Search results for "GRP"

showing 10 items of 32 documents

Thermal NDE of thick GRP panels by means of a Pulse Modulated Lock-In Thermography technique

2010

This work describes the development and implementation of an infrared thermal NDE procedure for the evaluation of subsurface defects. The approach is called Pulse-Modulated Lock-In Thermography (PMLT) and is based on the analysis of the frequency response of the measured temperature and comparison with the carrier frequencies launched by the external heat delivering source. The heat deposited on the object is in particular modulated as a train of square waves. This is easily achieved by periodically shuttering the heat source. The temperature is then sampled throughout the deposition of a few square waves. A lock-in algorithm is then implemented able to selectively filter out components at …

Frequency responseEngineeringbusiness.industryAcousticsPhysicsQC1-999Phase (waves)Filter (signal processing)Square waveSignalSettore ING-IND/14 - Progettazione Meccanica E Costruzione Di MacchineInfrared NDT Lock-In thermography GRP compositesNondestructive testingThermographyThermalElectronic engineeringbusiness
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GRP78 POLYMORPHISM rs430397 IS ASSOCIATED WITH HEPATOCELLULAR CARCINOMA IN A SOUTHERN ITALIAN POPULATION

2014

GRP78 POLYMORPHISM HEPATOCELLULAR CARCINOMA ITALIAN POPULATION
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Hypoxia Positively Regulates the Expression of pH-Sensing G-Protein–Coupled Receptor OGR1 (GPR68)

2016

Background & Aims: A novel family of proton-sensing G-proteinâcoupled receptors, including ovarian cancer G-proteinâcoupled receptor 1 (OGR1) (GPR68) has been identified to play a role in pH homeostasis. Hypoxia is known to change tissue pH as a result of anaerobic glucose metabolism through the stabilization of hypoxia-inducible factor-1α. We investigated how hypoxia regulates the expression of OGR1 in the intestinal mucosa and associated cells. Methods: OGR1 expression in murine tumors, human colonic tissue, and myeloid cells was determined by quantitative reverse-transcription polymerase chain reaction. The influence of hypoxia on OGR1 expression was studied in monocytes/macrophages and…

WT wild type0301 basic medicineMM6 MonoMac 6HV healthy volunteerSPARC secreted protein acidic and rich in cysteineNF-κB nuclear factor-κBInflammationBiologyIEC intestinal epithelial cell03 medical and health sciencesIntestinal mucosaTDAG8Ovarian Cancer G-Protein–Coupled ReceptormedicineOGR1 ovarian cancer G-protein–coupled receptor 1 (GPR68)IFN interferonlcsh:RC799-869ReceptorOriginal ResearchTh T-helperInflammationTNF tumor necrosis factorIBD inflammatory bowel diseaseHepatologyRT-qPCR quantitative reverse-transcription polymerase chain reactionAICAR 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranosideTDAG8 T-cell death-associated gene 8 (GPR65)Inflammatory Bowel DiseaseGRP65GastroenterologyHypoxia (medical)Molecular biologyGPR G-protein–coupled receptormRNA messenger RNAIL interleukinChIP chromatin immunoprecipitationHIF hypoxia-inducible factorUC ulcerative colitis030104 developmental biologyHypoxia-inducible factorsCancer researchCD Crohn's diseaselcsh:Diseases of the digestive system. GastroenterologyTumor necrosis factor alphaFCS fetal calf serummedicine.symptomChromatin immunoprecipitationHomeostasisCellular and Molecular Gastroenterology and Hepatology
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The GRP94 Inhibitor PU-WS13 Decreases M2-like Macrophages in Murine TNBC Tumors: A Pharmaco-Imaging Study with 99mTc-Tilmanocept SPECT

