Search results for "Roi"

showing 10 items of 11055 documents

A Network Involving Gut Microbiota, Circulating Bile Acids, and Hepatic Metabolism Genes That Protects Against Non-Alcoholic Fatty Liver Disease.

2019

Scope Gut microbiota contributes to non-alcoholic fatty liver disease (NAFLD) pathogenesis by multiple mechanisms not yet completely understood. Novel differential features between germ-free mice (GFm) transplanted with protective or non-protective cecal microbiota against NAFLD are investigated. Methods and results Gut microbiota composition, plasma, and fecal bile acids (BAs) and liver mRNAs are quantified in GFm recipients from four donor mice differing in NAFLD severity (control diet, high-fat diet [HFD]-responder, HFD-non-responder, and quercetin-supplemented HFD). Transplanted GFm are on control or HFD for 16-weeks. Multivariate analysis shows that GFm colonized with microbiota from H…

0301 basic medicineMalemedicine.medical_specialtyGut floraDiet High-Fatdigestive systemPathogenesisBile Acids and Salts03 medical and health sciencesMiceNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsFeces030109 nutrition & dieteticsbiologyEthanoldigestive oral and skin physiologyFatty livernutritional and metabolic diseasesTransporterbiology.organism_classificationmedicine.diseasePhenotypeGastrointestinal MicrobiomeMice Inbred C57BL030104 developmental biologyEndocrinologyLiverBacteroidesTranscriptomeDrug metabolismFood ScienceBiotechnologyMolecular nutritionfood research
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Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain.

2018

Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodege…

0301 basic medicineMalemedicine.medical_specialtyInflammationmedicine.disease_causeDiet High-FatSettore BIO/09 - FisiologiaNeuroprotectionlcsh:RC321-57103 medical and health sciences0302 clinical medicineNeuroinflammationInternal medicinemedicineGlucagon-Like Peptide 2AnimalsObesityNeurodegenerationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationTUNEL assayGlial fibrillary acidic proteinbiologyChemistryNeurodegenerationdigestive oral and skin physiologyBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyNeuroprotective AgentsNeurologyGliosisOxidative stressAstrocytesbiology.proteinGlucagon-Like Peptide-2 ReceptorOxidative streEncephalitismedicine.symptomInflammation MediatorsGLP-2030217 neurology & neurosurgeryOxidative stresshormones hormone substitutes and hormone antagonistsNeurobiology of disease
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The Gut Microbial Metabolite Trimethylamine-N-Oxide Is Present in Human Cerebrospinal Fluid

2017

Trimethylamine-N-oxide (TMAO) is a small organic molecule, derived from the intestinal and hepatic metabolism of dietary choline and carnitine. Although the involvement of TMAO in the framework of many chronic diseases has been recently described, no evidence on its putative role in the central nervous system has been provided. The aim of this study was to evaluate whether TMAO is present at detectable levels in human cerebrospinal fluid (CSF). CSF was collected for diagnostic purposes from 58 subjects by lumbar puncture and TMAO was quantified by using liquid chromatography coupled with multiple-reaction monitoring mass spectrometry. The molecule was detected in all samples, at concentrati…

0301 basic medicineMalemedicine.medical_specialtyMetaboliteCentral nervous systemTrimethylamine N-oxidelcsh:TX341-641Gut floraSpinal Puncturetrimethylamine-N-oxideMass Spectrometry03 medical and health scienceschemistry.chemical_compoundMethylamines0302 clinical medicineCerebrospinal fluidAlzheimer DiseasePredictive Value of TestsInternal medicinemedicineCholineHumansCarnitineAgedAged 80 and overNutrition and DieteticsbiologyBacteriagut microbiotaCommunicationMiddle Agedbiology.organism_classificationcentral nervous systemGastrointestinal MicrobiomeIntestines030104 developmental biologyEndocrinologymedicine.anatomical_structurechemistryBiochemistryDementiaFemalelcsh:Nutrition. Foods and food supply030217 neurology & neurosurgeryDrug metabolismFood Sciencemedicine.drugChromatography LiquidNutrients
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Activation of MORs in the VTA induces changes on cFos expression in different projecting regions: Effect of inflammatory pain.

