cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.10724477
title: Kinect dataset (Basic Data)

description: The "images", "depth", "pose" and "PointCloud" of Kinect sequences.
Dataset structure:
long_capture/depth
long_capture/images
long_capture/intrinsic
long_capture/PointCloud
long_capture/pose
longcapture/camera_parameters.txt
long_capture/test.txt
longcapture/transformations_colmap.json
long_capture/transformations.json
short_capture/depth
short_capture/images
short_capture/intrinsic
short_capture/PointCloud
short_capture/pose
short_capture/transformations_colmap.json
short_capture/transformations.json
DOI: 10.34740/kaggle/ds/4511657
title: DT/MARS CycleGAN for Crops detection
DOI: 10.21227/pd8n-d240
title: IEEEXtreme 14: Coupon Codes

description: This dataset contains a total of 3210 submissions, with 2% correct solutions and 58% partial solutions. Link to the original challenge: https://csacademy.com/ieeextreme-practice/task/coupon-codes/ See the included PDF document for details about the original challenge.
DOI: 10.6084/m9.figshare.8324588
title: Outcomes of Chronic Total Occlusions in Coronary Arteries According to Three Therapeutic Strategies: A Meta-analysis with 6985 Patients from 8 Published Observational Studies

description: Abstract Objective: To perform a systematic review and meta-analysis of studies comparing coronary artery bypass grafting (CABG), percutaneous coronary intervention (PCI), and medical treatment (MT) in patients with chronic total occlusions (CTOs). Methods: We identified eligible observational studies published in the China National Knowledge Infrastructure database, PubMed, Excerpta Medica database, Google Scholar, Cochrane Library, Web of Science, and "Clinical trials" registration from 1999 to October 2018. Main outcome measures were all-cause mortality, cardiac death, major adverse cardiac events (MACEs), and myocardial infarction (MI). Results: There were eight observational studies including 6985 patients. Patients' mean age was 64.4 years. Mean follow-up time was 4.3 years. Comparing with MT (2958 patients), PCI (3157 patients) presented decreased all-cause mortality (odd ratio [OR]: 0.46, 95% confidence interval [CI]: 0.36-0.60; P&lt;0.001), cardiac death (OR: 0.40, 95% CI: 0.31-0.52; P&lt;0.001), MACE (OR: 0.55, 95% CI: 0.43-0.71; P&lt;0.001), and MI (OR: 0.40, 95% CI: 0.26-0.62; P&lt;0.001). Comparing with MT, CABG (613 patients) presented lower all-cause mortality (OR: 0.50, 95% CI: 0.36-0.69; P&lt;0.001) and MACE (OR: 0.50, 95% CI: 0.26-0.96; P=0.04), but not lower MI (OR: 0.23, 95% CI: 0.03-1.54; P=0.13) and cardiac death (OR: 0.83, 95% CI: 0.51-1.35). Comparing with CABG, PCI did not present decreased risk for those outcomes. Conclusions: PCI or CABG was associated with better clinical outcome in patients with CTO than MT. PCI is not better than CABG in decreasing mortality, MI, cardiac death, and MACE in coronary CTO patients.
DOI: 10.6084/m9.figshare.8324588.v1
title: Outcomes of Chronic Total Occlusions in Coronary Arteries According to Three Therapeutic Strategies: A Meta-analysis with 6985 Patients from 8 Published Observational Studies

