cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.6021716
title: Supplementary Material for: Personalized Statin Therapy and Coronary Atherosclerotic Plaque Burden in Asymptomatic Low/Intermediate-Risk Individuals

description: <b><i>Background:</i></b> Current guidelines for the primary prevention of atherosclerotic cardiovascular disease are based on the estimation of a predicted 10-year cardiovascular disease risk and the average relative risk reduction estimates from statin trials. In the clinical setting, however, decision-making is better informed by the expected benefit for the individual patient, which is typically lacking. Consequently, a personalized statin benefit approach based on absolute risk reduction over 10 years (ARR<sub>10</sub> benefit threshold ≥2.3%) has been proposed as a novel approach. However, how this benefit threshold relates with coronary plaque burden in asymptomatic individuals with low/intermediate cardiovascular disease risk is unknown. <b><i>Aims:</i></b> In this study, we compared the predicted ARR<sub>10</sub> obtained in each individual with plaque burden detected by coronary computed tomography angiography. <b><i>Methods and Results:</i></b> Plaque burden (segment volume score, segment stenosis score, and segment involvement score) was assessed in prospectively recruited asymptomatic subjects (<i>n</i> = 70; 52% male; median age 56 years [interquartile range 51–64 years]) with low/intermediate Framingham risk score (&lt; 20%). The expected ARR<sub>10</sub> with statin in the entire cohort was 2.7% (1.5–4.6%) with a corresponding number needed to treat over 10 years of 36 (22–63). In subjects with an ARR<sub>10</sub> benefit threshold ≥2.3% (vs. &lt; 2.3%), plaque burden was significantly higher (<i>p</i> = 0.02). <b><i>Conclusion:</i></b> These findings suggest that individuals with higher coronary plaque burden are more likely to get greater benefit from statin therapy even among asymptomatic individuals with low cardiovascular risk.
DOI: 10.6084/m9.figshare.6021644
title: Transcriptional mechanisms linking hypoxia and expression of inositol 1,4,5-trisphosphate (IP3) receptors

description: Background and Purpose Glioblastoma multiforme (GBM) is the most clinically aggressive form of glioma. Hypoxic regions were observed in GBM biopsies. Hypoxia appeared to be correlated with the aggressiveness of glioma. Preliminary data showed that type 2 IP<sub>3</sub> receptor was downregulated following hypoxia. I hypothesised that the down-regulation is mediated through hypoxia-inducible factor (HIF)-1-mediated transcriptional effects. Experimental Approach Sub-confluent human U87 glioma cells were cultured in normoxia and treated with either vehicle control or the hypoxia-mimicking agent desferrioxamine (DFO; 0.5 mM) for 24 hours. Cells were also cultured in hypoxia and treated with either vehicle control or the HIF-1α translational inhibitor KC7F2 (40 μM). Two-step quantitative reverse transcription polymerase chain reaction was used to quantify the transcript levels of IP<sub>3</sub> receptor subtypes after the treatments. The levels were normalised to that of β-actin and TATA-binding protein. Key Results In contrast to previous reports, expression of β-actin was not stable in hypoxia and is on its own unsuitable to be used as the reference gene. Hypoxia did not significant alter expression of individual IP<sub>3</sub> receptor subtypes transcriptionally. Treatment with DFO upregulated transcript level of type 3 IP<sub>3</sub> receptor only (<i>p</i> = 0.0082). KC7F2 treatment reduced HIF-1α level by three-fold but did not affect the observed upregulation. Conclusions and Implications Hypoxia-mediated down-regulation of expression of type 2 IP<sub>3</sub> receptor does not rely on transcriptional mechanisms. Further studies of its expression on a protein level can be done to test the proposition that it is dependent on co-translational or post-translational mechanisms.
DOI: 10.6084/m9.figshare.6021644.v1
title: Transcriptional mechanisms linking hypoxia and expression of inositol 1,4,5-trisphosphate (IP3) receptors

