Search results for "Type"

showing 10 items of 10618 documents

H2-M polymorphism in mice susceptible to collagen-induced arthritis involves the peptide binding groove.

1996

The ability to develop type II collagen (CII)-induced arthritis (CIA) in mice is associated with the major histocompatibilityI-A gene and with as yet poorly defined regulatory molecules of the major histocompatibility complex (MHC) class II antigen processing and presentation pathway. H2-M molecules are thought to be involved in the loading of antigenic peptides into the MHC class II binding cleft. We sequencedH2-Ma, H2-Mb1, andH2-Mb2 genes from CIA-susceptible and-resistant mouse strains and identified four differentMa andMb2 alleles and three differentMb1 alleles defined by polymorphic residues within the predicted peptide binding groove. Most CIA-resistant mouse strains share commonMa, M…

musculoskeletal diseasesImmunologyGenes MHC Class IIMolecular Sequence DataGenes MHC Class IPeptide bindingMice Inbred StrainsMajor histocompatibility complexEpitopeMiceAntigenMHC class IGeneticsAnimalsAmino Acid SequencePhylogenyDNA PrimersMHC class IIPolymorphism GeneticbiologyBase SequenceSequence Homology Amino AcidAntigen processingH-2 AntigensHistocompatibility Antigens Class IIMolecular biologyArthritis ExperimentalHistocompatibilityHaplotypesbiology.proteinCollagenSequence AlignmentImmunogenetics
researchProduct

Altered (oxidized) C1q induces a rheumatoid arthritis-like destructive and chronic inflammation in joint structures in arthritis-susceptible rats.

1997

Previous studies have identified an altered C1q molecule in synovial fluids from the joints of rheumatoid arthritis patients. We therefore immunized arthritis-susceptible Lewis 1A.AVN rats with either native C1q (C1q nat), altered (oxidized) C1q (C1q ox), or type II collagen (CII, induces arthritis in these animals), in order to induce arthritis. Unlike C1q nat, both CII and C1q ox were able to induce swelling and erythema of joints consistent with an arthritis-like inflammatory reaction. Histopathological evaluation of individual joint sections revealed synovitis, bursitis and tendovaginitis, massive joint destruction, and severe pannus formation. In a time-course study, no differences in …

musculoskeletal diseasesImmunologyType II collagenArthritischemical and pharmacologic phenomenaInflammationPathology and Forensic Medicinefluids and secretionsAntigenimmune system diseasesSynovitismedicineImmunology and AllergyAnimalsskin and connective tissue diseasesAutoimmune diseaseInflammationbiologybusiness.industryArthritisComplement C1qmedicine.diseaseRatsRats Inbred LewRheumatoid arthritisImmunologybiology.proteinFemaleJointsmedicine.symptomAntibodybusinessOxidation-ReductionClinical immunology and immunopathology
researchProduct

Interleukin 10 polymorphisms in ankylosing spondylitis.

2003

Genetic polymorphisms of the IL10 promoter region have been implicated in many autoimmune diseases, including seronegative spondyloarthropathies. We studied three SNPs (IL10-1087, -824, and -597) and two microsatellites (IL10R and IL10G) lying within the promoter region of IL10 for association with susceptibility to and clinical manifestations of ankylosing spondylitis (AS), a common form of spondyloarthritis. Four hundred and sixty-eight individuals from 182 Finnish families affected with AS were studied. No association between individual IL10 promoter region polymorphisms or marker haplotype was observed with susceptibility to AS, but weak association was noted between the IL10-597 and -8…

musculoskeletal diseasesImmunologychemical and pharmacologic phenomenaSingle-nucleotide polymorphismBiologyPolymorphism Single Nucleotideimmune system diseasesparasitic diseasesGeneticsmedicineSNPHumansSpondylitis AnkylosingAlleleSpondylitisGenetics (clinical)AllelesGenetic associationGeneticsAnkylosing spondylitisPolymorphism GeneticHaplotypehemic and immune systemsmedicine.diseaseInterleukin-10ImmunologyBASFIMicrosatellite Repeats
researchProduct

Modulation of type II collagen-induced arthritis in DBA/1 mice by intravenous application of a peptide from the C1q-A chain.

