cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5353759.v2
title: Modeling <i>in vivo</i> relative biological effectiveness in particle therapy for clinically relevant endpoints

description: <b>Background:</b> The relative biological effectiveness (RBE) of particle therapy compared to photon radiotherapy is known to be variable but the exact dependencies are still subject to debate. <i>In vitro</i> data suggested that RBE is to a large extend independent of ion type if parametrized by the beam quality Q. This study analyzed the RBE dependence of pre-clinical data on late toxicity with an emphasis on the beam quality. <b>Material and methods:</b> Published pre-clinical RBE dose-response data of the spinal cord following one and two fractions of photon and carbon ion irradiation were compiled. The beam quality for each treatment condition was obtained from Monte Carlo simulations. The <i>α<sub>p</sub></i> and <i>β<sub>p</sub></i> parameters of the linear-quadratic (LQ) model for particle irradiation were determined from the pre-clinical data and was provided as a function of <i>Q</i>. An introduced model proposed <i>α<sub>p</sub></i> to increase linearly with <i>Q</i> and <i>β<sub>p</sub></i> to remain constant. RBE values predicted by the model were compared to the published data. <b>Results:</b> The α<sub>p</sub> parameter was highly correlated with <i>Q (R<sup>2</sup></i> = 0.96) with a linear slope of 0.019 Gy<sup>−1</sup>. No significant variation of <i>β<sub>p</sub></i> with <i>Q</i> was found. RBE and <i>Q</i> were also highly correlated (<i>R</i><sup>2</sup> = 0.98) for one and two fractions. The (extrapolated) RBE at <i>Q</i> = 0 (theoretical photon limit) for one and two fractions was 1.22 and significantly larger than 1 (<i>p</i> = .004). The model reproduced the dependence of RBE on fractionation well. <b>Conclusions</b>: Fraction dose and beam quality <i>Q</i> were sufficient to describe the RBE variability for a late toxicity model within a carbon ion treatment field. Assuming the independence of the identified RBE parameters on the ion type might suggest the translation of variable (pre-) clinical RBE data from carbon ion to proton therapy.
DOI: 10.6084/m9.figshare.10072379
title: Petrogenesis of post-collisional magmatism at the Carboniferous–Permian boundary in central Inner Mongolia, NE China: insights into when the Hegenshan Ocean closed?

description: The tectonic evolution of the Hegenshan Ocean is an important but poorly understood issue in the geology of the southeastern Central Asian Orogenic Belt (CAOB). Here we present an integrated study of petrology, geochronology, geochemistry, and Sr–Nd–Hf isotopes on a volcanic suite from the Baoligaomiao Formation near Dongwuqi, central Inner Mongolia, NE China. LA-ICP-MS zircon U–Pb dating indicates that the volcanic rocks formed at the Carboniferous–Permian boundary (ca. 301–297 Ma). Geochemistry data reveal that the rocks belong to alkaline to sub-alkaline series, and are characterized by enrichments in light rare earth elements (La<sub>N</sub>/Yb<sub>N</sub> = 13.01–39.30) and large ion lithophile elements and depletions in heavy rare earth elements and high field strength elements (e.g., Nb, Ta, and Ti). They have relatively low initial <sup>87</sup>Sr/<sup>86</sup>Sr ratios (0.702570–0.708084) and highly positive whole-rock Ԑ<sub>Nd</sub>(t) (2.27–2.72) and zircon Ԑ<sub>Hf</sub>(t) values (0.66–11.92). These geochemical characteristics and Sr–Nd–Hf isotopic compositions reveal that the rocks originated from partial melts of a juvenile, arc-type middle-lower crust, with fractional crystallization as a dominant factor controlling the magma differentiation. The rocks were generated in a post-collisional regime, and occurred as a magmatic response to the final closure of the Hegenshan Ocean at the Late Carboniferous (ca. 305 Ma). In addition, based on a review of the pre-existing literature data, a model of continental arc–back-arc basin system at the southern margin of South Mongolian microcontinent is proposed to explain the tectonic evolution of the Hegenshan Ocean.
DOI: 10.6084/m9.figshare.10072379.v1
title: Petrogenesis of post-collisional magmatism at the Carboniferous–Permian boundary in central Inner Mongolia, NE China: insights into when the Hegenshan Ocean closed?

