cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.14893108
title: Mutations of key driver genes in gastric cancer metastasis risk: a systematic review and meta-analysis

description: <b>Objective</b>: Associations between gene mutations and metastasis in gastric cancer (GC) remain contradictory, resulting in the inaccurate estimation of the magnitude of the risk associated with specific genotypes. <b>Methods</b>: In this study, we first screened out four key driver genes (TP53, PIK3CA, APC and ARID1A) by jointly analyzing the mutation levels and searching the literature for genes associated with GC metastasis. We then performed a meta-analysis to demonstrate the relationship between these key driver gene mutations and GC metastasis, including lymphatic and distance metastasis. <b>Results</b>: We found out four key driver genes (TP53, PIK3CA, APC and ARID1A), associated with risk of GC metastasis. The results showed that TP53 (OR 1.39, 95% CI 1.12–1.72) and APC mutations (OR 0.58, 95% CI 0.38–0.89) were associated with lymph node metastasis and distant metastasis in GC. And TP53 mutations (OR 1.65, 95% CI 1.25–2.18) were significantly related to GC metastasis in the Asian population. APC mutations (OR 0.54, 95% CI 0.29–1.00) were also related to GC metastasis in the European and American populations. There was no significant association with GC metastasis in PIK3CA or ARID1A mutations. <b>Expert opinion:</b>Mutations of TP53 and APC play important roles in lymph node metastasis and distant metastasis of GC and may be potential important biomarkers of progression and therapeutic targets. These observations should be further prospectively verified.
DOI: 10.6084/m9.figshare.14893108.v1
title: Mutations of key driver genes in gastric cancer metastasis risk: a systematic review and meta-analysis

description: <b>Objective</b>: Associations between gene mutations and metastasis in gastric cancer (GC) remain contradictory, resulting in the inaccurate estimation of the magnitude of the risk associated with specific genotypes. <b>Methods</b>: In this study, we first screened out four key driver genes (TP53, PIK3CA, APC and ARID1A) by jointly analyzing the mutation levels and searching the literature for genes associated with GC metastasis. We then performed a meta-analysis to demonstrate the relationship between these key driver gene mutations and GC metastasis, including lymphatic and distance metastasis. <b>Results</b>: We found out four key driver genes (TP53, PIK3CA, APC and ARID1A), associated with risk of GC metastasis. The results showed that TP53 (OR 1.39, 95% CI 1.12–1.72) and APC mutations (OR 0.58, 95% CI 0.38–0.89) were associated with lymph node metastasis and distant metastasis in GC. And TP53 mutations (OR 1.65, 95% CI 1.25–2.18) were significantly related to GC metastasis in the Asian population. APC mutations (OR 0.54, 95% CI 0.29–1.00) were also related to GC metastasis in the European and American populations. There was no significant association with GC metastasis in PIK3CA or ARID1A mutations. <b>Expert opinion:</b>Mutations of TP53 and APC play important roles in lymph node metastasis and distant metastasis of GC and may be potential important biomarkers of progression and therapeutic targets. These observations should be further prospectively verified.
DOI: 10.6084/m9.figshare.19611733
title: Identifying the shared genes and KEGG pathways of Resolvin D1-targeted network and osteoarthritis using bioinformatics

description: Osteoarthritis (OA) is a common chronic degenerative disease characterized by the loss of articular cartilage, which causes loss of joint function and reduce quality of life. Resolvin D1 (RvD1) has shown interesting anti-inflammatory effects; however, the mechanism of action of RvD1 in OA remains unclear. The aim of this study was to investigate the potential mechanism of RvD1 in OA by bioinformatics and partial in vitro mechanisms. Here, 106 shared differentially expressed genes (DEGs) were identified based on the GSE82107, GSE55235, GSE55457 dataset; 700 DEGs were identified based on GSE169077. Enrichment analyses of these genes were then successively conducted. RvD1-targeted genes and KEGG pathways are identified by STITCH. 27 shared KEGG pathways were identified among RvD1-targeted pathways and OA. Furthermore, cell apoptosis assay, western blotting, real-time fluorescent quantitative PCR (qRT-PCR), enzyme linked immunosorbent assay (ELISA) were used to confirm the expression levels of the key genes of shared Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways between RvD1-targeted and OA in IL-1β treated rat knee chondrocytes. The results showed that RvD1-targeted pathways and the expression of nuclear p65, p53, and p-JNK were inhibited in the RvD1 group compared with the IL-1β group. Thus, the findings indicate that RvD1 may inhibit the development of OA through NF/kB, p53, MAPK/JNK, PI3K-AKT signaling pathways, and act as a treatment for OA.
DOI: 10.6084/m9.figshare.19611735
title: Lamin B1 is a potential therapeutic target and prognostic biomarker for hepatocellular carcinoma