description: Background and Purpose Glioblastoma multiforme (GBM) is the most clinically aggressive form of glioma. Hypoxic regions were observed in GBM biopsies. Hypoxia appeared to be correlated with the aggressiveness of glioma. Preliminary data showed that type 2 IP<sub>3</sub> receptor was downregulated following hypoxia. I hypothesised that the down-regulation is mediated through hypoxia-inducible factor (HIF)-1-mediated transcriptional effects. Experimental Approach Sub-confluent human U87 glioma cells were cultured in normoxia and treated with either vehicle control or the hypoxia-mimicking agent desferrioxamine (DFO; 0.5 mM) for 24 hours. Cells were also cultured in hypoxia and treated with either vehicle control or the HIF-1α translational inhibitor KC7F2 (40 μM). Two-step quantitative reverse transcription polymerase chain reaction was used to quantify the transcript levels of IP<sub>3</sub> receptor subtypes after the treatments. The levels were normalised to that of β-actin and TATA-binding protein. Key Results In contrast to previous reports, expression of β-actin was not stable in hypoxia and is on its own unsuitable to be used as the reference gene. Hypoxia did not significant alter expression of individual IP<sub>3</sub> receptor subtypes transcriptionally. Treatment with DFO upregulated transcript level of type 3 IP<sub>3</sub> receptor only (<i>p</i> = 0.0082). KC7F2 treatment reduced HIF-1α level by three-fold but did not affect the observed upregulation. Conclusions and Implications Hypoxia-mediated down-regulation of expression of type 2 IP<sub>3</sub> receptor does not rely on transcriptional mechanisms. Further studies of its expression on a protein level can be done to test the proposition that it is dependent on co-translational or post-translational mechanisms.
DOI: 10.6084/m9.figshare.6021623
title: Expression levels of selected genes can predict individual rheumatoid arthritis patient response to tumor necrosis factor alpha blocker treatment

description: <b>Objectives:</b> Rheumatoid arthritis (RA) patients have many therapeutic options; however, tools to predict individual patient response are limited. The Genefron personal diagnostic kit, developed by analyzing large datasets, utilizes selected interferon stimulated gene expressions to predict treatment response. This study evaluates the kit’s prediction accuracy of individual RA patients’ response to tumor necrosis alpha (TNFα) blockers. <b>Methods:</b> A retrospective analysis was performed on RA patients reported in published datasets. A prospective analysis assessed RA patients, before and 3 months after starting a TNFα blocker. Clinical response was evaluated according to EULAR response criteria. Blood samples were obtained before starting treatment and were analyzed utilizing the kit which measures expression levels of selected genes by quantitative real time polymerase chain reaction (PCR). ROC analysis was applied to the published datasets and the prospective data. <b>Results:</b> The Genefron kit analysis of retrospective data predicted the response to a TNFα blocker in 53 of 61 RA patients (86.8% accuracy). In the prospective analysis, the kit predicted the response in 16 of 18 patients (89% accuracy) achieving a EULAR moderate response, and in 15 of 18 patients achieving a EULAR good response (83.3% accuracy). ROC analysis applied to the two published datasets yielded an AUC of 0.89. ROC analysis applied to the prospective data yielded an AUC of 0.83 (sensitivity – 100%, specificity – 75%) The statistical power obtained in the prospective study was .9. <b>Conclusion:</b> The diagnostic kit predicted the response to TNFα blockers in a high percentage of patients assessed retrospectively or prospectively. This personal kit may guide selection of a suitable biological drug for the individual RA patient.
DOI: 10.6084/m9.figshare.6021623.v1
title: Expression levels of selected genes can predict individual rheumatoid arthritis patient response to tumor necrosis factor alpha blocker treatment

description: <b>Objectives:</b> Rheumatoid arthritis (RA) patients have many therapeutic options; however, tools to predict individual patient response are limited. The Genefron personal diagnostic kit, developed by analyzing large datasets, utilizes selected interferon stimulated gene expressions to predict treatment response. This study evaluates the kit’s prediction accuracy of individual RA patients’ response to tumor necrosis alpha (TNFα) blockers. <b>Methods:</b> A retrospective analysis was performed on RA patients reported in published datasets. A prospective analysis assessed RA patients, before and 3 months after starting a TNFα blocker. Clinical response was evaluated according to EULAR response criteria. Blood samples were obtained before starting treatment and were analyzed utilizing the kit which measures expression levels of selected genes by quantitative real time polymerase chain reaction (PCR). ROC analysis was applied to the published datasets and the prospective data. <b>Results:</b> The Genefron kit analysis of retrospective data predicted the response to a TNFα blocker in 53 of 61 RA patients (86.8% accuracy). In the prospective analysis, the kit predicted the response in 16 of 18 patients (89% accuracy) achieving a EULAR moderate response, and in 15 of 18 patients achieving a EULAR good response (83.3% accuracy). ROC analysis applied to the two published datasets yielded an AUC of 0.89. ROC analysis applied to the prospective data yielded an AUC of 0.83 (sensitivity – 100%, specificity – 75%) The statistical power obtained in the prospective study was .9. <b>Conclusion:</b> The diagnostic kit predicted the response to TNFα blockers in a high percentage of patients assessed retrospectively or prospectively. This personal kit may guide selection of a suitable biological drug for the individual RA patient.
DOI: 10.6084/m9.figshare.6021599
title: Supplementary Material for: Effect of Sodium Thiosulfate on Arterial Stiffness in End-Stage Renal Disease Patients Undergoing Chronic Hemodialysis (Sodium Thiosulfate-Hemodialysis Study): A Randomized Controlled Trial