description: The tectonic evolution of the Hegenshan Ocean is an important but poorly understood issue in the geology of the southeastern Central Asian Orogenic Belt (CAOB). Here we present an integrated study of petrology, geochronology, geochemistry, and Sr–Nd–Hf isotopes on a volcanic suite from the Baoligaomiao Formation near Dongwuqi, central Inner Mongolia, NE China. LA-ICP-MS zircon U–Pb dating indicates that the volcanic rocks formed at the Carboniferous–Permian boundary (ca. 301–297 Ma). Geochemistry data reveal that the rocks belong to alkaline to sub-alkaline series, and are characterized by enrichments in light rare earth elements (La<sub>N</sub>/Yb<sub>N</sub> = 13.01–39.30) and large ion lithophile elements and depletions in heavy rare earth elements and high field strength elements (e.g., Nb, Ta, and Ti). They have relatively low initial <sup>87</sup>Sr/<sup>86</sup>Sr ratios (0.702570–0.708084) and highly positive whole-rock Ԑ<sub>Nd</sub>(t) (2.27–2.72) and zircon Ԑ<sub>Hf</sub>(t) values (0.66–11.92). These geochemical characteristics and Sr–Nd–Hf isotopic compositions reveal that the rocks originated from partial melts of a juvenile, arc-type middle-lower crust, with fractional crystallization as a dominant factor controlling the magma differentiation. The rocks were generated in a post-collisional regime, and occurred as a magmatic response to the final closure of the Hegenshan Ocean at the Late Carboniferous (ca. 305 Ma). In addition, based on a review of the pre-existing literature data, a model of continental arc–back-arc basin system at the southern margin of South Mongolian microcontinent is proposed to explain the tectonic evolution of the Hegenshan Ocean.
DOI: 10.6084/m9.figshare.23700657.v1
title: Additional file 4 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

description: Additional file 4:Antibodies information of Immunofluorescence.
DOI: 10.6084/m9.figshare.23700660
title: Additional file 5 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

description: Additional file 5:Antibodies information of Immunochemistry.
DOI: 10.6084/m9.figshare.23700660.v1
title: Additional file 5 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

description: Additional file 5:Antibodies information of Immunochemistry.
DOI: 10.6084/m9.figshare.23700663.v1
title: Additional file 6 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

description: Additional file 6:(A) qRT-PCR verifies that the mRNA expression of FAP in OEFAP-HFFs is significantly higher than in NCFAP-HFFs and T24 cells. (B, C) WB indicates that the protein expression of FAP in OEFAP-HFFs is significantly higher than in NCFAP-HFFs and T24 cells. (D, E) WB show that HFF-CM (stimulated or not stimulated) has a pro-EMT effect, with downregulated E-cadherin and upregulated N-cadherin and Vimentin. The pro-EMT effects of HFF-CM were significantly amplified after TGF-β1 induction or overexpression FAP, while the TGF-β1 neutralizing antibody reverses the pro-EMT effects of TGF-β1 induction.
DOI: 10.6084/m9.figshare.23700666.v1
title: Additional file 7 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

description: Additional file 7: (A) VCAN expression is significantly higher in BLCA tissues than in adjacent normal tissues. (B) Immunofluorescence shows that the fluorescence intensity of VCAN in CAFs is notably brighter than in NFs, and in OEFAP-HFFs it is notably brighter than in NCFAP-HFFs.
DOI: 10.6084/m9.figshare.23700669
title: Additional file 8 of TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells

description: Additional file 8: (A) Immunofluorescence shows that the fluorescence intensity of VCAN in HFFs is markedly enhanced under the induction of TGF-β1; TGF-β1 neutralizing antibody significantly reduces this enhanced fluorescence intensity. (B) qRT-PCR verifies that the expression of VCAN in OEVCAN-HFFs is significantly higher than in NCVCAN-HFFs and T24 cells. (C) Immunofluorescence reveals that the VCAN fluorescence intensity in OEVCAN-HFFs is notably brighter than in NCVCAN-HFFs and T24 cells. (D) ELISA shows that the concentration of VCAN in the OEVCAN-HFF supernatant is significantly higher than in NCVCAN-HFF and T24 cell supernatant. (E) WB show that OEVCAN-HFF-CM can downregulate E-cadherin as well as upregulate N-cadherin and Vimentin.
DOI: 10.6084/m9.figshare.22127853.v1
title: Hypoxia-induced GPCPD1 depalmitoylation triggers mitophagy via regulating PRKN-mediated ubiquitination of VDAC1

