Search results for "Hybridization"

showing 10 items of 812 documents

Increased Oxidative Damage Associated with Unfavorable Cytogenetic Subgroups in Chronic Lymphocytic Leukemia

2014

Oxidative stress contributes to genomic instability in chronic lymphocytic leukemia (CLL), but its relationship with the acquisition of specific chromosomal abnormalities is unknown. We recruited 55 untreated CLL patients and assessed 8-oxo-2′-deoxyguanosine (8-oxo-dG), glutathione, and malondialdehyde (MDA) levels, and we compared them among the cytogenetic subgroups established using fluorescence in situ hybridization (FISH). Significant increases in 8-oxo-dG and/or MDA were observed in patients with unfavorable cytogenetic aberrations (17p and 11q deletions) compared to the 13q deletion group.TP53deletion patients exhibited a diminished DNA repair efficiency. Finally, cases with normal F…

MaleGenome instabilityArticle SubjectDNA RepairDNA damageDNA repairChronic lymphocytic leukemialcsh:MedicineBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCohort Studieschemistry.chemical_compoundMalondialdehydemedicineHumansLymphocytesIn Situ Hybridization FluorescenceAgedAged 80 and overChromosome AberrationsGeneral Immunology and Microbiologymedicine.diagnostic_testlcsh:RDeoxyguanosineGeneral MedicineGlutathioneMiddle AgedMalondialdehydemedicine.diseaseGlutathioneLeukemia Lymphocytic Chronic B-CellOxidative Stresschemistry8-Hydroxy-2'-DeoxyguanosineImmunologyFemaleLipid PeroxidationReactive Oxygen SpeciesGene DeletionOxidative stressDNA DamageResearch ArticleFluorescence in situ hybridizationBioMed Research International
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Interstitial deletion of chromosome 2p15-16.1: Report of two patients and critical review of current genotype–phenotype correlation

2011

Abstract We report two individuals with developmental delay and dysmorphic features, in whom array-based comparative genomic hybridization (array CGH) led to the identification of a 2p15p16.1 de novo deletion. In the first patient (Patient 1) a familial deletion of 6q12, inherited from her father, was also detected. In the second patient (Patient 2) in addition to the 2p15p16.1 microdeletion a de novo deletion in Xq28 was detected. Both individuals shared dysmorphic features and developmental delay with the six reported patients with a 2p15p16.1 microdeletion described in medical literature. Conclusion: in the first patient a 642 kb 2p16.1 deletion (from 60.604 to 61.246 Mb), and a 930 kb 6…

MaleGenotypeDevelopmental delayDevelopmental DisabilitiesBioinformaticsContiguous gene syndromeGenotype phenotypeCorrelationGeneticsHumansChromosomal delectionMedicineAbnormalities MultipleClinical phenotypeGenetic Association StudiesIn Situ Hybridization FluorescenceSex Chromosome AberrationsGenetics (clinical)Sequence DeletionGeneticsChromosomes Human XComparative Genomic Hybridizationbusiness.industryInfantChromosomeSyndromeGeneral MedicineMicrodeletion syndromemedicine.diseaseXq28PhenotypeChild PreschoolChromosomes Human Pair 2FemaleChromosome DeletionbusinessComparative genomic hybridizationEuropean Journal of Medical Genetics
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Heterochromatin of the scarab beetle, Bubas bison (Coleoptera: Scarabaeidae) II. Evidence for AT-rich compartmentalization and a high amount of rDNA …

2005

An unexpected result arising from a previous characterization of the scarab beetle Bubas bison (Coleoptera: Scarabaeidae) heterochromatin was its unusual homogeneous reaction to different staining methods. In particular, silver stainability of heterochromatic ends of all chromosomes prevented identification of the number of rDNA transcriptionally active regions. Data formerly obtained using silver impregnation (Ag-NOR), C- G- and DAPI banding are here improved and completed by application of CMA(3) staining and rDNA FISH with the aim to investigate heterochromatin base composition and locate rDNA regions with respect to NOR-associated heterochromatin. Our results show that B. bison has a hi…

MaleHeterochromatinGeneral Physics and AstronomyDNA Ribosomalchemistry.chemical_compoundStructural BiologyHeterochromatinBotanyRNA Ribosomal 18SAnimalsGeneral Materials ScienceGeneIn Situ Hybridization FluorescenceScarabaeidaeStaining and LabelingbiologyRNAKaryotypeCell BiologyTelomereRibosomal RNAbiology.organism_classificationAT Rich SequenceChromosome BandingStainingColeopterachemistryEvolutionary biologyKaryotypingFemaleDNAMicron
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A Single Copy of the Recently Identified Dual Oxidase Maturation Factor (DUOXA) 1 Gene Produces Only Mild Transient Hypothyroidism in a Patient with …

