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showing 10 items of 2571 documents

Cytoprotective effects of the antioxidant phytochemical indicaxanthin in beta-thalassemia red blood cells

2006

Antioxidant phytochemicals are investigated as novel treatments for supportive therapy in beta-thalassemia. The dietary indicaxanthin was assessed for its protective effects on human beta-thalassemic RBCs submitted in vitro to oxidative haemolysis by cumene hydroperoxide. Indicaxanthin at 1.0-10 microM enhanced the resistance to haemolysis dose-dependently. In addition, it prevented lipid and haemoglobin (Hb) oxidation, and retarded vitamin E and GSH depletion. After ex vivo spiking of blood from thalassemia patients with indicaxanthin, the phytochemical was recovered in the soluble cell compartment of the RBCs. A spectrophotometric study showed that indicaxanthin can reduce perferryl-Hb ge…

congenital hereditary and neonatal diseases and abnormalitiesAntioxidantErythrocytesPyridinesmedicine.medical_treatmentindicaxanthinphytochemicalBiochemistryHemolysisAntioxidantschemistry.chemical_compoundHemoglobinsAntioxidants betalainhemic and lymphatic diseasesSettore BIO/10 - BiochimicamedicineBenzene DerivativesHumansVitamin ETraditional medicineDose-Response Relationship DrugChemistrybeta-ThalassemiaBeta thalassemiaGeneral Medicinemedicine.diseaseLipid MetabolismGlutathionehaemoglobinBetaxanthinsPhytochemicalBiochemistryCytoprotectionSpectrophotometryCase-Control StudiesHeminAntioxidants betalains haemoglobin indicaxanthin phytochemicals red blood cellsIndicaxanthinOxidation-Reductionred blood cells
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Sporadic and Familial Variants in NF1: An Explanation of the Wide Variability in Neurocognitive Phenotype?

2020

Background: Cognitive impairment is the most common neurological manifestation in NF1 and occurs in 30-70% of NF1 cases. The onset and severity of each specific cognitive deficit varies greatly from child to child, with no apparent external causes. The wide variability of phenotype is the most complex aspect in terms of management and care. Despite multiple research, the mechanism underlying the high heterogeneity in NF1 has not yet been elucidated. While many studies have focused on the effects of specific and precise genetic mutations on the NF1 phenotype, little has been done on the impact of NF1 transmission (sporadic vs. familial cases). We used a complete neuropsychological evaluation…

congenital hereditary and neonatal diseases and abnormalitiesCBCL[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticslcsh:RC346-42903 medical and health sciences0302 clinical medicinemedicineEffects of sleep deprivation on cognitive performanceEarly childhoodlcsh:Neurology. Diseases of the nervous systemCognitive deficit030304 developmental biologyOriginal Research0303 health scienceschildNeuropsychologyfamilial[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive SciencesCognition3. Good healthcognitive profileNeurology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNF1sporadicNeurology (clinical)medicine.symptomPsychologySESNeurocognitivePsychosocialhereditary030217 neurology & neurosurgery[SDV.NEU.SC] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive SciencesClinical psychology
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Safety of tiotropium and olodaterol fixed-dose combination for COPD in patients on β-blockers

2015

Introduction: The TONADO studies (NCT01431274; NCT01431287) established the efficacy and safety of a new once-daily fixed-dose combination (FDC) with tiotropium (T), a long-acting muscarinic antagonist, and olodaterol (O), a long-acting β 2 -agonist, for the treatment of COPD. This post hoc analysis evaluates T+O safety in the subgroup of patients (pts) receiving β-blockers (BBs) in these studies. Methods: These were randomised, double-blind, parallel-group, 52-week, Phase III trials comparing T+O FDC (2.5/5 µg; 5/5 µg) with the monocomponents. Adverse events (AEs) and serious AEs (SAEs) were recorded and SAEs independently adjudicated. Pooled safety data from pts receiving BBs at baseline …

congenital hereditary and neonatal diseases and abnormalitiesCOPDmedicine.medical_specialtybusiness.industryIncidence (epidemiology)Fixed-dose combinationOlodaterolMuscarinic antagonistmedicine.diseasechemistry.chemical_compoundchemistryInternal medicinePost-hoc analysisMedicineIn patientbusinessAdverse effectmedicine.drug5.1 Airway Pharmacology and Treatment
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Absence of mutation at the GAP-related domain of the neurofibromatosis type 1 gene in sporadic neurofibrosarcomas and other bone and soft tissue sarc…