2021

Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancers and is not eligible for hormone and anti-HER2 therapies. Identifying therapeutic targets and associated biomarkers in TNBC is a clinical challenge to improve patients’ outcome and management. High infiltration of CD206+ M2-like macrophages in the tumor microenvironment (TME) indicates poor prognosis and survival in TNBC patients. As we previously showed that membrane expression of GRP94, an endoplasmic reticulum chaperone, was associated with the anti-inflammatory profile of human PBMC-derived M2 macrophages, we hypothesized that intra-tumoral CD206+ M2 macrophages expressing GRP94 may represent innovative…

QH301-705.5GRP94M2-like macrophages03 medical and health sciences0302 clinical medicineBreast cancerIn vivoSpect imagingmedicineBiology (General)Triple-negative breast cancerGRP94; M2-like macrophages; triple-negative breast cancer; PU-WS13; SPECT imaging; biomarker; CD206; Tilmanocept030304 developmental biology0303 health sciencesTumor microenvironmentSPECT imagingbusiness.industryGeneral Medicinemedicine.diseasePU-WS133. Good health030220 oncology & carcinogenesisCancer researchtriple-negative breast cancerBiomarker (medicine)biomarkerbusinessCD8HormoneCells
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Migraine and cluster headache – the common link

2018

Abstract Although clinically distinguishable, migraine and cluster headache share prominent features such as unilateral pain, common pharmacological triggers such glyceryl trinitrate, histamine, calcitonin gene-related peptide (CGRP) and response to triptans and neuromodulation. Recent data also suggest efficacy of anti CGRP monoclonal antibodies in both migraine and cluster headache. While exact mechanisms behind both disorders remain to be fully understood, the trigeminovascular system represents one possible common pathophysiological pathway and network of both disorders. Here, we review past and current literature shedding light on similarities and differences in phenotype, heritability…

medicine.medical_specialtyNeurologyCluster headacheImplantable Neurostimulators/statistics & numerical dataPain medicineCalcitonin Gene-Related PeptideDeep Brain StimulationMigraine DisordersNitroglycerin/adverse effectsHypothalamuslcsh:MedicineTriptansReviewCalcitonin gene-related peptideBioinformatics03 medical and health sciencesNitroglycerin0302 clinical medicinemedicineHumans030212 general & internal medicineTryptamines/pharmacologyMigraineTrigeminovascular systembusiness.industryNeuromodulationCluster Headache/bloodCluster headacheAnti-CGRP (receptor) monoclonal antibodies – mAbsMigraine Disorders/bloodTrigeminovascular systemlcsh:RGeneral MedicineCalcitonin gene-related peptide (CGRP)medicine.diseaseDeep Brain Stimulation/statistics & numerical dataNeuromodulation (medicine)Tryptamines3. Good healthCalcitonin Gene-Related Peptide/antagonists & inhibitorsAnesthesiology and Pain MedicineImplantable NeurostimulatorsMigraineNeurology (clinical)business030217 neurology & neurosurgerymedicine.drugThe Journal of Headache and Pain
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Synthesis, characterization, and cytotoxic activity of copper(II) and platinum(II) complexes of 2-benzoylpyrrole and X-ray structure of bis[2-benzoyl…

2004

Copper(II) and platinum(II) complexes of 2-benzoylpyrrole (2-BZPH) were synthesized and characterized with IR, 1 H and 1 3 C NMR spectroscopies and coordination geometry with ligands arranged in transoid fashion. The crystal structure of [Cu I I (2-BZP) 2 ] was determined by X-ray diffraction. Death of complex treated Jurkat cells was measured by flow cytometry. The bis-chelate complexes [Cu I I (2-BZP) 2 ] and [Pt I I (2-BZP) 2 ] adopt square-planar coordination geometry with ligands, arranged in transoid fashion. Concentrations of 1-10 μM Platinum(II) complexes reduced cell survival from 100% to 20%, in contrast to the copper(II) complex which caused no cell death at a concentration of 10…

