Search results for "Cero"

showing 10 items of 691 documents

Redox lipidomics to better understand brain aging and function

2019

Human prefrontal cortex (PFC) is a recently evolutionary emerged brain region involved in cognitive functions. Human cognitive abilities decline during aging. Yet the molecular mechanisms that sustain the preservation or deterioration of neurons and PFC functions are unknown. In this review, we focus on the role of lipids in human PFC aging. As the evolution of brain lipid concentrations is particularly accelerated in the human PFC, conferring a specific lipid profile, a brief approach to the lipidome of PFC was consider along with the relationship between lipids and lipoxidative damage, and the role of lipids in human PFC aging. In addition, the specific targets of lipoxidative damage in h…

AdultAgingPrefrontal CortexGlycerophospholipidsBiologymedicine.disease_causeBiochemistryCognitionPhysiology (medical)LipidomicsmedicineHumansCognitive DysfunctionCognitive declineMitochondrionPrefrontal cortexExerciseCaloric RestrictionNeuronsSphingolipidsCognitionEnergy metabolismMiddle AgedLipidomeAdvanced lipoxidation end productsLipid MetabolismCytoskeletal ProteinsOxidative StressProteostasisnervous systemLipidomicsFatty Acids UnsaturatedEnergy MetabolismNeuroscienceFunction (biology)Oxidative stress
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Topographic heterogeneity of amyloid B-protein epitopes in brains with various forms of neuronal ceroid lipofuscinoses suggesting defective processin…

1990

To verify our hypothesis of defective protease inhibitor domains that are encoded by abnormal processing of amyloid precursor protein (APP) in brains of patients with neuronal ceroid lipofuscinoses (NCL), immunohistochemical and cytochemical studies were performed with monoclonal antibodies (mAbs) directed against various domains of APP. For the studies, 22 autopsy brains were used: 12 with different forms of NCL, and 10 control brains. The staining procedure for the avidin-biotin complex (ABC) technique and the postembedding gold-labelled procedure for electron microscopy (EM) were employed. Of all mAbs used for the study, only mAbs generated against amyloid B-protein bound to neural tissu…

AdultAmyloidPathologymedicine.medical_specialtyBatten diseaseAdolescentAmyloidImmunocytochemistryPathology and Forensic MedicineLipofuscinEpitopes03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineNeuronal Ceroid-LipofuscinosesAmyloid precursor proteinmedicineHumansSenile plaquesChildAged030304 developmental biology0303 health sciencesAmyloid beta-PeptidesbiologyAntibodies MonoclonalBrainInfantMiddle Agedmedicine.diseaseImmunohistochemistryMolecular biology3. Good healthChild Preschoolbiology.proteinNeuronal ceroid lipofuscinosisNeurology (clinical)Protein Processing Post-Translational030217 neurology & neurosurgeryImmunostainingActa Neuropathologica
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Effect of gut-derived acetate on glucose turnover in man

1988

1. The effect of acetate absorbed from the gut on glucose turnover has been determined in four healthy subjects during both fasting and an intravenous glucose infusion by using [U-13C]glucose. 2. In the first part of the study, after an overnight fast, a tracer dose of [U-13C]glucose was infused at a constant rate along with an infusion of saline for 7 h. In the second part the saline infusion was replaced by glucose at 4.25 mg min−1 kg−1. In both studies 15 mmol of sodium acetate was given by mouth at 15 min intervals from the fourth to the sixth hour. Glucose turnover, respiratory quotient, metabolic rate and blood levels of acetate, 3-hydroxybutyrate, lactate, insulin, glucagon and gastr…

AdultDietary FiberGlycerolMalemedicine.medical_specialtymedicine.medical_treatmentHydroxybutyratesGastric Inhibitory PolypeptideAcetatesFatty Acids NonesterifiedCarbohydrate metabolismGlucagonAcetic acidchemistry.chemical_compoundGastric inhibitory polypeptideLipid oxidationInternal medicinemedicineHumansInsulinCarbon RadioisotopesAcetic Acid3-Hydroxybutyric AcidChemistryRespirationInsulinGeneral MedicineMetabolismCarbon DioxideGlucagonRespiratory quotientGlucoseEndocrinologyLactatesFemaleClinical Science
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The Neuronal Ceroid-Lipofuscinoses. Recent Advances

1998

The neuronal ceroid lipofuscinoses (NCLs) represent a group of neurodegenerative disorders characterised by progressive visual failure, neurodegeneration, epilepsy and the accumulation of an autofluorescent lipopigment in neurons and other cells. The main childhood subtypes are infantile (INCL;CLN1), classical late infantile (LINCL;CLN2) and juvenile NCL (J NCL; CLN3), distinguished on the basis of age of onset, clinical course and ultrastructural morphology, and recently genetic analysis. In addition several variant forms of the disease complex have been described as well as a rare adult onset form. Advances in both genetics and biochemistry have led to the identification of the genes for …