description: <b><i>Background:</i></b> Arterial stiffness (AS) and vascular calcification are significantly related to a high cardiovascular mortality risk in hemodialysis (HD) patients. Intravenous sodium thiosulfate (IV STS) can prevent and delay the vascular calcification progression in uremic states; however, the STS effect on AS has not been assessed. This study aimed to evaluate the STS efficacy on vascular calcification and AS in HD patients. <b><i>Methods:</i></b> Fifty HD patients with abnormal AS, as measured via the cardio-ankle vascular index (CAVI ≥8), were prospectively randomized to open-label 12.5 g IV STS during the last HD hour twice weekly for 6 months (<i>n</i> = 24) or the usual care (control group; <i>n</i> = 26). Patients and treating physicians were not blinded. The CAVI, coronary artery calcification (CAC) score, hemodynamics, and biochemical parameters were measured at the baseline and at 3 and 6 months. <b><i>Results:</i></b> All the baseline parameters were comparable. The IV STS significantly reduced the CAVI when compared to the control group (mean CAVI difference = –0.53; 95% CI –1.00 to –0.06; <i>p</i> = 0.03). A significant CAVI improvement was seen in those patients without diabetes mellitus. The natural logarithm of the CAC volume score was significantly increased in the control group. The high sensitivity C-reactive protein level was slightly lowered in the IV STS group (not significant). <b><i>Conclusion:</i></b> The intradialytic STS treatment significantly reduced the AS, as measured by the CAVI, and stabilized the vascular calcification in the HD patients. STS may be a novel therapeutic strategy for delaying and treating the structural and functional vascular wall abnormalities in HD patients.
DOI: 10.6084/m9.figshare.6021599.v1
title: Supplementary Material for: Effect of Sodium Thiosulfate on Arterial Stiffness in End-Stage Renal Disease Patients Undergoing Chronic Hemodialysis (Sodium Thiosulfate-Hemodialysis Study): A Randomized Controlled Trial

description: <b><i>Background:</i></b> Arterial stiffness (AS) and vascular calcification are significantly related to a high cardiovascular mortality risk in hemodialysis (HD) patients. Intravenous sodium thiosulfate (IV STS) can prevent and delay the vascular calcification progression in uremic states; however, the STS effect on AS has not been assessed. This study aimed to evaluate the STS efficacy on vascular calcification and AS in HD patients. <b><i>Methods:</i></b> Fifty HD patients with abnormal AS, as measured via the cardio-ankle vascular index (CAVI ≥8), were prospectively randomized to open-label 12.5 g IV STS during the last HD hour twice weekly for 6 months (<i>n</i> = 24) or the usual care (control group; <i>n</i> = 26). Patients and treating physicians were not blinded. The CAVI, coronary artery calcification (CAC) score, hemodynamics, and biochemical parameters were measured at the baseline and at 3 and 6 months. <b><i>Results:</i></b> All the baseline parameters were comparable. The IV STS significantly reduced the CAVI when compared to the control group (mean CAVI difference = –0.53; 95% CI –1.00 to –0.06; <i>p</i> = 0.03). A significant CAVI improvement was seen in those patients without diabetes mellitus. The natural logarithm of the CAC volume score was significantly increased in the control group. The high sensitivity C-reactive protein level was slightly lowered in the IV STS group (not significant). <b><i>Conclusion:</i></b> The intradialytic STS treatment significantly reduced the AS, as measured by the CAVI, and stabilized the vascular calcification in the HD patients. STS may be a novel therapeutic strategy for delaying and treating the structural and functional vascular wall abnormalities in HD patients.
DOI: 10.6084/m9.figshare.6021584
title: Experimental data and Analysis

description: (a) Reflection spectrum of the FBG sensing array; (b) Hilbert transform of the reflection spectrum without de-noising; (c) The first derivative of the transformed signal.
DOI: 10.6084/m9.figshare.6021563
title: Simulation data and Analysis

description: (a) The reflection spectrum of 3 FBGs; (b) The Hilbert transform; (c) The first derivative of the transformed signal
DOI: 10.6084/m9.figshare.6021563.v1
title: Simulation data and Analysis

