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Träfflista för sökning "WFRF:(Czeiter Endre) srt2:(2007-2009)"

Sökning: WFRF:(Czeiter Endre) > (2007-2009)

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1.
  • Martens-Lobenhoffer, Jens, et al. (författare)
  • Determination of cerebrospinal fluid concentrations of arginine and dimethylarginines in patients with subarachnoid haemorrhage
  • 2007
  • Ingår i: Journal of Neuroscience Methods. - : Elsevier. - 0165-0270 .- 1872-678X. ; 164:1, s. 155-160
  • Tidskriftsartikel (refereegranskat)abstract
    • Elevated cerebrospinal fluid (CSF) concentrations of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), are assumed to be related to delayed vasospasm after subarachnoid haemorrhage (SAH). However, data on CSF concentrations of L-arginine, ADMA and its structural isomer symmetric dimethylarginine (SDMA) are very sparse in humans. We here present a new hydrophilic interaction chromatography-tandem mass spectrometry (HILIC-MS-MS) method for the precise determination of these substances in CSF. The method requires only minimal sample preparation and features isotope labeled internal standards. First data of patients with SAH showed that on the day of admission CSF concentration values of L-arginine and ADMA were not significantly different from controls, but increased markedly during the course of the hospital stay. The decrease of the L-arginine to ADMA ratio points to a progressive impairment of the NO production rate in the brain after SAH which is confirmed by a simultaneous decrease in nitrate and nitrite concentrations in CSF. 
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2.
  • Auer, Tibor, et al. (författare)
  • SÚLYOS KOPONYA-AGY SÉRÜLÉS VIZSGÁLATADIFFÚZIÓS TENZOR ÉS FUNKCIONÁLISMR-KÉPALKOTÁSSAL ALACSONY TÉRERÔN : [Diffusion tensor and functional MR imaging of severe traumatic craniocerebral injury at low magnetic field]
  • 2007
  • Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 60:11-12, s. 480-488
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim of the study: Presentation of diffusion tensor imaging (DTI) performed at low magnetic field (1 Tesla) in the algorithm of work-up of a patient suffering from severe traumatic brain injury (TBI).Method: DTI and functional MRI (fMRI) were applied at 1 Tesla for visualization of neural pathways and examination of sensory functions of a patient with severe TBI. DTI-measurement was also performed on a healthy patient for comparison.Results: DTI acquired at low magnetic field yielded appropriate visualization of neural pathways. DTI confirmed the results of the clinical and fMRI examinations in the patient suffering from severe TBI.Conclusion: An optimized DTI can be useful in the examination of patients with TBI, moreover, it may also help in the establishment of diagnoses of other central nervous system diseases affecting neuronal pathways. The presented results suggest that DTI of appropriate quality can be performed at low magnetic field.
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3.
  • Büki, Andras, 1966-, et al. (författare)
  • Clinical and model research of neurotrauma
  • 2009
  • Ingår i: Methods in Molecular Biology. - Totowa, NJ : Humana Press. - 1064-3745 .- 1940-6029. ; 566, s. 41-55
  • Tidskriftsartikel (refereegranskat)abstract
    • Modeling traumatic brain injury represents a major challenge for neuroscientists - to represent extremely complex pathobiological processes kept under close surveillance in the most complex organ of a laboratory animal. To ensure that such models also reflect those alterations evoked by and/or associated with traumatic brain injury (TBI) in man, well-defined, graded, simple injury paradigms should be used with clear endpoints that also enable us to assess the relevance of our findings to human observations. It is of particular importance that our endpoints should harbor clinical significance, and to this end, biological markers ultimately associated with the pathological processes operant in TBI are considered the best candidate. This chapter provides protocols for relevant experimental models of TBI and clinical materials for neuroproteomic analysis. 
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4.
