Search results for " Type II"

showing 10 items of 542 documents

Experimental inhibition of nitric oxide increases Plasmodium relictum (lineage SGS1) parasitaemia.

2012

7 pages; International audience; Malaria is a widespread vector-borne disease infecting a wide range of terrestrial vertebrates including reptiles, birds and mammals. In addition to being one of the most deadly infectious diseases for humans, malaria is a threat to wildlife. The host immune system represents the main defence against malaria parasites. Identifying the immune effectors involved in malaria resistance has therefore become a major focus of research. However, this has mostly involved humans and animal models (rodents) and how the immune system regulates malaria progression in non-model organisms has been largely ignored. The aim of the present study was to investigate the role of…

PlasmodiumCanariesNitric Oxide Synthase Type IIDiseaseParasitemia[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunologyGuanidinesImmune defencechemistry.chemical_compound0302 clinical medicineImmunopathology[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisEnzyme InhibitorsExperimental infection0303 health sciencesbiologyGeneral Medicine3. Good healthNitric oxide synthaseInfectious Diseases[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyAvian malariaSparrows[ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyMalaria Avian030231 tropical medicineImmunologyPlasmodium relictum lineage SGS1ImmunopathologyNitric oxide03 medical and health sciencesImmune systemAvian malariaparasitic diseasesmedicineAnimals[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology030304 developmental biology[ SDE.BE ] Environmental Sciences/Biodiversity and EcologyNitric oxidemedicine.diseasebiology.organism_classificationPlasmodium relictumchemistryImmunologybiology.proteinParasitology[SDE.BE]Environmental Sciences/Biodiversity and EcologyMalaria[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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Effectiveness of screening for known mutations in Sicilian patients with "probable" familial hypercholesterolemia.

2002

Background and Aim: More than 750 mutations in the low-density lipoprotein (LDL) receptor gene are currently known to cause familial hypercholesterolemia (FH), but the array of mutations varies considerably in different populations. The definition of essentially all the LDL receptor gene mutations in a population is therefore a prerequisite for the implementation of nation-wide genetic testing for FH. Methods and Results: In this study, a screening strategy based on PCR-enzymatic digestion and PCR-allele specific hybridisation procedures was used to evaluate the frequency distributions of 11 known mutations in a cohort of 214 unrelated subjects meeting the diagnostic criteria of "probable" …

Point mutationNutrition and DieteticsSettore MED/09 - Medicina InternaEndocrinology Diabetes and MetabolismMedicine (miscellaneous)ExonsPolymerase Chain ReactionFHCohort StudiesHyperlipoproteinemia Type IIGene FrequencyReceptors LDLMutationScreeningHumansGenetic TestingCardiology and Cardiovascular MedicineSicilyFood Science
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Resveratrol, a polyphenolic phytoalexin present in red wine, enhances expression and activity of endothelial nitric oxide synthase.

2002

Background— Estrogens can upregulate endothelial nitric oxide synthase (eNOS) in human endothelial cells by increasing eNOS promoter activity and enhancing the binding activity of the transcription factor Sp1. Resveratrol, a polyphenolic phytoalexin found in grapes and wine, has been reported to act as an agonist at the estrogen receptor. Therefore, we tested the effect of this putative phytoestrogen on eNOS expression in human endothelial cells. Methods and Results— Incubation of human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells with resveratrol for 24 to 72 hours upregulated eNOS mRNA expression in a time- and concentration-dependent manner (up to 2.8-fold)…

PolymersRNA StabilityElectrophoretic Mobility Shift AssayWineResveratrolUmbilical veinchemistry.chemical_compoundEnosStilbenesPromoter Regions GeneticCells Culturedchemistry.chemical_classificationbiologyPhytoalexinEstrogen Antagonistsfood and beveragesNitric Oxide Synthase Type IIIUp-RegulationNitric oxide synthasemedicine.anatomical_structureReceptors EstrogenEnzyme InductionCardiology and Cardiovascular MedicineSesquiterpenesmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIINuclease Protection AssaysEnzyme ActivatorsPhytoestrogensNitric OxidePhenolsPhytoalexinsPhysiology (medical)Internal medicinemedicineHumansEstrogens Non-SteroidalRNA MessengerFlavonoidsSp1 transcription factorPlant ExtractsTerpenesPolyphenolsbiology.organism_classificationMolecular biologyIsoflavonesEnzyme ActivationEndocrinologychemistryResveratrolbiology.proteinEndothelium VascularPlant PreparationsNitric Oxide SynthaseCirculation
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An interesting question of Pompe disease. A case report

2006

Glycogenosis type II or Pompe disease is an inherited autosomal recessive disorder known in 3 different clinical forms (infantile, juvenile and adult). We report on a case diagnosed as a classic infantile form with the worst outcome of all 3 described, if we had followed and executed a correct and complete diagnostic pathway. A 7 months old female child was admitted for fever and dyspnoea. At chest auscultation weepings and weezings were found; on the cardiac apex a murmur due to mitralic failure was retrieved. The thorax X-ray showed a greatly increased heart shadow with a cardiothoracic index of 0.75. ECG showed high voltages and signs of bilateral ventricular hypertrophy. Cardiac ultraso…

