cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5398558
title: Geochronology, geochemistry, Sr–Nd–Hf isotopic compositions, and petrogenetic and tectonic implications of Early Cretaceous intrusions associated with the Duolong porphyry–epithermal Cu–Au deposit, central Tibet

description: This article reports new zircon laser ablation-multicollector-inductively coupled plasma-mass spectrometry U–Pb and Hf isotope, whole-rock major and trace element, and Sr–Nd isotope data for mineralized and barren intrusions associated with the Duolong porphyry–epithermal copper–(gold) deposit (DPCD, a mining camp containing several individual deposits) in the western Qiangtang Terrane (QT), central Tibet. These data are used to further our understanding of the geological evolution of this region. The mineralized and barren DPCD intrusions are typical I-type granitoids that were synchronously emplaced at ca. 112.6–125.9 Ma. These igneous rocks show arc affinities that are characterized by enrichments in the light rare earth elements (La<sub>N</sub>/Yb<sub>N</sub> = 4.08–15.23) and the light ion lithophile elements (Rb, Th, U, K, and Pb), and depletions in the high field strength elements (Nb, Ta, and Ti). They have <sup>87</sup>Sr/<sup>86</sup>Sr<sub>(i)</sub> values of 0.7046–0.7079, <sub>Nd</sub>(<i>t</i>) values of –6.0 to +1.1, and two-stage Nd model ages of ca. 823–1410 Ma. Zircons from these intrusive rocks have variable but generally positive <i>ε</i><sub>Hf</sub>(<i>t</i>) values (–2.7 to +13.7) and relatively young zircon Hf crustal model ages of 335–1351 Ma. Combining these data with geochemical data reported in recent studies, we infer that the mineralized and barren DPCD intrusions formed in a continental marginal arc setting and likely originated from a common parental magma that was result of magma mixing of juvenile crust-derived basaltic melts and old lower crust-derived melts. The formation of the DPCD intrusions indicates that the Bangongco–Nujiang oceanic lithosphere was still undergoing northward subduction beneath the western QT at ca. 112.6–125.9 Ma, suggesting in turn that the oceanic basin have not closed completely during the Early Cretaceous. These new data also indicate that the processes that occur during the subduction of oceanic crust in continental marginal arc settings produce and preserve juvenile crustal material, leading to net continental crust vertical growth and thickening.
DOI: 10.6084/m9.figshare.8020196
title: Targeting autophagy enhances heat stress-induced apoptosis <i>via</i> the ATP-AMPK-mTOR axis for hepatocellular carcinoma

description: <b>Purpose:</b> Radiofrequency ablation (RFA) is widely accepted as a curative treatment for small hepatocellular carcinoma (HCC). However, insufficient RFA (IRFA) can lead to rapid local recurrence. The underlying mechanisms remain poorly understood. This study aimed to elucidate the role and regulatory mechanisms of autophagy in the recurrence of HCC after IRFA. <b>Materials and methods:</b> SMMC7721 and Huh7 cells were exposed to sublethal heat stress to stimulate the transition zone of IRFA treatment. The levels of autophagy were measured by western blot, immunofluorescence and transmission electron microscopy. Functional assays, such as CCK-8, EdU incorporation and flow cytometry, were performed to determine the role of heat-induced autophagy. The involved signaling pathways were explored by western blot. Finally, the antitumor effects of chloroquine (CQ) on heat-treated HCC cells were evaluated <i>via</i> an <i>in vivo</i> xenograft tumor model. <b>Results:</b> Sublethal heat stress induced autophagy in a temperature- and time-dependent manner in HCC cells. Furthermore, the inhibition of autophagy by CQ or siRNA targeting the autophagy-related genes Beclin-1 and Atg5 enhanced heat-induced apoptosis. The combination of CQ and heat treatment significantly suppressed tumor growth both <i>in vitro</i> and <i>in vivo</i>. Mechanistically, we reported for the first time that the ATP-AMPK-mTOR signaling pathway was involved in heat-induced autophagy. <b>Conclusions:</b> Heat stress induced protective autophagy against heat-induced apoptosis in HCC <i>via</i> the ATP-AMPK-mTOR axis, suggesting that targeting autophagy may be a promising strategy for improving the efficacy of RFA treatment for HCC.
DOI: 10.6084/m9.figshare.8020196.v1
title: Targeting autophagy enhances heat stress-induced apoptosis <i>via</i> the ATP-AMPK-mTOR axis for hepatocellular carcinoma

