cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.13385294
title: Supplementary Material for: MNSFβ Promotes the Proliferation and Migration of Human Extravillous Trophoblast Cells and the Villus Expression Level of MNSFβ Is Decreased in Recurrent Miscarriage Patients

description: <b><i>Aims:</i></b> The invasion of extravillous trophoblast (EVT) cells into maternal decidua is essential for the establishment and maintenance of pregnancy. Derangement of EVT cell invasion might cause pregnancy complications including recurrent miscarriage (RM). We previously reported that deficiency of monoclonal nonspecific suppressor factor beta (MNSFβ) led to the early pregnancy failure in mice and the decidual MNSFβ expression level in RM patients was significantly decreased, but the underlying molecular mechanism of the role that MNSFβ played at the maternal-fetal interface remains unclear. Thus, in the present study, we determined effects of downregulated MNSFβ expression on human EVT cell activities. <b><i>Methods:</i></b> The MNSFβ expression in first-trimester human decidual and placental villus tissues was detected, respectively, by immunofluorescence or immunohistochemical analyses. The MNSFβ expression level in the immortalized first-trimester human EVT cell line HTR8/SVneo was downregulated by transfecting the small interfering RNA against MNSFβ and upregulated by transfecting the recombinant pDsRed-MNSFβ plasmids. The proliferation, migration, invasion, and apoptosis activities of HTR8/SVneo cells were, respectively, determined by cytometry assay, scratch test, transwell assay, and FITC/PI staining. The expression levels of P53, RhoA, Bcl-2, Bax, and MMP-9 in HTR8/SVneo cells, as well as the expression levels of MNSFβ and RhoA in placental villi of RM patients and physically normal pregnant women (NP), were examined by Western blot analysis. <b><i>Results:</i></b> MNSFβ protein signals were observed in first-trimester human villus and extravillous trophoblast cells. The downregulated MNSFβ expression significantly attenuated the proliferation, migration, and invasion abilities of HTR8/SVneo cells, accompanied with the obviously decreased expression levels of P53, RhoA, Bcl-2, Bax, and MMP-9, whereas the upregulated MNSFβ expression in HTR8/SVneo cells represented the inverse effects. Furthermore, expression levels of MNSFβ and RhoA in first-trimester human placental villus tissues of RM patients were significantly decreased compared to that of NP women. <b><i>Conclusion:</i></b> These data suggested that MNSFβ promotes proliferation and migration of human EVT cells, probably via the P53 signaling pathway, and the deficiency of MNSFβ in placental villi might lead to early pregnancy loss by reducing proliferation and invasion activities of EVTs.
DOI: 10.6084/m9.figshare.13385294.v1
title: Supplementary Material for: MNSFβ Promotes the Proliferation and Migration of Human Extravillous Trophoblast Cells and the Villus Expression Level of MNSFβ Is Decreased in Recurrent Miscarriage Patients

description: <b><i>Aims:</i></b> The invasion of extravillous trophoblast (EVT) cells into maternal decidua is essential for the establishment and maintenance of pregnancy. Derangement of EVT cell invasion might cause pregnancy complications including recurrent miscarriage (RM). We previously reported that deficiency of monoclonal nonspecific suppressor factor beta (MNSFβ) led to the early pregnancy failure in mice and the decidual MNSFβ expression level in RM patients was significantly decreased, but the underlying molecular mechanism of the role that MNSFβ played at the maternal-fetal interface remains unclear. Thus, in the present study, we determined effects of downregulated MNSFβ expression on human EVT cell activities. <b><i>Methods:</i></b> The MNSFβ expression in first-trimester human decidual and placental villus tissues was detected, respectively, by immunofluorescence or immunohistochemical analyses. The MNSFβ expression level in the immortalized first-trimester human EVT cell line HTR8/SVneo was downregulated by transfecting the small interfering RNA against MNSFβ and upregulated by transfecting the recombinant pDsRed-MNSFβ plasmids. The proliferation, migration, invasion, and apoptosis activities of HTR8/SVneo cells were, respectively, determined by cytometry assay, scratch test, transwell assay, and FITC/PI staining. The expression levels of P53, RhoA, Bcl-2, Bax, and MMP-9 in HTR8/SVneo cells, as well as the expression levels of MNSFβ and RhoA in placental villi of RM patients and physically normal pregnant women (NP), were examined by Western blot analysis. <b><i>Results:</i></b> MNSFβ protein signals were observed in first-trimester human villus and extravillous trophoblast cells. The downregulated MNSFβ expression significantly attenuated the proliferation, migration, and invasion abilities of HTR8/SVneo cells, accompanied with the obviously decreased expression levels of P53, RhoA, Bcl-2, Bax, and MMP-9, whereas the upregulated MNSFβ expression in HTR8/SVneo cells represented the inverse effects. Furthermore, expression levels of MNSFβ and RhoA in first-trimester human placental villus tissues of RM patients were significantly decreased compared to that of NP women. <b><i>Conclusion:</i></b> These data suggested that MNSFβ promotes proliferation and migration of human EVT cells, probably via the P53 signaling pathway, and the deficiency of MNSFβ in placental villi might lead to early pregnancy loss by reducing proliferation and invasion activities of EVTs.
DOI: 10.6084/m9.figshare.13385261
title: Supplementary Material for: Pulp Vitality and Longevity of Adhesive Restorations Are Not Affected by Selective Carious Removal: A Multicenter Clinical Trial

