Search results for "cck"

showing 4 items of 4 documents

Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Hypothalamus-specific deletion of socs3 in adult mice enhances hindbrain sensitivity to endogenous satiety signals via oxytocin signaling

2011

Communication sans actes n° 469 (1 page) ; http://www.neurosciences.asso.fr/V2/colloques/SN11/; Leptin is a major contributor to long-term energy homeostasis, through an intracellular transduction pathway involving activation of Stat3 and its feedback inhibitor Socs3, which limits Stat3 activation. Previous studies have shown that Socs3 haploinsufficiency or socs3 deletion in the whole brain or in selective neuronal populations triggers an increased sensitivity to exogenous leptin, through increased Stat3 activation, and protects against diet-induced obesity in mice fed a high fat diet. Intriguingly however, no phenotype was detected when Socs3 mutant mice were maintained under standard die…

[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT][SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]digestive oral and skin physiologycck[ SDV.OT ] Life Sciences [q-bio]/Other [q-bio.OT]nucleus tractus solitariusComputingMilieux_MISCELLANEOUSdevazepide
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Cowbird versus cuckoo hosts: a comparative study of learned nest defense

2005

One of the best example of coevolutionaru adaptations is that of the interactions between avian brood parasites and their hosts. Brood parasites lay their eggs in nests of other specieis and leave the job of caring for their young with the hosts. Hosts of brood parasites tend to suffer high reproductive costs as often they raise few of no young of their own, an effect of being parasitizes. For this reason, many hosts have evolved strategies that reduces the cost of parasitism.

brood parasitism common cucckoo brown-headed cowbird nest defence coevolutionary mechanisms
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Association between CCK-AR gene and schizophrenia with auditory hallucinations

2007

[Objective]: Previous studies on a possible association between CCK-AR polymorphisms and schizophrenia have been controversial. The aim of the present study was to assess a potential association between schizophrenic patients with auditory hallucinations and polymorphisms of the CCK-AR gene.

medicine.medical_specialtyGenotypeHallucinationsSingle-nucleotide polymorphismAuditory hallucinationsRegulatory Sequences Nucleic Aciddigestive systemPolymorphism Single NucleotideGene FrequencyReference ValuesInternal medicineGenotypeGene expressionGeneticsmedicineHumansSNPCCK-AR geneAllelePsychiatryGeneBiological PsychiatryGenetics (clinical)DNA Primersbusiness.industrydigestive oral and skin physiologyHaplotypeDNAmedicine.diseaseReceptor Cholecystokinin APsychiatry and Mental healthEndocrinologySchizophreniaSchizophreniaSchizophrenic Psychologybusinesshormones hormone substitutes and hormone antagonistsPsychiatric Genetics
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