Search results for "PORT"

showing 10 items of 20457 documents

Impact of glucocorticoids on systemic sirtuin 1 expression and activity in rats with adjuvant-induced arthritis

2020

The class III histone deacetylase sirtuin 1 (SIRT1) plays a pivotal role in numerous biological and physiological functions, including inflammation. An association between SIRT1 and proinflammatory cytokines might exist. In addition to their important role in inflammation associated with rheumatoid arthritis (RA), proinflammatory cytokines mediate the development of systemic effects. Here, we evaluated systemic SIRT1 expression and enzymatic activity, in peripheral blood mononuclear cells (PBMCs) and in liver isolated from rats with adjuvant-induced arthritis (AIA), treated or not with low or high doses of glucocorticoids (GCs). We also measured the production of tumour necrosis factor alph…

0301 basic medicineCancer Researchmedicine.medical_specialtyArthritisInflammationPeripheral blood mononuclear cellProinflammatory cytokine03 medical and health sciences0302 clinical medicineSirtuin 1Internal medicinemedicineAnimalsBeta (finance)Molecular BiologyGlucocorticoidsbiologySirtuin 1Brief ReportDNA Methylationmedicine.diseaseArthritis ExperimentalRats030104 developmental biologyEndocrinology030220 oncology & carcinogenesisRheumatoid arthritisbiology.proteinLeukocytes MononuclearCytokinesTumor necrosis factor alphamedicine.symptom
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Trends in net survival from 15 cancers in six European Latin countries: the SUDCAN population-based study material

2016

The aim of the SUDCAN collaborative study was to compare the net survival from 15 cancers diagnosed in 2000-2004 in six European Latin countries and provide trends in net survival and dynamics of excess mortality rates up to 5 years after diagnosis from 1992 to 2004 in France, Italy, Spain, and Switzerland, and from 2000 to 2004 in Belgium and Portugal. This paper presents a detailed description of the data analyzed and quality indicators. Incident cases from Belgium, France, Italy, Portugal, Spain, and Switzerland were retrieved from 56 general or specialized population-based cancer registries that participated in the EUROCARE-5 database. Fifteen cancer sites were analyzed. The data were c…

0301 basic medicineCancer Researchmedicine.medical_specialtyDatabases FactualEpidemiology03 medical and health sciences0302 clinical medicineBelgiumNeoplasmsEpidemiologymedicineHumansSurvival rateNet SurvivalSurvival analysisPortugalMortality ratePublic Health Environmental and Occupational HealthSurvival Analysis3. Good healthCancer registryEuropeSurvival RateTrend analysis030104 developmental biologyGeographyItalyOncologySpainPopulation Surveillance030220 oncology & carcinogenesisFranceDeath certificateSwitzerlandFollow-Up StudiesDemographyEuropean Journal of Cancer Prevention
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Identification of clinical phenotypes and related survival in patients with large hccs

2021

Background. Hepatocellular carcinoma (HCC) factors, especially maximum tumor diameter (MTD), tumor multifocality, portal vein thrombosis (PVT), and serum alpha-fetoprotein (AFP), influence survival. Aim. To examine patterns of tumor factors in large HCC patients. Methods. A database of large HCC patients was examined. Results. A multiple Cox proportional hazard model on death identified low serum albumin levels and the presence of PVT and multifocality, with each having a hazard ratio ≥2.0. All combinations of these three parameters were examined in relation to survival. Using univariate Cox analysis, the combination of albumin &gt

0301 basic medicineCancer Researchmedicine.medical_specialtyPVTSettore MED/12 - GASTROENTEROLOGIASerum albuminlcsh:RC254-282GastroenterologyArticle03 medical and health sciences0302 clinical medicineInternal medicineMedicinePlateletHCCneoplasmsSurvival ratePVT.biologybusiness.industryProportional hazards modelAlbuminHazard ratioSettore MED/09 - MEDICINA INTERNAAlbuminMultifocalityHCC; large; phenotypes; PVT; multifocality; albuminlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesPortal vein thrombosisAlbumin; HCC; Large; Multifocality; Phenotypes; PVTPhenotypesPhenotype030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinLargebusiness
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Portal vein infiltration in patients with hepatocellular carcinoma: The relevance of correct classification.

