cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29844730.v1
title: Unveiling the Role of <i>Sdc4</i><sup>+</sup> Monocytes in NASH: A Single-Cell RNA Sequencing Study

description: Nonalcoholic steatohepatitis (NASH) involves liver inflammation and fibrosis. Monocytes, key immune cells differentiating into macrophages and dendritic cells, are understudied in NASH using single-cell RNA sequencing (scRNA-seq). Liver nonparenchymal cells from NASH and control mice underwent scRNA-seq to identify monocyte subsets and transcriptional profiles. Findings were validated via transfection, coculture, immunofluorescence, and qPCR. scRNA-seq analysis revealed that <i>Ly6c</i><sup>hi</sup> monocytes in Cluster 0 appeared to be converted into macrophages in the liver, potentially contributing to the progression of NASH inflammation. Similarly, <i>Ly6c</i><sup>lo</sup> monocytes in Cluster 1 seemed to differentiate into dendritic cells, possibly mediating T-cell immune responses in NASH. Notably, <i>Sdc4</i> was uniquely abundant in Cluster 0. <i>Sdc4</i><sup>+</sup> monocytes were elevated in NASH patients and mice versus controls. Under lipotoxic conditions, <i>Sdc4</i>-deficient (sh-<i>Sdc4</i>) monocytes exhibited upregulated expression of <i>CD206</i> (an M2 marker) and <i>IL-10</i>. When cocultured with sh-<i>Sdc4</i> monocytes under palmitic acid stimulation, HepG2 cells accumulated fewer lipid droplets and produced less TNF-α protein, along with increased <i>IL-10</i> genes, compared to controls. Our study elucidates the heterogeneity and functional transformation of two major monocyte subsets in NASH. We foundSdc4+ monocytes may exacerbate NASH through pro-inflammatory mechanisms.
DOI: 10.6084/m9.figshare.30256803
title: Profiling of Epstein-Barr Virus microRNAs in Whole Blood and Exosomes in Multiple Sclerosis

description: Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease with Epstein-Barr virus (EBV) suggested as a prerequisite for disease development. EBV expresses 44 microRNAs (miRNAs) with largely unknown functions, but they have been implicated in EBV-infected cell proliferation and immune evasion. This study investigates EBV miRNAs levels in whole blood and plasma exosomes at baseline and after treatment, and in relation to disease activity based on age-adjusted NfL ratios, in 50 newly diagnosed patients with relapsing-remitting MS (RRMS). EBV miRNAs purified from whole blood and isolated plasma exosomes were measured by qPCR, using TaqMan Array Cards, and correlated to mRNA of <i>GZMA</i>, <i>GZMH</i>, <i>IFN-γ</i>, <i>TNF-α</i>, <i>IL-10</i>, <i>IL-1B</i>, and <i>IL-1R1</i> in whole blood, measured by qPCR. Serum neurofilament light chain (NfL) and IL-6, plasma anti-EBNA1 antibody titers, occludin, and zonula occludens-1 were measured by various immunoassays. The miRNA profiling of whole blood revealed expression of BHRF1 miRNAs in most patients, indicating that EBV is in lytic phase or latency phase III. Higher levels of miR-BART14-3p were observed in patients classified with high disease activity. EBV miRNA levels correlated with anti-EBNA1 antibody titers, biomarkers of inflammation and tight junction proteins. Most patients with MS express EBV miRNAs that are present in the lytic phase, in which EBV replicates, and latency phase III, in which EBV promotes proliferation of infected B cells.The expression of EBV miR-BART14-3p in plasma exosomes is higher in patients with high compared to low disease activity.The expression of EBV miRNAs correlates with anti-EBNA1 antibody titers, cytotoxic molecules produced by NK and T cells, proinflammation, or blood-brain barrier integrity.Patients receiving high efficacy treatments had increased levels of EBV miR-BART10-3p and miR-BART16 in plasma exosomes. Most patients with MS express EBV miRNAs that are present in the lytic phase, in which EBV replicates, and latency phase III, in which EBV promotes proliferation of infected B cells. The expression of EBV miR-BART14-3p in plasma exosomes is higher in patients with high compared to low disease activity. The expression of EBV miRNAs correlates with anti-EBNA1 antibody titers, cytotoxic molecules produced by NK and T cells, proinflammation, or blood-brain barrier integrity. Patients receiving high efficacy treatments had increased levels of EBV miR-BART10-3p and miR-BART16 in plasma exosomes.
DOI: 10.6084/m9.figshare.30256803.v1
title: Profiling of Epstein-Barr Virus microRNAs in Whole Blood and Exosomes in Multiple Sclerosis

