Search results for "ice"

showing 10 items of 26338 documents

Age-related regulation of bone formation by the sympathetic cannabinoid CB1 receptor.

2017

The endocannabinoid (eCB) system, including its receptors, ligands, and their metabolizing enzymes, plays an important role in bone physiology. Skeletal cannabinoid type 1 (CB1) receptor signaling transmits retrograde signals that restrain norepinephrine (NE) release, thus transiently stimulating bone formation following an acute challenge, suggesting a feedback circuit between sympathetic nerve terminals and osteoblasts. To assess the effect of chronic in vivo occurrence of this circuit, we characterized the skeletal phenotype of mice with a conditional deletion of the CB1 receptor in adrenergic/noradrenergic cells, including sympathetic nerves. Whereas the deletion of the CB1 receptor did…

0301 basic medicineMalemedicine.medical_specialtySympathetic nervous systemAgingHistologyCannabinoid receptorSympathetic Nervous SystemPhysiologyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentDopamine beta-HydroxylaseBone resorptionBone remodeling03 medical and health sciencesNorepinephrineNorepinephrineReceptor Cannabinoid CB1OsteogenesisInternal medicinemedicineAnimalsNeuropeptide YBone ResorptionReceptorMice KnockoutChemistryEndocannabinoid systemMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyCannabinoidReceptors Adrenergic beta-2Gene Deletionmedicine.drugEndocannabinoidsBone
researchProduct

Software-based analysis of 1-hour Holter ECG to select for prolonged ECG monitoring after stroke.

2020

Abstract Objective Identification of ischemic stroke patients at high risk for paroxysmal atrial fibrillation (pAF) during 72 hours Holter ECG might be useful to individualize the allocation of prolonged ECG monitoring times, currently not routinely applied in clinical practice. Methods In a prospective multicenter study, the first analysable hour of raw ECG data from prolonged 72 hours Holter ECG monitoring in 1031 patients with acute ischemic stroke/TIA presenting in sinus rhythm was classified by an automated software (AA) into “no risk of AF” or “risk of AF” and compared to clinical variables to predict AF during 72 hours Holter‐ECG. Results pAF was diagnosed in 54 patients (5.2%; mean …

0301 basic medicineMalemedicine.medical_specialtyTime Factorsmedicine.medical_treatmentNeurosciences. Biological psychiatry. NeuropsychiatryBrain Ischemia03 medical and health sciencesElectrocardiography0302 clinical medicineRisk FactorsInternal medicineAtrial FibrillationMedicineHumansIn patientSinus rhythmcardiovascular diseasesProspective StudiesRC346-429Medical History TakingStrokeResearch ArticlesAgedAged 80 and overReceiver operating characteristicbusiness.industryGeneral NeuroscienceThrombolysisMiddle Agedmedicine.diseaseEcg monitoringStroke030104 developmental biologyMulticenter studyCardiologyElectrocardiography AmbulatoryFemaleNeurology. Diseases of the nervous systemNeurology (clinical)business030217 neurology & neurosurgeryRC321-571Holter ecgResearch ArticleAnnals of clinical and translational neurology
researchProduct

Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
researchProduct

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
researchProduct

Changes in CDKN2A/2B expression associate with T-cell phenotype modulation in atherosclerosis and type 2 diabetes mellitus.

2018

Previous studies indicate a role of CDKN2A/2B/2BAS genes in atherosclerosis and type 2 diabetes mellitus (T2DM). Progression of these diseases is accompanied by T-cell imbalance and chronic inflammation. Our main objective was to investigate a potential association between CDKN2A/2B/2BAS gene expression and T cell phenotype in T2DM and coronary artery disease (CAD) in humans, and to explore the therapeutic potential of these genes to restore immune cell homeostasis and disease progression. Reduced mRNA levels of CDKN2A (p16Ink4a), CDKN2B (p15Ink4b), and CDKN2BAS were observed in human T2DM and T2DM-CAD subjects compared with controls. Protein levels of p16Ink4a and p15Ink4b were also dimini…

0301 basic medicineMalemedicine.medical_specialtyendocrine system diseasesMice Knockout ApoECD3T cellCD14Inflammation03 medical and health sciencesMice0302 clinical medicinePhysiology (medical)Internal medicineNeointimamedicineAnimalsHumansIL-2 receptorInterleukin-7 receptorneoplasmsbiologybusiness.industryGenes p16Biochemistry (medical)CDKN2BASPublic Health Environmental and Occupational HealthType 2 Diabetes MellitusGeneral MedicineAtherosclerosis030104 developmental biologyEndocrinologymedicine.anatomical_structureDiabetes Mellitus Type 2030220 oncology & carcinogenesisbiology.proteinLeukocytes Mononuclearmedicine.symptombusinessTranslational research : the journal of laboratory and clinical medicine
researchProduct

Endothelial GLP-1 (Glucagon-Like Peptide 1) Receptor Mediates Cardiovascular Protection by Liraglutide In Mice With Experimental Arterial Hypertension

2019

Supplemental Digital Content is available in the text.