description: Abstract Objective: To perform a systematic review and meta-analysis of studies comparing coronary artery bypass grafting (CABG), percutaneous coronary intervention (PCI), and medical treatment (MT) in patients with chronic total occlusions (CTOs). Methods: We identified eligible observational studies published in the China National Knowledge Infrastructure database, PubMed, Excerpta Medica database, Google Scholar, Cochrane Library, Web of Science, and "Clinical trials" registration from 1999 to October 2018. Main outcome measures were all-cause mortality, cardiac death, major adverse cardiac events (MACEs), and myocardial infarction (MI). Results: There were eight observational studies including 6985 patients. Patients' mean age was 64.4 years. Mean follow-up time was 4.3 years. Comparing with MT (2958 patients), PCI (3157 patients) presented decreased all-cause mortality (odd ratio [OR]: 0.46, 95% confidence interval [CI]: 0.36-0.60; P&lt;0.001), cardiac death (OR: 0.40, 95% CI: 0.31-0.52; P&lt;0.001), MACE (OR: 0.55, 95% CI: 0.43-0.71; P&lt;0.001), and MI (OR: 0.40, 95% CI: 0.26-0.62; P&lt;0.001). Comparing with MT, CABG (613 patients) presented lower all-cause mortality (OR: 0.50, 95% CI: 0.36-0.69; P&lt;0.001) and MACE (OR: 0.50, 95% CI: 0.26-0.96; P=0.04), but not lower MI (OR: 0.23, 95% CI: 0.03-1.54; P=0.13) and cardiac death (OR: 0.83, 95% CI: 0.51-1.35). Comparing with CABG, PCI did not present decreased risk for those outcomes. Conclusions: PCI or CABG was associated with better clinical outcome in patients with CTO than MT. PCI is not better than CABG in decreasing mortality, MI, cardiac death, and MACE in coronary CTO patients.
DOI: 10.34740/kaggle/dsv/7723392
title: Gemma Replicator
DOI: 10.6084/m9.figshare.11994624
title: Table S1.xlsx

description: <b>Table
S1</b>. Sample description and
dating results for dolerites from the Dongchuan Group.
DOI: 10.6084/m9.figshare.12518873
title: Additional file 1 of Evaluating the association between feed efficiency and the fecal microbiota of early-life Duroc pigs using 16S rRNA sequencing

description: Additional file 1. Characteristics of the pigs used in this study.
DOI: 10.6084/m9.figshare.12518873.v1
title: Additional file 1 of Evaluating the association between feed efficiency and the fecal microbiota of early-life Duroc pigs using 16S rRNA sequencing

description: Additional file 1. Characteristics of the pigs used in this study.
DOI: 10.6084/m9.figshare.19858962
title: Oxymatrine induces anti-tumor response in cervical cancer by modulating circ_0008460/miR-197-3p/ribonucleotide reductase subunit M2 (RRM2)

description: Oxymatrine (OMT) has exhibited an anti-cancer role in human cancers, including cervical cancer (CC). The dysregulated circular RNAs (circRNAs) are key regulators in cancer biology, and circ_0008460 was upregulated in CC. This study was performed to investigate the circRNA-based molecular mechanism for OMT in CC. RNA detection for circ_0008460, microRNA-197-3p (miR-197-3p), or ribonucleotide reductase subunit M2 (RRM2) was completed using reverse transcription-quantitative polymerase chain reaction assay. Cell behaviors were assessed by Cell Counting Kit-8 assay for cell viability, colony formation assay or Edu assay for cell proliferation, flow cytometry for cell apoptosis, and wound healing assay/transwell assay for migration/invasion. Protein expression examination was conducted using western blot. Dual-luciferase reporter assay and RNA pull-down assay were applied to confirm target binding. Tumor xenograft assay was performed for OMT research <i>in vivo</i>. OMT induced circ_0008460 downregulation in CC cells. OMT-induced inhibitory effects on cell growth, migration, and invasion but promoting effect on cell apoptosis were attenuated by circ_0008460. Circ_0008460 directly interacted with miR-197-3p, and OMT inhibited malignant behaviors of CC cells via mediating circ_0008460/miR-197-3p axis. RRM2 acted as a target for miR-197-3p and circ_0008460 affected the RRM2 level through absorbing miR-197-3p. OMT upregulated miR-197-3p to inhibit RRM2 expression to impede CC cell development. CC tumorigenesis was suppressed by OMT via targeting circ_0008460/miR-197-3p/RRM2 axis <i>in vivo</i>. These results suggested that OMT restrained CC cell progression <i>in vitro</i> and tumor growth <i>in vivo</i> by downregulating circ_0008460 to mediate miR-197-3p/RRM2 axis.
DOI: 10.6084/m9.figshare.19858962.v1
title: Oxymatrine induces anti-tumor response in cervical cancer by modulating circ_0008460/miR-197-3p/ribonucleotide reductase subunit M2 (RRM2)

