Search results for "hyperammonemia"

showing 9 items of 19 documents

Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats.

2020

Minimal hepatic encephalopathy is associated with changes in the peripheral immune system which are transferred to the brain, leading to neuroinflammation and thus to cognitive and motor impairment. Mechanisms by which changes in the immune system induce cerebral alterations remain unclear. Extracellular vesicles (EVs) seem to play a role in this process in certain pathologies. The aim of this work was to assess whether EVs play a role in the induction of neuroinflammation in cerebellum and motor incoordination by chronic hyperammonemia. We characterized the differences in protein cargo of EVs from plasma of hyperammonemic and control rats by proteomics and Western blot. We assessed whether…

MaleCerebellumtnfαhepatic encephalopathyArticleExtracellular VesiclesImmune systemWestern blotmedicineAnimalsHumansHyperammonemiaRats WistarReceptorlcsh:QH301-705.5NeuroinflammationInflammationMicrogliamedicine.diagnostic_testbusiness.industryTumor Necrosis Factor-alphaHyperammonemiaGeneral Medicinetnfα receptor tnfr1medicine.diseaseRatsMotor Skills DisordersDisease Models Animalmedicine.anatomical_structurelcsh:Biology (General)glial activationTumor necrosis factor alphaNervous System DiseasesTNF alpha receptor TNFR1businessNeuroscienceTNF alpha
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Liver pathology in transient neonatal hyperammonemia.

1983

Ultrastructural investigations have been performed on two cases of transient neonatal hyperammonaemia (TNH). This newly recognized metabolic disorder is chiefly characterized by severe hyperammonaemia in the postnatal period, a comatous state, absence of abnormal organic aciduria, normal activity of urea cycle enzymes and, usually, complete recovery. The aetiology is presently unknown. Electron microscopy uncovered rather congruent alterations of hepatocyte structure, with a wide spectrum of mitochondrial lesions, an increase of autophagous bodies with organelle remnants, and changes in the excretory apparatus. Thus, in contrast to some of the hereditary disorders of the urea cycle, no spec…

MalePathologymedicine.medical_specialtyHistologyMitochondria LiverBiologyMitochondrionOrganic aciduriaUltrastructural PathologyPathology and Forensic MedicineAmmoniaInternal medicinemedicineHumansMolecular BiologyStaining and LabelingMetabolic disorderHepatobiliary diseaseInfant NewbornHyperammonemiaCell BiologyGeneral Medicinemedicine.diseaseMicroscopy Electronmedicine.anatomical_structureEndocrinologyLiverUrea cycleHepatocyteAnatomyMetabolism Inborn ErrorsVirchows Archiv. A, Pathological anatomy and histopathology
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Chronic Moderate Hyperammonemia Impairs Active and Passive Avoidance Behavior and Conditional Discrimination Learning in Rats

2000

Abstract The cerebral dysfunction associated with hepatic encephalopathy is generally considered to have hyperammonemia as one of its main causes. Hyperammonemia impairs the neuronal glutamate–nitric oxide–cyclic GMP pathway and the induction of NMDA receptor-dependent long-term potentiation in the hippocampus. We studied the performance of pre/neonatally and postnatally exposed rats to hyperammonemia on active avoidance, passive avoidance, and conditional discrimination tasks. Pre/neonatal hyperammonemia slowed learning of active avoidance behaviors and impaired memory for the passive avoidance task while postnatal hyperammonemia impaired learning on the conditional discrimination task. Hy…

MaleTime FactorsHippocampusAcetatesMotor ActivityDiscrimination LearningDevelopmental NeuroscienceAmmoniaPregnancyAvoidance LearningmedicineAnimalsRats WistarHepatic encephalopathyAnalysis of VarianceHyperammonemiaLong-term potentiationCognitionImpaired memorymedicine.diseaseAnimal FeedRatsAnimals NewbornNeurologyPrenatal Exposure Delayed EffectsAnesthesiaNMDA receptorFemalePassive avoidancePsychologyNeuroscienceExperimental Neurology
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Acute ammonia toxicity is mediated by the NMDA type of glutamate receptors

1992

AbstractPrevious experiments in our laboratory suggested that ammonium toxicity could be mediated by the NMDA type of glutamate receptors. To assess this hypothesis we tested if MK-801, a specific antagonist of the NMDA receptor, is able to prevent ammonium toxicity. Mice and rats were injected i.p. with 12 and 7 mmol/kg of ammonium acetate, respectively, 73% of the mice and 70% of the rats died. However, when the animals were injected i.p. with 2 mg/kg of MK-801, 15 min before ammonium injection, only 5% of the mice and 15% of the rats died. The remarkable protection afforded by MK-801 indicates that ammonia toxicity is mediated by the NMDA receptor.

Malemedicine.medical_specialtyBiophysicsGlutamic AcidReceptors N-Methyl-D-AspartateBiochemistryAmmonia toxicityMicechemistry.chemical_compoundGlutamatesAmmoniaStructural BiologyInternal medicineGeneticsmedicineAnimalsHyperammonemiaNeurotransmitter metabolismAmmoniumReceptorMolecular BiologyMK-801Glutamate receptorRats Inbred StrainsValineCell BiologyGlutamic acidNMDA receptorRatsReceptors NeurotransmitterEndocrinologyReceptors GlutamatechemistryToxicityNMDA receptorDizocilpine MaleateAmmonium acetateFEBS Letters
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Selective regional distribution of tubulin induced in cerebrum by hyperammonemia

1989

Ingestion of ammonium induces hyperammonemia which increases tubulin content in cerebrum but not in cerebellum. We have dissected 11 discrete areas of cerebrum and quantified the tubulin content in control and hyperammonemic rats. An heterogeneity in the induction of tubulin is shown. The areas more affected are ventral hippocampus, dorsal hippocampus, hypothalamus, septum, reticular formation and frontal cortex, in which tubulin content increased by 63%, 27%, 32%, 48%, 45%, and 25%, respectively, after two months of feeding the ammonium diet.