Pompe DiseaseLiverGlycogen Storage Disease Type IIHumansInfantGlycogen Glycogen storage disease Glycogen storage disease type IIFemaleChildren
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Genetic diagnosis of familial hypercholesterolemia in a South European outbreed population: influence of low-density lipoprotein (LDL) receptor gene …

2001

The aims of this study were to examine the presence of mutations in the low-density lipoprotein receptor gene among subjects clinically diagnosed with familial hypercholesterolemia and to analyze whether the molecular diagnosis helps to predict the response to simvastatin treatment in our familial hypercholesterolemia population. Fifty-five probands and 128 related subjects with familial hypercholesterolemia were studied. Genetic diagnosis was carried out following a three-step protocol based on Southern blot and PCR-single strand conformational polymorphism analysis. A randomized clinical trial with simvastatin was conducted in 42 genetically diagnosed subjects with familial hypercholester…

ProbandAdultMalemedicine.medical_specialtySimvastatinEndocrinology Diabetes and MetabolismClinical BiochemistryPopulationFamilial hypercholesterolemiaBiologyBiochemistryHyperlipoproteinemia Type IIchemistry.chemical_compoundEndocrinologyHigh-density lipoproteinApolipoproteins EInternal medicinemedicineHumanseducationAgedApolipoproteins Beducation.field_of_studyCholesterolBiochemistry (medical)Cholesterol HDLnutritional and metabolic diseasesCholesterol LDLMiddle Agedmedicine.diseaseEndocrinologychemistryReceptors LDLSimvastatinLow-density lipoproteinMutationlipids (amino acids peptides and proteins)FemaleHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteinmedicine.drugThe Journal of clinical endocrinology and metabolism
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Additive effect of mutations in LDLR and PCSK9 genes on the phenotype of familial hypercholesterolemia.

2006

Patients homozygous or Compound heterozygous for LDLR mutations or double heterozygous for LDLR and apo B R3500Q mutation have higher LDL-C levels. more extensive xanthomatosis and more severe premature coronary disease (pCAD) than simple heterozygotes for mutations in either these genes or for missense mutations in PCSK9 gene. It is not known whether combined mutations in LDLR and PKCS9 are associated with such a severe phenotype. We sequenced Apo B and PCSK9 genes in two patients with the clinical diagnosis of homozygous FH who were heterozygous for LDLR gene mutations. Proband Z.P. (LDL-C 13.39 mmol/L and pCAD) was heterozygous for an LDLR mutation (p.E228K) inherited from her father (LD…

ProbandLDLR geneAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemia (FH); Autosomal dominant hypercholesterolemia 3 (ADH3); LDLR gene; PCSK9 gene; Premature coronary artery diseasePremature coronary artery diseaseLDLR PCSK9Mutation MissenseFamilial hypercholesterolemiaCompound heterozygositymedicine.disease_causeHyperlipoproteinemia Type IIFamilial hypercholesterolemia (FH) Autosomal dominant hypercholesterolemia 3 (ADH3) LDLR gene PCSK9 gene Premature coronary artery diseaseFamilial hypercholesterolemia (FH)medicineMissense mutationHumansCells CulturedGeneticsMutationbiologybusiness.industrySerine EndopeptidasesHeterozygote advantageMiddle Agedmedicine.diseaseAutosomal dominant hypercholesterolemia 3 (ADH3)PedigreePhenotypeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionReceptors LDLPCSK9 geneLDL receptorbiology.proteinlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessAtherosclerosis
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Lack of phenotypic additive effect of familial defective apolipoprotein B3531 in familial hypercholesterolaemia.

2020

Familial defective apolipoprotein (apo) B (FDB) and familial hypercholesterolaemia (FH) are the two common genetic conditions that cause hypercholesterolaemia. R3531C mutation of the APOB gene is a rare cause of FDB. Individuals with both FDB and FH are rare. A 51-year-old man with hypercholesterolaemia (11.4 mmol/L) and his family were studied. Low-density lipoprotein (LDL) receptor (LDLR) and APOB genes were analysed by direct sequencing. LDL of four subjects were studied in a fibroblast LDL receptor-binding displacement assay. We found a mutation of the LDLR gene (p.Y398X) in the proband and in four other family members: the p.R3531C APOB gene mutation was also found in the proband, his …

ProbandMalemedicine.medical_specialtyApolipoprotein B030204 cardiovascular system & hematologyCompound heterozygosityHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compoundFDB35310302 clinical medicineInternal medicineInternal MedicinemedicineHumans030212 general & internal medicineApolipoproteins Bdouble heterozygotebiologybusiness.industryCholesterolLDL receptornutritional and metabolic diseasesHeterozygote advantageMiddle AgedEndocrinologychemistryItalyReceptors LDLLDL receptorMutation (genetic algorithm)Mutationfamilial hypercholesterolaemiabiology.proteinlipids (amino acids peptides and proteins)businessLipoproteinInternal medicine journalReferences
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Involvement of NO in contact hypersensitivity.

