Search results for " injury"

showing 10 items of 1007 documents

Waterjet Dissection of Peripheral Nerves: An Experimental Study of the Sciatic Nerve of Rats

2010

BACKGROUND: Although waterjet dissection has been well evaluated in intracranial pathologies, little is known of its qualities in peripheral nerve surgery. Theoretically, the precise dissection qualities could support the separation of nerves from adjacent tissues and improve the preservation of nerve integrity in peripheral nerve surgery. OBJECTIVE: To evaluate the potential of the new waterjet dissector in peripheral nerve surgery. METHODS: Waterjet dissection with pressures of 20 to 80 bar was applied on the sciatic nerves of 101 rats. The effect of waterjet dissection on the sciatic nerve was evaluated by clinical tests, neurophysiological examinations, and histopathological studies up …

MaleMicrosurgerySciatic Neuropathymedicine.medical_treatmentDissection (medical)Neurosurgical ProceduresRats Sprague-DawleyPressuremedicineAnimalsIntraoperative ComplicationsTherapeutic Irrigationbusiness.industryDissectionEquipment DesignAnatomyNerve injuryMicrosurgerySurgical Instrumentsmedicine.diseaseSciatic NerveNerve RegenerationRatsPeripheralmedicine.anatomical_structurePeripheral nervous systemModels AnimalSurgeryOccipital nerve stimulationNeurology (clinical)Sciatic nerveSciatic Neuropathymedicine.symptombusinessOperative Neurosurgery
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Preconditioning by Mitochondrial Reactive Oxygen Species Improves the Proangiogenic Potential of Adipose-Derived Cells-Based Therapy

2009

Objective— Transplantation of adipose-derived stroma cells (ADSCs) stimulates neovascularization after experimental ischemic injury. ADSC proangiogenic potential is likely mediated by their ability to differentiate into endothelial cells and produce a wide array of angiogenic and antiapoptotic factors. Mitochondrial reactive oxygen species (ROS) have been shown to control ADSC differentiation. We therefore hypothesized that mitochondrial ROS production may change the ADSC proangiogenic properties. Methods and Results— The use of pharmacological strategies (mitochondrial inhibitors, antimycin, and rotenone, with or without antioxidants) allowed us to specifically and precisely modulate mito…

MaleMitochondrial ROSProgrammed cell deathStromal Cells/cytology/metabolismAngiogenesisCellsReactive Oxygen Species/*metabolismNeovascularization PhysiologicBiologyMitochondrionmedicine.disease_causeMice03 medical and health sciences0302 clinical medicineAdipocytesmedicineAnimalsEndothelial Cells/*cytology/*physiologyCells CulturedNeovascularization030304 developmental biologyMitochondria/*metabolismchemistry.chemical_classificationReperfusion Injury/physiopathology0303 health sciencesReactive oxygen speciesCulturedEndothelial CellsCell DifferentiationMitochondriaCell biologyCell Differentiation/*physiologyTransplantationPhysiologic/*physiologychemistryReperfusion Injury030220 oncology & carcinogenesisImmunologyStromal CellsStem cellReactive Oxygen SpeciesCardiology and Cardiovascular MedicineOxidative stressArteriosclerosis, Thrombosis, and Vascular Biology
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Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury

2012

Disruption of the blood-brain barrier (BBB) results in cerebral edema formation, which is a major cause for high mortality after traumatic brain injury (TBI). As anesthetic care is mandatory in patients suffering from severe TBI it may be important to elucidate the effect of different anesthetics on cerebral edema formation. Tight junction proteins (TJ) such as zonula occludens-1 (ZO-1) and claudin-5 (cl5) play a central role for BBB stability. First, the influence of the volatile anesthetics sevoflurane and isoflurane on in-vitro BBB integrity was investigated by quantification of the electrical resistance (TEER) in murine brain endothelial monolayers and neurovascular co-cultures of the B…

