Search results for " and neonatal diseases and abnormalities"

showing 10 items of 344 documents

Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a target in LKB1 Mutant Lung Cancer

2013

Abstract The LKB1/STK11 tumor suppressor encodes a serine/threonine kinase, which coordinates cell growth, polarity, motility, and metabolism. In non–small cell lung carcinoma, LKB1 is somatically inactivated in 25% to 30% of cases, often concurrently with activating KRAS mutations. Here, we used an integrative approach to define novel therapeutic targets in KRAS-driven LKB1-mutant lung cancers. High-throughput RNA interference screens in lung cancer cell lines from genetically engineered mouse models driven by activated KRAS with or without coincident Lkb1 deletion led to the identification of Dtymk, encoding deoxythymidylate kinase (DTYMK), which catalyzes dTTP biosynthesis, as synthetica…

DNA Replicationcongenital hereditary and neonatal diseases and abnormalitiesLung NeoplasmsMutantSTK11BiologyAMP-Activated Protein KinasesProtein Serine-Threonine Kinasesmedicine.disease_causeArticleProto-Oncogene Proteins p21(ras)MiceDeoxythymidylate kinaseAMP-Activated Protein Kinase KinasesRNA interferenceCell Line TumorCarcinoma Non-Small-Cell LungmedicineMetabolomicsThymine NucleotidesAnimalsHumansMolecular Targeted TherapyLung cancerskin and connective tissue diseasesCell DeathModels GeneticKinaseCell growthGenomicsmedicine.diseaseMolecular biologyHigh-Throughput Screening AssaysOncologyGene Knockdown TechniquesCancer researchRNA InterferenceKRASNucleoside-Phosphate KinaseDNA Damage
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Core-Shell Arginine-Containing Chitosan Microparticles for Enhanced Transcorneal Permeation of Drugs

2019

Chitosan oligosaccharide (C) was functionalized with L-arginine (A) and short hydrocarbon chains (C-8) to design an amphiphilic copolymer, henceforth CAC(8), leading to microparticles (MPs) consisting of an arginine-decorated hydrophilic shell and inner hydrophobic domains allowing the encapsulation of high amount hydrophobic drugs such as sorafenib tosylate (>10% w/w). L-arginine side chains were selected in order to impart the final MPs enhanced transcorneal penetration properties, thus overcoming the typical biological barriers which hamper the absorption of drugs upon topical ocular administration. The mucoadhesive properties and drug release profile of the CAC(8) MPs (CAC(8)-MPs) were …

Drug3003congenital hereditary and neonatal diseases and abnormalitiesArginineSwinemedia_common.quotation_subjectamphiphilic copolymerPharmaceutical ScienceL-arginineAdministration Ophthalmic02 engineering and technologyArginine030226 pharmacology & pharmacyCorneaChitosan03 medical and health scienceschemistry.chemical_compoundDrug Delivery Systems0302 clinical medicineMucoadhesionSide chainAnimalsskin and connective tissue diseasesProtein Kinase Inhibitorsmedia_commonMucin-3microparticlesDrug CarriersMucinnutritional and metabolic diseasesSorafenibPermeation021001 nanoscience & nanotechnologyCombinatorial chemistryBioavailabilityDrug LiberationmicroparticlechemistrySettore CHIM/09 - Farmaceutico Tecnologico Applicativoocular administrationchitosan0210 nano-technologymucoadhesion
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Dérivé de la bléomycine générant moins de ROS ? Moins de fibrose ? Une alternative dans le développement d’une thérapie anticancéreuse efficace mais …

2010

Deglycobleomycin (DBLM), the aglycon of the glycopeptide antitumor drug bleomycin (BLM), was first used since 1980 during comparative studies between BLM and DBLM in order to elucidate the role of the sugar component in the mechanism of action of BLM. In fact, the deglycosylation of BLM reduce the toxicity of this molecule and fails to produce reactive oxygen species, responsible for pulmonary fibrosis, and for anti-neoplastic activity of BLM. This causes toxic DNA lesions and ultimately leads to cell death. The therapeutic use of BLM is limited by a dose-dependent lung toxicity that eventually leads to fibrosis. Testing BLM-derivative molecules and defining their molecular mechanisms invol…

Drugcongenital hereditary and neonatal diseases and abnormalitiesCancer Researchurogenital systemmedia_common.quotation_subjectnutritional and metabolic diseasesHematologyGeneral MedicineBleomycinmedicine.diseaseMolecular biologychemistry.chemical_compoundOncologychemistryMechanism of actionApoptosisFibrosisPulmonary fibrosisToxicitymedicineRadiology Nuclear Medicine and imagingmedicine.symptomCytotoxicitymedia_commonBulletin du Cancer
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Extensive molecular analysis of patients bearing CFTR-related disorders.

