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1,510 results for “Liver disease”
Figure S1. Mediation analysis on the effect of insulin resistance on intraocular pressure. Figure S2. Forest plot showing the OR (95% CI) for EIOP of ALD versus NAFLD and the OR (95% CI) for EIOP of drinkers versus non-drinkers. Abbreviations: OR, odds ratio; CI, confidence interval; ALD, alcoholic liver disease; NAFLD, non-alcoholic fatty liver disease.
<p>Figure S1. Mediation analysis on the effect of insulin resistance on intraocular pressure.</p> <p>Figure S2. Forest plot showing the OR (95% CI) for EIOP of ALD versus NAFLD and the OR (95% CI) for EIOP of drinkers versus non-drinkers. Abbreviations: OR, odds ratio; CI, confidence interval; ALD, alcoholic liver disease; NAFLD, non-alcoholic fatty liver disease.</p>
Metabolomics of pediatric fatty liver disease
<p>Fecal and plasma metabolite profiles of non-alcoholic fatty liver disease (NAFLD) in a pediatric cohort</p>
VISION Invited lecture - Bariatric surgery and non-alcoholic fatty liver disease
<p>Recording and presentation of the invited lecture that took place online on 16 June 2021 - <strong>Pantelis Antonakis, MD, PhD - Bariatric surgery and non-alcoholic fatty liver disease.</strong></p> <p>Bariatric surgery is a documented solution for morbid obesity. Additionally to excess weight loss, significant improvement in comorbidities is an established benefit after bariatric operations. In recent years, non-alcoholic fatty liver disease (NAFLD) has emerged as one of these comorbidities. Herein we will review the data supporting the positive effect of bariatric surgery in patients with NAFLD.</p>
Dihydrosphingolipids are associated with steatosis and increased fibrosis damage in human and animal models of non-alcoholic fatty liver disease
<p>Data sets used for the article entitled: "Accumulation of dihydrosphingolipids and neutral lipids is related to steatosis and fibrosis damage in human and animal models of non-alcoholic fatty liver disease"</p> <p>- Patient data: DATA Patients JLR.xlsx</p> <p>- Mouse data: DATA Mice.xlsx</p>
Statistics "Bioderived therapeutics for chronic liver diseases"
<p>Details to the statistics for the chapter 4 in the thesis "Bioderived therapeutics for chronic liver diseases"</p>
Fig. 1 in Infection with Toxoplasma gondii can promote chronic liver diseases in HIV-infected individuals
Fig. 1. Frequency of different liver pathologies in deceased patients from cohorts seropositive and seronegative to Toxoplasma gondii (Nicolle et Manceaux, 1908). * – difference between the indices for the entire cohort of seropositive patients and for the group of deceased patients from this cohort (p <0.05); ^ – difference between the indices for the entire cohort of seronegative patients and for the group of deceased patients from this cohort (p <0.05)
Study of Semaglutide for Non-Alcoholic Fatty Liver Disease (NAFLD), a Metabolic Syndrome With Insulin Resistance, Increased Hepatic Lipids, and Increased Cardiovascular Disease Risk (The SLIM LIVER St
ClinicalTrials.gov study NCT04216589. IPD Sharing: YES. Countries: 2. Publications: 2.
Alcohol Biosensor Monitoring for Alcoholic Liver Disease
ClinicalTrials.gov study NCT03533660. IPD Sharing: YES. Countries: 1. Publications: 1.
Study of Various Treatments in Non-alcoholic Fatty Liver Disease (NAFLD) Patients Who Have Aspects of Non-alcoholic Steatohepatitis (NASH)
ClinicalTrials.gov study NCT04147195. IPD Sharing: YES. Countries: 3. Publications: 1.
