cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.16851348.v1
title: Additional file 5 of The mitochondrial genomes of Tortricidae: nucleotide composition, gene variation and phylogenetic performance

description: Additional file 5: Table S5. Codon usage pattern in six tortricid tribes analyzed in this study.
DOI: 10.6084/m9.figshare.22617394.v1
title: Additional file 1 of Tumor microenvironment remodeling after neoadjuvant immunotherapy in non-small cell lung cancer revealed by single-cell RNA sequencing

description: Additional file 1: Table S1. Clinical information of tumor and blood samples used in the study.
DOI: 10.6084/m9.figshare.16851342
title: Additional file 3 of The mitochondrial genomes of Tortricidae: nucleotide composition, gene variation and phylogenetic performance

description: Additional file 3: Table S3. Reannotation and comparison of mitochondrial genome organizations of 27 previous sequenced tortricid species.
DOI: 10.6084/m9.figshare.11609778
title: Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation

description: Wound scarring remains a major challenge for plastic surgeons. Transforming growth factor (TGF)-β plays a key role in the process of scar formation. Previous studies have demonstrated that truncated TGF-β type II receptor (t-TGF-βRII) is unable to continue signal transduction but is still capable of binding to TGF-β, thereby blocking the TGF-β signaling pathway. Hepatocyte growth factor (HGF) is a multifunctional growth factor that promotes tissue regeneration and wound healing. Theoretically, the combination of HGF and t-TGF-βRII would be expected to exert a synergistic effect on promoting wound healing and reducing collagen formation. In the present study, lentivirus-mediated transfection of the two genes (t-TGF-βRII/HGF) into fibroblasts in vitro and in a rat model in vivo was used. The results demonstrated that the expression of t-TGF-βRII and HGF in NIH-3T3 cells was successfully induced. The expression of both molecules significantly reduced collagen I and III expression, and also inhibited fibroblast proliferation. Furthermore, histological examination and scar quantification revealed less scarring in the experimental wound in a rat model. Moreover, on macroscopic inspection, the experimental wound exhibited less visible scarring compared with the control. Therefore, the present study demonstrated that the combination gene therapy of t-TGF-βRII and HGF promoted wound healing, with less scarring and more epithelial tissue formation, not only by suppressing the overgrowth of collagen due to its antifibrotic effect, but also by promoting tissue regeneration.
DOI: 10.6084/m9.figshare.11609778.v1
title: Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation

description: Wound scarring remains a major challenge for plastic surgeons. Transforming growth factor (TGF)-β plays a key role in the process of scar formation. Previous studies have demonstrated that truncated TGF-β type II receptor (t-TGF-βRII) is unable to continue signal transduction but is still capable of binding to TGF-β, thereby blocking the TGF-β signaling pathway. Hepatocyte growth factor (HGF) is a multifunctional growth factor that promotes tissue regeneration and wound healing. Theoretically, the combination of HGF and t-TGF-βRII would be expected to exert a synergistic effect on promoting wound healing and reducing collagen formation. In the present study, lentivirus-mediated transfection of the two genes (t-TGF-βRII/HGF) into fibroblasts in vitro and in a rat model in vivo was used. The results demonstrated that the expression of t-TGF-βRII and HGF in NIH-3T3 cells was successfully induced. The expression of both molecules significantly reduced collagen I and III expression, and also inhibited fibroblast proliferation. Furthermore, histological examination and scar quantification revealed less scarring in the experimental wound in a rat model. Moreover, on macroscopic inspection, the experimental wound exhibited less visible scarring compared with the control. Therefore, the present study demonstrated that the combination gene therapy of t-TGF-βRII and HGF promoted wound healing, with less scarring and more epithelial tissue formation, not only by suppressing the overgrowth of collagen due to its antifibrotic effect, but also by promoting tissue regeneration.
DOI: 10.6084/m9.figshare.11609787
title: A Sufentanil-Based Rapid Cardiac Anesthesia Regimen in Children Undergoing Percutaneous Minimally-Invasive Intraoperative Device Closure of Ventricular Septal Defect

