Search results for "Abeta"

showing 10 items of 22 documents

Remarks on the Historiography of Mathematics

2021

In this paper, I examine aspects of the methodological debate that originated in 2010, when the distinguished historian of mathematics Sabetai Unguru reviewed Roshdi Rashed’s edition of the Arabic translation of Apollonius’ Conics. In his review, Unguru criticized what Rashed calls “l’usage instrumental d’une autre mathématique pour commenter une oeuvre ancienne”. I consider this debate very important and will try to place it within in the discussion of the so-called “geometric algebra” that goes back to the seventies, by tracing the contributions of the main figures who took part in it. Published Online (2021-04-30)Copyright © 2021 by Aldo Brigaglia Article PDF Link: https://jps.library.ut…

History of mathematicsTranslationSocial Sciences and HumanitiesRoshdi RashedHistoriographyGeneral MedicineGeometric algebraConic sectionSabetai UnguruHistory of mathematicsSciences Humaines et SocialesLink (knot theory)ClassicsArabic translationAestimatio: Sources and Studies in the History of Science
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Insulin activated Akt rescues Aβ oxidative stress-induced cell death by orchestrating molecular trafficking.

2011

Increasing evidence indicates that Alzheimer's disease, one of the most diffused aging pathologies, and diabetes may be related. Here, we demonstrate that insulin signalling protects LAN5 cells by amyloid-β42 (Aβ)-induced toxicity. Aβ affects both activation of insulin receptors and the levels of phospho-Akt, a critical signalling molecule in this pathway. In contrast, oxidative stress induced by Aβ can be antagonized by active Akt that, in turn, inhibits Foxo3a, a pro-apoptotic transcription factor activated by reactive oxygen species generation. Insulin cascade protects against mitochondrial damage caused by Aβ treatment, restoring the mitochondrial membrane potential. Moreover, we show t…

Insulin cell death Akt Abeta peptideSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)
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Microsomal triglyceride transfer protein gene mutations in Turkish children: A novel mutation and clinical follow up.

2016

Abetalipoproteinemia (ABL; OMIM 200100) is a rare autosomal recessive disease that affects the absorption of dietary fats and fat soluble vitamins. Here, we describe the clinical and genetic characteristics of three patients with ABL. Two patients (patients 1 and 2) who were carriers of the c.398-399delAA mutation (previously known mutation) had developmental delay and hepatic steatosis developed at the age of five in patient 1. Patient 3 was the carrier of a novel mutation (g.10886-10902delAAGgtaagtttgtgttg in intron 3 and c.506A>T exon 5) in microsomal triglyceride transfer protein (MTP) gene and had hepatic steatosis.

Male0301 basic medicineHeterozygotemedicine.medical_specialtySettore MED/09 - Medicina InternaTurkeyDevelopmental delayDevelopmental DisabilitiesTurkish030204 cardiovascular system & hematologyHepatic steatosimedicine.disease_causeMicrosomal triglyceride transfer protein03 medical and health sciencesExon0302 clinical medicineInternal medicineHumansMedicineGeneGenetic Association StudiesGeneticsMutationABLbiologyAbetalipoproteinemiaDevelopmental delayHepatic steatosisMicrosomal triglyceride transfer proteinTurkishbusiness.industryIntronGastroenterologyInfantAbetalipoproteinemiaMicrosomal triglyceride transfer proteinmedicine.diseaseIntronsAbetalipoproteinemiaFatty Liver030104 developmental biologyEndocrinologyMutationbiology.proteinFemaleSteatosisCarrier ProteinsbusinessFollow-Up Studies
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Molecular diagnosis of hypobetalipoproteinemia: an ENID review.

2007

Abstract Primary hypobetalipoproteinemia (HBL) includes a group of genetic disorders: abetalipoproteinemia (ABL) and chylomicron retention disease (CRD), with a recessive transmission, and familial hypobetalipoproteinemia (FHBL) with a co-dominant transmission. ABL and CRD are rare disorders due to mutations in the MTP and SARA2 genes, respectively. Heterozygous FHBL is much more frequent. FHBL subjects often have fatty liver and, less frequently, intestinal fat malabsorption. FHBL may be linked or not to the APOB gene. Most mutations in APOB gene cause the formation of truncated forms of apoB which may or may be not secreted into the plasma. Truncated apoBs with a size below that of apoB-3…

