Search results for " enzyme"

showing 10 items of 791 documents

Plasma derived protein C in severe sepsis: report of two cases

2008

Severe sepsis is defined as sepsis-associated organ dysfunction, (arterial hypoxemia, acute oliguria, coagulation abnormalities, thrombocytopenia, hyperbilirubinemia), hypoperfusion (hyperlactatemia) and arterial hypotension (mean arterial pressure \70 mmHg, or a systolic blood pressure decrease[40 mmHg) [3, 4]. Septic shock [3, 4] is defined as acute circulatory failure induced by sepsis with hypotension despite adequate fluid resuscitation. A dysfunction of the protein C (PC) pathway is always present in severe sepsis and contributes to the development of coagulopathy and necrosis [12, 13]. This decrease is caused by consumption of protein C during systemic activation of blood coagulation…

medicine.medical_specialtyMean arterial pressurebusiness.industrySeptic shockOrgan dysfunctionProteolytic enzymesmedicine.diseaseGastroenterologySepsisPlasmaInternal medicineEmergency MedicineInternal MedicinemedicineHyperlactatemiamedicine.symptombusinessProtein Cmedicine.drugPurpura fulminansInternal and Emergency Medicine
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In vivo antihypertensive mechanism of lactoferrin-derived peptides: Reversion of angiotensin I- and angiotensin II-induced hypertension in Wistar rats

2015

Novel peptides with antihypertensive effects in SHR rats have previously been identified in lactoferrin (LF) hydrolysates. To investigate their in vivo antihypertensive mechanism, we have assessed the blood pressure lowering effects of two of these LF-derived peptides (RPYL and DPYKLRP) in Wistar rats subjected to either angiotensin I- or angiotensin II-induced hypertension. Blood pressure was measured by the tail-cuff method, hypertension was induced by subcutaneous infusion of angiotensins, and then captopril, valsartan or LF-derived peptides orally administered. Angiotensin I- and angiotensin II-induced hypertension were reversed by captopril and valsartan, respectively. RPYL and DPYKLRP…

medicine.medical_specialtyMedicine (miscellaneous)Lactoferrin-derived peptidesPharmacologyWistar ratAntihypertensive peptidesInternal medicineRenin–angiotensin systemMedicineTX341-641Angiotensin-induced hypertensionNutrition and DieteticsAngiotensin II receptor type 1biologyNutrition. Foods and food supplybusiness.industryCaptoprilAngiotensin-converting enzymeAngiotensin IIBlood pressureEndocrinologyValsartanbiology.proteinRenin angiotensin systemmedicine.symptombusinessVasoconstrictionFood Sciencemedicine.drugIn vivo ACE inhibition
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The deubiquitinating enzyme CYLD regulates the differentiation and maturation of thymic medullary epithelial cells.

2014

The cross talk between thymocytes and the thymic epithelium is critical for T-cell development and the establishment of central tolerance. Medullary thymic epithelial cells (mTECs) are located in the thymic medulla and mediate the elimination of self-reactive thymocytes, thereby preventing the onset of autoimmunity. Previous studies identified the deubiquitinating enzyme CYLD as a critical regulator of T-cell development by activating proximal T-cell receptor signaling during the transition of double-positive to single-positive thymocytes. Here we evaluated the impact of the naturally occurring short-splice variant of the cyld gene (sCYLD) on the development and maturation of mTECs. We foun…

medicine.medical_specialtyMedullary cavityImmunologyReceptors Antigen T-CellCell CountThymus GlandBiologyDeubiquitinating Enzyme CYLDImmunophenotypingMiceInternal medicinemedicineImmunology and AllergyAnimalsMice KnockoutThymocytesUbiquitinationCell DifferentiationEpithelial CellsCell BiologyCell biologyDeubiquitinating Enzyme CYLDCysteine EndopeptidasesEndocrinologyPhenotypeAntigens SurfaceMutationFemaleSignal TransductionImmunology and cell biology
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Substance P Serum Degradation in Complex Regional Pain Syndrome – Another Piece of the Puzzle?

2021

In a previous study, we demonstrated that the serum peptidase system might be less efficient in complex regional pain syndrome (CRPS). Since the neuropeptide substanc P (SP) contributes to inflammation in CRPS, we now investigated the metabolism of SP in CRPS specifically. An SP metabolism assay was performed in 24 CRPS patients, which constitute a subgroup of our previous investigation on BK degradation. In addition, we included 26 healthy controls (24 newly recruited plus 2 from our previous investigation), and 13 patients after limb trauma, who did not fulfil the CRPS diagnostic criteria (trauma controls, TC) were included. We adapted a thin layer chromatography assay (TLC) to quantify S…

medicine.medical_specialtyNeuropeptideBradykininInflammationSubstance PPeptidyl-Dipeptidase ASubstance PBradykininchemistry.chemical_compoundInternal medicinemedicineHumansNeprilysinbiologybusiness.industryAngiotensin-converting enzymemedicine.diseaseAnesthesiology and Pain MedicineEndocrinologyComplex regional pain syndromeNeurologychemistrybiology.proteinNeurology (clinical)medicine.symptombusinessComplex Regional Pain SyndromesEx vivoPeptide HydrolasesThe Journal of Pain
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Oxidative Stress and DNA Damage in Human Gastric Carcinoma: 8-Oxo-7'8-dihydro-2'-deoxyguanosine (8-oxo-dG) as a Possible Tumor Marker