description: Abstract Objective: To assess the effectiveness and safety of fast-track cardiac anesthesia using the short-acting opioid sufentanil in children undergoing intraoperative device closure of ventricular septal defect (VSD). Methods: This retrospective clinical study included 65 children who underwent intraoperative device closure of VSD between January 2017 and June 2017. Patients were diagnosed with isolated perimembranous VSD by transthoracic echocardiography. Then, they were divided into two groups, group F (n=30), whose patients were given sufentanil-based fast-track cardiac anesthesia, and group C (n=35), whose patients were given conventional cardiac anesthesia. Perioperative clinical data were analyzed. Results: No significant differences were found between the preoperative clinical parameters and intraoperative hemodynamic indices between the two groups. In group C, compared with group F, the postoperative duration of mechanical ventilation, the length of stay in the intensive care unit, the length of hospital stay, and the hospital costs were significantly increased. Conclusion: In this retrospective study at a single center, sufentanil-based fast-track cardiac anesthesia was shown to be a safe and effective technique for minimally-invasive intraoperative device closure of VSD in children, which was performed with reduced in-hospital costs.
DOI: 10.6084/m9.figshare.11609787.v1
title: A Sufentanil-Based Rapid Cardiac Anesthesia Regimen in Children Undergoing Percutaneous Minimally-Invasive Intraoperative Device Closure of Ventricular Septal Defect

description: Abstract Objective: To assess the effectiveness and safety of fast-track cardiac anesthesia using the short-acting opioid sufentanil in children undergoing intraoperative device closure of ventricular septal defect (VSD). Methods: This retrospective clinical study included 65 children who underwent intraoperative device closure of VSD between January 2017 and June 2017. Patients were diagnosed with isolated perimembranous VSD by transthoracic echocardiography. Then, they were divided into two groups, group F (n=30), whose patients were given sufentanil-based fast-track cardiac anesthesia, and group C (n=35), whose patients were given conventional cardiac anesthesia. Perioperative clinical data were analyzed. Results: No significant differences were found between the preoperative clinical parameters and intraoperative hemodynamic indices between the two groups. In group C, compared with group F, the postoperative duration of mechanical ventilation, the length of stay in the intensive care unit, the length of hospital stay, and the hospital costs were significantly increased. Conclusion: In this retrospective study at a single center, sufentanil-based fast-track cardiac anesthesia was shown to be a safe and effective technique for minimally-invasive intraoperative device closure of VSD in children, which was performed with reduced in-hospital costs.
DOI: 10.6084/m9.figshare.7415579
title: Study on the photo-degradation stability of poly(butylene succinate-co-butylene adipate) / TiO2 nanocomposites

description: A poly(butylene succinate-co-butylene adipate)/TiO<sub>2</sub> (PBSA/TiO2) nanocomposite was prepared by a melt-blending process. The effect of TiO<sub>2</sub> nanoparticles on the photodegradation behaviors of the nanocomposite was investigated by transmission electron microscopy (TEM), differential scanning calorimetry (DSC), Fourier-transform infrared spectroscopy (FT-IR), field-emission scanning electron microscopy (FE-SEM), rheological measurements, and mechanical tests. TEM images of the PBSA/TiO<sub>2</sub> revealed that the TiO<sub>2</sub> nanoparticles were well dispersed in the matrix without obvious aggregation. The FT-IR results indicated that the TiO<sub>2</sub> nanoparticles can block high-energy ultraviolet (UV) light and reduce the degradation of the PBSA matrix. The viscosity analysis results indicated that the TiO<sub>2</sub> nanoparticles inhibited the chain scission of PBSA matrix under irradiation. In addition, the surface of the PBSA/TiO<sub>2</sub> films and their mechanical properties change less than that of untreated PBSA films during the photoaging process. The obtained results imply that the TiO<sub>2</sub> nanoparticles can be considered as an efficient photodegradation-resistant additive to PBSA for reducing photodegradation.
DOI: 10.6084/m9.figshare.23668564
title: Noncoding RNAs-based high KIF26B expression correlates with poor prognosis and tumor immune infiltration in colon cancer

