14 research outputs found
Phytate utilization of maize mediated by different nitrogen forms in a plant–arbuscular mycorrhizal fungus–phosphate-solubilizing bacterium system
<div><p>A pot experiment was conducted to investigate the organic phosphorus (P) (phytate) utilization of <i>Zea mays</i> L. with different nitrogen (N) forms (NH<sub>4</sub><sup>+</sup> and NO<sub>3</sub><sup>−</sup>) when both arbuscular mycorrhizal (AM) fungus (<i>Funelliformis mosseae</i>) and phosphate-solubilizing bacterium (PSB, <i>Pseudomonas alcaligenes</i>) are present. The soil was supplied with either KNO<sub>3</sub> or (NH<sub>4</sub>)<sub>2</sub>SO<sub>4</sub> (200 mg kg<sup>−1</sup> N) with or without phytin (75 mg P kg<sup>−1</sup>). Results showed that the application of NH<sub>4</sub><sup>+</sup> to the soil in a plant–AM fungus–PSB system decreased rhizosphere pH and increased phosphatase activity. It also enhanced the mineralization rate of phytin, which resulted in the release of more inorganic P. The application of NO<sub>3</sub><sup>−</sup> promoted mycorrhizal colonization and hyphal length density in the soil. The inorganic P in the hyphosphere decreased, but more P was transferred to the plant through the mycorrhizal hyphae. Hence, in addition, the application of the two different N forms did not significantly alter the content of plant P. The plant supplied with different N fertilizers acquired P through different mechanisms associated with other microbes. NH<sub>4</sub><sup>+</sup> application promoted phytin mineralization by decreasing soil pH, whereas NO<sub>3</sub><sup>−</sup> application increased inorganic P uptake by strengthening the mycorrhizal pathway.</p></div
DataSheet1_Non-coding ribonucleic acid-mediated CAMSAP1 upregulation leads to poor prognosis with suppressed immune infiltration in liver hepatocellular carcinoma.ZIP
Liver hepatocellular carcinoma (LIHC) is well-known for its unfavorable prognosis due to the lack of reliable diagnostic and prognostic biomarkers. Calmodulin-regulated spectrin-associated protein 1 (CAMSAP1) is a non-centrosomal microtubule minus-end binding protein that regulates microtubule dynamics. This study aims to investigate the specific role and mechanisms of CAMSAP1 in LIHC. We performed systematical analyses of CAMSAP1 and demonstrated that differential expression of CAMSAP1 is associated with genetic alteration and DNA methylation, and serves as a potential diagnostic and prognostic biomarker in some cancers, especially LIHC. Further evidence suggested that CAMSAP1 overexpression leads to adverse clinical outcomes in advanced LIHC. Moreover, the AC145207.5/LINC01748-miR-101–3p axis is specifically responsible for CAMSAP1 overexpression in LIHC. In addition to the previously reported functions in the cell cycle and regulation of actin cytoskeleton, CAMSAP1-related genes are enriched in cancer- and immune-associated pathways. As expected, CAMSAP1-associated LIHC is infiltrated in the suppressed immune microenvironment. Specifically, except for immune cell infiltration, it is significantly positively correlated with immune checkpoint genes, especially CD274 (PD-L1), and cancer-associated fibroblasts. Prediction of immune checkpoint blockade therapy suggests that these patients may benefit from therapy. Our study is the first to demonstrate that besides genetic alteration and DNA methylation, AC145207.5/LINC01748-miR-101-3p-mediated CAMSAP1 upregulation in advanced LIHC leads to poor prognosis with suppressed immune infiltration, representing a potential diagnostic and prognostic biomarker as well as a promising immunotherapy target for LIHC.</p
Flowchart of this systematic review.
<p>Flowchart of this systematic review.</p
Characteristics of 19 included studies.
<p>Characteristics of 19 included studies.</p
Increased Biological Effective Dose of Radiation Correlates with Prolonged Survival of Patients with Limited-Stage Small Cell Lung Cancer: A Systematic Review - Fig 2
<p><b>Association between BED and mOS (A), mPFS (B), 1-year OS (C), 3-year OS (D), 5-year OS (E), and LR (F) for all included studies.</b> Each point in the plot represents a value of one arm. The point size represents the sample size. All analyses were conducted by linear regression methods weighted by sample size. <b><i>BED</i></b>, biological effective dose; <b><i>mOS</i></b>, median overall survival; <b>1-, 3-, 5-year <i>OS</i></b>, 1-, 3, 5-year overall survival; <b><i>LR</i></b>, local relapse</p
MOESM1 of Epidermal growth factor receptor (EGFR) T790M mutation identified in plasma indicates failure sites and predicts clinical prognosis in non-small cell lung cancer progression during first-generation tyrosine kinase inhibitor therapy: a prospective observational study
Additional file 1: Figure S1. Design of the assay for detection of EGFR T790M mutations. (A) FAM- and VIC-labeled probes were designed to target mutant and wild-type EGFR alleles, respectively. (B) Sequence information of the primers and probes for the T790M ddPCR assay. (C) Selective sensitivity of the assay for T790M mutation. Up to 1:2,500 dilution of mutant to wild-type EGFR alleles; at least two positive droplets were stably detected by the ddPCR assay. The numbers shown in the positive area are the amounts of EGFR mutant allele-positive droplets by ddPCR. Mt, mutant allele; Wt, wild-type allele; ddPCR, droplet digital PCR
Therapeutical effect of intrapleural perfusion with hyperthermic chemotherapy on malignant pleural effusion under video-assisted thoracoscopic surgery
