cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.12886067
title: Additional file 4 of DLBCL with amplification of JAK2/PD-L2 exhibits PMBCL-like CNA pattern and worse clinical outcome resembling those with MYD88 L265P mutation

description: Additional file 4. The detailed information of DLBCL with JAK2/PD-L2 amplification. The detailed data about clinicopathological characteristics, morphology, immunohistochemistry and treatments of DLBCL with JAK2/PD-L2 amplification are showed in this file.
DOI: 10.6084/m9.figshare.12886058
title: Additional file 1 of DLBCL with amplification of JAK2/PD-L2 exhibits PMBCL-like CNA pattern and worse clinical outcome resembling those with MYD88 L265P mutation

description: Additional file 1. MLPA results and clinical follow-up data. The clinicopathological characteristics, clinical follow-up data and MLPA results are showed in this file.
DOI: 10.6084/m9.figshare.11314499
title: Retrospective analysis of risk factors for low 1-minute Apgar scores in term neonates

description: The current study was designed to investigate the perinatal risk factors for low 1-min Apgar scores in term neonates. We retrospectively analyzed the maternal and neonatal clinical data of 10,550 infants who were born through vaginal delivery from 37 weeks 0 days to 41 weeks 6 days of single gestation from January 2013 to July 2018. Because the 1-min Apgar score reflects neonatal status at birth, we analyzed the risk factors for low (score &lt;7) 1-min Apgar scores through logistic regression. Among these 10,550 neonates, 339 (3.2%) had low (score &lt;7) 1-min Apgar scores. Among them, 321 (94.7%) were admitted to the neonatology department for further observation or treatment. Multivariate analysis revealed that educational background, body mass index, gestational age, pathological obstetrics, longer duration of the second stage of labor, forceps delivery or vacuum extraction, neonatal weight, neonatal sex, and meconium-stained amniotic fluid were independent risk factors for 1-min Apgar scores &lt;7. Neonates who had low 1-min Apgar scores were more frequently admitted to the neonatology department for further observation or treatment. Early detection of risk factors and timely intervention to address these factors may improve neonatal outcomes at birth and reduce the rate of admission to the neonatology department.
DOI: 10.6084/m9.figshare.11314499.v1
title: Retrospective analysis of risk factors for low 1-minute Apgar scores in term neonates

description: The current study was designed to investigate the perinatal risk factors for low 1-min Apgar scores in term neonates. We retrospectively analyzed the maternal and neonatal clinical data of 10,550 infants who were born through vaginal delivery from 37 weeks 0 days to 41 weeks 6 days of single gestation from January 2013 to July 2018. Because the 1-min Apgar score reflects neonatal status at birth, we analyzed the risk factors for low (score &lt;7) 1-min Apgar scores through logistic regression. Among these 10,550 neonates, 339 (3.2%) had low (score &lt;7) 1-min Apgar scores. Among them, 321 (94.7%) were admitted to the neonatology department for further observation or treatment. Multivariate analysis revealed that educational background, body mass index, gestational age, pathological obstetrics, longer duration of the second stage of labor, forceps delivery or vacuum extraction, neonatal weight, neonatal sex, and meconium-stained amniotic fluid were independent risk factors for 1-min Apgar scores &lt;7. Neonates who had low 1-min Apgar scores were more frequently admitted to the neonatology department for further observation or treatment. Early detection of risk factors and timely intervention to address these factors may improve neonatal outcomes at birth and reduce the rate of admission to the neonatology department.
DOI: 10.6084/m9.figshare.9740648
title: Additional file 6: of Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs

description: Results for GO annotation and KEGG pathway enrichment analysis for predicted target genes of miR-3607-3p. (XLSX 215 kb)
DOI: 10.6084/m9.figshare.12362510
title: Additional file 8 of Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses

description: Additional file 8: Suppl. Table 8. MF result of the downregulated DEGs in CPIP.
DOI: 10.5281/zenodo.8307915
title: Forward-in-time simulation of chromosomal rearrangements: The invisible backbone that sustains long-term adaptation : simulated data

description: Data simulated with Aevol (www.aevol.fr), a software available on gitlab ( https://gitlab.inria.fr/aevol/aevol ), for our paper submitted to Molecular Ecology entitled "Forward-in-time simulation of chromosomal rearrangements: The invisible backbone that sustains long-term adaptation".
DOI: 10.5281/zenodo.8307916
title: Forward-in-time simulation of chromosomal rearrangements: The invisible backbone that sustains long-term adaptation : simulated data

