Search results for "AICAR"

showing 6 items of 6 documents

Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon Cancer

2016

Recent studies have correlated physical activity with a better prognosis in cachectic patients, although the underlying mechanisms are not yet understood. In order to identify the pathways involved in the physical activity-mediated rescue of skeletal muscle mass and function, we investigated the effects of voluntary exercise on cachexia in colon carcinoma (C26)-bearing mice. Voluntary exercise prevented loss of muscle mass and function, ultimately increasing survival of C26-bearing mice. We found that the autophagic flux is overloaded in skeletal muscle of both colon carcinoma murine models and patients, but not in running C26-bearing mice, thus suggesting that exercise may release the auto…

0301 basic medicineCachexiaColorectal cancerMuscle Fibers SkeletalMicevoluntary physical activityChloroquineMice Inbred BALB CMultidisciplinaryMuscle WeaknessMyogenesis3. Good healthmedicine.anatomical_structureColonic NeoplasmsFemalecancer cachexiamedicine.drugmedicine.medical_specialty[SDV.CAN]Life Sciences [q-bio]/Cancerautophagic fluxBiologyArticleCachexia03 medical and health sciencesAtrophyInternal medicineCell Line TumorPhysical Conditioning AnimalmedicineAutophagyAerobic exerciseAnimalsHumansMuscle SkeletalSirolimusrapamycinAutophagyAutophagosomesSkeletal musclemuscle wasting[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyRibonucleotidesmedicine.diseaseAminoimidazole CarboxamideSurvival Analysisexercise mimetics030104 developmental biologyEndocrinology5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR)LysosomesNeoplasm Transplantationmuscle wasting; cancer cachexia; voluntary physical activity; exercise mimetics; 5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR); rapamycin; autophagic flux
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RNase H2 Loss in Murine Astrocytes Results in Cellular Defects Reminiscent of Nucleic Acid-Mediated Autoinflammation

2018

Aicardi-Goutières syndrome (AGS) is a rare early onset childhood encephalopathy caused by persistent neuroinflammation of autoimmune origin. AGS is a genetic disorder and >50% of affected individuals bear hypomorphic mutations in ribonuclease H2 (RNase H2). All available RNase H2 mouse models so far fail to mimic the prominent CNS involvement seen in AGS. To establish a mouse model recapitulating the human disease, we deleted RNase H2 specifically in the brain, the most severely affected organ in AGS. Although RNase H2δGFAPmice lacked the nuclease in astrocytes and a majority of neurons, no disease signs were apparent in these animals. We additionally confirmed these results…

0301 basic medicinelcsh:Immunologic diseases. AllergyMaleEncephalomyelitis Autoimmune ExperimentalAicardi–Goutières syndromeRNase PDNA damageImmunologyRibonuclease HFluorescent Antibody TechniqueAicardi-goutières Syndrome ; Cellular Senescence ; Dna Damage ; Interferon Signature ; Rnase H2BiologyNervous System MalformationsAutoimmune Diseases03 medical and health sciencesMiceAutoimmune Diseases of the Nervous SystemNucleic AcidsmedicineImmunology and Allergycellular senescenceAnimalsRibonucleaseNeuroinflammationCells CulturedOriginal ResearchInflammationMice KnockoutInnate immune systemBrainmedicine.diseaseMolecular biologyImmunohistochemistryDisease Models Animal030104 developmental biologymedicine.anatomical_structurePhenotypeinterferon signatureAstrocytesKnockout mousebiology.proteinAicardi–Goutières syndromeDNA damageFemalelcsh:RC581-607RNase H2BiomarkersAstrocyteFrontiers in Immunology
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Case Report: The JAK-Inhibitor Ruxolitinib Use in Aicardi-Goutieres Syndrome Due to ADAR1 Mutation

