cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.7554063
title: : Dataset related to the article "Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study"

description: This record contains raw data related to the article “Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study”. <em><strong>Abstract</strong></em> <strong>Background: </strong>Advanced glycation end-products (AGEs) and their interaction with the receptor for advanced glycation end-products (RAGE) play a pivotal role in the development and progression of type 2 diabetes. In this retrospective cohort study, we explored the association of circulating levels of soluble RAGE (sRAGE) isoforms, i.e., endogenous secretory esRAGE and cleaved cRAGE, AGEs and their respective ratios with 15-year all-cause mortality in type 2 diabetes. <strong>Methods: </strong>Baseline AGEs and sRAGE isoforms concentration were measured by ELISA in 362 patients with type 2 diabetes and in 125 age- and gender-matched healthy control subjects (CTR). Independent predictors of mortality were determined using Cox proportional-hazards models and used to build and validate a nomogram for all-cause mortality prediction in type 2 diabetes. <strong>Results: </strong>AGEs, total sRAGE, cRAGE and the AGEs/sRAGE and AGEs/esRAGE ratios were significantly increased in patients with type 2 diabetes compared to CTR (p &lt; 0.001). In CTR subjects, but not in type 2 diabetes patients, a significant negative correlation between cRAGE and age was confirmed (p = 0.003), whereas the AGEs/sRAGE (p = 0.032) and AGEs/cRAGE (p = 0.006) ratios were positively associated with age. At an average follow-up of 15 years (4,982 person-years), 130 deaths were observed. The increase in the AGEs/cRAGE ratio was accompanied by a higher risk of all-cause mortality in patients with type 2 diabetes (HR per each SD increment = 1.30, 95% CI 1.15-1.47; p &lt; 0.001). Moreover, sRAGE was associated with the development of major adverse cardiovascular events (MACE) in type 2 diabetes patients without previous MACE (OR for each SD increase: 1.48, 95% CI 1.11-1.89). A nomogram based on age, sex, HbA1c, systolic blood pressure, and the AGEs/cRAGE ratio was built to predict 5-, 10- and 15-year survival in type 2 diabetes. Patients were categorized into quartiles of the monogram scores and Kaplan-Meier survival curves confirmed the prognostic accuracy of the model (log-rank p = 6.5 × 10<sup>- 13</sup>). <strong>Conclusions: </strong>The ratio between AGEs and the cRAGE isoform is predictive of 15-year survival in patients with type 2 diabetes. Our data support the assessment of circulating AGEs and soluble RAGE isoforms in patients with type 2 diabetes as predictors of MACE and all-cause mortality. Enable Ginger<em>Cannot connect to Ginger</em> Check your internet connection<br> or reload the browserDisable in this text fieldRephraseRephrase current sentence26Log in to edit with Ginger×
DOI: 10.5281/zenodo.7554064
title: : Dataset related to the article "Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study"

description: This record contains raw data related to the article “Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study”. <em><strong>Abstract</strong></em> <strong>Background: </strong>Advanced glycation end-products (AGEs) and their interaction with the receptor for advanced glycation end-products (RAGE) play a pivotal role in the development and progression of type 2 diabetes. In this retrospective cohort study, we explored the association of circulating levels of soluble RAGE (sRAGE) isoforms, i.e., endogenous secretory esRAGE and cleaved cRAGE, AGEs and their respective ratios with 15-year all-cause mortality in type 2 diabetes. <strong>Methods: </strong>Baseline AGEs and sRAGE isoforms concentration were measured by ELISA in 362 patients with type 2 diabetes and in 125 age- and gender-matched healthy control subjects (CTR). Independent predictors of mortality were determined using Cox proportional-hazards models and used to build and validate a nomogram for all-cause mortality prediction in type 2 diabetes. <strong>Results: </strong>AGEs, total sRAGE, cRAGE and the AGEs/sRAGE and AGEs/esRAGE ratios were significantly increased in patients with type 2 diabetes compared to CTR (p &lt; 0.001). In CTR subjects, but not in type 2 diabetes patients, a significant negative correlation between cRAGE and age was confirmed (p = 0.003), whereas the AGEs/sRAGE (p = 0.032) and AGEs/cRAGE (p = 0.006) ratios were positively associated with age. At an average follow-up of 15 years (4,982 person-years), 130 deaths were observed. The increase in the AGEs/cRAGE ratio was accompanied by a higher risk of all-cause mortality in patients with type 2 diabetes (HR per each SD increment = 1.30, 95% CI 1.15-1.47; p &lt; 0.001). Moreover, sRAGE was associated with the development of major adverse cardiovascular events (MACE) in type 2 diabetes patients without previous MACE (OR for each SD increase: 1.48, 95% CI 1.11-1.89). A nomogram based on age, sex, HbA1c, systolic blood pressure, and the AGEs/cRAGE ratio was built to predict 5-, 10- and 15-year survival in type 2 diabetes. Patients were categorized into quartiles of the monogram scores and Kaplan-Meier survival curves confirmed the prognostic accuracy of the model (log-rank p = 6.5 × 10<sup>- 13</sup>). <strong>Conclusions: </strong>The ratio between AGEs and the cRAGE isoform is predictive of 15-year survival in patients with type 2 diabetes. Our data support the assessment of circulating AGEs and soluble RAGE isoforms in patients with type 2 diabetes as predictors of MACE and all-cause mortality. Enable Ginger<em>Cannot connect to Ginger</em> Check your internet connection<br> or reload the browserDisable in this text fieldRephraseRephrase current sentence26Log in to edit with Ginger×
DOI: 10.5281/zenodo.7551792
title: Dataset related to the article "Enduring Reactive Oxygen Species Emission Causes Aberrant Protein S-Glutathionylation Transitioning Human Aortic Valve Cells from a Sclerotic to a Stenotic Phenotype"

