cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.23556877
title: Genetic variants of <i>FGFR</i> family associated with height, hypertension, and osteoporosis

description: Hypertension and osteoporosis are the most common types of health problems. A recent study suggested that the fibroblast growth factor receptor-like protein 1 (<i>FGFRL1</i>) gene in giraffes is the most promising candidate gene that may have direct effects on both the skeleton and the cardiovascular system. Our study purposed to replicate the finding that the <i>FGFR5</i> gene is related to giraffe-related characteristics (height, hypertension, and osteoporosis), and to assess the associations between genetic variants of the <i>FGFR</i> family and three phenotypes. An association study was performed to confirm the connections between hypertension, osteoporosis, and height and the <i>FGFR</i> family proteins (<i>FGFR1</i> to <i>FGFR5</i>). We identified a total of 192 genetic variants in the <i>FGFR</i> family and found six SNVs in the <i>FGFR2</i>, <i>FGFR3</i>, and <i>FGFR4</i> genes that were associated with two phenotypes simultaneously. Also, the <i>FGFR</i> family was found to be involved in calcium signalling, and three genetic variants of the <i>FGFR3</i> gene showed significant signals in the pituitary and hypothalamus. Taken together, these findings suggest that <i>FGFR</i> genes are associated with hypertension, height, and osteoporosis. In particular, the present study highlights the <i>FGFR3</i> gene, which influences two fundamental regulators of bone remodelling.
DOI: 10.6084/m9.figshare.23556877.v1
title: Genetic variants of <i>FGFR</i> family associated with height, hypertension, and osteoporosis

description: Hypertension and osteoporosis are the most common types of health problems. A recent study suggested that the fibroblast growth factor receptor-like protein 1 (<i>FGFRL1</i>) gene in giraffes is the most promising candidate gene that may have direct effects on both the skeleton and the cardiovascular system. Our study purposed to replicate the finding that the <i>FGFR5</i> gene is related to giraffe-related characteristics (height, hypertension, and osteoporosis), and to assess the associations between genetic variants of the <i>FGFR</i> family and three phenotypes. An association study was performed to confirm the connections between hypertension, osteoporosis, and height and the <i>FGFR</i> family proteins (<i>FGFR1</i> to <i>FGFR5</i>). We identified a total of 192 genetic variants in the <i>FGFR</i> family and found six SNVs in the <i>FGFR2</i>, <i>FGFR3</i>, and <i>FGFR4</i> genes that were associated with two phenotypes simultaneously. Also, the <i>FGFR</i> family was found to be involved in calcium signalling, and three genetic variants of the <i>FGFR3</i> gene showed significant signals in the pituitary and hypothalamus. Taken together, these findings suggest that <i>FGFR</i> genes are associated with hypertension, height, and osteoporosis. In particular, the present study highlights the <i>FGFR3</i> gene, which influences two fundamental regulators of bone remodelling.
DOI: 10.6084/m9.figshare.25450015.v1
title: Supplementary Material for: Incidence of Hyper Progressive Disease in Combination Immunotherapy and Anti-Programmed Cell Death Protein 1/Programmed Death-Ligand 1 Monotherapy for Unresectable Hepatocellular Carcinoma

description: <b><i>Introduction:</i></b> Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) signaling blockade is the most effective strategy for the treatment of immune evading hepatocellular carcinoma (HCC). While immune checkpoint inhibitor has revolutionized the concept of cancer treatment, it has also led to unexpected tumor growth. Regulatory T cells express PD-1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) receptors, which are proliferated and activated by antibody binding, and their ratio to CD8+ T cells is altered, which is one of the causes for hyper progressive disease (HPD). We examined the frequency of HPD in anti-PD-1/PD-L1 monotherapy and combination therapy with vascular endothelial growth factor (VEGF) antibody and anti-CTLA-4 antibodies. <b><i>Methods:</i></b> This was a prospective and retrospective cohort study which enrolled 198 patients with unresectable HCC from January 2015 to December 2021 at the Kindai University Hospital. Fifty-eight patients received anti-PD-1/PD-L1 monotherapy, 119 patients combination with VEGF antibody, and 21 patients combination with anti-CTLA-4 antibody. We defined HPD as tumor growth rate (TGR) ratio ≥4, ΔTGR ≥40%, and tumor growth kinetics ratio ≥4. <b><i>Results:</i></b> The HPD rate was 10.3% (6/58) in anti-PD-1/PD-L1 monotherapy, 1.7% (2/119) in combination with VEGF antibody, and 4.8% (1/21) in combination with anti-CTLA-4 antibody (<i>p</i> = 0.034). The odds ratio for HPD in the combined anti-CTLA-4 antibody group was 0.433 (95% confidence interval [CI]: 0.05–3.83) when compared to the anti-PD-1/PD-L1 monotherapy group and 2.93 (95% CI: 0.25–33.79) when compared to the combined VEGF antibody group. <b><i>Conclusion:</i></b> The frequency of HPD in unresectable HCC compared to anti-PD-1/PD-L1 monotherapy was decreased with the combination with anti-VEGF antibody and not increased with anti-CTLA-4 antibody. Anti-PD-1/PD-L1 combined with anti-CTLA-4 antibody is now available in real-world and needs to be further validated with accumulated clinical practice.
DOI: 10.6084/m9.figshare.25450015
title: Supplementary Material for: Incidence of Hyper Progressive Disease in Combination Immunotherapy and Anti-Programmed Cell Death Protein 1/Programmed Death-Ligand 1 Monotherapy for Unresectable Hepatocellular Carcinoma