description: The aim of this multicenter randomized clinical trial was to evaluate the pulp vitality and survival rate of adhesive restorations performed on posterior deciduous teeth after non-selective (NSCR) or selective (SCR) carious tissue removal over 33 months. One hundred and seven children (average age 4–8 years, SD 1.4) with at least two active moderate cavitated lesions in dentin were included. Teeth were randomized and submitted to NSCR or SCR before composite resin restoration. Restorations were clinically and radiographically assessed at baseline, 6, 12, 18, 24, and 33 months by a blinded, trained, and calibrated operator in each center. The characteristics of the restorations were recorded according to FDI criteria and were considered as restorative failures when scores 4 or 5 were presented. Pulp vitality was measured by clinical and radiographic examinations, and those teeth that presented any signs or symptoms of irreversible pulpitis or pulp necrosis were considered as failure. Data were analyzed by a Cox regression model with shared frailty, considering two outcomes: pulp and restorative. A total of 278 restorations (137 after NSCR and 141 after SCR) were performed at baseline in four different centers and there was no loss in the follow-up period. Survival rate was 97.1 and 87.1% for pulp and for restorative outcome, respectively. The overall annual failure rate was 7%. There were no differences in the failure risk according to the treatment group, center, and all the clinical and demographic variables, regardless of outcome. Composite restorations of active moderate deep carious lesions performed on posterior primary teeth show satisfactory survival for restorative and pulp outcome after a 33-month follow-up, regardless of the technique executed for carious tissue removal.
DOI: 10.6084/m9.figshare.13385261.v1
title: Supplementary Material for: Pulp Vitality and Longevity of Adhesive Restorations Are Not Affected by Selective Carious Removal: A Multicenter Clinical Trial

description: The aim of this multicenter randomized clinical trial was to evaluate the pulp vitality and survival rate of adhesive restorations performed on posterior deciduous teeth after non-selective (NSCR) or selective (SCR) carious tissue removal over 33 months. One hundred and seven children (average age 4–8 years, SD 1.4) with at least two active moderate cavitated lesions in dentin were included. Teeth were randomized and submitted to NSCR or SCR before composite resin restoration. Restorations were clinically and radiographically assessed at baseline, 6, 12, 18, 24, and 33 months by a blinded, trained, and calibrated operator in each center. The characteristics of the restorations were recorded according to FDI criteria and were considered as restorative failures when scores 4 or 5 were presented. Pulp vitality was measured by clinical and radiographic examinations, and those teeth that presented any signs or symptoms of irreversible pulpitis or pulp necrosis were considered as failure. Data were analyzed by a Cox regression model with shared frailty, considering two outcomes: pulp and restorative. A total of 278 restorations (137 after NSCR and 141 after SCR) were performed at baseline in four different centers and there was no loss in the follow-up period. Survival rate was 97.1 and 87.1% for pulp and for restorative outcome, respectively. The overall annual failure rate was 7%. There were no differences in the failure risk according to the treatment group, center, and all the clinical and demographic variables, regardless of outcome. Composite restorations of active moderate deep carious lesions performed on posterior primary teeth show satisfactory survival for restorative and pulp outcome after a 33-month follow-up, regardless of the technique executed for carious tissue removal.
DOI: 10.6084/m9.figshare.13385234
title: Supplementary Material for: The Expanding Phenotypic Spectrums Associated with <b><i>ATP1A3</i></b> Mutation in a Family with Rapid-Onset Dystonia Parkinsonism

