Search results for "FRAGMENTS"

showing 10 items of 422 documents

Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

2017

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches. Here, we report that hAPP-transgenic models of …

0301 basic medicineGenetically modified mouseMaleMurine amyloid-betaBACE1-ASMice TransgenicPlaque Amyloidlcsh:RC346-429Pathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein Precursor0302 clinical medicineMeningesAmyloid precursor proteinMedicineAnimalsHumansTransgenic miceSenile plaqueslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-Peptidesbiologybusiness.industryAmyloidosisResearchP3 peptideBrainAmyloidosismedicine.diseasePeptide FragmentsBiochemistry of Alzheimer's diseaseAstrogliosisCell biologyMice Inbred C57BL030104 developmental biologyCaspasesAmyloid precursor proteinMutationbiology.proteinAbetaFemaleNeurology (clinical)businessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgery
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sgp120 and the contact system in hereditary angioedema: A diagnostic tool in HAE with normal C1 inhibitor

2020

Mutations in Factor XII, plasminogen gene, angiopoietin-1 gene and kininogen 1 gene have been found in some patients with hereditary angioedema with normal C1 inhibitor (HAE-nl-C1inh), but the underlying disease mechanisms remain unclear. Additionally, there are no accepted biomarkers for this disease. Because the contact system has been implicated in hereditary angioedema with C1 inhibitor deficiency (HAE-C1inh), we studied the fragmentation patterns of serum glycoprotein 120 (sgp120), a protein that is highly susceptible to cleavage by kallikrein, in 31 HAE-C1inh and 13 HAE-nl-C1inh patient plasma samples. Compared to normal controls, the majority of plasma samples from patients with HAE-…

0301 basic medicineImmunologyProteinase Inhibitory Proteins SecretoryCleavage (embryo)C1-inhibitor03 medical and health sciences0302 clinical medicinemedicineHumansKaolinComplement ActivationMolecular BiologyGenechemistry.chemical_classificationChromatographyFactor XIIbiologyChemistryAngioedemas HereditaryPlasminogenKallikreinmedicine.diseaseMolecular biologyBlood Coagulation FactorsPeptide Fragments030104 developmental biologyFactor XIIProteolysisHereditary angioedemabiology.proteinBiomarker (medicine)KallikreinsGlycoproteinComplement C1 Inhibitor ProteinPlasticsBiomarkers030215 immunologyMolecular Immunology
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In Situ, Light-Guided Axon Growth on Biomaterials via Photoactivatable Laminin Peptidomimetic IK(HANBP)VAV

2018

The ability to guide the growth of neurites is relevant for reconstructing neural networks and for nerve tissue regeneration. Here, a biofunctional hydrogel that allows light-based directional control of axon growth in situ is presented. The gel is covalently modified with a photoactivatable derivative of the short laminin peptidomimetic IKVAV. This adhesive peptide contains the photoremovable group 2-(4′-amino-4-nitro-[1,1′-biphenyl]-3-yl)propan-1-ol (HANBP) on the Lys rest that inhibits its activity. The modified peptide is highly soluble in water and can be simply conjugated to -COOH containing hydrogels via its terminal -NH 2 group. Light exposure allows presentation of the IKVAV adhesi…

0301 basic medicineIn situMaterials scienceNeuritePeptidomimeticNeuronal OutgrowthPeptideINGENIERÍAS Y TECNOLOGÍAS02 engineering and technologyBiotecnología Industrial03 medical and health sciencesMiceCoated Materials BiocompatibleNeural Stem CellsDIRECTIONAL NEURONAL GROWTHLamininIKVAVNeuritesAnimalsGeneral Materials Sciencechemistry.chemical_classificationbiologyPHOTO-TRIGGERED CELL ADHESIONBioproductos Biomateriales Bioplásticos Biocombustibles Bioderivados etc.Hydrogels021001 nanoscience & nanotechnologyNeural stem cellPeptide FragmentsLAMININ PEPTIDOMIMETICS030104 developmental biologychemistryCell cultureSelf-healing hydrogelsbiology.proteinBiophysicsLamininPeptidomimetics0210 nano-technologyACS Applied Materials & Interfaces
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3d collagen hydrogel promotes in vitro langerhans islets vascularization through ad-mvfs angiogenic activity

2021

Adipose derived microvascular fragments (ad-MVFs) consist of effective vascularization units able to reassemble into efficient microvascular networks. Because of their content in stem cells and related angiogenic activity, ad-MVFs represent an interesting tool for applications in regenerative medicine. Here we show that gentle dissociation of rat adipose tissue provides a mixture of ad-MVFs with a length distribution ranging from 33–955 μm that are able to maintain their original morphology. The isolated units of ad-MVFs that resulted were able to activate transcriptional switching toward angiogenesis, forming tubes, branches, and entire capillary networks when cultured in 3D collagen type-…

