Search results for "57"

showing 10 items of 4186 documents

Tetraspanin CD63 controls basolateral sorting of organic cation transporter 2 in renal proximal tubules.

2016

CD63 is a ubiquitously expressed member of the tetraspanin superfamily. Using a mating-based split-ubiquitin-yeast 2-hybrid system, pull-down experiments, total internal reflection fluorescence microscopy, Forster resonance energy transfer, and biotinylation assays, we found that CD63 interacts with human organic cation transporter 2 (hOCT2), which transports endogenous and exogenous substrates, such as neurotransmitters and drugs in several epithelial cells. CD63 overexpression affects cellular localization of hOCT2 expressed in human embryonic kidney (HEK)293 cells. Studies with CD63-knockout mice indicate that in renal proximal tubules, CD63 determines the insertion of the mouse ortholog…

0301 basic medicineOrganic Cation Transport ProteinsEndosomeEndosomesBiochemistryMadin Darby Canine Kidney CellsKidney Tubules Proximal03 medical and health sciencesMiceDogsTetraspaninGeneticsAnimalsHumansMolecular BiologyCellular localizationEpithelial polarityChemistryTetraspanin 30rab4 GTP-Binding ProteinsHEK 293 cellsCell MembraneOrganic Cation Transporter 2TransporterEpithelial CellsTransfectionCell biologyMice Inbred C57BLProtein Transport030104 developmental biologyHEK293 CellsMembrane proteinBiotechnologyProtein BindingFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Vitamin D and Its Analogues Decrease Amyloid-β (Aβ) Formation and Increase Aβ-Degradation

2017

Alzheimer’s disease (AD) is characterized by extracellular plaques in the brain, mainly consisting of amyloid-β (Aβ), as derived from sequential cleavage of the amyloid precursor protein. Epidemiological studies suggest a tight link between hypovitaminosis of the secosteroid vitamin D and AD. Besides decreased vitamin D level in AD patients, an effect of vitamin D on Aβ-homeostasis is discussed. However, the exact underlying mechanisms remain to be elucidated and nothing is known about the potential effect of vitamin D analogues. Here we systematically investigate the effect of vitamin D and therapeutically used analogues (maxacalcitol, calcipotriol, alfacalcidol, paricalcitol, doxercalcife…

0301 basic medicineParicalcitolPlaque Amyloidvitamin Damyloid precursor proteinlcsh:ChemistrySecosteroidMicechemistry.chemical_compound0302 clinical medicinevitamin D analoguesvitamin D; vitamin D analogues; amyloid precursor protein; amyloid-β; secretases; Aβ-degradationAmyloid precursor proteinlcsh:QH301-705.5CalcipotriolSpectroscopybiologysecretasesBrainAlfacalcidolVitaminsGeneral Medicine3. Good healthComputer Science ApplicationsFemalemedicine.drugmedicine.medical_specialtyAβ-degradationNicastrinamyloid-βArticleCatalysisInorganic Chemistry03 medical and health sciencesCell Line TumorInternal medicinemedicineVitamin D and neurologyAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyAmyloid beta-PeptidesOrganic ChemistryMice Inbred C57BL030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999chemistryProteolysisbiology.proteinAmyloid Precursor Protein SecretasesAmyloid precursor protein secretase030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Alterations in White Matter Network and Microstructural Integrity Differentiate Parkinson’s Disease Patients and Healthy Subjects

2019

Parkinson’s disease (PD) is a neurodegenerative disease, neuropathologically characterized by progressive loss of neurons in distinct brain areas. We hypothesize that quantifiable network alterations are caused by neurodegeneration. The primary motivation of this study was to assess the specific network alterations in PD patients that are distinct but appear in conjunction with physiological aging. 178 subjects (130 females) stratified into PD patients, young, middle-aged and elderly healthy controls (age- and sex-matched with PD patients), were analyzed using 3D-T1 magnetization-prepared rapid gradient-echo (MPRAGE) and diffusion weighted images acquired in 3T MRI scanner. Diffusion modeli…