description: This record contains raw data related to the article "Enduring Reactive Oxygen Species Emission Causes Aberrant Protein S-Glutathionylation Transitioning Human Aortic Valve Cells from a Sclerotic to a Stenotic Phenotype" <strong><em>Aims:</em></strong> During calcific aortic valve stenosis (CAVS) progression, oxidative stress and endothelial dysfunction mark the initial pathogenic steps with a parallel dysregulation of the antioxidant systems. Here, we tested whether oxidation-induced protein S-glutathionylation (P-SSG) accounts for a phenotypic switch in human aortic valvular tissue, eventually leading to calcium deposition. Next, we tested whether countering this reactive oxygen species (ROS) surge would prevent these perturbations. <strong><em>Results:</em></strong> We employed state-of-the-art technologies, such as electron paramagnetic resonance (EPR), liquid chromatography-tandem mass spectrometry, imaging flow-cytometry, and live-cell imaging on human excised aortic valves and primary valve endothelial cells (VECs). We observed that a net rise in EPR-detected ROS emission marked the transition from fibrotic to calcific in human CAVS specimens, coupled to a progressive increment in P-SSG deposition. In human VECs (hVECs), treatment with 2-acetylamino-3-[4-(2-acetylamino-2-carboxyethylsulfanylthiocarbonylamino)phenylthiocarbamoylsulfanyl]propionic acid triggered highly oxidizing conditions prompting P-SSG accumulation, damaging mitochondria, and inducing endothelial nitric oxide synthase uncoupling. All the events conjured up in morphing these cells from their native endothelial phenotype into a damaged calcification-inducing one. As proof of principle, the use of the antioxidant N-acetyl-L-cysteine prevented these alterations. <strong><em>Innovation:</em></strong> Borne as a compensatory system to face excessive oxidative burden, with time, P-SSG contributes to the morphing of hVECs from their innate phenotype into a damaged one, paving the way to calcium deposition. <strong><em>Conclusion:</em></strong> Our data suggest that, in the human aortic valve, unremitted ROS emission along with a P-SSG build-up occurs and accounts, at least in part, for the morphological/functional changes leading to CAVS.
description: This work was supported by the Italian Ministry of Health funds (Ricerca Finalizzata: GR-2018-12366423) and by Fondazione Gigi e Pupa Ferrari ONLUS (FPF-14). G.K. is supported by the T32 NIH training grant (T32AG058527) and funds from the Johns Hopkins University Older American Independence Center of the National Institute on Aging (NIA) under award number P30AG021334. NP is supported by NIH (R01 HL136918).
DOI: 10.5281/zenodo.7551793
title: Dataset related to the article "Enduring Reactive Oxygen Species Emission Causes Aberrant Protein S-Glutathionylation Transitioning Human Aortic Valve Cells from a Sclerotic to a Stenotic Phenotype"

