cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.19497964.v1
title: Additional file 1 of CAR race to cancer immunotherapy: from CAR T, CAR NK to CAR macrophage therapy

description: Additional file 1.
DOI: 10.25582/data.2023-01.2718489/2291380
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2720834/2291381
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2718416/2291382
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2718652/2291383
title: Data for EMSL Project 51287 from January 2023
DOI: 10.25582/data.2023-01.2719835/2291384
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.13730850
title: MicroRNA-138 improves LPS-induced trophoblast dysfunction through targeting RELA and NF-κB signaling

description: Preeclampsia is a pregnancy complication classified by new onset of elevated blood pressure and proteinuria after 20 weeks of gestation. During preeclampsia, extra villous trophoblasts fail to adequately invade the myometrial spiral arteries, leading to incomplete and impaired vessel transformation and initiating or aggravating preeclampsia. Although NF-κB and proinflammatory cytokines have been reported to be related to trophoblast dysfunction, the underlying mechanism remains unclear. Herein, we demonstrated the miR-138/RELA axis modulating the migratory ability, and invasive ability of HTR-8/SVneo and JEG-3 cells, as well as the inflammatory factor levels in response to LPS stimulation. miR-138 expression was upregulated in preeclampsia placenta and LPS-stimulated HTR-8/SVneo and JEG-3 cell lines. miR-138 overexpression rescued the migratory and invasive ability of HTR-8/SVneo and JEG-3 cells inhibited by LPS stimulation, and decreased LPS-induced TNF-α and IL-6 levels. By binding the 3’-UTR of RELA, miR-138 negatively regulated p65 expression. The silencing of p65 also improved LPS-induced HTR-8/SVneo and JEG-3 cell dysfunction and TNF-α and IL-6 levels. More importantly, p65 overexpression partially reversed the functions of miR-138 overexpression upon both cells, indicating that miR-138 exerted its biological effects through targeting RELA. In conclusion, miR-138 improves LPS-induced inflammation and oxidative stress on trophoblasts through targeting RELA and affecting NF-κB signaling. The miR-138/RELA axis might be involved in preeclampsia pathogenesis, which requires further <i>in vivo</i> and clinical researches.
DOI: 10.6084/m9.figshare.13730850.v1
title: MicroRNA-138 improves LPS-induced trophoblast dysfunction through targeting RELA and NF-κB signaling

description: Preeclampsia is a pregnancy complication classified by new onset of elevated blood pressure and proteinuria after 20 weeks of gestation. During preeclampsia, extra villous trophoblasts fail to adequately invade the myometrial spiral arteries, leading to incomplete and impaired vessel transformation and initiating or aggravating preeclampsia. Although NF-κB and proinflammatory cytokines have been reported to be related to trophoblast dysfunction, the underlying mechanism remains unclear. Herein, we demonstrated the miR-138/RELA axis modulating the migratory ability, and invasive ability of HTR-8/SVneo and JEG-3 cells, as well as the inflammatory factor levels in response to LPS stimulation. miR-138 expression was upregulated in preeclampsia placenta and LPS-stimulated HTR-8/SVneo and JEG-3 cell lines. miR-138 overexpression rescued the migratory and invasive ability of HTR-8/SVneo and JEG-3 cells inhibited by LPS stimulation, and decreased LPS-induced TNF-α and IL-6 levels. By binding the 3’-UTR of RELA, miR-138 negatively regulated p65 expression. The silencing of p65 also improved LPS-induced HTR-8/SVneo and JEG-3 cell dysfunction and TNF-α and IL-6 levels. More importantly, p65 overexpression partially reversed the functions of miR-138 overexpression upon both cells, indicating that miR-138 exerted its biological effects through targeting RELA. In conclusion, miR-138 improves LPS-induced inflammation and oxidative stress on trophoblasts through targeting RELA and affecting NF-κB signaling. The miR-138/RELA axis might be involved in preeclampsia pathogenesis, which requires further <i>in vivo</i> and clinical researches.
DOI: 10.25582/data.2023-02.2731500/2291385
title: Data for EMSL Project 51287 from February 2023
DOI: 10.6084/m9.figshare.7963685
title: Competency-Based Medical Education implementation: Are we transforming the culture of assessment?