description: The protein kinesin family member 26B (KIF26B) is aberrantly expressed in various cancers. However, its particular role and association with tumor immune infiltration in colon adenocarcinoma (COAD) remain unclear. All original data were downloaded directly from The Cancer Genome Atlas (TCGA), UCSC Xena, and Gene Expression Omnibus (GEO) databases and processed with R 3.6.3. KIF26B expression was analyzed using Oncomine, TIMER, TCGA, GEO databases, and our clinical specimens. KIF26B expression at the protein level was explored with Human Protein Atlas (HPA) database. The upstream miRNAs and lncRNAs were predicted by StarBase and validated using RT-qPCR. Correlation of KIF26B expression with the expression of immune-related or immune checkpoint genes and GSEA analysis of KIF26B-related genes were investigated via R software. Relationship of KIF26B expression with immune biomarkers or tumor immune infiltration levels was studied through GEPIA2 and TIMER databases. KIF26B was upregulated, and its overexpression was closely related to overall survival (OS), disease-specific survival (DSS), progression-free interval (PFI), T stage, N stage, and CEA levels in COAD. MIR4435-2HG/hsa-miR−500a−3p/KIF26B axis was identified as the promising regulatory pathway of KIF26B. KIF26B expression was positively correlated with immune-related genes, tumor immune infiltration, and biomarker genes of immune cells in COAD, and KIF26B-related genes were significantly enriched in macrophage activation-related pathways. Expression of immune checkpoint genes, including PDCD1, CD274, and CTLA4, was also closely related to KIF26B expression. Our results clarified that ncRNA-based increased KIF26B expression was associated with a worse prognosis and high tumor immune infiltration in COAD.
DOI: 10.6084/m9.figshare.23668564.v1
title: Noncoding RNAs-based high KIF26B expression correlates with poor prognosis and tumor immune infiltration in colon cancer

description: The protein kinesin family member 26B (KIF26B) is aberrantly expressed in various cancers. However, its particular role and association with tumor immune infiltration in colon adenocarcinoma (COAD) remain unclear. All original data were downloaded directly from The Cancer Genome Atlas (TCGA), UCSC Xena, and Gene Expression Omnibus (GEO) databases and processed with R 3.6.3. KIF26B expression was analyzed using Oncomine, TIMER, TCGA, GEO databases, and our clinical specimens. KIF26B expression at the protein level was explored with Human Protein Atlas (HPA) database. The upstream miRNAs and lncRNAs were predicted by StarBase and validated using RT-qPCR. Correlation of KIF26B expression with the expression of immune-related or immune checkpoint genes and GSEA analysis of KIF26B-related genes were investigated via R software. Relationship of KIF26B expression with immune biomarkers or tumor immune infiltration levels was studied through GEPIA2 and TIMER databases. KIF26B was upregulated, and its overexpression was closely related to overall survival (OS), disease-specific survival (DSS), progression-free interval (PFI), T stage, N stage, and CEA levels in COAD. MIR4435-2HG/hsa-miR−500a−3p/KIF26B axis was identified as the promising regulatory pathway of KIF26B. KIF26B expression was positively correlated with immune-related genes, tumor immune infiltration, and biomarker genes of immune cells in COAD, and KIF26B-related genes were significantly enriched in macrophage activation-related pathways. Expression of immune checkpoint genes, including PDCD1, CD274, and CTLA4, was also closely related to KIF26B expression. Our results clarified that ncRNA-based increased KIF26B expression was associated with a worse prognosis and high tumor immune infiltration in COAD.
DOI: 10.6084/m9.figshare.6891395
title: MOESM4 of CRX directs photoreceptor differentiation by accelerating chromatin remodeling at specific target sites

description: Additional file 4. GO analysis describes differences in nearest gene to each regulatory site. Sheets within the table represent distinct comparisons referenced within the text.
DOI: 10.6084/m9.figshare.8987093
title: Association between elevated adiponectin level and adverse outcomes in patients with heart failure: a systematic review and meta-analysis

description: Studies regarding the prognostic value of circulating adiponectin level in patients with heart failure are conflicting. The aim of this meta-analysis was to evaluate the association between elevated circulating adiponectin level and adverse outcomes in patients with heart failure. We searched PubMed and Embase databases from their inception to June 2018. Original observational studies that investigated the prognostic value of adiponectin in heart failure patients and reported all-cause mortality or combined endpoints of death/readmission as outcome measure were included. Pooled risk ratio (RR) with 95% confidence intervals (CI) were estimated by higher versus lower circulating adiponectin level. A total of 7 studies involving 862 heart failure patients were identified. Meta-analysis showed that heart failure patients with higher adiponectin level had significantly increased risk of all-cause mortality (RR 2.05; 95%CI 1.22–3.43) after adjustment for potential confounders. In addition, higher adiponectin level was associated with an increased risk of the combined endpoints of death/readmission (RR 2.22; 95%CI 1.38–3.57). Elevated baseline circulating adiponectin level is possibly associated with an increased risk of all-cause mortality and the combined endpoints of death/readmission in patients with heart failure. Determination of circulating adiponectin level has potential to improve risk stratification in heart failure patients.
DOI: 10.6084/m9.figshare.8987129.v1
title: Henoch-Schönlein purpura nephritis associated with monoclonal gammopathy of renal significance: a case report