description: This record contains raw data related to the article "Enduring Reactive Oxygen Species Emission Causes Aberrant Protein S-Glutathionylation Transitioning Human Aortic Valve Cells from a Sclerotic to a Stenotic Phenotype" <strong><em>Aims:</em></strong> During calcific aortic valve stenosis (CAVS) progression, oxidative stress and endothelial dysfunction mark the initial pathogenic steps with a parallel dysregulation of the antioxidant systems. Here, we tested whether oxidation-induced protein S-glutathionylation (P-SSG) accounts for a phenotypic switch in human aortic valvular tissue, eventually leading to calcium deposition. Next, we tested whether countering this reactive oxygen species (ROS) surge would prevent these perturbations. <strong><em>Results:</em></strong> We employed state-of-the-art technologies, such as electron paramagnetic resonance (EPR), liquid chromatography-tandem mass spectrometry, imaging flow-cytometry, and live-cell imaging on human excised aortic valves and primary valve endothelial cells (VECs). We observed that a net rise in EPR-detected ROS emission marked the transition from fibrotic to calcific in human CAVS specimens, coupled to a progressive increment in P-SSG deposition. In human VECs (hVECs), treatment with 2-acetylamino-3-[4-(2-acetylamino-2-carboxyethylsulfanylthiocarbonylamino)phenylthiocarbamoylsulfanyl]propionic acid triggered highly oxidizing conditions prompting P-SSG accumulation, damaging mitochondria, and inducing endothelial nitric oxide synthase uncoupling. All the events conjured up in morphing these cells from their native endothelial phenotype into a damaged calcification-inducing one. As proof of principle, the use of the antioxidant N-acetyl-L-cysteine prevented these alterations. <strong><em>Innovation:</em></strong> Borne as a compensatory system to face excessive oxidative burden, with time, P-SSG contributes to the morphing of hVECs from their innate phenotype into a damaged one, paving the way to calcium deposition. <strong><em>Conclusion:</em></strong> Our data suggest that, in the human aortic valve, unremitted ROS emission along with a P-SSG build-up occurs and accounts, at least in part, for the morphological/functional changes leading to CAVS.
description: This work was supported by the Italian Ministry of Health funds (Ricerca Finalizzata: GR-2018-12366423) and by Fondazione Gigi e Pupa Ferrari ONLUS (FPF-14). G.K. is supported by the T32 NIH training grant (T32AG058527) and funds from the Johns Hopkins University Older American Independence Center of the National Institute on Aging (NIA) under award number P30AG021334. NP is supported by NIH (R01 HL136918).
DOI: 10.5281/zenodo.7551601
title: Dataset related to the article "Extraction-Free Absolute Quantification of Circulating miRNAs by Chip-Based Digital PCR"

description: This record contains raw data related to the article "Extraction-Free Absolute Quantification of Circulating miRNAs by Chip-Based Digital PCR" Circulating microRNAs (miRNA) have been proposed as specific biomarkers for several diseases. Quantitative Real-Time PCR (RT-qPCR) is the gold standard technique currently used to evaluate miRNAs expression from different sources. In the last few years, digital PCR (dPCR) emerged as a complementary and accurate detection method. When dealing with gene expression, the first and most delicate step is nucleic-acid isolation. However, all currently available protocols for RNA extraction suffer from the variable loss of RNA species due to the chemicals and number of steps involved, from sample lysis to nucleic acid elution. Here, we evaluated a new process for the detection of circulating miRNAs, consisting of sample lysis followed by direct evaluation by dPCR in plasma from healthy donors and in the cardiovascular setting. Our results showed that dPCR is able to detect, with high accuracy, low-copy-number as well as highly expressed miRNAs in human plasma samples without the need for RNA extraction. Moreover, we assessed a known myocardial infarction-related miR-133a in acute myocardial infarct patients vs. healthy subjects. In conclusion, our results show the suitability of the extraction-free quantification of circulating miRNAs as disease markers by direct dPCR.
description: This work was supported by Gigi e Pupa Ferrari ONLUS [FPF-14] and the Italian Ministry of Health [GR-2018-12366423].
DOI: 10.5281/zenodo.7551602
title: Dataset related to the article "Extraction-Free Absolute Quantification of Circulating miRNAs by Chip-Based Digital PCR"

