Search results for "Protective Agent"

showing 10 items of 226 documents

Erythropoietin in Traumatic Brain Injury: An Answer Will Come Soon

2015

Traumatic brain injury (TBI) is a major cause of morbidity and mortality in the United States. It is estimated that each year TBIs are associated with 1.1 million emergency department visits, 235,000 hospitalizations, and 50,000 deaths (1). Despite improvements in medical interventions, there are still no neuroprotective agents available to counteract secondary or delayed damage to the traumatically injured human brain or to promote its repair. TBI encompasses heterogeneous etiologic, anatomical, and molecular patterns of injury that exhibit different propensities to cause cerebral damage. Without careful consideration of individual injuries, the results of therapeutic trials remain difficu…

medicine.medical_specialtyClinical Trials as Topicbusiness.industryTraumatic brain injurySettore MED/27 - NeurochirurgiaMedicine (all)Neuroprotective AgentRecombinant Proteinmedicine.diseaseRecombinant ProteinsEpoetin AlfaNeuroprotective AgentsErythropoietinBrain InjuriesBrain InjurieReceptors ErythropoietinMedicineHumansSurgeryNeurology (clinical)businessIntensive care medicineErythropoietinmedicine.drugHuman
researchProduct

Will it ever become possible to prevent dopaminergic neuronal degeneration?

2008

Parkinsons disease (PD) is the second leading age-related degenerative brain disease in the world affecting millions of people. This neurological disorder disrupts the quality of life of patients and their families, exerts an enormous emotional and physical strain on caregivers, and has a large cost for society. Moreover, the increasing numbers of elderly people in the population will result in a sharp increase in the prevalence of PD. The understanding of its pathophysiology and treatment has advanced at a very impressive rate during past decades. Nevertheless, PD is still fatal and there is at present no cure for it. Furthermore, there are no proven therapies for prevention of PD and alth…

medicine.medical_specialtyDopaminePopulationNeurological disorderDiseaseNeuroprotectionSettore BIO/09 - FisiologiaNeuroprotective agentsRisk FactorsmedicineAnimalsHumansNeuronal degenerationNeurodegeneration Neuroprotection Parkinson's diseaseIntensive care medicineeducationPharmacologyNeuronseducation.field_of_studyCell Deathbusiness.industryGeneral NeuroscienceDopaminergicNeurodegenerative DiseasesParkinson's disease -- Treatmentmedicine.diseaseBrain diseaseNeuroprotective AgentsDrug developmentbusinessNervous system -- Degeneration
researchProduct

Neuroprotective Actions of Estradiol and Novel Estrogen Analogs in Ischemia: Translational Implications

2010

This review highlights our investigations into the neuroprotective efficacy of estradiol and other estrogenic agents in a clinically relevant animal model of transient global ischemia, which causes selective, delayed death of hippocampal CA1 neurons and associated cognitive deficits. We find that estradiol rescues a significant number of CA1 pyramidal neurons that would otherwise die in response to global ischemia, and this is true when hormone is provided as a long-term pretreatment at physiological doses or as an acute treatment at the time of reperfusion. In addition to enhancing neuronal survival, both forms of estradiol treatment induce measurable cognitive benefit in young animals. Mo…

medicine.medical_specialtyGPR30hippocampusIschemiaEstrogen receptorHippocampusNeuroprotectionArticleEstradiol CongenersIschemiaInternal medicineestradiolmedicineAnimalsHumansEndocrine and Autonomic Systemsbusiness.industryCREBEstrogen analogapoptosismedicine.diseasestrokeglobal ischemiainsulin-like growth factor-1EndocrinologyNeuroprotective AgentsneuroprotectionEstradiol CongenersbusinessGPERhormones hormone substitutes and hormone antagonistsHormoneestrogen receptor
researchProduct

Soy-derived phytoestrogens as preventive and acute neuroprotectors in experimental ischemic stroke: Influence of rat strain

