cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.17128371
title: Genetic diversity analysis of phenotypic traits among 37 <i>Xanthoceras sorbifolium</i> elite germplasms

description: <i>Xanthoceras sorbifolium</i> is one of the most economically important species cultivated in northern China. To analyze the phenotypic variation within <i>X. sorbifolium</i>, 35 phenotypic traits among 37 elite germplasms were analyzed using nested analysis of variance, coefficient of variation (CVs), principal component analysis (PCA), correlation analysis, and cluster analysis. Large variation and rich phenotypic diversity were found among and within germplasms of <i>X. sorbifolium</i>. The mean of coefficient of variation for 35 traits among 37 germplasms was 25.49%. It varied from 12.80% to 63.25%, and ranked as follows: branch traits (45.51%) &gt; inflorescence traits (31.01%) &gt; fruit traits (24.67%) &gt; flower traits (24.35%) &gt; seed traits (21.82%) &gt; leaf traits (21.45%). The mean heritability (H<sup>2</sup>) of 35 phenotypic traits was 75.94%. Significant correlations were observed within and among most branch, leaf, inflorescence, flower, fruit, and seed traits. The cumulative contribution rate of the first nine main principle components reached 80.333%. The 35 phenotypic traits were classified into two main categories and five subcategories by clustering analysis of phenotypic traits. Combined result of correlation, PCA, and clustering of phenotypic traits, 18 representative traits were selected. The 37 elite germplasms were classified into two main groups and six subgroups according to their characteristics by Ward’s method and reasonable utilization of each subgroup were suggested. These results provide useful information for genetic improvement, preservation, and evaluation of <i>X. sorbifolium</i> germplasms.
DOI: 10.6084/m9.figshare.17128371.v1
title: Genetic diversity analysis of phenotypic traits among 37 <i>Xanthoceras sorbifolium</i> elite germplasms

description: <i>Xanthoceras sorbifolium</i> is one of the most economically important species cultivated in northern China. To analyze the phenotypic variation within <i>X. sorbifolium</i>, 35 phenotypic traits among 37 elite germplasms were analyzed using nested analysis of variance, coefficient of variation (CVs), principal component analysis (PCA), correlation analysis, and cluster analysis. Large variation and rich phenotypic diversity were found among and within germplasms of <i>X. sorbifolium</i>. The mean of coefficient of variation for 35 traits among 37 germplasms was 25.49%. It varied from 12.80% to 63.25%, and ranked as follows: branch traits (45.51%) &gt; inflorescence traits (31.01%) &gt; fruit traits (24.67%) &gt; flower traits (24.35%) &gt; seed traits (21.82%) &gt; leaf traits (21.45%). The mean heritability (H<sup>2</sup>) of 35 phenotypic traits was 75.94%. Significant correlations were observed within and among most branch, leaf, inflorescence, flower, fruit, and seed traits. The cumulative contribution rate of the first nine main principle components reached 80.333%. The 35 phenotypic traits were classified into two main categories and five subcategories by clustering analysis of phenotypic traits. Combined result of correlation, PCA, and clustering of phenotypic traits, 18 representative traits were selected. The 37 elite germplasms were classified into two main groups and six subgroups according to their characteristics by Ward’s method and reasonable utilization of each subgroup were suggested. These results provide useful information for genetic improvement, preservation, and evaluation of <i>X. sorbifolium</i> germplasms.
DOI: 10.5281/zenodo.10680283
title: СРАВНИТЕЛЬНАЯ ОЦЕНКА АНТИБАКТЕРИАЛЬНОЙ ТЕРАПИИ ПРИ ОБОСТРЕНИИ ХРОНИЧЕСКОЙ ОБСТРУКТИВНОЙ БОЛЕЗНИ ЛЕГКИХ
DOI: 10.5281/zenodo.10680284
title: СРАВНИТЕЛЬНАЯ ОЦЕНКА АНТИБАКТЕРИАЛЬНОЙ ТЕРАПИИ ПРИ ОБОСТРЕНИИ ХРОНИЧЕСКОЙ ОБСТРУКТИВНОЙ БОЛЕЗНИ ЛЕГКИХ
DOI: 10.35097/1927
title: Codebook and Dataset of Paper "Effect of emotionalizing sounds on the estimation and evaluation of displayed safety distances"

