cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.8319902
title: Supplementary Material for: Socioeconomic Costs and Health Inequalities from Psoriasis: A Cohort Study

description: <b><i>Background:</i></b> To date, there are no nationwide studies of the social and economic burden of psoriasis to patients in Denmark. Incentives for health care management based on patient-related outcomes and value (IMPROVE) in psoriasis and psoriatic arthritis is a project aimed at assisting movement from activity-based to outcome-based health care management. One of the key objectives in IMPROVE is to describe the disease-associated socioeconomic burden of psoriasis. <b><i>Methods:</i></b> A case-matched study of the impact of psoriasis on patients’ income, employment and health care costs in Denmark was performed. The IMPROVE study was a retrospective analysis of patients with a hospital diagnosis of psoriasis identified from the Danish National Patient Registry (NPR). In total, 13,025 psoriasis patients and 25,629 matched controls were identified from the NPR. Data from psoriasis patients and matched controls were compared for social and economic factors including income, employment, health care costs and risk of comorbidities. <b><i>Results:</i></b> Psoriasis was associated with increased health care costs (mean annual costs +116% compared to control, <i>p</i> &lt; 0.001), peaking in the year of referral to hospital for psoriasis and sustained thereafter. Both direct and indirect costs were significantly higher for patients with psoriasis than controls (<i>p</i> &lt; 0.001). In the years before and immediately following hospital diagnosis, the rates of employment were lower in psoriasis patients than controls. Comorbidities, including cardiovascular (odds ratio 1.93 [95% CI 1.77–2.09]) and psychiatric conditions (odds ratio 2.61 [95% CI 2.30–2.97]), were more prevalent in patients with psoriasis than controls. <b><i>Conclusion:</i></b> In Denmark, psoriasis has a significant impact on health care costs, income and employment, and is associated with a range of comorbidities.
DOI: 10.6084/m9.figshare.8319902.v1
title: Supplementary Material for: Socioeconomic Costs and Health Inequalities from Psoriasis: A Cohort Study

description: <b><i>Background:</i></b> To date, there are no nationwide studies of the social and economic burden of psoriasis to patients in Denmark. Incentives for health care management based on patient-related outcomes and value (IMPROVE) in psoriasis and psoriatic arthritis is a project aimed at assisting movement from activity-based to outcome-based health care management. One of the key objectives in IMPROVE is to describe the disease-associated socioeconomic burden of psoriasis. <b><i>Methods:</i></b> A case-matched study of the impact of psoriasis on patients’ income, employment and health care costs in Denmark was performed. The IMPROVE study was a retrospective analysis of patients with a hospital diagnosis of psoriasis identified from the Danish National Patient Registry (NPR). In total, 13,025 psoriasis patients and 25,629 matched controls were identified from the NPR. Data from psoriasis patients and matched controls were compared for social and economic factors including income, employment, health care costs and risk of comorbidities. <b><i>Results:</i></b> Psoriasis was associated with increased health care costs (mean annual costs +116% compared to control, <i>p</i> &lt; 0.001), peaking in the year of referral to hospital for psoriasis and sustained thereafter. Both direct and indirect costs were significantly higher for patients with psoriasis than controls (<i>p</i> &lt; 0.001). In the years before and immediately following hospital diagnosis, the rates of employment were lower in psoriasis patients than controls. Comorbidities, including cardiovascular (odds ratio 1.93 [95% CI 1.77–2.09]) and psychiatric conditions (odds ratio 2.61 [95% CI 2.30–2.97]), were more prevalent in patients with psoriasis than controls. <b><i>Conclusion:</i></b> In Denmark, psoriasis has a significant impact on health care costs, income and employment, and is associated with a range of comorbidities.
DOI: 10.6084/m9.figshare.8319878
title: Shape files

description: Shape files for the code and analysis in "Landscape-level validation of allometric relationships for carbon stock estimation reveals bias driven by soil type"
DOI: 10.6084/m9.figshare.8319875
title: Supplementary Material for: Urotensin II Induces Mice Skeletal Muscle Atrophy Associated with Enhanced Autophagy and Inhibited Irisin Precursor (Fibronectin Type III Domain Containing 5) Expression in Chronic Renal Failure