2013

We characterized the oxidative stress (OS) status by the levels of reduced/oxidized glutathione (GSH/GSSG), malondialdehyde (MDA) and the mutagenic base 8-oxo-7′8-dihydro-2′-deoxyguanosine (8-oxo-dG) in human gastric carcinoma (HGC) samples and compared the results with normal tissue from the same patients. We also analyzed 8-oxo-dG in peripheral mononuclear cells (PMNC) and urine from healthy control subjects and in affected patients in the basal state and one, three, six, nine and twelve months after tumor resection. The levels of DNA repair enzyme mRNA expression (hOGG1, RAD51, MUYTH and MTH1) were determined in tumor specimens and compared with normal mucosa. Tumor specimens exhibited i…

medicine.medical_specialtyPathologyDNA damageDNA repair8-oxo-dGBiologymedicine.disease_causePeripheral blood mononuclear cellArticleCatalysisInorganic Chemistrychemistry.chemical_compoundInternal medicinemedicine8-oxo-dG; DNA repair enzymes; gastric cancer; oxidative stress; tumor markeroxidative stressDeoxyguanosinePhysical and Theoretical ChemistryMolecular BiologySpectroscopyTumor markergastric cancerOrganic ChemistryGeneral MedicineGlutathioneMalondialdehydeComputer Science ApplicationsEndocrinologyDNA repair enzymeschemistrytumor markerOxidative stressInternational Journal of Molecular Sciences; Volume 14; Issue 2; Pages: 3467-3486
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Pentobarbital-sensitive EDHF comediates ACh-induced arteriolar dilation in the hamster microcirculation

1999

It is unclear to what extent the endothelium-derived hyperpolarizing factor (EDHF) contributes to the control of microcirculatory blood flow in vivo. We analyzed, by intravital microscopy in hamster muscles, the potential role of EDHF along the vascular tree under stimulated (ACh) or basal conditions. Experiments were performed in conscious as well as anesthetized (pentobarbital, urethan) animals. Additionally, cellular effects of the potential EDHF were studied in isolated small arteries. In pentobarbital-anesthetized animals, treatment with N ω-nitro-l-arginine (l-NNA; 30 μmol/l) and indomethacin (3 μmol/l) reduced the dilation in response to 10 μmol/l ACh from 60 ± 6 to 20 ± 4%. This ni…

medicine.medical_specialtyPentobarbitalEndothelium-derived hyperpolarizing factorPotassium ChannelsCharybdotoxinPhysiologyVasodilator AgentsIndomethacinHamsterVasodilationNitroarginineMuscle Smooth VascularMicrocirculationGlibenclamideBiological FactorsCytochrome P-450 Enzyme SystemArterioleCricetinaePhysiology (medical)Internal medicinemedicine.arterymedicineAnimalsCyclooxygenase InhibitorsMuscle SkeletalPentobarbitalSkinMesocricetusChemistryMicrocirculationPenicillamineAcetylcholineArteriolesEndocrinologyAnesthesiaFatty Acids UnsaturatedPotassiumEndothelium VascularCardiology and Cardiovascular MedicineIntravital microscopyAdjuvants Anesthesiamedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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The metabolic syndrome in hypertension: European society of hypertension position statement.

2008

The metabolic syndrome considerably increases the risk of cardiovascular and renal events in hypertension. It has been associated with a wide range of classical and new cardiovascular risk factors as well as with early signs of subclinical cardiovascular and renal damage. Obesity and insulin resistance, beside a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with proinflammatory properties, have been implicated in the pathogenesis. The close relationships among the different components of the syndrome and their associated disturbances make it difficult to understand what the underlying causes and consequences are. At each of these …

medicine.medical_specialtyPhysiologySodium Chloride Symporter InhibitorsAdrenergic beta-AntagonistsPhysical exerciseAngiotensin-Converting Enzyme InhibitorsType 2 diabetesBioinformaticsInsulin resistanceWeight lossInternal medicineInternal MedicinemedicineHumansThiazideAntihypertensive AgentsMetabolic Syndromebusiness.industrymedicine.diseaseCalcium Channel BlockersObesityExercise TherapyEndocrinologyBlood pressureHypertensionmedicine.symptomMetabolic syndromeCardiology and Cardiovascular MedicinebusinessAngiotensin II Type 1 Receptor BlockersRisk Reduction Behaviormedicine.drugDiet TherapyJournal of hypertension
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Angiotensin-Converting Enzyme Inhibitor Ramiprilat Interferes With the Sequestration of the B 2 Kinin Receptor Within the Plasma Membrane of Native E…