description: Oxymatrine (OMT) has exhibited an anti-cancer role in human cancers, including cervical cancer (CC). The dysregulated circular RNAs (circRNAs) are key regulators in cancer biology, and circ_0008460 was upregulated in CC. This study was performed to investigate the circRNA-based molecular mechanism for OMT in CC. RNA detection for circ_0008460, microRNA-197-3p (miR-197-3p), or ribonucleotide reductase subunit M2 (RRM2) was completed using reverse transcription-quantitative polymerase chain reaction assay. Cell behaviors were assessed by Cell Counting Kit-8 assay for cell viability, colony formation assay or Edu assay for cell proliferation, flow cytometry for cell apoptosis, and wound healing assay/transwell assay for migration/invasion. Protein expression examination was conducted using western blot. Dual-luciferase reporter assay and RNA pull-down assay were applied to confirm target binding. Tumor xenograft assay was performed for OMT research <i>in vivo</i>. OMT induced circ_0008460 downregulation in CC cells. OMT-induced inhibitory effects on cell growth, migration, and invasion but promoting effect on cell apoptosis were attenuated by circ_0008460. Circ_0008460 directly interacted with miR-197-3p, and OMT inhibited malignant behaviors of CC cells via mediating circ_0008460/miR-197-3p axis. RRM2 acted as a target for miR-197-3p and circ_0008460 affected the RRM2 level through absorbing miR-197-3p. OMT upregulated miR-197-3p to inhibit RRM2 expression to impede CC cell development. CC tumorigenesis was suppressed by OMT via targeting circ_0008460/miR-197-3p/RRM2 axis <i>in vivo</i>. These results suggested that OMT restrained CC cell progression <i>in vitro</i> and tumor growth <i>in vivo</i> by downregulating circ_0008460 to mediate miR-197-3p/RRM2 axis.
DOI: 10.6084/m9.figshare.19858965
title: Stearoyl-CoA desaturase 1 regulates malignant progression of cervical cancer cells

description: The primary regulatory gene for fatty acid synthesis, stearoyl-CoA desaturase 1 (SCD1), has been linked to the progression of several malignancies. Its role in cervical cancer remains unclear till now. This paper aimed to explore the role and mechanism of SCD1 in cervical cancer. The GEPIA database was used to perform a bioinformatics analysis of the role of SCD1 in cervical cancer staging and prognosis. The influences of SCD1 knockdown on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progress were then investigated. Following transcription factor Kruppel like factor 9 (KLF9) was discovered to be negatively correlated with SCD1, the regulatory role of KLF9 in the effects of SCD1 on cervical cancer cells and the signaling pathway was evaluated. According to the GEPIA database, SCD1 level was associated with the cervical cancer stage, the overall survival level, and the disease-free survival level. Cell proliferation, migration, invasion, and EMT progress were all hindered when its expression was knocked down. Novelty, KLF9 reversed the effects of SCD1 on cells, as well as the Akt/glycogen synthase kinase 3β (GSK3β) signaling pathway. Together, SCD1 was negatively regulated by KLF9 and it activated the Akt/GSK3β signaling pathway to promote the malignant progression of cervical cancer cells. Developing SCD1 inhibitors offers novel ideas for the biological treatment of cervical cancer.
DOI: 10.6084/m9.figshare.19858965.v1
title: Stearoyl-CoA desaturase 1 regulates malignant progression of cervical cancer cells