description: Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease with Epstein-Barr virus (EBV) suggested as a prerequisite for disease development. EBV expresses 44 microRNAs (miRNAs) with largely unknown functions, but they have been implicated in EBV-infected cell proliferation and immune evasion. This study investigates EBV miRNAs levels in whole blood and plasma exosomes at baseline and after treatment, and in relation to disease activity based on age-adjusted NfL ratios, in 50 newly diagnosed patients with relapsing-remitting MS (RRMS). EBV miRNAs purified from whole blood and isolated plasma exosomes were measured by qPCR, using TaqMan Array Cards, and correlated to mRNA of <i>GZMA</i>, <i>GZMH</i>, <i>IFN-γ</i>, <i>TNF-α</i>, <i>IL-10</i>, <i>IL-1B</i>, and <i>IL-1R1</i> in whole blood, measured by qPCR. Serum neurofilament light chain (NfL) and IL-6, plasma anti-EBNA1 antibody titers, occludin, and zonula occludens-1 were measured by various immunoassays. The miRNA profiling of whole blood revealed expression of BHRF1 miRNAs in most patients, indicating that EBV is in lytic phase or latency phase III. Higher levels of miR-BART14-3p were observed in patients classified with high disease activity. EBV miRNA levels correlated with anti-EBNA1 antibody titers, biomarkers of inflammation and tight junction proteins. Most patients with MS express EBV miRNAs that are present in the lytic phase, in which EBV replicates, and latency phase III, in which EBV promotes proliferation of infected B cells.The expression of EBV miR-BART14-3p in plasma exosomes is higher in patients with high compared to low disease activity.The expression of EBV miRNAs correlates with anti-EBNA1 antibody titers, cytotoxic molecules produced by NK and T cells, proinflammation, or blood-brain barrier integrity.Patients receiving high efficacy treatments had increased levels of EBV miR-BART10-3p and miR-BART16 in plasma exosomes. Most patients with MS express EBV miRNAs that are present in the lytic phase, in which EBV replicates, and latency phase III, in which EBV promotes proliferation of infected B cells. The expression of EBV miR-BART14-3p in plasma exosomes is higher in patients with high compared to low disease activity. The expression of EBV miRNAs correlates with anti-EBNA1 antibody titers, cytotoxic molecules produced by NK and T cells, proinflammation, or blood-brain barrier integrity. Patients receiving high efficacy treatments had increased levels of EBV miR-BART10-3p and miR-BART16 in plasma exosomes.
DOI: 10.5517/ccdc.csd.cc1n0lx5
title: CCDC 1519927: Experimental Crystal Structure Determination

description: Related Article: David H. Woen, Guo P. Chen, Joseph W. Ziller, Timothy J. Boyle, Filipp Furche, William J. Evans|2017|Angew.Chem.,Int.Ed.|56|2050|doi:10.1002/anie.201611758
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.6084/m9.figshare.30071824
title: Molecular Mechanism of Butyrate Modulating Treg/Th17 Balance in UC Through cAMP-PKA/mTOR Axis

