Search results for " Metabolic diseases"

showing 10 items of 699 documents

International consensus guidelines for scoring the histopathological growth patterns of liver metastasis

2017

BACKGROUND: Liver metastases present with distinct histopathological growth patterns (HGPs), including the desmoplastic, pushing and replacement HGPs and two rarer HGPs. The HGPs are defined owing to the distinct interface between the cancer cells and the adjacent normal liver parenchyma that is present in each pattern and can be scored from standard haematoxylin-and-eosin-stained (H&E) tissue sections. The current study provides consensus guidelines for scoring these HGPs.METHODS: Guidelines for defining the HGPs were established by a large international team. To assess the validity of these guidelines, 12 independent observers scored a set of 159 liver metastases and interobserver var…

0301 basic medicineOncologycongenital hereditary and neonatal diseases and abnormalitiesCancer Researchmedicine.medical_specialtyPathologyIntraclass correlationmedicine.medical_treatmentcolorectal cancerGuidelineMetastasisangiogenesis03 medical and health sciencesbreast cancer0302 clinical medicineSDG 3 - Good Health and Well-beingInternal medicineJournal ArticlemedicineHumansNeoplasm Metastasisprognostic factorintegumentary systembusiness.industryLiver Neoplasmsnutritional and metabolic diseasesvessel co-optionGold standard (test)medicine.diseaseliver metastasis030104 developmental biologyTissue sectionsPractice GuidelineOncology030220 oncology & carcinogenesisCancer cellCohortBiomarker (medicine)Hepatectomytumour microenvironmentbusinessBritish Journal of Cancer
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A case report of Muir-Torre syndrome in a woman with breast cancer and MSI-Low skin squamous cell carcinoma.

2017

IF 1.590; International audience; Background: The tumor spectrum in the Lynch syndrome is well defined, comprising an increased risk of developing colonic and extracolonic malignancies. Muir-Torre syndrome is a variant with a higher risk of skin disease. Patients have been described carrying mutations in the mismatch repair genes and presenting tumors with unusual histology or affected organ not part of the Lynch syndrome spectrum. Hence, the real link between Lynch syndrome, or Muir-Torre syndrome, and these tumors remains difficult to assess.Case presentation: We present the case of a 45-year-old-woman, diagnosed with breast cancer at 39 years of age and skin squamous cell carcinoma (SCC)…

0301 basic medicinePathologymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitieslcsh:QH426-470Case Report[SDV.CAN]Life Sciences [q-bio]/CancerMLH1lcsh:RC254-282Sebaceous adenoma[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciences0302 clinical medicineSebaceous adenomaBreast cancerMuir–Torre syndromeSquamous cell carcinomaPMS2Skin Squamous Cell CarcinomaMedicineneoplasmsGenetics (clinical)MSIbusiness.industryMicrosatellite instabilitynutritional and metabolic diseasesMuir-Torre syndromeMSI-Llcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMMRLynch syndromedigestive system diseases3. Good healthMSH2lcsh:Genetics030104 developmental biologyLynch syndromeOncologyMSH2030220 oncology & carcinogenesisCancer researchbusiness
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High-fat diet-induced metabolic disorders impairs 5-HT function and anxiety-like behavior in mice

2015

BACKGROUND AND PURPOSE The link between type 2 diabetes mellitus (T2DM) and depression is bidirectional. However, the possibility that metabolic disorders may elicit anxiogenic-like/depressive-like symptoms or alter the efficacy of antidepressant drugs remains poorly documented. This study explored the influence of T2DM on emotionality and proposed a therapeutic strategy that might be used in depressed diabetic patients. EXPERIMENTAL APPROACH Mice were fed a high-fat diet (HFD) and subjected to a full comprehensive metabolic and behavioural analysis to establish correlations between metabolic and psychiatric disorders. In vivo intra-hippocampal microdialysis was also applied to propose a me…