description: The primary regulatory gene for fatty acid synthesis, stearoyl-CoA desaturase 1 (SCD1), has been linked to the progression of several malignancies. Its role in cervical cancer remains unclear till now. This paper aimed to explore the role and mechanism of SCD1 in cervical cancer. The GEPIA database was used to perform a bioinformatics analysis of the role of SCD1 in cervical cancer staging and prognosis. The influences of SCD1 knockdown on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progress were then investigated. Following transcription factor Kruppel like factor 9 (KLF9) was discovered to be negatively correlated with SCD1, the regulatory role of KLF9 in the effects of SCD1 on cervical cancer cells and the signaling pathway was evaluated. According to the GEPIA database, SCD1 level was associated with the cervical cancer stage, the overall survival level, and the disease-free survival level. Cell proliferation, migration, invasion, and EMT progress were all hindered when its expression was knocked down. Novelty, KLF9 reversed the effects of SCD1 on cells, as well as the Akt/glycogen synthase kinase 3β (GSK3β) signaling pathway. Together, SCD1 was negatively regulated by KLF9 and it activated the Akt/GSK3β signaling pathway to promote the malignant progression of cervical cancer cells. Developing SCD1 inhibitors offers novel ideas for the biological treatment of cervical cancer.
DOI: 10.6084/m9.figshare.19858964
title: Curcumin alleviates rheumatoid arthritis progression through the phosphatidylinositol 3-kinase/protein kinase B pathway: an <i>in vitro</i> and <i>in vivo</i> study

description: Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized by synovial inflammation and joint bone and cartilage destruction. Curcumin can improve joint inflammation in rats with arthritis and inhibit synovial revascularization and abnormal proliferation of fibroblasts. However, it is unclear whether curcumin affects the RA progression. The TNF-α-stimulated primary RA fibroblast-like synoviocytes (RA-FLS) and SV-40 transformed MH7A cells were used as the <i>in vitro</i> model of RA. A mouse model of collagen-induced arthritis (CIA) was used as the <i>in vivo</i> model. The effects of curcumin on cell proliferation, apoptosis, migration, invasion, and inflammatory response were assessed by colony formation, flow cytometry, wound scratch, Transwell assays, and western blotting analysis. Arthritis index scores and degree of paw swelling in mice were assessed to evaluate RA. Curcumin inhibited the TNF-α-induced proliferation, migration, invasion of MH7A and RA-FLS cells and promoted cell apoptosis. Administration with curcumin reversed the CIA-induced increase in arthritis scores, hind paw edema, and loss of appetite, while these effects were rescued by insulin-like growth factor 1, the upstream cytokine of PI3K/AKT. Moreover, curcumin suppressed the inflammatory response by reducing TNF-α, IL-6, and IL-17 secretion in CIA-stimulated mice. Curcumin has an excellent anti-RA effect <i>in vivo</i> and <i>in vitro</i>, which is exerted by inhibiting the expression of pro-inflammatory factors TNF-a, IL-6 and IL-17 and inhibiting the activation of PI3K/AKT signaling pathway. Thus, curcumin may be a promising candidate for anti-RA treatment.
DOI: 10.6084/m9.figshare.19858964.v1
title: Curcumin alleviates rheumatoid arthritis progression through the phosphatidylinositol 3-kinase/protein kinase B pathway: an <i>in vitro</i> and <i>in vivo</i> study

description: Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized by synovial inflammation and joint bone and cartilage destruction. Curcumin can improve joint inflammation in rats with arthritis and inhibit synovial revascularization and abnormal proliferation of fibroblasts. However, it is unclear whether curcumin affects the RA progression. The TNF-α-stimulated primary RA fibroblast-like synoviocytes (RA-FLS) and SV-40 transformed MH7A cells were used as the <i>in vitro</i> model of RA. A mouse model of collagen-induced arthritis (CIA) was used as the <i>in vivo</i> model. The effects of curcumin on cell proliferation, apoptosis, migration, invasion, and inflammatory response were assessed by colony formation, flow cytometry, wound scratch, Transwell assays, and western blotting analysis. Arthritis index scores and degree of paw swelling in mice were assessed to evaluate RA. Curcumin inhibited the TNF-α-induced proliferation, migration, invasion of MH7A and RA-FLS cells and promoted cell apoptosis. Administration with curcumin reversed the CIA-induced increase in arthritis scores, hind paw edema, and loss of appetite, while these effects were rescued by insulin-like growth factor 1, the upstream cytokine of PI3K/AKT. Moreover, curcumin suppressed the inflammatory response by reducing TNF-α, IL-6, and IL-17 secretion in CIA-stimulated mice. Curcumin has an excellent anti-RA effect <i>in vivo</i> and <i>in vitro</i>, which is exerted by inhibiting the expression of pro-inflammatory factors TNF-a, IL-6 and IL-17 and inhibiting the activation of PI3K/AKT signaling pathway. Thus, curcumin may be a promising candidate for anti-RA treatment.
DOI: 10.6084/m9.figshare.19858970
title: MicroRNA-1269 is downregulated in glioblastoma and its maturation is regulated by long non-coding RNA SLC16A1 Antisense RNA 1