0301 basic medicineParkinson's diseaseCognitive NeuroscienceSpleniumCorpus callosumcomputer.software_genrelcsh:RC321-571White matterdiffusion MRI03 medical and health sciences0302 clinical medicineVoxelMedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal Researchbusiness.industryagingmedicine.diseasenetwork connectivity analysis030104 developmental biologymedicine.anatomical_structureCorticospinal tractParkinson’s diseasebusinessNeuroscienceInsulacomputerwhite matter030217 neurology & neurosurgeryNeuroscienceDiffusion MRIFrontiers in Aging Neuroscience
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Acute Cortical Transhemispheric Diaschisis after Unilateral Traumatic Brain Injury

2017

Focal neocortical brain injuries lead to functional alterations, which can spread beyond lesion-neighboring brain areas. The undamaged hemisphere and its associated disturbances after a unilateral lesion, so-called transhemispheric diaschisis, have been progressively disclosed over the last decades; they are strongly involved in the pathophysiology and, potentially, recovery of brain injuries. Understanding the temporal dynamics of these transhemispheric functional changes is crucial to decipher the role of the undamaged cortex in the processes of functional reorganization at different stages post-lesion. In this regard, little is known about the acute-subacute processes after 24-48 h in th…

0301 basic medicinePatch-Clamp TechniquesTraumatic brain injurySomatosensory system03 medical and health sciences0302 clinical medicineCortex (anatomy)Unilateral lesionBrain Injuries TraumaticNeuroplasticitymedicineAnimalsDiaschisisNeuronal PlasticityMotor CortexElectroencephalographySomatosensory Cortexmedicine.diseaseMice Inbred C57BLDisease Models AnimalElectrophysiology030104 developmental biologymedicine.anatomical_structureBrain HemisphereNeurology (clinical)PsychologyNeuroscience030217 neurology & neurosurgeryJournal of Neurotrauma
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A longitudinal DTI and histological study of the spinal cord reveals early pathological alterations in G93A-SOD1 mouse model of amyotrophic lateral s…

2017

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective motor neuron degeneration in the motor cortex, brainstem and spinal cord. It is generally accepted that ALS is caused by death of motor neurons, however the exact temporal cascade of degenerative processes is not yet completely known. To identify the early pathological changes in spinal cord of G93A-SOD1 AIS mice we performed a comprehensive longitudinal analysis employing diffusion-tensor magnetic resonance imaging alongside histology and electron microscopy, in parallel with peripheral nerve histology. We showed the gradient of degeneration appearance in spinal cord white and gray matter, startin…

0301 basic medicinePathologyNeurologyTime FactorsMotor neuron diseasesSensory Receptor CellMice0302 clinical medicineImage Processing Computer-AssistedAxonAmyotrophic lateral sclerosisGray MatterAnthracenesWhite MatterMitochondriamedicine.anatomical_structureDiffusion Tensor ImagingNeurologySpinal CordG93A-SOD1 miceBrainstemHumanMotor cortexmedicine.medical_specialtyAxon degenerationTime FactorSensory Receptor CellsSOD1Mice TransgenicWhite matter03 medical and health sciencesMagnetic resonance imagingDevelopmental NeuroscienceMicroscopy Electron TransmissionmedicineElectron microscopyAnimalsHumansMotor neuron diseaseAmyotrophic lateral sclerosiAnimalbusiness.industrySuperoxide DismutaseAmyotrophic Lateral SclerosisSpinal cordmedicine.diseaseAmyotrophic lateral sclerosisMice Inbred C57BLDisease Models Animal030104 developmental biologyAnthracenebusinessNeuroscience030217 neurology & neurosurgeryExperimental neurology
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Increased liver carcinogenesis and enrichment of stem cell properties in livers of Dickkopf 2 (Dkk2) deleted mice.

