Publications by authors named "Xiumin Wu"

Objective: Despite growing interest in the application of machine learning (ML) in proteomics, a comprehensive and systematic mapping of this research domain has been lacking. This study addresses this gap by conducting the first large-scale bibliometric analysis focused exclusively on ML-driven proteomics, aiming to elucidate its knowledge structure, development trajectory, and emerging research trends.

Methods: A total of 5,156 publications from the Web of Science Core Collection (1997-2024) were retrieved and analyzed.

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Hepatocellular carcinoma (HCC) is the most prevalent primary malignant tumor, with sorafenib as the main treatment for advanced cases. However, the development of resistance to sorafenib, often driven by cancer stemness, significantly limits its therapeutic efficacy. Minichromosome maintenance complex component 10 (MCM10), a critical regulator of DNA replication and tumor progression, has been implicated in cancer stemness and therapeutic resistance.

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Objective: The assessment of immunotherapy plays a pivotal role in the clinical management of skin melanoma. Graph neural networks (GNNs), alongside other deep learning algorithms and bioinformatics approaches, have demonstrated substantial promise in advancing cancer diagnosis and treatment strategies.

Methods: GNNs models were developed to predict the response to immunotherapy and to pinpoint key pathways.

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Unlabelled: Type I IFN signaling is a crucial component of antiviral immunity that has been linked to promoting the efficacy of some chemotherapeutic drugs. We developed a reporter system in HCT116 cells that detects activation of the endogenous IFI27 locus, an IFN target gene. We screened a library of annotated compounds in these cells and discovered Aurora kinase inhibitors (AURKi) as strong hits.

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Immunological targeting of pathological cells has been successful in oncology and is expanding to other pathobiological contexts. Here, we present a flexible platform that allows labeling cells of interest with the surface-expressed model antigen ovalbumin (OVA), which can be eliminated via either antigen-specific T cells or newly developed OVA antibodies. We demonstrate that hepatocytes can be effectively targeted by either modality.

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Article Synopsis
  • Stem cells play a crucial role in maintaining rapidly renewing tissues like blood and intestines, and mutations affecting their proliferation and differentiation can lead to serious health issues.
  • Researchers conducted studies by genetically targeting Rho-kinases Rock1 and Rock2 in adult mice, discovering these enzymes are essential for the health of hematopoietic (blood-forming) and gastrointestinal systems.
  • Mice lacking Rho-kinases experienced cell cycle arrest in blood progenitors and impaired gut epithelial renewal, highlighting the importance of these kinases for stem cell function and overall organ integrity.
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The present study aims to investigate the effect of climatic and non-climatic factors on rice production by employing an annual time series data from the period of 1970 to 2018. The study employed an ARDL (Autoregressive Distributed Lag) approach, and the long-term equilibrium linkages between the variables have been discovered. Additionally, the study also used a regression model to determine the robustness for the authentication of results.

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This research attempts to evaluate the linkage among climatic change factors such as average temperature and rainfall patterns and non-climatic factors such as the area under major yield crops, fertilizer consumption, and formal credit on major food crop yield from 1985 to 2016 in Pakistan. For the first step, we checked the stationarity of the series by utilizing the unit root tests. An autoregressive distributed lag (ARDL) model was employed to identify the linkages between variables after verifying the properties over a specific period of time.

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Objective: To observe the effect of acupuncture combined with sertraline hydrochloride and sertraline hydrochloride alone on cancer-related depression (CRD), and to explore its action mechanism.

Methods: A total of 120 patients with CRD were randomly divided into an observation group and a control group, 60 cases in each group. Based on the routine treatment of oncology, the patients in the control group were treated with sertraline hydrochloride tablets, 50 mg per time, once a day, and the patients in the observation group were additionally treated with acupuncture at Zhongwan (CV 12), Baihui (GV 20), Shenting (GV 24), Xinshu (BL 15), Ganshu (BL 18), Pishu (BL 20), Shenmen (HT 7), Taichong (LR 3), Taixi (KI 3), 20 to 40 min per time, once a day, 5 times a week.

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Fibroblastic reticular cells (FRCs) are specialized stromal cells that define tissue architecture and regulate lymphocyte compartmentalization, homeostasis, and innate and adaptive immunity in secondary lymphoid organs (SLOs). In the present study, we used single-cell RNA sequencing (scRNA-seq) of human and mouse lymph nodes (LNs) to identify a subset of T cell-zone FRCs defined by the expression of Gremlin1 (Grem1) in both species. Grem1-CreER knock-in mice enabled localization, multi-omics characterization and genetic depletion of Grem1 FRCs.

