2010
Molecular and cellular mechanisms of pancreatic injury
Thrower EC, Gorelick FS, Husain SZ. Molecular and cellular mechanisms of pancreatic injury. Current Opinion In Gastroenterology 2010, 26: 484-489. PMID: 20651589, PMCID: PMC3023172, DOI: 10.1097/mog.0b013e32833d119e.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisEndoplasmic ReticulumHumansPancreasPancreatitis, Acute NecrotizingPancreatitis, ChronicTrypsinTrypsinogenConceptsPancreatic injuryCellular mechanismsFibroblast growth factor 21Antiapoptotic effectGrowth factor 21Ameliorate injuryEndoplasmic reticulum stressChronic pancreatitisFactor 21Immune cellsExendin-4Endogenous trypsin inhibitorBile acidsDisease severityInjuryPancreatitisCausative factorsSensitizing factorTrypsinogen activationProtein CReticulum stressTrypsinogen mutationsBcl-2Intracellular eventsUpregulation of proteins
2009
Impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis
Mareninova OA, Hermann K, French SW, O’Konski M, Pandol SJ, Webster P, Erickson AH, Katunuma N, Gorelick FS, Gukovsky I, Gukovskaya AS. Impaired autophagic flux mediates acinar cell vacuole formation and trypsinogen activation in rodent models of acute pancreatitis. Journal Of Clinical Investigation 2009, 119: 3340-3355. PMID: 19805911, PMCID: PMC2769194, DOI: 10.1172/jci38674.Peer-Reviewed Original ResearchAnimalsAutophagyCathepsinsDisease Models, AnimalFastingFemaleLysosomesMaleMicePancreasPancreatitis, Acute NecrotizingProteinsRatsTrypsinTrypsinogenVacuolesNew Insights Into the Mechanisms of Pancreatitis
Gaisano HY, Gorelick FS. New Insights Into the Mechanisms of Pancreatitis. Gastroenterology 2009, 136: 2040-2044. PMID: 19379751, DOI: 10.1053/j.gastro.2009.04.023.Peer-Reviewed Original Research
2008
Molecular basis for pancreatitis
Thrower E, Husain S, Gorelick F. Molecular basis for pancreatitis. Current Opinion In Gastroenterology 2008, 24: 580-585. PMID: 19122498, PMCID: PMC3030809, DOI: 10.1097/mog.0b013e32830b10e6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalHumansMiceMolecular BiologyPancreatitis, Acute NecrotizingPancreatitis, AlcoholicPancreatitis, ChronicPrognosisRisk AssessmentSensitivity and SpecificityConceptsChronic pancreatitisAcute pancreatitisPain responseAnimal modelsToll-like receptor 4Transient receptor potential vanilloid subtype 1Specific neural receptorsSevere acute pancreatitisBasic science studiesChymotrypsin CShock protein 70Neural receptorsReceptor 4Chronic diseasesPancreatitisAlcohol abuseReceptor 2Subtype 1Potential treatmentPilot studyProtective mechanismAcinar cellsProtein 70Genetic factorsYear findings
2002
Neutrophils and NADPH oxidase mediate intrapancreatic trypsin activation in murine experimental acute pancreatitis
Gukovskaya AS, Vaquero E, Zaninovic V, Gorelick FS, Lusis AJ, Brennan M, Holland S, Pandol SJ. Neutrophils and NADPH oxidase mediate intrapancreatic trypsin activation in murine experimental acute pancreatitis. Gastroenterology 2002, 122: 974-984. PMID: 11910350, DOI: 10.1053/gast.2002.32409.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesCeruletideEnzyme ActivationMaleMiceMice, Inbred BALB CMice, KnockoutNADPH OxidasesNeutrophilsPancreasPancreatitis, Acute NecrotizingPhosphoproteinsRatsRats, Sprague-DawleyTrypsinConceptsIntrapancreatic trypsin activationAcute pancreatitisNADPH oxidaseTrypsin activationAdenine Dinucleotide Phosphate OxidaseParenchymal cell injuryExperimental acute pancreatitisNADPH oxidase activityPancreatic acinar tissueDigestive enzymesWestern blot analysisAntineutrophil serumPathologic activationCell injuryPancreatitisExperimental pancreatitisHigh dosesMarked attenuationNeutrophilsAbstractTextAcinar tissuePancreatic homogenatesReactive oxygen speciesMyeloperoxidaseMice
2000
EARLY TRYPSINOGEN ACTIVATION IN ACUTE PANCREATITIS
Lerch M, Gorelick F. EARLY TRYPSINOGEN ACTIVATION IN ACUTE PANCREATITIS. Medical Clinics Of North America 2000, 84: 549-563. PMID: 10872413, DOI: 10.1016/s0025-7125(05)70239-x.Peer-Reviewed Original ResearchMeSH KeywordsCalcium SignalingEndopeptidasesEnzyme ActivationGenetic Predisposition to DiseaseHumansHydrogen-Ion ConcentrationPancreasPancreatitis, Acute NecrotizingTrypsinogen