2018
Cigarette toxin 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces experimental pancreatitis through α7 nicotinic acetylcholine receptors (nAChRs) in mice
Alahmari AA, Sreekumar B, Patel V, Ashat M, Alexandre M, Uduman AK, Akinbiyi EO, Ceplenski A, Shugrue CA, Kolodecik TR, Tashkandi N, Messenger SW, Groblewski GE, Gorelick FS, Thrower EC. Cigarette toxin 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces experimental pancreatitis through α7 nicotinic acetylcholine receptors (nAChRs) in mice. PLOS ONE 2018, 13: e0197362. PMID: 29870540, PMCID: PMC5988302, DOI: 10.1371/journal.pone.0197362.Peer-Reviewed Original ResearchConceptsNNK treatmentHuman acinar cellsNicotinic acetylcholine receptorsTrypsinogen activationAcetylcholine receptorsΑ7 nicotinic acetylcholine receptorIndependent risk factorMarkers of inflammationAcinar cellsΑ7nAChR knockout miceΑ7nAChR activationNeutrophil infiltrationWT miceAcute pancreatitisC57BL/6 miceCigarette smokingPancreatic edemaRisk factorsClinical studiesPancreatitisCigarette smokeKnockout miceExperimental pancreatitisΑ7 isoformPyknotic nuclei
2012
Tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone initiates and enhances pancreatitis responses
Alexandre M, Uduman AK, Minervini S, Raoof A, Shugrue CA, Akinbiyi EO, Patel V, Shitia M, Kolodecik TR, Patton R, Gorelick FS, Thrower EC. Tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone initiates and enhances pancreatitis responses. AJP Gastrointestinal And Liver Physiology 2012, 303: g696-g704. PMID: 22837343, PMCID: PMC3468532, DOI: 10.1152/ajpgi.00138.2012.Peer-Reviewed Original ResearchConceptsNicotinic acetylcholine receptorsAcetylcholine receptorsCigarette smoke toxinsParameters of pancreatitisPancreatitis responsesTobacco carcinogen 4Acinar cell responsesRat pancreatic aciniSmoke toxinsAcute pancreatitisCigarette smokingIntraperitoneal injectionAcinar cell preparationsClinical studiesLong-term effectsCarcinogen 4Pancreatitis modelAdrenergic receptorsReceptor typesCell responsesTobacco toxinsPyknotic nucleiNNKPancreatic aciniPancreatitis
2009
Reducing Extracellular pH Sensitizes the Acinar Cell to Secretagogue-Induced Pancreatitis Responses in Rats
Bhoomagoud M, Jung T, Atladottir J, Kolodecik TR, Shugrue C, Chaudhuri A, Thrower EC, Gorelick FS. Reducing Extracellular pH Sensitizes the Acinar Cell to Secretagogue-Induced Pancreatitis Responses in Rats. Gastroenterology 2009, 137: 1083-1092. PMID: 19454288, PMCID: PMC2736307, DOI: 10.1053/j.gastro.2009.05.041.Peer-Reviewed Original ResearchConceptsAcinar cellsAcute pancreatitisPancreatic acinar cellsSecretagogue-induced pancreatitisAcid loadAcid challengeAcute acid loadKey early eventPancreatic edemaClinical studiesCell injuryPancreatitisAmylase secretionIsolated aciniAbstractTextPhe effectTrypsinogen activationInjuryPancreatitis responsesZymogen activationAIMSEarly eventsRatsActivationRelevant concentrations
2008
Ethanol Exposure Depletes Hepatic Pigment Epithelium-Derived Factor, a Novel Lipid Regulator
Chung C, Shugrue C, Nagar A, Doll JA, Cornwell M, Gattu A, Kolodecik T, Pandol SJ, Gorelick F. Ethanol Exposure Depletes Hepatic Pigment Epithelium-Derived Factor, a Novel Lipid Regulator. Gastroenterology 2008, 136: 331-340.e2. PMID: 18996124, PMCID: PMC2833423, DOI: 10.1053/j.gastro.2008.09.065.Peer-Reviewed Original ResearchConceptsPigment epithelium-derived factorEthanol-induced hepatic steatosisEthanol-induced steatosisMMP-2/9 activityPEDF levelsHepatic steatosisEthanol feedingLoss of PEDFAnimal modelsTriglyceride contentRecombinant pigment epithelium-derived factorNovel lipid regulatorLiver triglyceride contentLiver biopsy specimensEpithelium-derived factorEthanol fed animalsNormal liver samplesAccumulation of lipidsHistologic steatosisBiopsy specimensClinical studiesEthanol exposureHepatocellular carcinomaSteatosisPigment epithelium
1999
ETIOPATHOGENESIS OF ACUTE PANCREATITIS
Karne S, Gorelick F. ETIOPATHOGENESIS OF ACUTE PANCREATITIS. Surgical Clinics Of North America 1999, 79: 699-710. PMID: 10470320, DOI: 10.1016/s0039-6109(05)70036-0.Peer-Reviewed Original ResearchConceptsAcute pancreatitisCourse of APPotent proteolytic enzymesCapillary leak syndromeAcinar cellsPreliminary clinical studySpecific clinical settingsSystemic complicationsLeak syndromeCytokine inhibitorsInflammatory moleculesCascade of eventsInflammatory cellsPancreatic edemaVasoactive moleculesClinical studiesParticular neutrophilsPancreatitisFurther secretionClinical settingNitric oxideComplement systemCytokinesPremature activationImmediate release