description: Data simulated with Aevol (www.aevol.fr), a software available on gitlab ( https://gitlab.inria.fr/aevol/aevol ), for our paper submitted to Molecular Ecology entitled "Forward-in-time simulation of chromosomal rearrangements: The invisible backbone that sustains long-term adaptation".
DOI: 10.6084/m9.figshare.21275438
title: Dexmedetomidine protects cells from Angiotensin II-induced smooth muscle cell phenotype switch and endothelial cell dysfunction

description: Abdominal aortic aneurysm (AAA) is a vascular disorder greatly threatening life of the elderly population. Dexmedetomidine (DEX), an α2-adrenergic receptor agonist, has been shown to suppress AAA development. Nevertheless, the signaling pathways that might be mediated by DEX in AAA has not been clarified. Vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) were treated with Angiotensin II (Ang II) to mimic AAA <i>in vitro</i>. BrdU, wound healing, and Transwell assays were utilized for measuring VSMC proliferation and migration. Western blotting was used for evaluating protein levels of contractile VSMC markers, collagens and matrix metalloproteinases (MMPs) in VSMCs as well as apoptosis- and HMGB1/TLR4/NF-κB signaling-related markers in ECs. Cell adhesion molecule expression and monocyte-endothelial adhesion were assessed by immunofluorescence staining and adhesion assays. Flow cytometry was implemented for analyzing EC apoptosis. Hematoxylin-eosin staining and ELISA were used to detect the effect of DEX <i>in vivo</i>. In this study, DEX inhibited Ang II-evoked VSMC phenotype switch and extracellular matrix degradation. DEX suppressed the inflammatory response and apoptosis of ECs induced by Ang II. DEX inhibited HMGB1/TLR4/NF-κB signaling pathway in Ang II-treated ECs. DEX attenuated Ang II-induced AAA and inflammation in mice. Overall, DEX ameliorates Ang II-induced VSMC phenotype switch, and inactivates HMGB1/TLR4/NF-κB signaling pathway to alleviate Ang II-induced EC dysfunction.
DOI: 10.6084/m9.figshare.21275438.v1
title: Dexmedetomidine protects cells from Angiotensin II-induced smooth muscle cell phenotype switch and endothelial cell dysfunction

description: Abdominal aortic aneurysm (AAA) is a vascular disorder greatly threatening life of the elderly population. Dexmedetomidine (DEX), an α2-adrenergic receptor agonist, has been shown to suppress AAA development. Nevertheless, the signaling pathways that might be mediated by DEX in AAA has not been clarified. Vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) were treated with Angiotensin II (Ang II) to mimic AAA <i>in vitro</i>. BrdU, wound healing, and Transwell assays were utilized for measuring VSMC proliferation and migration. Western blotting was used for evaluating protein levels of contractile VSMC markers, collagens and matrix metalloproteinases (MMPs) in VSMCs as well as apoptosis- and HMGB1/TLR4/NF-κB signaling-related markers in ECs. Cell adhesion molecule expression and monocyte-endothelial adhesion were assessed by immunofluorescence staining and adhesion assays. Flow cytometry was implemented for analyzing EC apoptosis. Hematoxylin-eosin staining and ELISA were used to detect the effect of DEX <i>in vivo</i>. In this study, DEX inhibited Ang II-evoked VSMC phenotype switch and extracellular matrix degradation. DEX suppressed the inflammatory response and apoptosis of ECs induced by Ang II. DEX inhibited HMGB1/TLR4/NF-κB signaling pathway in Ang II-treated ECs. DEX attenuated Ang II-induced AAA and inflammation in mice. Overall, DEX ameliorates Ang II-induced VSMC phenotype switch, and inactivates HMGB1/TLR4/NF-κB signaling pathway to alleviate Ang II-induced EC dysfunction.
DOI: 10.6084/m9.figshare.7120343
title: Additional file 4: of Transcriptional profiling of liver during the critical embryo-to-hatchling transition period in the chicken (Gallus gallus)

description: Canonical and biological pathways identified by the contrast of all embryos vs. all hatchlings. The AR-DEGs from the E vs. H contrast were assigned by Ingenuity Pathway Analysis (IPA) to canonical and functional and pathways. Fisher’s Exact Test is used in IPA to determine probability (P ≤ 0.05) that AR-DEGs belong to a particular canonical pathway or biological function accrued in the Ingenuity Knowledge Base. (XLSX 53 kb)
DOI: 10.6084/m9.figshare.7120343.v1
title: Additional file 4: of Transcriptional profiling of liver during the critical embryo-to-hatchling transition period in the chicken (Gallus gallus)

