Search results for "APOB"

showing 10 items of 32 documents

Frailty syndrome in community care – tips for patients and caregivers

2017

Zespół słabości (ZS) jest dynamicznym stanem charakteryzującym się zmniejszeniem fizjologicznych rezerw organizmu, osłabieniem odporności na czynniki stresogenne oraz zaburzeniami funkcjonowania układów ciała. W ZS dochodzi do zmniejszenia masy ciała i siły mięśniowej, problemów z poruszaniem się, utrzymaniem równowagi oraz do zmniejszenia aktywności fizycznej. Wyróżniamy trzy stadia zespołu słabości: wczesny ZS (pre- -frail), zespół słabości (frail) oraz powikłania zespołu słabości. Głównym czynnikiem ryzyka wystąpienia ZS jest wiek podeszły, ale znaczenie mają również czynniki genetyczne, środowiskowe, styl życia oraz choroby współistniejące. Do rozpoznania ZS stosuje się m.in. skalę Frie…

Gerontologycaregiversmedicine.medical_specialtyleczenietreatmentbusiness.industryzapobieganieFrailty syndromefrailtydiagnostykamedicine.diseaseopiekunowiepreventionEpidemiologydiagnosticsMedicineepidemiologyzespół słabościepidemiologiabusinessHIGHER SCHOOL’S PULSE
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Distinct immune evasion in APOBEC ‐enriched, HPV ‐negative HNSCC

2020

Immune checkpoint inhibition leads to response in some patients with head and neck squamous cell carcinoma (HNSCC). Robust biomarkers are lacking to date. We analyzed viral status, gene expression signatures, mutational load and mutational signatures in whole exome and RNA-sequencing data of the HNSCC TCGA dataset (n = 496) and a validation set (DKTK MASTER cohort, n = 10). Public single-cell gene expression data from 17 HPV-negative HNSCC were separately reanalyzed. APOBEC3-associated TCW motif mutations but not total single nucleotide variant burden were significantly associated with inflammation. This association was restricted to HPV-negative HNSCC samples. An APOBEC-enriched, HPV-negat…

MaleAPOBECCancer ResearchT-Lymphocytesmedicine.medical_treatment610BiologyCohort Studies03 medical and health sciences0302 clinical medicineGene expressionBiomarkers TumormedicineHumansExomeAPOBEC Deaminasestumor inflammationPapillomaviridaeExomeGeneImmune EvasionInflammationSequence Analysis RNASquamous Cell Carcinoma of Head and NeckPapillomavirus InfectionsAPOBECmutational signatureImmunotherapyMiddle Agedmedicine.diseaseHead and neck squamous-cell carcinomaPhenotypeImmune checkpointddc:Gene Expression Regulation Neoplasticstomatognathic diseasesOncologyHead and Neck Neoplasms030220 oncology & carcinogenesisMutationCancer researchimmune checkpoint inhibitionFemalehead and neck cancerTranscriptome600 Technik Medizin angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und GesundheitInternational Journal of Cancer
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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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Next-generation-sequencing-based identification of familial hypercholesterolemia-related mutations in subjects with increased LDL–C levels in a latvi…

2015

Background Familial hypercholesterolemia (FH) is one of the commonest monogenic disorders, predominantly inherited as an autosomal dominant trait. When untreated, it results in early coronary heart disease. The vast majority of FH remains undiagnosed in Latvia. The identification and early treatment of affected individuals remain a challenge worldwide. Most cases of FH are caused by mutations in one of four genes, APOB, LDLR, PCSK9, or LDLRAP1. The spectrum of disease-causing variants is very diverse and the variation detection panels usually used in its diagnosis cover only a minority of the disease-causing gene variants. However, DNA-based tests may provide an FH diagnosis for FH patients…

MaleNonsynonymous substitutionApolipoprotein BCoronary Artery DiseaseFamilial hypercholesterolemiaDiseaseCohort StudiesPCSK9Genetics(clinical)Family historyGenetics (clinical)Aged 80 and overGeneticseducation.field_of_studybiologySerine EndopeptidasesHigh-Throughput Nucleotide SequencingAutosomal dominant traitMiddle AgedLDLRAP1Apolipoprotein B-100Femalelipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9APOBResearch ArticleAdultPopulationPolymorphism Single NucleotideLDLHyperlipoproteinemia Type IIYoung AdultGeneticsmedicineHumanseducationAdaptor Proteins Signal TransducingAgedDiagnostic toolsPCSK9Cholesterol LDLmedicine.diseaseLatviaGenetics PopulationLDLRReceptors LDLMutationNext-generation sequencingbiology.proteinBMC Medical Genetics
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Effects of fluvastatin slow-release (XL 80 mg) versus simvastatin (20 mg) on the lipid triad in patients with type 2 diabetes.