description: <b><i>Background/Aims:</i></b> Skeletal muscle atrophy is one of the main manifestations of protein energy wasting. We hypothesized that urotensin II (UII) can lead to skeletal muscle atrophy through upregulating autophagy and affecting Irisin precursor fibronectin type III domain containing 5 (FNDC5) expressions. <b><i>Methods:</i></b> Three animal models (the sham operation, wild-type C57BL/6 mice with 5/6 nephrectomy, <i>UII</i> receptor (<i>UT</i>) gene knockout (UTKO) mice with 5/6 nephrectomy) were designed. Skeletal muscle weight, cross-sectional area (CSA) along with UII, FNDC5, LC3, and p62 expression were investigated. C2C12 cells were differentiated for up to 4 days into myotubes. These cells were then exposed to different UII concentrations (10<sup>–5</sup> to 10<sup>–7</sup> M) for 6–12 h and analyzed for the expressions of autophagic markers. These cells were also exposed to the same predetermined UII concentrations for 48–72 h and analyzed for the FNDC5 expression. Myotube diameter was measured. <b><i>Results:</i></b> Upregulation of UII expression in skeletal muscle tissue was accompanied by reduced muscle weight and skeletal muscle CSA in the 2 posterior limbs, upregulated autophagy markers expression, and downregulated FNDC5 expression in 5/6 nephrectomy mice. The decrease of skeletal muscle weight, skeletal muscle CSA, downregulation of FNDC5 expression, and the upregulation of autophagy markers were inhibited in UTKO with 5/6 nephrectomy mice. Our in vitro<i></i>study showed that UII could directly decrease myotube diameter, induce autophagy markers upregulation, and inhibit expression of FNDC5. When <i>UII</i> receptor gene was interfered by UT-specific siRNA, UII induced autophagy markers upregulation and FNDC5 downregulation were inhibited. <b><i>Conclusion:</i></b> We are the first to verify UII induces mice skeletal muscle atrophy associated with enhanced skeletal muscle autophagy and inhibited FNDC5 expression in chronic renal failure.
DOI: 10.6084/m9.figshare.8319872
title: Data subset for the analyses and figures

description: Data subset (16 of 102 sites) from the analysis and figures in "Landscape-level validation of allometric relationships for carbon stock estimation reveals bias driven by soil type"
DOI: 10.6084/m9.figshare.8319875.v1
title: Supplementary Material for: Urotensin II Induces Mice Skeletal Muscle Atrophy Associated with Enhanced Autophagy and Inhibited Irisin Precursor (Fibronectin Type III Domain Containing 5) Expression in Chronic Renal Failure

description: <b><i>Background/Aims:</i></b> Skeletal muscle atrophy is one of the main manifestations of protein energy wasting. We hypothesized that urotensin II (UII) can lead to skeletal muscle atrophy through upregulating autophagy and affecting Irisin precursor fibronectin type III domain containing 5 (FNDC5) expressions. <b><i>Methods:</i></b> Three animal models (the sham operation, wild-type C57BL/6 mice with 5/6 nephrectomy, <i>UII</i> receptor (<i>UT</i>) gene knockout (UTKO) mice with 5/6 nephrectomy) were designed. Skeletal muscle weight, cross-sectional area (CSA) along with UII, FNDC5, LC3, and p62 expression were investigated. C2C12 cells were differentiated for up to 4 days into myotubes. These cells were then exposed to different UII concentrations (10<sup>–5</sup> to 10<sup>–7</sup> M) for 6–12 h and analyzed for the expressions of autophagic markers. These cells were also exposed to the same predetermined UII concentrations for 48–72 h and analyzed for the FNDC5 expression. Myotube diameter was measured. <b><i>Results:</i></b> Upregulation of UII expression in skeletal muscle tissue was accompanied by reduced muscle weight and skeletal muscle CSA in the 2 posterior limbs, upregulated autophagy markers expression, and downregulated FNDC5 expression in 5/6 nephrectomy mice. The decrease of skeletal muscle weight, skeletal muscle CSA, downregulation of FNDC5 expression, and the upregulation of autophagy markers were inhibited in UTKO with 5/6 nephrectomy mice. Our in vitro<i></i>study showed that UII could directly decrease myotube diameter, induce autophagy markers upregulation, and inhibit expression of FNDC5. When <i>UII</i> receptor gene was interfered by UT-specific siRNA, UII induced autophagy markers upregulation and FNDC5 downregulation were inhibited. <b><i>Conclusion:</i></b> We are the first to verify UII induces mice skeletal muscle atrophy associated with enhanced skeletal muscle autophagy and inhibited FNDC5 expression in chronic renal failure.
DOI: 10.6084/m9.figshare.8319824
title: KUT Infrasound March 2018

