Search results for " Progression"

showing 10 items of 1092 documents

The membrane-bound O-acyltransferase domain-containing 7 variant rs641738 increases inflammation and fibrosis in chronic hepatitis B.

2017

Chronic hepatitis B (CHB) is characterized by hepatic inflammation that promotes progression to cirrhosis and predisposes to the development of hepatocellular carcinoma (HCC). Subtle interindividual genetic variation as well as viral and environmental factors interact to determine disease progression between individuals. Recently, the rs641738 membrane-bound O-acyltransferase domain-containing 7 (MBOAT7) polymorphism was demonstrated to influence histological liver damage in alcoholic liver disease, nonalcoholic fatty liver disease, and hepatitis C, but no data are available for CHB. We evaluated rs641738 influence on disease severity in a cohort of 1,101 patients with CHB. Forty-two patien…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCirrhosisSex FactorSeverity of Illness IndexCohort StudiesGene FrequencyFibrosisNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseAge FactorProspective StudiesChronicMembrane ProteinMultivariate AnalysiAge FactorsHepatitis CSingle NucleotideMiddle AgedHepatitis BPrognosisHepatocellular carcinomaDisease ProgressionFemaleHumanAdultmedicine.medical_specialtyLogistic ModelPrognosiAcyltransferaseLiver CirrhosiAcetyltransferases; Acyltransferases; Adult; Age Factors; Cohort Studies; Confidence Intervals; Disease Progression; Female; Gene Frequency; Genetic Predisposition to Disease; Hepatitis B Chronic; Humans; Liver Cirrhosis; Logistic Models; Male; Membrane Proteins; Middle Aged; Multivariate Analysis; Non-alcoholic Fatty Liver Disease; Polymorphism Single Nucleotide; Prognosis; Prospective Studies; Risk Assessment; Severity of Illness Index; Sex FactorsPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesHepatitis B ChronicSex FactorsSDG 3 - Good Health and Well-beingAcetyltransferasesInternal medicineAcetyltransferasemedicineConfidence IntervalsHumansGenetic Predisposition to DiseasePolymorphismHepatologybusiness.industryMembrane ProteinsHepatologymedicine.diseaseMinor allele frequencyProspective Studie030104 developmental biologyLogistic ModelsImmunologyMultivariate AnalysisCohort StudiebusinessConfidence IntervalAcyltransferasesHepatology (Baltimore, Md.)
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Renin-Angiotensin System Inhibitors, Type 2 Diabetes and Fibrosis Progression: An Observational Study in Patients with Nonalcoholic Fatty Liver Disea…

2016

Background The clinical determinants of fibrosis progression in nonalcoholic fatty liver disease (NAFLD) are still under definition. Aim To assess the clinical determinants of fibrosis progression rate (FPR) in NAFLD patients with baseline and follow-up histological evaluation, with a special focus on the impact of pharmacological therapy. Methods In an observational cohort of 118 Italian patients from tertiary referral centers, liver histology was evaluated according to Kleiner. Independent predictors of FPR were selected by a stepwise regression approach. Results Median follow-up was 36 months (IQR 24–77). Twenty-five patients (18%) showed some amelioration, 63 (53%) had stability, 30 (25…

0301 basic medicineLiver CirrhosisMalePeptide HormonesBiopsyTertiary Care Centerlcsh:MedicineBlood PressureAngiotensin-Converting Enzyme InhibitorsType 2 diabetesGastroenterologyVascular MedicineBiochemistryRenin-Angiotensin SystemTertiary Care Centers0302 clinical medicineFibrosisRetrospective StudieNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseMedicine and Health SciencesEthnicitieslcsh:ScienceDiureticsMultidisciplinarymedicine.diagnostic_testMedicine (all)Liver DiseasesFatty liverAngiotensin Receptor AntagonistMiddle AgedPrognosisMetforminMetforminItalian PeopleItalyLiverHypertensionDisease Progression030211 gastroenterology & hepatologyFemaleAnatomymedicine.drugHumanResearch ArticleAdultmedicine.medical_specialtyHistologyPrognosiLiver CirrhosiAdrenergic beta-AntagonistsSurgical and Invasive Medical ProceduresGastroenterology and HepatologyFollow-Up Studie03 medical and health sciencesAngiotensin Receptor AntagonistsInternal medicineDiabetes mellitusBiopsymedicineDiureticHumansRetrospective StudiesBiochemistry Genetics and Molecular Biology (all)business.industrylcsh:RAdrenergic beta-Antagonistnutritional and metabolic diseasesBiology and Life SciencesRetrospective cohort studyAngiotensin-Converting Enzyme Inhibitormedicine.diseaseFibrosisHormonesFatty Liver030104 developmental biologyEndocrinologyAgricultural and Biological Sciences (all)Diabetes Mellitus Type 2People and Placeslcsh:QPopulation GroupingsHydroxymethylglutaryl-CoA Reductase InhibitorHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessDevelopmental BiologyFollow-Up StudiesPLoS ONE
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Impact of virus eradication in patients with compensated hepatitis C virus-related cirrhosis: competing risks and multistate model

