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Feedstock properties play a crucial role in thermal conversion processes, where understanding the influence of these properties on treatment performance is essential for optimizing both feedstock selection and the overall process. In this study, a series of van Krevelen diagrams were generated to illustrate the impact of H/C and O/C ratios of feedstock on the products obtained from six commonly used thermal conversion techniques: torrefaction, hydrothermal carbonization, hydrothermal liquefaction, hydrothermal gasification, pyrolysis, and gasification. Machine learning methods were employed, utilizing data, methods, and results from corresponding studies in this field. Furthermore, the reliability of the constructed van Krevelen diagrams was analyzed to assess their dependability. The van Krevelen diagrams developed in this work systematically provide visual representations of the relationships between feedstock and products in thermal conversion processes, thereby aiding in optimizing the selection of feedstock and the choice of thermal conversion technique.

[Objective] In order to explore the changes of vegetation communities under different grazing intensities in grassland, the effects of community characteristics on soil aggregates were analyzed. [Methods] Taking the controlled grazing experimental area of Xilamuren desert steppe as the research object, the characteristics of vegetation community and soil aggregates under light grazing (LG), moderate grazing (MG), heavy grazing (HG), and no grazing (CK) and their relationship were analyzed by field investigation and indoor analysis, and the effects of plant community changes on soil aggregates were revealed. [Results] (1) The Shannon-Wiener diversity index (H′) and Simpson dominance index (D) of LG were significantly lower than those of other grazing intensities (p

To analyze the community characteristics of tropical monsoon forests with different succession stages, four different plant communities named A, B, C, and D were investigated in this study, respectively, in a typical monsoon forest of Ehuangzhang in Yangchun, Guangdong Province. The species composition, biodiversity and spatial structure were analyzed, their maturity levels’ differences were detemined, succession direction was predicted, and suggestions for optimization were put forward. The results were as follows: (1) The forest layers of the four communities were single. Small diameter at breast height (DBH) class trees and lower forest dominated these communities, owning 1-3 obvious dominant species. (2) The Shannon-Wiener index ranged from 2.72 to 3.74, Simpson index from 0.90 to 0.97, and Pielou evenness index from 0.74 to 0.89, suggesting that their diversity characteristics were significant differences. (3) Their dominance ranged from 0.49 to 0.51, uniform angle from 0.56 to 0.61, mingling from 0.54 to 0.83, forest spatial structure index from 60.57 to 71.44, forest spatial structure distance from 53.15 to 68.53. (4) The analysis of community basic characteristics, diversity characteristics and spatial structural characteristics indicated that the maturity levels in all community ranked D > A > C > B. In conclusion, four communities are currently in the pre- or mid-term succession stages and the development space of DBH and tree height is large. The four communities are in the moderate growth state. All trees show a slight aggregated distribution, and the tree species are moderately, strongly or very strongly mingling. Besides, there is a distance in spatial structure between four communities and ideal forest with the development of maturity levels. The four communities continue to succession with intolerant tree species as the main dominant tree species, and gradually and preliminarily have the typical vegetation characteristics of the district forest climax community. With the development of maturity levels, the four communities’ biodiversity and mingling will increase, the spatial structure will be optimized and the stability will be enhanced. The results of this study provide scientific basis for community construction mechanism and forest structure optimization. In the future, Ehuangzhang tropical monsoon forests should be more regulated and protected, while the ecology of vegetation and biodiversity conservation in the area should be widely monitored and studied in depth.

Clinically used inhibitors of mammalian target of rapamycin (mTOR) negatively impacts endothelial-dependent vasodilatation (EDD) through unidentified mechanisms. Here we show that either the endothelium-specific deletion of Mtor to inhibit both mTOR complexes, or depletion of Raptor or Rictor to disrupt mTORC1 or mTORC2, causes impaired EDD, accompanied by reduced NO in the serum of mice. Consistently, inhibition of mTOR decreases NO production by human and mouse EC. Specifically, inhibition of mTORC1 suppresses eNOS gene expression, due to impairment in p70S6K-mediated posttranscriptional regulation of the transcription factor KLF2 expression. In contrast to mTORC1 inhibition, a positive-feedback between MAPK (p38 and JNK) activation and Nox2 upregulation contributes to the excessive generation of reactive oxygen species (ROS), which causes eNOS uncoupling and decreased NO bioavailability in mTORC2-inhibited EC. Adeno-associated virus-mediated EC-specific overexpression of KLF2 or suppression of Nox2 restores EDD function in endothelial mTORC1- or mTORC2-inhibited mice.

Increased expression of vascular cell adhesion molecule (VCAM)-1 on the activated arterial endothelial cell (EC) surface critically contributes to atherosclerosis which may in part be regulated by epigenetic mechanisms. This study investigated whether and how the clinically available histone deacetylases 1 and 2 (HDAC1/2) inhibitor drug Romidepsin epigenetically modulates VCAM-1 expression to suppress atherosclerosis. Methods: VCAM-1 expression was analyzed in primary human aortic EC (HAEC) treated with Romidepsin or transfected with HDAC1/2-targeting siRNA. Methylation of GATA6 promoter region was examined with methylation-specific PCR assay. Enrichment of STAT3 to GATA6 promoter was detected with chromatin immunoprecipitation. Lys685Arg mutation was constructed to block STAT3 acetylation. The potential therapeutic effect of Romidepsin on atherosclerosis was evaluated in Apoe -/- mice fed with a high-fat diet. Results: Romidepsin significantly attenuated TNFα-induced VCAM-1 expression on HAEC surface and monocyte adhesion through simultaneous inhibition of HDAC1/2. This downregulation of VCAM-1 was attributable to reduced expression of transcription factor GATA6. Romidepsin enhanced STAT3 acetylation and its binding to DNA methyltransferase 1 (DNMT1), leading to hypermethylation of the GATA6 promoter CpG-rich region at +140/+255. Blocking STAT3 acetylation at Lys685 disrupted DNMT1-STAT3 interaction, decreased GATA6 promoter methylation, and reversed the suppressive effects of HDAC1/2 inhibition on GATA6 and VCAM-1 expression. Finally, intraperitoneal administration of Romidepsin reduced diet-induced atherosclerotic lesion development in Apoe -/- mice, accompanied by a reduction in GATA6/VCAM-1 expression in the aorta. Conclusions: HDAC1/2 contributes to VCAM-1 expression and atherosclerosis by suppressing STAT3 acetylation-dependent GATA6 promoter methylation. These findings may provide a rationale for HDAC1/2-targeting therapy in atherosclerotic heart disease.