1998

The NO synthases (NOS) generate NO from L-arginine. High concentrations of NO have been shown to be responsible for tissue injury and cell death, while low concentrations of NO induce vasodilatation and other signaling effects. We have investigated the involvement of NO in contact hypersensitivity (CHS) reactions. CHS induced by treatment of BALB/c mice with the contact allergen 2,4-dinitrofluorobenzene (DNFB) was significantly reduced by the NOS inhibitor N-methyl-L-arginine (L-NMA), but not by the stereoisomer D-NMA, as shown by reduced ear swelling responses and evaluation of ear tissue sections. The CHS response was also reduced by aminoguanidine, which is known to preferentially inhibi…

Programmed cell deathLangerhans cellArginineInjections IntradermalT-LymphocytesImmunologyNitric Oxide Synthase Type IIBiologyArginineDermatitis ContactNitric OxideGuanidineschemistry.chemical_compoundMicemedicineImmunology and AllergyAnimalsRNA MessengerEnzyme InhibitorsSkinMice Inbred BALB Cintegumentary systemEpidermis (botany)Histocompatibility Antigens Class IIGeneral MedicineAllergensMolecular biologyPimagedineNitric oxide synthasemedicine.anatomical_structurechemistryLangerhans Cellsbiology.proteinDinitrofluorobenzeneSignal transductionNitric Oxide SynthaseKeratinocyteHaptensInternational immunology
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Cytotoxicity of apigenin toward multiple myeloma cell lines and suppression of iNOS and COX-2 expression in STAT1-transfected HEK293 cells.

2020

Apigenin is one of the most abundant dietary flavonoids that possesses multiple bio-functions.This study was designed to determine the influence of apigenin on gene expressions, cancer cells, as well as STAT1/COX-2/iNOS pathway mediated inflammation and tumorigenesis in HEK293-STAT1 cells. Furthermore, the cytotoxic activity toward multiple myeloma (MM) cell lines was investigated.Bioinformatic analyses were used to predict the sensitivity and resistance of tumor cells toward apigenin and to determine cellular pathways influenced by this compound. The cytotoxic and ferroptotic activity of apigenin was examined by the resazurin reduction assay. Additionally, we evaluated apoptosis, and cell …

Programmed cell deathPharmaceutical ScienceNitric Oxide Synthase Type IIApoptosis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDrug DiscoveryAntineoplastic Combined Chemotherapy ProtocolsAutophagyCytotoxic T cellHumansDAPIApigenin030304 developmental biologyCell ProliferationPharmacology0303 health sciencesDose-Response Relationship DrugChemistryCell CycleComputational BiologyCell cycleAntineoplastic Agents PhytogenicHEK293 CellsSTAT1 Transcription FactorComplementary and alternative medicineApoptosisCell cultureCyclooxygenase 2Doxorubicin030220 oncology & carcinogenesisApigeninCancer cellCancer researchMolecular MedicineMultiple MyelomaReactive Oxygen SpeciesPhytomedicine : international journal of phytotherapy and phytopharmacology
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Relative contribution of different l-arginine sources to the substrate supply of endothelial nitric oxide synthase

2011

In certain cases of endothelial dysfunction l-arginine becomes rate-limiting for NO synthesis in spite of sufficiently high plasma concentrations of the amino acid. To better understand this phenomenon, we investigated routes of substrate supply to endothelial nitric oxide synthase (eNOS). Our previous data with human umbilical vein (HUVEC) and EA.hy.926 endothelial cells demonstrated that eNOS can obtain its substrate from the conversion of l-citrulline to l-arginine and from protein breakdown. In the present study, we determined the quantitative contribution of proteasomal and lysosomal protein degradation and investigated to what extent extracellular peptides and l-citrulline can provide…

Proteasome Endopeptidase ComplexNitric Oxide Synthase Type IIIArginineEndotheliumLeupeptinsPeptideArginineNitric OxideUmbilical veinCell LineGenes ReporterEnosLysosomeHuman Umbilical Vein Endothelial CellsmedicineExtracellularHumansHistidineProtease InhibitorsMolecular BiologyChromatography High Pressure LiquidHistidinechemistry.chemical_classificationbiologyMembrane Transport ProteinsBiological TransportChloroquineDipeptidesAtherosclerosisbiology.organism_classificationmedicine.anatomical_structureBiochemistrychemistryProteolysisCitrullineEndothelium VascularLysosomesCardiology and Cardiovascular MedicineOligopeptidesJournal of Molecular and Cellular Cardiology
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