Search results for "patho"

showing 10 items of 10772 documents

Tricho-dento-osseous syndrome and precocious eruption

2017

Tricho-dento-osseous syndrome (TDO), an uncommon form of ectodermal dysplasia is an autosomal dominant genetic disorder which is characterized by inherited defects in tissues arising from epithelial-mesenchymal interaction. Genetic studies have revealed that it is caused by mutation in the DLX3 gene. TDO presents with a great phenotypic heterogeneity and studies have suggested that this heterogeneity is the result of environmental factors or other genetic modifiers. In this article, we report a case of TDO in which the child had typical clinical features of hair, teeth and bone defects, as seen in TDO. Parents of the child were unaffected. Genetic analysis of the child revealed mutation in …

0301 basic medicineMutationPathologymedicine.medical_specialtyEctodermal dysplasiaOral Medicine and PathologyGenetic heterogeneityDLX3Genetic disorderCase ReportBiology:CIENCIAS MÉDICAS [UNESCO]medicine.diseasemedicine.disease_causeGenetic analysisTricho-Dento-Osseous Syndrome03 medical and health sciencesstomatognathic diseases030104 developmental biologyUNESCO::CIENCIAS MÉDICASmedicineGeneral DentistryJournal of Clinical and Experimental Dentistry
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Interleukin 1α: a comprehensive review on the role of IL-1α in the pathogenesis and treatment of autoimmune and inflammatory diseases.

2021

Abstract The interleukin (IL)-1 family member IL-1α is a ubiquitous and pivotal pro-inflammatory cytokine. The IL-1α precursor is constitutively present in nearly all cell types in health, but is released upon necrotic cell death as a bioactive mediator. IL-1α is also expressed by infiltrating myeloid cells within injured tissues. The cytokine binds the IL-1 receptor 1 (IL-1R1), as does IL-1β, and induces the same pro-inflammatory effects. Being a bioactive precursor released upon tissue damage and necrotic cell death, IL-1α is central to the pathogenesis of numerous conditions characterized by organ or tissue inflammation. These include conditions affecting the lung and respiratory tract, …

0301 basic medicineMyocarditisil-1βmedicine.medical_treatmentAutoimmunity Cancer Cytokines IL-1 IL-1αIL-1β Inflammation Interleukin 1 Receptor Antagonist Protein Receptors Interleukin-1 SARS-CoV-2 COVID-19 Interleukin-1alpha Humansil-1αImmunologyreceptorsInflammationmedicine.disease_causeAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicineSettore MED/38 - Pediatria Generale E Specialisticail-1Interleukin-1alphamedicinecancerImmunology and AllergyHumans030203 arthritis & rheumatologyAnakinrabusiness.industrySARS-CoV-2autoimmunityInterleukinCOVID-19Receptors Interleukin-1medicine.diseasecytokinesRilonaceptInterleukin 1 Receptor Antagonist Protein030104 developmental biologyCytokineinflammationImmunologyautoimmunity; cancer; cytokines; il-1; il-1α; il-1β; inflammation; humans; interleukin 1 receptor antagonist protein; receptors interleukin-1; SARS-COV-2; COVID-19; interleukin-1alphamedicine.symptombusinessinterleukin-1medicine.drugAutoimmunity reviews
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NOD-like receptors: major players (and targets) in the interface between innate immunity and cancer

2019

Innate immunity comprises several inflammation-related modulatory pathways which receive signals from an array of membrane-bound and cytoplasmic pattern recognition receptors (PRRs). The NLRs (NACHT (NAIP (neuronal apoptosis inhibitor protein), C2TA (MHC class 2 transcription activator), HET-E (incompatibility locus protein from Podospora anserina) and TP1 (telomerase-associated protein) and Leucine-Rich Repeat (LRR) domain containing proteins) relate to a large family of cytosolic innate receptors, involved in detection of intracellular pathogens and endogenous byproducts of tissue injury. These receptors may recognize pathogen-associated molecular patterns (PAMPs) and/or danger-associated…

