cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.9916490
title: RETRACTED ARTICLE: MicroRNA-3194-3p inhibits metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma by decreasing Wnt/β-catenin signaling through targeting BCL9

description: We, the Editors and Publisher of the journal <i>Artificial Cells, Nanomedicine, and Biotechnology</i>, have retracted the following article: Bowen Yao, Yazhao Li, Liang Wang, Tianxiang Chen, Yongshen Niu, Qingguang Liu & Zhikui Liu (2019) MicroRNA-3194-3p inhibits metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma by decreasing Wnt/β-catenin signaling through targeting BCL9. <i>Artificial Cells, Nanomedicine, and Biotechnology</i>, 47:1, 3885–3895, DOI: 10.1080/21691401.2019.1670190 Since publication, concerns have been raised about the integrity of the data in the article. In particular, Figures 3A, 5E, 6E and 6F appear to have been previously published in other journals with different author lists, specifically:Figure 3A appears to have been duplicated with Figure 3E, Yang et al., Cell Death & Disease (2017), DOI: 10.1038/cddis.2017.358Figure 5E appears to have been duplicated with Figure 10C, Liu et al., Journal of Experimental & Clinical Cancer Research (2019), DOI: 10.1186/s13046-019-1188-xFigure 6E and 6F appear to have been duplicated with Figure 10G and 10F, Liu et al., Journal of Experimental & Clinical Cancer Research (2018), DOI: 10.1186/s13046-018-0717-3 Figure 3A appears to have been duplicated with Figure 3E, Yang et al., Cell Death & Disease (2017), DOI: 10.1038/cddis.2017.358 Figure 5E appears to have been duplicated with Figure 10C, Liu et al., Journal of Experimental & Clinical Cancer Research (2019), DOI: 10.1186/s13046-019-1188-x Figure 6E and 6F appear to have been duplicated with Figure 10G and 10F, Liu et al., Journal of Experimental & Clinical Cancer Research (2018), DOI: 10.1186/s13046-018-0717-3 When approached for an explanation, the authors checked their data and confirmed there are fundamental errors present and that the images had been “manipulated”. Therefore, they have agreed to the retraction of this article. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted.”
DOI: 10.6084/m9.figshare.9916490.v2
title: RETRACTED ARTICLE: MicroRNA-3194-3p inhibits metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma by decreasing Wnt/β-catenin signaling through targeting BCL9

description: We, the Editors and Publisher of the journal <i>Artificial Cells, Nanomedicine, and Biotechnology</i>, have retracted the following article: Bowen Yao, Yazhao Li, Liang Wang, Tianxiang Chen, Yongshen Niu, Qingguang Liu & Zhikui Liu (2019) MicroRNA-3194-3p inhibits metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma by decreasing Wnt/β-catenin signaling through targeting BCL9. <i>Artificial Cells, Nanomedicine, and Biotechnology</i>, 47:1, 3885–3895, DOI: 10.1080/21691401.2019.1670190 Since publication, concerns have been raised about the integrity of the data in the article. In particular, Figures 3A, 5E, 6E and 6F appear to have been previously published in other journals with different author lists, specifically:Figure 3A appears to have been duplicated with Figure 3E, Yang et al., Cell Death & Disease (2017), DOI: 10.1038/cddis.2017.358Figure 5E appears to have been duplicated with Figure 10C, Liu et al., Journal of Experimental & Clinical Cancer Research (2019), DOI: 10.1186/s13046-019-1188-xFigure 6E and 6F appear to have been duplicated with Figure 10G and 10F, Liu et al., Journal of Experimental & Clinical Cancer Research (2018), DOI: 10.1186/s13046-018-0717-3 Figure 3A appears to have been duplicated with Figure 3E, Yang et al., Cell Death & Disease (2017), DOI: 10.1038/cddis.2017.358 Figure 5E appears to have been duplicated with Figure 10C, Liu et al., Journal of Experimental & Clinical Cancer Research (2019), DOI: 10.1186/s13046-019-1188-x Figure 6E and 6F appear to have been duplicated with Figure 10G and 10F, Liu et al., Journal of Experimental & Clinical Cancer Research (2018), DOI: 10.1186/s13046-018-0717-3 When approached for an explanation, the authors checked their data and confirmed there are fundamental errors present and that the images had been “manipulated”. Therefore, they have agreed to the retraction of this article. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted.”
DOI: 10.15468/dl.ejykka
title: Occurrence Download

description: A dataset containing 19 species occurrences available in GBIF matching the query:
{
 "and" : [
 "HasGeospatialIssue is false",
 "HasCoordinate is true",
 "OccurrenceStatus is Present",
 {
 "not" : {
 "BasisOfRecord" : [
 "is one of (Fossil, Living Specimen)"
 ]
 }
 },
 "TaxonKey is one of (Cobitis punctilineata)",
 "Geometry POLYGON((19.0 42.0, 19.0 34.5, 29.7 34.5, 29.7 42.0, 19.0 42.0))"
 ]
}