MaleCandidate geneSettore MED/09 - Medicina InternaApolipoprotein BGenotypeLocus (genetics)BiologyPolymorphism Single NucleotidePCSK9 GenemedicineHumansFamilial hypobetalipoproteinemiaGenetic TestingAPOB geneApolipoproteins BGeneticsPCSK9AbetalipoproteinemiaChylomicron retention diseasemedicine.diseaseEuropean Network for Inherited Dyslipidemia (ENID)AbetalipoproteinemiaPhenotypePCSK9 geneHypobetalipoproteinemia Familial Apolipoprotein BMutationbiology.proteinlipids (amino acids peptides and proteins)FemaleHypobetalipoproteinemiaMTP geneCardiology and Cardiovascular MedicineCarrier Proteinsuropean Network for Inherited Dyslipidemia (ENID)European Network for Inherited Dyslipidemia (ENID) Familial hypobetalipoproteinemia Abetalipoproteinemia Chylomicron retention disease.Chylomicron retention diseaseAtherosclerosis
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Labetalol absorption kinetics: Rat small intestine and colon studies

2006

Labetalol is a widely used drug for the management of hypertension, which is preferably administered by the oral route despite its low bioavailability. The objective of this study is to ascertain the mechanisms underlying its absorption as an approach to help in predicting the influence of dosage changes, possible drug-drug and drug-fruit juice interactions. Perfusion experiments have been performed in rats in two sites of absorption: the intestine and the colon. The nonlinearity of the process has been established by means of the assay of a wide range of concentrations (2-2000 microM). Fitting of the concentration versus time data allows the estimation of passive diffusion constant in the …

MalebiologyColonChemistryPharmaceutical ScienceAbsorption (skin)PharmacologyIntestinal absorptionSmall intestineRatsBioavailabilitymedicine.anatomical_structureIntestinal AbsorptionPharmacokineticsIntestine Smallmedicinebiology.proteinAnimalsLabetalolEffluxRats WistarLabetalolmedicine.drugP-glycoproteinJournal of Pharmaceutical Sciences
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Homozygous familial hypobetalipoproteinemia: two novel mutations in the splicing sites of apolipoprotein B gene and review of the literature.

2015

Objective: Familial hypobetalipoproteinemia (FHBL) is autosomal codominant disorder of lipoprotein metabolism characterized by low plasma levels of total cholesterol (TC), low-density lipoproteincholesterol (LDL-C) and apolipoprotein B (apoB) below the 5 th percentile of the distribution in the population. Patients with the clinical diagnosis of homozygous FHBL (Ho-FHBL) are extremely rare and few patients have been characterized at the molecular level. Here we report the medical history and the molecular characterization of one paediatric patient with clinical features of Ho-FHBL. Methods: A one month old infant with failure to thrive, severe hypocholesterolemia and acanthocytosis was clin…

ProbandAdultMaleAcanthocytosiSettore MED/09 - Medicina InternaApolipoprotein BPopulationDNA Mutational AnalysisBiologyHypobetalipoproteinemiasExonHumanseducationGeneGeneticseducation.field_of_studyHomozygoteIntronInfantCholesterol LDLAbetalipoproteinemiaIntronsAlternative SplicingHomozygous familial hypobetalipoproteinemiaCholesterolRNA splicingApolipoprotein B-100Mutationbiology.proteinlipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineApolipoprotein BMinigeneAtherosclerosis
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Mutations in MTP gene in abeta- and hypobeta-lipoproteinemia.

2005

Abstract Familial hypobetalipoproteinemia (FHBL) and abetalipoproteinemia (ABL) are inherited disorders of apolipoprotein B (apo B)-containing lipoproteins that result from mutations in apo B and microsomal triglyceride transfer protein (MTP) genes, respectively. Here we report three patients with severe deficiency of plasma low-density lipoprotein (LDL) and apo B. Two of them (probands F.A. and P.E.) had clinical and biochemical phenotype consistent with ABL. Proband F.A. was homozygous for a minute deletion/insertion (c.1228delCCCinsT) in exon 9 of MTP gene predicted to cause a truncated MTP protein of 412 amino acids. Proband P. E. was heterozygous for a mutation in intron 9 (IVS9-1G>A),…