1999

Background —ACE (kininase II) inhibitors have been shown to exert their beneficial cardiovascular effects via the inhibition of both angiotensin II formation and bradykinin breakdown. Because recent evidence suggests that ACE inhibitors may also interfere with B 2 kinin receptor signaling and thus enhance the vascular response to bradykinin, we examined whether the distribution of B 2 kinin receptors within the plasma membrane of native endothelial cells is affected by an ACE inhibitor. Methods and Results —Localization of the B 2 kinin receptor in membranes prepared from native porcine aortic endothelial cells was evaluated by means of specific [ 3 H]bradykinin binding and immunoprecipita…

medicine.medical_specialtyReceptor Bradykinin B2SwineBradykininAngiotensin-Converting Enzyme InhibitorsPharmacologyBradykininchemistry.chemical_compoundRamiprilPhysiology (medical)Internal medicinemedicineAnimalsCalcium SignalingBradykinin receptorReceptorAortaMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyReceptors BradykininMembrane ProteinsBiological TransportAngiotensin-converting enzymeKininAngiotensin IIEndothelial stem cellEndocrinologychemistryCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinEndothelium VascularMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineRamiprilatSignal TransductionCirculation
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A score model for the continuous grading of early allograft dysfunction severity

2014

Early allograft dysfunction (EAD) dramatically influences graft and patient outcomes. A lack of consensus on an EAD definition hinders comparisons of liver transplant outcomes and management of recipients among and within centers. We sought to develop a model for the quantitative assessment of early allograft function [Model for Early Allograft Function Scoring (MEAF)] after transplantation. A retrospective study including 1026 consecutive liver transplants was performed for MEAF score development. Multivariate data analysis was used to select a small number of postoperative variables that adequately describe EAD. Then, the distribution of these variables was mathematically modeled to assig…

medicine.medical_specialtyTime Factorsmedicine.medical_treatmentLiver transplantationModels BiologicalSeverity of Illness IndexDecision Support TechniquesLiver diseasePredictive Value of TestsRisk FactorsInternal medicineSeverity of illnessmedicineHumansInternational Normalized RatioBlood CoagulationProportional Hazards ModelsRetrospective StudiesPrincipal Component AnalysisTransplantationHepatologyProportional hazards modelbusiness.industryGraft SurvivalReproducibility of ResultsAlanine TransaminaseBayes TheoremBilirubinRetrospective cohort studyClinical Enzyme Testsmedicine.diseaseLiver TransplantationSurgeryTransplantationTreatment OutcomeNonlinear DynamicsPredictive value of testsMultivariate AnalysisSurgeryLiver functionPrimary Graft DysfunctionbusinessBiomarkersLiver Transplantation
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Liver specific deletion of CYLDexon7/8 induces severe biliary damage, fibrosis and increases hepatocarcinogenesis in mice

2012

Background & Aims CYLD is a tumor suppressor gene that is mutated in familial cylindromatosis, an autosomal dominant predisposition to tumors of skin appendages. Reduced CYLD expression has been observed in other tumor entities, including hepatocellular carcinoma. In the present study, we analyzed the role of CYLD in liver homeostasis and hepatocarcinogenesis in vivo . Methods Mice with liver-specific deletion of CYLDexon7/8 ( CYLD FF xAlbCre ) were generated. Liver tissues were histologically analyzed and oval cell activation was investigated. Hepatocarcinogenesis was induced by diethylnitrosamine/phenobarbital (DEN/PB). Microarray expression profiling of livers was performed in untreated …

medicine.medical_specialtyTumor suppressor geneBiliary Tract DiseasesIn Vitro TechniquesBiologymedicine.disease_causeDimethylnitrosamineDeubiquitinating Enzyme CYLDMiceRisk FactorsFibrosisInternal medicinemedicineAnimalsHomeostasisGenetic Predisposition to DiseaseHepatologyLiver NeoplasmsExonsTransforming growth factor betamedicine.diseaseFibrosisMice Mutant StrainsDeubiquitinating Enzyme CYLDMice Inbred C57BLGene expression profilingCysteine EndopeptidasesDisease Models AnimalPhenotypeEndocrinologyLiverPhenobarbitalHepatocellular carcinomaCancer researchbiology.proteinCell activationCarcinogenesisGene DeletionJournal of Hepatology
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