Malemedicine.medical_specialtyCerebellumHippocampusmacromolecular substancesReticular formationBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundAmmoniaTubulinInternal medicinemedicineAnimalsAmmoniumbiologyCerebrumBrainRats Inbred StrainsHyperammonemiaGeneral Medicinemedicine.diseaseRatsTubulinmedicine.anatomical_structureEndocrinologynervous systemchemistryHypothalamusbiology.proteinNeurochemical Research
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Hyperammonemic encephalopathy after urinary diversion. Diet therapy

2016

medicine.medical_specialtyDiet therapymedicine.medical_treatment030232 urology & nephrologyUrinary DiversionPlant Proteins DietaryGastroenterologyIntestinal absorption03 medical and health sciencesEpilepsy Complex Partial0302 clinical medicineAmmoniaInternal medicinemedicineHumansHyperammonemia030212 general & internal medicineAgedAcidosisCarcinoma Transitional CellCARCINOMA TRANSITIONAL CELLBrain Diseases Metabolicbusiness.industryUrinary diversionHyperammonemiaHydrogen-Ion Concentrationmedicine.diseaseSurgeryIntestinal AbsorptionUrinary Bladder NeoplasmsFemaleDietary Proteinsmedicine.symptomAcidosisHyperammonemic encephalopathybusinessEndocrinología y Nutrición (English Edition)
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A Look into Liver Mitochondrial Dysfunction as a Hallmark in Progression of Brain Energy Crisis and Development of Neurologic Symptoms in Hepatic Enc…

2020

Background: The relationship between liver disease and neuropathology in hepatic encephalopathy is well known, but the genesis of encephalopathy in liver failure is yet to be elucidated. Conceptually, the main cause of hepatic encephalopathy is the accumulation of brain ammonia due to impaired liver detoxification function or occurrence of portosystemic shunt. Yet, as well as taking up toxic ammonia, the liver also produces vital metabolites that ensure normal cerebral function. Given this, for insight into how perturbations in the metabolic capacity of the liver may be related to brain pathology, it is crucial to understand the extent of ammonia-related changes in the hepatic metabolism th…

medicine.medical_specialtyhyperammonemiaEncephalopathylcsh:MedicineMitochondrionliverArticle03 medical and health sciencesLiver disease0302 clinical medicineInternal medicinebrain energy crisisKetogenesisMedicineHepatic encephalopathy030304 developmental biology0303 health sciencesbusiness.industrylcsh:RHyperammonemiaGeneral Medicinemedicine.diseaseketogenesismitochondriaEndocrinologygluconeogenesisKetone bodies030211 gastroenterology & hepatologyPortosystemic shuntbusinessJournal of clinical medicine
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High Output Heart Failure in Multiple Myeloma: Pathogenetic Considerations.

2022

The high output heart failure is a clinical condition in which the systemic congestion is associated to a high output state, and it can be observed in a non-negligible percentage of hematological diseases, particularly in multiple myeloma, a condition in which the risk of adverse cardiovascular events may increase, with a worse prognosis for patients. For this reason, though an accurate literature search, we provided in this review a complete overview of different pathogenetic mechanisms responsible for high output heart failure in multiple myeloma. Indeed, this clinical finding is present in the 8% of multiple myeloma patients, and it may be caused by artero-venous shunts, enhanced angioge…

multiple myelomaangiogenesisCancer ResearchOncologyhyperammonemiahigh output heart failureNeoplasms. Tumors. Oncology. Including cancer and carcinogensangiogenesiglutamminolysiplasma viscosityglutamminolysisRC254-282artero-venous fistulaeCancers
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A single transient episode of hyperammonemia induces long-lasting alterations in protein kinase A.

2007

A single transient episode of hyperammonemia induces long-lasting alterations in protein kinase A. Am J Physiol Gastrointest Liver Physiol 292: G305-G314,2007; doi:10.1152/ajpgi.00100.2006.-Hepatic encephalopathy in patients with liver disease is associated with poor prognosis. This could be due to the induction by the transient episode of hepatic encephalopathy of long-lasting alterations making patients more susceptible. We show that a single transient episode of hyperammonemia induces long-lasting alterations in signal transduction. The content of the regulatory subunit of the protein kinase dependent on cAMP (PKA-RI) is increased in erythrocytes from cirrhotic patients. This increase is…

soluble guanylate cyclaseAdultLiver CirrhosisMalemedicine.medical_specialtyCirrhosisErythrocytesPhysiologyliver cirrhosisEncephalopathyhepatic encephalopathyBiologyHepatitisLiver diseaseLiver Function TestsReference ValuesPhysiology (medical)Internal medicinemedicineAnimalsHumansHyperammonemiaRats WistarProtein kinase AHepatic encephalopathyAgedHepatologyPortacaval anastomosisMetabolic disorderErythrocyte MembraneGastroenterologyAscitesHyperammonemiaMiddle Agedmedicine.diseaseCyclic AMP-Dependent Protein KinasesRatsDisease Models AnimalEndocrinologyChronic Diseaserat modelsFemaleLiver FailureAmerican journal of physiology. Gastrointestinal and liver physiology
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