description: <b>Purpose:</b> Radiofrequency ablation (RFA) is widely accepted as a curative treatment for small hepatocellular carcinoma (HCC). However, insufficient RFA (IRFA) can lead to rapid local recurrence. The underlying mechanisms remain poorly understood. This study aimed to elucidate the role and regulatory mechanisms of autophagy in the recurrence of HCC after IRFA. <b>Materials and methods:</b> SMMC7721 and Huh7 cells were exposed to sublethal heat stress to stimulate the transition zone of IRFA treatment. The levels of autophagy were measured by western blot, immunofluorescence and transmission electron microscopy. Functional assays, such as CCK-8, EdU incorporation and flow cytometry, were performed to determine the role of heat-induced autophagy. The involved signaling pathways were explored by western blot. Finally, the antitumor effects of chloroquine (CQ) on heat-treated HCC cells were evaluated <i>via</i> an <i>in vivo</i> xenograft tumor model. <b>Results:</b> Sublethal heat stress induced autophagy in a temperature- and time-dependent manner in HCC cells. Furthermore, the inhibition of autophagy by CQ or siRNA targeting the autophagy-related genes Beclin-1 and Atg5 enhanced heat-induced apoptosis. The combination of CQ and heat treatment significantly suppressed tumor growth both <i>in vitro</i> and <i>in vivo</i>. Mechanistically, we reported for the first time that the ATP-AMPK-mTOR signaling pathway was involved in heat-induced autophagy. <b>Conclusions:</b> Heat stress induced protective autophagy against heat-induced apoptosis in HCC <i>via</i> the ATP-AMPK-mTOR axis, suggesting that targeting autophagy may be a promising strategy for improving the efficacy of RFA treatment for HCC.
DOI: 10.6084/m9.figshare.23748960
title: A latest Mesoproterozoic arc–back-arc s in the southwestern Yangtze Block, South China: Implications for paleogeographic configuration of the Rodinia supercontinent

description: This dataset include zircon U–Pb ages, whole-rock geochemical compositions, and Sr-Nd–Hf isotope data of mafic rock samples from the Yonglang and Luji areas, SW Yangtze Block.
DOI: 10.6084/m9.figshare.19029492.v1
title: Additional file 2 of IDEAS: individual level differential expression analysis for single-cell RNA-seq data

description: Additional file 2 GSEA results for COVID data analysis.
DOI: 10.6084/m9.figshare.20078636.v1
title: Toll-like receptor 9 (TLR9) gene deletion-mediated fracture healing in type II diabetic osteoporosis associates with inhibition of the nuclear factor-kappa B (NF-κB) signaling pathway

description: Diabetes is characterized by increased fracture risk. Evidence from <i>in vivo</i> studies is lacking for anti-fracture strategies in diabetes. Our microarray analyses predicted association of Toll-like receptor 9 (TLR9) with both diabetes and osteoporosis, which was the focus of this work in a murine model of type II diabetic osteoporosis (T2DOP). A T2DOP model with fracture was established in TLR9 knockout (TLR9<sup>−/−</sup>) mice, which were then treated with the NF-κB signaling pathway inhibitor (PDTC) and activator (TNF-α). The obtained data suggested that TLR9 knockout augmented regeneration of bone tissues and cartilage area in the callus, and diminished fibrous tissues in T2DOP mice. Moreover, TLR9 depletion significantly affected bone mineral density (BMD), bone volume/tissue volume (BV/TV), connectivity density, trabecular number, trabecular separation and trabecular thickness, thus promoting fracture recovery. Bone morphology and structure were also improved in response to TLR9 depletion in T2DOP mice. TLR9 depletion inactivated NF-κB signaling in T2DOP mice. PDTC was found to enhance fracture healing in T2DOP mice, while TNF-α negated this effect. Collectively, these data indicate that TLR9 depletion may hold anti-fracture properties, making it a potential therapeutic target for T2DOP. <b>Abbreviations:</b> Diabetic osteoporosis (DOP); bone mineral density (BMD); Toll-like receptors (TLRs); type 2 diabetes (T2D); Toll-like receptor 9 (TLR9); nuclear factor-kappaB (NF-κB); streptozotocin (STZ); type 2 diabetic osteoporosis (T2DOP); Gene Expression Omnibus (GEO); Kyoto encyclopedia of genes and genomes (KEGG); pyrrolidine dithiocarbamate (PDTC); computed tomography (CT); Hematoxylin–eosin (HE); bone morphogenetic protein 7 (BMP7); analysis of variance (ANOVA);
DOI: 10.6084/m9.figshare.20078618
title: Sprouty-related proteins with EVH1 domain (SPRED2) prevents high-glucose induced endothelial–mesenchymal transition and endothelial injury by suppressing MAPK activation