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Article Synopsis
  • TRPA1 is a nonselective ion channel found in sensory neurons that plays a role in sensing various stimuli and is linked to conditions like neuropathic pain and respiratory diseases.* -
  • Researchers optimized a series of small molecule antagonists to inhibit TRPA1, discovering a new linker that enhances their effectiveness and bioavailability.* -
  • The effectiveness of one compound was tested in animal models, showing a significant reduction in inflammation, and its binding structure was elucidated using cryogenic electron microscopy.*
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Despite the development of effective therapies, a substantial proportion of asthmatics continue to have uncontrolled symptoms, airflow limitation, and exacerbations. Transient receptor potential cation channel member A1 (TRPA1) agonists are elevated in human asthmatic airways, and in rodents, TRPA1 is involved in the induction of airway inflammation and hyperreactivity. Here, the discovery and early clinical development of GDC-0334, a highly potent, selective, and orally bioavailable TRPA1 antagonist, is described.

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The deubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with a high risk for mesothelioma and melanocytic tumors. Here, we show that pancreatic intraepithelial neoplasia driven by oncogenic mutant KrasG12D progressed to pancreatic adenocarcinoma in the absence of BAP1. The Hippo pathway was deregulated in BAP1-deficient pancreatic tumors, with the tumor suppressor LATS exhibiting enhanced ubiquitin-dependent proteasomal degradation.

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Severe asthma patients with low type 2 inflammation derive less clinical benefit from therapies targeting type 2 cytokines and represent an unmet need. We show that mast cell tryptase is elevated in severe asthma patients independent of type 2 biomarker status. Active β-tryptase allele count correlates with blood tryptase levels, and asthma patients carrying more active alleles benefit less from anti-IgE treatment.

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Both common and rare genetic variants of laccase domain-containing 1 (, previously C13orf31) are associated with inflammatory bowel disease, leprosy, Behcet disease, and systemic juvenile idiopathic arthritis. However, the functional relevance of these variants is unclear. In this study, we use LACC1-deficient mice to gain insight into the role of LACC1 in regulating inflammation.

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Preclinical and clinical evidence indicates that a subset of asthma is driven by type 2 cytokines such as interleukin-4 (IL-4), IL-5, IL-9, and IL-13. Additional evidence predicts pathogenic roles for IL-6 and type I and type II interferons. Because each of these cytokines depends on Janus kinase 1 (JAK1) for signal transduction, and because many of the asthma-related effects of these cytokines manifest in the lung, we hypothesized that lung-restricted JAK1 inhibition may confer therapeutic benefit.

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The Hippo signaling pathway regulates organ size and plays critical roles in maintaining tissue growth, homeostasis, and regeneration. Dysregulated in a wide spectrum of cancers, in mammals, this pathway is regulated by two key effectors, YAP and TAZ, that may functionally overlap. We found that TAZ promoted liver inflammation and tumor development.

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The deubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with a high risk of mesothelioma and melanocytic tumors. Here, we show that Bap1 deletion in melanocytes cooperates with the constitutively active, oncogenic form of BRAF (BRAF ) and UV to cause melanoma in mice, albeit at very low frequency. In addition, Bap1-null melanoma cells derived from mouse tumors are more aggressive and colonize and grow at distant sites more than their wild-type counterparts.

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Loss of function of the nuclear deubiquitinating enzyme BRCA1-associated protein-1 (BAP1) is associated with a wide spectrum of cancers. We report that tamoxifen-induced BAP1 deletion in adult mice resulted in severe thymic atrophy. BAP1 was critical for T cell development at several stages.

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Diabetic foot ulcers (DFU) are one of the major complications in type II diabetes patients and can result in amputation and morbidity. Although multiple approaches are used clinically to help wound closure, many patients still lack adequate treatment. Here we show that IL-20 subfamily cytokines are upregulated during normal wound healing.

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Eosinophilic inflammation and Th2 cytokine production are central to the pathogenesis of asthma. Agents that target either eosinophils or single Th2 cytokines have shown benefits in subsets of biomarker-positive patients. More broadly effective treatment or disease-modifying effects may be achieved by eliminating more than one inflammatory stimulator.

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Proper regulation of cell death signaling is crucial for the maintenance of homeostasis and prevention of disease. A caspase-independent regulated form of cell death called necroptosis is rapidly emerging as an important mediator of a number of human pathologies including inflammatory bowel disease and ischemia-reperfusion organ injury. Activation of necroptotic signaling through TNF signaling or organ injury leads to the activation of kinases receptor-interacting protein kinases 1 and 3 (RIP1 and RIP3) and culminates in inflammatory cell death.

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The membrane-type matrix metalloproteinases (MT-MMPs) play an important role in degrading the extracellular matrix (ECM) and facilitating protease-dependent tumor progression and invasion. Here, we report that unlike MT1-MMP, MT3-MMP was down-regulated in esophageal squamous cell carcinoma (ESCC) as detected by real-time PCR (qPCR), Western blot analysis, and immunohistochemistry (IHC). Down-regulation of MT3-MMP was observed at protein level in 66.

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