Publications by authors named "Minghan Chen"

Mounting evidence has revealed that functional brain networks are intrinsically dynamic, undergoing changes over time, even in the rest-state environment. Notably, recent studies have highlighted the existence of a small number of critical brain regions within each functional brain network that exhibit a flexible role in adapting the geometric pattern of brain connectivity over time, referred to as "temporal hub" regions. Therefore, the identification of these temporal hubs becomes pivotal for comprehending the mechanisms that underlie the dynamic evolution of brain connectivity.

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Objectives: Deltex1 is a transcriptional target of NFAT that promotes T cell anergy. However, whether Deltex1 affects the properties of regulatory T cells (Tregs), which are involved in the pathogenesis of Sjögren's disease (SjD), is unknown.

Methods: T cells were purified from peripheral blood using a negative selection method.

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Background: This study sought to assess the risk factors of herpes zoster (HZ) in rheumatoid arthritis (RA) patients treated with tofacitinib (TOFA).

Methods: This retrospective study reviewed RA patients receiving TOFA. We compared clinical characteristics, laboratory profiles, concomitant medication use, and HZ incidence in patients with and without recent biologic synthetic disease-modifying antirheumatic drugs (bDMARDs) treatment, which is defined as their administration ≤180 days before the initiation of TOFA treatment.

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Alzheimer's disease (AD) is the most common neurodegenerative disease, and it consumes considerable medical resources with increasing number of patients every year. Mounting evidence show that the regulatory disruptions altering the intrinsic activity of genes in brain cells contribute to AD pathogenesis. To gain insights into the underlying gene regulation in AD, we proposed a graph learning method, Single-Cell based Regulatory Network (SCRN), to identify the regulatory mechanisms based on single-cell data.

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Objective: To evaluate the risk of end-stage kidney disease (ESKD) in LN patients using tubulointerstitial lesion scores.

Methods: Clinical profiles and histopathological presentations of 151 biopsy-proven LN patients were retrospectively examined. Risk factors of ESKD based on characteristics and scoring of their tubulointerstitial lesions [e.

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Article Synopsis
  • Inflammatory T cells play a role in autoimmune diseases, specifically systemic lupus erythematosus (SLE), with research identifying the pseudogene UHRF1P as a potential new biomarker for SLE.
  • The UHRF1P protein, which is overexpressed in SLE patients' T cells, lacks a key domain that affects its function, leading to increased levels of the inflammatory cytokine IL-17A.
  • In mouse models, UHRF1P promotes autoimmune inflammation by preventing the degradation of a kinase (MAP4K3) that contributes to IL-17A production, indicating a mechanism by which it influences autoimmune disease progression.
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Objectives: To assess the link between the administration of biologic disease-modifying antirheumatic drugs (bDMARDs) and the risk of malignancy in human leukocyte antigen B27 (HLA-B27)-positive patients with ankylosing spondylitis (AS) experiencing sustained inflammation.

Methods: Between 2006 and 2021, 1445 HLA-B27-positive patients with AS were retrospectively evaluated. Among them, 112 patients required bDMARD therapy.

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Eukaryotic chromatin is organized into either silenced heterochromatin or relaxed euchromatin regions, which controls the accessibility of transcriptional machinery and thus regulates gene expression. In fission yeast, Schizosaccharomyces pombe, Set1 is the sole H3K4 methyltransferase and is mainly enriched at the promoters of actively transcribed genes. In contrast, Clr4 methyltransferase initiates H3K9 methylation, which has long been regarded as a hallmark of heterochromatic silencing.

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Background: Immune-mediated diseases (IMDs) after nucleic acid-based vaccines have been sporadically reported since their introduction during the worldwide COVID-19 crisis. Confirming their cause-effect association remains challenging. We analysed the effects of AZD1222 (ChAdOx1 nCoV-19), BNT-162b2, and/or mRNA-1273 on the development &/or deterioration of IMDs in terms of the time of clinical onsets of IMDs after exposure to these vaccines.

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Dual-specificity phosphatase 8 (DUSP8) is a MAPK phosphatase that dephosphorylates and inactivates the kinase JNK. DUSP8 is highly expressed in T cells; however, the in vivo role of DUSP8 in T cells remains unclear. Using T cell-specific Dusp8 conditional KO (T-Dusp8 cKO) mice, mass spectrometry analysis, ChIP-Seq, and immune analysis, we found that DUSP8 interacted with Pur-α, stimulated interleukin-9 (IL-9) gene expression, and promoted Th9 differentiation.

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Objective: To evaluate the risk and protective factors of serious infection (SI) in patients with systemic lupus erythematosus (SLE) within 180 days of rituximab (RTX) treatment.

Methods: Patients with SLE treated with RTX were analyzed. SI was defined as any infectious disease requiring hospitalization.

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Objectives: This study aimed to investigate the clinical outcomes of granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) under rituximab induction and reinduction therapy in Taiwan.

Methods: We performed a retrospective study in patients with GPA or MPA receiving rituximab therapy from August 2008 to July 2020 in seven medical centers in Taiwan. The clinical characteristics and outcomes of these patients were analyzed.

