长三角地区城市生态旅游发展水平时空演变及其影响因素

城市生态旅游作为旅游可持续发展的一种理想模式,是对城市环境问题和旅游发展方式的一种回应。基于城市生态旅游核心要义,构建城市生态旅游发展水平评价指标体系,运用熵权TOPSIS法对2010-2019年长三角地区41个城市的城市生态旅游发展水平进行测度,通过标准差椭圆和马尔科夫链分析其时空演变特征,并利用地理探测器探析城市生态旅游发展的影响因素。结果表明:(1)长三角地区城市生态旅游各维度发展水平增速各异,供给和保障是影响综合发展水平的主要因素,各维度空间格局差异显著;(2)城市生态旅游综合发展水平呈波动上升态势,增速较缓;空间分布较不均衡,已初步形成"东南高-西北低"的分布格局;(3)城市生态旅游发展水平重心呈现"西北-东南-西北"的偏移规律,向东南部集聚程度逐渐增强,水平等级转移仅发生在相邻等级之间;(4)交通发展水平和城镇化水平对城市生态旅游发展的影响较为显著,经济发展水平和居民收入水平的影响逐渐增强,产业结构水平和环保重视程度的促进效果不显著;两因子的交互作用大于单因子的作用力,表现出双因子增强或非线性增强的交互关系。研究结果可为长三角地区提高城市生态旅游发展水平与全面推进旅游可持续发展提供一定的理论依据与科学参考。     

微塑料对稻田土壤温室气体排放和微生物群落的影响

微塑料因在土壤环境中广泛存在及其潜在的生态风险而受到越来越多的关注。微塑料的赋存会改变土壤理化性质,并对土壤微生物群落及其驱动的生物地球化学过程产生影响,而相关研究尚处于起步阶段。可生物降解塑料作为传统塑料的替代品,越来越多地应用于农业活动,并释放到土壤中。然而,可生物降解微塑料对土壤微生物特性产生影响的研究鲜有报道。基于此,本试验以我国三江平原水稻田土壤为研究对象,选取了2种常见的微塑料为试验材料,分别为传统型微塑料聚丙烯(Polypropylene,PP)和可降解微塑料聚乳酸(Polylactic acid,PLA),进行了为期41d的微宇宙培养实验,旨在分析不同浓度与类型的微塑料对土壤可溶性有机碳(Dissolved Organic Carbon,DOC)含量及官能团特征、温室气体排放以及微生物群落结构的差异性影响。结果表明,传统型微塑料PP与可降解微塑料PLA添加均对土壤理化性质与微生物群落产生显著影响。其中,微塑料添加大体上增加了土壤DOC含量,PLA的促进作用较为明显,且增加含量与微塑料添加量呈正相关;PP和PLA均影响土壤DOC分子结构,削弱了土壤团聚化程度并促进了大分子量DOC化合物的生成;微塑料的添加促进土壤CH₄排放,而有效抑制了土壤CO₂排放;微塑料显著改变了土壤细菌和真菌群落的丰富度与多样性。相关分析结果表明,土壤CO₂累计排放量与芳香族化合物结构及疏水性等官能团特征、变形菌门(Proteobacteria)与放线菌门(Actinobacteria)均呈显著正相关关系。以上结果表明,微塑料添加改变了土壤DOC含量及官能团特征与微生物环境,进而影响土壤温室气体排放。本研究为今后微塑料对土壤地球化学和微生物特性的影响研究提供了科学的思路,同时也有助于评估微塑料对土壤生态系统的生态风险。     