2-BenzoylpyrroleCopper(II) and platinum(II) complexesCytotoxicityMagnetic Resonance SpectroscopySpectrophotometry InfraredCell SurvivalMolecular Conformationchemistry.chemical_elementAntineoplastic AgentsCrystal structureCrystallography X-RayLigandsBiochemistryJurkat cellsInorganic ChemistryJurkat CellsOrganometallic CompoundsHumansPyrrolesCytotoxicityCoordination geometryPlatinumFormazansCell DeathDose-Response Relationship DrugMolecular StructureX-rayHydrogen Bonding2-benzoylpyrrole; copper(ii) and platinum(ii) complexes; cytotoxicityCarbon-13 NMRFlow CytometryCopperCrystallographycopper(ii) and platinum(ii) complexeschemistryxray cristallogrphycytotoxicityIndicators and ReagentsPlatinumCopper2-benzoylpyrroleJournal of inorganic biochemistry
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Endotoxin inhibits gastric emptying in rats via a capsaicin-sensitive afferent pathway.

2001

The effects of endotoxin on gastric emptying of a solid nutrient meal and the neural mechanisms involved in such a response were investigated in conscious rats. The intraperitoneal (i.p.) administration of E. coli endotoxin (40 mug/kg) significantly reduced the 4-h rate of gastric emptying of a standard solid nutrient meal. Ablation of primary afferent neurons by systemic administration of high doses of capsaicin (20+30+50 mg/kg s.c.) to adult rats did not modify the rate of gastric emptying in control animals but prevented the delay in gastric transit induced by endotoxin. Local application of capsaicin to the vagus nerve rather than application of capsaicin to the celiac ganglion signific…

AtropineLipopolysaccharidesMaleendotoxinmedicine.medical_specialtyCalcitonin Gene-Related PeptidePharmacology toxicologyMuscarinic AntagonistscapsaicinRats Sprague-Dawleychemistry.chemical_compoundgastric emptyingtransitNeurons EfferentCalcitonin Gene-Related Peptide Receptor AntagonistsInternal medicinemedicineAnimalsDrug InteractionsCGRPNeurons AfferenttachykininsPhentolamineAfferent PathwayAdrenergic alpha-AntagonistsPharmacologyMealAfferent PathwaysGastric emptyingdigestive oral and skin physiologyGeneral MedicinePeptide FragmentsRatsEndocrinologychemistryGastric EmptyingCapsaicinCapsaicinNaunyn-Schmiedeberg's archives of pharmacology
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Amide-to-triazole switch vs. in vivo NEP-inhibition approaches to promote radiopeptide targeting of GRPR-positive tumors

2017

Abstract Introduction Radiolabeled bombesin (BBN)-analogs have been proposed for diagnosis and therapy of gastrin-releasing peptide receptor (GRPR)-expressing tumors, such as prostate, breast and lung cancer. Metabolic stability represents a crucial factor for the success of this approach by ensuring sufficient delivery of circulating radioligand to tumor sites. The amide-to-triazole switch on the backbone of DOTA-PEG 4 -[Nle 14 ]BBN(7–14) ( 1 ) was reported to improve the in vitro stability of resulting 177 Lu-radioligands. On the other hand, in-situ inhibition of neutral endopeptidase (NEP) by coinjection of phosphoramidon (PA) was shown to significantly improve the in vivo stability and …

MaleCancer ResearchBiodistributionStereochemistryPharmacology[ CHIM ] Chemical Sciences030218 nuclear medicine & medical imagingPolyethylene Glycols03 medical and health scienceschemistry.chemical_compoundHeterocyclic Compounds 1-RingMice0302 clinical medicineIn vivoCell Line TumorRadioligandAnimalsHumans[CHIM]Chemical SciencesRadiology Nuclear Medicine and imagingTissue DistributionNeprilysinTumor targeting GRPR-radioligand 177Lu-bombesin Triazolyl-bombesin NEP-inhibitionPhosphoramidonGlycopeptidesBombesinTriazolesAmidesIn vitro3. Good healthBioavailabilityReceptors Bombesinchemistry030220 oncology & carcinogenesisMolecular MedicineBombesinNeprilysin
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Mitochondrial dynamics in type 2 diabetes: Pathophysiological implications

