Search results for "porter"

showing 10 items of 920 documents

Ketogenic diet for infants with epilepsy: A literature review.

2020

Abstract The ketogenic diet (KD) is an established, nonpharmacological treatment for drug-resistant epilepsy (DRE). Actually, KD and its variants have been shown to be elective and resolute for patients with glucose transporter type 1 (GLUT1) deficiency. The aim of this review was to study the use of KD and its variants in infancy, including the neonatal age, and demonstrate the safety and efficacy of this treatment in patients with the age of 0–23 months affected by DRE already subjected to pharmacological approach attempts. A literature search was conducted using PubMed as the medical database source. We used the age limit of 0–23 months, and we considered only articles published between …

MalePediatricsmedicine.medical_specialtyDrug Resistant EpilepsyKetogenicmedicine.medical_treatmentDrug-resistant epilepsyDrug-resistant epilepsy Epilepsy Glucose transporter type 1 deficiency Infant Ketogenic diet Diet Ketogenic Disease Management Drug Resistant Epilepsy Epilepsy Female Glucose Transporter Type 1 Humans Infant. Infant Newborn. Male Seizures Treatment OutcomeNeonatal ageNewborn. MaleAge limitlaw.invention03 medical and health sciencesBehavioral NeuroscienceEpilepsy0302 clinical medicineRandomized controlled triallawSeizuresmedicineGlucose transporter type 1 deficiencyHumans030212 general & internal medicineProspective cohort studyGlucose Transporter Type 1Epilepsybusiness.industryInfant NewbornDisease ManagementInfantRetrospective cohort studyKetogenic dietInfant. InfantDrug Resistant Epilepsymedicine.diseaseDietTreatment OutcomeNeurologyFemaleNeurology (clinical)businessDiet Ketogenic030217 neurology & neurosurgeryKetogenic dietEpilepsybehavior : EB
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ABCC transporters mediate insect resistance to multiple Bt toxins revealed by bulk segregant analysis

2014

[EN] Background: Relatively recent evidence indicates that ABCC2 transporters play a main role in the mode of action of Bacillus thuringiensis (Bt) Cry1A-type proteins. Mapping of major Cry1A resistance genes has linked resistance to the ABCC2 locus in Heliothis virescens, Plutella xylostella, Trichoplusia ni and Bombyx mori, and mutations in this gene have been found in three of these Bt-resistant strains. Results: We have used a colony of Spodoptera exigua (Xen-R) highly resistant to a Bt commercial bioinsecticide to identify regions in the S. exigua genome containing loci for major resistance genes by using bulk segregant analysis (BSA). Results reveal a region containing three genes fro…

MalePhysiologyGenes InsectPlant ScienceBt resistanceInsecticide ResistanceHemolysin ProteinsStructural BiologyBacillus thuringiensisChromosome SegregationPhylogenyGeneticsbiologyAgricultural and Biological Sciences(all)LarvaFemaleGeneral Agricultural and Biological SciencesBiotechnologyResearch ArticleMolecular Sequence DataBacillus thuringiensisSpodopteraSpodopteraABCC2 transporterPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyBacterial ProteinsExiguaAnimalsAmino Acid SequenceGeneEcology Evolution Behavior and SystematicsCrosses GeneticBombyxBacillus thuringiensis ToxinsBiochemistry Genetics and Molecular Biology(all)Gene Expression ProfilingfungiWild typeCell BiologySequence Analysis DNAbiology.organism_classificationBombyxMolecular biologyEndotoxinsKineticsGENETICACry1AcMembrane proteinATP-Binding Cassette TransportersCry toxinsDevelopmental Biology
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MiR-133 Modulates the β1Adrenergic Receptor Transduction Cascade.