2012

Cystic fibrosis transmembrane conductance regulator (CFTR)–related disorders (CFTR-RDs) may present with pancreatic sufficiency, normal sweat test results, and better outcome. The detection rate of mutations is lower in CFTR-RD than in classic CF: mutations may be located in genes encoding proteins that interact with CFTR or support channel activity. We tested the whole CFTR coding regions in 99 CFTR-RD patients, looking for gene mutations in solute carrier (SLC) 26A and in epithelial Na channel (ENaC) in 33 patients who had unidentified mutations. CFTR analysis revealed 28 mutations, some of which are rare. Of these mutations, RT-PCR demonstrated that the novel 1525-1delG impairs exon 10 s…

Epithelial sodium channelcongenital hereditary and neonatal diseases and abnormalitiesCystic fibrosis CFTR SLC26A SCNNCystic FibrosisAnion Transport ProteinsDNA Mutational Analysismolecular analysiCystic Fibrosis Transmembrane Conductance RegulatorGene mutationPathology and Forensic Medicinecongenital bilateral absence of vasa deferentesExonGene Frequencydisseminated bronchiectasiscongenital bilateral absence of vasa deferenteHumansTrypsinmolecular analysisEpithelial Sodium ChannelsGeneCells CulturedGenetic Association StudiesGeneticsbiologydisseminated bronchiectasiEpithelial Cellsrespiratory systemrecurrent pancreatitidigestive system diseasesCystic fibrosis transmembrane conductance regulatorrespiratory tract diseasesSolute carrier familyCFTR related disordersTrypsin Inhibitor Kazal PancreaticCase-Control StudiesRNA splicingMutationbiology.proteinMolecular MedicineCFTR related disorderSLC26 familyCarrier ProteinsNa channel ENaCMinigenerecurrent pancreatitis
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Clinical efficacy of highly purified, doubly virus-inactivated factor VIII/von Willebrand factor concentrate (Fanhdi® ) in the treatment of von Wille…

2002

Summary. The goal of therapy in patients with von Willebrand disease (vWD) is to correct the dual defect of primary haemostasis and intrinsic coagulation reflected by low levels of von Willebrand factor (vWF) and factor VIII coagulant activity (FVIII:C). Factor VIII/von Willebrand factor (FVIII/vWF) concentrates are currently the treatment of choice in vWD patients unresponsive to desmopressin (DDAVP). However, only few studies on their clinical use are available so far. The main objective of this study was to retrospectively evaluate the clinical efficacy of a highly purified, doubly virus-inactivated FVIII/vWF concentrate with a high content of FVIII/vWF (Fanhdi®). Twenty-two patients wit…

Excessive Bleedingcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtybiologybusiness.industryRetrospective cohort studyHematologyGeneral Medicinemedicine.diseaseGastroenterologyVirusSurgeryVon Willebrand factorCoagulationhemic and lymphatic diseasesInternal medicinebiology.proteinVon Willebrand diseaseMedicinebusinessAdverse effectDesmopressinGenetics (clinical)medicine.drugHaemophilia
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Can we compare haemophilia carriers with clotting factor deficiency to male patients with mild haemophilia?

2020

Introduction Certain haemophilia carriers demonstrate an increased bleeding tendency, mainly related to clotting factor deficiency. No study has so far formally compared the bleeding phenotype of women and girls with mild FVIII or FIX deficiency and associated management with that of male patients affected by mild haemophilia A and B. Material and methods We retrospectively evaluated 44 women and girls with mild FVIII or FIX deficiency (FVIII or FIX 0.05-0.5 IU/mL) and 77 male patients with mild haemophilia A or B and compared them with respect to clotting factor level, age at and trigger for diagnosis, as well as treatment modalities. Results After excluding gender-related haemorrhagic sym…

FVIIImild haemophiliaAdultMalePediatricsmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesHeterozygoteAdolescentMucocutaneous zonecarriersPlasma factorAge at diagnosis030204 cardiovascular system & hematologyHaemophiliaHemophilia AHemostatics03 medical and health sciencesYoung Adult0302 clinical medicinecarrierhemic and lymphatic diseasesmedicineHumansDeamino Arginine VasopressinClotting factor deficiencyChildGenetics (clinical)AgedClotting factorAged 80 and overbusiness.industryFIXHematologyGeneral MedicineMiddle Agedmedicine.diseaseBlood Coagulation Factorsbleeding phenotypebleeding phenotype carriers FIX FVIII mild haemophiliaMale patientChild PreschoolMild haemophilia AFemalebusiness030215 immunologyHaemophilia : the official journal of the World Federation of HemophiliaREFERENCES
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Localization of non-specific X-linked mental retardation gene (MRX73) to Xp22.2.

