24 research outputs found
Land Use Transition and Its Influencing Factors in Poverty-Stricken Mountainous Areas of Sangzhi County, China
Previous studies have rarely revealed the characteristics and influencing factors of land use transformation (LUT) in poverty-stricken areas, where multiple actions of cultivated land protection are undertaken. The land use conversion matrix and Spatial Durbin Model were used to analyze the characteristics and influence factors of LUT based on remote sensing interpretation data of Sangzhi County in 2010, 2015, and 2018. The results demonstrate the following: (1) From 2010–2018, cultivated land, forest land, waters, and urban and rural construction land in Sangzhi County increased by 4.91%, 0.03%, 58.99%, and 55.63%, respectively, and grassland decreased by 13.32%. (2) Terrain, territorial, and traffic conditions were common influence factors of the land use type conversion (i.e., forest land to cultivated land, grassland to forest land, cultivated land to forest land, grassland to cultivated land, and cultivated land to urban and rural construction land). The conversion of land use type has a negative effect on the land use type conversion of adjacent townships. Territorial and traffic conditions affect the land use type conversion of adjacent townships. The results illuminate LUT at the township scale in mountainous areas and are beneficial to promoting the sustainable use of land resources and poverty alleviation
Serine/Threonine Kinase CHEK1-Dependent Transcriptional Regulation of RAD54L Promotes Proliferation and Radio Resistance in Glioblastoma
Accumulating evidence indicates that Checkpoint kinase 1 (CHEK1) plays an essential role in tumor cells and that it could induce cell proliferation and could be related to prognosis in multiple types of cancer. However, the biological role and molecular mechanism of CHEK1 in GBM still remain unclear. In this study, we identified that CHEK1 expression was enriched in glioblastoma (GBM) tumors and was functionally required for tumor proliferation and that its expression was associated to poor prognosis in GBM patients. Mechanically, CHEK1 induced radio resistance in GBM cells, and CHEK1 knockdown increased cell apoptosis when combined with radiotherapy via regulation of the DNA repair/recombination protein 54L (RAD54L) expression. Therapeutically, we found that CHEK1 inhibitor attenuated tumor growth both in vitro and in vivo. Collectively, CHEK1 promotes proliferation, induces radio resistance in GBM, and could become a potential therapeutic target for GBM
CDC7-dependent transcriptional regulation of RAD54L is essential for tumorigenicity and radio-resistance of glioblastoma
Accumulating evidence indicates that cell division cycle 7-related protein kinase(CDC7) plays an essential role in tumor cells and it could induces cell proliferation and could be related to prognosis in multiple types of cancer. However, the biological role and molecular mechanism of CDC7 in GBM still remains unclear. In this study, we identified that CDC7 expression was enriched in glioblastoma (GBM) tumors and was functionally required for tumor proliferation and its expression was associated to poor prognosis in GBM patients. Mechanically, CDC7 induced radio resistance in GBM cells and CDC7 knock down increased cell apoptosis when combined with radiotherapy. Moreover, CDC7 regulated The DNA repair/recombination protein 54L (RAD54L) expression via regulation of RAD54L promoter activity. Therapeutically, we found that CDC7 inhibitor attenuated tumor growth both in vitro and in vivo. Collectively, CDC7 promotes proliferation, induces radio resistance in GBM, and could become a potential therapeutic target for GBM
Cyclin-Dependent Kinase 2 Promotes Tumor Proliferation and Induces Radio Resistance in Glioblastoma
Accumulating evidence indicates that CDK2 promotes hyperproliferation and is associated to poor prognosis in multiple cancer cells. However, the physiological role of CDK2 in GBM and the biological mechanism still remains unclear. In this study, we identified that CDK2 expression was significantly enriched in GBM tumors compared with normal brain. Additionally, CDK2 was functionally required for tumor proliferation and its expression was associated to poor prognosis in GBM patients. Mechanically, CDK2 induced radio resistance in GBM cells and CDK2 knock down increased cell apoptosis when combined with radiotherapy. Therapeutically, we found that CDK2 inhibitor attenuated tumor growth both in vitro and in vivo. Collectively, CDK2 promotes proliferation, induces radio resistance in GBM, and could become a therapeutic target for GBM
Polo‑like kinase�4 promotes tumorigenesis and induces resistance to radiotherapy in glioblastoma
Deep learning model to discriminate diverse infection types based on pairwise analysis of host gene expression
Summary: Accurate detection of pathogens, particularly distinguishing between Gram-positive and Gram-negative bacteria, could improve disease treatment. Host gene expression can capture the immune system’s response to infections caused by various pathogens. Here, we present a deep neural network model, bvnGPS2, which incorporates the attention mechanism based on a large-scale integrated host transcriptome dataset to precisely identify Gram-positive and Gram-negative bacterial infections as well as viral infections. We performed analysis of 4,949 blood samples across 40 cohorts from 10 countries using our previously designed omics data integration method, iPAGE, to select discriminant gene pairs and train the bvnGPS2. The performance of the model was evaluated on six independent cohorts comprising 374 samples. Overall, our deep neural network model shows robust capability to accurately identify specific infections, paving the way for precise medicine strategies in infection treatment and potentially also for identifying subtypes of other diseases
Unusual facet and co-catalyst effects in TiO2-based photocatalytic coupling of methane
Abstract Photocatalytic coupling of methane to ethane and ethylene (C2 compounds) offers a promising approach to utilizing the abundant methane resource. However, the state-of-the-art photocatalysts usually suffer from very limited C2 formation rates. Here, we report our discovery that the anatase TiO2 nanocrystals mainly exposing {101} facets, which are generally considered less active in photocatalysis, demonstrate surprisingly better performances than those exposing the high-energy {001} facet. The palladium co-catalyst plays a pivotal role and the Pd2+ site on co-catalyst accounts for the selective C2 formation. We unveil that the anatase {101} facet favors the formation of hydroxyl radicals in aqueous phase near the surface, where they activate methane molecules into methyl radicals, and the Pd2+ site participates in facilitating the adsorption and coupling of methyl radicals. This work provides a strategy to design efficient nanocatalysts for selective photocatalytic methane coupling by reaction-space separation to optimize heterogeneous-homogeneous reactions at solid-liquid interfaces