description: <b><i>Introduction:</i></b> Rapid-onset dystonia parkinsonism (RDP), also referred to as Dystonia 12, is a rare autosomal dominant genetic disease characterized by abrupt onset of a rostrocaudal gradient of dystonia with prominent bulbar symptoms, and parkinsonian features, primarily bradykinesia and postural instability without tremor. The purpose of this study was to identify the genetic defect in a Chinese pedigree with familial RDP and to explore genotype-phenotype correlation. <b><i>Methods:</i></b> A 3-generation Chinese Han pedigree consisting of 9 members and 3 patients with RDP, and 200 unrelated ethnically matched normal subjects were recruited in this study. Exome sequencing was performed in the proband, and Sanger sequencing was then conducted in other family members and 200 normal controls. <b><i>Results:</i></b> In addition to the typical clinical manifestations of RDP, the proband and her sister presented tongue tremor which developed at the onset, and intriguingly the proband showed a “re-emergent” tongue tremor. Both the proband and her sister had a medical history of hyperthyroidism, and at the psychiatric interview they both received diagnoses of depression and anxiety. Excessive grammar errors existed in most sentences written by the proband, and this written-expression disorder occurred years before the onset of RDP. The mother of the proband presented tongue enlargement, oromandibular dystonia, and limb dystonia, which were not observed in her 2 daughters at the time of study. A missense variant, c.1838C&gt;T (p.T613M), in the <i>ATP1A3</i> gene, was identified in the 3 patients in the family and in 2 young children but was absent in family members without RDP and in the 200 normal controls. <b><i>Conclusion:</i></b> These findings may broaden the phenotypic spectrums of RDP with mutations in the <i>ATP1A3</i> gene, provide new insights into the diagnosis of RDP, and have implications for genetic counseling.
DOI: 10.6084/m9.figshare.13385234.v1
title: Supplementary Material for: The Expanding Phenotypic Spectrums Associated with <b><i>ATP1A3</i></b> Mutation in a Family with Rapid-Onset Dystonia Parkinsonism

description: <b><i>Introduction:</i></b> Rapid-onset dystonia parkinsonism (RDP), also referred to as Dystonia 12, is a rare autosomal dominant genetic disease characterized by abrupt onset of a rostrocaudal gradient of dystonia with prominent bulbar symptoms, and parkinsonian features, primarily bradykinesia and postural instability without tremor. The purpose of this study was to identify the genetic defect in a Chinese pedigree with familial RDP and to explore genotype-phenotype correlation. <b><i>Methods:</i></b> A 3-generation Chinese Han pedigree consisting of 9 members and 3 patients with RDP, and 200 unrelated ethnically matched normal subjects were recruited in this study. Exome sequencing was performed in the proband, and Sanger sequencing was then conducted in other family members and 200 normal controls. <b><i>Results:</i></b> In addition to the typical clinical manifestations of RDP, the proband and her sister presented tongue tremor which developed at the onset, and intriguingly the proband showed a “re-emergent” tongue tremor. Both the proband and her sister had a medical history of hyperthyroidism, and at the psychiatric interview they both received diagnoses of depression and anxiety. Excessive grammar errors existed in most sentences written by the proband, and this written-expression disorder occurred years before the onset of RDP. The mother of the proband presented tongue enlargement, oromandibular dystonia, and limb dystonia, which were not observed in her 2 daughters at the time of study. A missense variant, c.1838C&gt;T (p.T613M), in the <i>ATP1A3</i> gene, was identified in the 3 patients in the family and in 2 young children but was absent in family members without RDP and in the 200 normal controls. <b><i>Conclusion:</i></b> These findings may broaden the phenotypic spectrums of RDP with mutations in the <i>ATP1A3</i> gene, provide new insights into the diagnosis of RDP, and have implications for genetic counseling.
DOI: 10.6084/m9.figshare.13385237
title: Supplementary Material for: Effect of Cryptotanshinone on Measures of Rat Cardiomyocyte Oxidative Stress and Gene Activation Associated with Apoptosis