description: Hepatocellular carcinoma (HCC) is an aggressive malignancy. Previous studies have found that lamin B1 (LMNB1) contributes to the development of human cancers. However, the biological functions and prognostic values of LMNB1 in HCC have not been adequately elucidated. In our present research, the expression pattern of LMNB1 was analyzed. The prognostic values of LMNB1 were evaluated by Kaplan–Meier survival analysis and Cox proportional hazards regression analysis. The effects of LMNB1 on HCC progression were assessed by Cell Counting Kit-8 (CCK-8), colony formation, wound healing, Transwell and in vivo xenograft assays. The mechanisms of LMNB1 in HCC progression were elucidated by gene set enrichment analysis (GSEA) and loss-of-function assays. Besides, a nomogram for predicting overall survival (OS) was constructed. The results demonstrated that LMNB1 was overexpressed in HCC and that increased LMNB1 expression predicted a dismal prognosis. Further experiments showed that LMNB1 facilitated cell proliferation and metastasis in HCC. Functional enrichment analysis revealed that LMNB1 modulated metastasis-associated biological functions such as focal adhesion, extracellular matrix, cell junctions and cell adhesion. Mechanistically, we revealed that LMNB1 promoted HCC progression by regulating the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways. Moreover, incorporating LMNB1, Ki67 and Barcelona Clinic Liver Cancer (BCLC) stage into a nomogram showed better predictive accuracy than the Tumor-Node-Metastasis (TNM) stage and BCLC stage. In conclusion, LMNB1 may serve as an effective therapeutic target as well as a reliable prognostic biomarker for HCC.
DOI: 10.6084/m9.figshare.19611735.v1
title: Lamin B1 is a potential therapeutic target and prognostic biomarker for hepatocellular carcinoma

description: Hepatocellular carcinoma (HCC) is an aggressive malignancy. Previous studies have found that lamin B1 (LMNB1) contributes to the development of human cancers. However, the biological functions and prognostic values of LMNB1 in HCC have not been adequately elucidated. In our present research, the expression pattern of LMNB1 was analyzed. The prognostic values of LMNB1 were evaluated by Kaplan–Meier survival analysis and Cox proportional hazards regression analysis. The effects of LMNB1 on HCC progression were assessed by Cell Counting Kit-8 (CCK-8), colony formation, wound healing, Transwell and in vivo xenograft assays. The mechanisms of LMNB1 in HCC progression were elucidated by gene set enrichment analysis (GSEA) and loss-of-function assays. Besides, a nomogram for predicting overall survival (OS) was constructed. The results demonstrated that LMNB1 was overexpressed in HCC and that increased LMNB1 expression predicted a dismal prognosis. Further experiments showed that LMNB1 facilitated cell proliferation and metastasis in HCC. Functional enrichment analysis revealed that LMNB1 modulated metastasis-associated biological functions such as focal adhesion, extracellular matrix, cell junctions and cell adhesion. Mechanistically, we revealed that LMNB1 promoted HCC progression by regulating the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways. Moreover, incorporating LMNB1, Ki67 and Barcelona Clinic Liver Cancer (BCLC) stage into a nomogram showed better predictive accuracy than the Tumor-Node-Metastasis (TNM) stage and BCLC stage. In conclusion, LMNB1 may serve as an effective therapeutic target as well as a reliable prognostic biomarker for HCC.
DOI: 10.6084/m9.figshare.14893344
title: An adaptive patch-based goldstein filter for interferometric phase denoising

