Search results for "HEREDITARY"

showing 10 items of 650 documents

Evidence against linkage of schizophrenia to chromosome 5q11-q13 markers in systematically ascertained families.

1992

Ten pedigrees systematically ascertained in Germany were tested for linkage to chromosome 5q11-q13. In order to replicate the previous report by Sherrington et al (1988), families with a bipolar family member were omitted from the lod score calculations, all diagnoses were based upon Research Diagnostic Criteria, and four different models of the affection status were calculated, including the model for which Sherrington et al calculated the highest lod scores. None of the families investigated showed a positive lod score. Using multipoint linkage analyses, we were able to exclude the region for which a positive linkage has been reported.

Linkage (software)GeneticsGenetic Markerscongenital hereditary and neonatal diseases and abnormalitiesGenetic LinkageResearch Diagnostic CriteriaPedigree chartmedicine.diseaseFamily memberChromosome (genetic algorithm)Psychotic DisordersSchizophreniamedicineSchizophreniaChromosomes Human Pair 5HumansFamilyLymphocytesLod ScorePsychologyBiological PsychiatryLod scoresLod scoreBiological psychiatry
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Inflammatory Characteristics of Monocytes from Pediatric Patients with Tuberous Sclerosis.

2015

Objective  Therapeutic options for the tuberous sclerosis complex (TSC) syndrome showed varying outcomes. Malfunctional tsc1 / tsc2 genes leave mTOR uninhibited, a positive downstream modulator of the innate proinflammatory immune system, which has not yet been described in pediatric patients with TSC. Methods  Using polymerase chain reaction (PCR) gene expression levels of monocytes after cultivation with lipopolysaccharide (LPS) or with LPS + mTOR inhibitor rapamycin, patients with TSC ( n  = 16) were compared with healthy subjects ( n  = 20). Results  Compared with monocytes from healthy controls, LPS showed a more prominent gene expression pattern in patients with TSC (CCL24, CXCL10, IL…

Lipopolysaccharidescongenital hereditary and neonatal diseases and abnormalitiesLipopolysaccharideGene ExpressionMonocytesProinflammatory cytokinechemistry.chemical_compoundTuberous sclerosisTuberous SclerosisGene expressionmedicineCXCL10HumansChildInflammationSirolimusbusiness.industryTOR Serine-Threonine KinasesInfant NewbornInfantGeneral Medicinemedicine.diseasemedicine.anatomical_structureCross-Sectional StudieschemistryChild PreschoolPediatrics Perinatology and Child HealthImmunologyCytokinesNeurology (clinical)TSC1TSC2Inflammation MediatorsbusinessCCL24Immunosuppressive AgentsNeuropediatrics
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A fractional viscoelastic non-local Timoshenko beam

2014

Long-range interactions Fractional hereditary nano beams Non-local hereditarinessSettore ICAR/08 - Scienza Delle Costruzioni
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mTORC1 activation in B cells confers impairment of marginal zone microarchitecture by exaggerating cathepsin activity

2018

Mammalian target of rapamycin complex 1 (mTORC1) is a key regulator of cell metabolism and lymphocyte proliferation. It is inhibited by the tuberous sclerosis complex (TSC), a heterodimer of TSC1 and TSC2. Deletion of either gene results in robust activation of mTORC1. Mature B cells reside in the spleen at two major anatomical locations, the marginal zone (MZ) and follicles. The MZ constitutes the first line of humoral response against blood‐borne pathogens and undergoes atrophy in chronic inflammation. In previous work, we showed that mice deleted for TSC1 in their B cells (TSC1(BKO)) have almost no MZ B cells, whereas follicular B cells are minimally affected. To explore potential underl…

Lymphotoxin-beta0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesImmunologyMice TransgenicSpleenCHO CellsmTORC1Lymphocyte proliferationMechanistic Target of Rapamycin Complex 1Tuberous Sclerosis Complex 1 ProteinCathepsin BCell LineMice03 medical and health sciencesCricetulus0302 clinical medicineLymphotoxin beta ReceptorTuberous Sclerosis Complex 2 ProteinmedicineAnimalsImmunology and AllergyReceptorLymphotoxin-alphaSirolimusCathepsinB-LymphocytesChemistryOriginal ArticlesMarginal zoneCathepsinsCell biology030104 developmental biologymedicine.anatomical_structureLymphotoxinSpleen030215 immunologyImmunology
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Clinical characteristics of pancreatic and biliary tract cancers in Lynch syndrome : A retrospective analysis from the Finnish National Lynch Syndrom…