description: This record contains raw data related to the article "Extraction-Free Absolute Quantification of Circulating miRNAs by Chip-Based Digital PCR" Circulating microRNAs (miRNA) have been proposed as specific biomarkers for several diseases. Quantitative Real-Time PCR (RT-qPCR) is the gold standard technique currently used to evaluate miRNAs expression from different sources. In the last few years, digital PCR (dPCR) emerged as a complementary and accurate detection method. When dealing with gene expression, the first and most delicate step is nucleic-acid isolation. However, all currently available protocols for RNA extraction suffer from the variable loss of RNA species due to the chemicals and number of steps involved, from sample lysis to nucleic acid elution. Here, we evaluated a new process for the detection of circulating miRNAs, consisting of sample lysis followed by direct evaluation by dPCR in plasma from healthy donors and in the cardiovascular setting. Our results showed that dPCR is able to detect, with high accuracy, low-copy-number as well as highly expressed miRNAs in human plasma samples without the need for RNA extraction. Moreover, we assessed a known myocardial infarction-related miR-133a in acute myocardial infarct patients vs. healthy subjects. In conclusion, our results show the suitability of the extraction-free quantification of circulating miRNAs as disease markers by direct dPCR.
description: This work was supported by Gigi e Pupa Ferrari ONLUS [FPF-14] and the Italian Ministry of Health [GR-2018-12366423].
DOI: 10.5281/zenodo.7525975
title: Supplementary data, Global strategy for the conservation and use of pea genetic resources

description: Supplementary data, Global strategy for the conservation and use of pea genetic resources
DOI: 10.5281/zenodo.7525974
title: Supplementary data, Global strategy for the conservation and use of pea genetic resources

description: Supplementary data, Global strategy for the conservation and use of pea genetic resources
DOI: 10.5281/zenodo.7107513
title: High resolution land cover 2016 Velika Gorica

description: 30cm Object based image analysis land cover dataset based on WorldView 3 and nDSM, stored as a .shp file. <strong>Class</strong> <strong>Vector </strong> <strong>NumCodec</strong> <strong>(16bit)</strong> <strong>Raster</strong> <strong>NumCodec</strong> <strong>(8bit)</strong> Building 100 10 0 Lowest rise building 110 11 1 Low rise building 120 12 2 Mid rise building 130 13 3 High rise building 140 14 4 Highest rise building 150 15 Mineral surface 210 21 Bare soil 220 22 Artificial grass 230 23 Grass 310 31 Shrub round 410 41 Shrub linear 420 42 Evergreen 510 51 Deciduous 520 52 Lake 610 61 River 620 62 Sea 630 63 Undergrowth 710 71 Agriculture, intensive temporary crops 810 81 Agriculture, intensive permanent crops 820 82 Agriculture, extensive 830 83 unclassified 999 99 NonAOI 999 99
DOI: 10.5281/zenodo.7551502
title: Dataset related to the article "Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation"

description: This record contains raw data related to the article "Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation" <strong>Background and aims:</strong> Post-operative atrial fibrillation (POAF), defined as new-onset AF in the immediate period after surgery, is associated with poor adverse cardiovascular events and a higher risk of permanent AF. Mechanisms leading to POAF are not completely understood and epicardial adipose tissue (EAT) inflammation could be a potent trigger. Here, we aim at exploring the link between EAT-secreted interleukin (IL)-1β, atrial remodeling, and POAF in a population of coronary artery disease (CAD) patients. <strong>Methods:</strong> We collected EAT and atrial biopsies from 40 CAD patients undergoing cardiac surgery. Serum samples and EAT-conditioned media were screened for IL-1β and IL-1ra. Atrial fibrosis was evaluated at histology. The potential role of NLRP3 inflammasome activation in promoting fibrosis was explored <em>in vitro</em> by exposing human atrial fibroblasts to IL-1β and IL-18. <strong>Results:</strong> 40% of patients developed POAF. Patients with and without POAF were homogeneous for clinical and echocardiographic parameters, including left atrial volume and EAT thickness. POAF was not associated with atrial fibrosis at histology. No significant difference was observed in serum IL-1β and IL-1ra levels between POAF and no-POAF patients. EAT-mediated IL-1β secretion and expression were significantly higher in the POAF group compared to the no-POAF group. The <em>in vitro</em> study showed that both IL-1β and IL-18 increase fibroblasts' proliferation and collagen production. Moreover, the stimulated cells perpetuated inflammation and fibrosis by producing IL-1β and transforming growth factor (TGF)-β. <strong>Conclusion:</strong> EAT could exert a relevant role both in POAF occurrence and in atrial fibrotic remodeling.
DOI: 10.5281/zenodo.7551503
title: Dataset related to the article "Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation"