2017

Mitochondria play a key role in maintaining cellular metabolic homeostasis. These organelles have a high plasticity and are involved in dynamic processes such as mitochondrial fusion and fission, mitophagy and mitochondrial biogenesis. Type 2 diabetes is characterised by mitochondrial dysfunction, high production of reactive oxygen species (ROS) and low levels of ATP. Mitochondrial fusion is modulated by different proteins, including mitofusin-1 (MFN1), mitofusin-2 (MFN2) and optic atrophy (OPA-1), while fission is controlled by mitochondrial fission 1 (FIS1), dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF). PARKIN and (PTEN)-induced putative kinase 1 (PINK1) partici…

MiD51 mitochondrial dynamics proteins of 51 kDaΔΨm mitochondrial membrane potential0301 basic medicineMitochondrial fission factorClinical BiochemistryMitochondrial DegradationMFN2Review ArticleTXNIP thioredoxin interacting proteinMitochondrial DynamicsBiochemistryAdenosine TriphosphateGRP78 78 kDa glucose-regulated proteinMFF mitochondrial fission factorMFN2 mitofusin 2TRX2 thioredoxin 2Redox biologylcsh:QH301-705.5NF-κB nuclear factor kappa Blcsh:R5-920MitophagyType 2 diabetesDRP1 dynamin-related protein 1FIS1 fission protein 1BNIP3 BCL2/adenovirus E1B 19 kDa interacting protein 3MitochondriaOPA1 optic atrophy 1SIRT1/3 sirtuin 1/3Biochemistrymitochondrial fusionTGF-β1 transforming growth factor-β1Mitochondrial fissionOMM outer mitochondrial membranelcsh:Medicine (General)MiD49 mitochondrial dynamics proteins of 49Nox 4 NADPH oxidase-4IMM inner mitochondrial membraneFIS1ATF6 activating transcription factor 6PINK1mTOR mammalian target of rapamycinCHOP C/EBP homologous proteinBiologymdivi-1 mitochondrial division inhibitor-1Mitochondrial Proteins03 medical and health sciencesROS reactive oxygen speciessXBP1 spliced X-box binding protein 1UCP-1 uncoupling protein-1MFN1 mitofusin 1SOD superoxide dismutaseLC3 1 A/1B-light chain 3HumansPINK1 (PTEN)-induced putative kinase 1S3 15-OxospiramilactoneOrganic ChemistrymtDNA mitochondrial DNAAMPK AMP-activated protein kinase030104 developmental biologyDiabetes Mellitus Type 2Mitochondrial biogenesislcsh:Biology (General)Oxidative stressp38 MAPK p38 mitogen-activated protein kinasep62/SQSTM1 ubiquitin and sequestosome-1Reactive Oxygen SpeciesRedox Biology
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Grp78 overexpression triggers pink1-ip3 r-mediated neuroprotective mitophagy

2021

An experimental model of spinal root avulsion (RA) is useful to study causal molecular programs that drive retrograde neurodegeneration after neuron-target disconnection. This neurode-generative process shares common characteristics with neuronal disease-related processes such as the presence of endoplasmic reticulum (ER) stress and autophagy flux blockage. We previously found that the overexpression of GRP78 promoted motoneuronal neuroprotection after RA. After that, we aimed to unravel the underlying mechanism by carrying out a comparative unbiased proteomic analysis and pharmacological and genetic interventions. Unexpectedly, mitochondrial factors turned out to be most altered when GRP78…

biologyQH301-705.5Endoplasmic reticulumAutophagyNeurodegenerationMitophagyMedicine (miscellaneous)PINK1Mitochondrionmedicine.diseaseNeuroprotectionGeneral Biochemistry Genetics and Molecular BiologyArticleNeuroprotectionCell biologyGRP78/BiPMotoneuronsChaperone (protein)Mitophagybiology.proteinmedicineBiology (General)Neurodegeneration
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