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7,327 results for “Pathway”
Dataset related to the article "Activation of Nrf2/HO-1 Pathway and Human Atherosclerotic Plaque Vulnerability: an In Vitro and In Vivo Study"
<p>This record contains raw data related to the article “Activation of Nrf2/HO-1 Pathway and Human Atherosclerotic Plaque Vulnerability: an In Vitro and In Vivo Study"</p> <p>Abstract: Reactive oxygen species (ROS) induce nuclear factor erythroid 2–related factor 2 (Nrf2) activation as an adaptive defense mechanism, determining the synthesis of antioxidant molecules, including heme-oxygenase-1 (HO-1). HO-1 protects cells against oxidative injury, degrading free heme and inhibiting ROS production. HO-1 is highly expressed in macrophages during plaque growth. Macrophages are morpho-functionally heterogeneous, and the prevalence of a specific phenotype may influence the plaque fate. This heterogeneity has also been observed in monocyte-derived macrophages(MDMs), a model of macrophages infiltrating tissue. The study aims to assess oxidative stress status and Nrf2/HO-1 axis in MDM morphotypes obtained from healthy subjects and coronary artery disease (CAD) patients, in relation to coronary plaque features evaluated in vivo by optical coherence tomography (OCT). We found that MDMs of healthy subjects exhibited a lower oxidative stress status, lower Nrf2 and HO-1 levels as compared to CAD patients. High HO-1 levels in MDMs were associated with the presence of a higher macrophage content, a thinner fibrous cap, and a ruptured plaque with thrombus formation, detected by OCT analysis. These findings suggest the presence of a relationship between in vivo plaque characteristics and in vitro MDM profile, and may help to identify patients with rupture-prone coronary plaque.</p> <p> </p>
Data and R scripts for: "Effect of introduction pathways on the invasion success of non-native plants along environmental gradients"
<p>Data and scripts that replicate the results for the publication: Marc Riera, Joan Pino, Llorenç Sáez, Pere Aymerich, Yolanda Melero (under review) Effect of introduction pathways on the invasion success of non-native plants along environmental gradients<br>The content of the files is described in a RedMe.txt file at the root directory, and in the main text of the manuscript.<br>Code developed and provided by Marc Riera. Contact: m.riera@creaf.uab.cat</p>
Up-regulation of miR-208a aggravates high-fat diet-induced cardiomyocytes injury by targeting IRS-2/PI3K/AKT pathway
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Supplementary material for "Identification of Protein Networks and Biological Pathways Driving the Progression of Atherosclerosis in Human Carotid Arteries through Mass Spectrometry-Based Proteomics"
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Dataset related to the article "An optimized MRM-based workflow of the L-arginine/nitric oxide pathway metabolites revealed disease- and sex-related differences in the cardiovascular field"
<p>This record contains raw data related to the article "An optimized MRM-based workflow of the L-arginine/nitric oxide pathway metabolites revealed disease- and sex-related differences in the cardiovascular field"</p> <p>Clinical data indicate that low circulating L-homoarginine (HArg) concentrations are associated with cardiovascular (CV) disease, CV mortality, and all-cause mortality. A high number of LC-based analytical methods for the quantification of HArg, in combination with the L-arginine (Arg)-related pathway metabolites, have been reported. However, these methods usually consider a limited panel of analytes. Thus, in order to achieve a comprehensive picture of the Arg metabolism, we described an improved targeted metabolomic approach based on a multiple reaction monitoring (MRM) mass spectrometry method for the simultaneous quantification of the Arg/nitric oxide (NO) pathway metabolites. This methodology was then employed to quantify plasma concentrations of these analytes in a cohort of individuals with different grades/types of coronary artery disease (CAD) in order to increase knowledge about the role of HArg and its associated metabolites in the CV field. Our results showed that the MRM method here implemented is suitable for the simultaneous assessment of a wide panel of amino acids involved in the Arg/NO metabolic pathway, in plasma samples from patients with CV disease. Further, the findings highlighted an impairment of the Arg/NO metabolic pathway, and suggest a sex-dependent regulation of this metabolic route.</p>
Loss of Serpina1 in mice leads to altered gene expression in inflammatory and metabolic pathways
<p>This is the data relating to Livers taken from age- and sex-matched at 8 to 14 weeks of age C57BL/6 wild-type (WT) and <em>Serpina1</em> knockout mice (KO), lacking all 5 serpin A1 a-e paralogues expressed in mice. Total RNA was isolated and performed RNA-sequencing and transcriptome analysis. <strong>The dataset contains the counts matrix for the mice samples mapped to the genes using HTSeq.</strong></p>
Dataset related to the article "Oxidized LDL-dependent pathway as new pathogenic trigger in Arrhythmogenic Cardiomyopathy."