2005

The lipid triad is the association of small, dense (sd) low-density lipoprotein (LDL), low high-density lipoprotein (HDL), and hypertriglyceridemia, all of which play a role in coronary artery disease in patients with type 2 diabetes. Although statins have demonstrated clear positive effects on cardiovascular morbidity/mortality in patients with diabetes and on single components of the lipid triad, it remains controversial whether they affect all components of the triad in these patients. Therefore, we performed a single-center, parallel-group, prospective, randomized, open-label, blinded-endpoint (PROBE)-type comparison of fluvastatin extended-release (XL) 80 mg (n=48) and simvastatin 20 m…

Malemedicine.medical_specialtySimvastatinIndolesHDLApolipoprotein BSmall dense LDLType 2 diabetesTriglycerideLDLFatty Acids MonounsaturatedFluvastatin XLInternal medicineDiabetes mellitusType 2 diabetes mellitusmedicineHumansPharmacology (medical)Prospective StudiesFluvastatinAgedHypertriglyceridemiabiologybusiness.industryAnticholesteremic AgentsApoA-IHypertriglyceridemianutritional and metabolic diseasesType 2 Diabetes MellitusGeneral MedicineMiddle Agedmedicine.diseaseLipoproteins LDLEndocrinologyDiabetes Mellitus Type 2SimvastatinDelayed-Action Preparationsbiology.proteinlipids (amino acids peptides and proteins)FemaleApoBbusinessLipoproteins HDLFluvastatinmedicine.drugLipoproteinAdvances in therapy
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Iedzimtu hiperholesterinēmiju izraisošo mutāciju noskaidrošana Latvijas populācijā

2015

Iedzimta hiperholesterinēmija (IH) ir nopietna ģenētiskā slimība, kurai raksturīgs paaugstināts zema blīvuma lipoproteīnu holesterīna daudzums asinīs. IH ir riska faktors sirds-asinsvadu slimībām. Šīs slimības cēlonis visbiežāk ir mutācijas četros gēnos – LDLR, APOB, PCSK9 un LDLRAP1. Darba mērķis bija noskaidrot IH fenotipu izraisošās mutācijas četros gēnos Latvijas populācijā, izmantojot liela apjoma paralēlās sekvenēšanas metodi. Darbā tika analizētas mutācijas 98 pacientos, kuriem ir aizdomas par IH. Ģenētisko variāciju noteikšanai tika izmantota jaunās paaudzes pusvadītāja sekvenēšanas metode. Rezultātā tika atrastas 97 dažādas nomaiņas, vairums no kurām ir APOB un LDLR gēnos, bet vism…

PCSK9LDLRIedzimta hiperholesterinēmijapusvadītāja sekvenēšanaBioloģijaAPOB
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Evaluation Of Massive Parallel Sequencing As A Diagnostic Tool For Familial Hypercholesterolemia

2015

Abstract Familial hypercholesterolemia (FH) is one of the most common single gene disorders, which is mostly inherited as an autosomal dominant trait. The physical signs of FH are elevated low density lipoprotein cholesterol (LDL-C), elevated total cholesterol (TC) levels and tendon xantomas. Identification and early treatment of affected individuals is desirable and in lack of physical symptoms DNA-based diagnosis provides confirmation of diagnosis and enables early patient management. The majority of FH cases are caused by mutations in four genes (APOB, LADLR, PCSK9, and LDLRAP1). There are commercial kits available for testing of the 20 most common FH causing mutations, but the spectrum …

Pediatricsmedicine.medical_specialtyldlrApolipoprotein Bldlrap1ScienceLow density lipoprotein cholesterolFamilial hypercholesterolemiachemistry.chemical_compoundngsmedicinepcsk9MultidisciplinaryMassive parallel sequencingfamilial hypercholesterolemiabiologyCholesterolPCSK9QAutosomal dominant traitmedicine.diseasechemistryapobLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.
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The production of 85 kDa N-terminal fragment of apolipoprotein B in mutant HepG2 cells generated by targeted modification of apoB gene occurs by ALLN…

2010

Abstract To study the mechanism of low levels of full length and truncated apoB in individuals heterozygous for apoB truncation, a non-sense mutation was introduced in one of the three alleles of apob gene of HepG2 cells by homologous recombination. Despite very low levels of apoB-82 (1–2%) in the media, a prominent N-terminal apoB protein of 85 kDa (apoB-15) was secreted that fractionated at d > 1.065 in density gradient ultracentrifugation. The mechanism of production of this short protein was studied by 35S-methionine pulse–chase experiment. Oleate prevented presecretory degradation of apoB-100 in the cell and resulted in increased secretion of newly synthesized apoB-100 with decreases i…

Protein FoldingHepG2Apolipoprotein BLeupeptinsmedicine.medical_treatmentMutantBiophysicsBiologyCysteine Proteinase Inhibitorsdigestive systemBiochemistry85 kDa N-terminalCysteine ProteasesapoBmedicineHumansSecretionMolecular BiologyApolipoproteins BProteasenutritional and metabolic diseasesCell BiologyHep G2 CellsCysteine proteaseMolecular biologyTransmembrane proteinProtein TransportCodon NonsenseHypobetalipoproteinemia Familial Apolipoprotein Bbiology.proteinlipids (amino acids peptides and proteins)Density gradient ultracentrifugationIntracellular
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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Liraglutide reduces postprandial hyperlipidaemia by increasing apoB48 catabolism and by reducing apoB48 production

2016

IF 6.080; International audience

[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismliraglutideapoB48Diabetic dyslipidemiaPostprandial hyperlipidemiaGLP1 agonist[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism
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