description: <b><i>Background:</i></b> Oxidative stress is a key factor that results in cardiomyocyte apoptosis and cardiovascular diseases. Cryptotanshinone (CTS), one of the major bioactive constitutes extracted from the root of the plant <i>Salvia miltiorrhiza</i>Bunge, has been widely studied for various disease treatments. However, the roles of CTS on cardiomyocytes remain unclear. <b><i>Methods:</i></b> In the present study, neonatal rat cardiomyocytes were pretreated with CTS for 4 h before being exposed to H<sub>2</sub>O<sub>2</sub>. Cell viability for the cells with or without pretreatment with CTS before exposure to H<sub>2</sub>O<sub>2</sub> was evaluated by the MTT assay. Production of lactate dehydrogenase (LDH), nitric oxide (NO), prostaglandin E<sub>2</sub> (PGE<sub>2</sub>), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxides (GSH-Px) was quantified by corresponding detection kits. The mRNA levels of Bcl-2 antiapoptotic and Bax-like proapoptotic genes were quantified with RT-PCR. Production of reactive oxygen species (ROS) was qualified and quantified with a dichlorofluorescein diacetate cellular ROS detection assay kit. The extracellular signal-related kinase (ERK) phosphorylation and nuclear factor κB (NF-κB) activation were measured by Western blot. <b><i>Results:</i></b> Our results revealed that the CTS pretreatment could enhance cell viability and promote Bcl-2 antiapoptotic gene expression. Additionally, CTS could abolish the H<sub>2</sub>O<sub>2</sub>-induced production of NO, LDH, and PGE<sub>2</sub>. Consistent with these findings, CTS could inhibit ROS and MDA production and promote SOD, CAT, and GSH-Px activities. Mechanistically, CTS may achieve these processes by inhibiting ERK and NF-κB signal pathways. <b><i>Conclusion:</i></b> CTS protects cardiomyocytes against the H<sub>2</sub>O<sub>2</sub>-induced cellular injuries through ERK and NF-κB inactivation and ROS scavenging. Therefore, CTS is a promising reagent against ROS-induced cardiomyopathy.
DOI: 10.6084/m9.figshare.11636676
title: Epigenome- and Transcriptome-wide Changes in Muscle Stem Cells from Low Birth Weight Men

description: <b>Background</b>: Being born with low birth weight (LBW) is a risk factor for muscle insulin resistance and type 2 diabetes (T2D), which may be mediated by epigenetic mechanisms programmed by the intrauterine environment. Epigenetic mechanisms exert their prime effects in developing cells. We hypothesized that muscle insulin resistance in LBW subjects may be due to early differential epigenomic and transcriptomic alterations in their immature muscle progenitor cells. <b>Results</b>: Muscle progenitor cells were obtained from 23 healthy young adult men born at term with LBW, and 15 BMI-matched normal birth weight (NBW) controls. The cells were subsequently cultured and differentiated into myotubes. DNA and RNA were harvested before and after differentiation for genome-wide DNA methylation and RNA expression measurements. After correcting for multiple comparisons (q ≤ 0.05), 56 CpG sites were found to be significantly, differentially methylated in myoblasts from LBW compared with NBW men, of which the top five gene-annotated CpG sites (<i>SKI, ARMCX3, NR5A2, NEUROG, ESRRG</i>) previously have been associated to regulation of cholesterol, fatty acid and glucose metabolism and muscle development or hypertrophy. LBW men displayed markedly decreased myotube gene expression levels of the AMPK-repressing tyrosine kinase gene <i>FYN</i> and the histone deacetylase gene <i>HDAC7</i>. Silencing of <i>FYN</i> and <i>HDAC7</i> was associated with impaired myotube formation, which for <i>HDAC7</i> reduced muscle glucose uptake. <b>Conclusions</b>: The data provides evidence of impaired muscle development predisposing LBW individuals to T2D is linked to and potentially caused by distinct DNA methylation and transcriptional changes including down regulation of <i>HDAC7</i> and <i>FYN</i> in their immature myoblast stem cells.
DOI: 10.6084/m9.figshare.11636676.v1
title: Epigenome- and Transcriptome-wide Changes in Muscle Stem Cells from Low Birth Weight Men

