Search results for " pig"

showing 10 items of 733 documents

Homozygous variants in the gene SCAPER cause syndromic intellectual disability

2019

The S-Phase Cyclin A Associated Protein In The ER (SCAPER) gene is a ubiquitously expressed gene with unknown function in the brain. Recently, biallelic SCAPER variants were described in four patients from three families with retinitis pigmentosa (RP) and intellectual disability (ID). Here, we expand the spectrum of pathogenic variants in SCAPER and report on 10 further patients from four families with ID, RP, and additional dysmorphic features carrying homozygous variants in SCAPER. The variants found comprise frameshift, nonsense, and missense variants as well as an intragenic homozygous deletion, which spans SCAPER exons 15 and 16 and introduces a frameshift and a premature stop codon. A…

AdultMale0301 basic medicineAdolescentmedia_common.quotation_subjectCyclin ANonsenseGene Expression030105 genetics & heredityFrameshift mutationConsanguinityMice03 medical and health sciencesExonNeural Stem CellsIntellectual DisabilityRetinitis pigmentosaGene expressionGeneticsmedicineAnimalsHumansMissense mutationFamilyChildGeneGenetics (clinical)media_commonCerebral CortexNeuronsGeneticsbiologyHomozygoteSyndromemedicine.diseasePedigree030104 developmental biologyMutationbiology.proteinFemaleCarrier ProteinsRetinitis PigmentosaAmerican Journal of Medical Genetics Part A
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Phenotypical features of two patients diagnosed with PHARC syndrome and carriers of a new homozygous mutation in the ABHD12 gene.

2018

Abstract PHARC (Polyneuropathy, Hearing loss, Ataxia, Retinitis pigmentosa and Cataracts) (MIM# 612674 ) is an autosomal recessive neurodegenerative disease caused by mutations in the ABHD12 gene. We evaluated two Spanish siblings affected with pes cavus, sensorimotor neuropathy, hearing loss, retinitis pigmentosa and juvenile cataracts in whom the genetic test of ABHD12 revealed a novel homozygous frameshift mutation, c.211_223del (p.Arg71Tyrfs*26). The earliest clinical manifestation in these patients was a demyelinating neuropathy manifested with a Charcot-Marie-Tooth phenotype over three decades. Progressive hearing loss, cataracts and retinitis pigmentosa appeared after the age of 30. …

AdultMaleARLID12 genecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAtaxiagenetic structuresHearing lossUsher syndromeCharcot-Marie-Tooth diseaseCataractFrameshift mutation03 medical and health sciencesPolyneuropathies0302 clinical medicineCataractsRetinitis pigmentosaotorhinolaryngologic diseasesmedicineHumansMuscle SkeletalDeaf-blindnessbusiness.industryPHARCBrainmedicine.diseaseDermatologyMagnetic Resonance Imagingeye diseasesMonoacylglycerol LipasesPedigreePhenotypeNeurologySpainMutation030221 ophthalmology & optometryAtaxiasense organsNeurology (clinical)medicine.symptombusinessUsher syndromePolyneuropathy030217 neurology & neurosurgeryRetinitis PigmentosaRetinopathyJournal of the neurological sciences
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Two Novel Deletions (Array CGH Findings) in Pigment Dispersion Syndrome

2007

Purpose: We report the first male with pigment dispersion syndrome and a balanced translocation t(10;15)(p11.1;q11.1). Methods: Cytogenetic analyses using Giemsa banding and FISH methods, and array CGH were performed. Results: Array CGH analyses did not show altered DNA sequences in the breakpoints of the translocation, but revealed two novel deletions in 2q22.1 and 18q22.1. Conclusion: We suppose that the coexistence of t(10;15) and pigment dispersion syndrome in our patient is a coincidence. The deletion in 2q22.1, where the gene LRP1B has been located, may play a major role in the dysembryogenesis of the eye and cause the disorder.

AdultMaleEye DiseasesLRP1BG bandingChromosomal translocationBiologyTranslocation GeneticDNA sequencingmedicineHumansPigment Epithelium of EyeGeneIn Situ Hybridization FluorescenceGenetics (clinical)Sequence DeletionGeneticsChromosomes Human Pair 15Chromosomes Human Pair 10BreakpointNucleic Acid Hybridizationmedicine.diseaseMolecular biologyOphthalmologyPediatrics Perinatology and Child HealthPigment dispersion syndromeFish <Actinopterygii>Retinal PigmentsOphthalmic Genetics
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Spontaneous regression of multiple melanocytic nevi after melanoma: report of 3 cases.