description: Diabetic retinopathy (DR) is a common complication of diabetes, and the leading cause of blindness in adults. Sprouty-related proteins with EVH1 domain (SPRED2) play an important role in diabetes and are closely related to the lens and eye morphogenesis. This study attempted to investigate the role and related mechanism of SPRED2 in DR. DR rat model was established by administration streptozocin. Human retinal endothelial cells (HRECs) were treated with high glucose (HG) to mimic DR. The results showed that SPRED2 expression was decreased in the retinal tissues of DR rats and HG-treated HRECs. MTT assay and flow cytometry data showed that SPRED2 overexpression reduced cell viability of HG-treated HRECs. SPRED2 overexpression enhanced Caspase-3 activity and promoted apoptosis of HG-treated HRECs. Furthermore, the expressions of endothelial cell markers CD31 and E-cad were down-regulated, whereas the expressions of mesenchymal cell markers FSP1, SM22, and α-SMA were up-regulated in the HG-treated HRECs. SPRED2 overexpression reversed HG-induced endothelial–mesenchymal transition in HRECs. The expressions of tight junction components claudin 3, occludin, and ZO-1 were increased in HG-treated HRECs following SPRED2 up-regulation. In addition, SPRED2 overexpression downregulated the expression of p-ERK1/2, p-p38, and p-JNK in the HG-treated HRECs. In conclusion, this study demonstrated that SPRED2 overexpression repressed endothelial–mesenchymal transition and endothelial injury in HG-treated HRECs by suppressing MAPK signaling pathway. These findings suggested that SPRED2 may be a novel potential therapeutic target implicated in DR progression.
DOI: 10.5281/zenodo.10649338
title: Dataset related to article "Preoperative diagnosis of periprosthetic infection in patients undergoing hip or knee revision arthroplasties: development and validation of machine learning algorithm".

description: This record contains raw data related to article "Preoperative diagnosis of periprosthetic infection in patients undergoing hip or knee revision arthroplasties: development and validation of machine learning algorithm"

Abstract: Background: Periprosthetic joint infection (PJI) following total hip and knee arthroplasty remains an extremely challenging and relatively high complication. This study aims to develop, validate and evaluate the use of machine learning (ML) algorithm to predict PJI in patients undergoing revision arthroplasties. Methods: A comprehensive review of patients undergoing hip or knee revision arthroplasty from 1 January 2015 to 31 March 2021 was conducted. Clinical data coming from preoperative patients history, laboratory analysis and demographic characteristics of patients were screened. Final data have been used to train a Logistic Regression model with the aim of predicting PJI preoperatively. Results: 1360 patients were enrolled, 1141 in the aseptic cohort and 219 in the infected cohort were included. ML demonstrated good discriminatory performance in predicting PJI in the selected patients (area under the curve 0.770 ± 0.006 in the training set and 0.720 ± 0.057 in the test set), and identified 3 significant predictors of PJI.  Conclusion: ML algorithm trained using preoperative clinical data accurately predicted PJI. The incorporation of ML models into preoperative assessment of patients undergoing prosthetic revision procedures are useful in providing specific risk assessment to aid individualised counselling, shared decision making and presurgical optimization.

 

Keywords: Artificial intelligence; Arthroplasty; Deep machine learning; Hip; Knee; Periprosthetic joint infection.
DOI: 10.5281/zenodo.10649339
title: Dataset related to article "Preoperative diagnosis of periprosthetic infection in patients undergoing hip or knee revision arthroplasties: development and validation of machine learning algorithm".

description: This record contains raw data related to article "Preoperative diagnosis of periprosthetic infection in patients undergoing hip or knee revision arthroplasties: development and validation of machine learning algorithm"

