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Understanding the impacts of human trampling on ecological environment is necessary for the utilization and management of recreational areas. Qilian Mountain National Park is one of the first pilot areas of the national park system in China, which is also the most popular tourist destinations suitable for hiking and camping. However, there have been very few studies on human trampling in the Qilian Mountains region. We conducted a controlled trampling experiment to explore the short-term impacts of different trampling intensities (0, 50, 200, 500, and 1000 passes) on soil and vegetation in a grassland in the park. At 0–5, 5–10 and 10–20 cm soil depth, some selected soil properties were measured. Human trampling had negative impacts on surface soil properties, aboveground plant cover and height in the study area. At 0–5 cm soil depth, compared to the control site, bulk density, soil organic matter and soil penetration resistance respectively increased from 0.66 to 0.79 g/cm3, 5.5–6.5% and 9.64–13.7 kg/cm2 after 1000 passes. Soil saturated hydraulic conductivity, water holding capacity and total porosity decreased from 0.29 to 0.23 mm/min, 31.62–24.07% and 46.22–34.67%, respectively. Soil properties were degraded both on the topsoil(0–5 cm) and midsoil(5–10 cm), with the greatest degradation occurring at 1000 passes, followed by 500 passes. The total vegetation cover and mean vegetation height decreased significantly with increasing trampling intensities. After different passes, the relative vegetation cover and height showed a curvilinear decrease. A reasonable threshold of visitors should be controlled between 500 and 1000 passes to ensure the quality of the landscape. Our findings suggest that human trampling of highly sensitive and fragile alpine grasslands has a significant impact and may further impede their function. Therefore, it is urgent to protect the ecological environment of alpine grasslands.

Background: Dysregulation of immune surveillance is tightly linked to the development of metabolic dysfunction-associated steatohepatitis (MASH)-driven hepatocellular carcinoma (HCC); however, its underlying mechanisms remain unclear. Herein, we aimed to determine the role of interleukin-21 receptor (IL-21R) in MASH-driven HCC. Methods: The clinical significance of IL-21R was assessed in human HCC specimens using immunohistochemistry staining. Furthermore, the expression of IL-21R in mice was assessed in the STAM model. Thereafter, two different MASH-driven HCC mouse models were applied between IL-21R-deficient mice and wild type controls to explore the role of IL-21R in MASH-driven HCC. To further elucidate the potential mechanisms by which IL-21R affected MASH-driven HCC, whole transcriptome sequencing, flow cytometry and adoptive lymphocyte transfer were performed. Finally, flow cytometry, enzyme-linked immunosorbent assay, immunofluorescent staining, chromatin immunoprecipitation assay and western blotting were conducted to explore the mechanism by which IL-21R induced IgA+ B cells. Results: HCC patients with high IL-21R expression exhibited poor relapse-free survival, advanced TNM stage and severe steatosis. Additionally, IL-21R was demonstrated to be upregulated in mouse liver tumors. Particularly, ablation of IL-21R impeded MASH-driven hepatocarcinogenesis with dramatically reduction of lipid accumulation. Moreover, cytotoxic CD8+ T lymphocyte activation was enhanced in the absence of IL-21R due to the reduction of immunosuppressive IgA+ B cells. Mechanistically, the IL-21R-STAT1-c-Jun/c-Fos regulatory axis was activated in MASH-driven HCC and thus promoted the transcription of Igha, resulting in the induction of IgA+ B cells. Conclusions: IL-21R plays a cancer-promoting role by inducing IgA+ B cells in MASH-driven hepatocarcinogenesis. Targeting IL-21R signaling represents a potential therapeutic strategy for cancer therapy. [ABSTRACT FROM AUTHOR]

Psoriasis is a severe disease associated with the disturbance of metabolism and inflammation, but the molecular mechanisms underlying these aspects of psoriasis pathology are poorly understood. Here, we report that glutaminase 1-mediated (GLS1mediated) glutaminolysis was aberrantly activated in patients with psoriasis and in psoriasis-like mouse models, which promoted Th17 and [gamma][delta] T17 (IL-17A-producing [gamma][delta] T) cell differentiation through enhancement of histone H3 acetylation of the Il17a promoter, thereby contributing to the immune imbalance and development of psoriasis. We further demonstrate that mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) protease was constitutively active in psoriatic [CD4.sup.+] and [gamma][delta] T cells, thereby supporting GLS1 expression by stabilizing c-Jun, which directly binds to the GLS1 promoter region. Blocking the activity of either GLS1 or MALT1 protease resolved Th17 and [gamma][delta] T17 cell differentiation and epidermal hyperplasia in the psoriasis-like mouse models. Finally, IL-17A enhanced GLS1 expression via the MALT1/cJun pathway in keratinocytes, resulting in hyperproliferation of and chemokine production by keratinocytes. Our findings identify the role of the MALT1/cJun/ GLS1/glutaminolysis/H3 acetylation/T17 axis in psoriasis pathogenesis and reveal potential therapeutic targets for this disease., Introduction Psoriasis is a chronic inflammatory disease affecting up to 3% of the world's population (1). Immune imbalance of T cells is believed to play a key role in psoriasis [...]