0301 basic medicinePharmacologymedicine.medical_specialtyMicrodialysisnutritional and metabolic diseasesPharmacologymedicine.disease3. Good healthImpaired glucose tolerance03 medical and health sciences030104 developmental biology0302 clinical medicineEndocrinologyInsulin resistanceDiabetes mellitusInternal medicinemedicineEscitalopramAntidepressantMajor depressive disorderPsychologyReuptake inhibitor030217 neurology & neurosurgerymedicine.drugBritish Journal of Pharmacology
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Associations between dietary polyphenols and type 2 diabetes in a cross-sectional analysis of the PREDIMED-Plus Trial: role of body mass index and sex

2019

Overweight and obesity are important risk factors for type 2 diabetes (T2D). Moving towards healthier diets, namely, diets rich in bioactive compounds, could decrease the odds of suffering T2D. However, those individuals with high body mass index (BMI) may have altered absorption or metabolism of some nutrients and dietary components, including polyphenols. Therefore, we aimed to assess whether high intakes of some classes of polyphenols are associated with T2D in a population with metabolic syndrome and how these associations depend on BMI and sex. This baseline cross-sectional analysis includes 6633 participants from the PREDIMED-Plus trial. Polyphenol intakes were calculated from food fr…

0301 basic medicinePhysiologyCross-sectional studyClinical BiochemistryHydroxycinnamic acidsType 2 diabetesOverweightBiochemistry0302 clinical medicinepreventionFlavonoidesmetabolitesrisk2. Zero hungereducation.field_of_studyDiabetisDiabetes1. No poverty3. Good healthObesitatDietamedicine.symptommanagementHydroxybenzoic acidHydroxybenzoic acidsPhenolic acidsPopulationmen030209 endocrinology & metabolismArticleLignansCatechins2 cohorts03 medical and health sciencesEnvironmental healthcatechins diet flavonoids hydroxybenzoic acids hydroxycinnamic acids lignans obesity phenolic acids proanthocyanidinsmedicineProanthocyanidinsObesityeducationMolecular BiologyFlavonoids030109 nutrition & dieteticsbusiness.industrylcsh:RM1-950biomarkersnutritional and metabolic diseasesCell Biologymedicine.diseaseObesityDietlcsh:Therapeutics. PharmacologyMetabolic syndromebusinessBody mass index
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Niemann-Pick type C2 protein supplementation in experimental non-alcoholic fatty liver disease

2017

BACKGROUND AND AIMS: Hepatic cholesterol deposition drives inflammation and fibrosis in non-alcoholic steatohepatitis (NASH). The Niemann-Pick type C2 (NPC2) protein plays an important role in regulating intracellular cholesterol trafficking and homeostasis. We hypothesized that intravenous NPC2 supplementation reduces cholesterol accumulation, hepatic inflammation and fibrogenesis in a nutritional NASH rat model.METHODS: Rats were fed a high-fat, high-cholesterol (HFHC) diet for four weeks resulting in moderately severe NASH. Animals were treated with intravenous NPC2 or placebo twice weekly for either the last two weeks or the entire four weeks. End-points were liver/body- and spleen/body…

0301 basic medicinePhysiologyGene Expressionlcsh:MedicinePathology and Laboratory MedicineBiochemistrychemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseSterol Regulatory Element Binding ProteinsInnate Immune SystemMultidisciplinarybiologyLiver DiseasesReverse cholesterol transportFatty liverIntracellular Signaling Peptides and ProteinsLipidsCholesterolLiverCytokinesLiver FibrosisFemale030211 gastroenterology & hepatologylipids (amino acids peptides and proteins)Research Articlemedicine.medical_specialtyImmunologyBiological Transport ActiveGastroenterology and HepatologyCollagen Type I03 medical and health sciencesSigns and SymptomsDiagnostic MedicineInternal medicineGeneticsmedicineAnimalsRats WistarGlycoproteinsNutritionInflammationbusiness.industryCholesterollcsh:RBiology and Life Sciencesnutritional and metabolic diseasesMolecular Developmentmedicine.diseaseDietary FatsFibrosisRatsDietCollagen Type I alpha 1 ChainPPAR gammaFatty LiverDisease Models Animal030104 developmental biologyEndocrinologychemistryImmune SystemABCA1LDL receptorbiology.proteinlcsh:QSteatohepatitisCarrier ProteinsbusinessDevelopmental BiologyLipoprotein
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Nutritional Intake and the Risk for Non-Alcoholic Fatty Liver Disease (NAFLD)

2019

The prevalence of non-alcoholic fatty liver disease (NAFLD) is rising worldwide, and it is estimated that approximately one billion individuals may be afflicted with NAFLD globally [...]