Abstract: Background: Periprosthetic joint infection (PJI) following total hip and knee arthroplasty remains an extremely challenging and relatively high complication. This study aims to develop, validate and evaluate the use of machine learning (ML) algorithm to predict PJI in patients undergoing revision arthroplasties. Methods: A comprehensive review of patients undergoing hip or knee revision arthroplasty from 1 January 2015 to 31 March 2021 was conducted. Clinical data coming from preoperative patients history, laboratory analysis and demographic characteristics of patients were screened. Final data have been used to train a Logistic Regression model with the aim of predicting PJI preoperatively. Results: 1360 patients were enrolled, 1141 in the aseptic cohort and 219 in the infected cohort were included. ML demonstrated good discriminatory performance in predicting PJI in the selected patients (area under the curve 0.770 ± 0.006 in the training set and 0.720 ± 0.057 in the test set), and identified 3 significant predictors of PJI.  Conclusion: ML algorithm trained using preoperative clinical data accurately predicted PJI. The incorporation of ML models into preoperative assessment of patients undergoing prosthetic revision procedures are useful in providing specific risk assessment to aid individualised counselling, shared decision making and presurgical optimization.

 

Keywords: Artificial intelligence; Arthroplasty; Deep machine learning; Hip; Knee; Periprosthetic joint infection.
DOI: 10.6084/m9.figshare.19029524
title: Additional file 5 of Open chromatin interaction maps reveal functional regulatory elements and chromatin architecture variations during wheat evolution

description: Additional file 5: Table S6 The interchromosomal open chromatin loops.
DOI: 10.6084/m9.figshare.19029530.v1
title: Additional file 7 of Open chromatin interaction maps reveal functional regulatory elements and chromatin architecture variations during wheat evolution

description: Additional file 7: Table S9 The differentially interacted intrachromosomal loops between bread wheat and Ae. tauschii.
DOI: 10.6084/m9.figshare.20078618.v1
title: Sprouty-related proteins with EVH1 domain (SPRED2) prevents high-glucose induced endothelial–mesenchymal transition and endothelial injury by suppressing MAPK activation

description: Diabetic retinopathy (DR) is a common complication of diabetes, and the leading cause of blindness in adults. Sprouty-related proteins with EVH1 domain (SPRED2) play an important role in diabetes and are closely related to the lens and eye morphogenesis. This study attempted to investigate the role and related mechanism of SPRED2 in DR. DR rat model was established by administration streptozocin. Human retinal endothelial cells (HRECs) were treated with high glucose (HG) to mimic DR. The results showed that SPRED2 expression was decreased in the retinal tissues of DR rats and HG-treated HRECs. MTT assay and flow cytometry data showed that SPRED2 overexpression reduced cell viability of HG-treated HRECs. SPRED2 overexpression enhanced Caspase-3 activity and promoted apoptosis of HG-treated HRECs. Furthermore, the expressions of endothelial cell markers CD31 and E-cad were down-regulated, whereas the expressions of mesenchymal cell markers FSP1, SM22, and α-SMA were up-regulated in the HG-treated HRECs. SPRED2 overexpression reversed HG-induced endothelial–mesenchymal transition in HRECs. The expressions of tight junction components claudin 3, occludin, and ZO-1 were increased in HG-treated HRECs following SPRED2 up-regulation. In addition, SPRED2 overexpression downregulated the expression of p-ERK1/2, p-p38, and p-JNK in the HG-treated HRECs. In conclusion, this study demonstrated that SPRED2 overexpression repressed endothelial–mesenchymal transition and endothelial injury in HG-treated HRECs by suppressing MAPK signaling pathway. These findings suggested that SPRED2 may be a novel potential therapeutic target implicated in DR progression.
DOI: 10.6084/m9.figshare.20078636
title: Toll-like receptor 9 (TLR9) gene deletion-mediated fracture healing in type II diabetic osteoporosis associates with inhibition of the nuclear factor-kappa B (NF-κB) signaling pathway