description: <b>Purpose:</b> Adopting CBME is challenging in medicine. It mandates a change in processes and approach, ultimately a change in institutional culture with stakeholders ideally embracing and valuing the new processes. Adopting the transformational change model, this study describes the shift in assessment culture by Academic Advisors (AAs) and preceptors over three years of CBME implementation in one Department of Family Medicine. <b>Methods:</b> A qualitative grounded theory method was used for this two-part study. Interviews were conducted with 12 AAs in 2013 and nine AAs in 2016 using similar interview questions. Data were analyzed through a constant comparative method. <b>Results:</b> Three overarching themes emerged from the data: (1) specific identified shifts in assessment culture, (2) factors supporting the shifts in culture, and (3) outcomes related to the culture shift. <b>Conclusions:</b> In both parts of the study, participants noted that assessment took more time and effort. In Part 2, however, the effort was mitigated by a sense of value for all stakeholders. With support from the mandate of regulatory bodies, local leadership, department, faculty development and an electronic platform, a cultural transformation occurred in assessment that enhanced learning and teaching, use of embedded standards for performance decisions, and tracking and documentation performance.
DOI: 10.6084/m9.figshare.7963685.v2
title: Competency-Based Medical Education implementation: Are we transforming the culture of assessment?

description: <b>Purpose:</b> Adopting CBME is challenging in medicine. It mandates a change in processes and approach, ultimately a change in institutional culture with stakeholders ideally embracing and valuing the new processes. Adopting the transformational change model, this study describes the shift in assessment culture by Academic Advisors (AAs) and preceptors over three years of CBME implementation in one Department of Family Medicine. <b>Methods:</b> A qualitative grounded theory method was used for this two-part study. Interviews were conducted with 12 AAs in 2013 and nine AAs in 2016 using similar interview questions. Data were analyzed through a constant comparative method. <b>Results:</b> Three overarching themes emerged from the data: (1) specific identified shifts in assessment culture, (2) factors supporting the shifts in culture, and (3) outcomes related to the culture shift. <b>Conclusions:</b> In both parts of the study, participants noted that assessment took more time and effort. In Part 2, however, the effort was mitigated by a sense of value for all stakeholders. With support from the mandate of regulatory bodies, local leadership, department, faculty development and an electronic platform, a cultural transformation occurred in assessment that enhanced learning and teaching, use of embedded standards for performance decisions, and tracking and documentation performance.
DOI: 10.25582/data.2023-02.2731844/2291386
title: Data for EMSL Project 51287 from February 2023
DOI: 10.6084/m9.figshare.7963685.v1
title: Competency-based medical education implementation: Are we transforming the culture of assessment?

description: <b>Purpose:</b> Adopting CBME is challenging in medicine. It mandates a change in processes and approach, ultimately a change in institutional culture with stakeholders ideally embracing and valuing the new processes. Adopting the transformational change model, this study describes the shift in assessment culture by Academic Advisors (AAs) and preceptors over three years of CBME implementation in one Department of Family Medicine. <b>Methods:</b> A qualitative grounded theory method was used for this two-part study. Interviews were conducted with 12 AAs in 2013 and nine AAs in 2016 using similar interview questions. Data were analyzed through a constant comparative method. <b>Results:</b> Three overarching themes emerged from the data: (1) specific identified shifts in assessment culture, (2) factors supporting the shifts in culture, and (3) outcomes related to the culture shift. <b>Conclusions:</b> In both parts of the study, participants noted that assessment took more time and effort. In Part 2, however, the effort was mitigated by a sense of value for all stakeholders. With support from the mandate of regulatory bodies, local leadership, department, faculty development and an electronic platform, a cultural transformation occurred in assessment that enhanced learning and teaching, use of embedded standards for performance decisions, and tracking and documentation performance.
DOI: 10.25582/data.2023-01.2719547/2291387
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.13730859
title: LncRNA Neat1 expedites the progression of liver fibrosis in mice through targeting miR-148a-3p and miR-22-3p to upregulate <i>Cyth3</i>