AimsMammalian target of rapamycin (mTOR) inhibitors used in drug-eluting stents (DES) to control restenosis have been found to delay endothelialization and increase incidence of late-stent thrombosis through mechanisms not completely understood. We revealed that mTOR inhibition (mTORi) upregulated the expression of cell growth suppressor IRF-1 in primary human arterial endothelial cells (HAEC). This study aimed to examine how mTOR-regulated IRF-1 expression contributes to the suppressive effect of mTORi on arterial endothelial proliferation.Methods and resultsWestern blotting, quantitative PCR, and a dual-luciferase reporter assay indicated that mTOR inhibitors rapamycin and torin 1 upregulated IRF-1 expression and increased its transcriptional activity. IRF-1 in turn contributed to the suppressive effect of mTORi by mediating HAEC apoptosis and cell cycle arrest in part through upregulation of caspase 1 and downregulation of cyclin D3, as revealed by CCK-8 assay, Annexin V binding assay, measurement of activated caspase 3, BrdU incorporation assay, and matrigel tube formation assay. In a mouse model of femoral artery wire injury, administration of rapamycin inhibited EC recovery, an effect alleviated by EC deficiency of IRF-1. Chromatin immunoprecipitation assay with HAEC and rescue expression of wild type or dominant-negative IRF-1 in EC isolated from Irf1-/- mice confirmed transcriptional regulation of IRF-1 on the expression of CASP1 and CCND3. Furthermore, mTORi activated multiple PKC members, among which PKCζ was responsible for the growth-inhibitory effect on HAEC. Activated PKCζ increased IRF1 transcription through JAK/STAT-1 and NF-κB signaling. Finally, overexpression of wild type or mutant raptor incapable of binding mTOR indicated that mTOR-free raptor contributed to PKCζ activation in mTOR-inhibited HAEC.ConclusionsThe study reveals an IRF-1-mediated mechanism that contributes to the suppressive effects of mTORi on HAEC proliferation. Further study may facilitate the development of effective strategies to reduce the side effects of DES used in coronary interventions.

Objective To investigate the role of Notch1 signaling pathway in Th1/Th2 imbalance induced by neonatal Streptococcus pneumoniae pneumonia (S.pp) infection. Methods Twelve Balb/c neonatal mice (1 week old) were randomly divided into neonatal S.pp group, neonatal S.pp with Notch1 inhibition treatment group (S.pp+DAPT, a γ-secretase inhibitor) and mock-infected control group (control group) (n=4). The S.pp group and the S.pp+DAPT group were infected with 1×107 CFU of S. pneumoniae in 10 μL of PBS intranasally, while the control group received equivalent PBS. In 7 d after infection, the S.pp+DAPT groups were given 0.3 mg/kg DAPT by nasal instillation, and the S.pp and the control groups were instilled equivalent PBS. In 5 weeks after infection, airway hyperresponsiveness (AHR) was evaluated by invasive body plethysmography system. Differential cell counts in bronchoalveolar lavage fluid (BALF) were analyzed. HE staining was used to observe the histopathological changes of the lung tissue. Western blotting was used to detect the protein expression of Notch1 protein, and RT-PCR to measure the mRNA levels of T-bet and GATA3. And the percentages of Th1 and Th2 cells in the lung tissue were determined by flow cytometry and Th1/Th2 ratio was calculated. Results Notch1 expression was significantly lower in the S.pp+ DAPT group than the S.pp group (0.23±0.09 vs 1.94±0.78, P < 0.01). The total cell count and counts of neutrophils, monocytes and lymphocytes in the BALF from the S.pp+DAPT group were remarkably lower than those in the S.pp group (P < 0.01). The S.pp+DAPT mice had obviously lower histologic scores of pulmonary peribronchiolitis, pulmonary perivasculitis and pulmonary alveolitis in lung tissue than the S.pp group (0.55±0.17 vs 1.52±0.27, P < 0.01; 0.05±0.10 vs 0.88±0.25, P < 0.01; 0.18±0.35 vs 1.57±0.25, P < 0.01). The mRNA level of GATA3 and percentage of Th2 cells were significantly lower in the S.pp+DAPT group than the S.pp group [19.11±9.79 vs 177.56±65.95, P < 0.01; (0.16±0.02)% vs (0.28±0.04)%, P < 0.01]. While the mRNA level of T-bet and percentage of Th1 cells were similar between the 2 groups. The S.pp+DAPT group had significantly higher Th1/Th2 when compared with the S.pp group (14.67±2.60 vs 7.89±0.82, P < 0.01). The AHR in the S.pp+DAPT group mice was significantly decreased when inhaled different concentrations of acetylcholine (3.125~50 mg/mL) as compared with the S.pp group (P < 0.01). Conclusion Neonatal S.pp may induce Th1/Th2 imbalance by activating Notch1 signal, and thus promote airway hyperreactivity and airway inflammation.