2019

Abstract Chronic pain is a worldwide major health problem and many pain-suffering patients are under opioid based therapy. Epidemiological data show that pain intensity correlates with the risk of misuse of prescription opioids, and other drugs of abuse including alcohol. This increased vulnerability to suffer Substance Use Disorders could be, in part, caused by functional changes that occur over the mesocorticolimbic system, a brain pathway involved in reward processing and addiction. Previous data in rats revealed that inflammatory pain desensitizes mu opioid receptors (MORs) in the ventral tegmental area (VTA). As a consequence, pain alters dopamine release in the nucleus accumbens (NAc)…

0301 basic medicineMalemedicine.medical_specialtyMicroinjectionsFreund's AdjuvantReceptors Opioid muPainNucleus accumbens03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineDopamineInternal medicinemental disordersNeural PathwaysMedicineAnimalsInflammationbusiness.industryVentral Tegmental AreaChronic painGenes fosCell BiologyEnkephalin Ala(2)-MePhe(4)-Gly(5)-medicine.diseaseImmunohistochemistryRatsVentral tegmental areaAnalgesics OpioidDAMGOStria terminalis030104 developmental biologymedicine.anatomical_structureEndocrinologynervous systemchemistryOpioidGene Expression Regulationbusiness030217 neurology & neurosurgerymedicine.drugBasolateral amygdalaNeurochemistry international
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The predictive power of transcranial sonography in movement disorders: a longitudinal cohort study.

2018

Transcranial sonography (TCS) is a noninvasive, easily performed, and commonly available neuroimaging technique useful for the study of brain parenchyma in movement disorders. This tool has been increasingly used in the diagnosis of Parkinson’s disease and atypical parkinsonism. The aim of the study was to evaluate the applicability of this technique as supportive tool in the early diagnosis of movement disorders. We performed TCS on 315 individuals which were diagnosed as healthy controls or affected by idiopathic Parkinson’s disease, monogenetic subtypes of Parkinson’s disease, atypical parkinsonism, and Dementia with Lewy bodies. Five TCS diagnostic patterns were defined on the basis of …

0301 basic medicineMalemedicine.medical_specialtyMovement disordersNeurologyUltrasonography Doppler TranscranialConcordanceDementia with Lewy bodiesDermatologyDiseaseCohort Studies03 medical and health sciences0302 clinical medicineNeuroimagingPredictive Value of TestsInternal medicineSubstantia nigramedicineLenticular nucleiHumansNeuroradiologyAgedMovement DisordersDementia with Lewy bodiesbusiness.industryfungiGeneral MedicineMiddle Agedmedicine.diseasePsychiatry and Mental health030104 developmental biologyAtypical parkinsonismIdiopathic Parkinson’s diseaseTranscranial sonographySettore MED/26 - NeurologiaFemaleNeurology (clinical)Neurosurgerymedicine.symptombusiness030217 neurology & neurosurgeryNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Recombinant human hepatocyte growth factor provides protective effects in cerulein-induced acute pancreatitis in mice.

2018

Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c-Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein-induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip…

0301 basic medicineMalemedicine.medical_specialtyNecrosisPhysiologyClinical BiochemistryInflammationApoptosismedicine.disease_causeProtective AgentsAntioxidantsProinflammatory cytokine03 medical and health sciencesMiceInternal medicineEdemamedicineAnimalsHumansbusiness.industryHepatocyte Growth FactorCell BiologyProto-Oncogene Proteins c-metmedicine.diseaseGlutathioneSurvival AnalysisRecombinant ProteinsDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyPancreatitisAcute pancreatitisPancreatitisHepatocyte growth factormedicine.symptombusinessOxidative stressCeruletidemedicine.drugSignal TransductionJournal of cellular physiology
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Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model.

2019

Traumatic brain injury (TBI) represents a significant risk factor for development of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The S100A9-driven amyloid-neuroinflammatory cascade occurring during primary and secondary TBI events can serve as a mechanistic link between TBI and Alzheimer’s as demonstrated recently in the human brain tissues. Here by using immunohistochemistry in the controlled cortical impact TBI mouse model we have found pro-inflammatory S100A9 in the brain tissues of all mice on the first and third post-TBI days, while 70% of mice did not show any S100A9 presence on seventh post-TBI day similar to controls. This indicates that defensive mechanisms effe…

0301 basic medicineMalemedicine.medical_specialtyNeurologyAmyloidTraumatic brain injuryPlaque AmyloidProtein Aggregation PathologicalS100A9Proinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsCalgranulin BSignificant riskNeuroinflammationNeuronsbusiness.industryGeneral NeuroscienceBrainmedicine.diseasenervous system diseasesDisease Models Animal030104 developmental biologyMicrogliabusinessAlzheimer’s disease Amyloid Neuroinflammation Oligomerization S100A9 Traumatic brain injuryNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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Effect of chondroitin sulphate on synovitis of knee osteoarthritic patients.