 The dataset includes 19 records from 4 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003489-260225131425191/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.7856834
title: Anti-tumour effects of red blood cell membrane-camouflaged black phosphorous quantum dots combined with chemotherapy and anti-inflammatory therapy

description: Conventional anti-tumour chemotherapy is facing the challenges of poor specificity, high toxicity and drug resistance. Tumour microenvironment (TME) plays a critical role in tumour development and drug resistance. To address this problem, we constructed a novel anti-tumour nanoparticle platform RBC@BPQDs-DOX/KIR, black phosphorus nanoparticle quantum dots (BPQDs) with one of the chemotherapeutics (doxorubicin, DOX) and an anti-inflammatory traditional Chinese medicine active component (Kirenol, KIR). Red blood cell membrane (RBCm) vesicles were used as the shell to envelop several nanocores. The combination of DOX and KIR may promote therapeutic efficacy, at which the anti-apoptotic effect of the tumour cells was inhibited (by downregulating Bcl-2 and upregulating Bax) and the tumour progression-related inflammatory factors, such as tumour necrosis factor α (TNF-α) and interleukin-6 (IL-6) were downregulated. Furthermore, TME was remodelled and the anti-tumour effect of DOX was magnified. RBCm imparts high biocompatibility and enhanced permeability and retention (EPR) effects to RBC@BPQDs-DOX/KIR, thus enhancing its tumour passively targetability. Overall, the RBCm-camouflaged drug delivery system RBC@BPQDs-DOX/KIR as a promising therapy for targeted chemotherapeutics and anti-inflammatory therapeutics may provide a specific and highly efficient anti-tumour treatment choice.
DOI: 10.6084/m9.figshare.7856834.v2
title: Anti-tumour effects of red blood cell membrane-camouflaged black phosphorous quantum dots combined with chemotherapy and anti-inflammatory therapy

description: Conventional anti-tumour chemotherapy is facing the challenges of poor specificity, high toxicity and drug resistance. Tumour microenvironment (TME) plays a critical role in tumour development and drug resistance. To address this problem, we constructed a novel anti-tumour nanoparticle platform RBC@BPQDs-DOX/KIR, black phosphorus nanoparticle quantum dots (BPQDs) with one of the chemotherapeutics (doxorubicin, DOX) and an anti-inflammatory traditional Chinese medicine active component (Kirenol, KIR). Red blood cell membrane (RBCm) vesicles were used as the shell to envelop several nanocores. The combination of DOX and KIR may promote therapeutic efficacy, at which the anti-apoptotic effect of the tumour cells was inhibited (by downregulating Bcl-2 and upregulating Bax) and the tumour progression-related inflammatory factors, such as tumour necrosis factor α (TNF-α) and interleukin-6 (IL-6) were downregulated. Furthermore, TME was remodelled and the anti-tumour effect of DOX was magnified. RBCm imparts high biocompatibility and enhanced permeability and retention (EPR) effects to RBC@BPQDs-DOX/KIR, thus enhancing its tumour passively targetability. Overall, the RBCm-camouflaged drug delivery system RBC@BPQDs-DOX/KIR as a promising therapy for targeted chemotherapeutics and anti-inflammatory therapeutics may provide a specific and highly efficient anti-tumour treatment choice.
DOI: 10.6084/m9.figshare.9287186
title: The use of TLR2 modified BMSCs for enhanced bone regeneration in the inflammatory micro-environment

description: The repair of periodontal bone tissue defects in patients with periodontitis is one of the major challenges for dentists. Stem cell-based bone regeneration has been considered as a promising strategy to restore the lost periodontal bone tissue. However, the local inflammatory environment of periodontal tissue affects stem cell-based periodontal bone regeneration. Toll-like receptor 2 (TLR2), a member of the TLR family, plays an important role in regulating immunoreaction. Previous studies have shown that the activation of TLR2 signaling pathway is involved in enhancing tissue vascularization and wound healing. However, the mechanisms underlying the therapeutic effects of TLR2 on regulating bone marrow stromal cells (BMSCs) mediated periodontal bone tissue regeneration still need to be further investigated. In this study, we tested the effect of TLR2 on regulating BMSCs mediated alveolar bone regeneration by establishing a TLR2 gene-modified canine BMSCs using a lentivirus. Activation of TLR2 significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and bone morphogenetic protein 2 (BMP-2) and then upregulated the expression of their downstream osteogenic and angiogenic related gene in BMSCs. TLR2-BMSCs mediated bone regeneration in canine tooth extraction sockets under an inflammatory environment demonstrated that activation of the TLR2 signaling pathway significantly stimulated BMSCs meditated angiogenesis and osteogenesis.
DOI: 10.6084/m9.figshare.9287186.v1
title: The use of TLR2 modified BMSCs for enhanced bone regeneration in the inflammatory micro-environment