description: <b>Background</b>: Being born with low birth weight (LBW) is a risk factor for muscle insulin resistance and type 2 diabetes (T2D), which may be mediated by epigenetic mechanisms programmed by the intrauterine environment. Epigenetic mechanisms exert their prime effects in developing cells. We hypothesized that muscle insulin resistance in LBW subjects may be due to early differential epigenomic and transcriptomic alterations in their immature muscle progenitor cells. <b>Results</b>: Muscle progenitor cells were obtained from 23 healthy young adult men born at term with LBW, and 15 BMI-matched normal birth weight (NBW) controls. The cells were subsequently cultured and differentiated into myotubes. DNA and RNA were harvested before and after differentiation for genome-wide DNA methylation and RNA expression measurements. After correcting for multiple comparisons (q ≤ 0.05), 56 CpG sites were found to be significantly, differentially methylated in myoblasts from LBW compared with NBW men, of which the top five gene-annotated CpG sites (<i>SKI, ARMCX3, NR5A2, NEUROG, ESRRG</i>) previously have been associated to regulation of cholesterol, fatty acid and glucose metabolism and muscle development or hypertrophy. LBW men displayed markedly decreased myotube gene expression levels of the AMPK-repressing tyrosine kinase gene <i>FYN</i> and the histone deacetylase gene <i>HDAC7</i>. Silencing of <i>FYN</i> and <i>HDAC7</i> was associated with impaired myotube formation, which for <i>HDAC7</i> reduced muscle glucose uptake. <b>Conclusions</b>: The data provides evidence of impaired muscle development predisposing LBW individuals to T2D is linked to and potentially caused by distinct DNA methylation and transcriptional changes including down regulation of <i>HDAC7</i> and <i>FYN</i> in their immature myoblast stem cells.
DOI: 10.6084/m9.figshare.13385267
title: IBTrACS

description: The trajectory of the 2017 TC HATO
DOI: 10.6084/m9.figshare.13385267.v1
title: IBTrACS

description: The trajectory of the 2017 TC HATO
DOI: 10.6084/m9.figshare.13385327
title: Geomagnetic and solar data

description: Geomagnetic and solar data during 16 - 26 August 2017<br>
DOI: 10.6084/m9.figshare.13385318
title: Sanya Ionosonde Data

description: Ionosonde data at the Sanya ionosonde station in 2017
DOI: 10.6084/m9.figshare.13385318.v1
title: Sanya Ionosonde Data

description: Ionosonde data at the Sanya ionosonde station in 2017
DOI: 10.6084/m9.figshare.13385279
title: GPS data in HATO

description: The GPS stations, including HKLT, HKNP, HKOH, HKSC, and HKWS from Hong Kong SatRef network stations.<br>Time duration is 16 - 26 August 2017<br>
DOI: 10.5281/zenodo.4326601
title: Processed TCGA BRCA and METABRIC datasets used in the Moanna manuscript

description: This dataset consists of the processed multi-omics data and clinical labels used for training and evaluating Moanna (https://github.com/rlupat/moanna). This dataset is processed based on raw files downloaded from cbioportal. (training) http://download.cbioportal.org/brca_metabric.tar.gz (testing) http://download.cbioportal.org/brca_tcga_pan_can_atlas_2018.tar.gz
description: {"references": ["Curtis, C., et al., The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups. Nature, 2012. 486(7403): p. 346-52.", "Pereira, B., et al., The somatic mutation profiles of 2,433 breast cancers refine their genomic and transcriptomic landscapes. Nature Communications, 2016. 7(1): p. 11479.", "The Cancer Genome Atlas Research Network, Comprehensive molecular portraits of human breast tumours. Nature, 2012. 490(7418): p. 61-70.", "Ciriello, G., et al., Comprehensive Molecular Portraits of Invasive Lobular Breast Cancer. Cell, 2015. 163(2): p. 506-19.", "Cerami, E., et al., The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data. Cancer Discov, 2012. 2(5): p. 401-4.", "Gao, J., et al., Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal. Sci Signal, 2013. 6(269): p. pl1."]}
DOI: 10.5281/zenodo.4326234
title: Near surface softening and healing in eastern Honshu associated with the 2011 Tohoku-Oki Earthquake: Research data and code

description: The zip file named 'mainshock.zip' contains the Matlab codes and seismic data for reproducing the results of Figure 2. The Excel file named 'Source Data.xls' contains the raw data of Figures 3 and 4.
DOI: 10.5281/zenodo.4325486
title: Near surface softening and healing in eastern Honshu associated with the 2011 Tohoku-Oki Earthquake: Research data and code

description: The zip file named 'mainshock.zip' contains the Matlab codes and seismic data for reproducing the results of Figure 2. The Excel file named 'Source Data.xls' contains the raw data of Figures 3 and 4.