2014

Complete spontaneous regression of multiple melanocytic nevi after melanoma is an extremely rare phenomenon. We report 3 cases of patients with a history of melanoma that showed regression of almost all melanocytic nevi over time. One of the patients had 2 simultaneous primary cutaneous melanomas without metastasis. In the other 2 patients, regression of the melanocytic nevi was seen after the development of metastasis in lymph nodes. These patients had spontaneously developed an efficient immune response against melanocytes, and they would represent paradigmatic examples of the spontaneous immune responses in melanoma patients. Better understanding of the mechanisms involved in the complet…

AdultMaleLymphatic metastasismedicine.medical_specialtySkin NeoplasmsTime FactorsAdolescentmedicine.medical_treatmentBiopsyDermoscopyDermatologyPathology and Forensic MedicineMetastasisFatal OutcomeComplete regressionBiopsymedicineNevusHumansneoplasmsMelanomaNevus Pigmentedmedicine.diagnostic_testbusiness.industryMelanomaGeneral MedicineImmunotherapymedicine.diseaseDermatologyRegressionTreatment OutcomeNeoplasm Regression SpontaneousLymphatic MetastasisDisease ProgressionLymph Node ExcisionMelanocytesFemalebusinessThe American Journal of dermatopathology
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Screening for celiac disease in non-Hodgkin's lymphoma patients: a serum anti-transglutaminase-based approach

2003

Several studies have shown the existence of an association between celiac disease (CD) and non-Hodgkin's lymphoma (NHL). Our aim was to evaluate the usefulness of the serum anti-tissue transglutaminase (anti-tTG) antibody assay in screening for CD in consecutive NHL patients. In all, 80 consecutive patients (median age 61 years) with a new diagnosis of NHL were included. To compare the frequency of CD and of positive results for the anti-tTG assay, we enrolled 500 blood donors. In all patients serum anti-tTG was determined with two different ELISA: one based on tTG from guinea pig (gp-tTG) and the other based on human recombinant t-TG (h-tTG) as the antigens. Serum anti-endomysial antibodie…

AdultMaleLymphoma B-CellSettore MED/09 - Medicina InternaAdolescentDuodenumBiopsyGuinea PigsImmunoenzyme TechniqueLymphoma T-CellGliadinGuinea PigImmunoenzyme TechniquesAnimalsHumansIntestinal MucosaFluorescent Antibody Technique IndirectAutoantibodiesAgedNeoplasm StagingAged 80 and overTransglutaminasesAnimalLymphoma Non-HodgkinMiddle AgedAutoantibodieImmunoglobulin ACeliac DiseaseFemaleHuman
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Clinical patterns and electrophysiological findings in retinal pigment epithelium diseases. Does a correlation exist?

1986

At present it is difficult to distinguish those human chorioretinal diseases in which the retinal pigment epithelium (RPE) is the primary site of dysfunction. This difficulty is caused by several factors such as scarcity of biochemical and histological information and a lack of correlation of basic science information available with the clinical body of knowledge. In the present study we examined 134 eyes at early or late stages of hereditary diseases involving the RPE. We tried to distinguish primary RPE involvement by using standard ERG (a- and b-wave) and EOG testing. We conclude that in general primary RPE damage can be better assessed by current electrophysiology in those diseases whic…

AdultMalePathologymedicine.medical_specialtyAdolescentBasic scienceEye diseasemacromolecular substancesBiologyCorrelationRetinal DiseasesPhysiology (medical)medicineElectroretinographyHumansChildPigment Epithelium of EyeAgedRetinaRetinal pigment epitheliummedicine.diagnostic_testMiddle Agedmedicine.diseaseSensory SystemsOphthalmologyElectrophysiologyElectrooculographymedicine.anatomical_structureFemalesense organsElectroretinographyRetinopathyDocumenta ophthalmologica. Advances in ophthalmology
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Differentiation in medulloblastomas: correlation between the immunocytochemical demonstration of photoreceptor markers (S-antigen, rod-opsin) and the…

1989

Biopsy specimens of 66 medulloblastomas were investigated by means of S-antigen and rod-opsin immunocytochemistry. The patients were operated between 1969 and 1988 and the medical records were retrospectively evaluated to correlate the immunocytochemical features of the tumors to the course of the disease. S-antigen- and rod-opsin-immunoreactive tumor cells were found in 19 out of 66 cases. Since in the normal non-neoplastic state immunoreactive S-antigen and rod-opsin are restricted to retinal photoreceptors and a class of pinealocytes derived from photoreceptor cells, the occurrence of these proteins in certain tumor cells of medulloblastomas suggests a differentiation of these cells alon…