0301 basic medicinePhysiologylcsh:TX341-641DiseaseGlobal Healthdigestive system03 medical and health sciences0302 clinical medicineFeeding behaviorNon-alcoholic Fatty Liver DiseaseGlobal healthMedicineHumans030109 nutrition & dieteticsNutrition and Dieteticsbusiness.industryFatty livernutritional and metabolic diseasesNon alcoholicFeeding BehaviorDietary patternmedicine.diseasedigestive system diseasesEditorialn/a030211 gastroenterology & hepatologybusinesslcsh:Nutrition. Foods and food supplyFood ScienceNutrients
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Metformin decreases progerin expression and alleviates pathological defects of Hutchinson–Gilford progeria syndrome cells

2016

Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disorder that causes systemic accelerated aging in children. This syndrome is due to a mutation in the LMNA gene that leads to the production of a truncated and toxic form of lamin A called progerin. Because the balance between the A-type lamins is controlled by the RNA-binding protein SRSF1, we have hypothesized that its inhibition may have therapeutic effects for HGPS. For this purpose, we evaluated the antidiabetic drug metformin and demonstrated that 48 h treatment with 5 mmol/l metformin decreases SRSF1 and progerin expression in mesenchymal stem cells derived from HGPS induced pluripotent stem cells (HGPS MSCs). The effect …

0301 basic medicinePremature agingcongenital hereditary and neonatal diseases and abnormalitiesAgingArticleLMNA03 medical and health sciencesProgeria0302 clinical medicinemedicineInduced pluripotent stem cellProgeriaintegumentary systembusiness.industryGenetic disordernutritional and metabolic diseasesmedicine.diseaseProgerinMetformin030104 developmental biology030220 oncology & carcinogenesisCancer researchGeriatrics and GerontologybusinessLaminmedicine.drugnpj Aging and Mechanisms of Disease
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Pathological modelling of pigmentation disorders associated with Hutchinson-Gilford Progeria Syndrome (HGPS) revealed an impaired melanogenesis pathw…

2018

AbstractHutchinson-Gilford Progeria Syndrome (HGPS) is a rare genetic disorder that leads to premature aging. In this study, we used induced pluripotent stem cells to investigate the hypopigmentation phenotypes observed in patients with progeria. Accordingly, two iPS cell lines were derived from cells from HGPS patients and differentiated into melanocytes. Measurements of melanin content revealed a lower synthesis of melanin in HGPS melanocytes as compared to non-pathologic cells. Analysis of the melanosome maturation process by electron microscopy revealed a lower percentage of mature, fully pigmented melanosomes. Finally, a functional rescue experiment revealed the direct role of progerin…

0301 basic medicinePremature agingcongenital hereditary and neonatal diseases and abnormalitiesInduced Pluripotent Stem Cellslcsh:MedicineBiologyModels BiologicalArticleMelanin03 medical and health sciencesProgeriamedicineHumansInduced pluripotent stem celllcsh:SciencePigmentation disorderMelanosomeHypopigmentationProgeriaMelanosomesMultidisciplinaryintegumentary systemlcsh:Rnutritional and metabolic diseasesmedicine.diseaseProgerinCell biology030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMelanocyteslcsh:Qmedicine.symptomPigmentation Disorders
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Metabolites related to purine catabolism and risk of type 2 diabetes incidence; modifying effects of the TCF7L2-rs7903146 polymorphism