Raw data related to: Randomised Clinical Trial: Calorie Restriction Regimen with Tomato Juice Supplementation Ameliorates Oxidative Stress and Preserves a Proper Immune Surveillance Modulating Mitochondrial Bioenergetics of T-Lymphocytes in Obese Children Affected by Non-Alcoholic Fatty Liver Disease (NAFLD)
<p><strong>Abstract</strong></p> <p>Fatty liver disease is a serious complication of childhood obesity. Calorie-restricted regimen (RCR) is one of the e ective therapy for this condition. Aim of the study was to evaluate the effect of lycopene-rich tomato sauce with oregano and basil extracts in obese children with fatty liver on RCR. 61 obese children with fatty liver were enrolled, 52 completed the study. A randomized cross over clinical trial was performed. Participants were assigned to RCR alone or with a supplement of lycopene-rich tomato juice for 60 days; subsequently, the groups were switched to the alternative regimen for the next 60 days. Reduction in BMI, HOMA-IR, cholesterol, triglycerides, liver size, and steatosis was more profound in tomato-supplemented group. Leptin decreased in both groups whereas adiponectin raised only after tomato supplementation. RCR is associated with the impaired engagement of T-cells glycolysis and proliferation, tomato-supplementation resulted in glycolytic metabolic activation of T-cells. Tomato juice ameliorates glucose and lipid metabolism in obese children, improve oxidative and inflammatory state and modulates the mitochondrial metabolism of T-cells contributing to a maintenance of a proper immune surveillance in children, impaired by RCR. The addition of tomato to RCR could be considered a protective and preventive support to obese child.</p> <p><strong>Progetto giovani ricercatori </strong>[GR-2016-02363725] dal titolo: "Immune Tolerance, Metabolism and Multiple Sclerosis: Novel Molecular Tools to Monitor Disease Pathogenesis and Progression"</p>
MERFISH and snRNAseq analysis of healthy and disease human liver
<p>Single-cell RNA sequencing (scRNA-seq) has advanced our understanding of cell types and their heterogeneity within the human liver, but the spatial organization at single-cell resolution has not yet been described. Here we apply multiplexed error robust fluorescent in situ hybridization (MERFISH) to map the zonal distribution of hepatocytes, resolve subsets of macrophage and mesenchymal populations, and investigate the relationship between hepatocyte ploidy and gene expression within the healthy human liver. We next integrated spatial information from MERFISH with the more complete transcriptome produced by single- nucleus RNA sequencing (snRNA-seq), revealing zonally enriched receptor-ligand interactions. Finally, analysis of fibrotic liver samples identified two hepatocyte populations that are not restricted to zonal distribution and expand with injury. Together these spatial maps of the healthy and fibrotic liver provide a deeper understanding of the cellular and spatial remodeling that drives disease which, in turn, could provide new avenues for intervention and further study.</p>
Transcriptomic atlas reveals organ-specific disease tolerance in sickle cell mice. Dataset for HbSS livers injected or not with heme
<p>The objective of this experiment was to explore the transcriptome of the HbSS Townes mouse model of sickle cell disease. Townes model mice carry several human hemoglobin knock-in genes replacing the endogenous mouse genes and may be useful in studying sickle cell disease. All mice were genotyped, age- and sex-matched littermates. All HbAA (control, normal human hemoglobin) vs HbSS (sickle cell disease, mutated human hemoglobin) mice were used for experimentations at 6-8 weeks of age, to limit intra-group heterogeneity. Hemin (Ferriprotoporphyrin IX) was purchased from Frontiers Scientific and injected intravenously (iv.) in a retroorbital sinus at a concentration of 24 µmol/kg. Control mice received PBS instead. Mice were anesthetized with isoflurane 2-3% for injections, blood collection and sacrifice. All mice were sacrificed by cervical dislocation, 4 hours after injection.