Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
6,650
datasets available to search
ShareScore release 0.9.0
Dataset results
6,650 results for “pancreatitis”
Metabolic syndrome for the prognosis of postoperative complications after open pancreatic surgery in Chinese adult: a propensity score matching study
<p><strong>Background: </strong>To investigate the relationship between metabolic syndrome (MS) and postoperative complications in Chinese adults after open pancreatic surgery.</p> <p><strong>Methods: </strong>Relevant data were retrieved from the Medicalsystem® database of Changhai hospital (MDCH). All patients who underwent pancreatectomy from January 2017 to May 2019 were included, and relevant data were collected and analyzed. A propensity score matching (PSM) and a multivariate generalized estimating equation were used to investigate the association between MS and composite compositions during hospitalization. Cox regression model was employed for survival analysis.</p> <p><strong>Results: </strong>1481 patients were finally eligible for this analysis. According to diagnostic criteria of Chinese MS, 235 patients were defined as MS, and the other 1246 patients were controls. After PSM, no association was found between MS and postoperative composite complications (OR: 0.958, 95%CI: 0.715-1.282, P=0.958). But MS was associated with postoperative acute kidney injury (OR: 1.730, 95%CI: 1.050-2.849, P=0.031). Postoperative AKI was associated with mortality in 30 days and 90 days after surgery (P<0.001).</p> <p><strong>Conclusions: </strong>MS is not an independent risk factor correlated with postoperative composite complications after open pancreatic surgery. But MS is an independent risk factor for postoperative AKI of pancreatic surgery in Chinese population, and AKI is associated with survival after surgery.</p>
Adipose-derived stromal cells preserve pancreatic islet function in a transplantable 3D bioprinted scaffold
<p><span>Intra-portal islet transplantation is the method of choice for treatment of insulin dependent type 1 diabetes, but its outcome is hindered by limited islet survival due to the immunological and metabolic stress post transplantation. Adipose-derived stromal cells (ASCs) promise to improve significantly the islet micro-environment but an efficient long-term delivery method has not been achieved. We therefore explore the potential of generating ASC enriched islet transplant structure by 3D bioprinting. Here, we fabricate a double-layered 3D bioprinted scaffold for islets and ASCs by using alginate-nanofibrillated cellulose bioink. We demonstrate the diffusion properties of the scaffold and report that human ASCs increase the islet viability, preserve the endocrine function, and reduce pro-inflammatory cytokines secretion <em>in vitro</em>. Intraperitoneal implantation of the ASCs and islets in 3D bioprinted scaffold improve the long-term function of islets in diabetic mice. Our data reveals an important role for ASCs on the islet micro-environment. We suggest a novel cell therapy approach of ASCs combined with islets in a 3D structure with a potential for clinical beta cell replacement therapies at extrahepatic sites. </span></p>
Single-cell transcriptomic profiling of human pancreatic islets reveals genes responsive to glucose exposure over 24 hours
<p><strong>Aims/hypothesis</strong>: Disruption of pancreatic islet function and glucose homeostasis can lead to the development of sustained hyperglycemia, beta cell glucotoxicity, and subsequently type 2 diabetes. In this study, we explored the effects of <em>in vitro</em> hyperglycemic conditions on human pancreatic islet gene expression across 24 hours in six pancreatic cell types: alpha, beta, gamma, delta, ductal, and acinar cells. We hypothesized that genes associated with hyperglycemic conditions may be relevant to the onset and progression of diabetes.</p> <p><strong>Methods</strong>: We exposed human pancreatic islets from two donors to low (2.8 mmol/l) and high (15.0 mmol/l) glucose concentrations over 24 hours <em>in vitro</em>. To assess the transcriptome, we performed single-cell RNA sequencing (scRNA-seq) at seven time points. We modeled time as both a discrete and continuous variable to determine momentary and longitudinal changes in transcription associated with islet time in culture or glucose exposure. Additionally, we integrated genomic features and genetic summary statistics to nominate candidate effector genes. For three of these genes, we functionally characterized the effect on insulin production and secretion using CRISPR interference to knockdown gene expression in EndoC-βH1 cells, followed by a glucose-stimulated insulin secretion assay.</p> <p><strong>Results</strong>: Across all cell types, we identified 1,447 genes associated with time, 680 genes associated with glucose exposure, and 418 genes associated with interaction effects between time and glucose. By integrating these expression profiles with summary statistics from genetic association studies, we identified 2,449 candidate effector genes for type 2 diabetes, HbA1c, random blood glucose, and fasting blood glucose. Of these candidate effector genes, we showed that three—<em>ERO1B</em>, <em>HNRNPA2B1</em>, and <em>RHOBTB3</em>—exhibited an effect on glucose-stimulated insulin secretion and production in EndoC-βH1 cells.</p> <p><strong>Conclusions/interpretation</strong>: The findings of our study provide an in-depth characterization of the 24-hour transcriptomic response of human pancreatic islets to glucose exposure at a single-cell resolution. By integrating differentially expressed genes with genetic signals for type 2 diabetes and glucose-related traits, we provide insights into the molecular mechanisms underlying glucose homeostasis. Finally, we provide functional evidence to support the role of three candidate effector genes in insulin secretion and production.</p>