2013

// Thorsten Maass 1 , Jens Marquardt 2 , Ju-Seog Lee 3 , Markus Krupp 4 , Peter Scholz-Kreisel 2 , Carolin Mogler 5 , Peter Schirmacher 5 , Martina Muller 1 , Heiner Westphal 6 , Peter R. Galle 2 , Andreas Teufel 1 1 Department of Internal Medicine I, University of Regensburg, Regensburg, Germany 2 I. Department of Medicine, University Medical Center Mainz, Mainz, Germany 3 Cancer Biology Program, MD Anderson Cancer Center, Houston, TX, USA 4 Department of Informatics, Johannes Gutenberg University Mainz, Mainz, Germany 5 Institute of Pathology, University of Heidelberg, Heidelberg, Germany 6 Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Develop…

0301 basic medicinePathologymedicine.medical_specialtyCarcinogenesisBiologymedicine.disease_causeTranscriptome03 medical and health sciencesMicestem cellsmedicineAtypiaAnimalsHumansGene Regulatory Networksprognostic signatureGeneWnt Signaling PathwayMice Knockouttranscriptomics profilingLiver CarcinogenesisDkk2Liver NeoplasmsGastroenterologyWnt signaling pathwaymedicine.diseaseMolecular biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureOncologyHepatocyteCancer researchNeoplastic Stem CellsIntercellular Signaling Peptides and ProteinsStem cellLiver cancerCarcinogenesisgenetic signatureResearch PaperOncotarget
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The quality of cortical network function recovery depends on localization and degree of axonal demyelination

2016

AbstractMyelin loss is a severe pathological hallmark common to a number of neurodegenerative diseases, including multiple sclerosis (MS). Demyelination in the central nervous system appears in the form of lesions affecting both white and gray matter structures. The functional consequences of demyelination on neuronal network and brain function are not well understood. Current therapeutic strategies for ameliorating the course of such diseases usually focus on promoting remyelination, but the effectiveness of these approaches strongly depends on the timing in relation to the disease state. In this study, we sought to characterize the time course of sensory and behavioral alterations induced…

0301 basic medicinePathologymedicine.medical_specialtyImmunologyCentral nervous systemSensationMedizinSensory systemBiologyAdaptive ImmunityWhite matter03 medical and health sciencesBehavioral NeuroscienceCuprizoneMice0302 clinical medicineWhite matter lesionmedicineBiological neural networkAnimalsRemyelinationGray MatterPathologicalMyelin SheathCerebral CortexBehavior AnimalEndocrine and Autonomic SystemsMultiple sclerosisLysophosphatidylcholinesThalamocortical systemRecovery of Functionmedicine.diseaseWhite MatterElectrodes ImplantedMice Inbred C57BLGray matter lesion030104 developmental biologymedicine.anatomical_structureRemyelinationDemyelinationTonotopyNerve NetNeuroscience030217 neurology & neurosurgeryDemyelinating Diseases
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NF1 microdeletion syndrome: case report of two new patients

2019

Abstract Background 17q11.2 microdeletions, which include the neurofibromatosis type 1 (NF1) gene region, are responsible for the NF1 microdeletion syndrome, observed in 4.2% of all NF1 patients. Large deletions of the NF1 gene and its flanking regions are associated with a more severe NF1 phenotype than the NF1 general population. Case presentation We hereby describe the clinical and molecular features of two girls (aged 2 and 4 years, respectively), with non-mosaic atypical deletions. Patient 1 showed fifteen café-au-lait spots and axillary freckling, as well as a Lisch nodule in the left eye, strabismus, high-arched palate, malocclusion, severe kyphoscoliosis, bilateral calcaneovalgus fo…