description: The Goldstein filter was a well-known approach of synthetic aperture radar interferogram filtering for its simplicity and high efficiency. The filtering performance of Goldstein and its improved filters is mostly affected by several parameters, such as the noise suppression parameter <i>α</i>, the sliding patch size, and the kernel window size. Yet, the fixed parameters will cause the filtering intensity to mismatch the noise levels of different regions. In this paper, we propose an adaptive patch-based Goldstein filter (AP-Goldstein filter), which takes the pseudo-variation coefficient as the measure of patch homogeneity and adaptively selects the patch sizes in different regions of interferogram. This filter controls the noise suppression parameter <i>α</i> by pseudo-coherence, which is a common and effective indicator applied to filter the interferogram phase. Meanwhile, the previously determined patch size of each pixel is used to confirm the kernel window size at the same region. The proposed and other advanced filters were tested on real and simulated interferograms. The qualitative and quantitative comparison of the experimental results shows that this new method can better restrain the phase noise of interferogram while maintaining the edge detailed information and can improve the automation of filtering.
DOI: 10.6084/m9.figshare.22757346.v1
title: Additional file 13 of Pan-cancer analysis revealed H3K4me1 at bivalent promoters premarks DNA hypermethylation during tumor development and identified the regulatory role of DNA methylation in relation to histone modifications

description: Additional file 13: Supplementary Table S1. Summary of 5 gene groups in different cancer types.
DOI: 10.6084/m9.figshare.22757349
title: Additional file 14 of Pan-cancer analysis revealed H3K4me1 at bivalent promoters premarks DNA hypermethylation during tumor development and identified the regulatory role of DNA methylation in relation to histone modifications

description: Additional file 14: Supplementary Table S2. Primer information used in this study.
DOI: 10.6084/m9.figshare.22757346
title: Additional file 13 of Pan-cancer analysis revealed H3K4me1 at bivalent promoters premarks DNA hypermethylation during tumor development and identified the regulatory role of DNA methylation in relation to histone modifications

description: Additional file 13: Supplementary Table S1. Summary of 5 gene groups in different cancer types.
DOI: 10.6084/m9.figshare.22757352
title: Additional file 15 of Pan-cancer analysis revealed H3K4me1 at bivalent promoters premarks DNA hypermethylation during tumor development and identified the regulatory role of DNA methylation in relation to histone modifications

description: Additional file 15: Supplementary Table S3. Public datasets used in this study.
DOI: 10.6084/m9.figshare.22757349.v1
title: Additional file 14 of Pan-cancer analysis revealed H3K4me1 at bivalent promoters premarks DNA hypermethylation during tumor development and identified the regulatory role of DNA methylation in relation to histone modifications

description: Additional file 14: Supplementary Table S2. Primer information used in this study.
DOI: 10.5281/zenodo.10656413
title: Vaje s programom jamovi

description: Vaje z Jamovi-jem.
DOI: 10.5281/zenodo.10656414
title: Vaje s programom jamovi

description: Vaje z Jamovi-jem.
DOI: 10.6084/m9.figshare.22757352.v1
title: Additional file 15 of Pan-cancer analysis revealed H3K4me1 at bivalent promoters premarks DNA hypermethylation during tumor development and identified the regulatory role of DNA methylation in relation to histone modifications

description: Additional file 15: Supplementary Table S3. Public datasets used in this study.
DOI: 10.6084/m9.figshare.7553189
title: CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma

description: Aberrant expression of CUL4B was identified in various types of solid cancers. Cumulative evidences support the oncogenic role of CUL4B in cancers, including regulation of cell proliferation and signal transduction. However, its clinical value and potential pathogenic mechanism in diffuse large B-cell lymphoma (DLBCL) have not been described previously. Therefore, we hypothesize that overexpressed CUL4B may contribute to the pathogenesis of DLBCL. The aim of this study is to assess the expression and the biological function of CUL4B in DLBCL progression. In our study, CUL4B overexpression was observed in DLBCL tissues, and its upregulation was closely associated with poor prognosis in patients. Furthermore, the functional roles of CUL4B was detected both <i>in vitro</i> and <i>in vivo</i>. We demonstrated that silencing CUL4B could not only induce cell proliferation inhibition, cell cycle arrest, and motility attenuation of DLBCL cells <i>in vitro</i>, but also decrease tumor growth in DLBCL xenografts mice. In addition, we identiﬁed that CUL4B may act as a potent inductor of JNK phosphorylation in regulation of autophagy. Our findings demonstrated a significant role of CUL4B in the development and progression of DLBCL. CUL4B may act as a useful biomarker and a novel therapeutic target in DLBCL.
DOI: 10.6084/m9.figshare.7553189.v1
title: CUL4B regulates autophagy via JNK signaling in diffuse large B-cell lymphoma

