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

Anti-inflammatory Effects of α7-nicotinic ACh Receptors are Exerted Through Interactions with Adenylyl Cyclase-6

Background and purpose Alpha 7 nicotinic acetylcholine receptors (CHRNA7) suppress inflammation through diverse pathways in immune cells, so is potentially involved in a number of inflammatory diseases. However, the detailed mechanisms underlying CHRNA7’s anti‐inflammatory effects remain elusive. Experimental approach The anti‐inflammatory effects of CHRNA7 agonists in both murine macrophages (RAW 264.7) and bone marrow‐derived macrophages (BMDM) stimulated with LPS were examined. The role of adenylyl cyclase 6 (AC6) in Toll‐like Receptor 4 (TLR4) degradation was explored via overexpression and knockdown. A mouse model of chronic obstructive pulmonary disease was used to confirm key findings. Results Anti‐inflammatory effects of CHRNA7 were largely dependent on AC6 activation, as knockdown of AC6 considerably abnegated the effects of CHRNA7 agonists while AC6 overexpression promoted them. We found that CHRNA7 and AC6 are co‐localized in lipid rafts of macrophages and directly interact. Activation of AC6 led to the promotion of TLR4 degradation. Administration of CHRNA7 agonist PNU‐282987 attenuated pathological and inflammatory end points in a mouse model of chronic obstructive pulmonary disease (COPD). Conclusion and implications CHRNA7 inhibits inflammation through activating AC6 and promoting degradation of TLR4. The use of CHRNA7 agonists may represent a novel therapeutic approach for treating COPD and likely other inflammatory diseases

Modulation of cardiac resident macrophages immunometabolism upon high-fat-diet feeding in mice

BackgroundA high-fat diet (HFD) contributes to various metabolic disorders and obesity, which are major contributors to cardiovascular disease. As an essential regulator for heart homeostasis, cardiac resident macrophages may go awry and contribute to cardiac pathophysiology upon HFD. Thus, to better understand how HFD induced cardiac dysfunction, this study intends to explore the transcriptional and functional changes in cardiac resident macrophages of HFD mice.MethodsC57BL/6J female mice that were 6 weeks old were fed with HFD or normal chow diet (NCD) for 16 weeks. After an evaluation of cardiac functions by echocardiography, mouse hearts were harvested and cardiac resident CCR2- macrophages were sorted, followed by Smart sequencing. Bioinformatics analysis including GO, KEGG, and GSEA analyses were employed to elucidate transcriptional and functional changes.ResultsHyperlipidemia and obesity were observed easily upon HFD. The mouse hearts also displayed more severe fibrosis and diastolic dysfunction in HFD mice. Smart sequencing and functional analysis revealed metabolic dysfunctions, especially lipid-related genes and pathways. Besides this, antigen-presentation-related gene such as Ctsf and inflammation, particularly for NF-κB signaling and complement cascades, underwent drastic changes in cardiac resident macrophages. GO cellular compartment analysis was also performed and showed specific organelle enrichment trends of the involved genes.ConclusionDysregulated metabolism intertwines with inflammation in cardiac resident macrophages upon HFD feeding in mice, and further research on crosstalk among organelles could shed more light on potential mechanisms

Characteristic of microencapsulated 1,3-dioleoyl-2-palmitoylglycerol and its application in infant formula powder

1,3-Dioleoyl-2-palmitoylglycerol (OPO) is used widely as a food additive. However, the structured lipid is sensitive to oxygen and light in the production process. This results in the loss of its original nutrition and production of harmful substances. In this study, the OPO was microencapsulated using whey protein isolate and maltodextrin as the wall material and monostearin as an emulsifier by spray-drying technology added to the infant formula milk, in order to improve its oxidative stability. The OPO microcapsules were released in vitro through the simulated gastrointestinal tract; sensory evaluation of microencapsulated OPO in infant formula powder and nutrition absorption of microencapsulated OPO in infant formula power by animal experiments were investigated. The results showed that OPO microcapsules have a slow-release effect; after 2 h of simulated gastric fluid digestion, only 16.1 ± 3.2% of the oil was released from microencapsulated OPO, and after another 2 h of simulated intestinal fluid digestion, there was 92.3 ± 2.8% of oil released from the microencapsulated OPO. The infant formula with microencapsulated OPO has a uniform colour and no odour. The quality of infant formula with microencapsulated OPO was obviously better than infant formula with OPO by storage test. Everted mice gut sac experiments confirmed that microencapsulation did not affect absorption of mice to OPO in infant formula and prevented the loss of calcium. The study confirmed that addition of microencapsulated OPO makes infant formula more efficient for product quality and nutrition absorption

A Novel Gene Signature Associated with Inflammatory Responses and Immune Status Assists in Prognosis and Intervention for Patients with HCC