2014

Rationale : The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, overactivation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors in cardiomyocytes and lead to increased heart rate and cardiac contractility. However, chronic stimulation of β-adrenergic receptors leads to impaired cardiac function, and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MicroRNA-133 (miR-133) is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of messenger RNA translation/stability. …

MalePhysiologyMessengerheart failureApoptosiscardiomyocytesInbred C57BLSecond Messenger SystemsTransgenicRats Sprague-DawleyBeta-1 adrenergic receptorMiceGenes ReporterReceptorsCyclic AMPGuanine Nucleotide Exchange FactorsMyocytes CardiacAlpha-1D adrenergic receptor3' Untranslated RegionsCells CulturedCulturedbiologyChemistryadrenergic beta-1 receptor antagonists; cardiac; cyclic AMP; heart failure; microRNAs; myocytes; 3' Untranslated Regions; Adenylyl Cyclases; Animals; Apoptosis; Cells Cultured; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Disease Progression; Gene Expression Regulation; Genes Reporter; Guanine Nucleotide Exchange Factors; Male; Metoprolol; Mice; Mice Inbred C57BL; Mice Transgenic; MicroRNAs; Myocardium; Myocytes Cardiac; RNA Messenger; Rats; Rats Sprague-Dawley; Receptors Adrenergic beta-1; Recombinant Fusion Proteins; Second Messenger Systems; Physiology; Cardiology and Cardiovascular Medicine; Medicine (all)Medicine (all)Cell biologyAdrenergicadrenergic beta-1 receptor antagonistsDisease ProgressionCARDIAC HYPERTROPHYSignal transductionCardiology and Cardiovascular MedicineAdenylyl CyclasesMetoprololmedicine.medical_specialtyAdrenergic receptorcardiacCellsRecombinant Fusion ProteinsMice Transgenicbeta-1Alpha-1B adrenergic receptorInternal medicinecAMPmedicineAnimalsRNA MessengerReporterPressure overloadalpha and beta adrenoceptorsMyocytesMyocardiumBeta adrenergic receptor kinaseCyclic AMP-Dependent Protein KinasesAlpha-1A adrenergic receptorRatsMice Inbred C57BLMicroRNAsEndocrinologyGenesGene Expression Regulationbiology.proteinRNASprague-DawleyReceptors Adrenergic beta-1MicroRNAs; alpha and beta adrenoceptors; cardiomyocytes; CARDIAC HYPERTROPHY; cAMP
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Effect of chronic citalopram on serotonin-related and stress-regulated genes in the dorsal raphe nucleus of the rat

2007

Using a model of depression in which chronic social stress induces depressive-like symptoms, we investigated effects of the selective serotonin-reuptake inhibitor (SSRI) citalopram on gene expression in the dorsal raphe nucleus of male rats. Expression of tryptophan hydroxylase (TPH) protein was found to be upregulated by the stress and normalized by citalopram, while mRNAs for genes TPH 1 and 2 were differentially affected. Citalopram had no effect on serotonin transporter mRNA but reduced serotonin-1A autoreceptor mRNA in stressed animals. The SSRI prevented the stress-induced upregulation of mRNA for CREB binding protein, synaptic vesicle glycoprotein 2b and the glial N-myc downstream-re…

MaleSerotoninendocrine systemmedicine.medical_specialtyCitalopramTryptophan HydroxylaseBiologyCitalopramPolymerase Chain Reactionbehavioral disciplines and activitiesGene Expression Regulation Enzymologic03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDorsal raphe nucleusStress PhysiologicalInternal medicinemental disordersmedicineAnimalsPharmacology (medical)Rats WistarSocial BehaviorNeurotransmitterBiological PsychiatrySerotonin transporter030304 developmental biologyPharmacology0303 health sciencesTryptophan hydroxylaseRatsPsychiatry and Mental healthEndocrinologyNeurologychemistryModels Animalbiology.proteinSynaptic vesicle glycoprotein 2BRNARaphe Nuclei5-HT1A receptorNeurology (clinical)SerotoninSelective Serotonin Reuptake Inhibitors030217 neurology & neurosurgerymedicine.drugEuropean Neuropsychopharmacology
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The effects of nitric oxide on striatal serotoninergic transmission involve multiple targets: an in vivo microdialysis study in the awake rat