description: Aberrant expression of CUL4B was identified in various types of solid cancers. Cumulative evidences support the oncogenic role of CUL4B in cancers, including regulation of cell proliferation and signal transduction. However, its clinical value and potential pathogenic mechanism in diffuse large B-cell lymphoma (DLBCL) have not been described previously. Therefore, we hypothesize that overexpressed CUL4B may contribute to the pathogenesis of DLBCL. The aim of this study is to assess the expression and the biological function of CUL4B in DLBCL progression. In our study, CUL4B overexpression was observed in DLBCL tissues, and its upregulation was closely associated with poor prognosis in patients. Furthermore, the functional roles of CUL4B was detected both <i>in vitro</i> and <i>in vivo</i>. We demonstrated that silencing CUL4B could not only induce cell proliferation inhibition, cell cycle arrest, and motility attenuation of DLBCL cells <i>in vitro</i>, but also decrease tumor growth in DLBCL xenografts mice. In addition, we identiﬁed that CUL4B may act as a potent inductor of JNK phosphorylation in regulation of autophagy. Our findings demonstrated a significant role of CUL4B in the development and progression of DLBCL. CUL4B may act as a useful biomarker and a novel therapeutic target in DLBCL.
DOI: 10.6084/m9.figshare.6504974
title: Additional file 2: of Dog vaccination with EgM proteins against Echinococcus granulosus

description: Table S1. A time course of eggs pre gram (EPG) in the faeces of dogs vaccinated with EgM9 and EgM123 compared with PBS against E. granulosus. (XLS 234Â kb)
DOI: 10.6084/m9.figshare.6504974.v1
title: Additional file 2: of Dog vaccination with EgM proteins against Echinococcus granulosus

description: Table S1. A time course of eggs pre gram (EPG) in the faeces of dogs vaccinated with EgM9 and EgM123 compared with PBS against E. granulosus. (XLS 234Â kb)
DOI: 10.6084/m9.figshare.22757389
title: Additional file 1 of EPRS1 correlates with malignant progression in hepatocellular carcinoma

description: Supplementary Material 1
DOI: 10.6084/m9.figshare.22757389.v1
title: Additional file 1 of EPRS1 correlates with malignant progression in hepatocellular carcinoma

description: Supplementary Material 1
DOI: 10.6084/m9.figshare.7029353.v1
title: Fig.3_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: High frequency characteristic signal extraction method for arc fault
DOI: 10.6084/m9.figshare.7029359.v1
title: Fig.7_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: Current waveform slope data of combined load
DOI: 10.6084/m9.figshare.23282708
title: node_shenzhen.csv

description: The nodes of road network graph in Shenzhen city
DOI: 10.6084/m9.figshare.23282708.v1
title: node_shenzhen.csv

description: The nodes of road network graph in Shenzhen city
DOI: 10.18465/8f293914-a6b1-497e-a8e3-eca9f57d5d27
title: MNS Nantes 2015

description: Modèle Numérique de Surface obtenu par LiDAR sur la ville de Nantes
DOI: 10.6084/m9.figshare.7029362
title: Fig.4_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: High frequency signal data for series arc fault
DOI: 10.6084/m9.figshare.7029362.v1
title: Fig.4_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: High frequency signal data for series arc fault
DOI: 10.6084/m9.figshare.23282774
title: node_jinan.csv

description: The nodes of road network graph in Jinan city
DOI: 10.6084/m9.figshare.23282774.v1
title: node_jinan.csv

description: The nodes of road network graph in Jinan city
DOI: 10.6084/m9.figshare.23282777
title: edge_jinan.csv

description: The edges of road network graph in Jinan city
DOI: 10.6084/m9.figshare.23282777.v1
title: edge_jinan.csv

description: The edges of road network graph in Jinan city
DOI: 10.6084/m9.figshare.23282780
title: traj_jinan.csv