Background: Tumor growth depends on tumor cells and the tumor microenvironment, which are regulated by inflammation and immune responses. However, the roles of inflammation and immune status in hepatocellular carcinoma (HCC) remain unclear. The aim of this study was to evaluate the prognostic value of an inflammatory response-related gene signature associated with immune status, which may provide insight into new treatment options for HCC patients.Materials and Methods: Differentially expressed genes associated with inflammation were obtained from The Cancer Genome Atlas (TCGA), the Gene Expression Omnibus, and the Molecular Signatures Database. An inflammation-associated prognostic gene signature was constructed and validated using TCGA and the International Cancer Genome Consortium datasets, respectively, using LASSO Cox regression analysis. Log-rank was performed to compare the overall survival of low-and high-risk score cohorts. Immune cell infiltration and immune-related functions were analyzed using single-sample gene enrichment analysis. The structures of the drugs identified by the prognostic model were predicted using PubChem. The drugs sensitivity of bleomycin, simvastatin and zoledronate detected by CCK8 colorimetric assay. The mRNA levels of 7 genes in HCC after drug treatment analyzed via qRT-PCR.Results: Inflammation-associated genes, including ITGA5, MEP1A, P2RX4, RIPK2, SLC7A1 and SRI, were identified and found to be associated with the prognosis of HCC. We further found that the high-risk patients experienced poor prognosis, which was observed to be an independent and significant risk factor for prognosis. Moreover, we observed elevated expression levels in multiple immune cell types and immune function. Lastly, we validated that bleomycin, simvastatin and zoledronate could regulate these genes in HCC.Conclusion: The inflammatory-response-associated gene signature could predict the prognosis and the immunological status of HCC patients. Additionally, bleomycin, simvastatin and zoledronate may represent potential drug candidates that could inhibit these genes. This may constitute a new approach for the treatment of HCC

Experimental sand burial and precipitation enhancement alter plant and soil carbon allocation in a semi-arid steppe in north China

Sand burial is a common phenomenon in inland semi-arid and arid areas, affecting plant growth and even plant community structure. Precipitation regime, including the variation of precipitation intensity and frequency, also drives community structure and functions in such areas. However, few studies have focused on the combined effect of sand burial and changed precipitation regime on community function, specifically its role in carbon storage. A 2-yr field experiment with factorial treatments of precipitation (control, slight enhancement and strong enhancement) and sand addition (control and 5 cm sand addition) was conducted to test the responses of plant and soil carbon content in a semi-arid typical steppe in N China. Results showed that sand burial had no significant effect on plant carbon density, but significantly changed the allocation of plant carbon from aboveground to belowground; these responses differed among species and life forms in the community. Precipitation enhancement had no significant effects on plant carbon and its allocation, perhaps because effects of precipitation on plants are due more to precipitation frequency than to precipitation intensity per event. Sand burial and precipitation enhancement decreased soil carbon, especially soil organic carbon, and promoted soil carbon to be distributed deeper down the soil profile. These findings will help to understand how sand deposition affects plant and soil carbon storage and their allocation in plant communities under a changing precipitation regime, and more generally, to understand carbon storage dynamics in early-successional sandy ecosystems in the context of global change

Differential plant species responses to interactions of sand burial, precipitation enhancement and climatic variation promote co-existence in Chinese steppe vegetation

Aims: Sand burial and precipitation play important roles in vegetation of inland deserts and desertified areas, and both are under strong influence of climate and land-use change. Sand deposition and precipitation both vary greatly in space and time, and different plant species, with diverse adaptations, occupy different niches along spatial gradients in the combination of sand and water availability dynamics. We hypothesized that species specificity in spatial and temporal niche occupation along such gradients is a mechanism for their co-existence and, thereby, a driver and stabilizer of biodiversity in dry, sandy areas. Location: Ordos Plateau, China. Methods: We conducted a 2-yr field experiment with factorial treatments of precipitation (control, slight enhancement, strong enhancement) and sand addition (control, medium addition, large addition). Plant cover of the six dominant species was followed over different seasons, as we expected different species to benefit from different treatments in different seasons and years with different weather regimes. Results: Sand burial alone significantly affected plant cover of all six dominant species, while precipitation enhancement had no significant effect. Effects of sand burial on plant cover changed overall during the two hydrologically contrasting years. Our key finding was that there were multiple significant two- and three-way interactions between species, sand burial and precipitation enhancement on plant cover, while there were also multiple two- and three-way interactions involving species, sand burial or precipitation treatment with year and/or season. Conclusion: Our results supported our hypothesis, i.e. the co-existence of species in a semi-arid sand dune can be explained from the different niches they occupy in terms of seasonal and year-to-year variation in precipitation in combination with sand deposition regime. The interactions of these drivers on plant cover with experimental enhancement of precipitation, mimicking a realistic scenario for this region, suggest that shifts in species composition are to be expected this century. More generally, our findings advance our understanding of what drives species co-existence and thereby biodiversity, now and in the future

Anti‐inflammatory effects of α7‐nicotinic ACh receptors are exerted through interactions with adenylyl cyclase‐6

Background and purpose Alpha 7 nicotinic acetylcholine receptors (CHRNA7) suppress inflammation through diverse pathways in immune cells, so is potentially involved in a number of inflammatory diseases. However, the detailed mechanisms underlying CHRNA7’s anti‐inflammatory effects remain elusive. Experimental approach The anti‐inflammatory effects of CHRNA7 agonists in both murine macrophages (RAW 264.7) and bone marrow‐derived macrophages (BMDM) stimulated with LPS were examined. The role of adenylyl cyclase 6 (AC6) in Toll‐like Receptor 4 (TLR4) degradation was explored via overexpression and knockdown. A mouse model of chronic obstructive pulmonary disease was used to confirm key findings. Results Anti‐inflammatory effects of CHRNA7 were largely dependent on AC6 activation, as knockdown of AC6 considerably abnegated the effects of CHRNA7 agonists while AC6 overexpression promoted them. We found that CHRNA7 and AC6 are co‐localized in lipid rafts of macrophages and directly interact. Activation of AC6 led to the promotion of TLR4 degradation. Administration of CHRNA7 agonist PNU‐282987 attenuated pathological and inflammatory end points in a mouse model of chronic obstructive pulmonary disease (COPD). Conclusion and implications CHRNA7 inhibits inflammation through activating AC6 and promoting degradation of TLR4. The use of CHRNA7 agonists may represent a novel therapeutic approach for treating COPD and likely other inflammatory diseases