinal cord injury, providing new treatment ideas

Ubiquitin ligase RNF125 targets PD-L1 for ubiquitination and degradation

As a critical immune checkpoint molecule, PD-L1 is expressed at significantly higher levels in multiple neoplastic tissues compared to normal ones. PD-L1/PD-1 axis is a critical target for tumor immunotherapy, blocking the PD-L1/PD-1 axis is recognized and has achieved unprecedented success in clinical applications. However, the clinical efficacy of therapies targeting the PD-1/PD-L1 pathway remains limited, emphasizing the need for the mechanistic elucidation of PD-1/PD-L1 expression. In this study, we found that RNF125 interacted with PD-L1 and regulated PD-L1 protein expression. Mechanistically, RNF125 promoted K48-linked polyubiquitination of PD-L1 and mediated its degradation. Notably, MC-38 and H22 cell lines with RNF125 knockout, transplanted in C57BL/6 mice, exhibited a higher PD-L1 level and faster tumor growth than their parental cell lines. In contrast, overexpression of RNF125 in MC-38 and H22 cells had the opposite effect, resulting in lower PD-L1 levels and delayed tumor growth compared with parental cell lines. In addition, immunohistochemical analysis of MC-38 tumors with RNF125 overexpression showed significantly increased infiltration of CD4+, CD8+ T cells and macrophages. Consistent with these findings, analyses using The Cancer Genome Atlas (TCGA) public database revealed a positive correlation of RNF125 expression with CD4+, CD8+ T cell and macrophage tumor infiltration. Moreover, RNF125 expression was significantly downregulated in several human cancer tissues, and was negatively correlated with the clinical stage of these tumors, and patients with higher RNF125 expression had better clinical outcomes. Our findings identify a novel mechanism for regulating PD-L1 expression and may provide a new strategy to increase the efficacy of immunotherapy