description: Diabetes is characterized by increased fracture risk. Evidence from <i>in vivo</i> studies is lacking for anti-fracture strategies in diabetes. Our microarray analyses predicted association of Toll-like receptor 9 (TLR9) with both diabetes and osteoporosis, which was the focus of this work in a murine model of type II diabetic osteoporosis (T2DOP). A T2DOP model with fracture was established in TLR9 knockout (TLR9<sup>−/−</sup>) mice, which were then treated with the NF-κB signaling pathway inhibitor (PDTC) and activator (TNF-α). The obtained data suggested that TLR9 knockout augmented regeneration of bone tissues and cartilage area in the callus, and diminished fibrous tissues in T2DOP mice. Moreover, TLR9 depletion significantly affected bone mineral density (BMD), bone volume/tissue volume (BV/TV), connectivity density, trabecular number, trabecular separation and trabecular thickness, thus promoting fracture recovery. Bone morphology and structure were also improved in response to TLR9 depletion in T2DOP mice. TLR9 depletion inactivated NF-κB signaling in T2DOP mice. PDTC was found to enhance fracture healing in T2DOP mice, while TNF-α negated this effect. Collectively, these data indicate that TLR9 depletion may hold anti-fracture properties, making it a potential therapeutic target for T2DOP. <b>Abbreviations:</b> Diabetic osteoporosis (DOP); bone mineral density (BMD); Toll-like receptors (TLRs); type 2 diabetes (T2D); Toll-like receptor 9 (TLR9); nuclear factor-kappaB (NF-κB); streptozotocin (STZ); type 2 diabetic osteoporosis (T2DOP); Gene Expression Omnibus (GEO); Kyoto encyclopedia of genes and genomes (KEGG); pyrrolidine dithiocarbamate (PDTC); computed tomography (CT); Hematoxylin–eosin (HE); bone morphogenetic protein 7 (BMP7); analysis of variance (ANOVA);
DOI: 10.5281/zenodo.10647455
title: Data supporting publication: Probing the micro- and nanoscopic properties of dental materials using infrared spectroscopy: A proof-of-principle study

description: This repository includes the data corresponding to the figures shown in the journal article entitled Probing the micro- and nanoscopic properties of dental materials using infrared spectroscopy: A proof-of-principle study, published in Acta Biomaterialia.
DOI: 10.5281/zenodo.10647456
title: Data supporting publication: Probing the micro- and nanoscopic properties of dental materials using infrared spectroscopy: A proof-of-principle study

description: This repository includes the data corresponding to the figures shown in the journal article entitled Probing the micro- and nanoscopic properties of dental materials using infrared spectroscopy: A proof-of-principle study, published in Acta Biomaterialia.
DOI: 10.5281/zenodo.10650880
title: Data supporting publication: Probing the micro- and nanoscopic properties of dental materials using infrared spectroscopy: A proof-of-principle study

description: This repository includes the data corresponding to the figures shown in the journal article entitled Probing the micro- and nanoscopic properties of dental materials using infrared spectroscopy: A proof-of-principle study, published in Acta Biomaterialia.
DOI: 10.6084/m9.figshare.20078635
title: The function of Sphingosine-1-phosphate receptor 2 (S1PR2) in maintaining intestinal barrier and inducing ulcerative colitis

description: Sphingosine-1-phosphate receptor 2 (S1PR2) was highly expressed in intestinal epithelial cells (IECs) and facilitated the proliferation of IECs. However, the specific function of S1PR2 in intestinal diseases, such as ulcerative colitis (UC), remains unclear. Accordingly, the current study set out to investigate the function of S1PR2 in maintaining intestinal barrier and inducing UC. S1PR2-overexpressed and knockdown Caco-2 cells were established to explore the function of S1PR2 on the permeability of IECs barrier. The UC-like mouse model in which UC is induced by dextran sulfate sodium (DSS) was established and utilized to investigate the role for S1PR2. The results showed that S1PR2 functioned as a maintainer of IECs permeability and a pathogenic factor for UC. A series of in vitro and in vivo experiments were conducted, and it was found that S1PR2 played an important role in intestinal epithelial cell proliferation and maintenance of intestinal epithelial cell barrier, possibly by the regulation on the expression level of SphK2, HDAC1, HDAC2, and ERK1/2 signaling pathway. The expression of S1PR2 was upregulated in UC mice and the colonic pathological damage in UC mice could be alleviated by the inhibition of S1PR2. Collectively, these results suggest that S1PR2 functions as a maintainer of IECs permeability and a pathogenic factor for UC. The research suggests S1PR2 may be an effective target for developing therapeutic strategies against UC. <b>Abbreviations:</b> S1PR2, Sphingosine-1-phosphate receptor 2; UC, ulcerative colitis; IECs, intestinal epithelial cells; DSS, dextran sulfate sodium; IBD, inflammation bowel disease; CD, Crohn’s disease; S1P, sphingosin-1-phosphate; SphK, sphingosine kinase; HIECs, human IECs; siRNA, small interfering RNA; CCK-8, cell counting kit-8; TEER, transepithelial electrical resistance; TEM, transmission electron microscope; RT-PCR, real-time reverse transcriptase polymerase-chain reaction; ELISA, enzyme-linked immunosorbent assay; HE, hematoxylin and eosin.