MaleMouse610 MedizinBrain EdemaPharmacologyCardiovascularMiceAnesthesiology610 Medical sciencesEdemaMolecular Cell BiologyClaudin-5MultidisciplinaryIsofluraneQRAnimal ModelsHead Injurymedicine.anatomical_structureNeurologyBlood-Brain BarrierAnesthesiaAnesthetics InhalationMedicineCellular Typesmedicine.symptomResearch Articlemedicine.drugMethyl EthersTraumatic brain injuryCerebrovascular DiseasesScienceBrain damageBlood–brain barrierSevofluraneCell LineTight JunctionsCerebral edemaSevofluraneModel OrganismsVascular BiologymedicineAnimalsBiologybusiness.industryEndothelial Cellsmedicine.diseaseCoculture TechniquesIsofluraneBrain InjuriesAnestheticZonula Occludens-1 ProteinMolecular NeurosciencebusinessNeurosciencePLoS ONE
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Influence of a Brief Episode of Anesthesia during the Induction of Experimental Brain Trauma on Secondary Brain Damage and Inflammation

2011

It is unclear whether a single, brief, 15-minute episode of background anesthesia already modulates delayed secondary processes after experimental brain injury. Therefore, this study was designed to characterize three anesthesia protocols for their effect on molecular and histological study endpoints. Mice were randomly separated into groups that received sevoflurane (sevo), isoflurane (iso) or an intraperitoneal anesthetic combination (midazolam, fentanyl and medetomidine; comb) prior to traumatic brain injury (controlled cortical impact, CCI; 8 m/s, 1 mm impact depth, 3 mm diameter). Twenty-four hours after insult, histological brain damage, neurological function (via neurological severit…

MaleMouseGeneral AnesthesiaNitric Oxide Synthase Type IIFentanylMiceAnesthesiologyAnesthesiaNeurosurgical CareMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionMicrofilament ProteinsQRAnimal ModelsSurvival RateHead InjuryNeurologyNeurointensive CareAnesthesiaMedicineRegional Anesthesiamedicine.symptomResearch Articlemedicine.drugTraumatic brain injuryScienceBlotting WesternImmunologyBrain damageAnesthetic MechanismsMicrobiologySevofluraneModel OrganismsNeuropharmacologymedicineAnimalsRNA MessengerBiologyInflammationInterleukin-6business.industryCalcium-Binding ProteinsImmunityBrain Contusionmedicine.diseaseMice Inbred C57BLIsofluraneCyclooxygenase 2Brain InjuriesAnestheticMidazolamClinical ImmunologybusinessPLoS ONE
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Inhibition of myosin light chain kinase reduces brain edema formation after traumatic brain injury.

2010

The role of the endothelial contractile apparatus in the process of brain edema formation after brain trauma is not characterized. Phosphorylation of myosin light chains by myosin light chain kinases (MLCK) activates endothelial contractile elements and results in a rearrangement of the cytoskeleton. This may enhance post-traumatic blood-brain barrier dysfunction. In order to investigate the role of the MLCK on brain edema formation and blood-brain barrier permeability after brain injury, mice were anesthetized and subjected to a controlled cortical impact (CCI). MLCK expression is significantly up-regulated after CCI with a maximum 12 h post-injury. Specific inhibition of MLCK by ML-7 resu…

MaleMyosin light-chain kinaseMyosin Light ChainsTime FactorsEndotheliumIntracranial PressureTraumatic brain injuryCentral nervous systemBrain Edemamacromolecular substancesBrain damageNaphthalenesBlood–brain barrierBiochemistryNeuroprotectionDrug Administration ScheduleFunctional LateralityStatistics NonparametricCerebral edemaCellular and Molecular NeuroscienceMicemedicineAnimalsEnzyme InhibitorsMyosin-Light-Chain KinaseNeurologic Examinationbusiness.industryAzepinesmedicine.diseaseConstrictionCell biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureGene Expression RegulationBlood-Brain BarrierBrain Injuriesmedicine.symptombusinessNeuroscienceEvans BlueJournal of neurochemistry
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Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits

2001

Abstract Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic agents, adhesion molecule expression, release of cytokines and oxygen-derived free radicals, and subsequent neutrophil accumulation. In the present study the cardioprotective effects of a novel highly selective small molecule C1s inhibitor (C1s-INH-248, Knoll) were examined in a rabbit model of myocardial ischemia (I) and reperfusion (R; i.e., 60 min I + 180 min R). In in vitro tests (enzyme activity and SRBC lysis) C1s-INH-248 demonstrated profound inhibitory potency. In vivo C1s-INH-248 (1 mg/kg body weight) administered 5 min before reperfusion significantly attenuated m…

MaleNecrosisEndotheliumNeutrophilsG proteinImmunologyMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryComplement C1 Inactivator ProteinsPharmacologyHemolysisLeukocyte CountClassical complement pathwaySuperoxidesIn vivomedicineAnimalsImmunology and AllergyComplement Activationbusiness.industryHemodynamicsmedicine.diseaseComplement systemmedicine.anatomical_structureAnesthesiaEndothelium VascularRabbitsmedicine.symptombusinessReperfusion injuryThe Journal of Immunology
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The 15-Country Collaborative Study of Cancer Risk among Radiation Workers in the Nuclear Industry: Estimates of Radiation-Related Cancer Risks

2007

International audience; A 15-Country collaborative cohort study was conducted to provide direct estimates of cancer risk following protracted low doses of ionizing radiation. Analyses included 407,391 nuclear industry workers monitored individually for external radiation and 5.2 million person-years of follow-up. A significant association was seen between radiation dose and all-cause mortality [excess relative risk (ERR) 0.42 per Sv, 90% CI 0.07, 0.79; 18,993 deaths]. This was mainly attributable to a dose-related increase in all cancer mortality (ERR/Sv 0.97, 90% CI 0.28, 1.77; 5233 deaths). Among 31 specific types of malignancies studied, a significant association was found for lung cance…

MaleNeoplasms Radiation-InducedInternational Cooperation[SDV]Life Sciences [q-bio]Radiation inducedradiation exposurenuclear industrycancer riskWhole-Body Counting030218 nuclear medicine & medical imagingCohort Studiescause of death0302 clinical medicineNuclear industryNuclear ReactorsRisk FactorsNeoplasmscancer mortalityMedicineRadiation injuryRadiationindustryadultarticleleukemiarisk assessmentmethodologycohort analysis3. Good healthmultiple myelomaOccupational DiseasesSurvival Ratefemalepriority journalrisk factorstatistics030220 oncology & carcinogenesisemploymentFemaleionizing radiationradiation doseCohort studyradiation injuryAdultEmploymentBiophysicsRadiation DosageRisk Assessmentsurvival03 medical and health sciencessocioeconomicsOccupational ExposureIndustryfollow upHumansRadiology Nuclear Medicine and imaginghumanRisk factorindustrial workerWhole body countingbusiness.industryNicotiana tabacumCancermedicine.diseasemortalitySurvival Analysislung cancerwhole body countingconfidence intervalRadiation-Inducedoccupational diseasenuclear reactorbusinessNuclear medicineCancer riskDemography
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Renal involvement in psychological eating disorders

2011

Psychological eating disorders – anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder – are an increasing public health problem with severe clinical manifestations: hypothermia, hypotension, electrolyte imbalance, endocrine disorders and kidney failure; they are of interest to nephrologists, but pathophysiological mechanisms in determining the renal involvement are still unclear. We describe pathophysiology, histological features and clinical manifestations of the most frequent psychological eating disorders: AN and BN. Regarding AN, we analyze the recent literature, and identify 3 principal pathways towards renal involvement: chronic dehydration-hypokalemia, nephrocalcinosis …