0301 basic medicineMMP2QH301-705.5Angiogenesis0206 medical engineeringMedicine (miscellaneous)Adipose tissue3D coculture02 engineering and technologyRegenerative medicineGeneral Biochemistry Genetics and Molecular BiologyArticleExtracellular matrix03 medical and health sciencesmedicineBiology (General)Islet of LangerhansTransplantationChemistry020601 biomedical engineeringCell biologyTransplantationMicrovascular fragments030104 developmental biologymedicine.anatomical_structureBasal laminaAngiogenesisStem cell3D coculture; Angiogenesis; Islet of Langerhans; Microvascular fragments; Transplantation
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The concerted amyloid-beta clearance of LRP1 and ABCB1/P-gp across the blood-brain barrier is linked by PICALM

2018

The accumulation of neurotoxic amyloid-beta (Aβ) in the brain is a characteristic hallmark of Alzheimer's disease (AD). The blood-brain barrier (BBB) provides a large surface area and has been shown to be an important mediator for removal of brain Aβ. Both, the ABC transporter P-glycoprotein (ABCB1/P-gp) and the receptor low-density lipoprotein receptor-related protein 1 (LRP1) have been implicated to play crucial roles in Aβ efflux from brain. Here, with immunoprecipitation experiments, co-immunostainings and dual inhibition of ABCB1/P-gp and LRP1, we show that both proteins are functionally linked, mediating a concerted transcytosis of Aβ through endothelial cells. Late-onset AD risk fact…

0301 basic medicineMaleAmyloid betaSwineImmunologyPrimary Cell CultureATP-binding cassette transporterBlood–brain barrierClathrinArticlePICALM03 medical and health sciencesBehavioral NeuroscienceMice0302 clinical medicineAlzheimer DiseasemedicineAnimalsATP Binding Cassette Transporter Subfamily B Member 1Mice KnockoutAmyloid beta-PeptidesbiologyEndocrine and Autonomic SystemsChemistryTumor Suppressor ProteinsPhosphatidylinositol bindingBrainEndothelial CellsLRP1Peptide FragmentsCell biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureTranscytosisReceptors LDLBlood-Brain BarrierMonomeric Clathrin Assembly Proteinsbiology.proteinTranscytosis030217 neurology & neurosurgeryLow Density Lipoprotein Receptor-Related Protein-1Brain, Behavior, and Immunity
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Muscle and serum metabolomes are dysregulated in colon-26 tumor-bearing mice despite amelioration of cachexia with activin receptor type 2B ligand bl…

2019

Cancer-associated cachexia reduces survival, which has been attenuated by blocking the activin receptor type 2B (ACVR2B) ligands in mice. The purpose of this study was to unravel the underlying physiology and novel cachexia biomarkers by use of the colon-26 (C26) carcinoma model of cancer cachexia. Male BALB/c mice were subcutaneously inoculated with C26 cancer cells or vehicle control. Tumor-bearing mice were treated with vehicle (C26+PBS) or soluble ACVR2B either before (C26+sACVR/b) or before and after (C26+sACVR/c) tumor formation. Skeletal muscle and serum metabolomics analysis was conducted by gas chromatography-mass spectrometry. Cancer altered various biologically functional groups …

0301 basic medicineMaleCachexiaPhysiologyEndocrinology Diabetes and MetabolismActivin Receptors Type IIlihaksetMyostatinMice0302 clinical medicineAmino Acidsta315Activin Receptor Type-2BbiologyOrganophosphatesRecombinant Proteins3. Good healthmedicine.anatomical_structureribosome030220 oncology & carcinogenesismyostatinColonic NeoplasmsMetabolomesyöpätauditC26Metabolic Networks and Pathwaysmedicine.medical_specialtyPhenylalanineCachexia03 medical and health sciencesribosomitPhysiology (medical)Internal medicineCell Line TumormedicineAnimalsskeletal muscleMuscle SkeletalPI3K/AKT/mTOR pathwaybusiness.industrySkeletal muscleCancermedicine.diseaseta3122BlockadeImmunoglobulin Fc Fragments030104 developmental biologyEndocrinologyProtein Biosynthesisbiology.proteinaineenvaihduntatuotteetPyrimidine NucleotidesproteiinitbusinesslihassurkastumasairaudetACVR2BAmerican journal of physiology. Endocrinology and metabolism
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Antibody–Fc/FcR Interaction on Macrophages as a Mechanism for Hyperprogressive Disease in Non–small Cell Lung Cancer Subsequent to PD-1/PD-L1 Blockade