description: Mitophagy, which selectively eliminates the dysfunctional and excess mitochondria by autophagy, is crucial for cellular homeostasis under stresses such as hypoxia. Dysregulation of mitophagy has been increasingly linked to many disorders including neurodegenerative disease and cancer. Triple-negative breast cancer (TNBC), a highly aggressive breast cancer subtype, is reported to be characterized by hypoxia. However, the role of mitophagy in hypoxic TNBC as well as the underlying molecular mechanism is largely unexplored. Here, we identified GPCPD1 (glycerophosphocholine phosphodiesterase 1), a key enzyme in choline metabolism, as an essential mediator in hypoxia-induced mitophagy. Under the hypoxic condition, we found that GPCPD1 was depalmitoylated by LYPLA1, which facilitated the relocating of GPCPD1 to the outer mitochondrial membrane (OMM). Mitochondria-localized GPCPD1 could bind to VDAC1, the substrate for PRKN/PARKIN-dependent ubiquitination, thus interfering with the oligomerization of VDAC1. The increased monomer of VDAC1 provided more anchor sites to recruit PRKN-mediated polyubiquitination, which consequently triggered mitophagy. In addition, we found that GPCPD1-mediated mitophagy exerted a promotive effect on tumor growth and metastasis in TNBC both <i>in vitro</i> and <i>in vivo</i>. We further determined that GPCPD1 could serve as an independent prognostic indicator in TNBC. In conclusion, our study provides important insights into a mechanistic understanding of hypoxia-induced mitophagy and elucidates that GPCPD1 could act as a potential target for the future development of novel therapy for TNBC patients.
DOI: 10.4121/uuid:622905c5-d760-49e9-96c2-b116a679ec33.v1
title: Supplementary data for the article: External human-machine interfaces on automated vehicles: Effects on pedestrian crossing decisions.

description: Supplementary data for the article: De Clercq, G. K., Dietrich, A., Núñez Velasco, P., De Winter, J. C F., & Happee, R. (in press). External human-machine interfaces on automated vehicles: Effects on pedestrian crossing decisions. Human Factors.
DOI: 10.6084/m9.figshare.13212635
title: Additional file 2 of Temporal transcriptomic differences between tolerant and susceptible genotypes contribute to rice drought tolerance

description: Additional file 2: Supplementary Table S1. Basic information of RNA-seq for all samples. Supplementary Table S2. Total expressed genes (FPKM&gt; 0.001) detected in twelve rice genotypes. Supplementary Table S3. Function-studied drought-tolerant genes, their correlation with drought-tolerance index by biomass (DTIB) and biomass measured in well-watered fields. Supplementary Table S4. Number of enriched GOBPs by upregulated and downregulated DRGs in various classifications of biological processes. Number in shade indicates the GO classification preferred by upregulated or downregulated DRGs. Supplementary Table S5. Correlations of fold changes from common drought-responsive genes between the tolerant and the susceptible groups during drought. Supplementary Table S6. Number of biological processes in various GO classifications enriched by recovery related genes in different clusters. Supplementary Table S7. Distributions of GO biological processes of different types in various GO classifications. Percentage in shade indicates the GO classification preferred by the type of GO biological processes. Supplementary Table S8. Enrichments of GO biological processes by osmolality- and H2O2-correlated drought responsive genes. Supplementary Table S9. Distribution of biological processes enriched by osmolality- and H2O2-correlated drought responsive genes in various GO classification. Supplementary Table S10. The enrichment of DT-featured biological processes in Gene Ontology for nine modules. Supplementary Table S11. Distribution of genes relevant to photosynthesis and phytohormones in the modules. Supplementary Table S12. Information of candidate genes of drought-tolerance. Supplementary Table S13. Information of candidate genes for drought-recovery.
DOI: 10.25549/usctheses-ouc11666585
title: Microsoft Word - Tashman Thesis v3.docx
DOI: 10.4121/uuid:622905c5-d760-49e9-96c2-b116a679ec33.v2
title: Supplementary data for the article: External human-machine interfaces on automated vehicles: Effects on pedestrian crossing decisions

description: Unity implementation of the virtual reality environment used in the experiment presented in the paper: De Clercq, K., Dietrich, A., Núñez Velasco, P., De Winter, J. C. F., & Happee, R. (2019). External human-machine interfaces on automated vehicles: Effects on pedestrian crossing decisions. Human Factors, 61, 1353–1370. https://doi.org/10.1177/0018720819836343
DOI: 10.5281/zenodo.7704680
title: Dataset from RNAseq analysis of differential gene expression among developmental stages of two non-marine ostracods

