Search results for "tlast"

showing 2 items of 2 documents

In vitro evaluation of poloxamer in situ forming gels for bedaquiline fumarate salt and pharmacokinetics following intramuscular injection in rats

2019

Graphical abstract

In situPO Propylene oxideIV IntravenousP338 Poloxamer 338lcsh:RS1-441Pharmaceutical Sciencechemistry.chemical_compoundn Sample sizeSD Standard deviationIM Intramuscularchemistry.chemical_classificationC0 Analyte plasma concentration at time zeroDoE Design of experimentsUV UltravioletPharmacology. TherapyK2.EDTA Potassium ethylenediaminetetraacetic acidLC–MS/MS Liquid chromatography-tandem mass spectrometryH&E Hematoxylin and eosintmax Sampling time to reach the maximum observed analyte plasma concentrationIn situ forming gelsCMC Critical micellar concentrationCmax Maximum observed analyte plasma concentrationIntramuscular injectionDN Dose normalizedGPT Gel point temperaturePLGA Poly-(DL-lactic-co-glycolic acid)TFA Trifluoroacetic acidCAN AcetonitrileATP Adenosine 5′ triphosphateSalt (chemistry)Polyethylene glycolPoloxamerArticlelcsh:Pharmacy and materia medicaPharmacokineticsIn vivoUHPLC Ultra-high performance liquid chromatographyPharmacokineticsAUClast Area under the analyte concentration versus time curve from time zero to the time of the last measurable (non-below quantification level) concentrationEO Ethylene oxideNMP N-methyl-2-pyrrolidoneComputingMethodologies_COMPUTERGRAPHICSAUC∞ Area under the analyte concentration vs time curve from time zero to infinite timeP407 Poloxamer 407In vitro releasePoloxamerCMT Critical micellar temperatureGel erosionIn vitrot1/2 Apparent terminal elimination half-lifechemistryMDR-TB Multi-drug resistant tuberculosisAUC80h Area under the analyte concentration versus time curve from time zero to 80 htlast Sampling time until the last measurable (non-below quantification level) analyte plasma concentrationMRM Multiple reaction monitoringNuclear chemistrySustained releaseInternational Journal of Pharmaceutics: X
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Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3.

2014

Many neurodegenerative disorders present with sensory loss. In the group of hereditary sensory and autonomic neuropathies loss of nociception is one of the disease hallmarks. To determine underlying factors of sensory neurodegeneration we performed whole-exome sequencing in affected individuals with the disorder. In a family with sensory neuropathy with loss of pain perception and destruction of the pedal skeleton we report a missense mutation in a highly conserved amino acid residue of atlastin GTPase 3 (ATL3), an endoplasmic reticulum-shaping GTPase. The same mutation (p.Tyr192Cys) was identified in a second family with similar clinical outcome by screening a large cohort of 115 patients …

AtlastinAdultMaleIntracellular SpaceMutation MissenseSensory systemBiologymedicine.disease_causeEndoplasmic ReticulumGTP PhosphohydrolasesCohort StudiesFractures BoneYoung AdultmedicineMissense mutationHumansExomenociceptionAxonAge of OnsetHereditary Sensory and Autonomic NeuropathiesGenes DominantaxonGeneticsMutationEndoplasmic reticulumNeurodegenerationneurodegenerationmedicine.diseasePenetrancePedigreeHSANsensory neuronsmedicine.anatomical_structurePhenotypeCoughHaplotypesMutationGastroesophageal RefluxFemaleNeurology (clinical)Human medicineBone DiseasesNeuroscienceBrain : a journal of neurology
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