2017

Abstract Objective To evaluate by ultrasonography the effect of chondroitin sulfate (CS) on synovitis in patients with knee osteoarthritis (KOA). To collaborate in the understanding of the biochemical mechanisms involved in the synovial inflammation process. Methods Randomized, single-blind, controlled trial involving 70 patients with primary KOA treated for 6 months with CS or acetaminophen (ACT). Evaluation of KOA status at baseline, 6 weeks, 3 and 6 months included: ultrasonography to assess synovitis (following the OMERACT expertise group definition), visual analogue scale and Lequesne index to measure pain and function, and ELISA to quantify inflammatory mediators in serum and synovial…

0301 basic medicineMalemedicine.medical_specialtyVisual analogue scaleInflammationPilot ProjectsOsteoarthritisGastroenterologylaw.invention03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRandomized controlled triallawInternal medicineSynovitisMedicineSynovial fluidHumansSingle-Blind MethodChondroitin sulfateAcetaminophenAgedPain MeasurementUltrasonography030203 arthritis & rheumatologyAged 80 and overSynovitisbusiness.industryAnti-Inflammatory Agents Non-SteroidalChondroitin SulfatesMiddle AgedOsteoarthritis Kneemedicine.diseaseAcetaminophenBiomechanical Phenomena030104 developmental biologyTreatment OutcomechemistryFemalemedicine.symptombusinessBiomarkersmedicine.drugFollow-Up StudiesMedicina clinica
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Sex hormones modulate pathogenic processes in experimental traumatic brain injury.

2018

Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…

0301 basic medicineMalemedicine.medical_specialtyanimal structuresmedicine.drug_classmedicine.medical_treatmentTropomyosin receptor kinase BTropomyosin receptor kinase ABiochemistryNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineInternal medicineBrain Injuries TraumaticmedicineAnimalsNerve Growth FactorsSex CharacteristicsbiologyEstradiolbusiness.industryEstrogen AntagonistsBrainDihydrotestosteroneAndrogennervous system diseasesMice Inbred C57BLSteroid hormoneDisease Models Animal030104 developmental biologyEndocrinologynervous systemSex steroidDihydrotestosteronebiology.proteinFemalebusiness030217 neurology & neurosurgeryNeurotrophinmedicine.drugJournal of neurochemistry
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Indomethacin counteracts the effects of chronic social defeat stress on emotional but not recognition memory in mice

2017

We have previously observed the impairing effects of chronic social defeat stress (CSDS) on emotional memory in mice. Given the relation between stress and inflammatory processes, we sought to study the effectiveness of the anti-inflammatory indomethacin in reversing the detrimental effects of CSDS on emotional memory in mice. The effects of CSDS and indomethacin on recognition memory were also evaluated. Male CD1 mice were randomly divided into four groups: non-stressed + saline (NS+SAL); non-stressed + indomethacin (NS+IND); stressed + saline (S+SAL); and stressed + indomethacin (S+IND). Stressed animals were exposed to a daily 10 min agonistic confrontation (CSDS) for 20 days. All subjec…

0301 basic medicineMalemedicine.medical_treatmentEmotionsIndomethacinlcsh:MedicineSocial SciencesAnxietySocial defeatMice0302 clinical medicineCognitionLearning and MemoryMedicine and Health SciencesPsychologylcsh:ScienceSalineObject RecognitionMammalsCognitive ImpairmentMultidisciplinaryAnimal BehaviorBehavior AnimalCognitive NeurologyAnti-Inflammatory Agents Non-SteroidalNeurologyAnimal SocialityVertebratesAnxietymedicine.symptomResearch ArticleElevated plus mazemedicine.medical_specialtyCognitive NeurosciencePsychological StressRodents03 medical and health sciencesEmotionalityMemoryInternal medicineMental Health and PsychiatrymedicineAvoidance LearningMemory impairmentAnimalsInterpersonal RelationsRecognition memorySocial stressBehaviorbusiness.industrylcsh:RCognitive PsychologyOrganismsBiology and Life SciencesDisease Models Animal030104 developmental biologyEndocrinologyAmniotesChronic DiseaseCognitive Sciencelcsh:QPerceptionbusinessZoology030217 neurology & neurosurgeryStress PsychologicalNeurosciencePLoS ONE
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