2016

BACKGROUND & AIMS No published study to date has provided a careful analysis of the effects of a sustained viral response (SVR) on the outcomes of patients with compensated hepatitis C virus (HCV)-related cirrhosis in relation to the degree of portal hypertension. Therefore, we estimated the impact of achieving SVR on disease progression, hepatocellular carcinoma (HCC) development and mortality in a large cohort of HCV patients with cirrhosis with or without oesophageal varices (OVs) at the start of antiviral therapy. METHODS A total of 535 Caucasian patients were prospectively recruited to this study. All patients had a clinical or histological diagnosis of compensated HCV-related cirrhosi…

0301 basic medicineLiver CirrhosisMalemedicine.medical_specialtyCirrhosisCarcinoma HepatocellularSVRSustained Virologic ResponseHepatitis C virusHepacivirusmedicine.disease_causeEsophageal and Gastric VaricesGastroenterologyAntiviral Agents03 medical and health sciencesLiver diseasemultistate0302 clinical medicineInternal medicinemedicineHumansProspective StudiesAgedCirrhosiHepatologybusiness.industryLiver Neoplasmsvirus diseasesHepatitis CHepatitis C ChronicMiddle Agedmedicine.diseasedigestive system diseases030104 developmental biologyItalyLiverHepatocellular carcinomaHCVDisease Progression030211 gastroenterology & hepatologyFemaleViral hepatitisLiver cancerbusinessViral load
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Myeloid cells do not contribute to gender-dependent differences in disease outcome in murine cutaneous leishmaniasis.

2015

Gender-associated differences in the outcome of infections are well known. Apart from behavior-released differences in their incidence, immunological factors also contribute to disease outcome. The underlying mechanisms are often unknown. Here, we show that in murine experimental leishmaniasis, female mice develop larger skin lesions that harbor significantly more parasites, exhibit increased parasite dissemination to visceral organs associated with a shift towards T helper (Th) 2 immunity with increased levels of IL-4. Antigen presenting cells (APC) responsible for T cell priming, such as macrophages or dendritic cells, were not involved in the process. Additionally, in adoptive transfer e…

0301 basic medicineMaleAdoptive cell transferMyeloidStromal cellT cellImmunologyLeishmaniasis CutaneousBiology03 medical and health sciencesMice0302 clinical medicineImmune systemTh2 CellsCutaneous leishmaniasismedicineAnimalsHumansCell LineageMyeloid CellsAntigen-presenting cellTh1-Th2 BalanceCells CulturedCell DifferentiationDendritic cellmedicine.diseaseHormonesMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureImmunologyDisease ProgressionFemaleSexDisease SusceptibilityInterleukin-4Stromal Cells030215 immunologyCellular immunology
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Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin.

2021

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. A minority of affected patients develops inflammation, subsequently fibrosis, cirrhosis and hepatocellular carcinoma (HCC). HCC is a leading cause of cancer-related death. An increased number of senescent cells correlate with age-related tissue degeneration during NAFLD-induced HCC. Senolytics are promising agents that target selectively senescent cells. Previous studies showed that whereas a combination of the senolytic drugs dasatinib and quercetin (D + Q) reduced NAFLD in mice, D + Q lacked efficacy in removing doxorubicin-induced…

0301 basic medicineMaleAgingCirrhosisDasatiniblcsh:MedicineBiochemistrySenolytics.Liver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseSenotherapeuticsNonalcoholic fatty liver diseaseDiethylnitrosamineCancerlcsh:CytologyLiver Diseases3. Good healthDasatinib030220 oncology & carcinogenesisHepatocellular carcinomaDisease ProgressionQuercetinmedicine.symptomLiver diseasemedicine.drugShort ReportInflammationDiet High-Fat03 medical and health sciencesmedicineAnimalsObesitylcsh:QH573-671SenolyticMolecular BiologyInflammationbusiness.industrySenolyticslcsh:RCell Biologymedicine.diseasedigestive system diseasesMice Inbred C57BLDisease Models Animal030104 developmental biologyGene Expression RegulationCancer researchbusinessCell communication and signaling : CCS
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Lifespan Changes of the human brain in Alzheimer's disease