1995

The NF1 gene encodes neurofibromin, a GTPase-activating protein containing a GAP-related domain (NF1-GRD) that is capable of downregulating ras by stimulating ras intrinsic GTPase activity. We tested 44 sarcomas, nine of which corresponded to sporadic neurofibrosarcomas, for mutations at the NF1-GRD by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) technique, finding no mutation in every sample tested. We suggest that inactivation of the NF1-GRD by gene mutation seems not to be an important event in the tumorigenesis of sarcomas.

congenital hereditary and neonatal diseases and abnormalitiesCancer ResearchNeurofibromatosis 1DNA Mutational AnalysisBone NeoplasmsSoft Tissue NeoplasmsGTPaseBiologyGene mutationmedicine.disease_causePolymerase Chain ReactionGeneticsmedicineHumansneoplasmsMolecular BiologyGenePolymorphism Single-Stranded ConformationalGeneticsMutationNeurofibromin 1ProteinsSarcomaSingle-strand conformation polymorphismmedicine.diseaseNeurofibromin 1eye diseasesnervous system diseasesNeurofibrosarcomaCancer researchbiology.proteinSarcomaCarcinogenesisCancer Genetics and Cytogenetics
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In the literature: April 2020

2020

Deficient DNA mismatch repair (dMMR) may be caused by germline or somatic mutations in mismatch repair genes ( MLH1 , MSH2 , MSH3 , MSH6 and PMS2 ) or through epigenetic silencing of MLH1 .1 dMMR induces a hypermutator phenotype, also known as microsatellite instability (MSI). Next-generation sequencing identifies MSI in 12 cancer types. The highest prevalence is seen in endometrial cancer (31.4%), followed by colorectal cancer (19.7%) and gastric cancer (GC, 19.1%). MSI was related to better prognosis for colorectal cancer and GC . Moreover, the dMMR/MSI hypermutator phenotype is thought to produce large numbers of immunogenic neoantigens that can be recognised by immune cells, leading to …

congenital hereditary and neonatal diseases and abnormalitiesCancer Researchbusiness.industryCancerMicrosatellite instabilityNewsmedicine.diseaseMLH1digestive system diseasesnot applicableMSH6OncologyMSH3MSH2medicineCancer researchPMS2DNA mismatch repair1506businessneoplasmsESMO Open
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First analysis of the National Lung Cancer Register in Spain (RTT).

2018

e13608Background: The Spanish Lung Cancer Group (GECP) initiated a Tumor Thoracic Register (RTT) in September 2016 with the aim of evaluating accurate, basic data concerning this oncological pathol...

congenital hereditary and neonatal diseases and abnormalitiesCancer Researchmedicine.medical_specialtyintegumentary systemOncologyRegister (music)business.industryInternal medicinemedicineLung cancermedicine.diseasebusinessJournal of Clinical Oncology
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A ceRNA analysis on LMNA gene focusing on the Hutchinson-Gilford progeria syndrome