2023

IntroductionPatients with Lynch syndrome (LS) have an increased lifetime risk of pancreatic cancer (PC) and biliary tract cancer (BTC). These cancers have a notoriously pessimistic prognosis due to late diagnosis and limited therapeutic options. There are limited data based on small cohorts reviewing PC and BTC in LS patients.MethodsIn this retrospective study of the Lynch Syndrome Registry of Finland (LSRFi), records of genetically verified LS patients diagnosed with PC or BTC between 1982 and 2020 were analyzed.ResultsThirty-nine patients were included: tumor(s) were in the pancreas in 26 patients, in the biliary tract in 10, and in the ampulla of Vater in three. A pathogenic germline var…

Lynch syndrome (LS)Cancer Researchhereditary nonpolyposis colon cancermicrosatellite instability (MSI)3122 Cancerspancreatic cancerPancreatic cancer3121 Internal medicinemikrosatelliititLynch syndromeOncologyhereditary nonpolyposis colon cancer (HNPCC)biliary tract cancerBiliary tract cancermicrosatellite instabilityLynchin oireyhtymähaimasyöpäpaksusuolisyöpä
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Abstract LB-085: A new role for LKB1 to regulate Heat Shock Protein 90 activity

2018

Abstract Approximately 30% of human non-small cell lung cancer (NSCLC) patients harbor a somatic KRAS mutation resulting, in aberrant activation of downstream signaling pathways that control cell proliferation, cell growth, and cell survival. Importantly, alleles of LKB1, a serine/threonine kinase that functions as a tumor suppressor, are somatically inactivated in ~30% of NSCLCs within KRAS-mutant NSCLC. The loss of LKB1 gives rise to aggressive, highly metastatic, and highly drug resistant tumors. We have previously demonstrated that the inactivation of the tumor suppressor lkb1 rendered mutant kras murine NSCLC resistant to targeted agents including BET bromodomain and kinase inhibitors.…

MAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchCell signalingChemistryKinaseCell growthIsogenic human disease modelsOncologyHeat shock proteinCancer researchKinase activityskin and connective tissue diseasesPI3K/AKT/mTOR pathwayCancer Research
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IC3D Classification of Corneal Dystrophies—Edition 2

2015

To update the 2008 International Classification of Corneal Dystrophies (IC3D) incorporating new clinical, histopathologic, and genetic information.The IC3D reviewed worldwide peer-reviewed articles for new information on corneal dystrophies published between 2008 and 2014. Using this information, corneal dystrophy templates and anatomic classification were updated. New clinical, histopathologic, and confocal photographs were added.On the basis of revisiting the cellular origin of corneal dystrophy, a modified anatomic classification is proposed consisting of (1) epithelial and subepithelial dystrophies, (2) epithelial-stromal TGFBI dystrophies, (3) stromal dystrophies, and (4) endothelial d…

