Effects of Severe Water Stress on Maize Growth Processes in the Field

In this study, we investigated the effects of water stress on the growth and yield of summer maize (Zea mays L.) over four phenological stages: Seedling, jointing, heading, and grain-filling. Water stress treatments were applied during each of these four stages in a water-controlled field in the Guanzhong Plain, China between 2013 and 2016. We found that severe water stress during the seedling stage had a greater effect on the growth and development of maize than stress applied during the other three stages. Water stress led to lower leaf area index (LAI) and biomass owing to reduced intercepted photosynthetically active radiation (IPAR) and radiation-use efficiency (RUE). These effects extended to the reproductive stage and eventually reduced the unit kernel weight and yield. In addition, the chlorophyll content in the leaf remained lower, even though irrigation was applied partially or fully after the seedling stage. Severe and prolonged water stress in maize plants during the seedling stage may damage the structure of the photosynthetic membrane, resulting in lower chlorophyll content, and therefore RUE, than those in the plants that did not experience water stress at the seedling stage. Maize plants with such damage did not show a meaningful recovery even when irrigation levels during the rest of the growth period were the same as those applied to the plants not subjected to water stress. The results of our field experiments suggest that an unrecoverable yield loss could occur if summer maize were exposed to severe and extended water stress events during the seedling stage

Hypergraph-based analysis of weighted gene co-expression hypernetwork

BackgroundWith the rapid advancement of gene sequencing technologies, Traditional weighted gene co-expression network analysis (WGCNA), which relies on pairwise gene relationships, struggles to capture higher-order interactions and exhibits low computational efficiency when handling large, complex datasets.MethodsTo overcome these challenges, we propose a novel Weighted Gene Co-expression Hypernetwork Analysis (WGCHNA) based on weighted hypergraph, where genes are modeled as nodes and samples as hyperedges. By calculating the hypergraph Laplacian matrix, WGCHNA generates a topological overlap matrix for module identification through hierarchical clustering.ResultsResults on four gene expression datasets show that WGCHNA outperforms WGCNA in module identification and functional enrichment. WGCHNA identifies biologically relevant modules with greater complexity, particularly in processes like neuronal energy metabolism linked to Alzheimer’s disease. Additionally, functional enrichment analysis uncovers more comprehensive pathway hierarchies, revealing potential regulatory relationships and novel targets.ConclusionWGCHNA effectively addresses WGCNA’s limitations, providing superior accuracy in detecting gene modules and deeper insights for disease research, making it a powerful tool for analyzing complex biological systems

Advancements in unraveling and enhancing bacterial wilt resistance in Solanaceous crops

Ralstonia solanacearum significantly threatens Solanaceous crops, necessitating efficient genetic control strategies. With advancements in genomics, untapped resources for disease resistance are expected to be identified soon. Intensified research in remote hybridization and somatic cell fusion is crucial to enhance resistance to bacterial wilt. The application of effectors could enable high-throughput methodologies for bacterial wilt resistance identification and promote screening in wild species. For difficult-to-identify receptors, resistant varieties could be developed by incorporating resistance genes from Arabidopsis thaliana and other Solanaceous plants. The use of genome-editing techniques and the completion of whole-genome sequencing for key Solanaceous crops should expedite resistance gene cloning. Methods such as Resistance gene enrichment sequencing (RenSeq) could expedite receptor identification, promising a future where R. solanacearum-resistant crop development is within reach

The mechanism underlying B-cell developmental dysfunction in Kawasaki disease based on single-cell transcriptomic sequencing

BackgroundKawasaki disease (KD) is an acute systemic vasculitis that can lead to acquired heart disease in children mostly from in developed countries. The previous research showed that B cells in KD patients underwent a profound change in both the cell numbers and types after intravenous immunoglobulin (IVIG) therapy.MethodsWe performed the single-cell RNA-sequencing for the peripheral blood mononuclear cells (PBMCs) from three febrile patients and three KD patients to investigate the possible mechanism underlying B cell developmental dysfunction in KD. The pseudo-time analysis was employed to study the developmental trajectories of the PBMCs in febrile control and KD patients.ResultsOverall single-cell expression profiles show that the biological processes of immunity, B cell activation pathway and their related biological entities are repressed in KD patients before IVIG treatment compared to febrile patient and KD patients after IVIG treatment. The differentially expressed gene analyses further demonstrate that B cell signaling pathway is downregulated in B cells and plasma blast cells of KD patients before treatment while cell cycle genes and MYC gene are upregulated in dendritic cells (DCs) and hematopoietic stem and progenitor cells (HSPCs) of KD patients before treatment. The biological process of immune response is upregulated in the HSPCs of KD patients before treatment in our dataset while the biological process of inflammatory response is upregulated in the HSPCs of KD patients before treatment in GSE168732 dataset. Single-cell trajectory analyses demonstrate that KD patients before treatment have a shortened developmental path in which B cells and T cells are failed to differentiate into separate lineages. HSPD1 and HSPE1 genes show an elevated expression level in the early cell development stage of KD patients before treatment accompanied with the repression of MYC, SPI1, MT2A and UBE2C genes. Our analyses of all B cells from KD patients before treatment show most of B cells are arrested in a transitional state with an ill developmental path compared with febrile patients and KD patients after treatment.ConclusionOur results indicate that the immune premature HSPCs accompanied with the abnormal expression dynamics of cell cycle and SPI1 genes are the mechanism underlying B cell developmental dysfunction in KD patients

FISH+CD34+CD38- cells detected in newly diagnosed acute myeloid leukemia patients can predict the clinical outcome

