Search results for "pancreas"

showing 10 items of 231 documents

Overexpression of glucose 6 phosphate dehydrogenase preserves mouse pancreatic beta cells function until late in life.

2021

NAD(P)H donates electrons for reductive biosynthesis and antioxidant defense across all forms of life. Glucose-6- phosphate dehydrogenase (G6PD) is a critical enzyme to provide NADPH. G6PD deficiency is present in more than 400 million people worldwide. This enzymopathy provides protection against malaria but sensitizes cells to oxidative stressors. Oxidative stress has been involved in the pathogenesis of the diabetic complications and several studies have provided evidences of a link between G6PD deficiency and type 2 diabetes (T2D). We hypothesized that a moderate overexpression of G6PD (G6PD-Tg) could protect β-cells from age-associated oxidative stress thus reducing the risk of develop…

0301 basic medicineAgingmedicine.medical_specialtyOxidative phosphorylationType 2 diabetesGlucosephosphate Dehydrogenasemedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinehemic and lymphatic diseasesPhysiology (medical)Internal medicineDiabetes mellitusInsulin-Secreting Cellsparasitic diseasesNADPHmedicineGlucose-6-phosphate dehydrogenaseAnimalsPancreatic isletsDiabetesWild typenutritional and metabolic diseasesmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structureGlucosephosphate Dehydrogenase DeficiencychemistryDiabetes Mellitus Type 2Oxidative stressPancreas030217 neurology & neurosurgeryOxidative stressFree radical biologymedicine
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Circulating Tumor DNA Detection by Digital-Droplet PCR in Pancreatic Ductal Adenocarcinoma: A Systematic Review

2021

Simple Summary Pancreatic cancer is a digestive tumor that is most difficult to treat and carries one of the worst prognoses. The anatomical location of the pancreas makes it very difficult to obtain enough tumor material to establish a molecular diagnosis, so knowing the biology of this tumor and implementing new targeted-therapies is still a pending issue. The use of liquid biopsy, a blood sample test to detect circulating-tumor DNA fragments (ctDNA), is key to overcoming this difficulty and improving the evolution of this tumor. Liquid biopsies are equally representative of the tissue from which they come and allow relevant molecular and diagnostic information to be obtained in a faster …

0301 basic medicineCancer Researchpancreatic cancerpancreatic ductal adenocarcinoma (PDAC)lcsh:RC254-28203 medical and health sciences0302 clinical medicineCirculating tumor cellPancreatic cancerBiopsydigital-droplet PCR (ddPCR)MedicineLiquid biopsymedicine.diagnostic_testbusiness.industryctDNAmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMinimal residual disease030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellCancer researchBiomarker (medicine)Systematic ReviewbusinessPancreasCancers
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Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis

2016

Ductal occlusion has been postulated to precipitate focal pancreatic inflammation, while the nature of the primary occluding agents has remained elusive. Neutrophils make use of histone citrullination by peptidyl arginine deiminase-4 (PADI4) in contact to particulate agents to extrude decondensed chromatin as neutrophil extracellular traps (NETs). In high cellular density, NETs form macroscopically visible aggregates. Here we show that such aggregates form inside pancreatic ducts in humans and mice occluding pancreatic ducts and thereby driving pancreatic inflammation. Experimental models indicate that PADI4 is critical for intraductal aggregate formation and that PADI4-deficiency abrogates…

0301 basic medicineExtracellular TrapsHydrolasesNeutrophilsScienceGeneral Physics and AstronomyBiologyExtracellular TrapsArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciencesPancreatic JuiceProtein-Arginine Deiminase Type 4medicineAnimalsHumansPancreasCeruletideMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionQInterleukin-17Pancreatic DuctsGeneral ChemistryNeutrophil extracellular trapsFlow Cytometrymedicine.diseaseImmunohistochemistryChromatinCell biologyChromatinDisease Models AnimalHistone citrullination030104 developmental biologymedicine.anatomical_structurePancreatitisChronic DiseasePancreatic juiceImmunologyProtein-Arginine DeiminasesCytokinesPancreatitisPancreasCeruletideNature Communications
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Histone macroH2A1.2 promotes metabolic health and leanness by inhibiting adipogenesis

2016

Background Obesity has tremendous impact on the health systems. Its epigenetic bases are unclear. MacroH2A1 is a variant of histone H2A, present in two alternatively exon-spliced isoforms macroH2A1.1 and macroH2A1.2, regulating cell plasticity and proliferation, during pluripotency and tumorigenesis. Their role in adipose tissue plasticity is unknown. Results Here, we show evidence that macroH2A1.1 protein levels in the visceral adipose tissue of obese humans positively correlate with BMI, while macroH2A1.2 is nearly absent. We thus introduced a constitutive GFP-tagged transgene for macroH2A1.2 in mice, and we characterized their metabolic health upon being fed a standard chow diet or a hig…