高寒半干旱区沙地植被土壤水分变化特征及其影响因素

为揭示高寒半干旱区不同降雨强度对植被差异下沙化土地土壤含水量变化过程的影响。以青海共和盆地东缘黄沙头乔木、灌木和裸地为研究对象,基于2020、2021和2022年5月-9月植物生长季土壤含水量、降雨量和细根分布监测数据,分析2020年、2021年、2022年各生境0-200 cm深度土壤水分对小雨、中雨、大雨的响应。连续动态监测结果表明,大雨、中雨条件下,随土层深度的增加土壤水分对降雨的响应时间延长。乔木林和灌木林土壤水分对中雨、大雨最大响应深度为70 cm、100 cm,裸地对中雨、大雨最大响应深度为50 cm、100 cm。随土层深度的增加,小雨对乔木、灌木、裸地土壤水分的补充作用逐渐降低;中雨对灌木林土壤水分的补充作用逐渐降低,乔木林与之相反;大雨时乔木林、灌木林变异系数呈现S型变化,因此大雨对其土壤水分的补充存在明显的分层利用现象。不同植被类型土壤水分空间变化差异以及对降雨的响应受植被冠层截留对降水再分配的影响,土壤含水量与环境因子间的主成分分析表明,郁闭度、叶面积指数、150-200 cm土壤容重、细根生物量密度、根表面积密度、根长密度、比根长是反映研究区土壤水分的显著因子(P ＜ 0.05)。研究表明不同降雨强度植被土壤含水量存在明显差异,高寒半干旱区沙化土地乔、灌植被的建植可提升深层土壤储水能力;结果可为沙化土地恢复和水土流失防控提供科学依据。     

Tetrahedral framework nucleic acids promote diabetic wound healing via the Wnt signalling pathway

ObjectivesTo determine the therapeutic effect of tetrahedral framework nucleic acids (tFNAs) on diabetic wound healing and the underlying mechanism.Materials and MethodsThe tFNAs were characterized by polyacrylamide gel electrophoresis (PAGE), atomic force microscopy (AFM), transmission electron microscopy (TEM), dynamic light scattering (DLS) and zeta potential assays. Cell Counting Kit‐8 (CCK‐8) and migration assays were performed to evaluate the effects of tFNAs on cellular proliferation and migration. Quantitative polymerase chain reaction (Q‐PCR) and enzyme‐linked immunosorbent assay (ELISA) were used to detect the effect of tFNAs on growth factors. The function and role of tFNAs in diabetic wound healing were investigated using diabetic wound models, histological analyses and western blotting.ResultsCellular proliferation and migration were enhanced after treatment with tFNAs in a high‐glucose environment. The expression of growth factors was also facilitated by tFNAs in vitro. During in vivo experiments, tFNAs accelerated the healing process in diabetic wounds and promoted the regeneration of the epidermis, capillaries and collagen. Moreover, tFNAs increased the secretion of growth factors and activated the Wnt pathway in diabetic wounds.ConclusionsThis study indicates that tFNAs can accelerate diabetic wound healing and have potential for the treatment of diabetic wounds.

Tetrahedral framework nucleic acids (tFNAs) can facilitate the proliferation and migration of HaCaTs, HDFs and HUVECs in a high‐glucose environment. tFNAs can accelerate diabetic wound healing by promoting epithelialization, vascularization, collagen synthesis and the secretion of growth factors via the Wnt pathway.     

Mutant C/EBPα p30 alleviates immunosuppression of CD8+ T cells by inhibiting autophagy‐associated secretion of IL‐1β in AML

ObjectivesMutant C/EBPα p30 (mp30), the product of C/EBPα double mutations (DM), lacks transactivation domain 1 and has C‐terminal loss‐of‐function mutation. Acute myeloid leukaemia (AML) patients harbouring C/EBPα DM could be classified as a distinct subgroup with favourable prognosis. However, the underlying mechanism remains elusive.Materials and MethodsAutophagy regulated by mp30 was detected by western blot and immunofluorescence. Immune infiltration analysis and GSEA were performed to investigate autophagic and inflammatory status of AML patients from the {"type":"entrez-geo","attrs":{"text":"GSE14468","term_id":"14468"}}GSE14468 cohort. Flow cytometry was applied to analyse T cell activation.ResultsMp30 inhibited autophagy by suppressing nucleus translocation of NF‐κB. Autophagy‐associated secretion of IL‐1β was decreased in mp30‐overexpressed AML cells. Bioinformatic analysis revealed that inflammatory status was attenuated, while CD8⁺ T cell infiltration was upregulated in C/EBPα DM AML patients. Consistently, the proportion of CD8⁺CD69⁺ T cells in peripheral blood mononuclear cells (PBMCs) was upregulated after co‐culture with mp30 AML cell conditional culture medium. Knock‐out of IL‐1β in AML cells also enhanced CD8⁺ T cell activation. Accordingly, IL‐1β expression was significantly reduced in the bone marrow (BM) cells of C/EBPα DM AML patients compared to the wildtype, while the CD8⁺CD69⁺ T cell proportion was specifically elevated.ConclusionsC/EBPα DM alleviates immunosuppression of CD8⁺ T cells by inhibiting the autophagy‐associated secretion of IL‐1β, which elucidated that repression of autophagy‐related inflammatory response in AML patients might achieve a favourable clinical benefit.