<p>This record contains raw data related to the article “Oxidized LDL-dependent pathway as new pathogenic trigger in Arrhythmogenic Cardiomyopathy".</p> <p>Arrhythmogenic Cardiomyopathy (ACM) is hallmarked by ventricular fibro-adipogenic alterations, contributing to cardiac dysfunctions and arrhythmias. Although genetically-determined (e.g. <em>PKP2</em> mutations), ACM phenotypes are highly variable. More data on phenotype modulators, clinical prognosticators, and etiological therapies are awaited. We hypothesized that oxidized low-density-lipoproteins (oxLDL)-dependent activation of PPARγ, a recognized effector of ACM adipogenesis, contribute to disease pathogenesis.</p> <p>ACM patients showing high plasma concentration of oxLDL display severe clinical phenotypes in terms of fat infiltration, ventricular dysfunction, and major arrhythmic event risk.</p> <p>In ACM patient-derived cardiac cells, we demonstrated that oxLDL are major cofactors of adipogenesis. Mechanistically, the increased lipid accumulation is mediated by oxLDL cell internalization through CD36, ultimately resulting in PPARγ upregulation.</p> <p>By boosting oxLDL in a <em>Pkp2</em> heterozygous knock-out mice through high-fat-diet feeding, we confirmed <em>in vivo</em> the oxidized lipids dependency of cardiac adipogenesis and right ventricle systolic impairment, which are counteracted by atorvastatin treatment.</p> <p>The modulatory role of oxidized lipids on ACM adipogenesis, demonstrated at cellular, mouse, and patient levels, represents a novel risk stratification tool and a target for ACM pharmacological strategies.</p>
Table S1: Relative abundance of KEGG pathways obtained by PICRUSt
<p>Relative abundance of KEGG pathways obtained by PICRUSt</p>
Dataset relate to the article "Oxidative Stress and Arginine/Nitric Oxide Pathway in Red Blood Cells Derived from Patients with Prediabetes"
<p>This record contains row data relaed to the article "Oxidative Stress and Arginine/Nitric Oxide Pathway in Red Blood Cells Derived from Patients with Prediabetes"</p> <p><strong>Abstract: </strong>The effects of the oral glucose tolerance test (OGTT) on red blood cells (RBCs) have not been thoroughly investigated, although it is known that the<strong> </strong>ingestion of<strong> </strong>75-g<strong> </strong>glucose during OGTT results in a systemic state of inflammation and oxidative stress. Therefore, we evaluated the effect of OGTT on oxidative stress and L-Arginine/Nitric Oxide (L-Arg/NO) metabolic pathway in RBCs obtained from patients with prediabetes. Blood samples were collected from all participants before (T0) and at 10 (T1), 20 (T2), 30 (T3), 60 (T4), 90 (T5), 120 (T6), 150 (T7), and 180 (T8) minutes after glucose loading. Results showed a significant increase in oxidative stress status characterized by a rise in the GSSG/GSH ratio at T4 and T6 that went in parallel with a reduction of NO production in RBCs. In addition, in this time frame, increased exposure of phosphatidylserine on RBCs membrane was observed. These metabolic modifications were rescued at T8, together with an increase in activated RBC NO synthase expression.<strong> T</strong>hese findings provide a possible explanation of the phenomena occurring after glucose loading and suggest that, even in the early stages of diabetes, it may be important to avoid acute variations in glycemia in order to prevent diabetic complications.</p>
This record contains raw data related to the article "Sex-Specific Cell Types and Molecular Pathways Indicate Fibro-Calcific Aortic Valve Stenosis"
<p>This record contains raw data related to the article "Sex-Specific Cell Types and Molecular Pathways Indicate Fibro-Calcific Aortic Valve Stenosis"</p> <p><strong>Background:</strong> Aortic stenosis (AS) is the most common valve disorder characterized by fibro-calcific remodeling of leaflets. Recent evidence indicated that there is a sex-related difference in AS development and progression. Fibrotic remodeling is peculiar in women’s aortic valves, while men’s leaflets are more calcified. Our study aimed to assess aortic valve fibrosis (AVF) in a severe AS cohort using non-invasive diagnostic tools and determine whether sex-specific pathological pathways and cell types are associated with severe AS.