description: Canonical and biological pathways identified by the contrast of all embryos vs. all hatchlings. The AR-DEGs from the E vs. H contrast were assigned by Ingenuity Pathway Analysis (IPA) to canonical and functional and pathways. Fisher’s Exact Test is used in IPA to determine probability (P ≤ 0.05) that AR-DEGs belong to a particular canonical pathway or biological function accrued in the Ingenuity Knowledge Base. (XLSX 53 kb)
DOI: 10.6084/m9.figshare.12362495.v1
title: Additional file 3 of Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses

description: Additional file 3: Suppl. Table 3. BP result of the upregulated DEGs in CPIP.
DOI: 10.6084/m9.figshare.12362507
title: Additional file 7 of Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses

description: Additional file 7: Suppl. Table 7. MF result of the upregulated DEGs in CPIP.
DOI: 10.6084/m9.figshare.12886067.v1
title: Additional file 4 of DLBCL with amplification of JAK2/PD-L2 exhibits PMBCL-like CNA pattern and worse clinical outcome resembling those with MYD88 L265P mutation

description: Additional file 4. The detailed information of DLBCL with JAK2/PD-L2 amplification. The detailed data about clinicopathological characteristics, morphology, immunohistochemistry and treatments of DLBCL with JAK2/PD-L2 amplification are showed in this file.
DOI: 10.6084/m9.figshare.9740660.v1
title: Additional file 2 of Molecular characterization of bovine leukemia virus reveals existence of genotype 4 in Chinese dairy cattle

description: Figure S2. Alignment of full-length of BLV env gene nucleotide sequences (S2-A: 6–769 bp; S2-B: 777–1543 bp) between sequences obtained in this study together with 10 reference sequences and all Chinese sequences available in the GenBank database. Strains identified in this study are in red (cluster into genotype 4) and green (cluster into genotype 6). Numbers above the sequences are nucleotide number indicated by the env gene of AB934282. The countries of the strains are marked with abbreviations in parentheses to the right of the GenBank accession numbers. Dots indicate nucleotides identical to the reference sequences. The mark above the square frames indicate unique mutations for our isolates of BLV genotype 4 (▼) and genotype 6 (▽). The BLV reference strains from GenBank have accession numbers AF933703 (G1), AF257515 (G2), EF065647 (G3), JN695878 (G4), EF065635 (G5), LC080656 (G6), KF801457 (G7), JQ675759 (G8), LC080659 (G9), and LC154066 (G10). The Chinese sequences available in the GenBank database have the accession numbers: MH040198-MH040203, MH040205, MH040207-MH040209, MF574053-MF574068. The seven Chinese strains from this study have the accession numbers MK820044 and MK840875-MK840880. JPN = Japan; CHN = China; BRA = Brazil; ARG = Argentina; USA = United States of America; RUS = Russia; CRC = Costa Rica; PAR = Paraguay; MDA = Moldova; BOL = Bolivia; MYA = Myanmar. (ZIP 5157 kb)
DOI: 10.6084/m9.figshare.17079541.v1
title: Additional file 1 of Are we there yet? A machine learning architecture to predict organotropic metastases

description: Additional file 1. MOT data tables. Table S1: Tumor vs. Normal metrics: For six tumor types we show the model can detect tumor vs. normal transcriptomic expression profiles. Table S2: Site Specific classification: Site specific metastatic classification metrics. Table S3: Positive and Negative metrics for T/N transcriptomes site specific metastases. Table S4: All binary classification confusion matrices. Table S5: Top 1K selected features for site specific metastases predictions. Table S6: Enriched GO IDs in organotropic metastases. Table S7: Intersection of overrepresented GO processes measured by Fisher’s exact test.
DOI: 10.6084/m9.figshare.12886114.v1
title: Additional file 1 of The top 100 most cited articles on bronchoscopy: a bibliometric analysis

description: Additional file 1.
DOI: 10.6084/m9.figshare.9740642
title: Additional file 5: of Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs

description: Detailed results of microarray screening profiles using kidney biopsy samples. (XLS 348 kb)
DOI: 10.6084/m9.figshare.9740642.v1
title: Additional file 5: of Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs

description: Detailed results of microarray screening profiles using kidney biopsy samples. (XLS 348 kb)
DOI: 10.6084/m9.figshare.9740648.v1
title: Additional file 6: of Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs

description: Results for GO annotation and KEGG pathway enrichment analysis for predicted target genes of miR-3607-3p. (XLSX 215 kb)
DOI: 10.6084/m9.figshare.9740654.v1
title: Additional file 7: of Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs

description: Results for GO annotation and KEGG pathway enrichment analysis for predicted target genes of miR-4709-3p. (XLSX 111 kb)
DOI: 10.6084/m9.figshare.12362489
title: Additional file 1 of Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses

description: Additional file 1: Suppl. Table 1. All expressed transcripts.
DOI: 10.6084/m9.figshare.12362498
title: Additional file 4 of Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses

description: Additional file 4: Suppl. Table 4. BP result of the downregulated DEGs in CPIP.
DOI: 10.6084/m9.figshare.12362501
title: Additional file 5 of Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses

description: Additional file 5: Suppl. Table 5. CC result of the upregulated DEGs in CPIP.
DOI: 10.6084/m9.figshare.9740657.v1
title: Additional file 8: of Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs

description: Data of validation of putative targets genes of selective miRNAs by qPCR. (XLSX 13 kb)
DOI: 10.6084/m9.figshare.9740660
title: Additional file 2 of Molecular characterization of bovine leukemia virus reveals existence of genotype 4 in Chinese dairy cattle

description: Figure S2. Alignment of full-length of BLV env gene nucleotide sequences (S2-A: 6–769 bp; S2-B: 777–1543 bp) between sequences obtained in this study together with 10 reference sequences and all Chinese sequences available in the GenBank database. Strains identified in this study are in red (cluster into genotype 4) and green (cluster into genotype 6). Numbers above the sequences are nucleotide number indicated by the env gene of AB934282. The countries of the strains are marked with abbreviations in parentheses to the right of the GenBank accession numbers. Dots indicate nucleotides identical to the reference sequences. The mark above the square frames indicate unique mutations for our isolates of BLV genotype 4 (▼) and genotype 6 (▽). The BLV reference strains from GenBank have accession numbers AF933703 (G1), AF257515 (G2), EF065647 (G3), JN695878 (G4), EF065635 (G5), LC080656 (G6), KF801457 (G7), JQ675759 (G8), LC080659 (G9), and LC154066 (G10). The Chinese sequences available in the GenBank database have the accession numbers: MH040198-MH040203, MH040205, MH040207-MH040209, MF574053-MF574068. The seven Chinese strains from this study have the accession numbers MK820044 and MK840875-MK840880. JPN = Japan; CHN = China; BRA = Brazil; ARG = Argentina; USA = United States of America; RUS = Russia; CRC = Costa Rica; PAR = Paraguay; MDA = Moldova; BOL = Bolivia; MYA = Myanmar. (ZIP 5157 kb)
DOI: 10.6084/m9.figshare.12362510.v1
title: Additional file 8 of Expression profiling of spinal cord dorsal horn in a rat model of complex regional pain syndrome type-I uncovers potential mechanisms mediating pain and neuroinflammation responses

description: Additional file 8: Suppl. Table 8. MF result of the downregulated DEGs in CPIP.
DOI: 10.6084/m9.figshare.9740657
title: Additional file 8: of Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs

description: Data of validation of putative targets genes of selective miRNAs by qPCR. (XLSX 13 kb)
DOI: 10.6084/m9.figshare.17079232
title: Additional file 1 of Identification of a novel prognosis-associated ceRNA network in lung adenocarcinoma via bioinformatics analysis

description: Additional file 1. 255 overlapping genes.
DOI: 10.6084/m9.figshare.17079232.v1
title: Additional file 1 of Identification of a novel prognosis-associated ceRNA network in lung adenocarcinoma via bioinformatics analysis

description: Additional file 1. 255 overlapping genes.
DOI: 10.6084/m9.figshare.19703489
title: Salvianolic acid A (Sal A) suppresses malignant progression of glioma and enhances temozolomide (TMZ) sensitivity via repressing transgelin-2 (TAGLN2) mediated phosphatidylinositol-3-kinase (PI3K) / protein kinase B (Akt) pathway