description: This data is the original data from the KISONS database website (Kochi University of Technology Infrasound Observation Network System), hhtp://infrasound.kochi-tech.ac.jp/<br>
DOI: 10.6084/m9.figshare.8319872.v2
title: Data subset for the analyses and figures

description: Data subset (16 of 102 sites) from the analysis and figures in "Landscape-level validation of allometric relationships for carbon stock estimation reveals bias driven by soil type"
DOI: 10.6084/m9.figshare.8319872.v1
title: Data subset for the analyses and figures

description: Data subset (16 of 102 sites) from the analysis and figures in "Landscape-level validation of allometric relationships for carbon stock estimation reveals bias driven by soil type"
DOI: 10.6084/m9.figshare.8319824.v2
title: KUT Infrasound March 2018

description: This data is the original data from the KISONS database website (Kochi University of Technology Infrasound Observation Network System), hhtp://infrasound.kochi-tech.ac.jp/<br>
DOI: 10.6084/m9.figshare.8319824.v1
title: KUT_Infrasound_March2018

description: This data is the original data from the KISONS database website (Kochi University of Technology Infrasound Observation Network System), hhtp://infrasound.mydns.jp/infrasound/graph.php<br>
DOI: 10.6084/m9.figshare.8319758
title: Travel times between SA2s and hospitals (pkl)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the travel time in seconds to each hospital (time_to_X columns, where X is the Hospital_ID).
DOI: 10.6084/m9.figshare.8319755
title: Travel times between SA2s and hospitals (csv)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the travel time in seconds to each hospital (time_to_X columns, where X is the Hospital_ID).
DOI: 10.6084/m9.figshare.8319800
title: Empathic accuracy

description: The datasets contains information on empathic accuracy, personality, and health status of chronic pain patients and informal caregivers
DOI: 10.6084/m9.figshare.8319758.v1
title: Travel times between SA2s and hospitals (pkl)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the travel time in seconds to each hospital (time_to_X columns, where X is the Hospital_ID).
DOI: 10.6084/m9.figshare.8319755.v1
title: Travel times between SA2s and hospitals (csv)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the travel time in seconds to each hospital (time_to_X columns, where X is the Hospital_ID).
DOI: 10.6084/m9.figshare.8319800.v1
title: Empathic accuracy

description: The datasets contains information on empathic accuracy, personality, and health status of chronic pain patients and informal caregivers
DOI: 10.6084/m9.figshare.8319752
title: Shortest travel time between SA2s and any hospital (pkl)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the average shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) to any hospital for the residents of a SA2.
DOI: 10.6084/m9.figshare.8319749
title: Shortest travel time between SA2s and any hospital (csv)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the average shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) to any hospital for the residents of a SA2.
DOI: 10.6084/m9.figshare.8319746
title: Shortest travel time between MBs and any hospital (csv)

description: Contains the 2016 mesh block codes (MB_CODE16) and the shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) from the mesh block’s centroid to any hospital.
DOI: 10.6084/m9.figshare.8319752.v1
title: Shortest travel time between SA2s and any hospital (pkl)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the average shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) to any hospital for the residents of a SA2.
DOI: 10.6084/m9.figshare.8319743
title: Shortest travel time between MBs and any hospital (pkl)

description: Contains the 2016 mesh block codes (MB_CODE16) and the shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) from the mesh block’s centroid to any hospital.
DOI: 10.6084/m9.figshare.8319749.v1
title: Shortest travel time between SA2s and any hospital (csv)

description: Contains the 2016 statistical area level 2 codes (SA2_5DIG16) and the average shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) to any hospital for the residents of a SA2.
DOI: 10.6084/m9.figshare.8319743.v1
title: Shortest travel time between MBs and any hospital (pkl)

description: Contains the 2016 mesh block codes (MB_CODE16) and the shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) from the mesh block’s centroid to any hospital.
DOI: 10.6084/m9.figshare.8319746.v1
title: Shortest travel time between MBs and any hospital (csv)

description: Contains the 2016 mesh block codes (MB_CODE16) and the shortest time in seconds (shortest_time_sec) and minutes (shortest_time_min) from the mesh block’s centroid to any hospital.
DOI: 10.6084/m9.figshare.8319737
title: Hospital IDs, names and coordinates (csv)

description: Names of hospitals in Australia, their geographic coordinates (Longitude and Latitude) and an assigned hospital identifier between 1 and 1,011 (Hospital_ID).
DOI: 10.6084/m9.figshare.8319740
title: Travel times between MBs and hospitals (pkl)