MaleNephrologymedicine.medical_specialtyAnorexia NervosaHypokalemiaBioinformaticsRhabdomyolysisAdipokinesBinge-eating disorderInternal medicineAnimalsHumansMedicineObesityBulimiaInflammationDehydrationGlomerulosclerosis Focal Segmentalbusiness.industryBulimia nervosaBulimia Nervosa.Acute kidney injuryGeneral MedicineKidney diseasemedicine.diseaseKidney diseases; Anorexia Nervosa; Bulimia Nervosa.NephrocalcinosisEating disordersEndocrinologyNephrologyAnorexia nervosa (differential diagnoses)CytokinesIntercellular Signaling Peptides and ProteinsFemaleKidney DiseasesNephrocalcinosisbusinessKidney disease
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Erythropoietin and erythropoietin receptor expression after experimental spinal cord injury encourages therapy by exogenous erythropoietin

2005

OBJECTIVE: Erythropoietin (EPO) is a pleiotropic cytokine originally identified for its role in erythropoiesis. Recent studies have demonstrated that EPO and its receptor (EPO-R) are expressed in the central nervous system, where EPO exerts neuroprotective functions. Because the expression of the EPO and EPO-R network is poorly investigated in the central nervous system, the aim of the present study was to investigate whether the resident EPO and EPO-R network is activated in the injured nervous system. METHODS: A well-standardized model of compressive spinal cord injury in rats was used. EPO and EPO-R expression was determined by immunohistochemical analysis at 8 hours and at 2, 8, and 14 …

MaleNervous systemmedicine.medical_specialtyCentral nervous systemSpinal cord injuryNeuroprotectionErythropoietin receptorRats Sprague-Dawleyhemic and lymphatic diseasesInternal medicineReceptors ErythropoietinmedicineAnimalsSpinal cord injuryErythropoietinSpinal Cord InjuriesNeuronsbusiness.industryNervous tissuemedicine.diseaseAneurysmRecombinant ProteinsNeuroprotectionRatsErythropoietin receptorDisease Models Animalmedicine.anatomical_structureEndocrinologyGene Expression Regulationerythropoietin; erythropoietin receptor; neuroprotection; spinal cord injuryErythropoietinImmunologyNeurogliaSurgeryNeurology (clinical)businessSpinal Cord Compressionmedicine.drug
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Inhibitors of poly (ADP-ribose) synthetase reduce renal ischemia-reperfusion injury in the anesthetized rat in vivo.

2000

The activation of poly (ADP-ribose) synthetase (PARS) subsequent to DNA damage caused by reactive oxygen or nitrogen species has been implicated in several pathophysiological conditions, including ischemia-reperfusion injury and shock. The aim of this study was to investigate whether PARS inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo. Male Wistar rats were subjected to 45 min bilateral clamping of the renal pedicles, followed by 6 h reperfusion (control animals). Animals were administered the PARS inhibitors 3-aminobenzamide, 1, 5-dihydroxyisoquinoline, or nicotinamide during the reperfusion period. Ischemia, followed by reperfusion, produc…

MaleNiacinamideIschemiaRenal functionNatriuresisKidney; Poly (ADP-ribose) synthetase inhibitors; Proximal tubule; Reactive oxygen species; Reperfusion injuryPharmacologyPoly(ADP-ribose) Polymerase InhibitorsKidneyBiochemistryExcretionchemistry.chemical_compoundIn vivoGeneticsmedicineAnimalsUreaAnesthesiaEnzyme InhibitorsRats WistarMolecular BiologyKidneyCreatinineNicotinamidemedicine.diseaseIsoquinolinesRatsOxidative Stressmedicine.anatomical_structurechemistryCreatinineReperfusion InjuryBenzamidesReactive Oxygen SpeciesReperfusion injuryBiotechnologyGlomerular Filtration RateFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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