description: (a) The reflection spectrum of 3 FBGs; (b) The Hilbert transform; (c) The first derivative of the transformed signal
DOI: 10.6084/m9.figshare.6021545
title: Simulation data and Analysis

description: (a) The reflection spectrum of 3 FBGs; (b) The Hilbert transform; (c) The first derivative of the transformed signal
DOI: 10.6084/m9.figshare.6021545.v1
title: Simulation data and Analysis.xlsx

description: (a) The reflection spectrum of 3 FBGs; (b) The Hilbert transform; (c) The first derivative of the transformed signal
DOI: 10.6084/m9.figshare.6021491
title: Male specific Dmrt1 is a candidate sex determination gene in spotted scat (Scatophagus argus)

description: Supplymentary sequences, figures and tables.
DOI: 10.6084/m9.figshare.6021491.v1
title: Male specific Dmrt1 is a candidate sex determination gene in spotted scat (Scatophagus argus)

description: Supplymentary sequences, figures and tables.
DOI: 10.6084/m9.figshare.6021401
title: Additional file 4: of The DNA methylation profile of liver tumors in C3H mice and identification of differentially methylated regions involved in the regulation of tumorigenic genes

description: Table S3. Datasets of DNA methylation and gene expression downloaded from TCGA database. (XLSX 13Â kb)
DOI: 10.6084/m9.figshare.6021401.v1
title: Additional file 4: of The DNA methylation profile of liver tumors in C3H mice and identification of differentially methylated regions involved in the regulation of tumorigenic genes

description: Table S3. Datasets of DNA methylation and gene expression downloaded from TCGA database. (XLSX 13Â kb)
DOI: 10.6084/m9.figshare.6021377
title: Additional file 3: of The DNA methylation profile of liver tumors in C3H mice and identification of differentially methylated regions involved in the regulation of tumorigenic genes

description: Table S2. List of DMRs position and methylation difference between normal and tumor liver tissues. (XLSX 317Â kb)
DOI: 10.6084/m9.figshare.6021377.v1
title: Additional file 3: of The DNA methylation profile of liver tumors in C3H mice and identification of differentially methylated regions involved in the regulation of tumorigenic genes

description: Table S2. List of DMRs position and methylation difference between normal and tumor liver tissues. (XLSX 317Â kb)
DOI: 10.6084/m9.figshare.6021356
title: Additional file 1: of Increased circulating resistin levels in early-onset breast cancer patients of normal body mass index correlate with lymph node negative involvement and longer disease free survival: a multi-center POSH cohort serum proteomics study

description: Sections 1A and 1B presenting POSH Serum Procurement SOPs. (ZIP 244 kb)
DOI: 10.6084/m9.figshare.6021356.v1
title: Additional file 1: of Increased circulating resistin levels in early-onset breast cancer patients of normal body mass index correlate with lymph node negative involvement and longer disease free survival: a multi-center POSH cohort serum proteomics study

description: Sections 1A and 1B presenting POSH Serum Procurement SOPs. (ZIP 244 kb)
DOI: 10.6084/m9.figshare.6021347
title: Additional file 1: of The DNA methylation profile of liver tumors in C3H mice and identification of differentially methylated regions involved in the regulation of tumorigenic genes

description: Table S1. Primers for bisulfite sequencing and qRT-PCR. (XLSX 10Â kb)
DOI: 10.6084/m9.figshare.6021347.v1
title: Additional file 1: of The DNA methylation profile of liver tumors in C3H mice and identification of differentially methylated regions involved in the regulation of tumorigenic genes

description: Table S1. Primers for bisulfite sequencing and qRT-PCR. (XLSX 10Â kb)
DOI: 10.6084/m9.figshare.6021284
title: Additional file 1: of Geographic assessment of access to health care in patients with cardiovascular disease in South Africa

description: Graphs showing mean distance to a health facility from a household with subject diagnosed with a heart condition for each of the waves by district. Part 1: Codes of district municipalities. Map of South Africa displaying district codes. Part 2: Mean distance in kilometres to a health facility from a household with subject diagnosed with a heart condition in the 2008 and 2010–2011 NIDS Survey wave by district, South Africa. Mean distance to health facility by district for each wave. Part 3: Mean distance in kilometres to a health facility from a household with subject diagnosed with a heart condition in the 2012 and 2014–2015 NIDS Survey wave by district, South Africa. Mean distance to health facility by district for each wave. (ZIP 707 kb)
DOI: 10.6084/m9.figshare.6021284.v1
title: Additional file 1: of Geographic assessment of access to health care in patients with cardiovascular disease in South Africa