description: Liver fibrosis is a common response to chronic liver injury, ultimately leading to cirrhosis. The activation of hepatic stellate cells (HSCs) plays a dominant role in liver fibrosis. The regulatory roles of long noncoding RNAs (lncRNAs) in multiple human diseases have been observed. This study was dedicated to investigating the regulatory effects of the lncRNA nuclear paraspeckle assembly transcript 1 (Neat1) on liver fibrosis and HSC activation. Upregulation of Neat1 and cytohesin 3 (<i>Cyth3</i>) and downregulation of miR-148a-3p and miR-22-3p were observed in mouse fibrotic liver tissues. Knockdown of Neat1 or <i>Cyth3</i> attenuated liver fibrosis and collagen deposition <i>in vivo</i> and the activation of HSCs <i>in vitro</i>. An miR-148a-3p and miR-22-3p inhibitor facilitated HSC activation and collagen fiber expression. Neat1 directly targeted miR-148a-3p and miR-22-3p to modulate <i>Cyth3</i> expression. Knockdown of Neat1 inhibited <i>Cyth3</i> expression via the competing endogenous RNA (ceRNA) mechanism of sponging miR-148a-3p and miR-22-3p to regulate liver fibrosis and HSC activation. The ceRNA regulatory network may promote a better understanding of liver fibrogenesis, contribute to an original agreement of liver fibrosis etiopathogenesis and provide insights into the development of a novel domain of lncRNA-directed therapy against liver fibrosis.
DOI: 10.6084/m9.figshare.13730859.v1
title: LncRNA Neat1 expedites the progression of liver fibrosis in mice through targeting miR-148a-3p and miR-22-3p to upregulate <i>Cyth3</i>

description: Liver fibrosis is a common response to chronic liver injury, ultimately leading to cirrhosis. The activation of hepatic stellate cells (HSCs) plays a dominant role in liver fibrosis. The regulatory roles of long noncoding RNAs (lncRNAs) in multiple human diseases have been observed. This study was dedicated to investigating the regulatory effects of the lncRNA nuclear paraspeckle assembly transcript 1 (Neat1) on liver fibrosis and HSC activation. Upregulation of Neat1 and cytohesin 3 (<i>Cyth3</i>) and downregulation of miR-148a-3p and miR-22-3p were observed in mouse fibrotic liver tissues. Knockdown of Neat1 or <i>Cyth3</i> attenuated liver fibrosis and collagen deposition <i>in vivo</i> and the activation of HSCs <i>in vitro</i>. An miR-148a-3p and miR-22-3p inhibitor facilitated HSC activation and collagen fiber expression. Neat1 directly targeted miR-148a-3p and miR-22-3p to modulate <i>Cyth3</i> expression. Knockdown of Neat1 inhibited <i>Cyth3</i> expression via the competing endogenous RNA (ceRNA) mechanism of sponging miR-148a-3p and miR-22-3p to regulate liver fibrosis and HSC activation. The ceRNA regulatory network may promote a better understanding of liver fibrogenesis, contribute to an original agreement of liver fibrosis etiopathogenesis and provide insights into the development of a novel domain of lncRNA-directed therapy against liver fibrosis.
DOI: 10.25582/data.2023-02.2732113/2291388
title: Data for EMSL Project 51287 from February 2023
DOI: 10.25582/data.2023-01.2718498/2291389
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.14921230
title: Additional file 2 of Integration of metabolomics, genomics, and immune phenotypes reveals the causal roles of metabolites in disease

description: Additional file 2. Table S2
DOI: 10.6084/m9.figshare.14921230.v1
title: Additional file 2 of Integration of metabolomics, genomics, and immune phenotypes reveals the causal roles of metabolites in disease

description: Additional file 2. Table S2
DOI: 10.6084/m9.figshare.14921236
title: Additional file 4 of Integration of metabolomics, genomics, and immune phenotypes reveals the causal roles of metabolites in disease

description: Additional file 4. Table S4
DOI: 10.6084/m9.figshare.14921251
title: Additional file 9 of Integration of metabolomics, genomics, and immune phenotypes reveals the causal roles of metabolites in disease

description: Additional file 9. Table S8
DOI: 10.25582/data.2023-02.2731871/2291390
title: Data for EMSL Project 51287 from February 2023
DOI: 10.6084/m9.figshare.19498054
title: Additional file 10 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 10.
DOI: 10.6084/m9.figshare.19498054.v1
title: Additional file 10 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 10.
DOI: 10.6084/m9.figshare.14921236.v1
title: Additional file 4 of Integration of metabolomics, genomics, and immune phenotypes reveals the causal roles of metabolites in disease