2019

Studies examining associations between purine metabolites and type 2 diabetes (T2D) are limited. We prospectively examined associations between plasma levels of purine metabolites with T2D risk and the modifying effects of transcription factor-7-like-2 (TCF7L2) rs7903146 polymorphism on these associations. This is a case-cohort design study within the PREDIMED study, with 251 incident T2D cases and a random sample of 694 participants (641 non-cases and 53 overlapping cases) without T2D at baseline (median follow-up: 3.8 years). Metabolites were semi-quantitatively profiled with LC-MS/MS. Cox regression analysis revealed that high plasma allantoin levels, including allantoin-to-uric acid rat…

0301 basic medicinePurineMalePolymorphism (Crystallography)endocrine system diseaseslcsh:MedicineType 2 diabetesDiabetis no-insulinodependentchemistry.chemical_compound0302 clinical medicineBlood plasmaMetabolitesNon-insulin-dependent diabetesProspective Studieslcsh:ScienceMultidisciplinaryDiabetisIncidencePrognosisMetabòlits3. Good healthMetabolomeFemaleTranscription Factor 7-Like 2 Proteinmedicine.drugmedicine.medical_specialtyendocrine systemPolymorphism Single NucleotideArticle03 medical and health sciencesAllantoin:Ciencias de la Salud::Medicina preventiva [Materias Investigacion]Diabetes mellitusInternal medicinemedicineHumansGenetic Predisposition to DiseaseInosineAgedbusiness.industrylcsh:Rnutritional and metabolic diseasesPolimorfisme (Cristal·lografia)Xanthinemedicine.disease030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2PurinesSpainCase-Control Studieslcsh:QbusinessTCF7L2030217 neurology & neurosurgeryBiomarkersFollow-Up Studies
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Nuclear inclusions of pathogenic ataxin-1 induce oxidative stress and perturb the protein synthesis machinery

2020

Spinocerebellar ataxia type-1 (SCA1) is caused by an abnormally expanded polyglutamine (polyQ) tract in ataxin-1. These expansions are responsible for protein misfolding and self-assembly into intranuclear inclusion bodies (IIBs) that are somehow linked to neuronal death. However, owing to lack of a suitable cellular model, the downstream consequences of IIB formation are yet to be resolved. Here, we describe a nuclear protein aggregation model of pathogenic human ataxin-1 and characterize IIB effects. Using an inducible Sleeping Beauty transposon system, we overexpressed the ATXN1(Q82) gene in human mesenchymal stem cells that are resistant to the early cytotoxic effects caused by the expr…

0301 basic medicineSCA1 Spinocerebellar ataxia type-1Intranuclear Inclusion BodiesClinical BiochemistryMSC mesenchymal stem cellProtein aggregationBiochemistry0302 clinical medicineMutant proteinProtein biosynthesisDE differentially expressed genesNuclear proteinlcsh:QH301-705.5FTIR Fourier-transform infrared spectroscopyAtaxin-1lcsh:R5-920biologyChemistryNuclear ProteinspolyQ polyglutamineRibosomeCell biologySB Sleeping BeautyRibosome ; Polyglutamine ; Ataxin-1 ; Oxidative stress ; Transposon ; Sleeping beauty transposon ; Protein networkSpinocerebellar ataxiaProtein foldingCellular modelFunction and Dysfunction of the Nervous Systemlcsh:Medicine (General)Research PaperiPSC induced pluripotent stem cellAtaxin 1Nerve Tissue ProteinsPPI protein-protein interaction03 medical and health sciencesROS reactive oxygen speciesProtein networkSleeping beauty transposonGSEA Gene Set Enrichment AnalysismedicineHumansNPC neural progenitor cellOrganic Chemistrymedicine.diseaseAFM atomic force microscopyOxidative Stress030104 developmental biologylcsh:Biology (General)IIBs intranuclear inclusion bodiesMS mass spectrometryCardiovascular and Metabolic Diseasesbiology.proteinPolyglutamine030217 neurology & neurosurgery
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