</p> <p><strong>Materials and Methods:</strong> We have included 28 men and 28 women matched for age with severe AS who underwent echocardiography and cardiac contrast-enhanced computed tomography (CT) before intervention. The calcium and fibrosis volumes were assessed and quantified using the ImageJ thresholding method, indexed calcium and fibrosis volume were calculated by dividing the volume by the aortic annular area. For a deeper understanding of molecular mechanisms characterizing AS disorder, differentially expressed genes and functional inferences between women and men’s aortic valves were carried out on a publicly available microarray-based gene expression dataset (GSE102249). Cell types enrichment analysis in stenotic aortic valve tissues was used to reconstruct the sex-specific cellular composition of stenotic aortic valves.</p> <p><strong>Results:</strong> In agreement with the literature, our CT quantifications showed that women had significantly lower aortic valve calcium content compared to men, while fibrotic tissue composition was significantly higher in women than men. The expression profiles of human stenotic aortic valves confirm sex-dependent processes. Pro-fibrotic processes were prevalent in women, while pro-inflammatory ones, linked to the immune response system, were enhanced in men. Cell-type enrichment analysis showed that mesenchymal cells were over-represented in AS valves of women, whereas signatures for monocytes, macrophages, T and B cells were enriched men ones.</p> <p><strong>Conclusions:</strong> Our data provide the basis that the fibro-calcific process of the aortic valve is sex-specific, both at gene expression and cell type level. The quantification of aortic valve fibrosis by CT could make it possible to perform population-based studies and non-invasive assessment of novel therapies to reduce or halt sex-related calcific aortic valve stenosis (CAVS) progression, acting in an optimal window of opportunity early in the course of the disease.</p>
A Wide-Proteome Analysis to Identify Molecular Pathways Involved in Kidney Response to High-Fat Diet in Mice
<p>Dozio E, Maffioli E, Vianello E, Nonnis S, Grassi Scalvini F, Spatola L, Roccabianca P, Tedeschi G, Corsi Romanelli MM. A Wide-Proteome Analysis to Identify Molecular Pathways Involved in Kidney Response to High-Fat Diet in Mice. Int J Mol Sci. 2022 Mar 30;23(7):3809. doi: 10.3390/ijms23073809. PMID: 35409168; PMCID: PMC8999052.</p> <p>Abstract</p> <p>The etiopathogenesis of obesity-related chronic kidney disease (CKD) is still scarcely understood. To this aim, we assessed the effect of high-fat diet (HF) on molecular pathways leading to organ damage, steatosis, and fibrosis. Six-week-old male C57BL/6N mice were fed HF diet or normal chow for 20 weeks. Kidneys were collected for genomic, proteomic, histological studies, and lipid quantification. The main findings were as follows: (1) HF diet activated specific pathways leading to fibrosis and increased fatty acid metabolism; (2) HF diet promoted a metabolic shift of lipid metabolism from peroxisomes to mitochondria; (3) no signs of lipid accumulation and/or fibrosis were observed, histologically; (4) the early signs of kidney damage seemed to be related to changes in membrane protein expression; (5) the proto-oncogene MYC was one of the upstream transcriptional regulators of changes occurring in protein expression. These results demonstrated the potential usefulness of specific selected molecules as early markers of renal injury in HF, while histomorphological changes become visible later in obesity-related CDK. The integration of these information with data from biological fluids could help the identification of biomarkers useful for the early detection and prevention of tissue damage in clinical practice.</p>
Sex-dimorphic pathways in the associations between maternal trait anxiety, infant BDNF methylation and negative emotionality