1992

In this report we are able to show that intravenous (i.v.) application (day 0) of a nonapeptide (residues 26-34) from the human C1q A-chain (designated peptide A-C1q) prior to intradermal (i.d.) administration of chicken type II collagen (CII) in arthritis-susceptible DBA/1 mice (H2q), leads to abrogation of polymorphonuclear neutrophil (PMN) invasion into the joints. This nonapeptide exhibits epitope characteristics and high homology to residues 137-147 of CB11 (a cyanogen bromide fragment of chicken CII, known to contain both arthritis inducing and suppressing determinants). Arthritis index was lowest in animals pretreated i.v. with CII (as internal control), though animals pretreated i.v…

musculoskeletal diseasesMaleInjections IntradermalImmunologyMolecular Sequence DataType II collagenArthritischemical and pharmacologic phenomenaPeptideEpitopechemistry.chemical_compoundMiceAntigenAdjuvants ImmunologicmedicineImmunology and AllergyAnimalsAmino Acid Sequenceskin and connective tissue diseasesPeptide sequencechemistry.chemical_classificationbiologyArthritisComplement C1qHematologymedicine.diseaseMolecular biologyPeptide FragmentschemistryMice Inbred DBAImmunologyAntibody FormationInjections Intravenousbiology.proteinCyanogen bromideCollagenAntibodyOligopeptidesImmunobiology
researchProduct

FGFR2mutation in 46,XY sex reversal with craniosynostosis

2015

Patients with 46,XY gonadal dysgenesis (GD) exhibit genital anomalies, which range from hypospadias to complete male-to-female sex reversal. However, a molecular diagnosis is made in only 30% of cases. Heterozygous mutations in the human FGFR2 gene cause various craniosynostosis syndromes including Crouzon and Pfeiffer, but testicular defects were not reported. Here, we describe a patient whose features we would suggest represent a new FGFR2-related syndrome, craniosynostosis with XY male-to-female sex reversal or CSR. The craniosynostosis patient was chromosomally XY, but presented as a phenotypic female due to complete GD. DNA sequencing identified the FGFR2c heterozygous missense mutatio…

musculoskeletal diseasesMalemedicine.medical_specialtyGonadAdolescentDNA Mutational AnalysisMutation MissenseGonadal dysgenesisBiologymedicine.disease_causeCraniosynostosisXY gonadal dysgenesisCraniosynostosesMiceInternal medicineGeneticsmedicineAnimalsHumansMissense mutationGene Knock-In TechniquesReceptor Fibroblast Growth Factor Type 2Molecular BiologyGenetics (clinical)Gonadal Dysgenesis 46XYGeneticsMutationArticlesSyndromeGeneral MedicineSex reversalmedicine.diseaseMice Mutant StrainsDisease Models AnimalEndocrinologymedicine.anatomical_structurePfeiffer syndromeFemaleHuman Molecular Genetics
researchProduct

COL1A1 Sp1 polymorphism associates with bone density in early puberty.

2006

Optimal acquisition of bone mass in puberty is a key determinant of the lifetime risk of osteoporosis and has a strong genetic basis. We investigated the relationship between the COL1A1 Sp1 polymorphism and BMD in early puberty, and how the genotypes relate to bone size and geometry as well as bone turnover and material properties in 247 10- to 13-year-old girls. Bone properties were measured using DXA, pQCT, and ultrasound. Also, serum P1NP, OC, B-ALP, and TRACP 5b were assessed. Our results showed that girls with the TT genotype had significantly lower BMC and BMD of the total body, lumbar spine, and proximal femur, as well as BUA at the calcaneus, than those with the GT and GG genotype. …

musculoskeletal diseasesPeak bone massmedicine.medical_specialtyHistologyTime FactorsBone densityAdolescentGenotypePhysiologyEndocrinology Diabetes and MetabolismOsteoporosisPuberty PrecociousCollagen Type IBone remodelingBone DensityInternal medicineGenotypeMedicineHumansChildPolymorphism GeneticProximal femurbusiness.industrymusculoskeletal systemmedicine.diseaseCollagen Type I alpha 1 ChainEndocrinologyFemaleCalcaneusbusinessBiomarkersEarly pubertyBone
researchProduct

Type V collagen counteracts osteo-differentiation of human mesenchymal stem cells

2014

In search of novel gene signatures for osteo-differentiation of mesenchymal stem cells (MSCs), we submitted cDNA preparations from undifferentiated and differentiating MSCs to differential display- and semiquantitative-PCR and found down-regulation of COL5A1 in osteo-induced cultures at days 21 and 28, when the mineralized matrix accumulates. We also cultured osteo-differentiating MSCs onto type V collagen substrates and found a decrease in the accumulation of extracellular calcium compared to those grown in uncoated flasks. To our knowledge, this is first evidence that type V collagen might represent a stromal component that impairs osteogenesis.