description: MicroRNA-1269 (miR-1296) promotes esophageal cancer. However, its role in other cancers, such as glioblastoma (GBM) is unclear. We predicted that miR-1269 might interact with long non-coding RNA (lncRNA) SLC16A1 Antisense RNA 1 (SLC16A1-AS1), a critical player in GBM. We then studied the interaction between SLC16A1-AS1 and miR-1269 in GBM. In this study, paired GBM and non-tumor tissues were used to analyze the expression of SLC16A1-AS1 and premature and mature miR-1269. The interaction of SLC16A1-AS1 with premature miR-1269 was analyzed with RNA pull-down assay and dual-luciferase reporter assay. Cellular fractionation assay was applied to determine the subcellular location of SLC16A1-AS1. Overexpression assays were applied to determine the role of SLC16A1-AS1 in miR-1269 maturation. BrdU, Transwell and cell apoptosis assays were performed to analyze the role of SLC16A1-AS1 and miR-1269 in GBM cell proliferation, migration, and invasion. Interestingly, we observed the upregulation of premature miR-1269 and downregulation of mature miR-1269 in GBM. SLC16A1-AS1 was also overexpressed in GBM. The direct interaction of SLC16A1-AS1 with premature miR-1269 was observed. SLC16A1-AS1 suppressed miR-1269 maturation and promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, while miR-1269 displayed the opposite trend. SLC16A1-AS1 partly reversed the effects of miR-1269 on GBM cell proliferation, movement and apoptosis. Moreover, SLC16A1-AS1 overexpression increased the level of ki-67, CDK4 and Bcl-2 in LN-229 and LN-18 cells. However, miR-1269 could partly reverse the effect of SLC16A-AS1 on protein levels. Overall, miR-1269 is downregulated in GBM and its maturation is regulated by SLC16A1-AS1.
DOI: 10.6084/m9.figshare.19858970.v1
title: MicroRNA-1269 is downregulated in glioblastoma and its maturation is regulated by long non-coding RNA SLC16A1 Antisense RNA 1

description: MicroRNA-1269 (miR-1296) promotes esophageal cancer. However, its role in other cancers, such as glioblastoma (GBM) is unclear. We predicted that miR-1269 might interact with long non-coding RNA (lncRNA) SLC16A1 Antisense RNA 1 (SLC16A1-AS1), a critical player in GBM. We then studied the interaction between SLC16A1-AS1 and miR-1269 in GBM. In this study, paired GBM and non-tumor tissues were used to analyze the expression of SLC16A1-AS1 and premature and mature miR-1269. The interaction of SLC16A1-AS1 with premature miR-1269 was analyzed with RNA pull-down assay and dual-luciferase reporter assay. Cellular fractionation assay was applied to determine the subcellular location of SLC16A1-AS1. Overexpression assays were applied to determine the role of SLC16A1-AS1 in miR-1269 maturation. BrdU, Transwell and cell apoptosis assays were performed to analyze the role of SLC16A1-AS1 and miR-1269 in GBM cell proliferation, migration, and invasion. Interestingly, we observed the upregulation of premature miR-1269 and downregulation of mature miR-1269 in GBM. SLC16A1-AS1 was also overexpressed in GBM. The direct interaction of SLC16A1-AS1 with premature miR-1269 was observed. SLC16A1-AS1 suppressed miR-1269 maturation and promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, while miR-1269 displayed the opposite trend. SLC16A1-AS1 partly reversed the effects of miR-1269 on GBM cell proliferation, movement and apoptosis. Moreover, SLC16A1-AS1 overexpression increased the level of ki-67, CDK4 and Bcl-2 in LN-229 and LN-18 cells. However, miR-1269 could partly reverse the effect of SLC16A-AS1 on protein levels. Overall, miR-1269 is downregulated in GBM and its maturation is regulated by SLC16A1-AS1.
DOI: 10.6084/m9.figshare.19858973
title: Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88