Macular corneal dystrophygenetic structuresEndothelial dystrophiesGenetic diseaseStromaEpitheliumGelatinousdrop-like corneal dystrophyCorneaLisch Epithelial Corneal DystrophyCornea pathologyPosteror polymorphous corneal dystrophyCorneal Dystrophies HereditaryPosterior amorphous corneal dystrophyEpithelial-stromal TGFBI dystrophiesMacular corneal dystrophyFleck corneal dystrophyLattice corneal dystrophyPre-Descemet corneal dystrophyCongenital stromal corneal dystrophySubepithelialmucinous corneal dystrophySchnyder corneal dystrophyThiel-Behnke corneal dystrophyPosterior polymorphous corneal dystrophyEpithelial and subepithelial dystrophiesFuchsendothelial corneal dystrophyFleck corneal dystrophyReis-Bücklers corneal dystrophyCongenital hereditary endothelial dystrophyCentralcloudy dystrophy of FrançoisCongenital stromal corneal dystrophyPosterior amorphous corneal dystrophymedicine.medical_specialtyHistologyeducationHereditary diseaseHistopathologyBiologyKeratoconusLisch epithelial corneal dystrophyMeesmann dystrophyNOBowman membraneDescemetmembraneInternational Classification of DiseasesTerminology as TopicOphthalmologyGeneticsmedicineHumansBowman membrane; Centralcloudy dystrophy of François; Confocal microscopy; Confocal microscopy; Congenital corneal endothelial dystrophy and X-linked endothelialdystrophy; Congenital stromal corneal dystrophy; Cornea; Cornea; Cornea dystrophy; Cornea pathology; Descemetmembrane; Endothelial dystrophies; Endothelium; Epithelial and subepithelial dystrophies; Epithelial basement membranedystrophy; Epithelial recurrent erosion dystrophies; Epithelial-stromal TGFBI dystrophies; Epithelium; Fleck corneal dystrophy; Fuchsendothelial corneal dystrophy; Gelatinousdrop-like corneal dystrophy; Genetic disease; Genetics; Granular corneal dystrophy type 1; Granular corneal dystrophy type 2; Hereditary disease; Histology; Histopathology; Keratoconus; Lattice corneal dystrophy; Lisch epithelial corneal dystrophy; Macular corneal dystrophy; Meesmann dystrophy; Posterior amorphous corneal dystrophy; Posteror polymorphous corneal dystrophy; Pre-Descemet corneal dystrophy; Reis-Bücklers corneal dystrophy; Schnyder corneal dystrophy; Stroma; Stromal dystrophies; Subepithelialmucinous corneal dystrophy; TGFBI; Thiel-Behnke corneal dystrophy; OphthalmologyEndotheliumEpithelial basement membranedystrophyCornea dystrophyCongenital corneal endothelial dystrophy and X-linked endothelialdystrophymedicine.diseaseeye diseasesConfocal microscopyOphthalmologyGranular corneal dystrophy type 2Granular corneal dystrophy type 1Stromal dystrophiesLattice corneal dystrophysense organsTGFBIEpithelial recurrent erosion dystrophiesCornea
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G6PD protects from oxidative damage and improves healthspan in mice

2016

S.N.-P. and P.J.F.-M. have been funded by the Spanish Association Against Cancer(aecc). Work in the laboratory of M.S. is funded by the CNIO and by grants from the Spanish Ministry of Economy co-funded by the European Regional Development Fund(SAF project), the European Research Council (ERC Advanced Grant), the Regional Government of Madrid co-funded by the European Social Fund (ReCaRe project), the European Union (RISK-IR project), the Botin Foundation and Banco Santander(Santander Universities Global Division), the Ramon Areces Foundation, and the AXA Foundation. Work in the laboratory of J.V. was supported by grants SAF2013-44663-R,from the Spanish Ministry of Education and Science (MEC…

Male0301 basic medicineAgingCellGeneral Physics and AstronomyDehydrogenaseEndogenymedicine.disease_causestressMicehemic and lymphatic diseasesratmécanismegenesreactive oxygen specieschemistry.chemical_classificationMultidisciplinary[SDV.BA]Life Sciences [q-bio]/Animal biologyQvieillissementCell biologymedicine.anatomical_structureanimal transgéniqueFemaleGenetically modified mouse[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]congenital hereditary and neonatal diseases and abnormalitiesScienceTransgeneLongevityMice TransgenicGlucosephosphate DehydrogenaseBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesparasitic diseasesmedicineAnimalsHumansReactive oxygen speciesgènenutritional and metabolic diseasesGeneral ChemistrycellMolecular biologytransgenic mouseOxidative Stress030104 developmental biologymechanistic theorychemistryageingenzyme antioxydanteAgeingespèce reactive de l'oxygènecelluleReactive Oxygen SpeciesNADPOxidative stressNature Communications
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A Typical Immune T/B Subset Profile Characterizes Bicuspid Aortic Valve: In an Old Status?