description: Contains the 2016 mesh block codes (MB_CODE16) and the travel time in seconds to each hospital (time_to_X columns, where X is the Hospital_ID).
DOI: 10.6084/m9.figshare.8319734
title: Mesh block centroids (csv)

description: 2016 mesh block codes (MB_CODE16 column), names and codes of the corresponding SA2 (SA2_NAME16 and SA2_5DIG16), centroid longitude (xcoord) and latitude (ycoord).
DOI: 10.6084/m9.figshare.8319740.v1
title: Travel times between MBs and hospitals (pkl)

description: Contains the 2016 mesh block codes (MB_CODE16) and the travel time in seconds to each hospital (time_to_X columns, where X is the Hospital_ID).
DOI: 10.6084/m9.figshare.8319737.v1
title: Hospital IDs, names and coordinates (csv)

description: Names of hospitals in Australia, their geographic coordinates (Longitude and Latitude) and an assigned hospital identifier between 1 and 1,011 (Hospital_ID).
DOI: 10.6084/m9.figshare.8319704
title: Supplementary Material for: Markers of Oxidative Stress and Endothelial Dysfunction Predict Haemodialysis Patients Survival

description: <b><i>Introduction:</i></b> Overall survival of patients with end-stage renal disease (ESRD) remains poor. Oxidative stress is one of the major risk factors associated with mortality in this patient group. As glutathione S-transferases (GST) are well-established antioxidants, we hypothesized that a model including GST gene polymorphisms, oxidative damage byproducts and cell adhesion markers has a prognostic role in ESRD patient survival. <b><i>Methods:</i></b> A prospective study of 199 patients with ESRD on haemodialysis was conducted. GST genotype, oxidative stress byproducts and cell adhesion molecules were measured in plasma. Multivariate Cox regression and Kaplan-Meier survival analyses were performed to test the predictive ability of these parameters in the 8-year follow-up period. <b><i>Results:</i></b> GSTM1-null genotype was associated with significantly shorter overall (HR 1.6, <i>p</i> = 0.018) and cardiovascular-specific (HR 2.1, <i>p</i> = 0.010) survival. Oxidative stress byproducts (advanced oxidation protein products [AOPP], prooxidant-antioxidant balance [PAB], malondialdehyde [MDA]) and cell adhesion molecules (soluble vascular cell adhesion molecule-1 [sVCAM-1] and soluble intercellular adhesion molecule-1 [sICAM-1]) demonstrated a significant predictive role in terms of overall and cardiovascular survival. When 6 biomarkers (GSTM1 genotype, high AOPP/PAB/MDA/­sVCAM-1/sICAM-1) were combined into a scoring model, a significantly shorter overall and cardiovascular survival was observed for patients with the highest score (<i>p</i> &lt; 0.001). <b><i>Conclusion:</i></b> We identified a novel panel of biomarkers that can be utilized in predicting survival in ESRD patients. This biomarker signature could enable better monitoring of patients and stratification into appropriate treatment groups.
DOI: 10.6084/m9.figshare.8319734.v1
title: Mesh block centroids (csv)

description: 2016 mesh block codes (MB_CODE16 column), names and codes of the corresponding SA2 (SA2_NAME16 and SA2_5DIG16), centroid longitude (xcoord) and latitude (ycoord).
DOI: 10.6084/m9.figshare.8319695
title: Supplementary Material for: GFR-Specific versus GFR-Agnostic Cutoffs for Parathyroid Hormone and Fibroblast Growth Factor-23 in Advanced Chronic Kidney Disease