description: Vehicle trajectories in Jinan city on October 17, 2022
DOI: 10.6084/m9.figshare.23282780.v1
title: traj_jinan.csv

description: Vehicle trajectories in Jinan city on October 17, 2022
DOI: 10.6084/m9.figshare.7029365.v1
title: Fig.6_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: Current waveform slope data of single load
DOI: 10.6084/m9.figshare.7029410
title: Supplementary Datasets from Impact of the 2015–2016 El Nino on the terrestrial carbon cycle constrained by bottom-up and top-down approaches

description: Evaluating the response of the land carbon sink to the anomalies in temperature and drought imposed by El-Niño events provides insights into the present-day carbon cycle and its climate-driven variability. It is also a necessary step to build confidence in terrestrial ecosystems models' response to the warming and drying stresses expected in the future over many continents, and particularly in the tropics. Here we present an in-depth analysis of the response of the terrestrial carbon cycle to the 2015/2016 El-Niño that imposed extreme warming and dry conditions in the tropics and other sensitive regions. First, we provide a synthesis of the spatio-temporal evolution of anomalies in net land-atmosphere CO<sub>2</sub> fluxes estimated by two <i>in situ</i> measurements based on atmospheric inversions and 16 land-surface models (LSMs) from TRENDYv6. Simulated changes in ecosystem productivity, decomposition rates and fire emissions are also investigated. Inversions and LSMs generally agree on the decrease and subsequent recovery of the land sink in response to the onset, peak and demise of El-Niño conditions and point to the decreased strength of the land carbon sink: by 0.4–0.7 PgC yr<sup>−1</sup> (inversions) and by 1.0 PgC yr<sup>−1</sup> (LSMs) during 2015/2016. LSM simulations indicate that a decrease in productivity, rather than increase in respiration, dominated the net biome productivity anomalies in response to ENSO throughout the tropics, mainly associated with prolonged drought conditions.This article is part of a discussion meeting issue ‘The impact of the 2015/2016 El Nino on the terrestrial tropical carbon cycle: patterns, mechanisms and implications’.
DOI: 10.6084/m9.figshare.23807211
title: <b>Pupal and adult experience-induced preference for food odour components in the flower-visiting butterfly </b><i><b>Tirumala limniace</b></i>

description: <i><b>Tirumala limniace</b></i> (Danaidae) adult learning; pupal learning; male and female learning efficiency; effects of adult learning on pupal learning
DOI: 10.6084/m9.figshare.7029356
title: Fig.8_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: Arc faults in low-voltage electrical circuits are the main hidden cause of electric fires. Accurate identification of arc faults is essential for safe power consumption. In this paper, a detection algorithm for arc faults is tested in a low-voltage circuit. With capacitance coupling and a logarithmic detector, the high-frequency radiation characteristics of arc faults can be extracted. A rapid method for computing the current waveform slope characteristics of an arc fault provides another characteristic. Current waveform periodic integral characteristics can be extracted according to asymmetries of the arc faults. These three characteristics are used to develop a detection algorithm of arc faults based on multiinformation fusion and support vector machine learning models. The tests indicated that for series arc faults with single and combination loads and for parallel arc faults between metallic contacts and along carbonization paths, the recognition algorithm could effectively avoid the problems of crosstalk and signal loss during arc fault detection.
DOI: 10.6084/m9.figshare.7029365
title: Fig.6_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: Current waveform slope data of single load
DOI: 10.6084/m9.figshare.7029350
title: Fig.5_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: High frequency signal extraction data of parallel arc fault
DOI: 10.6084/m9.figshare.7029350.v1
title: Fig.5_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: High frequency signal extraction data of parallel arc fault
DOI: 10.6084/m9.figshare.7029353
title: Fig.3_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: High frequency characteristic signal extraction method for arc fault
DOI: 10.6084/m9.figshare.7029359
title: Fig.7_data from An arc fault diagnosis algorithm using multiinformation fusion and support vector machines

description: Current waveform slope data of combined load
DOI: 10.6084/m9.figshare.14368883.v1
title: Additional file 1 of Tropomyosin in mugwort cross-reacts to house dust mite, eliciting non-Th2 response in allergic rhinitis patients sensitized to house dust mite

description: Additional file 1: Table S1. Identified corresponding proteins in Artemisia sieversian.