description: Dataset comprising tree files and alignments used for phylogenetic validation of data, assemblies of reference transcriptomes and draft genomes, annotation of draft genomes, as well as supplementary tables.
DOI: 10.6084/m9.figshare.16888450
title: Targeting USP11 may alleviate radiation-induced pulmonary fibrosis by regulating endothelium tight junction

description: Radiation-induced pulmonary fibrosis (RIPF) is a major side effect after radiotherapy for thoracic malignancies. However, rare anti-RIPF therapeutics show definitive effects for treating this disease. Ubiquitin-specific peptidase 11 (USP11) has been reported to promote transforming growth factor β (TGFβ) signaling which plays an essential role underlying RIPF. Herein, we explored the role of USP11 on RIPF. In the present study, USP11-knockout (<i>Usp11<sup>-/-</sup></i>) mice were used to explore the effects of USP11 on RIPF. The lung tissue was obtained after receiving 30 Gy X-ray irradiation. The expression of USP11, TGF-β1, and a-SMA was determined by immunohistochemical and Western Blot, respectively. γ-H<sub>2</sub>AX foci and TUNEL positive cells were detected by fluorescent technique to assess DNA damage and apoptosis. High-throughput proteomic analysis was applied to further explore the related mechanisms. The transwell co-culture method was used to investigate bystander effects in HELF cells induced by irradiated HMEC-1 cells <i>in vitro</i>. Here we found that radiation activated USP11 <i>in vivo</i> and <i>in vitro</i>. Our results showed that USP11 deficiency effectively decreased serum TGF-β1 level, suppressed α-SMA expression, and mitigated pulmonary fibrosis. In addition, fewer γ-H<sub>2</sub>AX foci and decreased apoptotic cells were identified after irradiation in the primary cells isolated from the lungs of <i>Usp11<sup>-/-</sup></i> mice. High-throughput proteomics analysis results showed that 22-upregulated and 158-downregulated proteins were identified in the lung tissues of <i>Usp11<sup>-/-</sup></i> mice after irradiation. Furthermore, gene set enrichment analysis (GSEA) revealed that USP11 deficiency affects the tight junction signaling pathway. We verified that USP11 deficiency remarkably reinforced tight junction in the endothelial cells and alleviated TGF-β1 to inhibit fibrosis of fibroblast cells. The present study preliminarily showed that USP11-knockout mitigated RIPF via reinforcement endothelial barrier function.
DOI: 10.6084/m9.figshare.14791347
title: In vitro activities of the tetrazole VT-1161 compared with itraconazole and fluconazole against <i>Cryptococcus</i> and non-<i>albicans Candida</i> species

description: Recently, <i>Cryptococcus</i> and non-<i>albicans Candida</i> (NAC) have emerged as health-threatening pathogens for clinical fungal infections. Due to their increased resistance to existing antifungal drugs, novel antifungals are urgently needed. In this study, we evaluated the antifungal effect of VT-1161 and its comparators itraconazole and fluconazole against common fluconazole-sensitive or -resistant <i>Cryptococcus</i> and NAC strains. The tested strains were obtained from Chinese patients by the Invasive Fungal Infection Group within the past 2 years. The minimum inhibitory concentrations (MICs) of VT-1161 and other triazoles were measured according to the Clinical and Laboratory Standards Institute (CLSI) M27-Ed4 guidelines. We found that VT-1161 exhibited strong in vitro activity against <i>Cryptococcus</i> spp.. VT-1161 (geometric mean MIC = 0.024 μg/mL) was 21.7-fold and 104.5-fold more potent than itraconazole and fluconazole, respectively. Against the seven <i>Cryptococcus neoformans</i> isolates with higher fluconazole MICs (≥8 μg/mL based on the MIC<sub>90</sub> value of this azole), VT-1161 maintained potent activities, with MICs ranging between 0.031 and 0.5 μg/mL. For NAC spp., VT-1161 (geometric mean MIC = 0.099 μg/mL) was 6.0-fold and 11.4-fold more effective than itraconazole and fluconazole, respectively. There is a positive correlation of the MICs between VT-1161 and itraconazole/fluconazole. The MIC values of VT-1161 against <i>Candida glabrata</i> and <i>Candida tropicalis</i> were significantly lower than those of fluconazole, whereas for <i>Candida parapsilosis</i> the differences in the MIC values between VT-1161 and fluconazole were not statistically significant. The results showed that tetrazole VT-1161 might be a promising candidate for treating <i>Cryptococcus</i> and NAC infections.
DOI: 10.6084/m9.figshare.23700875
title: Additional file 7 of Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients

description: Additional file 7: Table S4. The summary of differentially altered genes between HPV-positvie and HPV-negative groups.
DOI: 10.6084/m9.figshare.23700869.v1
title: Additional file 5 of Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients

description: Additional file 5: Table S2. The summary of somatic SNV and InDel.
DOI: 10.6084/m9.figshare.23700866.v1
title: Additional file 4 of Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients

description: Additional file 4: Table S1. The summary of WES quality control.
DOI: 10.6084/m9.figshare.23700872.v1
title: Additional file 6 of Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients

description: Additional file 6: Table S3. CNV information in our cohort. Related to Fig. 3.
DOI: 10.6084/m9.figshare.23700866
title: Additional file 4 of Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients

description: Additional file 4: Table S1. The summary of WES quality control.
DOI: 10.6084/m9.figshare.23700731.v1
title: Additional file 1 of Whole-genome sequencing and functional annotation of pathogenic Paraconiothyrium brasiliense causing human cellulitis

description: Additional file 1: Table S1. KEGG functional annotation of P. brasiliense GGX 413
DOI: 10.6084/m9.figshare.23700872
title: Additional file 6 of Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients

description: Additional file 6: Table S3. CNV information in our cohort. Related to Fig. 3.
DOI: 10.6084/m9.figshare.7975778
title: Small molecule-driven NLRP3 inflammation inhibition via interplay between ubiquitination and autophagy: implications for Parkinson disease

description: Aging-related, nonresolving inflammation in both the central nervous system (CNS) and periphery predisposes individuals to the development of neurodegenerative disorders (NDDs). Inflammasomes are thought to be especially relevant to immune homeostasis, and their dysregulation contributes to inflammation and NDDs. However, few agents have been clinically shown to reduce NDD incidence by targeting inflammasomes. Our study indicated that NLRP3 (NLR family, pyrin domain containing 3) inflammasome is involved in Parkinson disease (PD) progression in patients and various murine models. In addition, the small molecule kaempferol (Ka) protected mice against LPS- and SNCA-induced neurodegeneration by inhibiting NLRP3 inflammasome activation as evidenced by the fact that Ka reduced cleaved CASP1 expression and disrupted NLRP3-PYCARD-CASP1 complex assembly with concomitant decreased IL1B secretion. Mechanically, Ka promoted macroautophagy/autophagy in microglia, leading to reduced NLRP3 protein expression, which in turn deactivated the NLRP3 inflammasome. Intriguingly, ubiquitination was involved in Ka-induced autophagic NLRP3 degradation. These findings were further confirmed <i>in vivo</i> as knockdown of <i>Atg5</i> expression or autophagy inhibitor treatment significantly inhibited the Ka-mediated NLRP3 inflammasome inhibition and neurodegeneration amelioration. Thus, we demonstrated that Ka promotes neuroinflammatory inhibition via the cooperation of ubiquitination and autophagy, suggesting that Ka is a promising therapeutic strategy for the treatment of NDDs. <b>Abbreviations:</b> 3-MA: 3-methyladenine; AAV: adeno-associated virus; ACTB: actin, beta; AIF1/IBA1: allograft inflammatory factor 1; ATG5: autophagy related 5; ATG7: autophagy related 7; BafA1: bafilomycin A<sub>1;</sub> BECN1: beclin 1, autophagy related; CASP1: caspase 1; CNS: central nervous system; CQ: chloroquine; DA neurons: dopaminergic neurons; DAMPS: damage-associated molecular patterns; DAPI: 4’,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; GFAP: glial fibrillary acidic protein; IP: immunoprecipitation; i.p.: intraperitoneally; Ka: kaempferol; KD: knockdown; KO: knockout; LPS: lipopolysaccharide; IL1B: interleukin 1 beta; IL6: interleukin 6; Ly: lysate; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; NC: negative control; NDD: neurodegenerative diseases; NLRP3: NLR family, pyrin domain containing 3; OE: overexpression; PD: Parkinson disease; poly-Ub: poly-ubiquitin; PTM: post-translational modification; PYCARD/ASC: PYD and CARD domain containing; Rapa: rapamycin; RFP: red fluorescent protein; SN: supernatant; SNCA: synuclein alpha; SNpc: substantia nigra pars compacta; SQSTM1: sequestosome 1; TH: tyrosine hydroxylase; TNF/TNF-alpha: tumor necrosis factor; Ub: ubiquitin; WT: wild type