description: This record contains raw data related to the article "Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation" <strong>Background and aims:</strong> Post-operative atrial fibrillation (POAF), defined as new-onset AF in the immediate period after surgery, is associated with poor adverse cardiovascular events and a higher risk of permanent AF. Mechanisms leading to POAF are not completely understood and epicardial adipose tissue (EAT) inflammation could be a potent trigger. Here, we aim at exploring the link between EAT-secreted interleukin (IL)-1β, atrial remodeling, and POAF in a population of coronary artery disease (CAD) patients. <strong>Methods:</strong> We collected EAT and atrial biopsies from 40 CAD patients undergoing cardiac surgery. Serum samples and EAT-conditioned media were screened for IL-1β and IL-1ra. Atrial fibrosis was evaluated at histology. The potential role of NLRP3 inflammasome activation in promoting fibrosis was explored <em>in vitro</em> by exposing human atrial fibroblasts to IL-1β and IL-18. <strong>Results:</strong> 40% of patients developed POAF. Patients with and without POAF were homogeneous for clinical and echocardiographic parameters, including left atrial volume and EAT thickness. POAF was not associated with atrial fibrosis at histology. No significant difference was observed in serum IL-1β and IL-1ra levels between POAF and no-POAF patients. EAT-mediated IL-1β secretion and expression were significantly higher in the POAF group compared to the no-POAF group. The <em>in vitro</em> study showed that both IL-1β and IL-18 increase fibroblasts' proliferation and collagen production. Moreover, the stimulated cells perpetuated inflammation and fibrosis by producing IL-1β and transforming growth factor (TGF)-β. <strong>Conclusion:</strong> EAT could exert a relevant role both in POAF occurrence and in atrial fibrotic remodeling.
DOI: 10.25403/upresearchdata.21716900.v1
title: Parentage analyses, selection of single nucleotide polymorphisms (SNPs) and design of panels for pedigree verification of the Bonsmara and Drakensberger cattle

description: The dataset was generated from the GeneSeek® Genomic Profiler (GGP) Bovine 150K BeadChip single nucleotide polymorphism (SNP) panel using 1 563 and 1 022 animals of the Bonsmara and Drakensberger, respectively. Data edits and calculations were all performed using the<em> R</em> software. After removing duplicate SNPs, those on the X, Y, and MT chromosomes, and those with unknown locations, a total of 119 375 autosomal SNPs based on the UMD3.1 bovine genome remained. Only animal genotypes with call rate more than 90% were considered for downstream analysis. The dataset only included 185 of the 200 parentage SNPs of the International Society for Animal Genetics (ISAG). The 185 SNPs were then evaluated for effectiveness in the Bonsmara and Drakensberger cattle populations. Results showed that the 185 ISAG were not sufficient for parentage testing in the two South African breeds. The primary dataset consisting of 119 375 number of SNPs was used to validate the parent-offspring relationships recorded in pedigree and to detect regions exhibiting hemizygous deletions. <br> Additional quality control edits applied to the 119 375 SNPs included the removal of genotypes with median GenCall (GC), GenTrain (GT) scores lower than 0.60 and 0.55, respectively. All SNPs that departed from Hardy–Weinberg equilibrium (p &lt; 0.001), with missing genotype rate of more than 5% and where the minor allele frequency (MAF) was &lt;0.05 across the populations were discarded. After edits, 2 585 animals (BON = 1 563 and DRB = 1 022) with 92 835 autosomal SNPs remained. This dataset was then used for parentage assignment and reconstruction of pedigree records using the gawk and <em>Hsphase</em> R package scripts, respectively. <br> Finally, the design of low-cost genotype parentage panels consisting of 200 SNPs per breed were selected from 78 286 SNP markers that had a GT score and GC score of 0.60&gt;= and 0.55&gt;=, respectively; a call rate of 0.99%&gt;=, MAF 0.05&gt;=, and those that had a HWE p-value &gt; 0.001. To minimize linkage disequilibrium (LD) among selected SNPs, the selected SNPs had to be at least 1 Mb apart and with a LogRRatio &gt; 0.001. <br>