musculoskeletal diseasesStromal cellchemistry.chemical_elementDown-RegulationBioengineeringBiologyMatrix (biology)CalciumApplied Microbiology and BiotechnologyOsteogenesisGene expressionExtracellularHumansSettore BIO/06 - Anatomia Comparata E CitologiaCells CulturedPharmacologyDifferential displayOsteoblastsGeneral Immunology and MicrobiologyMesenchymal stem cellCell DifferentiationMesenchymal Stem CellsGeneral MedicineMolecular biologychemistryembryonic structurescollagen stem cells osteogenesis gene expressionStem cellCollagen Type VBiotechnology
researchProduct

CRT-724 Can the Aortic Wall Communicate with Us?

2014

Association between aortic aneurysm wall and risk of rupture or dissection. Aortic specimens were obtained from 73 patients (51 men and 22 women, whose median age 61.7± 10.7 years) undergoing surgical repair of thoracic ascending aneurysm (TAA). Histopathological and immunohistochemical analyses

musculoskeletal diseasesSurgical repairmedicine.medical_specialtybusiness.industrygenotypeaortic wallSettore MED/23 - Chirurgia CardiacaDissection (medical)medicine.diseaseAneurysmSurgeryAortic wallAneurysm aortic wall genotypeAortic aneurysmAneurysmcardiovascular systemmedicineCardiology and Cardiovascular MedicinebusinessJACC: Cardiovascular Interventions
researchProduct

Interleukin 1 Gene Polymorphisms Presumably Participate in the Pathogenesis of Chronic Spontaneous Autocreative Urticaria

2020

Recent studies underline a potential role of autoimmune and genetic disturbances in this disorder pathogenesis. Variants in genes related to inflammatory processes may possibly predispose to chronic spontaneous urticaria (CSU) occurrence. The objective of this study was to search for an association of Il1 genes polymorphisms with the pathogenesis of CSU. The examined group consisted of 153 unrelated chronic spontaneous autoreactive urticaria patients. The control group consisted of 104 unrelated healthy volunteers. In all studied subjects, IL1 rs1304037 and rs180058 polymorphisms were examined. The Urticaria Activity Score was used to assess disease intensity. The age of disease onset was a…

musculoskeletal diseasesbusiness.industryImmunologyHaplotypeInterleukinCell BiologyDiseaseinterleukin 1chronic urticariapolymorphismPathogenesis030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineVirologyImmunologyGenotypeMedicineAllelebusinessGeneChronic urticaria030215 immunologyJournal of Interferon and Cytokine Research
researchProduct

Combined effect of AAV-U7-induced dystrophin exon skipping and soluble activin Type IIB receptor in mdx mice.

2012

Adeno-associated virus (AAV)-U7-mediated skipping of dystrophin-exon-23 restores dystrophin expression and muscle function in the mdx mouse model of Duchenne muscular dystrophy. Soluble activin receptor IIB (sActRIIB-Fc) inhibits signaling of myostatin and homologous molecules and increases muscle mass and function of wild-type and mdx mice. We hypothesized that combined treatment with AAV-U7 and sActRIIB-Fc may synergistically improve mdx muscle function. Bioactivity of sActRIIB-Fc on skeletal muscle was first demonstrated in wild-type mice. In mdx mice we show that AAV-U7-mediated dystrophin restoration improved specific muscle force and resistance to eccentric contractions when applied a…

musculoskeletal diseasesmdx mousemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesDuchenne muscular dystrophyActivin Receptors Type IIGenetic VectorsMyostatinBiologyDystrophin03 medical and health sciencesMice0302 clinical medicineInternal medicineGeneticsmedicineMyocyteAnimalsMuscular dystrophyMuscle SkeletalMolecular Biology030304 developmental biology0303 health sciencesBody WeightSkeletal muscleExonsGenetic TherapyDependovirusMuscular Dystrophy Animalmedicine.diseasemusculoskeletal system3. Good healthMice Inbred C57BLEndocrinologymedicine.anatomical_structureImmunologybiology.proteinMice Inbred mdxMolecular MedicineITGA7Dystrophin030217 neurology & neurosurgeryMuscle ContractionHuman gene therapy
researchProduct