2011

The ability of a soy-based high-phytoestrogen diet (nutritional intervention) or genistein (pharmacological intervention), to limit ischemic brain damage in Wistar, Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats, has been assessed. As to the nutritional intervention, two groups from each strain received either a phytoestrogen-free (PE-0) or a high-phytoestrogen (PE-600) diet from weaning to adulthood. As to the pharmacological intervention, all animals were fed the standard soy-free AIN-93G diet and subsequently separated into two groups from each strain to receive either pure genistein (aglycone form, 1mg/kg/day intraperitoneal) or vehicle at 30 min reperfusion. After an epis…

medicine.medical_specialtyIschemiaPharmaceutical ScienceGenisteinBlood PressurePhytoestrogensBrain IschemiaBrain ischemiachemistry.chemical_compoundInternal medicineDrug DiscoveryAnimalsMedicineWeaningcardiovascular diseasesPharmacologyPlant Extractsbusiness.industryRats Inbred StrainsCerebral InfarctionIsoflavonesmedicine.diseaseGenisteinRatsStrokeNeuroprotective AgentsEndocrinologyBlood pressureComplementary and alternative medicinechemistryReperfusion InjuryMolecular MedicinePhytoestrogensSoybeansbusinessReperfusion injuryPhytotherapyPhytomedicine
researchProduct

Practical importance of neuroprotection in Parkinson's disease.

2003

Consensus could be reached that there is overwhelming evidence of preclinical neuroprotection. However, the evidence of neuroprotection/neurorescue under clinical conditions is limited. Lessons from clinical trials designed to show neuroprotection (selegiline, amantadine, dopamine agonists) demonstrate that with the drugs available neuroprotection/neurorescue has to start as early as possible. A PET-controlled clinical trial with ropinirole shows that there seems to be a good chance for neuroprotection in the early phase of Parkinson's disease in patients treated from the very beginning of the disease while there is no such benefit in patients with a late start of a neuroprotective therapeu…

medicine.medical_specialtyNeurologyParkinson's diseaseIndolesBioinformaticsNeuroprotectionAntiparkinson AgentsDegenerative diseaseSelegilineAmantadineMedicineHumansbusiness.industrySelegilineAmantadineParkinson Diseasemedicine.diseaseClinical trialRopiniroleNeuroprotective AgentsNeurologyDopamine AgonistsNeurology (clinical)businessNeurosciencemedicine.drugJournal of neurology
researchProduct

Viability and function of the cryopreserved whole rat ovary: comparison between slow-freezing and vitrification

2011

Objective To investigate four different protocols for cryopreservation of the whole rat ovary with intact vasculature to evaluate whether differences exist in post-thawing viability of the ovary after either vitrification or slow freezing. Design Experimental study. Setting Obstetrics and gynecology department. Animal(s) Immature Sprague-Dawley female rats. Intervention(s) Ovaries were isolated with the vascular tree intact up to the bifurcation of the abdominal aorta and were subsequently cannulated. The ovaries were flushed with increasing concentrations of the cryoprotectant dimethyl sulfoxide (DMSO) to either 1.5 or 7 M. The ovaries underwent cryopreservation by vitrification or passive…

medicine.medical_specialtyNeutral redTime FactorsCryoprotectantApoptosisOvaryBiologyCryopreservationRats Sprague-DawleyTissue Culture TechniquesAndrologychemistry.chemical_compoundCryoprotective AgentsOvarian FollicleFreezingFollicular phasemedicineAnimalsDimethyl SulfoxideVitrificationIncubationCryopreservationTissue SurvivalGynecologyDose-Response Relationship DrugEstradiolCaspase 3Dimethyl sulfoxideOvaryFertility PreservationObstetrics and GynecologyOrgan PreservationImmunohistochemistryVitrificationRatsPerfusionmedicine.anatomical_structureReproductive MedicinechemistryFemaleFertility and Sterility
researchProduct

Oxygen and glucose deprivation induces major dysfunction in the somatosensory cortex of the newborn rat

2005

The mechanisms and functional consequences of ischemia-induced injury during perinatal development are poorly understood. Subplate neurons (SPn) play a central role in early cortical development and a pathophysiological impairment of these neurons may have long-term detrimental effects on cortical function. The acute and long-term consequences of combined oxygen and glucose deprivation (OGD) were investigated in SPn and compared with OGD-induced dysfunction of immature layer V pyramidal cortical neurons (PCn) in somatosensory cortical slices from postnatal day (P)0-4 rats. OGD for 50 min followed by a 10-24-h period of normal oxygenation and glucose supply in vitro or in culture led to pron…

medicine.medical_specialtyPatch-Clamp TechniquesTolbutamideIn Vitro TechniquesBiologySomatosensory systemMembrane PotentialsInternal medicineSubplatemedicineExtracellularAnimalsHypoglycemic AgentsMagnesiumEnzyme InhibitorsHypoxiaOuabainNeuronsMembrane potentialCaspase 3General NeuroscienceDose-Response Relationship RadiationDepolarizationSomatosensory CortexHyperpolarization (biology)ImmunohistochemistryElectric StimulationRatsGlucoseNeuroprotective AgentsEndocrinologymedicine.anatomical_structureAnimals Newbornnervous systemApoptosisCaspasesNMDA receptorDizocilpine MaleateEuropean Journal of Neuroscience
researchProduct