description: <b><i>Introduction:</i></b> Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) signaling blockade is the most effective strategy for the treatment of immune evading hepatocellular carcinoma (HCC). While immune checkpoint inhibitor has revolutionized the concept of cancer treatment, it has also led to unexpected tumor growth. Regulatory T cells express PD-1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) receptors, which are proliferated and activated by antibody binding, and their ratio to CD8+ T cells is altered, which is one of the causes for hyper progressive disease (HPD). We examined the frequency of HPD in anti-PD-1/PD-L1 monotherapy and combination therapy with vascular endothelial growth factor (VEGF) antibody and anti-CTLA-4 antibodies. <b><i>Methods:</i></b> This was a prospective and retrospective cohort study which enrolled 198 patients with unresectable HCC from January 2015 to December 2021 at the Kindai University Hospital. Fifty-eight patients received anti-PD-1/PD-L1 monotherapy, 119 patients combination with VEGF antibody, and 21 patients combination with anti-CTLA-4 antibody. We defined HPD as tumor growth rate (TGR) ratio ≥4, ΔTGR ≥40%, and tumor growth kinetics ratio ≥4. <b><i>Results:</i></b> The HPD rate was 10.3% (6/58) in anti-PD-1/PD-L1 monotherapy, 1.7% (2/119) in combination with VEGF antibody, and 4.8% (1/21) in combination with anti-CTLA-4 antibody (<i>p</i> = 0.034). The odds ratio for HPD in the combined anti-CTLA-4 antibody group was 0.433 (95% confidence interval [CI]: 0.05–3.83) when compared to the anti-PD-1/PD-L1 monotherapy group and 2.93 (95% CI: 0.25–33.79) when compared to the combined VEGF antibody group. <b><i>Conclusion:</i></b> The frequency of HPD in unresectable HCC compared to anti-PD-1/PD-L1 monotherapy was decreased with the combination with anti-VEGF antibody and not increased with anti-CTLA-4 antibody. Anti-PD-1/PD-L1 combined with anti-CTLA-4 antibody is now available in real-world and needs to be further validated with accumulated clinical practice.
DOI: 10.6084/m9.figshare.25450015.v2
title: Supplementary Material for: Incidence of Hyper Progressive Disease in Combination Immunotherapy and Anti-Programmed Cell Death Protein 1/Programmed Death-Ligand 1 Monotherapy for Unresectable Hepatocellular Carcinoma