description: The repair of periodontal bone tissue defects in patients with periodontitis is one of the major challenges for dentists. Stem cell-based bone regeneration has been considered as a promising strategy to restore the lost periodontal bone tissue. However, the local inflammatory environment of periodontal tissue affects stem cell-based periodontal bone regeneration. Toll-like receptor 2 (TLR2), a member of the TLR family, plays an important role in regulating immunoreaction. Previous studies have shown that the activation of TLR2 signaling pathway is involved in enhancing tissue vascularization and wound healing. However, the mechanisms underlying the therapeutic effects of TLR2 on regulating bone marrow stromal cells (BMSCs) mediated periodontal bone tissue regeneration still need to be further investigated. In this study, we tested the effect of TLR2 on regulating BMSCs mediated alveolar bone regeneration by establishing a TLR2 gene-modified canine BMSCs using a lentivirus. Activation of TLR2 significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and bone morphogenetic protein 2 (BMP-2) and then upregulated the expression of their downstream osteogenic and angiogenic related gene in BMSCs. TLR2-BMSCs mediated bone regeneration in canine tooth extraction sockets under an inflammatory environment demonstrated that activation of the TLR2 signaling pathway significantly stimulated BMSCs meditated angiogenesis and osteogenesis.
DOI: 10.6084/m9.figshare.9916490.v1
title: MicroRNA-3194-3p inhibits metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma by decreasing Wnt/β-catenin signaling through targeting BCL9

description: Local and systemic metastasis of hepatocellular carcinoma (HCC) causes the poor prognosis and increasing evidence confirms that aberrant miRNAs were involved in cancer progression. However, the expression and mechanisms of a specific miR-3194-3p in HCC remains unknown. In this research, we demonstrated that miR-3194-3p, significantly down-regulated in HCC tissues and cell lines, was associated with metastasis and recurrence of HCC. Notably, gain- and loss-of-function assays demonstrated that miR-3194-3p inhibited the migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i>. BCL9, up-regulated in HCC tissues, was a direct downstream target of miR-3194-3p and mediated the functional influence of miR-3194-3p. Most importantly, miR-3194-3p exerted its function by regulating β-catenin pathway. Moreover, miR-3194-3p and BCL9 expression were markedly correlated with adverse clinical features and poor prognosis of HCC patients. We showed that hypoxia was responsible for the down-expression of miR-3194-3p in HCC. Also, the promoting effects of hypoxia on metastasis and EMT of HCC cells were reversed by miR-3194-3p. Altogether, our study suggested that miR-3194-3p inhibits HCC EMT via decreasing Wnt/β-catenin signaling through targeting BCL9 and might be a therapeutic target for HCC.
DOI: 10.13018/bmr28112
title: 1H, 13C, and 15N chemical shift assignments of the Gp4 from the Pseudomonas phage LUZ24
DOI: 10.6084/m9.figshare.7856834.v1
title: Anti-tumour effects of red blood cell membrane-camouflaged black phosphorous quantum dots combined with chemotherapy and anti-inflammatory therapy

description: Conventional anti-tumour chemotherapy is facing the challenges of poor specificity, high toxicity and drug resistance. Tumour microenvironment (TME) plays a critical role in tumour development and drug resistance. To address this problem, we constructed a novel anti-tumour nanoparticle platform RBC@BPQDs-DOX/KIR, black phosphorus nanoparticle quantum dots (BPQDs) with one of the chemotherapeutics (doxorubicin, DOX) and an anti-inflammatory traditional Chinese medicine active component (Kirenol, KIR). Red blood cell membrane (RBCm) vesicles were used as the shell to envelop several nanocores. The combination of DOX and KIR may promote therapeutic efficacy, at which the anti-apoptotic effect of the tumour cells was inhibited (by downregulating Bcl-2 and upregulating Bax) and the tumour progression-related inflammatory factors, such as tumour necrosis factor α (TNF-α) and interleukin-6 (IL-6) were downregulated. Furthermore, TME was remodelled and the anti-tumour effect of DOX was magnified. RBCm imparts high biocompatibility and enhanced permeability and retention (EPR) effects to RBC@BPQDs-DOX/KIR, thus enhancing its tumour passively targetability. Overall, the RBCm-camouflaged drug delivery system RBC@BPQDs-DOX/KIR as a promising therapy for targeted chemotherapeutics and anti-inflammatory therapeutics may provide a specific and highly efficient anti-tumour treatment choice.
DOI: 10.13018/bmr28113
title: revmodN_ACC
DOI: 10.13018/bmr28114
title: AILVproS stereospecific methyl chemical shift assignments of HLA-A*01:01, a human class I major histocompatibility complex heavy chain, bound to NRASQ61K neoepitope and human beta-2 microglobulin
DOI: 10.6084/m9.figshare.9906659
title: Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis

description: Sinomenine (Sino) is diffusely applied in heal rheumatoid arthritis and neuralgia. Howbeit, the activities of Sino in breast cancer cells remain confused. The research attempted to probe the anti-tumor function of Sino in breast cancer cells and divulge the feasible molecular mechanism. Sion at the 1–16 μM concentrations was exploited for the exposure of MDA-MB-231 or MCF7 cells, and cell growth, migration, invasion, cell cycle-relevant and apoptosis-correlative factors were estimated. Micro RNA (miR)-29 expression was evaluated via enforcing qRT-PCR, and the actions of miR-29 in MDA-MB-231 cells growth, migration and invasion were appraised after the overexpressed or suppressed vectors transfection. The functions of PDCD-4 in JNK and MEK/ERK pathways were estimated by employing western blot. We found that, Sino exposure impeded cell proliferation, provoked cell apoptosis and barricaded cell migration and invasion in MDA-MB-231 and MCF7 cells. Enhancement of miR-29 was observed in Sino-managed cells, and miR-29 overexpression further potentiated the activities of Sino in MDA-MB-231 cells. Additionally, Sino remarkably enhanced PCDC-4 expression via adjusting miR-29 in MDA-MB-231 cells. Beyond that, overexpressed PCDC-4 obstructed JNK and MEK/ERK pathways in MDA-MB-231 cells. Taken together, the explorations unveiled that Sino restrained MDA-MB-231 cells proliferation, migration, invasion, and provoked apoptosis through modulation of miR-29/PDCD-4 axis.HighlightSino inhibits MDA-MB-231 and MCF7 cells proliferation and provokes apoptosis;Sino restrains MDA-MB-231 and MCF7 cells migration and invasion;Sino ascends miR-29 expression in MDA-MB-231 and MCF7 cells;Sino adjusts cell growth, migration and invasion via modulating miR-29;Sino up-regulates PDCD-4 expression through mediating miR-29;PDCD-4 obstructs JNK and MEK/ERK pathways in MDA-MB-231 cells. Sino inhibits MDA-MB-231 and MCF7 cells proliferation and provokes apoptosis; Sino restrains MDA-MB-231 and MCF7 cells migration and invasion; Sino ascends miR-29 expression in MDA-MB-231 and MCF7 cells; Sino adjusts cell growth, migration and invasion via modulating miR-29; Sino up-regulates PDCD-4 expression through mediating miR-29; PDCD-4 obstructs JNK and MEK/ERK pathways in MDA-MB-231 cells.
DOI: 10.6084/m9.figshare.9906659.v1
title: Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis

description: Sinomenine (Sino) is diffusely applied in heal rheumatoid arthritis and neuralgia. Howbeit, the activities of Sino in breast cancer cells remain confused. The research attempted to probe the anti-tumor function of Sino in breast cancer cells and divulge the feasible molecular mechanism. Sion at the 1–16 μM concentrations was exploited for the exposure of MDA-MB-231 or MCF7 cells, and cell growth, migration, invasion, cell cycle-relevant and apoptosis-correlative factors were estimated. Micro RNA (miR)-29 expression was evaluated via enforcing qRT-PCR, and the actions of miR-29 in MDA-MB-231 cells growth, migration and invasion were appraised after the overexpressed or suppressed vectors transfection. The functions of PDCD-4 in JNK and MEK/ERK pathways were estimated by employing western blot. We found that, Sino exposure impeded cell proliferation, provoked cell apoptosis and barricaded cell migration and invasion in MDA-MB-231 and MCF7 cells. Enhancement of miR-29 was observed in Sino-managed cells, and miR-29 overexpression further potentiated the activities of Sino in MDA-MB-231 cells. Additionally, Sino remarkably enhanced PCDC-4 expression via adjusting miR-29 in MDA-MB-231 cells. Beyond that, overexpressed PCDC-4 obstructed JNK and MEK/ERK pathways in MDA-MB-231 cells. Taken together, the explorations unveiled that Sino restrained MDA-MB-231 cells proliferation, migration, invasion, and provoked apoptosis through modulation of miR-29/PDCD-4 axis.HighlightSino inhibits MDA-MB-231 and MCF7 cells proliferation and provokes apoptosis;Sino restrains MDA-MB-231 and MCF7 cells migration and invasion;Sino ascends miR-29 expression in MDA-MB-231 and MCF7 cells;Sino adjusts cell growth, migration and invasion via modulating miR-29;Sino up-regulates PDCD-4 expression through mediating miR-29;PDCD-4 obstructs JNK and MEK/ERK pathways in MDA-MB-231 cells. Sino inhibits MDA-MB-231 and MCF7 cells proliferation and provokes apoptosis; Sino restrains MDA-MB-231 and MCF7 cells migration and invasion; Sino ascends miR-29 expression in MDA-MB-231 and MCF7 cells; Sino adjusts cell growth, migration and invasion via modulating miR-29; Sino up-regulates PDCD-4 expression through mediating miR-29; PDCD-4 obstructs JNK and MEK/ERK pathways in MDA-MB-231 cells.
DOI: 10.5281/zenodo.18786809
title: labeo_batesii_zanfona_01.fasta.gz
DOI: 10.5281/zenodo.18786810
title: labeo_batesii_zanfona_01.fasta.gz
DOI: 10.6084/m9.figshare.7828370.v24
title: <i>Inonotus obliquus</i> polysaccharide ameliorates dextran sulphate sodium induced colitis involving modulation of Th1/Th2 and Th17/Treg balance

description: Inflammatory bowel disease (IBD) is an intestinal chronic inflammatory disease, and is related to imbalance of CD4<sup>+</sup>T subsets. However, the current treatments of chronic colitis are not ideal and have potential side effects. Therefore, more effective and safer biologically active substances which are extracted from natural plants have been widely concerned. In this study, it was found that <i>Inonotus obliquus</i> polysaccharides (IOP), the main bioactive constituent of <i>Inonotus obliquus</i>, can alleviate dextran sodium sulfate-induced chronic murine intestinal inflammation. Oral administration of IOP (100, 200, 300 mg/kg) can significantly reduce the disease active index and alleviate the pathological changes in colitis mice, where the tight junction proteins Occludin and ZO-1 losses in colon tissues were reduced. It can also regulate imbalanced Th1/Th2 and Th17/Treg in colon tissues, mesenteric lymph nodes and spleen using Reverse Transcription-Polymerase Chain Reaction detection and flow cytometry. Immunohistochemistry and western blot assays further revealed the modulatory effect of IOP on the p-STAT1, p-STAT6, p-STAT3 expression, which promoted the balance of Th1/Th2, Th17/Treg in the colon of chronic colitis mice. In short, these results indicated that IOP was potentially effective therapeutic agent for IBD.
DOI: 10.13018/bmr28115
title: Sequence-specific Backbone Resonance Assignments of Human PrP(23-144) at pH 4.5
DOI: 10.6084/m9.figshare.7828370
title: <i>Inonotus obliquus</i> polysaccharide ameliorates dextran sulphate sodium induced colitis involving modulation of Th1/Th2 and Th17/Treg balance

description: Inflammatory bowel disease (IBD) is an intestinal chronic inflammatory disease, and is related to imbalance of CD4<sup>+</sup>T subsets. However, the current treatments of chronic colitis are not ideal and have potential side effects. Therefore, more effective and safer biologically active substances which are extracted from natural plants have been widely concerned. In this study, it was found that <i>Inonotus obliquus</i> polysaccharides (IOP), the main bioactive constituent of <i>Inonotus obliquus</i>, can alleviate dextran sodium sulfate-induced chronic murine intestinal inflammation. Oral administration of IOP (100, 200, 300 mg/kg) can significantly reduce the disease active index and alleviate the pathological changes in colitis mice, where the tight junction proteins Occludin and ZO-1 losses in colon tissues were reduced. It can also regulate imbalanced Th1/Th2 and Th17/Treg in colon tissues, mesenteric lymph nodes and spleen using Reverse Transcription-Polymerase Chain Reaction detection and flow cytometry. Immunohistochemistry and western blot assays further revealed the modulatory effect of IOP on the p-STAT1, p-STAT6, p-STAT3 expression, which promoted the balance of Th1/Th2, Th17/Treg in the colon of chronic colitis mice. In short, these results indicated that IOP was potentially effective therapeutic agent for IBD.