COMMUNI.CARE (Communication and Patient Engagement at Diagnosis of Pancreatic Cancer): Study Protocol
<div> <div> <div> <div> <p>Consecutive PDAC patients were enrolled at the time of diagnosis after obtaining informed consent in a single-center study for a total of 32 doctor-patient interactions. Data were audio-recorded, fully anonymized, and then transcribed. All data are in Italian.</p> </div> </div> </div> </div>
Development of human pancreatic cancer avatars as a model for dynamic immune landscape profiling and personalised therapy
<div> <div> <div> <p>Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer, a disease with dismal overall survival. Advances in treatment are hindered by a lack of preclinical models. Here we show how a personalised organotypic 'avatar' created from resected tissue, allows spatial and temporal reporting on a complete in situ tumour microenvironment, and mirrors clinical responses. Our perfusion culture method extends tumour slice viability, maintaining stable tumour content, metabolism, stromal composition, and immune cell populations for 12 days. Using multiplexed immunofluorescence and spatial transcriptomics, we identify immune neighbourhoods and potential for immunotherapy. We employed avatars to assess the impact of a pre-clinically validated metabolic therapy and show recovery of stromal and immune phenotypes and tumour re-differentiation. To determine clinical relevance, we monitored avatar response to gemcitabine treatment and identified a patient avatar-predicable response from clinical follow-up. Thus, avatars provide valuable information for the syngeneic testing of novel therapeutics and a truly personalised therapeutic assessment platform for patients.</p> </div> </div> </div>
AL589863.1 inhibits the progression of pancreatic cancer through regulating miR-671-5p/THBS1 axis
<p><span>We obtained <a name="OLE_LINK1"></a>mRNA and lncRNA expression profiles from 178 PC tissues and 4 normal pancreatic tissues in the TCGA database. We further downloaded the high throughput database of 167 normal tissues of the pancreas in the GTEx database. Then, the TCGA and GTEx datasets were integrated for further analysis. Three microarray datasets, including mRNA (GSE15471 and GSE62165) and miRNA (<a name="OLE_LINK2"></a>GSE32678), were downloaded from the GEO database. GSE15471 contained 39 pairs of <a name="OLE_LINK41"></a>pancreatic ductal adenocarcinoma tumors (PDAC) and adjacent normal tissues. GSE62165 included 118 PDAC and 13 adjacent normal samples. GSE32678 covered 25 PC samples and 7 adjacent normal samples. </span></p> <p><span>The Limma package in R was carried out to identify DEGs, <a name="_Hlk146015254"></a>DEmiRNAs, and DEl<a name="OLE_LINK4"></a><span>ncRNAs</span>. We identified the DEGs with threshold values of </span><span>|log 2 FC|> 1.5 and adjusted. <a name="OLE_LINK3"></a><em>p</em>-value< 0.05. </span><span>DEmiRNAs and DElncRNAs were determined with </span><a name="_Hlk146015501"></a><span>|log 2 FC|> 1.5/2.0 and <em>p</em>-value< 0.05</span><span>. Additionally, volcano plots were drawn to better visualize these DElncRNAs, DEmiRNAs, and DEGs using R software.</span></p>
Machine Learning and Network Analyses Reveals Disease Subtypes of Pancreatic Cancer and their Molecular Characteristics
<p>Supplementary information for the thesis chapter: Machine Learning and Network Analyses Reveals Disease Subtypes of Pancreatic Cancer and their Molecular Characteristics</p>
Synergistic activity of Hsp90 inhibitors and anticancer agents in pancreatic cancer cell cultures (raw data)
<p>This data set includes raw data supporting the paper "<strong>Synergistic activity of Hsp90 inhibitors and anticancer agents in pancreatic cancer cell cultures</strong>".</p> <p><strong>The files include the following data</strong>:</p> <p>1. MTT assay results used for calculation of <strong><em>EC</em><sub>50</sub> values</strong> of tested compounds and their combinations in cancer cells;</p> <p>2. The data used for calculating <strong>combination index</strong> in order to evaluate synergistic activity;</p> <p>3. The raw data from compound activity evaluation in <strong>3D tumor spheroid assay</strong>;</p> <p>4. The data from <strong>compound and hyperthermia </strong>effect evaluation in cancer cells.</p>
TNM classification-based framework for the identification of metastatic progression biomarkers in pancreatic cancer dataset
<p>This data was curated from TCGA and used in the research article titled "TNM classification-based framework for the identification of metastatic progression biomarkers in pancreatic cancer". Gene sets used from MSigDB were also included.</p>
Human pancreatic cancer single cell atlas reveals association of CXCL10+ fibroblasts and basal subtype tumor cells
Open the record for dataset details and reuse information.
Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling
<p class="MsoNormal"><span>Endogenous </span><span>humoral factors </span><span>that</span><span> link systemic and/or local insulin demand to pancreatic β-cells have not been identified. Here</span><span>,</span><span> we demonstrated that T-cadherin, a unique glycosylphosphatidylinositol-anchored cadherin primarily expressed in vascular endothelial cells and cardiac and skeletal muscle cells, but not in pancreatic β-cells, was secreted as soluble forms and was important for β-cell proliferation. <em>Cdh13</em> (T-cadherin) knockout mice exhibited impaired glucose handling due to attenuated β-cell proliferation under high-fat diet conditions. The gene expression analyses indicated the impairment in cell cycle and Notch signaling in the islets of T-cadherin knockout mice under high-fat diet conditions. In streptozotocin-induced diabetes, the replacement of soluble T-cadherin improved β-cell mass and blood glucose </span><span>levels</span><span> in T-cadherin knockout mice. </span><span>R</span><span>ecombinant soluble T-cadherin upregulated Notch signaling in cultured murine islets. We concluded that soluble T-cadherin could work as an endogenous humoral factor whose signaling pathways including Notch signaling regulate β-cell proliferation under diabetic conditions in mice.</span></p>
Single-Cell Mapping Reveals Several Immune Subsets Associated with Liver Metastasis of Pancreatic Ductal Adenocarcinoma
<p>Identifying a metastasis-correlated immune cell composition within the tumor microenvironment (TME) of pancreatic ductal adenocarcinoma (PDAC) will help to develop promising and innovative therapeutic strategies. Twenty-six samples from 11 patients (including 11 primary tumor tissues, 10 blood, and 5 lymph nodes) with different stages were used to develop a multiscale immune profile. High-dimensional single-cell analysis with mass cytometry was performed to search for metastasis-correlated immune changes in the microenvironment.</p> <p>The details about the files uploaded are as follows:</p> <p>1. panelA_Blood.zip includes 10 .fcs files from blood samples in Panel A;</p> <p>2. panelA_LN.zip includes 5 .fcs files from lymph node samples in Panel A;</p> <p>3. panelA_Tumor.zip includes 11 .fcs files from tumor tissue samples in Panel A;</p> <p>4. panelB_Tumor.zip includes 11 .fcs files from tumor tissue samples in Panel B;</p> <p>5. panel_metadata.xlsx describes marker used in Panel A and B;</p> <p>6. sample_metadata.xlsx describes detailed sample information.</p>
Individualized Drug Treatment for Treating Patients With Pancreatic Cancer
ClinicalTrials.gov study NCT00276744. IPD Sharing: NO. Countries: 1. Publications: 1.
Gemcitabine and Paclitaxel vs Gemcitabine Alone After FOLFIRINOX Failure in Metastatic Pancreatic Ductal Adenocarcinoma
ClinicalTrials.gov study NCT03943667. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Capecitabine and Docetaxel in Treating Patients With Recurrent or Progressive Metastatic Pancreatic Cancer
ClinicalTrials.gov study NCT00290693. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Study of Proton Therapy in Adjuvant Pancreatic Cancer
ClinicalTrials.gov study NCT03885284. IPD Sharing: NO. Countries: 1. Publications: 0.
Gemcitabine Hydrochloride and Cisplatin With or Without Veliparib or Veliparib Alone in Treating Patients With Locally Advanced or Metastatic Pancreatic Cancer
ClinicalTrials.gov study NCT01585805. IPD Sharing: Not stated. Countries: 3. Publications: 1.
Fecal Microbiota Transplantation for Pancreatitis
ClinicalTrials.gov study NCT02318134. IPD Sharing: Not stated. Countries: 1. Publications: 12.
Rectal Indomethacin to Prevent Post-Endoscopic Retrograde Cholangiopancreatography (ERCP) Pancreatitis
ClinicalTrials.gov study NCT01774604. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Combination Chemotherapy Before and After Surgery in Treating Patients With Localized Pancreatic Cancer
ClinicalTrials.gov study NCT02047474. IPD Sharing: Not stated. Countries: 1. Publications: 1.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.