BACKGROUND: In acute myeloid leukemia (AML), the leukemia initiating cells (LICs) or leukemia stem cells (LSCs) is found within the CD34(+)CD38(-) cell compartment. The LICs subpopulation survives chemotherapy and is most probable the cause of minimal residual disease (MRD), which in turn is thought to cause relapse. The aim of this study was to determine the prognostic value of the percentage of LICs in blasts at diagnosis. DESIGN AND METHODS: The percentage of LICs in the blast population was determined at diagnosis using a unique Flow-FISH analysis, which applies fluorescent in situ hybridization (FISH) analysis on flow cytometry sorted cells to distinguish LICs within the CD34(+)CD38(-) cell compartment. Fourty-five AML patients with FISH-detectable cytogenetic abnormalities treated with standardized treatment program were retrospectively included in the study. Correlations with overall survival (OS), events-free survival (EFS) and cumulative incidence of relapse (CIR) were evaluated with univariate and multivariate analysis. RESULTS: The percentage of LICs is highly variable in patients with acute myeloid leukemia, ranged from 0.01% to 52.8% (median, 2.1%). High LIC load (≥1%) negatively affected overall survival (2-year OS: 72.57% vs. 16.75%; P = 0.0037) and events-free survival (2-year EFS: 67.23% vs. 16.33%; P = 0.0018), which was due to an increased cumulative incidence of relapse (2-year CIR: 56.7% vs. 18.0%; P = 0.021). By multivariate analysis, high LIC load retained prognostic significance for OS and EFS. CONCLUSIONS: In the present study, we established the Flow-FISH protocol as a useful method to distinguish normal and leukemic cells within the CD34(+)CD38(-) cell subpopulation. The high percentage of LICs at diagnosis was significantly correlated with increased risk of poor clinical outcome

Overexpression of sphingosine kinase 1 is associated with salivary gland carcinoma progression and might be a novel predictive marker for adjuvant therapy

<p>Abstract</p> <p>Background</p> <p>Overexpression of sphingosine kinase-1 (SPHK1) has been demonstrated to be associated with the development and progression in various types of human cancers. The current study was to characterize the expression of SPHK1 in salivary gland carcinomas (SGC) and to investigate the association between SPHK1 expression and progression of SGC.</p> <p>Methods</p> <p>The expression of SPHK1 was examined in 2 normal salivary gland tissues, 8 SGC tissues of various clinical stages, and 5 pairs of primary SGC and adjacent salivary gland tissues from the same patient, using real-time PCR and western blot analysis. Furthermore, the SPHK1 protein expression was analyzed in 159 clinicopathologically characterized SGC cases by immunohistochemistry. Statistical analyses were performed to determine the prognostic and diagnostic associations.</p> <p>Results</p> <p>SPHK1 expression was found to be markedly upregulated in SGC tissues than that in the normal salivary gland tissues and paired adjacent salivary gland tissues, at both mRNA and protein levels. Statistical analysis revealed a significant correlation of SPHK1 expression with the clinical stage (<it>P </it>= 0.005), T classification (<it>P </it>= 0.017), N classification (<it>P </it>= 0.009), M classification (<it>P </it>= 0.002), and pathological differentiation (<it>P </it>= 0.013). Patients with higher SPHK1 expression had shorter overall survival time, whereas patients with lower SPHK1 expression had better survival. Importantly, patients in the group without adjuvant therapy who exhibited high SPHK1 expression had significantly lower overall survival rates compared with those with low SPHK1 expression. Moreover, multivariate analysis suggested that SPHK1 expression might be an independent prognostic indicator for the survival of SGC patients.</p> <p>Conclusions</p> <p>Our results suggest that SPHK1 expression is associated with SGC progression, and might represent as a novel and valuable predictor for adjuvant therapy to SGC patients.</p

Discovery and Validation of Molecular Biomarkers for Colorectal Adenomas and Cancer with Application to Blood Testing

BACKGROUND & AIMS: Colorectal cancer incidence and deaths are reduced by the detection and removal of early-stage, treatable neoplasia but we lack proven biomarkers sensitive for both cancer and pre-invasive adenomas. The aims of this study were to determine if adenomas and cancers exhibit characteristic patterns of biomarker expression and to explore whether a tissue-discovered (and validated) biomarker is differentially expressed in the plasma of patients with colorectal adenomas or cancer. METHODS: Candidate RNA biomarkers were identified by oligonucleotide microarray analysis of colorectal specimens (222 normal, 29 adenoma, 161 adenocarcinoma and 50 colitis) and validated in a previously untested cohort of 68 colorectal specimens using a custom-designed oligonucleotide microarray. One validated biomarker, KIAA1199, was assayed using qRT-PCR on plasma extracted RNA from 20 colonoscopy-confirmed healthy controls, 20 patients with adenoma, and 20 with cancer. RESULTS: Genome-wide analysis uncovered reproducible gene expression signatures for both adenomas and cancers compared to controls. 386/489 (79%) of the adenoma and 439/529 (83%) of the adenocarcinoma biomarkers were validated in independent tissues. We also identified genes differentially expressed in adenomas compared to cancer. KIAA1199 was selected for further analysis based on consistent up-regulation in neoplasia, previous studies and its interest as an uncharacterized gene. Plasma KIAA1199 RNA levels were significantly higher in patients with either cancer or adenoma (31/40) compared to neoplasia-free controls (6/20). CONCLUSIONS: Colorectal neoplasia exhibits characteristic patterns of gene expression. KIAA1199 is differentially expressed in neoplastic tissues and KIAA1199 transcripts are more abundant in the plasma of patients with either cancer or adenoma compared to controls