description: Additional file 4. Table S4
DOI: 10.6084/m9.figshare.19498060
title: Additional file 2 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 2.
DOI: 10.25582/data.2023-02.2731946/2291391
title: Data for EMSL Project 51287 from February 2023
DOI: 10.6084/m9.figshare.14921251.v1
title: Additional file 9 of Integration of metabolomics, genomics, and immune phenotypes reveals the causal roles of metabolites in disease

description: Additional file 9. Table S8
DOI: 10.6084/m9.figshare.19498060.v1
title: Additional file 2 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 2.
DOI: 10.6084/m9.figshare.19498063
title: Additional file 3 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 3.
DOI: 10.6084/m9.figshare.19498063.v1
title: Additional file 3 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 3.
DOI: 10.25582/data.2023-02.2731505/2291392
title: Data for EMSL Project 51287 from February 2023
DOI: 10.6084/m9.figshare.19498066
title: Additional file 4 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 4.
DOI: 10.25582/data.2023-02.2731715/2291393
title: Data for EMSL Project 51287 from February 2023
DOI: 10.6084/m9.figshare.19498066.v1
title: Additional file 4 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 4.
DOI: 10.6084/m9.figshare.19498069
title: Additional file 5 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 5.
DOI: 10.6084/m9.figshare.19498069.v1
title: Additional file 5 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 5.
DOI: 10.25582/data.2023-01.2717330/2291394
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.19498072
title: Additional file 6 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 6.
DOI: 10.6084/m9.figshare.19498072.v1
title: Additional file 6 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 6.
DOI: 10.6084/m9.figshare.19498075
title: Additional file 7 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 7.
DOI: 10.25582/data.2023-01.2717343/2291395
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.19498075.v1
title: Additional file 7 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 7.
DOI: 10.6084/m9.figshare.19498078
title: Additional file 8 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 8.
DOI: 10.25582/data.2023-01.2718752/2291396
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.19498078.v1
title: Additional file 8 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 8.
DOI: 10.25582/data.2023-01.2713508/2291397
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.19498081
title: Additional file 9 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 9.
DOI: 10.6084/m9.figshare.19498081.v1
title: Additional file 9 of A risk model of gene signatures for predicting platinum response and survival in ovarian cancer

description: Additional file 9.
DOI: 10.25582/data.2023-02.2731550/2291398
title: Data for EMSL Project 51287 from February 2023
DOI: 10.25582/data.2023-01.2716619/2291399
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.14779494
title: The expression and clinical prognostic value of protein phosphatase 1 catalytic subunit beta in pancreatic cancer

description: Pancreatic cancer (PAAD) is a common malignancy with a poor survival rate. The identification of novel biomarkers could improve clinical outcomes for patients with PAAD. Here we evaluated the expression and clinical significance of <i>PPP1CB</i> in PAAD. <i>PPP1CB</i> expression was higher in PAAD tissue than in matched paracancerous tissue (<i>P &lt; 0.05</i>). We predicted a network of regulatory targets and protein interaction partners of <i>PPP1CB</i>, and identified a PPI network consisting of 39 node genes. The expression of 33 node genes was higher in PAAD tissue than in matching paracancerous tissue. High expression of the node genes <i>ACTN4, ANLN, CLTB, IQGAP1, SPTAN1</i>, and <i>TMOD3</i> was associated with improved overall survival (<i>P &lt; 0.05</i>). SiRNA knockdown of <i>PPP1CB</i> significantly reduced the migration and invasion of PAAD cells. A <i>PPP1CB</i> immunohistochemical staining was performed using a tissue microarray (TMA), consisting of tumor samples collected from 91 patients with PAAD (88 of which contained matched paracancerous tissues). The expression of <i>PPP1CB</i> in PAAD was significantly higher than in the matched paracancerous tissue, (<i>P = 0.016</i>). High <i>PPP1CB</i> expression was associated with patient sex (<i>P = 0.048</i>), alcohol use (<i>P = 0.039</i>), CEA <b>(</b><i>P<b>= 0.038</b></i>), N stage <b>(</b><i>P = 0.001</i>), and invasion of nerve (<i>P = 0.036</i>). Furthermore, high <i>PPP1CB</i> expression was associated with significantly poorer overall survival (<i>P = 0.022</i>). Our data demonstrate that <i>PPP1CB</i> is associated with the migration and invasion of PAAD cells, and may be useful as an independent prognostic indicator for clinical outcome in patients with PAAD.
DOI: 10.6084/m9.figshare.14779494.v1
title: The expression and clinical prognostic value of protein phosphatase 1 catalytic subunit beta in pancreatic cancer