0301 basic medicineNOD1InflammasomesBiophysicsNLR ProteinsReview ArticleRECEPTORESBiochemistry46NOD2NLR Proteins45NLRInflammasome03 medical and health sciences0302 clinical medicineNeoplasmsMHC class INOD1medicineAnimalsHumansNF-kBReceptorMolecular BiologyReview ArticlesCancerInflammationInnate immune systembiologyPathogen-Associated Molecular Pattern MoleculesPattern recognition receptorNF-kappa BInflammasomeCell Biology3910Immunity InnateCell biology030104 developmental biology030220 oncology & carcinogenesisReceptors Pattern Recognitionbiology.proteinNAIPmedicine.drug
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Approaching Sex Differences in Cardiovascular Non-Coding RNA Research

2020

International audience; Cardiovascular disease (CVD) is the biggest cause of sickness and mortality worldwide in both males and females. Clinical statistics demonstrate clear sex differences in risk, prevalence, mortality rates, and response to treatment for different entities of CVD. The reason for this remains poorly understood. Non-coding RNAs (ncRNAs) are emerging as key mediators and biomarkers of CVD. Similarly, current knowledge on differential regulation, expression, and pathology-associated function of ncRNAs between sexes is minimal. Here, we provide a state-of-the-art overview of what is known on sex differences in ncRNA research in CVD as well as discussing the contributing biol…

0301 basic medicineNcRNAER-BETARNA Untranslatedexperimental modelsreceptorsReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular Systemlcsh:Chemistry0302 clinical medicineSex hormone-binding globulinlncRNAestrogenMedicinePROMOTER METHYLATIONlcsh:QH301-705.5DNA METHYLATIONSpectroscopyGENE-EXPRESSIONSex CharacteristicsbiologyMortality rateGeneral MedicineMOUSE MODELNon-coding RNA[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthComputer Science ApplicationsHEART-FAILUREESTROGEN-RECEPTOR-ALPHAandrogenvascular cells.vascular cellsCatalysisMICRORNA THERAPEUTICSInorganic Chemistry03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansEpigeneticsPhysical and Theoretical ChemistryX-INACTIVATIONMolecular BiologySocioeconomic statusmiRNAbusiness.industryOrganic ChemistryPOSTMENOPAUSAL HORMONE-THERAPYcardiovascular diseasesSexual dimorphism030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinbusinessBiomarkersInternational journal of molecular sciences
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Stem Cells and Other Emerging Agents as Innovative "Drugs" in Neurodegenerative Diseases: Benefits and Limitations.

2018

The brain has a limited process of repair/regeneration linked to the restricted and localized activity of neuronal stem cells. Consequently, it shows a reduced capacity to counteract the age-related loss of neural and glial cells and to repair the consequent injuries/lesions of nervous system. This progressively determines nervous dysfunction and onset/progression of neurodegenerative diseases, which represent a serious social (and economic) problem of our populations. Thus, the research of efficient treatments is encouraged. Stem cell therapy might represent a solution. Today, it, indeed, represents the object of intensive research with the hope of using it, in a near future, as effective …

0301 basic medicineNervous systemAgingPathologymedicine.medical_specialtyself‐repair/regenerative processmedicine.medical_treatmentbrainneurodegenerative pathologiestem cell therapyinnovative intervention measures03 medical and health sciences0302 clinical medicineIntervention (counseling)medicineSettore MED/05 - Patologia ClinicaAnimalsHumansbrain self‐repair/regenerative process innovative intervention measuresbusiness.industryRegeneration (biology)Stem CellsNeurodegenerative DiseasesStem-cell therapyneuronal stem cell030104 developmental biologymedicine.anatomical_structureTreatment Outcomeself-repair/regenerative proceGeriatrics and GerontologyStem cellbusinessNeuroscience030217 neurology & neurosurgeryinnovative intervention measureStem Cell TransplantationRejuvenation research
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Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction

2016

Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confoca…

0301 basic medicineNervous systemCentral Nervous SystemProteomicsScaffoldMouseProteomeNeural ConductionSeptinNerve Fibers MyelinatedMyelinGene Knockout TechniquesMiceContractile ProteinsAxonBiology (General)CytoskeletonMicroscopy ImmunoelectronCytoskeletonMyelin SheathMicroscopy ConfocalGeneral NeuroscienceQRGeneral MedicineAnatomyCell biologyglial cellsmedicine.anatomical_structureGene TargetingMedicineResearch ArticleQH301-705.5ScienceCentral nervous systemmyelinated axonsmacromolecular substancesBiologyGeneral Biochemistry Genetics and Molecular Biologymyelin structure03 medical and health sciencesSeptin/anillin filaments; central nervous system; myelinlabel-free proteomicsmedicineAnimalsneuropathologyGeneral Immunology and Microbiology030104 developmental biologynervous systemseptin cytoskeletonProtein MultimerizationSeptinsSeptin cytoskeletonNeuroscienceeLife
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Fabry disease and multiple sclerosis misdiagnosis: the role of family history and neurological signs