2011

Dual oxidases (DUOX1 and DUOX2) play a crucial role in the generation of hydrogen peroxide required in the oxidation of iodide and the synthesis of thyroid hormone. Heterodimerization with specific maturation factors (DUOXA1 and DUOXA2) is essential for the maturation and function of the DUOX enzyme complexes. Biallelic loss-of-function mutations of DUOX2 result in congenital hypothyroidism (CH), whereas a single reported case of homozygous DUOXA2 mutation (Y246X) has been associated with mild CH.We now report an infant with transient CH due to a complex genetic alteration of the DUOX/DUOXA system.Our patient was born to euthyroid nonconsanguineous parents and presented with an elevated TSH…

MaleHeterozygoteendocrine system diseasesEndocrinology Diabetes and MetabolismBlotting WesternGenetic VectorsClinical BiochemistryGene DosageMutation MissenseThyrotropinBiologyTransfectionmedicine.disease_causePolymorphism Single NucleotideBiochemistryGene dosageEndocrinologyHypothyroidismPolymorphism (computer science)medicineHumansMissense mutationAlleleGeneAllelesCells CulturedOligonucleotide Array Sequence AnalysisGeneticsMutationfungiBiochemistry (medical)Infant NewbornMembrane ProteinsNADPH OxidasesNucleic Acid Hybridizationfood and beveragesHeterozygote advantageJCEM Online: Brief ReportsDNADual OxidasesMolecular biologyMembrane proteinGene DeletionThe Journal of Clinical Endocrinology & Metabolism
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Regional distribution of the leucine-rich glioma inactivated (LGI) gene family transcripts in the adult mouse brain

2009

25 p., figuras y bibliografía

MaleHippocampusSubstantia nigraNerve Tissue ProteinsHippocampal formationGene mutationBiologyReticular formationMiceC57BL/6J micemedicineGene familyAnimalsMolecular BiologyThalamic reticular nucleusBrain MappingGeneral NeuroscienceDentate gyrusIntracellular Signaling Peptides and ProteinsBrainProteinsMice Inbred C57BLmedicine.anatomical_structureLGI2LGI1Neurology (clinical)LGI4LGI3NeuroscienceIn situ hybridizationDevelopmental Biology
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Expression of the rat connexin 39 (rCx39) gene in myoblasts and myotubes in developing and regenerating skeletal muscles: an in situ hybridization st…

2005

We report a detailed analysis of the expression pattern of the recently identified rat connexin gene, named rat connexin 39 (rCx39), both during embryonic development and in adult life. Qualitative and quantitative reverse transcription/polymerase chain reaction analysis showed intense expression of rCx39 restricted to differentiating skeletal muscles, with a peak of expression detected at 18 days of embryonic life, followed by a rapid decline to undetectable levels within the first week of postnatal life. A combination of the in situ hybridization technique for the detection of rCx39 mRNA and immunohistochemistry for myogenin, a myoblast-specific marker, allowed us to establish that the mR…

MaleHistologyTime FactorsGap junctionMyoblasts SkeletalMolecular Sequence DataMuscle Fibers SkeletalConnexinIn situ hybridizationBiologyConnexinsPathology and Forensic MedicineSatellite cellsmedicineMyocyteAnimalsCell LineageTissue DistributionAmino Acid SequenceRNA MessengerRats WistarMuscle SkeletalMyogeninIn Situ HybridizationPhylogenyMessenger RNABase SequenceSequence Homology Amino AcidMyogenesisReverse Transcriptase Polymerase Chain ReactionRegeneration (biology)Skeletal muscleGene Expression Regulation DevelopmentalCell BiologyMolecular biologyImmunohistochemistryProtein Structure TertiaryRatsmedicine.anatomical_structureMyogenesiMyogeninMyogenic cell lineageCell and tissue research
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A Polymorphism in the Crhr1 Gene Determines Stress Vulnerability in Male Mice

2014

Chronic stress is a risk factor for psychiatric disorders but does not necessarily lead to uniform long-term effects on mental health, suggesting modulating factors such as genetic predispositions. Here we address the question whether natural genetic variations in the mouse CRH receptor 1 (Crhr1) locus modulate the effects of adolescent chronic social stress (ACSS) on long-term stress hormone dysregulation in outbred CD1 mice, which allows a better understanding of the currently reported genes × environment interactions of early trauma and CRHR1 in humans. We identified 2 main haplotype variants in the mouse Crhr1 locus that modulate the long-term effects of ACSS on basal hypothalamic-pitui…