description: <b><i>Introduction:</i></b> Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) signaling blockade is the most effective strategy for the treatment of immune evading hepatocellular carcinoma (HCC). While immune checkpoint inhibitor has revolutionized the concept of cancer treatment, it has also led to unexpected tumor growth. Regulatory T cells express PD-1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) receptors, which are proliferated and activated by antibody binding, and their ratio to CD8+ T cells is altered, which is one of the causes for hyper progressive disease (HPD). We examined the frequency of HPD in anti-PD-1/PD-L1 monotherapy and combination therapy with vascular endothelial growth factor (VEGF) antibody and anti-CTLA-4 antibodies. <b><i>Methods:</i></b> This was a prospective and retrospective cohort study which enrolled 198 patients with unresectable HCC from January 2015 to December 2021 at the Kindai University Hospital. Fifty-eight patients received anti-PD-1/PD-L1 monotherapy, 119 patients combination with VEGF antibody, and 21 patients combination with anti-CTLA-4 antibody. We defined HPD as tumor growth rate (TGR) ratio ≥4, ΔTGR ≥40%, and tumor growth kinetics ratio ≥4. <b><i>Results:</i></b> The HPD rate was 10.3% (6/58) in anti-PD-1/PD-L1 monotherapy, 1.7% (2/119) in combination with VEGF antibody, and 4.8% (1/21) in combination with anti-CTLA-4 antibody (<i>p</i> = 0.034). The odds ratio for HPD in the combined anti-CTLA-4 antibody group was 0.433 (95% confidence interval [CI]: 0.05–3.83) when compared to the anti-PD-1/PD-L1 monotherapy group and 2.93 (95% CI: 0.25–33.79) when compared to the combined VEGF antibody group. <b><i>Conclusion:</i></b> The frequency of HPD in unresectable HCC compared to anti-PD-1/PD-L1 monotherapy was decreased with the combination with anti-VEGF antibody and not increased with anti-CTLA-4 antibody. Anti-PD-1/PD-L1 combined with anti-CTLA-4 antibody is now available in real-world and needs to be further validated with accumulated clinical practice.
DOI: 10.6084/m9.figshare.25450015.v3
title: Supplementary Material for: Incidence of Hyper Progressive Disease in Combination Immunotherapy and Anti-Programmed Cell Death Protein 1/Programmed Death-Ligand 1 Monotherapy for Unresectable Hepatocellular Carcinoma

description: <b><i>Introduction:</i></b> Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) signaling blockade is the most effective strategy for the treatment of immune evading hepatocellular carcinoma (HCC). While immune checkpoint inhibitor has revolutionized the concept of cancer treatment, it has also led to unexpected tumor growth. Regulatory T cells express PD-1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) receptors, which are proliferated and activated by antibody binding, and their ratio to CD8+ T cells is altered, which is one of the causes for hyper progressive disease (HPD). We examined the frequency of HPD in anti-PD-1/PD-L1 monotherapy and combination therapy with vascular endothelial growth factor (VEGF) antibody and anti-CTLA-4 antibodies. <b><i>Methods:</i></b> This was a prospective and retrospective cohort study which enrolled 198 patients with unresectable HCC from January 2015 to December 2021 at the Kindai University Hospital. Fifty-eight patients received anti-PD-1/PD-L1 monotherapy, 119 patients combination with VEGF antibody, and 21 patients combination with anti-CTLA-4 antibody. We defined HPD as tumor growth rate (TGR) ratio ≥4, ΔTGR ≥40%, and tumor growth kinetics ratio ≥4. <b><i>Results:</i></b> The HPD rate was 10.3% (6/58) in anti-PD-1/PD-L1 monotherapy, 1.7% (2/119) in combination with VEGF antibody, and 4.8% (1/21) in combination with anti-CTLA-4 antibody (<i>p</i> = 0.034). The odds ratio for HPD in the combined anti-CTLA-4 antibody group was 0.433 (95% confidence interval [CI]: 0.05–3.83) when compared to the anti-PD-1/PD-L1 monotherapy group and 2.93 (95% CI: 0.25–33.79) when compared to the combined VEGF antibody group. <b><i>Conclusion:</i></b> The frequency of HPD in unresectable HCC compared to anti-PD-1/PD-L1 monotherapy was decreased with the combination with anti-VEGF antibody and not increased with anti-CTLA-4 antibody. Anti-PD-1/PD-L1 combined with anti-CTLA-4 antibody is now available in real-world and needs to be further validated with accumulated clinical practice.
DOI: 10.21934/baua.jemetb18.puf.1
title: Public Use File zur Job-Exposure-Matrix auf Basis der BIBB/BAuA-Erwerbstätigenbefragung 2018: BAuA_JEM_ETB2018_PUF_1
DOI: 10.6084/m9.figshare.25436551
title: Phenotype data

description: Phenotype data for plants.
DOI: 10.6084/m9.figshare.23306198
title: Effect of visual cortex anodal tDCS on Chinese reading performance in normal peripheral vision.

description: Effect of visual cortex anodal tDCS on Chinese reading performance in normal peripheral vision.
DOI: 10.6084/m9.figshare.23306198.v1
title: Effect of visual cortex anodal tDCS on Chinese reading performance in normal peripheral vision.