description: Monoclonal gammopathy of renal significance (MGRS) can present with different morphologic features and lead to kidney failure. The Henoch-Schönlein purpura nephritis (HSPN) that cannot be relieved by treatment with glucocorticoid and immunosuppressive agents suggests the presence of monoclonal gammopathy in adult patients. The present study reports on a single case of HSPN associated with IgA-κMGRS. The patient who suffered from recurrent skin purpura for 6 months and nephrotic syndrome for 2 months was admitted to our hospital. Bone marrow biopsy showed monoclonal gammopathy of undetermined significance. Kidney biopsy indicated a Henoch-Schönlein purpura nephritis (HSPN, ISKDC classified as type III) with positive staining with κ-light chain in the glomeruli and renal tubular epithelial cells. Furthermore, skin biopsy showed leukocytoclastic vasculitis and negative staining for Congo red and light chain. Given both the renal and cutaneous involvement, the patient was considered to have HSPN associated with IgA-κMGRS. The patient experienced an exacerbation in his purpura-like lesions and clinical status after treatment with glucocorticoid and immunosuppressive agents. Consequently, the patient was put on a regimen that included dexamethasone (20 mg on the 1st, 4th, 8th, and 11th days of each month, iv) and bortezomib (2.4 mg on the 1st, 4th, 8th, and 11th days of each month, iv). Eight weeks after treatment, he had complete resolution of his cutaneous purpura and his biochemical parameters improved. The latent presence of MGRS in cases of HSPN should be considered in adult patients. Increased cognizance and correct treatment options could improve patient outcomes.
DOI: 10.6084/m9.figshare.8987084.v1
title: Carotid intima-media thickness and plaques in internal carotid artery as surrogate markers of lower limb arterial lesions in Chinese patients with diabetic foot

description: Peripheral arterial disease (PAD) can impair healing of diabetic foot (DF) in patients with diabetes mellitus. To determine whether carotid intima-media thickness (CIMT) can predict lower limb arterial lesions in patients with DF, this cross-sectional study enrolled patients with DF at West China Hospital (China) between January 2012 and December 2015. Ultrasonography was used to measure CIMT, assess the internal carotid arteries (ICA) for plaques, and evaluate lower limb segmental arteries for stenosis. The optimal CIMT cutoff for detecting lower limb PAD was determined by receiver operating characteristic (ROC) curve analysis. Factors associated with PAD were identified by logistic regression analyses. A total of 167 patients (mean age: 69.7±10.3 years; 102 men) were included. Patients with PAD were older and had higher levels of total cholesterol and low-density lipoprotein than patients without PAD (P&lt;0.05). The area under the ROC curve was 0.747 (P&lt;0.001). At the optimal CIMT cutoff of 0.71 mm, the sensitivity, specificity, positive predictive value, and negative predictive value were 79.65, 61.11, 81.08, and 58.93%, respectively. Compared with those without PAD, more patients with PAD had CIMT ≥0.71 mm (79.65 vs 38.89%; P&lt;0.001) and ICA plaques (66.37vs 11.11%; P&lt;0.001). Multivariate logistic regression revealed that age (odds ratio [OR]: 1.118; 95% confidence interval [95%CI]: 1.056–1.183; P&lt;0.001), ICA plaques (OR: 13.452; 95%CI: 4.450–40.662; P&lt;0.001), and CIMT ≥0.71 mm (OR: 2.802; 95%CI: 1.092–7.188; P=0.032) were associated with PAD.CIMT may be a surrogate marker of PAD in patients with DF.
DOI: 10.6084/m9.figshare.12132909.v1
title: Identifying the hub gene in gastric cancer by bioinformatics analysis and in vitro experiments

description: Gastric cancer (GC) is one of the main causes of the high death rate in the world. But the molecular mechanisms of GC carcinogenesis remain little known. This study aimed to identify novel promising biomarkers of GC and reveal its potential molecular mechanisms by integrating bioinformatics analysis. We screened the overlapped differentially expressed genes (DEGs) of TCGA and several GEO datasets. Among these DEGs, we used protein-protein interactions network analysis to recognize the hub genes. Moreover, functional enrichment analysis including GO and KEGG pathway analysis and gene set enrichment analysis (GSEA) were performed to study the role of DEGs and potential underlying mechanisms of GC. Based on integrated bioinformatics analysis, SERPINH1, COL1A2, COL8A1, COL4A1, COL5A1, COL12A1, and COL1A1 were screened as candidate diagnostic marker genes. In addition, SERPINH1 was identified as a core gene in the regulation of GC development. Furthermore, we confirmed that SERPINH1 could promote the proliferation, migration, and cell cycle of GC cells. Our present study demonstrated that SERPINH1 was a core therapeutic biomarker in the regulation of candidate genes involved in GC progression.
DOI: 10.6084/m9.figshare.12132909.v3
title: Identifying the hub gene in gastric cancer by bioinformatics analysis and in vitro experiments