<p><b>Background:</b> Patients with malignant pleural effusions (MPEs) have limited life expectancy. This study aims to investigate the feasibility of intrapleural perfusion with hyperthermic chemotherapy (IPHC) under video-assisted thoracoscopic surgery on MPE patients.</p> <p><b>Methods:</b> MPE patients were enrolled in the study and treated with IPHC. The treatment response was classified as complete response (CR, no re-accumulation of pleural fluid for 4 weeks), partial response (PR, re-accumulation above the post-IPHC level but below the pre-IPHC level for four weeks), no response (NR; re-accumulation or above the pre-IPHC level). The change of Karnofsky performance score (KPS) and tumour markers were also recorded. Follow-up was done every two weeks during first month and monthly thereafter until death.</p> <p><b>Results:</b> Eighty patients included 46 males and 34 females were included in the study. The total response rate was 100%, with 71.3% of CR and 28.7% of PR. The KPS scores were significantly elevated and the level of tumour markers in pleural effusion were dramatically decreased after IPHC. The median survival was 16.8 months ranged from 2.1 to 67.4 months. One-year and two-year survival rates were 82.5% and 23.8%, respectively. There were no serious clinical compilations during IPHC treatment.</p> <p><b>Conclusions:</b> IPHC is a safety, effective and promising approach for MPE patients. It provides well survival benefit and minor toxicities.</p
Image_4_A robust CD8+ T cell-related classifier for predicting the prognosis and efficacy of immunotherapy in stage III lung adenocarcinoma.tif
Patients with stage III lung adenocarcinoma (LUAD) have significant survival heterogeneity, meanwhile, CD8+ T cell has a remarkable function in immunotherapy. Therefore, developing novel biomarkers based on CD8+ T cell can help evaluate the prognosis and guide the strategy of immunotherapy for patients with stage III LUAD. Thus, we abstracted twelve datasets from multiple online databases and grouped the stage III LUAD patients into training and validation sets. We then used WGCNA and CIBERSORT, while univariate Cox analysis, LASSO analysis, and multivariate Cox analysis were performed. Subsequently, a novel CD8+ T cell-related classifier including HDFRP3, ARIH1, SMAD2, and UPB1 was developed, which could divide stage III LUAD patients into high- and low-risk groups with distinct survival probability in multiple cohorts (all P + T cells included in the model by immunohistochemistry and validated the validity of the model in a real-world cohort. Overall, we constructed a robust CD8+ T cell-related risk model originally which could predict the survival rates in stage III LUAD. What’s more, this model suggested that patients in the high-risk group could benefit from immunotherapy, which has significant implications for accurately predicting the effect of immunotherapy and evaluating the prognosis for patients with stage III LUAD.</p
Image_2_A robust CD8+ T cell-related classifier for predicting the prognosis and efficacy of immunotherapy in stage III lung adenocarcinoma.tif
Patients with stage III lung adenocarcinoma (LUAD) have significant survival heterogeneity, meanwhile, CD8+ T cell has a remarkable function in immunotherapy. Therefore, developing novel biomarkers based on CD8+ T cell can help evaluate the prognosis and guide the strategy of immunotherapy for patients with stage III LUAD. Thus, we abstracted twelve datasets from multiple online databases and grouped the stage III LUAD patients into training and validation sets. We then used WGCNA and CIBERSORT, while univariate Cox analysis, LASSO analysis, and multivariate Cox analysis were performed. Subsequently, a novel CD8+ T cell-related classifier including HDFRP3, ARIH1, SMAD2, and UPB1 was developed, which could divide stage III LUAD patients into high- and low-risk groups with distinct survival probability in multiple cohorts (all P + T cells included in the model by immunohistochemistry and validated the validity of the model in a real-world cohort. Overall, we constructed a robust CD8+ T cell-related risk model originally which could predict the survival rates in stage III LUAD. What’s more, this model suggested that patients in the high-risk group could benefit from immunotherapy, which has significant implications for accurately predicting the effect of immunotherapy and evaluating the prognosis for patients with stage III LUAD.</p
Table_2_A robust CD8+ T cell-related classifier for predicting the prognosis and efficacy of immunotherapy in stage III lung adenocarcinoma.docx
Patients with stage III lung adenocarcinoma (LUAD) have significant survival heterogeneity, meanwhile, CD8+ T cell has a remarkable function in immunotherapy. Therefore, developing novel biomarkers based on CD8+ T cell can help evaluate the prognosis and guide the strategy of immunotherapy for patients with stage III LUAD. Thus, we abstracted twelve datasets from multiple online databases and grouped the stage III LUAD patients into training and validation sets. We then used WGCNA and CIBERSORT, while univariate Cox analysis, LASSO analysis, and multivariate Cox analysis were performed. Subsequently, a novel CD8+ T cell-related classifier including HDFRP3, ARIH1, SMAD2, and UPB1 was developed, which could divide stage III LUAD patients into high- and low-risk groups with distinct survival probability in multiple cohorts (all P + T cells included in the model by immunohistochemistry and validated the validity of the model in a real-world cohort. Overall, we constructed a robust CD8+ T cell-related risk model originally which could predict the survival rates in stage III LUAD. What’s more, this model suggested that patients in the high-risk group could benefit from immunotherapy, which has significant implications for accurately predicting the effect of immunotherapy and evaluating the prognosis for patients with stage III LUAD.</p