2013

Background: Hutchinson-Gilford progeria syndrome is a rare dominant human disease of genetic origin. The average life expectancy is about 20 years, patients’ life quality is still very poor and no efficient therapy has yet been developed. It is caused by mutation of the LMNA gene, which results in accumulation in the nuclear membrane of a particular splicing form of Lamin-A called progerin. The mechanism by which progerin perturbs cellular homeostasis and leads to the symptoms is still under debate. Micro-RNAs are able to negatively regulate transcription by coupling with the 3’ UnTranslated Region of messenger RNAs. Several Micro-RNAs recognize the same 3’ UnTranslated Region and each Micr…

congenital hereditary and neonatal diseases and abnormalitiesCandidate geneCeRNA Hutchinson-Gilford Progeria LMNA Lamin-A 3’ UTR MiRNALMNACellular homeostasisHealth InformaticsLamin-ABiologySettore MED/13 - EndocrinologiaLMNAProgeriaCeRNAmedicineHutchinson-GilfordGeneticsProgeriaintegumentary systemCompeting endogenous RNAThree prime untranslated regionResearchnutritional and metabolic diseasesmedicine.diseaseProgerinSettore BIO/18 - GeneticaRNA splicing3’ UTRMiRNAJournal of Clinical Bioinformatics
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Tissue‐dependent differences in Bardet–Biedl syndrome gene expression

2019

BACKGROUND INFORMATION Primary cilia are highly conserved multifunctional cell organelles that extend from the cell membrane. A range of genetic disorders, collectively termed ciliopathies, is attributed to primary cilia dysfunction. The archetypical ciliopathy is the Bardet-Biedl syndrome (BBS), patients of which display virtually all symptoms associated with dysfunctional cilia. The primary cilium acts as a sensory organelle transmitting intra- and extracellular signals thereby transducing various signalling pathways facilitated by the BBS proteins. Growing evidence suggests that cilia proteins also have alternative functions in ciliary independent mechanisms, which might be contributing …

congenital hereditary and neonatal diseases and abnormalitiesContext (language use)BiologyCiliopathiesMice03 medical and health sciences0302 clinical medicineBardet–Biedl syndromeGene expressionOrganellemedicineAnimalsBardet-Biedl Syndrome030304 developmental biologyMice KnockoutRegulation of gene expression0303 health sciencesCiliumCell BiologyGeneral Medicinemedicine.diseaseCell biologyDisease Models AnimalCiliopathyGene Expression RegulationOrgan Specificity030217 neurology & neurosurgerySignal TransductionBiology of the Cell
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Phosphorylation of mismatch repair proteins MSH2 and MSH6 affecting MutSα mismatch-binding activity

2002

Mismatch repair (MMR) is involved in the removal of mispaired bases from DNA and thus plays an important role in the maintenance of genomic stability and the prevention of mutations and cancer. Moreover, MMR triggers genotoxicity and apoptosis upon processing of DNA lesions such as O6-methylguanine. Whereas the enzymology of MMR has been elucidated in great detail, only limited data are available concerning its regulation. Here we show that the major mismatch-binding proteins MSH2 and MSH6, forming the MutSalpha complex, are phosphorylated in vitro by protein kinase C and casein kinase II, but not by protein kinase A. Phosphorylation of MSH2 and MSH6 was also found within the cell, with MSH…

congenital hereditary and neonatal diseases and abnormalitiesDNA RepairDNA repairBase Pair MismatchMacromolecular SubstancesActive Transport Cell NucleusBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene ProteinsGeneticsHumansProtein phosphorylationPhosphorylationProtein kinase ACasein Kinase IIneoplasmsProtein kinase CProtein Kinase CCell Nucleusnutritional and metabolic diseasesdigestive system diseasesDNA-Binding ProteinsMutS Homolog 2 ProteinBiochemistryMSH2PhosphorylationDNA mismatch repairCasein kinase 2HeLa Cells
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"Table 1" of "Cross-sections and leptonic forward-backward asymmetries from the Z0 running of LEP."

2000

Hadronic cross section measured with the 1993 data. Additional systematic error of 0.10 PCT (efficiencies and backgrounds) and 0.29 PCT (absolute luminosity).

congenital hereditary and neonatal diseases and abnormalitiesE+ E- --> HADRONSE+ E- Scatteringparasitic diseasesIntegrated Cross SectionExclusive89.431-93.015Cross SectionR measurementbacterial infections and mycosesSIGhormones hormone substitutes and hormone antagonists
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