2018

Bicuspid valve disease is associated with the development of thoracic aortic aneurysm. The molecular mechanisms underlying this association still need to be clarified. Here, we evaluated the circulating levels of T and B lymphocyte subsets associated with the development of vascular diseases in patients with bicuspid aortic valve or tricuspid aortic valve with and without thoracic aortic aneurysm. We unveiled that the circulating levels of the MAIT, CD4+IL−17A+, and NKT T cell subsets were significantly reduced in bicuspid valve disease cases, when compared to tricuspid aortic valve cases in either the presence or the absence of thoracic aortic aneurysm. Among patients with tricuspid aortic…

Male0301 basic medicineAortic valveAgingT-LymphocytesLymphocyteHeart Valve Diseases030204 cardiovascular system & hematologyBiochemistryImmunoglobulin D0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseBicuspid aortic valve aneurysm B cellsb-cellsnotch1Invariant t-cells; aneurysm formation; angiotensin-ii; signaling pathway; genetic-variants; apoptotic cells; b-cells; mechanisms; mutations; notch1B-Lymphocytesmechanismsbiologylcsh:Cytologyhemic and immune systemsGeneral MedicineMiddle Agedmedicine.anatomical_structureAortic ValveCardiologycardiovascular systemFemaleResearch Articlesignaling pathwaymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesaneurysm formationInvariant t-cellsArticle SubjectBicuspid aortic valveT cellNaive B cellchemical and pharmacologic phenomenaThoracic aortic aneurysm03 medical and health sciencesBicuspid valveInternal medicinemedicineHumansSettore MED/05 - Patologia Clinicacardiovascular diseaseslcsh:QH573-671angiotensin-iigenetic-variantsB cellsbusiness.industrySettore MED/23 - Chirurgia Cardiacaapoptotic cellsCell Biologymutationsmedicine.disease030104 developmental biologybiology.proteinaneurysmbusinessA Typical Immune T/B Subset Profile Bicuspid Aortic Valve
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Canakinumab for the Treatment of Autoinflammatory Recurrent Fever Syndromes.

2018

BACKGROUND: Familial Mediterranean fever, mevalonate kinase deficiency (also known as the hyperimmunoglobulinemia D syndrome), and the tumor necrosis factor receptor-associated periodic syndrome (TRAPS) are monogenic autoinflammatory diseases characterized by recurrent fever flares. METHODS: We randomly assigned patients with genetically confirmed colchicine-resistant familial Mediterranean fever, mevalonate kinase deficiency, or TRAPS at the time of a flare to receive 150 mg of canakinumab subcutaneously or placebo every 4 weeks. Patients who did not have a resolution of their flare received an add-on injection of 150 mg of canakinumab. The primary outcome was complete response (resolution…

Male0301 basic medicineInterleukin-1betaFamilial Mediterranean fever0302 clinical medicineMonoclonalChildMedicine(all)Mevalonate kinase deficiencySubcutaneousMedicine (all)Interleukin-1betaAntibodies MonoclonalGeneral MedicineFamilial Mediterranean FeverRecurrent feverChild PreschoolFemaleTumor necrosis factor alphaDrugInflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5]medicine.drugAdultAdolescentFeverInjections SubcutaneousHereditary Autoinflammatory DiseasesAntibodies Monoclonal HumanizedAdolescent; Adult; Antibodies Monoclonal/administration & dosage; Antibodies Monoclonal/adverse effects; Antibodies Monoclonal/therapeutic use; Child; Child Preschool; Dose-Response Relationship Drug; Double-Blind Method; Familial Mediterranean Fever/drug therapy; Female; Fever/drug therapy; Hereditary Autoinflammatory Diseases/drug therapy; Humans; Injections Subcutaneous; Interleukin-1beta/antagonists & inhibitors; Male; Mevalonate Kinase Deficiency/drug therapy; Young AdultAntibodiesInjectionsDose-Response RelationshipYoung Adult03 medical and health sciencesAll institutes and research themes of the Radboud University Medical CenterDouble-Blind MethodGeneral & Internal MedicinemedicineHumansPreschoolAdolescent; Adult; Antibodies Monoclonal; Child; Child Preschool; Dose-Response Relationship Drug; Double-Blind Method; Familial Mediterranean Fever; Female; Fever; Hereditary Autoinflammatory Diseases; Humans; Injections Subcutaneous; Interleukin-1beta; Male; Mevalonate Kinase Deficiency; Young Adult; Medicine (all)030203 arthritis & rheumatologyDose-Response Relationship Drugbusiness.industryHereditary Autoinflammatory DiseasesHyperimmunoglobulinemia Dmedicine.diseaseCanakinumab030104 developmental biologyImmunologyMevalonate Kinase Deficiencybusiness
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