2004

Abstract The role of endogenous nitric oxide (NO) in N -methyl- d -aspartate (NMDA)-induced modulation of serotonin (5-HT) release in the striatum of freely moving rats has been studied using microdialysis technique. NMDA-induced increase in 5-HT release was significantly inhibited by selective nitric oxide synthase (nNOS) inhibitor S -methylthiocitrulline (S-Me-TC), ONOO − scavenger l -cysteine ( l -cys), and guanylate cyclase (GC) inhibitor 1 H [1,2,4]oxadiazolo[4,3- a ]quinoxalin-1-one (ODQ). These data suggest that modulation of 5-HT levels is linked to the formation of NO produced by NMDA receptor activation and that endogenously produced NO increases 5-HT concentrations both by stimul…

MaleSerotoninmedicine.medical_specialtyMicrodialysisN-MethylaspartateMicrodialysisNitric Oxide Synthase Type IPharmacologyNitric OxideSerotonergicSynaptic TransmissionNitric oxidechemistry.chemical_compoundSuperoxidesPeroxynitrous AcidInternal medicinemedicineAnimalsEnzyme InhibitorsRats WistarNeurotransmitterCyclic GMPMolecular Biologyneurotransmitters; modulators; transporters; and receptors; nitric oxide; serotonin; striatumbiologyGeneral NeuroscienceFree Radical ScavengersRatsNeostriatumNitric oxide synthasePeroxynitrous acidEndocrinologychemistryGuanylate Cyclasebiology.proteinNMDA receptorNeurology (clinical)SerotoninNitric Oxide SynthaseSignal TransductionDevelopmental Biology
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The atypical dopamine transport inhibitor, JHW 007, prevents amphetamine-induced sensitization and synaptic reorganization within the nucleus accumbe…

2013

Benztropine (BZT) analogs, a family of agents with high affinity for the dopamine transporter have been postulated as potential treatments in stimulant abuse due to their ability to attenuate a wide range of effects evoked by psychomotor stimulants such as cocaine and amphetamine (AMPH). Repeating administration of drugs, including stimulants, can result in behavioral sensitization, a progressive increase in their psychomotor activating effects. We examined in mice the sensitizing effects and the neuroplasticity changes elicited by chronic AMPH exposure, and the modulation of these effects by the BZT derivative and atypical dopamine uptake inhibitor, JHW007, a candidate medication for stimu…

MaleSilver Stainingmedicine.medical_treatmentDopamine transportMotor ActivityNucleus accumbensPharmacologyMedium spiny neuronNucleus AccumbensDendritic spinesSensitizationMiceDopamine Uptake InhibitorsMicroscopy Electron TransmissionDopaminemedicineAnimalsAsymmetric synapsesAmphetamineBiological PsychiatrySensitizationDopamine transporterBenztropineNeuronsPharmacologyAnalysis of VariancebiologyBenztropine analogStimulantAmphetaminemedicine.anatomical_structurebiology.proteinDopamine AntagonistsNucleus accumbensPsychologyNeurosciencemedicine.drug
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Changes in the expression of cation-Cl- cotransporters, NKCC1 and KCC2, during cortical malformation induced by neonatal freeze-lesion.