2001

Clinical and molecular studies are reported on a family (MRX73) of five males with non-specific X-linked mental retardation (XLMR). A total of 33 microsatellite and RFLP markers was typed. The gene for this XLMR condition was been linked to DXS1195, with a lod score of 2.36 at theta = 0. The haplotype and multipoint linkage analyses suggest localization of the MRX73 locus to an interval of 2 cM defined by markers DXS8019 and DXS365, in Xp22.2. This interval contains the gene of Coffin-Lowry syndrome (RSK2), where a missense mutation has been associated with a form of non-specific mental retardation. Therefore, a search for RSK2 mutations was performed in the MRX73 family, but no causal muta…

Family HealthMaleGeneticscongenital hereditary and neonatal diseases and abnormalitiesCoffin–Lowry syndromeX ChromosomeGenetic LinkageHaplotypeChromosome MappingLocus (genetics)Biologymedicine.diseasePedigreeGenetic linkageIntellectual DisabilitymedicineHumansMissense mutationMicrosatelliteFemaleLod ScoreRestriction fragment length polymorphismGenetics (clinical)X chromosomeMicrosatellite Repeats
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Charcot-Marie-Tooth disease: Genetic and clinical spectrum in a Spanish clinical series

2013

Objectives: To determine the genetic distribution and the phenotypic correlation of an extensive series of patients with Charcot-Marie-Tooth disease in a geographically well-defined Mediterranean area. Methods: A thorough genetic screening, including most of the known genes involved in this disease, was performed and analyzed in this longitudinal descriptive study. Clinical data were analyzed and compared among the genetic subgroups. Results: Molecular diagnosis was accomplished in 365 of 438 patients (83.3%), with a higher success rate in demyelinating forms of the disease. The CMT1A duplication (PMP22 gene) was the most frequent genetic diagnosis (50.4%), followed by mutations in the GJB1…

Foot DeformitiesMalecongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyDNA Mutational AnalysisNerve Tissue ProteinsDiseaseArticleConnexinsCentral nervous system diseaseDegenerative diseasestomatognathic systemCharcot-Marie-Tooth DiseaseGene duplicationHumansMedicineLongitudinal StudiesMuscle StrengthGeneRetrospective StudiesGeneticsSeries (stratigraphy)business.industryRetrospective cohort studymedicine.diseasePhenotypeMuscular Atrophystomatognathic diseasesSpainMutationSensation DisordersFemaleNeurology (clinical)businessMyelin ProteinsNeurology
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WT1 isoform expression pattern in acute myeloid leukemia.

2013

WT1 plays a dual role in leukemia development, probably due to an imbalance in the expression of the 4 main WT1 isoforms. We quantify their expression and evaluate them in a series of AML patients. Our data showed a predominant expression of isoform D in AML, although in a lower quantity than in normal CD34+ cells. We found a positive correlation between the total WT1 expression and A, B and C isoforms. The overexpression of WT1 in AML might be due to a relative increase in A, B and C isoforms, together with a relative decrease in isoform D expression.

Gene isoformAdultMalecongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchAdolescentCD34HL-60 CellsBiologyurologic and male genital diseasesPositive correlationCohort StudiesYoung AdultDual roleExpression patternhemic and lymphatic diseasesmedicineTumor Cells CulturedHumansProtein IsoformsWT1 ProteinsAgedAged 80 and overurogenital systemGene Expression Regulation LeukemicGene Expression ProfilingMyeloid leukemiaHematologyMiddle Agedmedicine.diseaseMolecular biologyfemale genital diseases and pregnancy complicationsLeukemiaLeukemia Myeloid AcuteOncologyCase-Control StudiesFemaleK562 CellsLeukemia research
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An autosomal dominant retinitis pigmentosa family with close linkage to D7S480 on 7q.

1995

Retinitis pigmentosa is the most prevalent inherited disorder of the retina. It can be autosomal dominant (adRP), autosomal recessive (arRP) or X-linked (XLRP). A form of adRP mapping to chromosome 7q was reported in a large Spanish pedigree. We have typed DNA from the members of another Spanish family for polymorphic markers from the known candidate genes. Positive lod scores were obtained only for the markers located on 7q31-35, giving a maximum lod score of 2.98 (3.01 by multipoint analysis) at theta = 0.00 for D7S480. A brief clinical evaluation is given.

Genetic MarkersMaleCandidate genecongenital hereditary and neonatal diseases and abnormalitiesgenetic structuresBiologyAutosomal dominant retinitis pigmentosaGene mappingRetinitis pigmentosaGeneticsmedicineHumansGeneGenetics (clinical)Genes DominantLinkage (software)GeneticsChromosome Mappingmedicine.diseaseHuman geneticseye diseasesPedigreeGenetic markerFemaleLod ScoreChromosomes Human Pair 7Retinitis PigmentosaHuman genetics
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