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Pores and old root‐channels are preferentially used by roots to allow them to penetrate hard soils. However, there are few studies that have accounted for the effects of pore‐rhizosheath on root growth. In this study, we developed an approach by adding the synthetic root exudates using a porous stainless tube with 0.1‐mm micropores through a peristaltic pump to reproduce the rhizosheath around the artificial pore, and investigated the effects of pores with and without rhizosheaths on maize root growth in a dense soil. The results indicated that the artificial rhizosheath was about 2.69 mm wide in the region surrounding the pores. The rhizosheath had a higher content of organic carbon, total nitrogen, and abundance of Actinobacteria than that of the bulk soil. Compared with the artificial macropores, the artificial root‐pores with a rhizosheath increased the opportunities for root utilisation of the pores space, promoting steeper and deeper root growth. It is concluded that the pore‐rhizosheath has a significant impact on root architecture by enhancing root distribution in macropores. Summary statement: There are few studies that have accounted for the effects of pore‐rhizosheath on root growth. This study reported that the artificial root‐pores with a rhizosheath increased the opportunities for maize root utilisation of the pores space, promoting steeper and deeper root growth. [ABSTRACT FROM AUTHOR]

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]

Glioblastoma (GBM) is the most common and malignant primary brain tumor in adults that originates from glial cells. The prognosis of patients with high-grade glioma is poor. It is therefore crucial to develop effective therapeutic strategies. Long non-coding RNAs (lncRNAs) have been reported as potential inducers or suppressors of tumor progression. Previous studies have indicated that the lncRNA Feline Leukemia Virus Subgroup C Cellular Receptor 1 Antisense RNA 1 (FLVCR1-AS1) is involved in the development and progression of gastric and lung cancer, as well as hepatocellular carcinoma and cholangiocarcinoma; however, the biological effect of FLVCR1-AS1 in glioma is not completely understood. The aim of the present study was to investigate how FLVCR1-AS1 modulates cell proliferation and invasion in glioma. FLVCR1-AS1 expression was significantly upregulated in GBM tissues compared with adjacent normal brain samples, and was higher in GBM cell lines compared with normal human astrocyte cells. Furthermore, the microRNA (miR)-30b-3p was revealed to be a putative target of FLVCR1-AS1, and the suppressive effects of miR-30b-3p on cellular proliferation and invasion were reversed following FLVCR1-AS1-knockdown. The results from Cell Counting Kit-8 and Transwell assays confirmed that FLVCR1-AS1-knockdown inhibited GBM cell proliferation and invasion ability. In addition, FLVCR1-AS1 was found to directly interact with miR-30b-3p, and a rescue experiment further established that FLVCR1-AS1 contributed to glioma progression by inhibiting miR-30b-3p. The results from the present study demonstrated that FLVCR1-AS1 may serve an oncogenic role in GBM and promote disease progression by interacting with miR-30b-3p. These findings suggested that FLVCR1-AS1 may be considered as a novel therapeutic target and diagnostic biomarker for GBM. [ABSTRACT FROM AUTHOR]

Background/Aims: Alcohol consumption has been shown to cause neuroinflammation and increase a variety of immune-related signaling processes. Microglia are a crucial part of alcohol-induced neuroinflammation and undergo apoptosis. Even though the importance of these inflammatory processes in the effects of alcohol-related neurodegeneration have been established, the mechanism of alcohol-induced microglia apoptosis is unknown. In prior research, we discovered that alcohol increases expression of salt-inducible kinase 1 (SIK1) in rodent brain tissue. In this study, we sought to determine what role SIK1 expression plays in alcohol-induced neuroinflammation as well as whether and by what mechanism it regulates microglia apoptosis. Methods: Adult C57BL/6 mice were divided into four groups and for 3 weeks treated with either 0%, 5%, 10%, or 15% alcohol during 3 hour periods. The mice were sacrificed and their brains excised for analysis. Additionally, primary microglia were isolated from neonatal mice. SIK1 expression in alcohol-treated brain tissue and microglia was analyzed via RT-PCR and western blotting. TUNEL staining, caspase-3, and caspase-9 activity assays were performed to evaluate microglial apoptosis. Cell fluorescence staining and NF-κB luciferase activity assays were used to evaluate the effects of SIK1 expression on the NF-κB signaling pathway. Results:SIK1 expression was increased in the brains of mice that consumed alcohol, and this effect was seen in mouse primary microglia. SIK1 knockdown in microglia increased alcohol-induced apoptosis in these cells. Furthermore, SIK1 reduced NF-κB signaling pathway factors, and SIK1 knockdown in microglia promoted alcohol-induced NF-κB activity. TUNEL staining, caspase-3, and caspase-9 activity assays consistently revealed that alcohol-induced microglial apoptosis was inhibited by depletion of p65. Finally, we determined that NF-κB signaling is required for alcohol-induced, SIK1-mediated apoptosis in microglia. Conclusion: This study establishes for the first time not only that SIK1 is crucial to regulating alcohol-induced microglial apoptosis, but also that the NF-κB signaling pathway is required for its activity. Overall, our results help elucidate mechanisms of alcohol-induced neuroinflammation. [ABSTRACT FROM AUTHOR]