AdultDiseaseBiologyGenetic analysisArticlePathology and Forensic MedicineEpilepsyNeuronal Ceroid-LipofuscinosesPrenatal DiagnosismedicineAnimalsHumansChildGeneFinlandNeuronal Ceroid-LipofuscinosesGeneticsTripeptidyl-Peptidase 1General NeuroscienceNeurodegenerationInfant Newbornmedicine.diseaseDisease Models AnimalCLN3Neurology (clinical)Age of onsetNeuroscienceForecastingBrain Pathology
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Human pathology in NCL

2013

AbstractIn childhood the neuronal ceroid lipofuscinoses (NCL) are the most frequent lysosomal diseases and the most frequent neurodegenerative diseases but, in adulthood, they represent a small fraction among the neurodegenerative diseases. Their morphology is marked by: (i) loss of neurons, foremost in the cerebral and cerebellar cortices resulting in cerebral and cerebellar atrophy; (ii) an almost ubiquitous accumulation of lipopigments in nerve cells, but also in extracerebral tissues. Loss of cortical neurons is selective, indiscriminate depletion in early childhood forms occurring only at an advanced stage, whereas loss of neurons in subcortical grey-matter regions has not been quantit…

AdultElectron microscopy; Brain; Extracerebral tissues; Granular osmiophilic deposits; Curvilinear; FingerprintPathologymedicine.medical_specialtyBatten diseaseFingerprintContext (language use)Extracerebral tissuesProgressive myoclonus epilepsyBiologyNeuronal Ceroid-LipofuscinosesCurvilinearElectron microscopymedicineHumansMolecular BiologyTripeptidyl-Peptidase 1BrainPPT1Anatomymedicine.diseaseCLN3DNAJC5Molecular MedicineGranular osmiophilic depositsNeuronal ceroid lipofuscinosisCerebellar atrophyBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Lack of association between gene polymorphisms of Angiotensin converting enzyme, Nod-like receptor 1, Toll-like receptor 4, FAS/FASL and the presence…

2011

Abstract Background Several polymorphisms of genes involved in the immunological recognition of Helicobacter pylori and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding Angiotensin converting enzyme (ACE), Nod-like receptor 1 (NOD1), Toll-like receptor 4 (TLR4) and FAS/FASL. Methods Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. ACE I/D (rs4646994), NOD1 796G>…

AdultGastritis AtrophicMaleFas Ligand ProteinGenotypeAtrophic gastritisPeptidyl-Dipeptidase AWhite PeopleFas ligandHelicobacter InfectionsRisk FactorsStomach NeoplasmsNod1 Signaling Adaptor ProteinNOD1GenotypemedicineGeneticsHumansGenetics(clinical)fas ReceptorAllelesGenetics (clinical)AgedAged 80 and overPolymorphism GeneticHelicobacter pyloribiologyCancerAngiotensin-converting enzymeMiddle AgedHelicobacter pylorimedicine.diseasebiology.organism_classificationToll-Like Receptor 4ApoptosisImmunologybiology.proteinFemalePrecancerous ConditionsResearch ArticleBMC Medical Genetics
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Prevalence of Helicobacter pylori infection and atrophic gastritis in Latvia.

2012

Helicobacter pylori infection and atrophic gastritis are related to an increased risk for gastric cancer. There is a decrease in global H. pylori prevalence. We analyzed the prevalence of H. pylori infection in Latvia by the plasma IgG test and the presence of atrophy by means of pepsinogen testing.This subanalysis was carried out on a randomly selected cross-sectional sample of a general population of adults to access cardiovascular risk factors. Plasma samples were screened for H. pylori IgG (cutoff value 24 U/ml), and pepsinogens (Pg) I and II. Pg cutoff values of PgI/PgII ≤ 3 and PgI ≤ 70 ng/ml were used to assess the prevalence of atrophy of any grade and PgI/PgII ≤ 2 and PgI ≤ 30 ng/m…

AdultGastritis AtrophicMalemedicine.medical_specialtyHelicobacter pylori infectionAdolescentCross-sectional studyAtrophic gastritisGastroenterologySeverity of Illness IndexHelicobacter InfectionsYoung AdultAtrophySex FactorsPredictive Value of TestsRisk FactorsStomach NeoplasmsInternal medicinePepsinogen AmedicinePepsinogen CPrevalenceHumansYoung adultAgedAged 80 and overChi-Square DistributionHepatologybiologyHelicobacter pyloribusiness.industryGastroenterologyAge FactorsCancerMiddle Agedbacterial infections and mycosesmedicine.diseaseAntibodies BacterialLatviaCross-Sectional Studiesbiology.proteinLinear ModelsFemaleGastritismedicine.symptomAntibodybusinessPrecancerous ConditionsBiomarkersEuropean journal of gastroenterologyhepatology
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The phenotype of gastric mucosa coexisting with Barrett's oesophagus.