2007

Focal cortical malformations comprise a heterogeneous group of disturbances in brain development, often associated with intractable epilepsy. A focal freeze-lesion of cerebral cortex in newborn rat produces a cortical malformation that resembles human polymicrogyria, clinical conditions that results from abnormal neuronal migration. The change in GABAergic functions that occurs during early brain development is induced by an alteration in Cl(-) homeostasis and plays important roles in neocortical development by modulating such events as laminar organization and synaptogenesis. We therefore investigated the relationship between pathogenesis of polymicrogyria and ontogeny of Cl(-) homeostasis…

MaleSodium-Potassium-Chloride SymportersSynaptogenesisDown-RegulationBiologyNervous System MalformationsLaminar organizationChloridesCell MovementChloride ChannelsCortex (anatomy)Parietal LobeGlial Fibrillary Acidic ProteinmedicinePolymicrogyriaAnimalsSolute Carrier Family 12 Member 2RNA MessengerRats Wistargamma-Aminobutyric AcidCerebral CortexSymportersGeneral NeuroscienceColocalizationCell DifferentiationGeneral Medicinemedicine.diseaseDenervationImmunohistochemistryMicrogyrusRatsUp-RegulationCold Temperaturemedicine.anatomical_structureNeuronal migration disorderBromodeoxyuridineCerebral cortexPhosphopyruvate HydrataseNeuroscienceBiomarkersNeuroscience research
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Differential effect of beta-N-oxalylamino-L-alanine, the Lathyrus sativus neurotoxin, and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate …

2000

We studied the effect of beta-oxalylamino-L-alanine, a glutamate analog present in Lathyrus sativus seeds and implicated in the etiopathogenesis of neurolathyrism, and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate on the extracellular levels of aspartate, glutamate and taurine in the primary motor cortex of freely moving rats. We found that while both neurotoxins increase the level of aspartate and glutamate, only (+/-)-alpha(-amino-3-hydroxy-5-methylisoxazole-4-propionate is able to modulate the level of taurine. GYKI-52466, a non-competitive non-NMDA antagonist, inhibited beta-oxalylamino-L-alanine-induced increase of aspartate, but not that of glutamate. Conversely, this ant…

MaleTaurineTaurineMicrodialysisGlutamic AcidTetrodotoxinReceptors N-Methyl-D-AspartateRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundGlutamate aspartate transporterNeurotoxinAnimalsNeurotransmitteralpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAlaninechemistry.chemical_classificationAspartic AcidbiologyGlutamate receptorMotor CortexAmino Acids DiaminoBrainCell BiologyCorpus StriatumAmino acidRatschemistryBiochemistrybiology.proteinPotassiumbeta-AlanineNMDA receptorExtracellular SpaceExcitatory Amino Acid AntagonistsNeurochemistry international
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Mutations in the PDS Gene in German Families with Pendred’s Syndrome: V138F Is a Founder Mutation

2003

Pendred's syndrome, an autosomal-recessive condition characterized by congenital sensorineural hearing loss and goiter, is caused by mutations in the PDS gene. Located on chromosome 7q22-q31, it encodes a chloride-iodide transporter expressed in the thyroid, inner ear, and kidney. We investigated the PDS gene of six affected individuals from four unrelated families with Pendred's syndrome by direct sequencing. PDS mutations were identified in homozygous or compound heterozygous state in all six cases. A homozygous missense mutation leading to the amino acid substitution S133T was detected in a family of Turkish origin. The mutations found in the other affected individuals, who originate fro…

MaleThreoninemedicine.medical_specialtyAdolescentTurkeyHearing Loss SensorineuralEndocrinology Diabetes and MetabolismClinical BiochemistryMutation MissenseBiologyCompound heterozygositymedicine.disease_causeBiochemistryGenetic determinismEndocrinologyHypothyroidismGermanyInternal medicineSerinemedicineHumansMissense mutationAlleleChildPendred syndromeGeneticsMutationBase SequenceBiochemistry (medical)HaplotypeInfant NewbornMembrane Transport Proteinsfood and beveragesSyndromemedicine.diseaseFounder EffectPedigreeEndocrinologyAmino Acid SubstitutionHaplotypesSulfate TransportersChild PreschoolMicrosatelliteFemaleCarrier ProteinsThe Journal of Clinical Endocrinology & Metabolism
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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