Publications by authors named "Ling-Yun Wu"

Spatial transcriptomics (ST) technologies revolutionize biomedical research by providing unprecedented insights into tissue architecture and disease mechanisms. While imaging-based ST technologies achieve single-cell spatial resolution, they face inherent limitations in gene detection capacity and measurement accuracy of expression profiles. Although computational approaches make notable progress, current methods remain challenged by insufficient integration of spatial context and systematic biases toward the single-cell RNA sequencing distribution.

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Domain identification is a critical problem in spatially resolved transcriptomics data analysis, which aims to identify distinct spatial domains within a tissue that maintain both spatial continuity and expression consistency. The degree of coupling between expression data and spatial information in different datasets often varies significantly. Some regions have intact and clear boundaries, while others exhibit blurred boundaries with high intra-domain expression similarity.

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Purpose: This study primarily elucidating the specific mechanism of SIRT2 on neuroinflammation and microglial pyroptosis in a mouse model of SAH.

Patients And Methods: CSF were collected from 57 SAH patients and 11 healthy individuals. C57BL/6 mouse SAH model was established using prechiasmatic cistern blood injection and the in vitro hemoglobin (Hb) stimulation microglia model.

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The immune system undergoes progressive functional remodeling from neonatal stages to old age. Therefore, understanding how aging shapes immune cell function is vital for precise treatment of patients at different life stages. Here, we constructed the first transcriptomic atlas of immune cells encompassing human lifespan, ranging from newborns to supercentenarians, and comprehensively examined gene expression signatures involving cell signaling, metabolism, differentiation, and functions in all cell types to investigate immune aging changes.

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Reproductive strategies of sexually dimorphic plants vary in response to the environment. Here, we ask whether the sexual systems of species (i.e.

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Motivation: Gene regulatory networks (GRNs) are vital tools for delineating regulatory relationships between transcription factors and their target genes. The boom in computational biology and various biotechnologies has made inferring GRNs from multi-omics data a hot topic. However, when networks are constructed from gene expression data, they often suffer from false-positive problem due to the transitive effects of correlation.

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Single-cell assay for transposase-accessible chromatin using sequencing (scATAC-seq) data provided new insights into the understanding of epigenetic heterogeneity and transcriptional regulation. With the increasing abundance of dataset resources, there is an urgent need to extract more useful information through high-quality data analysis methods specifically designed for scATAC-seq. However, analyzing scATAC-seq data poses challenges due to its near binarization, high sparsity and ultra-high dimensionality properties.

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Myelodysplastic syndrome (MDS) is a group of clonal hematopoietic neoplasms originating from hematopoietic stem progenitor cells (HSPCs). We previously identified frequent roundabout guidance receptor 1 () mutations in patients with MDS, while the exact role of in hematopoiesis remains poorly delineated. Here, we report that deficiency confers MDS-like disease with anemia and multilineage dysplasia in mice and predicts poor prognosis in patients with MDS.

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Background: In the field of biology and medicine, the interpretability and accuracy are both important when designing predictive models. The interpretability of many machine learning models such as neural networks is still a challenge. Recently, many researchers utilized prior information such as biological pathways to develop neural networks-based methods, so as to provide some insights and interpretability for the models.

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The occurrence of autophagy dysregulation is vital in the development of myelodysplastic syndrome and its transformation to acute myeloid leukemia. However, the mechanisms are largely unknown. Here, we have investigated the mechanism of the bcl6 corepressor mutation in myelodysplastic syndrome development and its transformation to acute myeloid leukemia.

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Article Synopsis
  • The study investigates how microglia, a type of immune cell in the brain, clear blood and maintain homeostasis after a subarachnoid hemorrhage (SAH), focusing on LC3-associated phagocytosis (LAP) and its regulation through specific gene pathways.
  • Researchers utilized an in vitro model simulating SAH to explore key signaling pathways, particularly emphasizing the P38 MAPK and DAPK1 pathways, which were linked to inhibited LAP and increased inflammation in microglia.
  • Findings revealed that the P38-DAPK1 signaling axis influences the expression of the gene BECN1, thereby affecting both the phagocytic ability and overall health of microglia in the context of SAH.
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The bone marrow microenvironment (BMM) can regulate leukemia stem cells (LSCs) via secreted factors. Increasing evidence suggests that dissecting the mechanisms by which the BMM maintains LSCs may lead to the development of effective therapies for the eradication of leukemia. Inhibitor of DNA binding 1 (ID1), a key transcriptional regulator in LSCs, previously identified by us, controls cytokine production in the BMM, but the role of ID1 in acute myeloid leukemia (AML) BMM remains obscure.