AdultMalePathologymedicine.medical_specialtyAdolescentgenetic structuresCellular differentiationImmunocytochemistryBiologyPhotoreceptor cellPathology and Forensic MedicinePinealocyteCellular and Molecular NeuroscienceAntigenBiopsymedicineHumansPhotoreceptor CellsAntigensCerebellar NeoplasmsChildEye ProteinsSurvival rateRetrospective StudiesMedulloblastomaArrestinmedicine.diagnostic_testInfantMiddle AgedPrognosismedicine.diseaseeye diseasesmedicine.anatomical_structureChild PreschoolFemalesense organsNeurology (clinical)Retinal PigmentsMedulloblastomaActa Neuropathologica
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Mutations in ARL2BP, Encoding ADP-Ribosylation-Factor-Like 2 Binding Protein, Cause Autosomal-Recessive Retinitis Pigmentosa

2013

Retinitis pigmentosa (RP) is a genetically heterogeneous retinal degeneration characterized by photoreceptor death, which results in visual failure. Here, we used a combination of homozygosity mapping and exome sequencing to identify mutations in ARL2BP, which encodes an effector protein of the small GTPases ARL2 and ARL3, as causative for autosomal-recessive RP (RP66). In a family affected by RP and situs inversus, a homozygous, splice-acceptor mutation, c.101−1G>C, which alters pre-mRNA splicing of ARLBP2 in blood RNA, was identified. In another family, a homozygous c.134T>G (p.Met45Arg) mutation was identified. In the mouse retina, ARL2BP localized to the basal body and cilium-associated…

AdultMaleRetinal degenerationCentrioleMolecular Sequence DataGenes RecessiveBiologymedicine.disease_causeMice03 medical and health sciences0302 clinical medicineBardet–Biedl syndromeGTP-Binding ProteinsReportRetinitis pigmentosaGeneticsmedicineAnimalsHumansBasal bodyGenetics(clinical)Photoreceptor CellsGenetics (clinical)030304 developmental biologyPrimary ciliary dyskinesiaGenetics0303 health sciencesMutationBase SequenceADP-Ribosylation FactorsCiliumHomozygoteMembrane Transport ProteinsEpithelial Cellsmedicine.diseasePedigreeCell biologyMutationFemalesense organsCarrier ProteinsRetinitis Pigmentosa030217 neurology & neurosurgeryProtein BindingTranscription FactorsThe American Journal of Human Genetics
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Gly114Asp mutation of rhodopsin in autosomal dominant retinitis pigmentosa

1995

Two autosomal dominant retinitis pigmentosa families of different origin were screened for rhodopsin mutations using the method of single strand conformation polymorphism and direct sequencing. We found a CGG-CAG substitution in codon 114 of rhodopsin in both families. This change predicted the replacement of a glycine by an aspartic acid and suggested that this change is the cause of the disease in these families.

AdultMaleRhodopsincongenital hereditary and neonatal diseases and abnormalitiesAdolescentgenetic structuresMolecular Sequence DataGlycinemedicine.disease_causeAutosomal dominant retinitis pigmentosaRetinitis pigmentosaAspartic acidmedicineHumansPoint MutationAmino Acid SequenceCodonMolecular BiologyGenes DominantGeneticsAspartic AcidMutationPolymorphism GeneticBase SequencebiologyDirect sequencingSingle-strand conformation polymorphismCell BiologyMiddle Agedmedicine.diseasePedigreeRhodopsinGlycinebiology.proteinFemalesense organsRetinitis PigmentosaMolecular and Cellular Probes
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A 66-kilodalton heat shock protein of Salmonella typhimurium is responsible for binding of the bacterium to intestinal mucus

1992

Salmonella typhimurium infections have increased during the last few years. However, the interplay of virulence factors in S. typhimurium pathogenesis is still poorly understood, particularly with regard to the mechanisms and components of the bacterium which are involved in its interaction with the intestinal mucus. We have observed that S. typhimurium is aggregated by incubation with colonic mucus (guinea pig model). To quantify this phenomenon, an aggregation assay was established. By using this assay, it was found that the aggregation profile of S. typhimurium strains freshly isolated from patients (age 9 and older) with salmonellosis correlated with the severity of the disease. An isol…

AdultMaleSalmonella typhimuriumSalmonellaAdolescentGuinea PigsImmunologyVirulencemedicine.disease_causeMicrobiologyBacterial AdhesionMicrobiologyFecesBacterial ProteinsIntestinal mucosaHeat shock proteinCentrifugation Density GradientmedicineAnimalsHumansIntestinal MucosaChildHeat-Shock ProteinsbiologyTemperatureAntibodies MonoclonalMiddle Agedbiology.organism_classificationEnterobacteriaceaeMucusInfectious DiseasesPolyclonal antibodiesbiology.proteinFemaleParasitologyBacteriaResearch ArticleInfection and Immunity
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