0301 basic medicineGenetically modified mouseCyclin-Dependent Kinase Inhibitor p21macroh2a1.2TransgeneAdipose tissueAdipose tissueMice TransgenicBiologyCarbohydrate metabolismDiet High-FatBody Mass IndexCell LineHistones03 medical and health sciencesMiceHistone variantGeneticsAnimalsHumansInsulinEpigeneticsAdipose tissue Histone variants Obesity macroh2a1.2ObesityTranscription factorPancreasMolecular BiologyUncoupling Protein 1SkinHistone variantsAdipogenesisResearchCell DifferentiationGlucose Tolerance TestMolecular biologyCell biologyMice Inbred C57BL030104 developmental biologyPhenotypeLiverMetabolic EngineeringAdipogenesisDNA methylationAdipose tissue; Histone variants; macroh2a1.2; Obesity; Molecular Biology; Genetics
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Telomerase and pluripotency factors jointly regulate stemness in pancreatic cancer stem cells

2021

© 2021 by the authors.

0301 basic medicineHomeobox protein NANOGCancer ResearchTelomerasePancreatic neoplasmsMedicinaBiologyStammzelleArticle03 medical and health sciences0302 clinical medicineSOX2Cancer stem cellPancreatic cancermedicineddc:610BauchspeicheldrüsenkrebsStemnessTelomeraseRC254-282Telomere lengthPancreas; CancerCancer stem cellsNeoplastic stem cellsCancer stem cells; Pancreatic cancer; Self-renewal; Stemness; Telomerase; Telomere lengthNeoplasms. Tumors. Oncology. Including cancer and carcinogensPancreatic cancermedicine.disease3. Good healthTelomere030104 developmental biologyOncologyKLF4030220 oncology & carcinogenesisCancer researchSelf-renewalStem cellDDC 610 / Medicine & health
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Sunitinib in patients with pre-treated pancreatic neuroendocrine tumors: A real-world study.

2018

Abstract Introduction Besides data reported in a Phase-III trial, data on sunitinib in pancreatic Neuroendocrine Tumors (panNETs) are scanty. Aim To evaluate sunitinib efficacy and tolerability in panNETs patients treated in a real-world setting. Patients and methods Retrospective analysis of progressive panNETs treated with sunitinib. Efficacy was assessed by evaluating progression-free survival, overall survival, and disease control (DC) rate (stable disease (SD) + partial response + complete response). Data are reported as median (25th–75th IQR). Results Eighty patients were included. Overall, 71.1% had NET G2, 26.3% had NET G1, and 2.6% had NET G3 neoplasms. A total of 53 patients (66.3…

0301 basic medicineIndolesEndocrinology Diabetes and MetabolismNeuroendocrine tumorsPyrroleGastroenterologyTarget therapyEfficacyAntineoplastic Agent0302 clinical medicineEndocrinologyRetrospective StudieSunitinibPancreadiabetes and metabolismSunitinibGastroenterologyPancreatic NeoplasmMiddle AgedDiabetes and MetabolismNeuroendocrine TumorsTreatment OutcomeTolerabilityNeuroendocrine tumors; Pancreas; Progressive disease; Sunitinib; Target therapy; Endocrinology Diabetes and Metabolism; Hepatology; EndocrinologyItaly030220 oncology & carcinogenesisNeuroendocrine tumorsmedicine.drugHumanAdultmedicine.medical_specialtyAntineoplastic AgentsNeutropenia03 medical and health sciencesNeuroendocrine tumorInternal medicinemedicineHumansPyrrolesProgression-free survivalPancreasCancer stagingAgedRetrospective StudiesHepatologybusiness.industryProgressive diseasemedicine.diseasePancreatic Neoplasms030104 developmental biologyNeuroendocrine tumors; pancreas; progressive disease; Sunitinib; target therapy; endocrinology; diabetes and metabolism; hepatology; endocrinologyIndolebusinessProgressive diseasePancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
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Elevated Serum Fibroblast Growth Factor 21 in Humans with Acute Pancreatitis.