description: Effect of visual cortex anodal tDCS on Chinese reading performance in normal peripheral vision.
DOI: 10.6084/m9.figshare.14388443
title: Multi-omics reveals novel prognostic implication of SRC protein expression in bladder cancer and its correlation with immunotherapy response

description: This study aims to identify potential prognostic biomarkers of bladder cancer (BCa) based on large-scale multi-omics data and investigate the role of SRC in improving predictive outcomes for BCa patients and those receiving immune checkpoint therapies (ICTs). Large-scale multi-comic data were enrolled from the Cancer Proteome Atlas, the Cancer Genome Atlas and gene expression omnibus based on machining-learning methods. Immune infiltration, survival and other statistical analyses were implemented using R software in cancers (<i>n</i> = 12,452). The predictive value of SRC was performed in 81 BCa patients receiving ICT from aa validation cohort (<i>n</i> = 81). Landscape of novel candidate prognostic protein signatures of BCa patients was identified. Differential BECLIN, EGFR, PKCALPHA, ANNEXIN1, AXL and SRC expression significantly correlated with the outcomes for BCa patients from multiply cohorts (<i>n</i> = 906). Notably, risk score of the integrated prognosis-related proteins (IPRPs) model exhibited high diagnostic accuracy and consistent predictive ability (AUC = 0.714). Besides, we tested the clinical relevance of baseline SRC protein and mRNA expression in two independent confirmatory cohorts (<i>n</i> = 566) and the prognostic value in pan-cancers. Then, we found that elevated SRC expression contributed to immunosuppressive microenvironment mediated by immune checkpoint molecules of BCa and other cancers. Next, we validated SRC expression as a potential biomarker in predicting response to ICT in 81 BCa patient from FUSCC cohort, and found that expression of SRC in the baseline tumour tissues correlated with improved survival benefits, but predicts worse ICT response. This study first performed the large-scale multi-omics analysis, distinguished the IPRPs (<i>BECLIN, EGFR, PKCALPHA, SRC, ANNEXIN1</i> and <i>AXL</i>) and revealed novel prediction model, outperforming the currently traditional prognostic indicators for anticipating BCa progression and better clinical strategies. Additionally, this study provided insight into the importance of biomarker SRC for better prognosis, which may inversely improve predictive outcomes for patients receiving ICT and enable patient selection for future clinical treatment.
DOI: 10.6084/m9.figshare.14388443.v1
title: Multi-omics reveals novel prognostic implication of SRC protein expression in bladder cancer and its correlation with immunotherapy response

description: This study aims to identify potential prognostic biomarkers of bladder cancer (BCa) based on large-scale multi-omics data and investigate the role of SRC in improving predictive outcomes for BCa patients and those receiving immune checkpoint therapies (ICTs). Large-scale multi-comic data were enrolled from the Cancer Proteome Atlas, the Cancer Genome Atlas and gene expression omnibus based on machining-learning methods. Immune infiltration, survival and other statistical analyses were implemented using R software in cancers (<i>n</i> = 12,452). The predictive value of SRC was performed in 81 BCa patients receiving ICT from aa validation cohort (<i>n</i> = 81). Landscape of novel candidate prognostic protein signatures of BCa patients was identified. Differential BECLIN, EGFR, PKCALPHA, ANNEXIN1, AXL and SRC expression significantly correlated with the outcomes for BCa patients from multiply cohorts (<i>n</i> = 906). Notably, risk score of the integrated prognosis-related proteins (IPRPs) model exhibited high diagnostic accuracy and consistent predictive ability (AUC = 0.714). Besides, we tested the clinical relevance of baseline SRC protein and mRNA expression in two independent confirmatory cohorts (<i>n</i> = 566) and the prognostic value in pan-cancers. Then, we found that elevated SRC expression contributed to immunosuppressive microenvironment mediated by immune checkpoint molecules of BCa and other cancers. Next, we validated SRC expression as a potential biomarker in predicting response to ICT in 81 BCa patient from FUSCC cohort, and found that expression of SRC in the baseline tumour tissues correlated with improved survival benefits, but predicts worse ICT response. This study first performed the large-scale multi-omics analysis, distinguished the IPRPs (<i>BECLIN, EGFR, PKCALPHA, SRC, ANNEXIN1</i> and <i>AXL</i>) and revealed novel prediction model, outperforming the currently traditional prognostic indicators for anticipating BCa progression and better clinical strategies. Additionally, this study provided insight into the importance of biomarker SRC for better prognosis, which may inversely improve predictive outcomes for patients receiving ICT and enable patient selection for future clinical treatment.
DOI: 10.6084/m9.figshare.16803523
title: Transcriptomic analysis of human endometrial stromal cells during early embryo invasion