description: <b><i>Background:</i></b> In the majority of patients with advanced chronic kidney disease (CKD), values of parathyroid hormone (PTH1–84) and fibroblast growth factor 23 (FGF-23) exceed the normal reference range, potentially as an appropriate adaptation to reduced glomerular filtration rate (GFR). We tested whether GFR-specific cutoffs for PTH1–84 and FGF-23 could better identify patients with inappropriately high PTH1–84 and FGF-23 for their degree of CKD and thereby improve prognostication of clinical outcomes compared to a uniform threshold. <b><i>Methods:</i></b> Prospective pan-Canadian cohort of 1,812 patients with mean estimated GFR (eGFR) 28.9 mL/min/1.73 m<sup>2</sup> followed for a median of 52 months. Repeated log-rank tests were used to identify optimal cutoffs for PTH1–84 and FGF-23 within eGFR strata (&lt;20, 20–29 and ≥30 mL/min/1.73 m<sup>2</sup>) that maximally differentiated high- and low-risk populations for (1) cardiovascular (CV) events (fatal or nonfatal myocardial infarction, coronary revascularization, stroke, heart failure) and (2) renal events (initiation of chronic renal replacement therapy). In multivariable models, we examined the association between ­GFR-specific cutoffs and outcomes and compared their added prognostic value to existing uniform thresholds. <b><i>Results:</i></b> Risk-based cutoffs for PTH1–84 and FGF-23 increased in a graded fashion with decreasing eGFR. Among patients with eGFR &lt;20 mL/min/1.73 m<sup>2</sup>, CV risk-based cutoffs for PTH1–84 and FGF-23 were 3.4 and 5.5 times the upper limit of normal, respectively, and reclassified 31.9 and 35.1% of patients when added to a multivariable base model for CV events. In contrast, the addition of PTH1–84 and FGF-23 to the base model using uniform cutoffs failed to reclassify such patients. Similar findings were demonstrated for renal outcomes. <b><i>Conclusion:</i></b> GFR-specific risk-based cutoffs for PTH1–84 and FGF-23 may facilitate more meaningful risk stratification in advanced CKD than current GFR-agnostic reference ranges derived from healthy adults. This may be most applicable in those with severely reduced GFR.
DOI: 10.6084/m9.figshare.8319704.v1
title: Supplementary Material for: Markers of Oxidative Stress and Endothelial Dysfunction Predict Haemodialysis Patients Survival

description: <b><i>Introduction:</i></b> Overall survival of patients with end-stage renal disease (ESRD) remains poor. Oxidative stress is one of the major risk factors associated with mortality in this patient group. As glutathione S-transferases (GST) are well-established antioxidants, we hypothesized that a model including GST gene polymorphisms, oxidative damage byproducts and cell adhesion markers has a prognostic role in ESRD patient survival. <b><i>Methods:</i></b> A prospective study of 199 patients with ESRD on haemodialysis was conducted. GST genotype, oxidative stress byproducts and cell adhesion molecules were measured in plasma. Multivariate Cox regression and Kaplan-Meier survival analyses were performed to test the predictive ability of these parameters in the 8-year follow-up period. <b><i>Results:</i></b> GSTM1-null genotype was associated with significantly shorter overall (HR 1.6, <i>p</i> = 0.018) and cardiovascular-specific (HR 2.1, <i>p</i> = 0.010) survival. Oxidative stress byproducts (advanced oxidation protein products [AOPP], prooxidant-antioxidant balance [PAB], malondialdehyde [MDA]) and cell adhesion molecules (soluble vascular cell adhesion molecule-1 [sVCAM-1] and soluble intercellular adhesion molecule-1 [sICAM-1]) demonstrated a significant predictive role in terms of overall and cardiovascular survival. When 6 biomarkers (GSTM1 genotype, high AOPP/PAB/MDA/­sVCAM-1/sICAM-1) were combined into a scoring model, a significantly shorter overall and cardiovascular survival was observed for patients with the highest score (<i>p</i> &lt; 0.001). <b><i>Conclusion:</i></b> We identified a novel panel of biomarkers that can be utilized in predicting survival in ESRD patients. This biomarker signature could enable better monitoring of patients and stratification into appropriate treatment groups.
DOI: 10.6084/m9.figshare.8319668
title: Strand-specific affinity of host factor hnRNP C1/C2 guides positive to negative-strand ratio in Coxsackievirus B3 infection

description: Coxsackievirus B3 is an enterovirus, with positive-sense single-stranded RNA genome containing ‘Internal Ribosome Entry Site’ (IRES) in the 5ʹUTR. Once sufficient viral proteins are synthesized in the cell from the input RNA, viral template switches from translation to replication to synthesize negative-strand RNA. Inhibition of translation is a key step in regulating this switch as the positive-strand RNA template should be free of ribosomes to enable polymerase movement. In this study, we show how a host protein hnRNP C1/C2 inhibits viral RNA translation. hnRNP C1/C2 interacts with stem-loop V in the IRES and displaces poly-pyrimidine tract binding protein, a positive regulator of translation. We further demonstrate that hnRNP C1/C2 induces translation to replication switch, independently from the already known role of the ternary complex (PCBP2-3CD-cloverleaf RNA). These results suggest a novel function of hnRNP C1/C2 in template switching of positive-strand from translation to replication by a new mechanism. Using mathematical modelling, we show that the differential affinity of hnRNP C1/C2 for positive and negative-strand RNAs guides the final ± RNA ratio, providing first insight in the regulation of the positive to negative-strand RNA ratio in enteroviruses.