description: Codebook and Dataset for Study: "Effect of emotionalizing sounds on the estimation and evaluation of displayed safety distances"
DOI: 10.6084/m9.figshare.5594221
title: NUPR1 maintains autolysosomal efflux by activating <i>SNAP25</i> transcription in cancer cells

description: In the advanced stages of cancer, autophagy is thought to promote tumor progression through its ability to mitigate various cellular stresses. However, the details of how autophagy is homeostatically regulated in such tumors are unknown. Here, we report that NUPR1 (nuclear protein 1, transcriptional regulator), a transcriptional coregulator, is aberrantly expressed in a subset of cancer cells and predicts low overall survival rates for lung cancer patients. NUPR1 regulates the late stages of autolysosome processing through the induction of the SNARE protein SNAP25, which forms a complex with the lysosomal SNARE-associated protein VAMP8. NUPR1 depletion deregulates autophagic flux and impairs autolysosomal clearance, inducing massive cytoplasmic vacuolization and premature senescence <i>in vitro</i> and tumor suppression <i>in vivo</i>. Collectively, our data show that NUPR1 is a potent regulator of autolysosomal dynamics and is required for the progression of some epithelial cancers.
DOI: 10.6084/m9.figshare.5594221.v1
title: NUPR1 maintains autolysosomal efflux by activating <i>SNAP25</i> transcription in cancer cells

description: In the advanced stages of cancer, autophagy is thought to promote tumor progression through its ability to mitigate various cellular stresses. However, the details of how autophagy is homeostatically regulated in such tumors are unknown. Here, we report that NUPR1 (nuclear protein 1, transcriptional regulator), a transcriptional coregulator, is aberrantly expressed in a subset of cancer cells and predicts low overall survival rates for lung cancer patients. NUPR1 regulates the late stages of autolysosome processing through the induction of the SNARE protein SNAP25, which forms a complex with the lysosomal SNARE-associated protein VAMP8. NUPR1 depletion deregulates autophagic flux and impairs autolysosomal clearance, inducing massive cytoplasmic vacuolization and premature senescence <i>in vitro</i> and tumor suppression <i>in vivo</i>. Collectively, our data show that NUPR1 is a potent regulator of autolysosomal dynamics and is required for the progression of some epithelial cancers.
DOI: 10.5255/ukda-sn-856958
title: Effects of Empathy of Apology and Monetary Compensation on Customers’ Revenge desires After Double Deviations, 2021

description: The data supporting the thesis "An empirical investigation of the effects of empathy of apology and monetary compensation on customers’ revenge desires after double deviations" is made open and accessible in the University of Birmingham Institutional Research Archive (UBIRA). The data contained in the UBIRA archive contain the data from a set of online, hypothetical scenario-based experiments in which participants responded to a series of Likert-type measures concerning their subsequent perceptions, emotions and behaviours. The experiments concern service recovery scenarios and customers' perceptions of firms' actions to recover from service failures. The details of the measures are provided in the data set. The details of the protocols are provided in the PhD thesis.
DOI: 10.6084/m9.figshare.19750116
title: Assessing the Impacts of Cluster Effects and Covariate Imbalance in Cluster Randomized Equivalence Trials

description: Equivalence tests establish whether treatments are similar in their intended outcomes. This is in contrast to superiority tests, which establish whether a new treatment is better than a standard treatment or placebo. Few equivalence trials have employed a cluster randomized design, but they are subject to some of the same analysis pitfalls that are common to superiority trials—namely, a failure to adjust for either cluster effects or covariate imbalances resulting from randomization. Using real and simulated data from a cluster randomized trial comparing exercise protocols among U.S. Army soldiers, this study empirically demonstrates the consequences for power and Type I error rates when either or both of these effects have been ignored in the analysis. Analysis of real trial data showed that equivalence test outcomes can change depending on whether appropriate adjustments are applied. Simulations demonstrated that failing to adjust for important baseline covariates severely reduces statistical power, and failing to adjust for cluster effects increases the risk of false declarations of equivalence. As cluster randomized designs are increasingly employed for equivalence trials, analysts must be aware of the importance of adjusting for cluster effects and covariate imbalances to avoid false conclusions.
DOI: 10.6084/m9.figshare.19750116.v2
title: Assessing the Impacts of Cluster Effects and Covariate Imbalance in Cluster Randomized Equivalence Trials