description: Pancreatic cancer (PAAD) is a common malignancy with a poor survival rate. The identification of novel biomarkers could improve clinical outcomes for patients with PAAD. Here we evaluated the expression and clinical significance of <i>PPP1CB</i> in PAAD. <i>PPP1CB</i> expression was higher in PAAD tissue than in matched paracancerous tissue (<i>P &lt; 0.05</i>). We predicted a network of regulatory targets and protein interaction partners of <i>PPP1CB</i>, and identified a PPI network consisting of 39 node genes. The expression of 33 node genes was higher in PAAD tissue than in matching paracancerous tissue. High expression of the node genes <i>ACTN4, ANLN, CLTB, IQGAP1, SPTAN1</i>, and <i>TMOD3</i> was associated with improved overall survival (<i>P &lt; 0.05</i>). SiRNA knockdown of <i>PPP1CB</i> significantly reduced the migration and invasion of PAAD cells. A <i>PPP1CB</i> immunohistochemical staining was performed using a tissue microarray (TMA), consisting of tumor samples collected from 91 patients with PAAD (88 of which contained matched paracancerous tissues). The expression of <i>PPP1CB</i> in PAAD was significantly higher than in the matched paracancerous tissue, (<i>P = 0.016</i>). High <i>PPP1CB</i> expression was associated with patient sex (<i>P = 0.048</i>), alcohol use (<i>P = 0.039</i>), CEA <b>(</b><i>P<b>= 0.038</b></i>), N stage <b>(</b><i>P = 0.001</i>), and invasion of nerve (<i>P = 0.036</i>). Furthermore, high <i>PPP1CB</i> expression was associated with significantly poorer overall survival (<i>P = 0.022</i>). Our data demonstrate that <i>PPP1CB</i> is associated with the migration and invasion of PAAD cells, and may be useful as an independent prognostic indicator for clinical outcome in patients with PAAD.
DOI: 10.25582/data.2023-01.2722695/2291400
title: Data for EMSL Project 51287 from January 2023
DOI: 10.6084/m9.figshare.14779497
title: Construction of lncRNA-related ceRNA regulatory network in diabetic subdermal endothelial cells

description: Long non-coding RNAs (lncRNAs) were considered to be involved in vascular complications in diabetes mellitus, but still only limited knowledge in this regard has been obtained. Herein, we further explored the roles of lncRNAs and mRNAs in diabetic vasculopathy (DV) through conducting bioinformatics analysis using data set downloaded from GEO database. The differentially expressed lncRNAs and mRNAs were identified by edge package. GO enrichment analysis and KEGG pathway analysis were performed based on clusterprofiler package. The relationship between lncRNA and miRNA was predicted using starBase database, and the potential mRNAs targeted by miRNAs were predicted by TargetScan, miRTarbase and miRDB database. The string database was used to analyze the protein-protein interaction (PPI). As a result, a total of 12 lncRNAs and 711 mRNAs were found to be differentially expressed in the diabetic subdermal endothelial cells compared with normal controls. A ceRNA network was established, which was composed of seven lncRNA nodes, 49 miRNA nodes, 58 mRNA nodes and 183 edges, and MSC-AS1 and LINC01550 may serve as key nodes. GO function enrichment analysis showed enrichments of epithelial cell proliferation, intercellular junction, and cell adhesion molecule binding. KEGG pathway analysis revealed 33 enriched pathways. PPI protein interaction analysis identified 57 potential ceRNA-related proteins. Overall, this study suggests that multiple lncRNAs, specifically MSC-AS1 and LINC01550, may play an important role in DV development and they are like to be developed as the therapeutic targets for DV. However, further experiments in vitro and in vivo should be conducted to validate our results.