description: This study aims to elucidate how butyrate, a short-chain fatty acid, regulates the Treg/Th17 balance in ulcerative colitis (UC) via the cAMP-PKA/mTOR signaling pathway, offering novel treatment strategies. Dextran sulfate sodium (DSS) was used to induce ulcerative colitis in a mouse model. Various butyrate dosages were administered to the mice. The mice’s body weight, colon length, spleen index (SI), and disease activity index (DAI) were all assessed.HE staining and Masson staining were used for histopathological evaluation. Immunohistochemistry and RT-qPCR were applied to detect fibrosis markers. Flow cytometry, RT-qPCR, and ELISA were employed to analyze immune cell subsets and cytokines. RT-qPCR and Western blotting were utilized to explore the cAMP-PKA/mTOR signaling pathway. Specific inhibitors were used to further confirm the mechanism of its action. Butyrate treatmentreduced DAI and SI, and reversed pathological changes (weight loss, colon shortening, splenomegaly) in DSS-induced UC model mice, with the high-dose group showing the best recovery. It inhibited colon fibrosis,and decreased fibrosis markers. By regulating the regulatory T cell (Treg)/T helper 17 cell (Th17) balance, butyrate restored immune homeostasis. Flow cytometry showed DSS-induced immune imbalance was reversed in a dose-dependent manner. Additionally, butyrate modulated the cAMP-PKA/mTOR signaling pathway, reversing DSS-induced gene and protein expression changes. Specific inhibitor experiments confirmed that butyrate exerted its therapeutic effects via this pathway. Butyrate can markedly alleviate acute UC intestinal inflammation and block chronic fibrosis progression. The bidirectional regulation of the cAMP-PKA/mTOR signaling pathway is the key mechanism for butyrate to restore immune homeostasis. Butyrate dose-dependently improves the pathological state of UC mice, reducing DAI and SI and restoring colon length.Butyrate effectively alleviates acute-phase inflammation in UC, blocks chronic fibrosis, and inhibits collagen proliferation and the expression of fibrosis markers.Butyrate regulates theTreg/Th17 balance and reshapes immune homeostasis by bidirectionally regulatingthe cAMP-PKA/mTOR signaling pathway. Butyrate dose-dependently improves the pathological state of UC mice, reducing DAI and SI and restoring colon length. Butyrate effectively alleviates acute-phase inflammation in UC, blocks chronic fibrosis, and inhibits collagen proliferation and the expression of fibrosis markers. Butyrate regulates theTreg/Th17 balance and reshapes immune homeostasis by bidirectionally regulatingthe cAMP-PKA/mTOR signaling pathway.
DOI: 10.6084/m9.figshare.30071824.v1
title: Molecular Mechanism of Butyrate Modulating Treg/Th17 Balance in UC Through cAMP-PKA/mTOR Axis

description: This study aims to elucidate how butyrate, a short-chain fatty acid, regulates the Treg/Th17 balance in ulcerative colitis (UC) via the cAMP-PKA/mTOR signaling pathway, offering novel treatment strategies. Dextran sulfate sodium (DSS) was used to induce ulcerative colitis in a mouse model. Various butyrate dosages were administered to the mice. The mice’s body weight, colon length, spleen index (SI), and disease activity index (DAI) were all assessed.HE staining and Masson staining were used for histopathological evaluation. Immunohistochemistry and RT-qPCR were applied to detect fibrosis markers. Flow cytometry, RT-qPCR, and ELISA were employed to analyze immune cell subsets and cytokines. RT-qPCR and Western blotting were utilized to explore the cAMP-PKA/mTOR signaling pathway. Specific inhibitors were used to further confirm the mechanism of its action. Butyrate treatmentreduced DAI and SI, and reversed pathological changes (weight loss, colon shortening, splenomegaly) in DSS-induced UC model mice, with the high-dose group showing the best recovery. It inhibited colon fibrosis,and decreased fibrosis markers. By regulating the regulatory T cell (Treg)/T helper 17 cell (Th17) balance, butyrate restored immune homeostasis. Flow cytometry showed DSS-induced immune imbalance was reversed in a dose-dependent manner. Additionally, butyrate modulated the cAMP-PKA/mTOR signaling pathway, reversing DSS-induced gene and protein expression changes. Specific inhibitor experiments confirmed that butyrate exerted its therapeutic effects via this pathway. Butyrate can markedly alleviate acute UC intestinal inflammation and block chronic fibrosis progression. The bidirectional regulation of the cAMP-PKA/mTOR signaling pathway is the key mechanism for butyrate to restore immune homeostasis. Butyrate dose-dependently improves the pathological state of UC mice, reducing DAI and SI and restoring colon length.Butyrate effectively alleviates acute-phase inflammation in UC, blocks chronic fibrosis, and inhibits collagen proliferation and the expression of fibrosis markers.Butyrate regulates theTreg/Th17 balance and reshapes immune homeostasis by bidirectionally regulatingthe cAMP-PKA/mTOR signaling pathway. Butyrate dose-dependently improves the pathological state of UC mice, reducing DAI and SI and restoring colon length. Butyrate effectively alleviates acute-phase inflammation in UC, blocks chronic fibrosis, and inhibits collagen proliferation and the expression of fibrosis markers. Butyrate regulates theTreg/Th17 balance and reshapes immune homeostasis by bidirectionally regulatingthe cAMP-PKA/mTOR signaling pathway.
DOI: 10.5517/ccdc.csd.cc1n0ly6
title: CCDC 1519928: Experimental Crystal Structure Determination