2018

Fabry disease (FD) is an X-linked inherited lysosomal storage disorder caused by a galactosidase A (a-gal A) deficiency. Central nervous system involvement and chronic white matter lesions are observed in both FD and multiple sclerosis (MS), which can confound the differential diagnosis. We analyzed the GLA gene, which encodes a-gal A, in 86 patients with clinical and neuroradiological findings consistent with MS to determine whether they had FD. We identified four women initially diagnosed with MS who had GLA mutations associated with FD. Our results indicate that family history besides neurological findings should be evaluated in patients with an uncertain diagnosis of MS. Also the involv…

0301 basic medicineNeurological signsPathologymedicine.medical_specialtyCentral nervous systemmultiple sclerosis03 medical and health sciences0302 clinical medicineα galactosidase aMedicinemisdiagnosisFamily historyfabry diseasebusiness.industryMultiple sclerosismedicine.diseaseFabry diseaseResearch Paper: PathologyHyperintensity3. Good health030104 developmental biologymedicine.anatomical_structureOncologyMisdiagnosiDifferential diagnosisbusiness030217 neurology & neurosurgeryOncotarget
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Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts

2018

Introduction: Even though our understanding of the antiphospholipid syndrome (APS) has improved tremendously over the last decades, we are still not in a position to replace symptomatic anticoagulation by pathogenesis based causal treatments. Areas covered: Recent years have provided further insights into pathogenetically relevant mechanisms. These include a differentiation of pathogenic subtypes of antiphospholipid antibodies (aPL), novel mechanisms modulating disease activity, for example, extracellular vesicles and microRNA, and novel players in pathogenesis, for example, neutrophils and neutrophil extracellular traps (NETs). Expert commentary: It is evident that aPL induce a proinflamma…

0301 basic medicineNeutrophilsImmunologyBioinformaticsExtracellular TrapsExtracellular vesiclesProinflammatory cytokinePathogenesisExtracellular VesiclesGenetic Heterogeneity03 medical and health sciences0302 clinical medicineimmune system diseasesAntiphospholipid syndromemicroRNAHumansImmunology and AllergyMedicineFetal lossBlood CoagulationComplement Activation030203 arthritis & rheumatologybusiness.industryNeutrophil extracellular trapsAntiphospholipid Syndromemedicine.diseaseMicroRNAs030104 developmental biologyAntibodies AntiphospholipidSignal transductionbusinessExpert Review of Clinical Immunology
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Update of the statements on biology and clinical impact of occult hepatitis B virus infection

2019

In October 2018 a large number of international experts with complementary expertise came together in Taormina to participate in a workshop on occult hepatitis B virus infection (OBI). The objectives of the workshop were to review the existing knowledge on OBI, to identify issues that require further investigation, to highlight both existing controversies and newly emerging perspectives, and ultimately to update the statements previously agreed in 2008. This paper represents the output from the workshop.

0301 basic medicineOccult HBV infectionHepatitis B virusmedicine.medical_specialtyCarcinoma HepatocellularHepatocellular carcinomaHbv reactivationMEDLINEHBV reactivationOBImedicine.disease_cause03 medical and health sciences0302 clinical medicineHBV S variantRisk FactorsmedicineHumansHepatitis B AntibodiesIntensive care medicineComputingMilieux_MISCELLANEOUSHepatitis B virusHepatitis B Surface AntigensHepatologyHBV cccDNALiver Neoplasmsvirus diseasesHBV cccDNA; HBV reactivation; HBV S variants; HBV transmission; Hepatocellular carcinoma; OBI; Occult HBV infectionHBV S variantsHepatitis Bmedicine.diseaseOccultdigestive system diseases3. Good healthHBV S variants; HBV cccDNA; HBV reactivation; HBV transmission; Hepatocellular carcinoma; OBI; Occult HBV infection030104 developmental biologyLiverHepatocellular carcinomaDNA Viral030211 gastroenterology & hepatologyHBV transmission[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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