description: Glioma originated from excessively proliferative and highly invaded glial cells is a common intracranial malignant tumor with poor prognosis. Resistance to temozolomide (TMZ) is a clinical challenge in glioma treatment due to the fact that chemoresistance remains a main obstacle in the improvement of drug efficacy. Salvianolic acid A (Sal A), originated from traditional Chinese herbal medicine <i>Salvia miltiorrhiza</i>, possesses anti-tumor effects and could facilitate the delivery of drugs to brain tumor tissues. In the present work, effects of Sal A on the viability, proliferation, migration, invasion and apoptosis of human glioma cell line U87 cells as well as influence of Sal A on TMZ resistance were measured, so as to identify the biological function of Sal A in the malignant behaviors and chemoresistance of glioma cells. Additionally, activation of TAGLN2/PI3K/Akt pathway in glioma cells was also detected to investigate whether Sal A could regulate TAGLN2/PI3K/Akt to manipulate the progression of glioma and TMZ resistance. Results discovered that Sal A treatment reduced the viability, repressed the proliferation, migration and invasion of glioma cells as well as promoted the apoptosis of glioma cells. Besides, Sal A treatment suppressed TAGLN2/PI3K/Akt pathway in glioma cells. Sal A treatment strengthened the suppressing effect of TMZ on glioma cell proliferation and reinforced the promoting effect of TMZ on glioma cell apoptosis, which were abolished by upregulation of TAGLN2. To conclude, Sal A treatment could suppress the malignant behaviors of glioma cells and improve TMZ sensitivity through inactivating TAGLN2/PI3K/Akt pathway.
DOI: 10.6084/m9.figshare.19703489.v1
title: Salvianolic acid A (Sal A) suppresses malignant progression of glioma and enhances temozolomide (TMZ) sensitivity via repressing transgelin-2 (TAGLN2) mediated phosphatidylinositol-3-kinase (PI3K) / protein kinase B (Akt) pathway

description: Glioma originated from excessively proliferative and highly invaded glial cells is a common intracranial malignant tumor with poor prognosis. Resistance to temozolomide (TMZ) is a clinical challenge in glioma treatment due to the fact that chemoresistance remains a main obstacle in the improvement of drug efficacy. Salvianolic acid A (Sal A), originated from traditional Chinese herbal medicine <i>Salvia miltiorrhiza</i>, possesses anti-tumor effects and could facilitate the delivery of drugs to brain tumor tissues. In the present work, effects of Sal A on the viability, proliferation, migration, invasion and apoptosis of human glioma cell line U87 cells as well as influence of Sal A on TMZ resistance were measured, so as to identify the biological function of Sal A in the malignant behaviors and chemoresistance of glioma cells. Additionally, activation of TAGLN2/PI3K/Akt pathway in glioma cells was also detected to investigate whether Sal A could regulate TAGLN2/PI3K/Akt to manipulate the progression of glioma and TMZ resistance. Results discovered that Sal A treatment reduced the viability, repressed the proliferation, migration and invasion of glioma cells as well as promoted the apoptosis of glioma cells. Besides, Sal A treatment suppressed TAGLN2/PI3K/Akt pathway in glioma cells. Sal A treatment strengthened the suppressing effect of TMZ on glioma cell proliferation and reinforced the promoting effect of TMZ on glioma cell apoptosis, which were abolished by upregulation of TAGLN2. To conclude, Sal A treatment could suppress the malignant behaviors of glioma cells and improve TMZ sensitivity through inactivating TAGLN2/PI3K/Akt pathway.
DOI: 10.5285/92383dba-8b6e-43da-9d78-e8784b97124c
title: Spatial and temporal datasets for 11 different small-scale laboratory experiments of fluid-driven fractures

description: These data consist of spatial and temporal datasets for 11 different small-scale laboratory experiments of fluid-driven fractures, described in the paper Up, down, and round again: the circulating flow dynamics of flux-driven fractures (Chalk and Kavanagh, accepted in Physics of Fluids, February 2024). These experiments, conducted at the University of Liverpool, are analogue models of natural fluid-driven fractures in glacial and magmatic settings. 

Fractures were created by injecting water or silicone oil into transparent gelatine at a constant rate. The total experimental data set consists of 11 different experiments named: S1,S2,S3,S4,S5,W1,W2,W3,W4,SH,WH. S experiments involve the injection of silicone oil, and W experiments involve the injection of water. The raw data consist of a temporal series of jpegs from camera recordings of each experiment, located in the subdirectory "frames". For all experiments except for WH and SH, the data also consist of a temporal series of csv files containing spatial velocity data of the internal fluid flow, located in the subdirectory "PIV". These data are described in further detail in the metadata file in the raw data directory.