</p> <p>The results of livers <span>(indicated foie)</span> from HbSS mice injected or not with heme are presented here. </p> <p>The results of livers <span>(indicated foie)</span> from HbAA mice injected or not with heme can be found at number 10.5281/zenodo.10963640. </p> <p>Thirty μm-thick frozen tissue sections of livers were cut as above and homogenized in 200μL of 1-Thioglycerol/Homogenization Solution (Maxwell® 16 LEV simplyRNA Tissue Kit Promega AS1280). The quality and quantity of mRNA were evaluated using a 2100 bioanalyzer with TNA 6000 NanoKits (all Agilent Technologies, Palo Alto, CA, USA). RNA Integrity Numbers superior to 7 were eligible for subsequent reverse transcription into cDNA. RNAseq was performed at the GenomIC plateform Cochin Institute INSERM U1016. After RNA extraction, RNA quality (RNA integrity number) was estimated. 1μg of high-quality total RNA sample (RIN &gt;7) was processed to build up the libraries, using TruSeq Stranded mRNA kit (Illumina) according to manufacturer instructions. Briefly, purified poly-A containing mRNA molecules were fragmented and reverse-transcribed using random primers. Replacement of dTTP by dUTP during second strand synthesis allowed us to achieve strand specificity. Addition of a single A base to the cDNA was followed by ligation of Illumina adapters.<br>Libraries were quantified by qPCR using KAPA Library Quantification Kits for Illumina Libraries (KapaBiosystems, Wilmington, MA). Library profiles were assessed using DNA High Sensitivity LabChip kits on an Agilent Bioanalyzer. Libraries were sequenced on an Illumina Nextseq 500 instrument using 75 base-lengths read V2 chemistry in a paired-end mode. After sequencing, primary analysis based on AOZAN software (ENS, Paris), was applied to demultiplex and control the quality of the raw data (based of FastQC modules / version 0.11.5).</p> <p>The dataset here represents 4 groups of mice, 4 mice per group as follows: HbAA PBS, HbAA heme, HbSS PBS, HbSS heme. </p> <p> </p>
Transcriptomic atlas reveals organ-specific disease tolerance in sickle cell mice. Dataset for HbAA livers injected or not with heme
<p>The objective of this experiment was to explore the <span>transcriptome</span> of the <span>HbSS Townes</span> <span>mouse model</span> of <span>sickle cell disease</span>.<span>Townes model mice carry several human hemoglobin <span>knock-in</span> genes replacing the endogenous mouse genes and may be useful in studying <span>sickle cell disease</span>.</span>All mice were <span>genotyped</span>, age- and sex-matched littermates. All <span>HbAA</span> (control, normal human hemoglobin) vs HbSS (<span>sickle cell disease</span>, mutated human hemoglobin) mice were used for experimentations at 6-8 weeks of age, to limit intra-group <span>heterogeneity</span>. <span>Hemin</span> (<span>Ferriprotoporphyrin IX</span>) was purchased from <span>Frontiers Scientific</span> and injected <span>intravenously</span> (iv.) in a retroorbital sinus at a concentration of 24 µmol/kg. Control mice received <span>PBS</span> instead. Mice were anesthetized with <span>isoflurane</span> 2-3% for injections, blood collection and sacrifice. All mice were sacrificed by cervical dislocation, 4 hours after injection.</p> <p>The results of <span>livers (indicated foie)</span> from HbAA mice injected or not with <span>heme</span> are presented here . </p> <p>The results of <span>livers <span>(indicated foie)</span></span> from <span>HbSS</span> mice injected or not with <span>heme</span> can be found at number <a href="https://doi.org/10.5281/zenodo.10962971">10.5281/zenodo.10962971</a>. </p> <p>Thirty μm-thick frozen tissue sections of <span>livers</span> were cut as above and homogenized in 200μL of 1-Thioglycerol/Homogenization Solution (Maxwell® 16 LEV simplyRNA Tissue Kit <span>Promega</span> AS1280). The quality and quantity of mRNA were evaluated using a 2100 bioanalyzer with TNA 6000 NanoKits (all <span>Agilent Technologies</span>, <span>Palo Alto, CA</span>, <span>USA</span>). RNA Integrity Numbers superior to 7 were eligible for subsequent <span>reverse transcription</span> into <span>cDNA</span>. <span>RNAseq</span> was performed at the GenomIC plateform <span>Cochin</span> Institute INSERM U1016. After <span>RNA extraction</span>, RNA quality (<span>RNA integrity number</span>) was estimated. 