2017

e15651 Background: Portal vein invasion (PVI) is has a significant impact on the prognosis of patients with hepatocellular carcinoma (HCC). Patients with PVI are classified as stage C in the BCLC score and systemic therapy is recommended. Patients with minor PVI are frequently misclassified due to radiological challenges in determining malignant PVI or non-adherence to guidelines. The concept of resection or TACE in limited PVI is sometimes followed with the assumption of a negligible influence on survival. Aim of this study is the reevaluation of PVI and the analysis of the impact of a misclassification. Methods: 763 patients with HCC of a total of 1413 were extracted from the clinical re…

0301 basic medicineCancer Researchmedicine.medical_specialtyPathologybusiness.industryPortal veinmedicine.disease03 medical and health sciences030104 developmental biologyOncologyHepatocellular carcinomamedicineIn patientRadiologybusinessInfiltration (medical)Journal of Clinical Oncology
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Fatal Liver and Bone Marrow Toxicity by Combination Treatment of Dichloroacetate and Artesunate in a Glioblastoma Multiforme Patient: Case Report and…

2016

A 52-year-old male patient was treated with standard radiochemotherapy with temozolomide for glioblastoma multiforme (GBM). After worsening of his clinical condition, further tumor-specific treatment was unlikely to be successful, and the patient seeked help from an alternative practitioner, who administered a combination of dichloroacetate (DCA) and artesunate (ART). A few days later, the patient showed clinical and laboratory signs of liver damage and bone marrow toxicity (leukopenia, thrombocytopenia). Despite successful restoration of laboratory parameters upon symptomatic treatment, the patient died 10 days after the infusion. DCA bears a well-documented hepatotoxic risk, while ART can…

0301 basic medicineCancer Researchmedicine.medical_specialtymedicine.medical_treatmentCase ReportToxicologychemotherapyGastroenterologylcsh:RC254-28203 medical and health scienceschemistry.chemical_compound0302 clinical medicineMedizinische FakultätInternal medicineadverse effectmedicineddc:610Adverse effectCancerLiver injuryChemotherapyLeukopeniaTemozolomidebusiness.industrymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensSurgeryClinical trial030104 developmental biologychemistryOncologyArtesunate030220 oncology & carcinogenesisadverse side effectsErythropoiesismedicine.symptombusinessmedicine.drugcomplementary and alternative medicine
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Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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C 4 -Dicarboxylate Utilization in Aerobic and Anaerobic Growth

2016

C 4 -dicarboxylates and the C 4 -dicarboxylic amino acid l -aspartate support aerobic and anaerobic growth of Escherichia coli and related bacteria. In aerobic growth, succinate, fumarate, D - and L -malate, L -aspartate, and L -tartrate are metabolized by the citric acid cycle and associated reactions. Because of the interruption of the citric acid cycle under anaerobic conditions, anaerobic metabolism of C 4 -dicarboxylates depends on fumarate reduction to succinate (fumarate respiration). In some related bacteria (e.g., Klebsiella ), utilization of C 4 -dicarboxylates, such as tartrate, is independent of fumarate respiration and uses a Na + -dependent membrane-bound oxaloacetate decarbo…

0301 basic medicineCarboxy-LyasesCitric Acid Cycle030106 microbiologySuccinic AcidContext (language use)medicine.disease_causeMicrobiology03 medical and health sciencesFumaratesKlebsiellaEscherichia colimedicineHumansDicarboxylic AcidsAnaerobiosisEscherichia coliDicarboxylic Acid TransportersbiologyEscherichia coli ProteinsMembrane Transport ProteinsBiological TransportGene Expression Regulation BacterialMetabolismFumarate reductasebiology.organism_classificationAerobiosisCitric acid cycle030104 developmental biologyOxaloacetate decarboxylaseBiochemistryAnaerobic exerciseBacteriaEcoSal Plus
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Homozygous Resistance to Thyroid Hormone β: Can Combined Antithyroid Drug and Triiodothyroacetic Acid Treatment Prevent Cardiac Failure?