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Vitiligo is a common skin depigmentation disorder characterized by the patchy loss of skin color. Nowadays, it is recognized as being correlated with multiple genetic factors as well as the psychological conditions of individuals. Long noncoding RNAs have been reported to underlie the pathogenesis of vitiligo; however, the role of long noncoding RNAs in the stress-related depigmentation process remains largely unknown.

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Background: Despite the striking efforts in investigating neurobiological factors behind the acquisition of amyloid-β (A), protein tau (T), and neurodegeneration ([N]) biomarkers, the mechanistic pathways of how AT[N] biomarkers spreading throughout the brain remain elusive.

Objective: To disentangle the massive heterogeneities in Alzheimer's disease (AD) progressions and identify vulnerable/critical brain regions to AD pathology.

Methods: In this work, we characterized the interaction of AT[N] biomarkers and their propagation across brain networks using a novel bistable reaction-diffusion model, which allows us to establish a new systems biology underpinning of AD progression.

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Background: Alzheimer's disease (AD) is a heterogeneous, multifactorial neurodegenerative disorder characterized by three neurobiological factors beta-amyloid, pathologic tau, and neurodegeneration. There are no effective treatments for AD at a late stage, urging for early detection and prevention. However, existing statistical inference approaches in neuroimaging studies of AD subtype identification do not take into account the pathological domain knowledge, which could lead to ill-posed results that are sometimes inconsistent with the essential neurological principles.

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Article Synopsis
  • - The study investigates rare cases of systemic hyper-inflammation with multi-organ involvement observed in two patients after receiving the ChAdOx1 nCoV-19 vaccine, while comparing their immune responses to healthy vaccinated controls.
  • - Blood samples were analyzed for biochemical parameters and immune profiles, revealing significant elevations in various cytokine levels in the patients, indicating a strong inflammatory response.
  • - The findings suggest that systemic inflammation can be a rare adverse effect of the ChAdOx1 nCoV-19 vaccine and identify specific immune markers that might play a role in the inflammation process.
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Recently, the fast development of single-cell RNA-seq (scRNA-seq) techniques has enabled high-resolution transcriptomic statistical analysis of individual cells in heterogeneous tissues, which can help researchers to explore the relationship between genes and human diseases. The emerging scRNA-seq data results in new analysis methods aiming to identify cell-level clustering and annotations. However, there are few methods developed to gain insights into the gene-level clusters with biological significance.

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Background: Dual-specificity phosphatases (DUSPs) can dephosphorylate both tyrosine and serine/threonine residues of their substrates and regulate T cell-mediated immunity and autoimmunity. The aim of this study was to investigate the potential roles of DUSPs in ankylosing spondylitis (AS).

Methods: Sixty AS patients and 45 healthy controls were enrolled in this study.

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Signaling driven by nucleic acid sensors participates in interferonopathy-mediated autoimmune diseases. NLRP12, a pyrin-containing NLR protein, is a negative regulator of innate immune activation and type I interferon (IFN-I) production. Peripheral blood mononuclear cells (PBMCs) derived from systemic lupus erythematosus (SLE) patients expressed lower levels of NLRP12, with an inverse correlation with IFNA expression and high disease activity.

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The rapid development of scRNA-seq technology in recent years has enabled us to capture high-throughput gene expression profiles at single-cell resolution, reveal the heterogeneity of complex cell populations, and greatly advance our understanding of the underlying mechanisms in human diseases. Traditional methods for gene co-expression clustering are limited to discovering effective gene groups in scRNA-seq data. In this paper, we propose a novel gene clustering method based on convolutional neural networks called Dual-Stream Subspace Clustering Network (DS-SCNet).

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Background: Overall survival of systemic lupus erythematosus (SLE) patients significantly increased in recent decades, however, the relative risk of mortality is still high. Long-term survival outcome of pediatric SLE remains unclear. This study aims to explore the long-term survival rate and its predictors in patients with systemic lupus erythematosus (SLE).

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Understanding the interfacial behaviors of biomolecules is crucial to applications in biomaterials and nanoparticle-based biosensing technologies. In this work, we utilized autoencoder-based graph clustering to analyze discontinuous molecular dynamics (DMD) simulations of lysozyme adsorption on a graphene surface. Our high-throughput DMD simulations integrated with a Go̅-like protein-surface interaction model makes it possible to explore protein adsorption at a large temporal scale with sufficient accuracy.

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Lung cancer is one of the leading causes of cancer-related death, with a five-year survival rate of 18%. It is a priority for us to understand the underlying mechanisms affecting lung cancer therapeutics' implementation and effectiveness. In this study, we combine the power of Bioinformatics and Systems Biology to comprehensively uncover functional and signaling pathways of drug treatment using bioinformatics inference and multiscale modeling of both scRNA-seq data and proteomics data.

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Unravelling the regulatory programs from single-cell multi-omics data has long been one of the major challenges in genomics, especially in the current emerging single-cell field. Currently there is a huge gap between fast-growing single-cell multi-omics data and effective methods for the integrative analysis of these inherent sparse and heterogeneous data. In this study, we have developed a novel method, Single-cell Multi-omics Gene co-Regulatory algorithm (SMGR), to detect coherent functional regulatory signals and target genes from the joint single-cell RNA-sequencing (scRNA-seq) and single-cell assay for transposase-accessible chromatin using sequencing (scATAC-seq) data obtained from different samples.

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