1μg of high-quality total RNA sample (RIN &gt;7) was processed to build up the libraries, using TruSeq Stranded mRNA kit (<span>Illumina</span>) according to manufacturer instructions. Briefly, purified <span>poly-A</span> containing mRNA molecules were fragmented and <span>reverse-transcribed</span> using random <span>primers</span>. Replacement of dTTP by dUTP during second strand synthesis allowed us to achieve strand specificity. Addition of a single A base to the <span>cDNA</span> was followed by <span>ligation</span> of <span>Illumina</span> adapters.<br>Libraries were quantified by <span>qPCR</span> using <span>KAPA Library Quantification</span> Kits for <span>Illumina</span> Libraries (KapaBiosystems, <span>Wilmington</span>, MA). Library profiles were assessed using DNA High Sensitivity LabChip kits on an <span>Agilent</span> Bioanalyzer. Libraries were sequenced on an <span>Illumina</span> Nextseq 500 instrument using 75 base-lengths read V2 chemistry in a <span>paired-end</span> mode. After sequencing, primary analysis based on AOZAN software (ENS, <span>Paris</span>), was applied to <span>demultiplex</span> and control the quality of the <span>raw data</span> (based of FastQC modules / version 0.11.5).</p> <p>The dataset here represents 4 groups of mice, 4 mice per group as follows: HbAA <span>PBS</span>, HbAA <span>heme</span>, HbSS <span>PBS</span>, <span>HbSS</span> <span>heme</span>. </p>
Data from: Steatotic liver disease induced by TCPOBOP-activated hepatic constitutive androstane receptor: Primary and secondary gene responses with links to disease progression
<p>Constitutive Androstane Receptor (CAR, <em>Nr1i3</em>), a liver nuclear receptor and xenobiotic sensor, induces drug, steroid and lipid metabolizing enzymes, stimulates liver hypertrophy and hyperplasia, and ultimately, hepatocellular carcinogenesis. The mechanisms linking early CAR responses to later disease development are poorly understood. Here we show that exposure of CD-1 mice to TCPOBOP, a halogenated xenochemical and selective CAR agonist ligand, induces pericentral steatosis marked by hepatic accumulation of cholesterol and neutral lipid, and elevated circulating alanine aminotransferase, indicating hepatocyte damage. TCPOBOP-induced steatosis was weaker in the pericentral region but stronger in the periportal region in females compared to males. Early (1-day) TCPOBOP transcriptional responses were enriched for CAR-bound primary response genes, and for lipogenesis and xenobiotic metabolism and oxidative stress protection pathways; late (2-wk) TCPOBOP responses included many CAR binding-independent secondary response genes, with enrichment for macrophage activation, immune response and cytokine and reactive oxygen species production. Late upstream regulators specific to TCPOBOP-exposed male liver were linked to pro-inflammatory responses and hepatocellular carcinoma progression. TCPOBOP administered weekly to male mice using a high corn oil vehicle activated carbohydrate-responsive transcription factor (MLXIPL)-regulated target genes, dysregulated mitochondrial respiratory and translation regulatory pathways, and induced more advanced liver pathology. Overall, TCPOBOP exposure recapitulates histological and gene expression changes characteristic of emerging steatotic liver disease, including secondary gene responses in liver non-parenchymal cells indicative of transition to a more advanced disease state. Upstream regulators of both the early and late TCPOBOP response genes include novel biomarkers for foreign chemical-induced metabolic dysfunction-associated steatotic liver disease.</p>
Raw Data for the article: Risk factors for bile leakage after liver resection for neoplastic disease