2017

Resistance to thyroid hormone β (RTHβ) due to homozygous THRB defects is exceptionally rare, with only five kindreds reported worldwide. Cardiac dysfunction, which can be life-threatening, is recognized in the disorder. Here we describe the clinical, metabolic, ophthalmic, and cardiac findings in a 9-year-old boy harboring a biallelic THRB mutation (R243Q), along with biochemical, physiologic, and cardiac responses to carbimazole and triiodothyroacetic acid (TRIAC) therapy. The patient exhibits recognized features (goiter, nonsuppressed thyroid-stimulating hormone levels, upper respiratory tract infections, hyperactivity, low body mass index) of heterozygous RTHβ, with additional characteri…

0301 basic medicineCardiac function curvemedicine.medical_specialtyendocrine systemGoiterendocrine system diseasesEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismCase ReportsCardiovascularthyroidresistance to thyroid hormonehomozygous THRB mutation03 medical and health sciences0302 clinical medicineClinical ResearchInternal medicinemedicine2.1 Biological and endogenous factorsDecompensation2. Zero hungercardiac thyrotoxicosisbusiness.industryThyroidDilated cardiomyopathymedicine.disease3. Good health030104 developmental biologyEndocrinologymedicine.anatomical_structureCarbimazoleHeart Disease6.1 PharmaceuticalsBasal metabolic ratebusinessHormonemedicine.drug
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mRNA-binding protein tristetraprolin is essential for cardiac response to iron deficiency by regulating mitochondrial function

2018

Cells respond to iron deficiency by activating iron-regulatory proteins to increase cellular iron uptake and availability. However, it is not clear how cells adapt to conditions when cellular iron uptake does not fully match iron demand. Here, we show that the mRNA-binding protein tristetraprolin (TTP) is induced by iron deficiency and degrades mRNAs of mitochondrial Fe/S-cluster-containing proteins, specifically Ndufs1 in complex I and Uqcrfs1 in complex III, to match the decrease in Fe/S-cluster availability. In the absence of TTP, Uqcrfs1 levels are not decreased in iron deficiency, resulting in nonfunctional complex III, electron leakage, and oxidative damage. Mice with deletion of Ttp …

0301 basic medicineCardiac responseCardiac function curveIron-Sulfur ProteinsTristetraprolinMitochondria HeartCell Line03 medical and health sciencesElectron Transport Complex IIIMiceTristetraprolinmedicineAnimalschemistry.chemical_classificationMice KnockoutReactive oxygen speciesMultidisciplinaryNDUFS1MyocardiumNADH DehydrogenaseIron deficiencyIron Deficienciesmedicine.diseaseCell biology030104 developmental biologychemistryPNAS PlusCoenzyme Q – cytochrome c reductaseOxidation-ReductionFunction (biology)
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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

2017

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective…

0301 basic medicineCarotid Artery DiseasesMalePathologymedicine.medical_specialtyNecrosisCardiology030204 cardiovascular system & hematologyBiologyC-Mer Tyrosine KinaseProinflammatory cytokine03 medical and health sciencesMiceNecrosis0302 clinical medicineProto-Oncogene ProteinsmedicineAnimalsHumansEfferocytosisMice Knockoutc-Mer Tyrosine KinaseBrief ReportFibrous capReceptor Protein-Tyrosine KinasesGeneral MedicineMERTKPlaque Atherosclerotic030104 developmental biologymedicine.anatomical_structureReceptors LDLApoptosisProteolysisFemalemedicine.symptomTyrosine kinase
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