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Plant roots release various organic materials that may modify soil structure and affect heat and mass transfer processes. The objective of this study was to determine the effects of a synthetic root exudate (SRE) on penetrometer resistance (PR), thermal conductivity (λ), hydraulic conductivity (k) and evaporation of water in a sandy soil. Soil samples, mixed with either distilled water or the SRE, were packed into columns at a designated bulk density and water content, and incubated for 7 days at 18°C. Soil PR, λ, k and evaporation rate were monitored during drying processes. Compared with those incubated with water, samples incubated with SRE had visible hyphae, greater PR (0.7–5.5 MPa in the water content range of 0.11 to 0.22 m3 m−3) and λ (0.2–0.7 W m−1 K−1 from 0.05 to 0.22 m3 m−3), and increased k in the wet region but decreased k in the dry region. SRE treatment also reduced the overall soil water evaporation rate and cumulative water loss. Analysis of X‐ray computed tomography (CT) scanning showed that the SRE‐treated samples had a greater proportion of small pores (<60 μm). These changes were attributed mainly to SRE‐stimulated microbial activities. Highlights: The effects of incubating a sandy soil with a synthetic root exudate (SRE) on soil physical properties and evaporation are examined.SRE incubation increased the fraction of small pores.SRE incubation increased soil penetrometer resistance and thermal conductivity.Soil hydraulic conductivity was increased in the wet region but was reduced in the dry region.SRE incubation reduced the overall evaporation rate and cumulative water loss. [ABSTRACT FROM AUTHOR]

Summary: Iron is virtually an essential nutrient for all organisms, to understand how iron contributes to virulence of plant pathogenic fungi, we identified ClFTR1 and ClNPS6 in maize pathogen Curvularia lunata (Cochliobolus lunatus) in this study. Disruption of ClNPS6 significantly impaired siderophore biosynthesis. ClFTR1 and ClNPS6 did mediate oxidative stress but had no significant impact on vegetative growth, conidiation, cell wall integrity and sexual reproduction. Conidial germination delayed and appressoria formation reduced in ΔClftr1 comparing with wild type (WT) CX‐3. Genes responsible for conidial germination, appressoria formation, non‐host selective toxin biosynthesis and cell wall degrading enzymes were also downregulated in the transcriptome of ΔClftr1 and ΔClnps6 compared with WT. The conidial development, toxin biosynthesis and polygalacturonase activity were impaired in the mutant strains with ClFTR1 and ClNPS6 deletion during their infection to maize. ClFTR1 and ClNPS6 were upregulated expression at 12–24 and 48–120 hpi in WT respectively. ClFTR1 positively regulated conidial germination, appressoria formation in the biotrophy‐specific phase. ClNPS6 positively regulates non‐host selective toxin biosynthesis and cell wall degrading enzyme activity in the necrotrophy‐specific phase. Our results indicated that ClFTR1 and ClNPS6 were key genes of pathogen known to conidia development and virulence factors. [ABSTRACT FROM AUTHOR]

Background: In recent years, miRNAs have been suggested to play key roles in the formation and development of human glioma. The aim of this study is to investigate the effect and mechanism of miR-184 expression on the malignant behavior of human glioma cells. Methods: The relative quantity of miR-184 was determined in human glioma cell lines, and the expression of hypoxia-inducible factor-1 alpha (HIF-1α) was explored using western blotting. The effects of miR-184 inhibition on cell viability and apoptosis were explored, and the miR-184 target gene was determined using a luciferase assay and western blotting. Flow cytometry and Hoechst staining were used to evaluate cell growth and apoptosis. Matrigel invasion and scratch assays were performed to measure the ability of cell invasion and migration. Results: miR-184 and HIF-1α protein levels were significantly upregulated in human glioma cells. Downregulation of miR-184 inhibited cell viability and increased the HEB cell apoptotic rate. Luciferase and western blot assays verified that FIH-1 was the target gene of miR-184 and negatively controlled the protein level of HIF-1α. Inhibition of HIF-1α by siRNA facilitated the apoptosis of HEB cells and suppressed A172 cell invasion and migration. Conclusion: miR-184 upregulation enhanced the malignant phenotype of human glioma cancer cells by reducing FIH-1 protein expression. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Glioblastoma (GBM) is an aggressive malignancy. The inherent resistance of GBM to radiotherapy poses great challenges for clinical treatment., Objectives: The primary objective of this study is to explore the molecular mechanisms of radiotherapy resistance in GBM and identify the key influencing factors that contribute to this phenomenon., Methods: The single-cell RNA sequencing (scRNA-seq) data of GBM were downloaded from the Gene Expression Omnibus (GEO) database. Cells were clustered using the Seurat R package, and the clusters were annotated using the CellMarker database. Pseudotime analysis was conducted using Monocle2. Marker scores were calculated based on the RNA-seq data of GBM from the UCSC database, and the enrichment of Hallmark gene sets was measured with the AUCell package. Furthermore, the most frequently mutated genes were identified using the simple nucleotide variation data from The Cancer Genome Atlas (TCGA) applying the maftools package., Results: This study identified two oligodendrocyte subsets (ODC3 and ODC4) as radiotherapy-resistant groups in GBM. Enrichment and Pseudotime analysis revealed that the inflammatory response and immune activation pathways were enriched in ODC3, while the cell division and interferon response pathways were enriched in ODC4. The enrichment scores of hallmark gene sets further confirmed that ODC3 and ODC4 subpopulations developed radiotherapy resistance via distinct molecular mechanisms. Analysis of gene mutation frequencies showed that TP53 exhibited the most significant change in mutation frequency, indicating that it was an important risk factor involved in radiotherapy resistance in GBM., Conclusion: We identified two ODC subpopulations that exhibited resistance to radiotherapy, providing a new perspective and potential targets for personalized treatment strategies for GBM., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Necroptosis is a type of programmed cell death involved in the pathogenesis of cancers. This work developed a prognostic glioblastoma (GBM) model based on necroptosis-related genes., Methods: RNA-Seq data were collected from the TCGA database. The "WGCNA" method was used to identify co-expression modules, based on which GO and KEGG analyses were conducted. A protein-protein interaction (PPI) network was compiled. The number of key prognostic genes was reduced applying COX regression and least absolute shrinkage and selection operator (LASSO) analysis to build a RiskScore model. Differences in immune microenvironments were assessed using CIBERSORT, ESTIMATE, MCP-count, and TIMER databases. The potential impact of key prognostic genes on GBM was validated by cellular experiments., Results: GBM patients in the higher necroptosis score group had higher immune scores and worse survival. The Brown module, which was closely related to the necroptosis score, was considered as a key gene module. Three key genes (GZMB, PLAUR, SOCS3) were obtained by performing regression analysis on the five clusters. The RiskScore model was significantly, positively, correlated with necroptosis score. Low-risk patients could benefit from immunotherapy, while high-risk patients may be more suitable to take multiple chemotherapy drugs. The nomogram showed strong performance in survival prediction. GZMB, PLAUR, and SOCS3 played key roles in GBM development. Among them, high-expressed GZMB was related to the invasive and migratory abilities of GBM cells., Conclusions: A genetic signature associated with necroptosis was developed, and we constructed a RiskScore model to provide reference for predicting clinical outcomes and immunotherapy responses of patients with GBM., (© 2024 Wiley Periodicals LLC.)