MaleHypothalamo-Hypophyseal SystemGenotypeGene ExpressionPituitary-Adrenal SystemLocus (genetics)Single-nucleotide polymorphismRegulatory Sequences Nucleic AcidBiologyBinding CompetitivePolymorphism Single NucleotideReceptors Corticotropin-Releasing HormoneMiceEndocrinologyGene FrequencyGenetic predispositionAnimalsHumansGenetic Predisposition to DiseaseChronic stressCRHR1 GeneGeneIn Situ HybridizationSocial stressGeneticsBehavior AnimalTriazinesHaplotypeHaplotypesPituitary GlandPyrazolesFemaleGene-Environment InteractionCorticosteroneStress PsychologicalSignal TransductionEndocrinology
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Novel LRPPRC compound heterozygous mutation in a child with early-onset Leigh syndrome French-Canadian type: Case report of an Italian patient

2020

Abstract Background Mitochondrial diseases, also known as oxidative phosphorylation (OXPHOS) disorders, with a prevalence rate of 1:5000, are the most frequent inherited metabolic diseases. Leigh Syndrome French Canadian type (LSFC), is caused by mutations in the nuclear gene (2p16) leucine-rich pentatricopeptide repeat-containing (LRPPRC). It is an autosomal recessive neurogenetic OXPHOS disorder, phenotypically distinct from other types of Leigh syndrome, with a carrier frequency up to 1:23 and an incidence of 1:2063 in the Saguenay-Lac-St Jean region of Quebec. Recently, LSFC has also been reported outside the French-Canadian population. Patient presentation We report a male Italian (Sic…

MaleHypotonia - developmental delayPediatricsmedicine.medical_specialtyPopulationEncephalopathyCytochrome-c Oxidase DeficiencyCase ReportHypotoniaCompound heterozygosityDiagnosis Differential03 medical and health sciences0302 clinical medicineWhole-genome-sequencingHypotonia; developmental delay; Mitochondrial disease; Whole-exome sequencing; CCT5030225 pediatricsmedicineMissense mutationHumansGlobal developmental delayeducationeducation.field_of_studyComparative Genomic Hybridizationbusiness.industrylcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseHypotoniaHypoplasiaMitochondrial diseaseNeoplasm Proteinsdevelopmental delayNeonatal hypotoniaPhenotypeItalyWhole-exome sequencingMutationLSFCmedicine.symptomLeigh DiseaseCCT5business030217 neurology & neurosurgeryInfant Premature
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Complement C1q is dramatically up-regulated in brain microglia in response to transient global cerebral ischemia.

2000

Abstract Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marke…

MaleImmunologyIschemiaInflammationIn situ hybridizationBiologySulfur RadioisotopesProinflammatory cytokineRNA ComplementaryCerebrospinal fluidDownregulation and upregulationmedicineImmunology and AllergyAnimalsTransient (computer programming)Rats WistarComplement C1qIn Situ HybridizationPharmacologyMicrogliaComplement C1qBrainRNA Probesmedicine.diseaseImmunohistochemistryCell biologyComplement systemRatsUp-Regulationmedicine.anatomical_structureIschemic Attack TransientImmunologyMicrogliamedicine.symptomNeuroscienceDigoxigeninJournal of immunology (Baltimore, Md. : 1950)
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Differential expression of the murine mannose-binding lectins A and C in lymphoid and nonlymphoid organs and tissues.

2003

Abstract Mannose-binding lectin (MBL), a member of the collectin family, binds to carbohydrate structures on the surfaces of micro-organisms and may serve as a recognition molecule of the lectin pathway of complement activation. In rodents two forms, MBL-A and MBL-C, were described and shown to be products of two related, but uncoupled, genes. The liver is the main source of MBL biosynthesis. For rat MBL-A, expression has also been described in the kidney. Here we report that the two forms of murine MBL are differentially expressed in a number of nonhepatic tissues. Real-time RT-PCR revealed that the liver is the major site of expression for both MBL genes. Lower copy numbers were found in …

MaleLymphoid TissueImmunologyCollectinchemical and pharmacologic phenomenaIn situ hybridizationMannose-Binding LectinMiceIntestine SmallImmunology and AllergyAnimalsProtein IsoformsIn Situ HybridizationMannan-binding lectinMice Inbred BALB CInnate immune systembiologyLectinbacterial infections and mycosesAcquired immune systemMolecular biologyImmunohistochemistryComplement systemAnimals NewbornLiverOrgan SpecificityLectin pathwaybiology.proteinFemaleSpleenJournal of immunology (Baltimore, Md. : 1950)
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