description: Related Article: David H. Woen, Guo P. Chen, Joseph W. Ziller, Timothy J. Boyle, Filipp Furche, William J. Evans|2017|Angew.Chem.,Int.Ed.|56|2050|doi:10.1002/anie.201611758
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc1n0lz7
title: CCDC 1519929: Experimental Crystal Structure Determination

description: Related Article: David H. Woen, Guo P. Chen, Joseph W. Ziller, Timothy J. Boyle, Filipp Furche, William J. Evans|2017|Angew.Chem.,Int.Ed.|56|2050|doi:10.1002/anie.201611758
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.6084/m9.figshare.30052371
title: Biased Usage of V/D/J Genes and Clonal Diversity in IgG Repertoires Correlates with Disease Activity and Clinical Features in Systemic Autoimmune Diseases

description: To examine whether features of the B cell receptor (BCR) IgG repertoire correlate with disease activity and clinical phenotypes in systemic autoimmune diseases (SAIDs). High-throughput sequencing was performed on IgG heavy chain repertoires from 138 patients with SAIDs, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), scleroderma (SSc), and idiopathic inflammatory myopathy (IIM), as well as 36 healthy controls (HC). We analyzed V/D/J gene usage, clonal distribution and diversity, CDR3 length distribution and amino acid usage, and the correlation between specific BCR features and clinical features. SAIDs showed skewed usage of V/D/J genes and V-D-J combinations, with altered CDR3 length distributions and amino acid usage in SLE, RA, SSc, and IIM. Notably, SLE and RA exhibited a pronounced expansion of mid-ranked clones and significantly higher clonal diversity compared to HC. Specific genes, including IGHD2-15, IGHV1-24, IGHV1-69-2, IGHV1-8, and IGHV4 family members, along with increased clonal diversity, were closely associated with disease activity and clinical phenotypes in SLE and RA. IgG repertoire features reflect disease-related immune perturbations and may serve as potential biomarkers for disease progression, diagnostics and targeted therapies in SAIDs.
DOI: 10.6084/m9.figshare.30052371.v2
title: Biased Usage of V/D/J Genes and Clonal Diversity in IgG Repertoires Correlates with Disease Activity and Clinical Features in Systemic Autoimmune Diseases

description: To examine whether features of the B cell receptor (BCR) IgG repertoire correlate with disease activity and clinical phenotypes in systemic autoimmune diseases (SAIDs). High-throughput sequencing was performed on IgG heavy chain repertoires from 138 patients with SAIDs, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), scleroderma (SSc), and idiopathic inflammatory myopathy (IIM), as well as 36 healthy controls (HC). We analyzed V/D/J gene usage, clonal distribution and diversity, CDR3 length distribution and amino acid usage, and the correlation between specific BCR features and clinical features. SAIDs showed skewed usage of V/D/J genes and V-D-J combinations, with altered CDR3 length distributions and amino acid usage in SLE, RA, SSc, and IIM. Notably, SLE and RA exhibited a pronounced expansion of mid-ranked clones and significantly higher clonal diversity compared to HC. Specific genes, including IGHD2-15, IGHV1-24, IGHV1-69-2, IGHV1-8, and IGHV4 family members, along with increased clonal diversity, were closely associated with disease activity and clinical phenotypes in SLE and RA. IgG repertoire features reflect disease-related immune perturbations and may serve as potential biomarkers for disease progression, diagnostics and targeted therapies in SAIDs.
DOI: 10.5517/ccdc.csd.cc1n0m09
title: CCDC 1519930: Experimental Crystal Structure Determination

description: Related Article: David H. Woen, Guo P. Chen, Joseph W. Ziller, Timothy J. Boyle, Filipp Furche, William J. Evans|2017|Angew.Chem.,Int.Ed.|56|2050|doi:10.1002/anie.201611758
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc1n0m1b
title: CCDC 1519931: Experimental Crystal Structure Determination

description: Related Article: David H. Woen, Guo P. Chen, Joseph W. Ziller, Timothy J. Boyle, Filipp Furche, William J. Evans|2017|Angew.Chem.,Int.Ed.|56|2050|doi:10.1002/anie.201611758
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.6084/m9.figshare.29876143
title: Induction Condition Optimization of the M-CSF-Induced Mouse Bone Marrow-Derived Macrophage and the Mechanism Exploration Based on RNA-Seq Analysis