ProbandApolipoprotein EAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BGenotypeDNA Mutational AnalysisGene mutationCompound heterozygosityHypobetalipoproteinemiasApo B genemedicineMissense mutationHumansGene mutationApo E genotypeGeneticsbiologyAbetalipoproteinemia; Hypobetalipoproteinemia; MTP gene; Apo B gene; Gene mutations; Apo E genotypeAbetalipoproteinemiamedicine.diseaseAbetalipoproteinemiaPedigreePhenotypeChild Preschoolbiology.proteinlipids (amino acids peptides and proteins)FemaleHypobetalipoproteinemiaMTP geneCardiology and Cardiovascular MedicineCarrier ProteinsHypobetalipoproteinemia
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New Lipid Modulating Drugs: The Role of Microsomal Transport Protein Inhibitors

2011

Microsomal triglyceride transfer protein (MTP) is involved in the synthesis of very low density lipoprotein in the liver. Its deficiency results in abetalipoproteinemia. MTP inhibitors target the assembly and secretion of apolipoprotein B-containing lipoproteins. These agents may potentially play a role, alone or in combination, in the treatment of hypercholesterolemia or hypertriglyceridemia. Clinical applications of MTP inhibitors initially focused primarily on high-dose monotherapy in order to produce substantial reductions in LDL-cholesterol levels but these proved to induce significant hepatic steatosis and transaminase elevations. However, likely orphan indications for MTP inhibitors,…

Very low-density lipoproteinApolipoprotein BHypercholesterolemiaFamilial hypercholesterolemiaLipoproteins VLDLPharmacologyMicrosomal triglyceride transfer proteinHyperlipoproteinemia Type IIchemistry.chemical_compoundMicrosomesDrug DiscoveryClinical endpointHumansMedicineApolipoproteins BHypertriglyceridemiaPharmacologybiologybusiness.industryCholesterolAbetalipoproteinemiamedicine.diseaseAbetalipoproteinemiaBiochemistrychemistryMTP-inhibitors lipids lipoproteins atherosclerosis cardiovascular prevention.biology.proteinlipids (amino acids peptides and proteins)SteatosisCarrier ProteinsbusinessCurrent Pharmaceutical Design
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Thioflavin T Promotes Aβ(1−40) Amyloid Fibrils Formation

2015

Fibrillogenesis of the small peptide Aβ(1-40) is considered to be the hallmark of Alzheimer's disease. Some evidence indicates small oligomers, rather than mature fibrils, as the key cytotoxic agents. The fluorescent dye Thioflavin T (ThT) is often used to detect amyloid deposits in both in vivo and in vitro experiments, and it is used to study kinetic measurements, under the fundamental hypothesis that this probe does not influence the aggregation processes. We report experimental data showing that ThT may promote the Aβ(1-40) peptide amyloid aggregation changing solvent-peptide interactions and stabilizing more ordered β-like conformation. This finding has a two-fold importance: It is a f…

chemistry.chemical_classificationAbeta(1-40)Amyloidthioflavin TP3 peptideNanotechnologyPeptideFibrillogenesisFibrilIn vitroSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)chemistry.chemical_compoundchemistryIn vivoBiophysicsGeneral Materials ScienceThioflavinfluorescencePhysical and Theoretical Chemistryfibrillation
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Genetics of familial hypobetalipoproteinemia

2007

Primary hypobetalipoproteinemias include three monogenic disorders: the relatively frequent codominant familial hypobetalipoproteinemia (FHBL), the rare recessive conditions abetalipoproteinemia (ABL) and chylomicron retention disease (CMRD). Approximately 50% of FHBL patients are carriers of mutations in the APOB gene, mostly causing the formation of truncated forms of ApoB. In some kindred, FHBL is linked to a locus on chromosome 3 (3p21), but the candidate gene is still unknown. Recently, a FHBL-like phenotype was observed in carriers of mutations of the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene causing loss-of-function of the encoded protein, a proprotein convertase tha…

hypobetalipoproteinemia; abetalipoproteinemia; Chylomicron retention diaseaseSettore MED/09 - Medicina InternaApolipoprotein BAssembly and secretion of ApoB-containing lipoproteinsApoB-containing lipoproteinsBiochemistryMicrosomal triglyceride transfer proteinabetalipoproteinemiaChylomicron retention diaseasemedicineFamilial hypobetalipoproteinemiaGeneticsbiologyPCSK9AbetalipoproteinemiahypobetalipoproteinemiaChylomicron retention diseasemedicine.diseaseProprotein convertaseAbetalipoproteinemiaLDL receptorbiology.proteinlipids (amino acids peptides and proteins)HypobetalipoproteinemiaAbetalipoproteinemia; ApoB-containing lipoproteins; Assembly and secretion of ApoB-containing lipoproteins; Chylomicron retention disease; Familial hypobetalipoproteinemiaChylomicron retention disease
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