  • Czeiter, Endre, et al. (författare)
  • Calpain inhibition reduces axolemmal leakage in traumatic axonal injury
  • 2009
  • Ingår i: Molecules. - : MDPI. - 1431-5157 .- 1420-3049. ; 14:12, s. 5115-5123
  • Tidskriftsartikel (refereegranskat)abstract
    • Calcium-induced, calpain-mediated proteolysis (CMSP) has recently been implicated to the pathogenesis of diffuse (traumatic) axonal injury (TAI). Some studies suggested that subaxolemmal CMSP may contribute to axolemmal permeability (AP) alterations observed in TAI. Seeking direct evidence for this premise we investigated whether subaxolemmal CMSP may contribute to axolemmal permeability alterations (APA) and pre-injury calpain-inhibition could reduce AP in a rat model of TAI. Horseradish peroxidase (HRP, a tracer that accumulates in axons with APA) was administered one hour prior to injury into the lateral ventricle; 30 min preinjury a single tail vein bolus injection of 30 mg/kg MDL-28170 (a calpain inhibitor) or its vehicle was applied in Wistar rats exposed to impact acceleration brain injury. Histological detection of traumatically injured axonal segments accumulating HRP and statistical analysis revealed that pre-injury administration of the calpain inhibitor MDL-28170 significantly reduced the average length of HRP-labeled axonal segments. The axono-protective effect of pre-injury calpain inhibition recently demonstrated with classical immunohistochemical markers of TAI was further corroborated in this experiment; significant reduction of the length of labeled axons in the drug-treated rats implicate CMSP in the progression of altered AP in TAI. 
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5.
  • Czeiter, Endre, et al. (författare)
  • Traumatic axonal injury in the spinal cord evoked by traumatic brain injury
  • 2008
  • Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 25:3, s. 205-213
  • Tidskriftsartikel (refereegranskat)abstract
    • Although it is well known that traumatic brain injury (TBI) evokes traumatic axonal injury (TAI) within the brain, TBI-induced axonal damage in the spinal cord (SC) has been less extensively investigated. Detection of such axonal injury in the spinal cord would further the complexity of TBI while also challenging some functional neurobehavioral endpoints frequently used to assess recovery in various models of TBI. To assess TAI in the spinal cord associated with TBI, we analyzed the craniocervical junction (CCJ), cervico-thoracic (CT), and thoraco-lumber (ThL) spinal cord in a rodent model of impact acceleration of TBI of varying severities. Rats were transcardially fixed with aldehydes at 2, 6, and 24 h post-injury (n = 36); each group included on sham-injured rodent. Semi-serial vibratome sections were reacted with antibodies targeting TAI via alteration in cytoskeletal integrity or impaired axonal transport. Consistent with previous observations in this model, the CCJ contained numerous injured axons. Immunoreactive, damaged axonal profiles were also detected as caudal, as the ThL spinal cord displayed morphological characteristics entirely consistent with those described in the brainstem and the CCJ. Quantitative analyses demonstrated that the occurrence and extent of TAI is positively associated with the impact/energy of injury and negatively with the distance from the brainstem. These observations show that TBI can evoke TAI in regions remote from the injury site, including the spinal cord itself. This finding is relevant to shaken baby syndrome as well as during the analysis of data in functional recovery in various models of TBI. 
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6.
  • Lückl, Jááos, et al. (författare)
  • Protein biomarkerek szerepe a koponyasérüles kísérletes modelljeiben és a klinikumban : [Protein biomarkers in experimental models and in clinical care of traumatic brain injury]
  • 2007
  • Ingår i: Ideggyogyaszati Szemle. - : Literatura Medica Kiado. - 0019-1442 .- 2498-6208. ; 60:7-8, s. 284-294
  • Forskningsöversikt (refereegranskat)abstract
    • Traumatic brain injury is the leading cause of mortality in Hungary in the population under 40 years of age. In Western societies, like the United Sates, traumatic brain injury represents an extreme social-economic burden, expected to become the third leading cause of mortality until 2020. Despite its' epidemiological significance, experimental therapeutic modalities developed in the last few decades did not prove efficient in the clinical care of severe traumatic brain injury. The reason for such a lack of success in terms of translating experimental results to clinical treatment at least partially could be explained by the paucity and the low sensitivity and specificity of clinical parameters endowing us to monitor the efficacy of the therapy. The drive for finding clinical parameters and monitoring tools that enable us to monitor treatment efficacy as well as outcome focused recent attention on biomarkers (and) surrogate markers that are based on rational pathological processes associated with/operant in traumatic brain injury. This review summarizes those biomarkers that could purportedly be used to monitor the treatment of the severely head injured while also providing information on salvageability facilitating the conduction of more rationally designed clinical studies. 
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