description: Bone marrow-derived macrophage (BMDM) is key tool cell for studying biological processes such as immunity and inflammation. It is also known as a cell drug that can be used for cytotherapy of many diseases such as liver fibrosis. Given the high demand for BMDMs in research, this study explored the most cost-effective, high-productivity method and its molecular mechanism for obtaining Macrophage Colony-Stimulating Factor (M-CSF)-induced mouse BMDM. A factorial experimental design was employed to examine different induction conditions on BMDM phenotype proportion and productivity, including bone marrow cell (BMC) seeding density, M-CSF concentration, induction time, and removal of bone marrow resident macrophage. Neutral red phagocytosis assay was used to measure phagocytic capacity of BMDM. The mechanism of BMDM proliferation and differentiation was investigated by RNA-seq technology. The most cost-effective and high-productivity BMDM induction protocol is 2 × 10<sup>5</sup> cells/cm<sup>2</sup> BMDM seeding density, 80 ng/ml M-CSF induction for 4 days with medium changing once on day 3. BMDM productivity reaches 75.6%. Furthermore, 4-day BMDM showed the strongest phagocytic capacity. RNA-Seq analysis revealed that Cd4, Smad6, Acta2, and Lrrc32 were key target genes regulating BMDM proliferation. Jun, Smad6, Cd4, Fhl2, Hspb1, Id1, and Inhbb were key target genes regulating BMDM differentiation. MAPK, mTOR, TGF-β, and NF-kappa B signaling pathways were the key proliferation or differentiation-related pathways. This study proposes an efficient and economical protocol for BMDM induction. Besides, it explores the regulatory mechanism of M-CSF on BMDM proliferation and differentiation.
DOI: 10.6084/m9.figshare.29876143.v1
title: Induction Condition Optimization of the M-CSF-Induced Mouse Bone Marrow-Derived Macrophage and the Mechanism Exploration Based on RNA-Seq Analysis

description: Bone marrow-derived macrophage (BMDM) is key tool cell for studying biological processes such as immunity and inflammation. It is also known as a cell drug that can be used for cytotherapy of many diseases such as liver fibrosis. Given the high demand for BMDMs in research, this study explored the most cost-effective, high-productivity method and its molecular mechanism for obtaining Macrophage Colony-Stimulating Factor (M-CSF)-induced mouse BMDM. A factorial experimental design was employed to examine different induction conditions on BMDM phenotype proportion and productivity, including bone marrow cell (BMC) seeding density, M-CSF concentration, induction time, and removal of bone marrow resident macrophage. Neutral red phagocytosis assay was used to measure phagocytic capacity of BMDM. The mechanism of BMDM proliferation and differentiation was investigated by RNA-seq technology. The most cost-effective and high-productivity BMDM induction protocol is 2 × 10<sup>5</sup> cells/cm<sup>2</sup> BMDM seeding density, 80 ng/ml M-CSF induction for 4 days with medium changing once on day 3. BMDM productivity reaches 75.6%. Furthermore, 4-day BMDM showed the strongest phagocytic capacity. RNA-Seq analysis revealed that Cd4, Smad6, Acta2, and Lrrc32 were key target genes regulating BMDM proliferation. Jun, Smad6, Cd4, Fhl2, Hspb1, Id1, and Inhbb were key target genes regulating BMDM differentiation. MAPK, mTOR, TGF-β, and NF-kappa B signaling pathways were the key proliferation or differentiation-related pathways. This study proposes an efficient and economical protocol for BMDM induction. Besides, it explores the regulatory mechanism of M-CSF on BMDM proliferation and differentiation.
DOI: 10.5517/ccdc.csd.cc1n0m2c
title: CCDC 1519932: Experimental Crystal Structure Determination

description: Related Article: Peter C.Healy|2016|CSD Communication|||
description: Related Article: Graham A. Bowmaker,  Peter C. Healy,  Alexandre N. Sobolev,  Allan H. White|2020|Aust.J.Chem.|73|497|doi:10.1071/CH19340
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc1mkh5v
title: CCDC 1506357: Experimental Crystal Structure Determination

description: Related Article: Ken Takaki, Makoto Hino, Akira Ohno, Kimihiro Komeyama, Hiroto Yoshida and Hiroshi Fukuoka|2017|Beilstein J.Org.Chem.|13|1816|doi:10.3762/bjoc.13.176
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.