2001

Barrett's oesophagus complicates the gastro-oesophageal acid reflux. Helicobacter pylori infection, particularly with cagA positive strains, induces inflammatory/atrophic lesions of the gastric mucosa, which may impair acid output. No systematic study has investigated the phenotype of the gastric mucosa coexisting with Barrett's oesophagus. This study was designed to identify the phenotype of gastric mucosa associated with Barrett's oesophagus.In this retrospective case control study, the phenotype of the gastric mucosa was histologically characterised in 53 consecutive patients with Barrett's oesophagus and in 53 (sex and age matched) non-ulcer dyspeptic controls. Both patients and control…

AdultGastritis AtrophicMalemedicine.medical_specialtyPathologyAtrophic gastritisBiopsySpirillaceaeBarrett's oesophagus gastritis in Barrett's oesophagus Barrett's oesophagus and gastric precancerous lesionsdigestive systemGastroenterologyHelicobacter InfectionsPathology and Forensic MedicineBarrett's oesophagus and gastric precancerous lesionsBarrett EsophagusInternal medicineotorhinolaryngologic diseasesGastric mucosamedicineHumansCagAAgedRetrospective StudiesAged 80 and overHelicobacter pyloribiologybusiness.industrygastritis in Barrett's oesophagusStomachdigestive oral and skin physiologyIntestinal metaplasiaGeneral MedicineMiddle AgedHelicobacter pyloribiology.organism_classificationmedicine.diseasedigestive system diseasesBarrett's oesophagussurgical procedures operativePhenotypemedicine.anatomical_structureGastric MucosaCase-Control StudiesPapersFemaleGastritismedicine.symptombusiness
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Effects of an ultra-long-distance (1000 km) race on lipid metabolism

1989

The influence was examined of ultra-long-distance running (1000 km race lasting 20 days) on changes in serum lipids. The 110 participants received two types of diet, a conventional Western diet and a wholesome vegetarian diet. Of the 55 finishers the serum concentration of total cholesterol, low density lipoprotein (LDL)-cholesterol, apolipoprotein B and triglycerides decreased significantly during the first 8 days of the run, but rose again towards the end of the race without reaching pre-race levels. The high density lipoprotein (HDL)-cholesterol increased initially but decreased in the final days of the run. The values for apolipoprotein A-I were not correlated with HDL-cholesterol. The …

AdultGlycerolMalemedicine.medical_specialtyApolipoprotein BPhysiologyBlood lipidsFatty Acids NonesterifiedRunningchemistry.chemical_compoundHigh-density lipoproteinPhysiology (medical)Internal medicinemedicineHumansOrthopedics and Sports MedicineApolipoproteins ATriglyceridesAgedApolipoproteins BbiologyTriglycerideCholesterolCholesterol HDLPublic Health Environmental and Occupational HealthLipid metabolismGeneral MedicineMiddle AgedLipid MetabolismDietCholesterolEndocrinologychemistryLow-density lipoproteinbiology.proteinFemalelipids (amino acids peptides and proteins)LipoproteinEuropean Journal of Applied Physiology and Occupational Physiology
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AISF update on the diagnosis and management of adult-onset lysosomal storage diseases with hepatic involvement.

2020

Lysosomal storage diseases (LSDs) are a heterogeneous group of inherited disorders caused by loss-of-function mutations in genes encoding for lysosomal enzymes/proteins. The consequence is a progressive accumulation of substrates in these intracellular organelles, resulting in cellular and tissue damage. The overall incidence is about 1/8000 live births, but is likely underestimated. LSDs are chronic progressive multi-systemic disorders, generally presenting with visceromegaly, and involvement of the central nervous system, eyes, the skeleton, and the respiratory and cardiovascular systems. The age at onset and phenotypic expression are highly variable, according to the specific enzymatic d…

AdultHepatosplenomegalyLysosomal acid lipase deficiencyBioinformaticsOrganomegaly03 medical and health sciencesLiver disease0302 clinical medicinemedicineCholesteryl ester storage disease Enzyme replacement therapy Gaucher disease Lysosomal acid lipase Niemann–Pick disease deficiency Substrate reduction therapyHumansSubstrate reduction therapyEnzyme Replacement TherapySocieties MedicalNiemann-Pick DiseasesAcid sphingomyelinase deficiencyGaucher DiseaseHepatologybusiness.industryGastroenterologyWolman DiseaseEnzyme replacement therapymedicine.diseaseLysosomal Storage DiseasesSphingomyelin PhosphodiesteraseItaly030220 oncology & carcinogenesis030211 gastroenterology & hepatologymedicine.symptombusinessNiemann–Pick diseaseLysosomesVisceromegalyDigestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
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