<p>This database includes the raw data linked with the paper “Sex-dimorphic pathways in the associations between maternal trait anxiety, infant BDNF methylation and negative emotionality” accepted for publication on Development and Psychopathology. This study is part of the longitudinal and multi-centric “Measuring the outcomes of maternal COVID-19-related prenatal exposure (MOM-COPE)” study. Here, we report on the sex-dependent effects of antenatal exposure to maternal anxiety on infants’ methylation levels of the BDNF gene at birth and on negative emotionality trajectories from 3 to 6 months of age.</p> <p>Procedures</p> <p>Mother–infant dyads (N = 276) were recruited at delivery. Maternal trait anxiety, as a marker of antenatal chronic stress exposure, was assessed soon after delivery using the Stait-Trait Anxiety Inventory (STAI-Y). Infants’ BDNF DNAm at birth was assessed in 11 CpG sites in buccal cells whereas infants’ NE was assessed at 3 (N = 225) and 6 months (N = 189) using the Infant Behavior Questionnaire-Revised (IBQ-R).</p> <p>Analytical plan</p> <p>Principal component analysis (PCA) was used to reduce the number of CpG sites into a smaller set of factors. The PCA yielded 2 principal components: PC1 (composed of 6 CpG sites) and PC2 (composed of 5 CpG sites). Separate hierarchical regression analyses were performed to evaluate the independent and interactive effects of infant gender and maternal anxiety on infant methylation levels.</p> <p>Hierarchical linear models (HLMs) were performed to investigate sex-dimorphic associations between infant NE trajectory from 3 to 6 months and maternal trait anxiety or infant BDNF methylation.</p> <p>Findings in brief</p> <p>Higher maternal antenatal anxiety was associated with greater 6-month-olds’ NE. Furthermore, maternal antenatal anxiety predicted greater infants’ BDNF methylation in five CpG sites in males but not in females. Higher methylation at these sites was associated with greater 3-to-6-month NE increase, independently of infants’ sex.</p>
Data Set of the Study "Fostering transdisciplinary research for sustainability in the global south: Pathways to impact for funding programmes "
<p>Supplementary survey data to the project "LIRA 2030 – Fostering Transdisciplinarity in Africa". The data set contains a survey that was conducted in three cohorts to find out about the transdisciplinarity competence and learning within projects funded by the Leading Integrated Research for Agenda 2030 in Africa (LIRA2030) programme of the International Science Council. The survey encompassed 13 rating questions and 9 open questions.</p>
Raw data for "Effects of sacubitril/valsartan on exercise capacity: a prognostic improvement that starts during uptitration. Eur J Clin Pharmacol. 2023;79:1173-1184." and "Looking into the Kinetics of NT-proBNP and sST2 Changes in Patients with Heart Failure Treated with Sacubitril/Valsartan: A Hint to Different Therapeutic Pathways;Drugs R D. 2023 Sep 13. doi: 10.1007/s40268-023-00438-2."
<p><strong>Looking into the Kinetics of NT-proBNP and sST2 Changes in Patients with Heart Failure Treated with Sacubitril/Valsartan: A Hint to Different Therapeutic Pathways:</strong></p> <p><strong>Background and objective: </strong>N-terminal pro-B-type natriuretic peptide (NT-proBNP) and soluble interleukin 1 receptor-like 1 ST2 (sST2) are biomarkers used to grade heart failure with reduced ejection fraction (HFrEF) severity. Both are potential targets of HFrEF treatment, but the first is associated with the patient's hemodynamic status, while the second is more indicative of the inflammatory status and of myocardial fibrosis. The aim of this study was to assess the kinetics of these biomarkers after treatment with sacubitril/valsartan in HFrEF.</p> <p><strong>Methods: </strong>We analyzed blood samples of patients with HFrEF at baseline (before sacubitril/valsartan treatment), after 1, 2, and 3 months (respectively, after a month taking the 24/26 - 49/51 - 97/103 mg twice daily, or b.i.d., doses), and 6 months after the maximum-tolerated dose was reached (end study).</p> <p><strong>Results: </strong>We obtained samples from 72 patients with HFrEF (age 64.0 ± 10.5 years, 83% males). NT-proBNP and sST2 values progressively and significantly reduced to 37% and 16%, respectively, with a greater reduction for NT-proBNP (p < 0.001). Specifically, NT-proBNP reduced from 1144 [593-2586] pg/mL to 743 [358-1524] pg/mL and sST2 from 27.3 [20.5-35.0] ng/mL to 23.1 [15.9-30.7] ng/mL, p for trend < 0.001 in both cases. The reduction of the two biomarkers over time occurred with statistically significant different kinetics: deferred for sST2 and faster for NT-proBNP. No significant changes in renal function and potassium levels were recorded.