0301 basic medicinePathologymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesGenotype-phenotype correlationNeurofibromatosesLisch noduleContiguous gene syndromePopulationCase ReportContiguous gene syndromeChromosomesCraniofacial Abnormalities03 medical and health sciences0302 clinical medicineAtypical deletionIntellectual DisabilitymedicineHumansMultiplex ligation-dependent probe amplificationNeurofibromatosiseducationChildPreschoolNeurofibromatoseseducation.field_of_studybusiness.industryLearning DisabilitiesPair 17lcsh:RJ1-570Axillary frecklinglcsh:Pediatricsmedicine.diseaseeye diseasesMLPA030104 developmental biologyNF1 geneChild PreschoolFemalemedicine.symptomChromosome DeletionbusinessAtypical deletion; Contiguous gene syndrome; Genotype-phenotype correlation; MLPA; NF1 gene; Child Preschool; Chromosome Deletion; Chromosomes Human Pair 17; Craniofacial Abnormalities; Female; Humans; Intellectual Disability; Learning Disabilities; Neurofibromatoses030217 neurology & neurosurgeryChromosomes Human Pair 17Comparative genomic hybridizationHumanItalian Journal of Pediatrics
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Disturbed Glucose Metabolism in Rat Neurons Exposed to Cerebrospinal Fluid Obtained from Multiple Sclerosis Subjects

2017

Axonal damage is widely accepted as a major cause of permanent functional disability in Multiple Sclerosis (MS). In relapsing-remitting MS, there is a possibility of remyelination by myelin producing cells and restoration of neurological function. The purpose of this study was to delineate the pathophysiological mechanisms underpinning axonal injury through hitherto unknown factors present in cerebrospinal fluid (CSF) that may regulate axonal damage, remyelinate the axon and make functional recovery possible. We employed primary cultures of rat unmyelinated cerebellar granule neurons and treated them with CSF obtained from MS and Neuromyelitis optica (NMO) patients. We performed microarray …

0301 basic medicinePathologymedicine.medical_specialtyglucose metabolismneuromyelitis opticaBiologymultiple sclerosisArticlecerebrospinal fluidlcsh:RC321-57103 medical and health sciencesMyelin0302 clinical medicineCerebrospinal fluidDownregulation and upregulationGene expressionmedicineRemyelinationAxonlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymultiple sclerosis; glucose metabolism; neuromyelitis optica; cerebrospinal fluid; gene expressionNeuromyelitis opticaGeneral NeuroscienceMultiple sclerosismedicine.disease030104 developmental biologymedicine.anatomical_structurenervous systemgene expression030217 neurology & neurosurgery
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Lymphatic Endothelial Cells Control Initiation of Lymph Node Organogenesis

2017

Lymph nodes (LNs) are strategically situated throughout the body at junctures of the blood vascular and lymphatic systems to direct immune responses against antigens draining from peripheral tissues. The current paradigm describes LN development as a programmed process that is governed through the interaction between mesenchymal lymphoid tissue organizer (LTo) cells and hematopoietic lymphoid tissue inducer (LTi) cells. Using cell-type-specific ablation of key molecules involved in lymphoid organogenesis, we found that initiation of LN development is dependent on LTi-cell-mediated activation of lymphatic endothelial cells (LECs) and that engagement of mesenchymal stromal cells is a succeedi…

0301 basic medicinePathologymedicine.medical_specialtygovernment.form_of_governmentOrganogenesis[SDV]Life Sciences [q-bio]Immunology610 Medicine & healthMice TransgenicBiologyChoristoma10263 Institute of Experimental Immunology03 medical and health sciencesMiceImmune systemLymphotoxin beta ReceptormedicineLymph node stromal cellImmunology and AllergyAnimalsLymph nodeCells CulturedComputingMilieux_MISCELLANEOUS2403 ImmunologyReceptor Activator of Nuclear Factor-kappa BMesenchymal stem cellNF-kappa BEndothelial CellsCell DifferentiationMesenchymal Stem Cells2725 Infectious DiseasesEmbryo MammalianCell biologyMice Inbred C57BLHaematopoiesisLymphatic EndotheliumReceptors Lysosphingolipid030104 developmental biologyInfectious Diseasesmedicine.anatomical_structureLymphatic system2723 Immunology and Allergygovernment570 Life sciences; biology[SDV.IMM]Life Sciences [q-bio]/ImmunologyLymphLymph NodesSignal Transduction
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