description: Gastric cancer (GC) is one of the main causes of the high death rate in the world. But the molecular mechanisms of GC carcinogenesis remain little known. This study aimed to identify novel promising biomarkers of GC and reveal its potential molecular mechanisms by integrating bioinformatics analysis. We screened the overlapped differentially expressed genes (DEGs) of TCGA and several GEO datasets. Among these DEGs, we used protein-protein interactions network analysis to recognize the hub genes. Moreover, functional enrichment analysis including GO and KEGG pathway analysis and gene set enrichment analysis (GSEA) were performed to study the role of DEGs and potential underlying mechanisms of GC. Based on integrated bioinformatics analysis, SERPINH1, COL1A2, COL8A1, COL4A1, COL5A1, COL12A1, and COL1A1 were screened as candidate diagnostic marker genes. In addition, SERPINH1 was identified as a core gene in the regulation of GC development. Furthermore, we confirmed that SERPINH1 could promote the proliferation, migration, and cell cycle of GC cells. Our present study demonstrated that SERPINH1 was a core therapeutic biomarker in the regulation of candidate genes involved in GC progression.
DOI: 10.6084/m9.figshare.20521407
title: Additional file 2 of Weighted single-step GWAS and RNA sequencing reveals key candidate genes associated with physiological indicators of heat stress in Holstein cattle

description: Additional file 2: Table S1. Differential gene expression between non-heat stress group and heat stress group.
DOI: 10.6084/m9.figshare.12132909
title: Identifying the hub gene in gastric cancer by bioinformatics analysis and in vitro experiments

description: Gastric cancer (GC) is one of the main causes of the high death rate in the world. But the molecular mechanisms of GC carcinogenesis remain little known. This study aimed to identify novel promising biomarkers of GC and reveal its potential molecular mechanisms by integrating bioinformatics analysis. We screened the overlapped differentially expressed genes (DEGs) of TCGA and several GEO datasets. Among these DEGs, we used protein-protein interactions network analysis to recognize the hub genes. Moreover, functional enrichment analysis including GO and KEGG pathway analysis and gene set enrichment analysis (GSEA) were performed to study the role of DEGs and potential underlying mechanisms of GC. Based on integrated bioinformatics analysis, SERPINH1, COL1A2, COL8A1, COL4A1, COL5A1, COL12A1, and COL1A1 were screened as candidate diagnostic marker genes. In addition, SERPINH1 was identified as a core gene in the regulation of GC development. Furthermore, we confirmed that SERPINH1 could promote the proliferation, migration, and cell cycle of GC cells. Our present study demonstrated that SERPINH1 was a core therapeutic biomarker in the regulation of candidate genes involved in GC progression.
DOI: 10.4121/f369d289-c89f-4750-9ce0-5dc35b68ac07
title: Data of winter field research in Paulina Saltmarsh

description: Field data collected in Paulina Saltmarsh on the mudflat, in the marsh creek, and at the marsh edge between 26 January and 29 March 2023 are deposited here. The data includes velocities, pressure, bed level change at measuring points, suspended sediment concentration data sets. This datasets were used to unravel when and how sediment is transported into or out of the salt marsh system. Date sets were used for the manuscript entitled "Conditional effects of tides and waves on sediment supply to salt marshes".<br>
DOI: 10.4121/f369d289-c89f-4750-9ce0-5dc35b68ac07.v1
title: Data of winter field research in Paulina Saltmarsh

description: Field data collected in Paulina Saltmarsh on the mudflat, in the marsh creek, and at the marsh edge between 26 January and 29 March 2023 are deposited here. The data includes velocities, pressure, bed level change at measuring points, suspended sediment concentration data sets. This datasets were used to unravel when and how sediment is transported into or out of the salt marsh system. Date sets were used for the manuscript entitled "Conditional effects of tides and waves on sediment supply to salt marshes".<br>