</p> <p><strong>Conclusion: </strong>These findings suggest that, in patients with HF, sacubitril/valsartan effects on the cardiovascular system share a double pathway: a first, hemodynamic, faster pathway and a second, non-hemodynamic anti-fibrotic, delayed one. Both likely contribute to the sacubitril/valsartan benefits in HFrEF.</p> <p> </p> <p><strong>Effects of sacubitril/valsartan on exercise capacity: a prognostic improvement that starts during uptitration</strong></p> <p><strong>Purpose: </strong>Sacubitril/valsartan is a mainstay of the treatment of heart failure with reduced ejection fraction (HFrEF); however, its effects on exercise performance yielded conflicting results. Aim of our study was to evaluate the impact of sacubitril/valsartan on exercise parameters and echocardiographic and biomarker changes at different drug doses.</p> <p><strong>Methods: </strong>We prospectively enrolled consecutive HFrEF outpatients eligible to start sacubitril/valsartan. Patients underwent clinical assessment, cardiopulmonary exercise test (CPET), blood sampling, echocardiography, and completed the Kansas City Cardiomyopathy Questionnaire (KCCQ-12). Sacubitril/valsartan was introduced at 24/26 mg b.i.d. dose and progressively uptitrated in a standard monthly-based fashion to 97/103 mg b.i.d. or maximum tolerated dose. Study procedures were repeated at each titration visit and 6 months after reaching the maximum tolerated dose.</p> <p><strong>Results: </strong>Ninety-six patients completed the study, 73 (75%) reached maximum sacubitril/valsartan dose. We observed a significant improvement in functional capacity across all study steps: oxygen intake increased, at peak exercise (from 15.6 ± 4.5 to 16.5 ± 4.9 mL/min/kg; p trend = 0.001), while minute ventilation/carbon dioxide production relationship reduced in patients with an abnormal value at baseline. Sacubitril/valsartan induced positive left ventricle reverse remodeling (EF from 31 ± 5 to 37 ± 8%; p trend < 0.001), while NT-proBNP reduced from 1179 [610-2757] to 780 [372-1344] pg/ml (p trend < 0.0001). NYHA functional class and the subjective perception of limitation in daily life at KCCQ-12 significantly improved. The Metabolic Exercise Cardiac Kidney Index (MECKI) score progressively improved from 4.35 [2.42-7.71] to 2.35% [1.24-4.96], p = 0.003.</p> <p><strong>Conclusions: </strong>A holistic and progressive HF improvement was observed with sacubitril/valsartan in parallel with quality of life. Likewise, a prognostic enhancement was observed.</p>
Synergistic Protective Effects of Ginsenoside Rb1 and Berberine Against Type 2 Diabetes Mellitus via the GDF15/HAMP Signaling Pathway Throughout the Liver Lobules: Insights from Spatial Transcriptomic
GEO Series GSE285791. Mus musculus. 171 samples. Type: Other.
Expression data from Drosophila melanogaster E2f/Rb genetic pathway manipulation
GEO Series GSE7655. Drosophila melanogaster. 18 samples. Type: Expression profiling by array.
Transcriptome and metabolome profiling reveals key pathways and metabolites involved in defense response of upland cotton against Verticillium dahliae
GEO Series GSE221845. Gossypium hirsutum. 12 samples. Type: Expression profiling by high throughput sequencing.
CHLORELLA, chloroplast-targeted long noncoding RNA, mediates the chloroplast functional transition during leaf lifespan through anterograde signaling pathway
GEO Series GSE255867. Arabidopsis thaliana. 12 samples. Type: Expression profiling by high throughput sequencing.
microRNA-252 and FoxO repress inflammaging by a dual inhibitory mechanism on Dawdle mediated TGF-β pathway in Drosophila muscle
GEO Series GSE142655. Drosophila melanogaster. 5 samples. Type: Expression profiling by high throughput sequencing.
Continuous activation of the IL-17F driven inflammatory pathway in acute and chronic digital dermatitis lesions in dairy cattle
GEO Series GSE196166. Bos taurus. 29 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.