0301 basic medicineMalemedicine.medical_specialtyhypertensionBlotting WesternInflammationBlood Pressure030204 cardiovascular system & hematologyangiotensin IImedicine.disease_causeGlucagon-Like Peptide-1 Receptor1005403 medical and health sciencesMice0302 clinical medicine10030Internal medicinemedicineoxidative stressAnimalsHypoglycemic AgentsReceptor10111Cells CulturedMice KnockoutliraglutideLiraglutidebusiness.industryBasic SciencesType 2 Diabetes MellitusEndothelial CellsAtherosclerosisGlucagon-like peptide-1Angiotensin II3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology10040inflammationComputingMethodologies_DOCUMENTANDTEXTPROCESSINGRNAmedicine.symptomCardiology and Cardiovascular Medicinebusiness10024Oxidative stressmedicine.drug
researchProduct

Decrease in αβ/γδ T-cell ratio is accompanied by a reduction in high-fat diet-induced weight gain, insulin resistance, and inflammation.

2018

The implication of αβ and γδ T cells in obesity-associated inflammation and insulin resistance (IR) remains uncertain. Mice lacking γδ T cells show either no difference or a decrease in high-fat diet (HFD)-induced IR, whereas partial depletion in γδ T cells does not protect from HFD-induced IR. αβ T-cell deficiency leads to a decrease in white adipose tissue (WAT) inflammation and IR without weight change, but partial depletion of these cells has not been studied. We previously described a mouse model overexpressing peroxisome proliferator-activated receptor β (PPAR-β) specifically in T cells [transgenic (Tg) T-PPAR-β] that exhibits a partial depletion in αβ T cells and no change in γδ T-ce…

0301 basic medicineMalemedicine.medical_specialtymedicine.medical_treatmentT cellReceptors Antigen T-Cell alpha-betaT-LymphocytesAdipose tissueInflammationWhite adipose tissueDiet High-FatWeight GainBiochemistry03 medical and health sciencesMice0302 clinical medicineImmune systemInsulin resistanceInternal medicineGlucose IntoleranceGeneticsmedicineAnimalsObesityMolecular BiologyInflammationChemistryInsulinWeight changeBody Weightfood and beveragesnutritional and metabolic diseasesReceptors Antigen T-Cell gamma-deltamedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologymedicine.anatomical_structurelipids (amino acids peptides and proteins)medicine.symptomInsulin Resistancehormones hormone substitutes and hormone antagonists030217 neurology & neurosurgeryBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
researchProduct

Influence of endogenous glucagon-like peptide-2 on lipid disorders in mice fed a high-fat diet

2016

Aim: The purpose of the present study was to investigate the influence of endogenous glucagon-like peptide-2 (GLP-2) on lipid profile in mice fed a standard diet (STD) or a high-fat diet (HFD). Materials and methods: HFD- and age-matched STD mice were injected once a day with GLP-2 (3-33), a GLP-2 receptor (GLP-2R) antagonist, or vehicle for 4 weeks. Results: HFD mice displayed increased intrahepatic lipid concentration and hepatic steatosis and higher plasma concentrations of cholesterol, LDL, AST, and ALT than STD mice. No difference was observed in lipid fecal elimination. In STD mice, the chronic treatment with GLP-2 (3-33) did not affect any parameter, while in HFD mice, it enhanced pl…

0301 basic medicineMalemedicine.medical_specialtyobesityEndogenyBiologyDiet High-FatliverSettore BIO/09 - Fisiologia03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineInsulin resistanceEndocrinologyMetabolic DiseaseslipidInternal medicineinsulin resistancemedicineGlucagon-Like Peptide 2AnimalsReceptormedicine.diagnostic_testCholesterolSettore BIO/16 - Anatomia Umanadigestive oral and skin physiologyAntagonistGeneral Medicinemedicine.diseaseGlucagon-like peptide-2LipidsPeptide FragmentsMice Inbred C57BL030104 developmental biologyEndocrinologychemistrylipids (amino acids peptides and proteins)030211 gastroenterology & hepatologySteatosisLipid profileGLP-2hormones hormone substitutes and hormone antagonists
researchProduct

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
researchProduct

Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
researchProduct