2019

Abstract Purpose: Hyperprogression (HP), a paradoxical boost in tumor growth, was described in a subset of patients treated with immune checkpoint inhibitors (ICI). Neither clinicopathologic features nor biological mechanisms associated with HP have been identified. Experimental Design: Among 187 patients with non–small cell lung cancer (NSCLC) treated with ICI at our institute, cases with HP were identified according to clinical and radiologic criteria. Baseline histologic samples from patients treated with ICI were evaluated by IHC for myeloid and lymphoid markers. T-cell–deficient mice, injected with human lung cancer cells and patient-derived xenografts (PDX) belonging to specific mutat…

0301 basic medicineMaleCancer ResearchMyeloidLung NeoplasmsCD33Programmed Cell Death 1 ReceptorFc receptorMice NudeMice SCIDReceptors Fcnon-small cell lung cancer Hyperprogression immune checkpoint inhibitors.B7-H1 AntigenArticle03 medical and health sciences0302 clinical medicineImmunophenotypingAntineoplastic Agents ImmunologicalPD-L1Carcinoma Non-Small-Cell LungCell Line TumormedicineAnimalsHumansLung cancerAntibodies Blockingbiologybusiness.industryMacrophagesmedicine.diseaseXenograft Model Antitumor Assays3. Good healthImmunoglobulin Fc FragmentsTumor Burden030104 developmental biologymedicine.anatomical_structureNivolumabOncology030220 oncology & carcinogenesisbiology.proteinCancer researchImmunohistochemistryFemaleAntibodybusinessClinical Cancer Research
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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Diagnostic accuracy of cerebrospinal fluid biomarkers measured by chemiluminescent enzyme immunoassay for Alzheimer disease diagnosis.

2020

In the last decades, an important role of cerebrospinal fluid (CSF) biomarkers for Alzheimer disease (AD) diagnosis has emerged. The evaluation of the triad consisting of 42 aminoacid-long amyloid-beta peptide (Aβ42), total Tau (tTau) and Tau phosphorylated at threonine 181 (pTau) have been recently integrated into the research diagnostic criteria of AD. For a long time, the enzyme-linked immunosorbent assay (ELISA) has represented the most commonly used method for the measurement of CSF biomarkers levels. This study aimed to assess the diagnostic accuracy of CSF biomarkers, namely Aβ42, tTau and pTau and their ratio, measured by fully automated CLEIA assay (Lumipulse). We included 96 patie…

0301 basic medicineMalePathologymedicine.medical_specialtyAmyloidClinical Biochemistrychemiluminescent enzyme immunoassay methodCSF biomarkerDiagnostic accuracyEnzyme-Linked Immunosorbent Assaytau Proteinslaw.invention03 medical and health sciences0302 clinical medicineCerebrospinal fluidliquorlawAlzheimer DiseasemedicineHumansPhosphorylationChemiluminescenceAgedchemistry.chemical_classificationAutomation LaboratoryAmyloid beta-Peptidesmedicine.diagnostic_testbusiness.industryGeneral MedicineCLEIAMiddle Agedmedicine.diseasePeptide Fragments030104 developmental biologyEnzymechemistryROC CurveImmunoassayArea Under CurveCase-Control StudiesCsf biomarkersLuminescent MeasurementsFemaleAlzheimer's diseasebusiness030217 neurology & neurosurgeryBiomarkersScandinavian journal of clinical and laboratory investigation
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Mast cells are associated with the onset and progression of celiac disease

2017

Background Celiac disease (CD) is an immune-mediated disorder characterized by an accumulation of immune cells in the duodenal mucosa as a consequence of both adaptive and innate immune responses to undigested gliadin peptides. Mast cells (MCs) are innate immune cells that are a major source of costimulatory signals and inflammatory mediators in the intestinal mucosa. Although MCs have previously been associated with CD, functional studies have never been performed. Objective We aimed at evaluating the role of MCs in the pathogenesis of CD. Methods Intestinal biopsy specimens of patients with CD were scored according to the Marsh classification and characterized for leukocyte infiltration a…

0301 basic medicineMaleSettore MED/09 - Medicina InternaImmunologygliadin immunologyFluorescent Antibody TechniqueBiologyCell DegranulationGliadinProinflammatory cytokinePathogenesis03 medical and health sciencesMice0302 clinical medicineImmune systemIntestinal mucosamedicineImmunology and AllergyAnimalsHumansCeliac diseaseMast CellsIntestinal Mucosap31-43 fragmentToll-like receptorInnate immune systemCeliac disease; gliadin immunology; mast cell; p31-43 fragment; mast cellFOXP3Mast cellImmunohistochemistryhumanitiesPeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisImmunologyDisease ProgressionFemalemast cell
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