description: Circular RNA (circRNA) had been confirmed to participate in ulcerative colitis (UC) development. Circular RNA_0001187 (Circ_0001187) had been found to be overexpressed in patients with Crohn disease. Therefore, circ_0001187 might be an important circRNA regulating intestinal inflammatory diseases. However, the role and mechanism of circ_0001187 in UC progression remains unclear. The colonic mucosal tissues were obtained from 23 UC patients and 23 healthy normal controls. Tumor necrosis factor-α (TNF-α) was used to mimic UC cell model <i>in vitro</i>. Cell function was assessed by cell counting kit 8 assay, EdU assay, flow cytometry, ELISA assay and oxidative stress detection. RNA interaction was confirmed by dual-luciferase reporter assay and RIP assay. Serum exosomes were isolated by ultracentrifugation and identified by transmission electron microscope. Circ_0001187 was overexpressed in UC patients. Circ_0001187 knockdown enhanced the proliferation, while suppressed apoptosis, inflammation and oxidative stress of TNF-α-induced FHC cells. Circ_0001187 acted as miR-1236-3p sponge, and the effects of circ_0001187 downregulation on TNF-α-induced FHC cell injury were overturned by miR-1236-3p inhibitor. MYD88 was targeted by miR-1236-3p, and circ_0001187 sponged miR-1236-3p to regulate MYD88. MYD88 knockdown alleviated TNF-α-induced FHC cell injury, and its upregulation revoked the inhibition effect of miR-1236-3p on TNF-α-induced FHC cell injury. High expression of circ_0001187 also was observed in the serum exosomes of UC patients. Our data confirmed that circ_0001187 facilitated UC progression through miR-1236-3p/MYD88 axis, which might be a potential treatment and diagnosis biomarker for UC.
DOI: 10.6084/m9.figshare.19858973.v1
title: Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88

description: Circular RNA (circRNA) had been confirmed to participate in ulcerative colitis (UC) development. Circular RNA_0001187 (Circ_0001187) had been found to be overexpressed in patients with Crohn disease. Therefore, circ_0001187 might be an important circRNA regulating intestinal inflammatory diseases. However, the role and mechanism of circ_0001187 in UC progression remains unclear. The colonic mucosal tissues were obtained from 23 UC patients and 23 healthy normal controls. Tumor necrosis factor-α (TNF-α) was used to mimic UC cell model <i>in vitro</i>. Cell function was assessed by cell counting kit 8 assay, EdU assay, flow cytometry, ELISA assay and oxidative stress detection. RNA interaction was confirmed by dual-luciferase reporter assay and RIP assay. Serum exosomes were isolated by ultracentrifugation and identified by transmission electron microscope. Circ_0001187 was overexpressed in UC patients. Circ_0001187 knockdown enhanced the proliferation, while suppressed apoptosis, inflammation and oxidative stress of TNF-α-induced FHC cells. Circ_0001187 acted as miR-1236-3p sponge, and the effects of circ_0001187 downregulation on TNF-α-induced FHC cell injury were overturned by miR-1236-3p inhibitor. MYD88 was targeted by miR-1236-3p, and circ_0001187 sponged miR-1236-3p to regulate MYD88. MYD88 knockdown alleviated TNF-α-induced FHC cell injury, and its upregulation revoked the inhibition effect of miR-1236-3p on TNF-α-induced FHC cell injury. High expression of circ_0001187 also was observed in the serum exosomes of UC patients. Our data confirmed that circ_0001187 facilitated UC progression through miR-1236-3p/MYD88 axis, which might be a potential treatment and diagnosis biomarker for UC.