2016

Background The metabolic regulator Fibroblast Growth Factor 21 (FGF21) is highly expressed in the acinar pancreas, but its role in pancreatic function is obscure. It appears to play a protective role in acute experimental pancreatitis in mice. The aim of this study was to define an association between FGF21 and the course and resolution of acute pancreatitis in humans. Methods and Principal Findings Twenty five subjects with acute pancreatitis admitted from May to September 2012 to the Beth Israel Deaconess Medical Center (BIDMC) were analyzed. Serial serum samples were collected throughout hospitalization and analyzed for FGF21 levels by ELISA. Twenty healthy subjects sampled three times o…

0301 basic medicineMaleAbdominal painFGF21Fibroblast Growth FactorPhysiologyHydrolaseslcsh:MedicineFibroblast growth factorPathology and Laboratory MedicineGastroenterologyBiochemistryEndocrinologyMedicine and Health SciencesLipasesIsraellcsh:ScienceFluidsMultidisciplinaryLiver DiseasesPhysicsFatty liverMiddle AgedEnzymesmedicine.anatomical_structurePhysical SciencesAcute DiseaseAcute pancreatitisFemalemedicine.symptomAnatomyPancreasResearch Articlemedicine.medical_specialtyStates of MatterPainEndocrine SystemGastroenterology and Hepatology03 medical and health sciencesExocrine GlandsSigns and SymptomsDiagnostic MedicineInternal medicineGrowth FactorsmedicineEndocrine systemHumansPancreasDemographyEndocrine Physiologybusiness.industrylcsh:RBiology and Life SciencesProteinsmedicine.diseaseAbdominal PainFatty LiverFibroblast Growth Factors030104 developmental biologyEndocrinologyPancreatitisPeople and PlacesEnzymologyPancreatitislcsh:QbusinessPLoS ONE
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Unexpected subcellular distribution of a specific isoform of the Coxsackie and adenovirus receptor, CAR-SIV, in human pancreatic beta cells

2018

Aims/hypothesis: The Coxsackie and adenovirus receptor (CAR) is a transmembrane cell-adhesion protein that serves as an entry receptor for enteroviruses and may be essential for their ability to infect cells. Since enteroviral infection of beta cells has been implicated as a factor that could contribute to the development of type 1 diabetes, it is often assumed that CAR is displayed on the surface of human beta cells. However, CAR exists as multiple isoforms and it is not known whether all isoforms subserve similar physiological functions. In the present study, we have determined the profile of CAR isoforms present in human beta cells and monitored the subcellular localisation of the princi…

0301 basic medicineMaleviruksetEndocrinology Diabetes and MetabolismInsulin-Secreting CellsProtein IsoformsReceptorChildProinsulinEnterovirusMicroscopy ConfocalChemistryNuclear ProteinsImmunogold labellingMiddle AgedFlow CytometryImmunohistochemistryTransmembrane protein3. Good healthCell biologyEndocrinologieenteroviruksetMédecine interneProtein interacting with C-kinase 1 (PICK1)medicine.anatomical_structureChild PreschoolCoxsackievirus BFemalePancreasPICK1Gene isoformBeta cells; Coxsackie and adenovirus receptor; Coxsackievirus B; Enterovirus; Insulin granule; Pancreas; Protein interacting with C-kinase 1 (PICK1)AdultCoxsackie and Adenovirus Receptor-Like Membrane ProteinAdolescentImmunoprecipitationBlotting WesterninsuliiniArticle03 medical and health sciencesYoung AdultMétabolismeInternal MedicinemedicineHumansImmunoprecipitationPancreasCoxsackie and adenovirus receptorInsulin granuleDiabétologieBeta cellshaima030104 developmental biologyDiabetes Mellitus Type 1Carrier ProteinsDiabetologia
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Molecular aspects of pancreatic β-cell dysfunction: Oxidative stress, microRNA, and long noncoding RNA.

2018

Metabolic syndrome is known as a frequent precursor of type 2 diabetes mellitus (T2D). This disease could affect 8% of the people worldwide. Given that pancreatic β-cell dysfunction and loss have central roles in the initiation and progression of the disease, the understanding of cellular and molecular pathways associated with pancreatic β-cell dysfunction can provide more information about the underlying pathways involved in T2D. Multiple lines evidence indicated that oxidative stress, microRNA, and long noncoding RNA play significant roles in various steps of diseases. Oxidative stress is one of the important factors involved in T2D pathogenesis. This could affect the function and surviva…

0301 basic medicinePhysiologyClinical BiochemistryCellDiseaseBiologymedicine.disease_causePathogenesis03 medical and health sciences0302 clinical medicineInsulin-Secreting CellsGene expressionmicroRNAmedicineHumansEpigeneticsPancreasCell BiologyLong non-coding RNACell biologyMicroRNAsOxidative Stress030104 developmental biologymedicine.anatomical_structureDiabetes Mellitus Type 2030220 oncology & carcinogenesisRNA Long NoncodingOxidative stressSignal TransductionJournal of cellular physiology
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