<p>Biliary leakage (BL) remains the most frequent and feared complication after hepatoresective surgery. Placement of the abdominal drainage at the end of liver surgery remains controversial due to the delicate balance between risks and potential benefits in case of BL. The study was aimed to detect possible risk factors for BL occurrence after liver surgery. We enrolled all oncologic patients who underwent liver resection from June 2016 to March 2021. BL was diagnosed according to the ISGLS definition. We have examined demographic characteristics of the patients, type of neoplasia, presence of cirrhosis, neoadjuvant chemotherapy and type of intervention. Uni- and multivariable analyses were performed to assess the predictive value of potential predictor of BL. A total of 379 patients were enrolled in the study, 16 (4.2%) of which developed BL. Among others, at univariate analysis the occurrence of BL was found to be associated with bilio-digestive anastomosis (OR: 9.75, C.I. 2.7-34.7, p < 0.001) and neoadjuvant chemotherapy (OR: 0.09, C.I 0.01,-0.88, p = 0.039). Multivariable analysis selected the body mass index (OR: 1.21, 95%C.I.: 1.04-1.41, p = 0.015), anatomical resection (OR: 8.35, 95% C.I.: 2.01-34.74, p = 0.004), and blood loss (OR: 1.09, 95%C.I.: 1.05-1.13, p < 0.001). Identification of patients at greater risk of BL can help in the choice of positioning the drainage at the end of liver surgery.</p>
Association of fat-to-muscle ratio with non-alcoholic fatty liver disease: a single-centre retrospective study
<p><strong>Objectives</strong>: Sarcopenia is a known risk factor for non-alcoholic fatty liver disease (NAFLD). Studies evaluating the association between the fat-to-muscle ratio (FMR) and NAFLD are limited. Therefore, the aim of our study was to investigate the association between FMR and NAFLD.</p> <p><strong>Design:</strong> A retrospective study was conducted on the individuals who underwent health examination in Wuhan Union Hospital between January 2020 and November 2021. Clinical data were collected from electronic medical records.</p> <p><strong>Setting:</strong> Our study was conducted in a hospital in China.</p> <p><strong>Participants:</strong> A total of 1,592 participants aged ≥40 years who underwent body composition analysis and liver ultrasonography were retrospectively reviewed.</p> <p><strong>Primary outcome measures:</strong> Liver ultrasonography was used to assess liver steatosis, and the Fibrosis-4 Index (FIB-4) was used to calculate the risk scores for liver fibrosis. The 10-year atherosclerotic cardiovascular disease (ASCVD) risk prediction model was used to calculate ASCVD risk scores.</p> <p><strong>Results:</strong> The FMR was significantly higher in individuals with NAFLD than in those without NAFLD (P<0.001). The prevalence of NAFLD gradually increased from FMR tertile 1 (reference) to tertile 2 (OR=1.49, 95% CI: 1.13–1.97) and tertile 3 (OR=2.85, 95% CI: 2.08–3.90). In addition, patients with NAFLD in FMR tertile 3 had a significantly higher risk of liver fibrosis (OR=4.48, 95% CI: 2.12–9.50) and ASCVD (OR=4.63, 95% CI: 2.62–8.19) than those in FMR tertile 1 after adjustment for multiple confounders.</p> <p><strong>Conclusion:</strong> In this study, we found a significant association between FMR and NAFLD. A higher FMR indicates a higher risk of NAFLD in the study population and a higher risk of liver fibrosis and ASCVD in NAFLD patients.</p>
Treatment of Nonalcoholic Fatty Liver Disease in Children (TONIC)
ClinicalTrials.gov study NCT00063635. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Study Comparing Tenofovir Disoproxil Fumarate (TDF), Emtricitabine (FTC)/TDF, and Entecavir (ETV) in the Treatment of Chronic HBV in Subjects With Decompensated Liver Disease.
ClinicalTrials.gov study NCT00298363. IPD Sharing: Not stated. Countries: 11. Publications: 1.
Prevalence of Non-alcoholic Fatty Liver Disease (NAFLD) in Hispanics With Diabetes Mellitus Type 2 (T2DM) and Role of Treatment
ClinicalTrials.gov study NCT01002547. IPD Sharing: NO. Countries: 1. Publications: 1.
Phase 2a, Dose-ranging Study With PF-05221304 in Nonalcoholic Fatty Liver Disease (NAFLD)
ClinicalTrials.gov study NCT03248882. IPD Sharing: YES. Countries: 6. Publications: 2.
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Annotated Behaviour and Observability Dataset (ABODe)
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