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Understanding the effect of the soil carbon "source-sink" in cropland in China under future warming scenarios is the basis for making reasonable carbon neutralization policies. This study focused on the paddy soil in Fujian Province, a typical subtropical region in China including 84 counties (cities and districts). We employed the 1:50000 soil database and biogeochemical process model (DNDC) to simulate the dynamic changes in paddy soil organic carbon under different warming scenarios for the period of 2017-2053.

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Accurately identifying phenotype-relevant cell subsets from heterogeneous cell populations is crucial for delineating the underlying mechanisms driving biological or clinical phenotypes. Here, by deploying a learning with rejection strategy, we developed a novel supervised learning framework called PENCIL to identify subpopulations associated with categorical or continuous phenotypes from single-cell data. By embedding a feature selection function into this flexible framework, for the first time, we were able to select informative features and identify cell subpopulations simultaneously, which enables the accurate identification of phenotypic subpopulations otherwise missed by methods incapable of concurrent gene selection.

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Aberrant self-renewal of leukemia initiation cells (LICs) drives aggressive acute myeloid leukemia (AML). Here, we report that UHRF1, an epigenetic regulator that recruits DNMT1 to methylate DNA, is highly expressed in AML and predicts poor prognosis. UHRF1 is required for myeloid leukemogenesis by maintaining self-renewal of LICs.

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Gene-based transcriptome analysis, such as differential expression analysis, can identify the key factors causing disease production, cell differentiation and other biological processes. However, this is not enough because basic life activities are mainly driven by the interactions between genes. Although there have been already many differential network inference methods for identifying the differential gene interactions, currently, most studies still only use the information of nodes in the network for downstream analyses.

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Seed priming is an effective method for imparting stress tolerance to plants. This study aimed to analyze the effects of solid matrix priming (SMP) on cauliflower and broccoli seed germination and early seedling growth under suboptimal temperature conditions. The SMP method used in this study included the following steps: (1) mixing seeds with vermiculite and water at a ratio of 2:3:2.

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The presence of aneurysmal subarachnoid hemorrhage (aSAH) is usually accompanied by excessive inflammatory response leading to damage of the central nervous system, and the sialic acid-binding Ig-like lectin 10 (Siglec-10) is a recognized factor being able to modify the inflammatory reaction. To investigate the potential role of Siglec-10 in aSAH, we collected the cerebrospinal fluid (CSF) of control ( = 11) and aSAH ( = 14) patients at separate times and measured the Siglec-10 concentration utilizing the enzyme-linked immunosorbent assay (ELISA) and evaluated the alterations of GOS and GCS during the disease process. In accordance with the STROBE statement, results showed that Siglec-10 in CSF rose quickly in response aSAH attack and then fell back to a slightly higher range above baseline, while it remained at relative high concentration and last longer in several severely injured patients.

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Pyruvate dehydrogenase (PDH), a key enzyme on the mitochondrial outer membrane, has been found to decrease activity notably in early brain injury (EBI) after subarachnoid hemorrhage (SAH). It has been demonstrated that PDH is associated with the production of reactive oxygen species (ROS) and apoptosis. Hence, in this study, we aimed to determine the cause of the decreased PDH activity and explore the potential role of PDH in EBI.

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Background: Cancer survivors have a higher risk of developing secondary cancer, with previous studies showing heterogeneous effects of prior cancer on cancer survivors.

Aim: To describe the features and clinical significance of a prior malignancy in patients with gastric cancer (GC).

Methods: We identified eligible patients from the Surveillance, Epidemiology, and End Results (SEER) database, and compared the clinical features of GC patients with/without prior cancer.

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Mounting evidence has suggested that modulating microglia polarization from pro-inflammatory M1 phenotype to anti-inflammatory M2 state might be a potential therapeutic approach in the treatment of subarachnoid hemorrhage (SAH) injury. Our previous study has indicated that sirtuin 1 (SIRT1) could ameliorate early brain injury (EBI) in SAH by reducing oxidative damage and neuroinflammation. However, the effects of SIRT1 on microglial polarization and the underlying molecular mechanisms after SAH have not been fully illustrated.

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