description: Equivalence tests establish whether treatments are similar in their intended outcomes. This is in contrast to superiority tests, which establish whether a new treatment is better than a standard treatment or placebo. Few equivalence trials have employed a cluster randomized design, but they are subject to some of the same analysis pitfalls that are common to superiority trials—namely, a failure to adjust for either cluster effects or covariate imbalances resulting from randomization. Using real and simulated data from a cluster randomized trial comparing exercise protocols among U.S. Army soldiers, this study empirically demonstrates the consequences for power and Type I error rates when either or both of these effects have been ignored in the analysis. Analysis of real trial data showed that equivalence test outcomes can change depending on whether appropriate adjustments are applied. Simulations demonstrated that failing to adjust for important baseline covariates severely reduces statistical power, and failing to adjust for cluster effects increases the risk of false declarations of equivalence. As cluster randomized designs are increasingly employed for equivalence trials, analysts must be aware of the importance of adjusting for cluster effects and covariate imbalances to avoid false conclusions.
DOI: 10.6084/m9.figshare.19750116.v1
title: Assessing the impacts of cluster effects and covariate imbalance in cluster randomized equivalence trials

description: Equivalence tests establish whether treatments are similar in their intended outcomes. This is in contrast to superiority tests, which establish whether a new treatment is better than a standard treatment or placebo. Few equivalence trials have employed a cluster randomized design, but they are subject to some of the same analysis pitfalls that are common to superiority trials — namely, a failure to adjust for either cluster effects or covariate imbalances resulting from randomization. Using real and simulated data from a cluster randomized trial comparing exercise protocols among U.S. Army soldiers, this study empirically demonstrates the consequences for power and Type I error rates when either or both of these effects have been ignored in the analysis. Analysis of real trial data showed that equivalence test outcomes can change depending on whether appropriate adjustments are applied. Simulations demonstrated that failing to adjust for important baseline covariates severely reduces statistical power, and failing to adjust for cluster effects increases the risk of false declarations of equivalence. As cluster randomized designs are increasingly employed for equivalence trials, analysts must be aware of the importance of adjusting for cluster effects and covariate imbalances to avoid false conclusions.
DOI: 10.6084/m9.figshare.15031594
title: Integrated multi-omics analysis of the clinical relevance and potential regulatory mechanisms of splicing factors in hepatocellular carcinoma

description: Splicing factors (SFs) have been increasingly documented to perturb the genome of cancers. However, little is known about the alterations of SFs in hepatocellular carcinoma (HCC). This study comprehensively delineated the genomic and epigenomic characteristics of 404 SFs in HCC based on the multi-omics data from the Cancer Genome Atlas database. The analysis revealed several clinically relevant SFs that could be effective biomarkers for monitoring the onset and prognosis of HCC (such as, HSPB1, DDX39A, and NELFE, which were the three most significant clinically relevant SFs). Functional enrichment analysis of these indicators showed the enrichment of pathways related to splicing and mRNA processes. Furthermore, the study found that SF copy number variation is common in HCC and could be a typical characteristic of hepato-carcinogenesis; the complex expression regulation of SFs was significantly affected by copy number variant and methylation. Several SFs with significant mutation patterns were identified (such as, RNF213, SF3B1, SPEN, NOVA1, and EEF1A1), and the potential regulatory network of SFs was constructed to identify their potential mechanisms for regulating clinically relevant alternative splicing events. Therefore, this study established a foundation to uncover the broad molecular spectrum of SFs for future functional and therapeutic studies of HCC.
DOI: 10.6084/m9.figshare.15031594.v1
title: Integrated multi-omics analysis of the clinical relevance and potential regulatory mechanisms of splicing factors in hepatocellular carcinoma

description: Splicing factors (SFs) have been increasingly documented to perturb the genome of cancers. However, little is known about the alterations of SFs in hepatocellular carcinoma (HCC). This study comprehensively delineated the genomic and epigenomic characteristics of 404 SFs in HCC based on the multi-omics data from the Cancer Genome Atlas database. The analysis revealed several clinically relevant SFs that could be effective biomarkers for monitoring the onset and prognosis of HCC (such as, HSPB1, DDX39A, and NELFE, which were the three most significant clinically relevant SFs). Functional enrichment analysis of these indicators showed the enrichment of pathways related to splicing and mRNA processes. Furthermore, the study found that SF copy number variation is common in HCC and could be a typical characteristic of hepato-carcinogenesis; the complex expression regulation of SFs was significantly affected by copy number variant and methylation. Several SFs with significant mutation patterns were identified (such as, RNF213, SF3B1, SPEN, NOVA1, and EEF1A1), and the potential regulatory network of SFs was constructed to identify their potential mechanisms for regulating clinically relevant alternative splicing events. Therefore, this study established a foundation to uncover the broad molecular spectrum of SFs for future functional and therapeutic studies of HCC.
DOI: 10.6084/m9.figshare.15031597
title: Construction of an immune-related lncRNA pairs model to predict prognosis and immune landscape of lung adenocarcinoma patients