2021

Type I Interferonopathies comprise inherited inflammatory diseases associated with perturbation of the type I IFN response. Use of Janus kinase (JAK) inhibitors has been recently reported as possible tools for treating some of those rare diseases. We describe herein the clinical picture and treatment response to the JAK-inhibitor ruxolitinib in a 5-year-old girl affected by Aicardi-Goutières Syndrome type 6 (AGS6) due to ADAR1 mutation. The girl's interferon score (IS) was compared with that of her older brother, suffering from the same disorder, who was not treated. We observed a limited, but distinct neurological improvement (Gross Motor Function and Griffiths Mental Development Scales). …

Mental developmentRuxolitinibMutationTreatment responseAicardi-Goutières syndrome; JAK-inhibitor; interferonopathies; ruxolitinib; type I interferonbusiness.industryOlder brotherruxolitinibJAK-inhibitorCase ReportAicardi-Goutières syndromemedicine.diseasemedicine.disease_causePediatricsRJ1-570interferonopathiesInterferonImmunologyPediatrics Perinatology and Child HealthmedicineAicardi–Goutières syndrometype I interferonJanus kinasebusinessmedicine.drugFrontiers in Pediatrics
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Early stimulation: psychomotor development of two girls with Aicardi syndrome.

1987

Summary The psychomotor development achieved by two girls with the Aicardi syndrome is described. Until now this syndrome has been considered to produce a total dissociation from the environment in those affected. The results of early intervention, although not spectacular, are sufficient to recommend early stimulation in these children.

Psychomotor learningPediatricsmedicine.medical_specialtyDissociation (neuropsychology)business.industryPublic Health Environmental and Occupational HealthInfantStimulationSyndromemedicine.diseaseLanguage DevelopmentDevelopmental psychologyAicardi syndromeBehavior TherapyIntervention (counseling)Pediatrics Perinatology and Child HealthDevelopmental and Educational PsychologymedicineHumansFemaleEye AbnormalitiesAgenesis of Corpus CallosumbusinessSpasms InfantilePsychomotor PerformanceChild: care, health and development
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Hypoxia Positively Regulates the Expression of pH-Sensing G-Protein–Coupled Receptor OGR1 (GPR68)

2016

Background & Aims: A novel family of proton-sensing G-proteinâcoupled receptors, including ovarian cancer G-proteinâcoupled receptor 1 (OGR1) (GPR68) has been identified to play a role in pH homeostasis. Hypoxia is known to change tissue pH as a result of anaerobic glucose metabolism through the stabilization of hypoxia-inducible factor-1α. We investigated how hypoxia regulates the expression of OGR1 in the intestinal mucosa and associated cells. Methods: OGR1 expression in murine tumors, human colonic tissue, and myeloid cells was determined by quantitative reverse-transcription polymerase chain reaction. The influence of hypoxia on OGR1 expression was studied in monocytes/macrophages and…

WT wild type0301 basic medicineMM6 MonoMac 6HV healthy volunteerSPARC secreted protein acidic and rich in cysteineNF-κB nuclear factor-κBInflammationBiologyIEC intestinal epithelial cell03 medical and health sciencesIntestinal mucosaTDAG8Ovarian Cancer G-Protein–Coupled ReceptormedicineOGR1 ovarian cancer G-protein–coupled receptor 1 (GPR68)IFN interferonlcsh:RC799-869ReceptorOriginal ResearchTh T-helperInflammationTNF tumor necrosis factorIBD inflammatory bowel diseaseHepatologyRT-qPCR quantitative reverse-transcription polymerase chain reactionAICAR 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranosideTDAG8 T-cell death-associated gene 8 (GPR65)Inflammatory Bowel DiseaseGRP65GastroenterologyHypoxia (medical)Molecular biologyGPR G-protein–coupled receptormRNA messenger RNAIL interleukinChIP chromatin immunoprecipitationHIF hypoxia-inducible factorUC ulcerative colitis030104 developmental biologyHypoxia-inducible factorsCancer researchCD Crohn's diseaselcsh:Diseases of the digestive system. GastroenterologyTumor necrosis factor alphaFCS fetal calf serummedicine.symptomChromatin immunoprecipitationHomeostasisCellular and Molecular Gastroenterology and Hepatology
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Autophagic flux restoration by exercise or pharmacological treatment counteracts cancer cachexia

2014

cachexia exercise AICAR.
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