2018

[EN] Brain imaging studies have shown that slow and progressive cerebral atrophy characterized the development of Alzheimer's Disease (AD). Despite a large number of studies dedicated to AD, key questions about the lifespan evolution of AD biomarkers remain open. When does the AD model diverge from the normal aging model? What is the lifespan trajectory of imaging biomarkers for AD? How do the trajectories of biomarkers in AD differ from normal aging? To answer these questions, we proposed an innovative way by inferring brain structure model across the entire lifespan using a massive number of MRI (N = 4329). We compared the normal model based on 2944 control subjects with the pathological …

0301 basic medicineMaleAgingLongevityHippocampuslcsh:MedicineTrastorns de la cognició en la vellesaAmygdalaArticle03 medical and health sciencesLateral ventricles0302 clinical medicineNeuroimagingmedicine[INFO.INFO-IM]Computer Science [cs]/Medical ImagingHumanslcsh:ScienceAgedCerebral atrophyAged 80 and overMultidisciplinarybusiness.industryNeurodegenerationlcsh:RBrainTrastorns de la memòriaHuman brainMiddle Agedmedicine.disease3. Good health030104 developmental biologymedicine.anatomical_structureFISICA APLICADADisease Progressionlcsh:QFemaleAbnormalitybusinessNeuroscience030217 neurology & neurosurgery
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Liver and Cardiovascular Damage in Patients With Lean Nonalcoholic Fatty Liver Disease, and Association With Visceral Obesity.

2017

Background & Aims Lean nonalcoholic fatty liver disease (NAFLD) is defined as NAFLD that develops in patients with a body mass index (BMI) less than 25 kg/m2. We investigated the differences between lean NAFLD and NAFLD in overweight and obese persons, factors associated with the severity of liver and cardiovascular disease, and the effects of visceral obesity. Methods We performed a retrospective cohort study of 669 consecutive patients with biopsy-proven NAFLD seen at 3 liver centers in Italy. We collected anthropometric, clinical, and biochemical data, as well as information on carotid atherosclerosis (artery intima-media thickness and plaque), liver histology (nonalcoholic steatohepatit…

0301 basic medicineMaleBiopsyOverweightGastroenterologyLiver disease0302 clinical medicineNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseMedicineGastroenterologyWaist SizeMiddle AgedCarotid ArteriesItalyLiverObesity AbdominalDisease Progression030211 gastroenterology & hepatologyFemalemedicine.symptomAdultmedicine.medical_specialtyWaistdigestive systemPolymorphism Single Nucleotide03 medical and health sciencesDiabetes mellitusInternal medicineDiabetes MellitusHumansAgedRetrospective StudiesHepatologybusiness.industryRisk FactorBody Weightnutritional and metabolic diseasesMembrane ProteinsOdds ratioLipasemedicine.diseaseAtherosclerosisdigestive system diseases030104 developmental biologyEndocrinologyMetabolic syndromeInsulin ResistancebusinessBody mass indexClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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A phase I dose-escalation study of IMAB362 (Zolbetuximab) in patients with advanced gastric and gastro-oesophageal junction cancer

2018

Introduction IMAB362 (Zolbetuximab) is a chimeric monoclonal antibody that binds to Claudin-18.2, a target antigen specific to cancer cells. In vitro, IMAB362 mediates cell death through antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity; thus, IMAB362 may serve as a potent, targeted immunotherapeutic agent. Methods This first-in-human phase I study enroled adult patients (N = 15) with advanced gastric or gastro-oesophageal junction cancer into five sequential single dose-escalation cohorts (33, 100, 300, 600, and 1000 mg/m2) following a 3 + 3 design. Safety/tolerability, including determination of maximum tolerated dose and recommended phase II dose, were the pr…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyTime FactorsEsophageal NeoplasmsMaximum Tolerated Dosemedicine.medical_treatmentMedizinGastroenterologyAntibodies Monoclonal/administration & dosage03 medical and health sciences0302 clinical medicineAntineoplastic Agents ImmunologicalPharmacokineticsAntineoplastic Agents Immunological/administration & dosageStomach NeoplasmsInternal medicineGermanymedicineHumansDrug Dosage CalculationsAdverse effectInfusions IntravenousAgedbusiness.industryCancerAntibodies MonoclonalEsophagogastric Junction/drug effectsImmunotherapyMiddle Agedmedicine.diseaseLatviaddc:030104 developmental biologyTreatment OutcomeOncologyTolerabilityResponse Evaluation Criteria in Solid Tumors030220 oncology & carcinogenesisToxicityDisease ProgressionFemaleStomach Neoplasms/drug therapyEsophagogastric JunctionEsophageal Neoplasms/drug therapybusinessProgressive disease
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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