It was reported that γ-irradiation had a controversial therapeutic effect on glioma cells. We aimed to investigate the cytotoxic effect on the glioma cells induced by γ-irradiation and explore the treatment to rescue the phenotype alteration of remaining cells. We used transwell assay to detect the glioma cell invasion and migration capacity. Cell proliferation and apoptosis were tested by the CCK-8 assay and flow cytometry respectively. Western Blot was used to detect the activity of Hedgehog signaling pathway and Epithelial-to-Mesenchymal Transition (EMT) status. γ-irradiation showed cytotoxic effect on LN229 cellsin vitro, whereas this contribution was limited in U251 cells. However, it could significantly stimulated EMT process in both LN229 and U251. Curcumin (CCM) could rescue EMT process induced by γ-irradiation via the suppression of Gli1 and the upregulation of Sufu. The location and expression of EMT markers were also verified by Immunofluorescence. Immunohistochemistry assay was used on intracranial glioma tissues of nude mice. The capacities of cell migration and invasion were suppressed with combined therapy. This research showed Curcumin could rescue the EMT process induced by γ-irradiation via inhibiting the Hedgehog signaling pathway and potentiate the cell cytotoxic effectin vivoandin vitro. [ABSTRACT FROM PUBLISHER]

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]

Soil compaction has become a global concern that reduces soil quality and may jeopardize agricultural sustainability. The objective of this study is to evaluate if the freezing–thawing process can alleviate the negative effects of soil compaction during overwinter time in Northeast China. The field experiment was a split plot design including two surface treatments (bare and mulch) and three compaction levels (low, moderate, and high compactions with initial bulk densities of 1.2, 1.4 and 1.6 g cm−3). Results showed that compared with initial values in the fall, freezing–thawing events increased soil porosity (by 4.28% to 25.68%) and the ratio of large-size pores (by 44.5% to 387.6%) after thawing in the spring. The greatest changes were observed in the high compaction treatment, and mulch-enhanced soil structural transformation. Additionally, the ratio of large-size aggregates (>1 mm) was increased and the fraction of small-size aggregates (<1 mm) was decreased. These changes in soil structural characteristics were attributed mainly to the modification of ice-filled pores space during the overwinter period. We concluded that the freezing–thawing process was an effective natural force for ameliorating soil compaction in Northeast China. [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.)

A light-field endoscope can simultaneously capture the three-dimensional information of in situ lesions and enables single-shot quantitative depth perception with minimal invasion for improving surgical and diagnostic accuracy. However, due to oversized rigid probes, clinical applications of current techniques are limited by their cumbersome devices. To minimize the size and enhance the flexibility, here we report a highly flexible and compact volumetric endoscope by employing precision-machined multiple micro-imaging devices (MIRDs). To further protect the flexibility, the designed MIRD with a diameter and height of 5 mm is packaged in pliable polyamide, using soft data cables for data transmission. It achieves the optimal lateral resolvability of 31 µm and axial resolvability of 255 µm, with an imaging volume over 2.3 × 2.3 × 10 mm 3 . Our technique allows easy access to the organism interior through the natural entrance, which has been verified through observational experiments of the stomach and rectum of a rabbit. Together, we expect this device can assist in the removal of tumors and polyps as well as the identification of certain early cancers of the digestive tract.

Maize eyespot, caused by Kabatiella zeae , has become a major yield-limiting factor in maize planting areas in northeast China. Limited information is available on pathotypes, virulence, and the genetic diversity of the K. zeae population. We analyzed virulence and genetic diversity of 103 K. zeae isolates collected from six provinces in China with differential hosts and the amplified fragment length polymorphism (AFLP) technique, respectively. To evaluate the virulence, 103 isolates were inoculated on nine differential hosts (maize inbred lines)-E28, Shen137, Qi319, B73, Danhuang34, Zi330, Mo17, Huangzaosi, and CN165-and grouped into 23 pathotypes and three virulence groups according to the coded triplet nomenclature system on differential hosts. AFLP analysis resolved the set of isolates into four genetic diversity clusters (DICE similarity values of 76%). Genetic variation of K. zeae among and between pathotypes revealed that the pathogen population had a high genotypic diversity. The correlation between pathotypes, virulence, and genetic diversity grouping was low. A correlation between AFLP groups and geographic locations was detected.

The role of NADPH oxidases (NOXs) in pathogenesis and development in the Curvularia leaf spot agent Curvularia lunata remains poorly understood. In this study, we identified C . lunata ClNOX2, which localized to the plasma membrane and was responsible for reactive oxygen species (ROS) generation. Scavenging the ROS production inhibited the conidial germination and appressorial formation. The ClNOX2 and ClBRN1 deletion mutants were defective in 1,8-dihydroxynaphthalene (DHN) melanin accumulation, appressorial formation, and cellulase synthesis and exhibited lower virulence. However, disruption of the ClNOX2 and ClBRN1 genes facilitated hyphal growth, enhanced stress adaptation to cell-wall-disrupting agents, and promoted developmental processes such as conidiation, conidial germination, and pseudothecium and ascus formation. Interestingly, loss of ClM1 , the cell wall integrity (CWI) mitogen-activated protein kinase gene in C . lunata , led to morphology and pathogenicity phenotypes similar to ClNOX2 and ClBRN1 deletion mutants such as abnormal conidia, fewer appressoria, less melanin, increased hyphal growth, and enhanced tolerance to Congo red (CR). These results indicated that the ClNOX2 gene plays an important role in C. lunata development and virulence via regulating intracellular DHN melanin biosynthesis. Quantitative reverse-transcription PCR revealed that the ClNOX2 -related ROS signaling pathway and ClM1 -mediated CWI signaling pathway are cross-linked in regulating DHN melanin biosynthesis. Our findings provide new insights into how ClNOX2 participates in pathogenesis and development in hemibiotrophic plant fungal pathogens.[Formula: see text] Copyright © 2020 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.