description: Graphs showing mean distance to a health facility from a household with subject diagnosed with a heart condition for each of the waves by district. Part 1: Codes of district municipalities. Map of South Africa displaying district codes. Part 2: Mean distance in kilometres to a health facility from a household with subject diagnosed with a heart condition in the 2008 and 2010–2011 NIDS Survey wave by district, South Africa. Mean distance to health facility by district for each wave. Part 3: Mean distance in kilometres to a health facility from a household with subject diagnosed with a heart condition in the 2012 and 2014–2015 NIDS Survey wave by district, South Africa. Mean distance to health facility by district for each wave. (ZIP 707 kb)
DOI: 10.6084/m9.figshare.6021080
title: Additional file 1: of Integrative genomics identifies new genes associated with severe COPD and emphysema

description: Supplementary Methods. Table S1. Colocalization probability and regulatory annotations for colocalized variants using corresponding GWAS and Lung-eQTL consortium datasets (see Excel file). Table S2. Colocalization probability and regulatory annotations for colocalized variants using corresponding GWAS and GTEx eQTL (blood and lung) datasets (see Excel file). Table S3. Additional imputed gene expression association results at previously described GWAS significant loci. Table S4. Result of association analysis between imputed gene expression and moderate to severe COPD of reported genes from severe COPD. Table S5. Differential expression analysis between COPD and controls using blood RNA-seq in COPDGene. Table S6. Differential expression analysis of quantitative emphysema using blood RNA-seq in COPDGene. Table S7. Differential expression analysis between severe COPD and controls using lung tissues. Table S8. Differential expression analysis of %LAA-950 and Perc15 using lung tissues. Table S9. T-cell-associated gene sets from Reactome using a ranked gene list from associations of %LAA-950 (DGN-Blood). Table S10. Covariate adjustments for differential expression analysis. Figure S1. Regional association plots within 50kb of LILRA3. GWAS of %LAA-950 and blood eQTL were shown in upper panel. Chromatin states and epigenomic marks of normal human lung fibroblast were shown in lower panel (see Supplementary Methods). Figure S2. Regional association plots within 50kb of DCBLD1. GWAS of %LAA-950 and lung eQTL were shown in upper panel. Chromatin states and epigenomic marks of normal human lung fibroblast were shown in lower panel (see Supplementary Methods). Figure S3. Scatter plot of effect size of significant SNPs from eQTL studies of blood and lung tissue for FAM13A. Figure S4. Contribution of each FAM13A SNP in prediction models to overall association statistics. (ZIP 758 kb)
DOI: 10.6084/m9.figshare.6021080.v1
title: Additional file 1: of Integrative genomics identifies new genes associated with severe COPD and emphysema

description: Supplementary Methods. Table S1. Colocalization probability and regulatory annotations for colocalized variants using corresponding GWAS and Lung-eQTL consortium datasets (see Excel file). Table S2. Colocalization probability and regulatory annotations for colocalized variants using corresponding GWAS and GTEx eQTL (blood and lung) datasets (see Excel file). Table S3. Additional imputed gene expression association results at previously described GWAS significant loci. Table S4. Result of association analysis between imputed gene expression and moderate to severe COPD of reported genes from severe COPD. Table S5. Differential expression analysis between COPD and controls using blood RNA-seq in COPDGene. Table S6. Differential expression analysis of quantitative emphysema using blood RNA-seq in COPDGene. Table S7. Differential expression analysis between severe COPD and controls using lung tissues. Table S8. Differential expression analysis of %LAA-950 and Perc15 using lung tissues. Table S9. T-cell-associated gene sets from Reactome using a ranked gene list from associations of %LAA-950 (DGN-Blood). Table S10. Covariate adjustments for differential expression analysis. Figure S1. Regional association plots within 50kb of LILRA3. GWAS of %LAA-950 and blood eQTL were shown in upper panel. Chromatin states and epigenomic marks of normal human lung fibroblast were shown in lower panel (see Supplementary Methods). Figure S2. Regional association plots within 50kb of DCBLD1. GWAS of %LAA-950 and lung eQTL were shown in upper panel. Chromatin states and epigenomic marks of normal human lung fibroblast were shown in lower panel (see Supplementary Methods). Figure S3. Scatter plot of effect size of significant SNPs from eQTL studies of blood and lung tissue for FAM13A. Figure S4. Contribution of each FAM13A SNP in prediction models to overall association statistics. (ZIP 758 kb)