description: The model of immune-related lncRNA pairs (IRLPs) seems to be an available predictor in lung adenocarcinoma (LUAD) patients. The aim of our study was to construct a model with IRLPs to predict the survival status and immune landscape of LUAD patients. Based on TCGA-LUAD dataset, a risk assessment model with IRLPs was established. Then, ROC curves were used to assess the predictive accuracy and effectiveness of our model. Next, we identified the difference of survival, immune cell infiltration, immune checkpoint inhibitor-related (ICI-related) biomarkers, and chemotherapeutics between high-risk group and low-risk group. Finally, A nomogram was built for predicting the survival rates of LUAD patients. 464 LUAD samples were randomly and equally divided into a training set and a test set. Six IRLPs were screened out to construct a risk model. K-M analysis and risk-plot suggested the prognosis of high-risk group was worse than low-risk group (p &lt; 0.001). Multivariate analysis shows risk score was independent risk factor of LUAD (p &lt; 0.001). In addition, the expression of immune cell infiltration, ICI-related biomarkers, chemotherapeutics all demonstrate significant difference in two groups. A nomogram was built that could predict the 1-, 3-, and 5-year survival rates of LUAD patients. Our immune-related lncRNA pairs risk model is expected to be a reliable model for predicting the prognosis and immune landscape of LUAD patients.
DOI: 10.6084/m9.figshare.15031597.v1
title: Construction of an immune-related lncRNA pairs model to predict prognosis and immune landscape of lung adenocarcinoma patients

description: The model of immune-related lncRNA pairs (IRLPs) seems to be an available predictor in lung adenocarcinoma (LUAD) patients. The aim of our study was to construct a model with IRLPs to predict the survival status and immune landscape of LUAD patients. Based on TCGA-LUAD dataset, a risk assessment model with IRLPs was established. Then, ROC curves were used to assess the predictive accuracy and effectiveness of our model. Next, we identified the difference of survival, immune cell infiltration, immune checkpoint inhibitor-related (ICI-related) biomarkers, and chemotherapeutics between high-risk group and low-risk group. Finally, A nomogram was built for predicting the survival rates of LUAD patients. 464 LUAD samples were randomly and equally divided into a training set and a test set. Six IRLPs were screened out to construct a risk model. K-M analysis and risk-plot suggested the prognosis of high-risk group was worse than low-risk group (p &lt; 0.001). Multivariate analysis shows risk score was independent risk factor of LUAD (p &lt; 0.001). In addition, the expression of immune cell infiltration, ICI-related biomarkers, chemotherapeutics all demonstrate significant difference in two groups. A nomogram was built that could predict the 1-, 3-, and 5-year survival rates of LUAD patients. Our immune-related lncRNA pairs risk model is expected to be a reliable model for predicting the prognosis and immune landscape of LUAD patients.
DOI: 10.6084/m9.figshare.25245436
title: treefile in the Fig. 2

description: treefile in the Fig. 2Bacteria: bac_output.treefileArchaea: ar53_output.treefile
DOI: 10.6084/m9.figshare.15031612
title: WT1 inhibits AML cell proliferation in a p53-dependent manner

description: WT1 has been reported to function as an oncogene and a tumor suppressor in acute myeloid leukemia (AML). The molecular mechanisms have not yet been fully elucidated. Here, we report that p53, served as a tumor suppressor, plays a critical role in regulating the function of WT1 in AML. For details, we performed a meta-analysis on 1131 AML cases, showing that WT1 gene mutation and TP53 gene exhibited a mutually exclusive predisposition in AML. p53 can be recruited to the promoter region of WT1’s target genes to modulate their expression by physically interacting with WT1. The AML-derived p53 mutation (p53<sup>R248Q</sup>) can disrupt the interaction between WT1 and p53, resulting in the loss of modulation of WT1’s target genes. Furthermore, wild-type p53 maintained the anti-proliferation activity of WT1 in AML cells. In contrast, WT1 promoted AML cell proliferation in the absence of p53 (or mutated p53). In conclusion, we demonstrated a novel explanation of the controversial function of WT1 in AML. These results provided a mechanism by which WT1 inhibited AML cell proliferation in a p53-dependent manner.
DOI: 10.6084/m9.figshare.15031612.v1
title: WT1 inhibits AML cell proliferation in a p53-dependent manner