Mp30 suppresses autophagy‐associated IL‐β secretion, which ultimately alleviates the immunosuppression of CD8⁺ T cells in the microenvironment, contributing to favourable prognosis of AML patients.     

Thioredoxin 1 supports colorectal cancer cell survival and promotes migration and invasion under glucose deprivation through interaction with G6PD

Overcoming energy stress is a critical step for cells in solid tumors. Under this stress microenvironment, cancer cells significantly alter their energy metabolism to maintain cell survival and even metastasis. Our previous studies have shown that thioredoxin-1 (Trx-1) expression is increased in colorectal cancer (CRC) and promotes cell proliferation. However, the exact role and mechanism of how Trx-1 is involved in energy stress are still unknown. Here, we observed that glucose deprivation of CRC cells led to cell death and promoted the migration and invasion, accompanied by upregulation of Trx-1. Increased Trx-1 supported CRC cell survival under glucose deprivation. Whereas knockdown of Trx-1 sensitized CRC cells to glucose deprivation-induced cell death and reversed glucose deprivation-induced migration, invasion, and epithelial-mesenchymal transition (EMT). Furthermore, we identified glucose-6-phosphate dehydrogenase (G6PD) interacting with Trx-1 by HuPortTM human protein chip, co-IP and co-localization. Trx-1 promoted G6PD protein expression and activity under glucose deprivation, thereby increasing nicotinamide adenine dinucleotide phosphate (NADPH) generation. Moreover, G6PD knockdown sensitized CRC cells to glucose deprivation-induced cell death and suppressed glucose deprivation-induced migration, invasion, and EMT. Inhibition of Trx-1 and G6PD, together with inhibition of glycolysis using 2-deoxy-D-glucose (2DG), resulted in significant anti-tumor effects in CRC xenografts in vivo. These findings demonstrate a novel mechanism and may represent a new effective therapeutic regimen for CRC.     

Myopia Development in Tree Shrew Is Associated with Chronic Inflammatory Reactions

In this study, we aimed to investigate whether chronic retinal inflammation is involved in the pathogenesis of form-deprivation myopia (FDM) using tree shrews as an animal model. Twenty-one tree shrews were randomly divided into 7-day/14-day FDM (FDM7/FDM14) groups and their corresponding 7-day/14-day control groups. Refraction and axial length were measured. To determine the effects of form deprivation on inflammation, we used real-time polymerase chain reaction (PCR) and immunohistochemistry to assess the expression levels of several proinflammatory cytokines. At day 0, the eyes in the FDM and control groups were hyperopic. However, after 7 and 14 days of form deprivation, the refractive error of the eyes in the FDM7 and FDM14 groups shifted from +6.6 ± 0.3 diopters (D) to +4.0 ± 0.5 D and from +6.4 ± 0.3 D to +5.0 ± 0.3 D, respectively. The levels of tumor necrosis factor-α, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and nuclear factor κB were increased in the FDM eyes, compared with those in the control eyes. The increase in matrix metalloproteinase-2 expression was greater in the FDM eyes than in the contralateral and control eyes, whereas collagen type I expression was downregulated. In conclusion, chronic inflammation may play a crucial pathogenic role in form-deprivation myopia in tree shrews.