description: During early embryo invasion (48 h after embryo attachment), what functional changes accompany dynamic gene expression alterations in human endometrial stromal cells? In the present study, primary human endometrial stromal cells (phESCs) were cultured. After <i>in vitro</i> decidualization, primary human endometrial stromal cells (phESCs) were cultured with blastocysts for 48 h. During this process, blastocysts attached and invaded the phESCs (embryo-invaded primary human endometrial stromal cells, ehESCs). We performed comprehensive transcriptomic profiling of phESCs (two replicates) and ehESCs (five replicates) and analyzed the differentially expressed gene (DEGs) sets for gene ontology (GO) terms and Kyoto encyclopaedia of genes and genomes (KEGG) pathway enrichment. To analyse potential connectivity patterns between the transcripts in these DEG sets, a protein-protein interaction (PPI) network was constructed using the STRING database. A total of 592 DEGs were identified between phESCs and ehESCs after embryo invasion. Primary human endometrial stromal cells underwent significant transcriptomic changes that occur in a stepwise fashion. Oxidative phosphorylation, mitochondrial organization, and P53 signalling pathways were significantly altered in phESCs after embryo invasion. EP300 may play a key role in regulating transcription <i>via</i> chromatin remodelling to facilitate the adaptive gene expression changes that occur during embryo invasion. Our data identify dynamic transcriptome changes that occur in endometrial stromal cells within 48 h after embryo invasion. The pathways that we found to be enriched in phESCs after embryo invasion (oxidative phosphorylation, mitochondrial organization, and P53 signalling) may represent novel mechanisms underlying embryo implantation, and may illuminate the reasons that some women experience reproductive failure.Key messagesHuman endometrial stromal cells have undergone changes in gene expression regulation and signalling pathways during the embryo invasion.Mitochondrial-oxidative phosphorylation changes in human stromal cells manifested as down-regulation of gene expression in the electron transport chain.TP53 signalling pathway and transcriptional regulator EP300 assist stromal cells to get adaptive changes during embryo invasion phase. Human endometrial stromal cells have undergone changes in gene expression regulation and signalling pathways during the embryo invasion. Mitochondrial-oxidative phosphorylation changes in human stromal cells manifested as down-regulation of gene expression in the electron transport chain. TP53 signalling pathway and transcriptional regulator EP300 assist stromal cells to get adaptive changes during embryo invasion phase.
DOI: 10.6084/m9.figshare.16803523.v1
title: Transcriptomic analysis of human endometrial stromal cells during early embryo invasion

description: During early embryo invasion (48 h after embryo attachment), what functional changes accompany dynamic gene expression alterations in human endometrial stromal cells? In the present study, primary human endometrial stromal cells (phESCs) were cultured. After <i>in vitro</i> decidualization, primary human endometrial stromal cells (phESCs) were cultured with blastocysts for 48 h. During this process, blastocysts attached and invaded the phESCs (embryo-invaded primary human endometrial stromal cells, ehESCs). We performed comprehensive transcriptomic profiling of phESCs (two replicates) and ehESCs (five replicates) and analyzed the differentially expressed gene (DEGs) sets for gene ontology (GO) terms and Kyoto encyclopaedia of genes and genomes (KEGG) pathway enrichment. To analyse potential connectivity patterns between the transcripts in these DEG sets, a protein-protein interaction (PPI) network was constructed using the STRING database. A total of 592 DEGs were identified between phESCs and ehESCs after embryo invasion. Primary human endometrial stromal cells underwent significant transcriptomic changes that occur in a stepwise fashion. Oxidative phosphorylation, mitochondrial organization, and P53 signalling pathways were significantly altered in phESCs after embryo invasion. EP300 may play a key role in regulating transcription <i>via</i> chromatin remodelling to facilitate the adaptive gene expression changes that occur during embryo invasion. Our data identify dynamic transcriptome changes that occur in endometrial stromal cells within 48 h after embryo invasion. The pathways that we found to be enriched in phESCs after embryo invasion (oxidative phosphorylation, mitochondrial organization, and P53 signalling) may represent novel mechanisms underlying embryo implantation, and may illuminate the reasons that some women experience reproductive failure.Key messagesHuman endometrial stromal cells have undergone changes in gene expression regulation and signalling pathways during the embryo invasion.Mitochondrial-oxidative phosphorylation changes in human stromal cells manifested as down-regulation of gene expression in the electron transport chain.TP53 signalling pathway and transcriptional regulator EP300 assist stromal cells to get adaptive changes during embryo invasion phase. Human endometrial stromal cells have undergone changes in gene expression regulation and signalling pathways during the embryo invasion. Mitochondrial-oxidative phosphorylation changes in human stromal cells manifested as down-regulation of gene expression in the electron transport chain. TP53 signalling pathway and transcriptional regulator EP300 assist stromal cells to get adaptive changes during embryo invasion phase.