description: WT1 has been reported to function as an oncogene and a tumor suppressor in acute myeloid leukemia (AML). The molecular mechanisms have not yet been fully elucidated. Here, we report that p53, served as a tumor suppressor, plays a critical role in regulating the function of WT1 in AML. For details, we performed a meta-analysis on 1131 AML cases, showing that WT1 gene mutation and TP53 gene exhibited a mutually exclusive predisposition in AML. p53 can be recruited to the promoter region of WT1’s target genes to modulate their expression by physically interacting with WT1. The AML-derived p53 mutation (p53<sup>R248Q</sup>) can disrupt the interaction between WT1 and p53, resulting in the loss of modulation of WT1’s target genes. Furthermore, wild-type p53 maintained the anti-proliferation activity of WT1 in AML cells. In contrast, WT1 promoted AML cell proliferation in the absence of p53 (or mutated p53). In conclusion, we demonstrated a novel explanation of the controversial function of WT1 in AML. These results provided a mechanism by which WT1 inhibited AML cell proliferation in a p53-dependent manner.
DOI: 10.6084/m9.figshare.15031612.v2
title: WT1 inhibits AML cell proliferation in a p53-dependent manner

description: WT1 has been reported to function as an oncogene and a tumor suppressor in acute myeloid leukemia (AML). The molecular mechanisms have not yet been fully elucidated. Here, we report that p53, served as a tumor suppressor, plays a critical role in regulating the function of WT1 in AML. For details, we performed a meta-analysis on 1131 AML cases, showing that WT1 gene mutation and TP53 gene exhibited a mutually exclusive predisposition in AML. p53 can be recruited to the promoter region of WT1’s target genes to modulate their expression by physically interacting with WT1. The AML-derived p53 mutation (p53<sup>R248Q</sup>) can disrupt the interaction between WT1 and p53, resulting in the loss of modulation of WT1’s target genes. Furthermore, wild-type p53 maintained the anti-proliferation activity of WT1 in AML cells. In contrast, WT1 promoted AML cell proliferation in the absence of p53 (or mutated p53). In conclusion, we demonstrated a novel explanation of the controversial function of WT1 in AML. These results provided a mechanism by which WT1 inhibited AML cell proliferation in a p53-dependent manner.
DOI: 10.6084/m9.figshare.16604508
title: Identification and verification of vascular cell adhesion protein 1 as an immune-related hub gene associated with the tubulointerstitial injury in diabetic kidney disease

description: Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD), but the pathogenesis is not completely understood. Tubulointerstitial injury plays critical roles in the development and progression of DKD. The present study aimed to investigate the profile of tubulointerstitial immune cell infiltration and reveal the underlying mechanisms between tubular cell injury and interstitial inflammation in DKD using bioinformatics strategies. First, xCell analysis identified immune cells displaying significant changes in the DKD tubulointerstitium, including upregulated CD4<sup>+</sup> T cells, Th2 cells, CD8<sup>+</sup> T cells, M1 macrophages, activated dendritic cells (DCs) and conventional DCs, as well as downregulated Tregs. Second, pyroptosis was identified as the main form of cell death compared with other forms of programmed cell death. Vascular cell adhesion protein 1 (VCAM1) was identified as the top ranked hub gene. The correlation analysis showed that VCAM1 was significantly positively correlated with pyroptosis and infiltrated immune cells in the tubulointerstitium. Upregulation of VCAM1 in the DKD tubulointerstitium was further verified in European Renal cDNA Bank cohort and was observed to negatively correlate with the glomerular filtration rate (GFR). Our <i>in vitro</i> study validated increased VCAM1 expression in HK-2 cells under diabetic conditions, and pyroptosis inhibition by disulfiram decreased VCAM1 expression, inflammatory cytokine release and fibrosis. In conclusion, our study identified upregulated VCAM1 expression in renal tubular cells, which might interact with infiltrated immune cells, thus promoting fibrosis. The FDA-approved drug disulfiram might improve fibrosis in DKD by targeting tubular pyroptosis and VCAM1 expression.