The addition of simvastatin administration to cold storage solution of explanted whole liver grafts for facing ischemia/reperfusion injury in an area…

2018

Abstract Background Liver transplantation is the best treatment for end-stage liver disease. The interruption of the blood supply to the donor liver during cold storage damages the liver, affecting how well the liver will function after transplant. The drug Simvastatin may help to protect donor livers against this damage and improve outcomes for transplant recipients. The aim of this study is to evaluate the benefits of treating the donor liver with Simvastatin compared with the standard transplant procedure. Patient and methods We propose a prospective, double-blinded, randomized phase 2 study of 2 parallel groups of eligible adult patients. We will compare 3-month, 6-month, and 12-month g…

medicine.medical_specialtySimvastatinmedicine.medical_treatmentlcsh:SurgeryCold storageIschemia/reperfusion injury030230 surgeryLiver transplantationDonor after brain deathPlaceboProtective Agents03 medical and health sciencesLiver diseaseStudy Protocol0302 clinical medicineDouble-Blind MethodDonor after brain death; Ischemia/reperfusion injury; Liver transplantation; SimvastatinMedicineHumansProspective StudiesLiver transplantationbusiness.industrylcsh:RD1-811General Medicinemedicine.diseaseSurgeryTransplantationFatty LiverRegimenLiverSimvastatinReperfusion Injury030211 gastroenterology & hepatologySurgerybusinessReperfusion injurymedicine.drugBMC surgery
researchProduct

Erythropoietin for Subarachnoid Hemorrhage: Is There a Reason for Hope?

2011

I b S a r a S ubarachnoid hemorrhage (SAH) associated with a ruptured cerebral aneurysm remains a source of significant morbidity and mortality, not only from the initial hemorrhage but lso from the delayed complications, such as cerebral vasospasm ften severe enough to induce irreversible changes in cerebral erfusion. Several drugs have been developed that have the otential to limit cerebral vasospasm and delayed ischemic eurologic deficit, thus improving outcome for patients. Howver, although numerous agents that can prevent arterial narrowng and/or block the excitatory cascade of events leading to schemic neuronal death in experimental conditions, there is still o pharmacologic agent tha…

medicine.medical_specialtySubarachnoid hemorrhageErythropoietin subarachnoid hemorrhageBlood volumeAneurysm RupturedNeuroprotectionAneurysmCerebral vasospasmInternal medicinemedicineErythropoietin; Neuroprotection; Subarachnoid hemorrhageHumansSubarachnoid hemorrhageErythropoietinSettore MED/27 - Neurochirurgiabusiness.industryEpoetin alfaPharmacologic Agentmedicine.diseaseRecombinant ProteinsNeuroprotectionEpoetin AlfaNeuroprotective AgentsErythropoietinCardiologySurgeryNeurology (clinical)businessmedicine.drug
researchProduct

Increased Connexin 43 Expression as a Potential Mediator of the Neuroprotective Activity of the Corticotropin-Releasing Hormone

2009

CRH is a major central stress mediator, but also a potent neuroprotective effector. The mechanisms by which CRH mediates its neuroprotective actions are largely unknown. Here, we describe that the gap junction molecule connexin43 (Cx43) mediates neuroprotective effects of CRH toward experimentally induced oxidative stress. An enhanced gap junction communication has been reported to contribute to neuroprotection after neurotoxic insults. We show that CRH treatment up-regulates Cx43 expression and gap junctional communication in a CRH receptor-dependent manner in IMR32 neuroblastoma cells, primary astrocytes, and organotypic hippocampal slice cultures. MAPKs and protein kinase A-cAMP response…

medicine.medical_specialtyendocrine systemCorticotropin-Releasing HormoneMAP Kinase Signaling SystemCarbenoxoloneConnexinBiologyNeuroprotectionModels BiologicalArticleRats Sprague-DawleyCorticotropin-releasing hormoneMiceEndocrinologyMediatorInternal medicineCell Line Tumormedicinepolycyclic compoundsAnimalsHumansProtein kinase AMolecular BiologyGap junctionBrainGap JunctionsGeneral MedicineCell biologyRatsEndocrinologyNeuroprotective Agentsnervous systemGene Expression RegulationConnexin 43cardiovascular systemSignal transductionhormones hormone substitutes and hormone antagonistsmedicine.drugSignal Transduction
researchProduct