oalib

Publish in OALib Journal

ISSN: 2333-9721

APC: Only $99

Submit

Any time

2018 ( 1 )

2016 ( 1 )

2015 ( 6 )

2014 ( 24 )

Custom range...

Search Results: 1 - 10 of 1278 matches for " Vesna Selakovi? "
All listed articles are free for downloading (OA Articles)
Page 1 /1278
Display every page Item
Neuron-specific enolase in cerebrospinal fluid and plasma of patients with acute ischemic brain disease
SelakoviVesna M.
Medicinski Pregled , 2003, DOI: 10.2298/mpns0308326s
Abstract: The objective of this research was to determine the dynamics of change of neuron-specific enolase concentration in patients with acute ischemic brain disease in cerebrospinal fluid and plasma. The study included 103 patients, their mean age 58-66 years. The control group consisted of 16 patients, of matching age and sex, with radicular lesions of discal origin, subjected to diagnostic radiculography. Concentration of neuron-specific enolase was measured by a flouroimmunometric method. The results showed that the concentration of neuron-specific enolase in cerebrospinal fluid and plasma of patients with brain ischemic disease within first seven days significantly increased compared to the control. The highest increase of concentration was established in brain infarction, somewhat lower in reversible ischemic attack, and the lowest in transient ischemic attack. Maximal concentration was established on the 3rd-4th day upon the brain infarction. Neuron-specific enolase concentration in cerebrospinal fluid and plasma may be an indicator of pathophysiological processes in the acute phase of brain ischemia and is significant in early diagnostics and therapy of the disease.
Cortisol in plasma and cerebrospinal fluid of patients with brain ischemia
SelakoviVesna M.
Medicinski Pregled , 2004, DOI: 10.2298/mpns0408354s
Abstract: Introduction One of the reactions to ischemia is increased release of glucocorticoid hormones, included in regulation of effects of numerous mediators/modulators that could be released in the acute phase of brain ischemia. The aim of our investigation was to define temporal dynamics of cortisol concentrations in plasma and cerebrospinal fluid of patients with different types of ischemic brain disease. Material and methods The study included 263 patients of both sexes, aged 55-68 years. History, clinical examination and cerebral computerized tomography were performed to establish the diagnosis. 97 patients had brain infarction, 66 had a reversible ischemic attack, 66 had a transient ischemic attack, and 34 patients had chronic encephalopathy. The control group included 22 age- and sex- matched patients, subjected to diagnostic lumbar radiculography, without disturbances in the cerebrospinal fluid passage. Cortisol concentrations were measured by direct radioimmunoassay. Results and discussion Results obtained in this research showed that in acute brain ischemic period there was a significant increase of cortisol concentration in plasma and cerebrospinal fluid. The increase was highest in patients with brain infarction, somewhat lower in reversible ischemic attack, and the lowest in transient ischemic attack compared to controls (331.7±92.8 pmol/ml of plasma and 2.5±1.1 pmol/ml of cerebrospinal fluid). Maximum concentrations were found during the first two days after insult. The main potentially protective effects of increased cortisol concentrations in patients with acute stroke could be the decrease of effects of deleterious reactions induced by ischemia. This mechanism might be an attempt of organism to compensate for disturbed homeostasis. Conclusion Measurement of cortisol in plasma and cerebrospinal fluid in patients with acute stroke is significant for monitoring the intensity of response of an organism to acute brain damage.
Mitochondrial superoxide production and MnSOD activity following exposure to an agonist and antagonists of ionotropic receptors in rat brain
Radenovi? Lidija Lj.,SelakoviVesna
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0501001r
Abstract: The involvement of NMDA and AMPA/kainate receptors in the induction of superoxide production in the rat brain was examined after intrahippocampal injection of kainate, a non-NMDA receptor agonist; kainate plus CNQX, a selective AMPA/kainate receptor antagonist; or kainate plus APV, a selective NMDA receptor antagonist. The measurements took place at different times in the ipsi- and contralateral hippocampus, forebrain cortex, striatum, and cerebellum homogenates. The used glutamate antagonists both ensured sufficient neuroprotection in the sense of lowering superoxide production and raising MnSOD levels, but in the mechanisms and time dynamics of their effects were different. Our findings suggest that NMDA and AMPA/kainate receptors are differentially involved in superoxide production. UDC 612.815 612.82.
Kainate-induced oxidative stress and neurotoxicity in the rat brain
Radenovi? Lidija Lj.,SelakoviVesna
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0504259r
Abstract: We investigated superoxide production and MnSOD activity after kainate injection into the CA3 region of the rat hippocampus. The measurements took place at different times in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. Free radicals including superoxide are responsible for post-lesional cytotoxicity. Neuronal cells responded to oxidative stress in kainate-induced neurotoxicity and caused the protective mechanism to increase MnSOD levels. The increase of MnSOD in distinct brain regions functionally connected via afferents and efferent suggests that these regions are affected by the injury. It implies that MnSOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity.
Does occupational exposure to low-dose ionizing radiation induce cell membrane damage?
?urovi? Branka 1,SelakoviVesna M.,Spasi?-Joki? Vesna M.
Archive of Oncology , 2004, DOI: 10.2298/aoo0404197d
Abstract: BACKGROUND: Chronic exposure to low-dose radiation doses could be much more harmful than high, short-term doses because of lipid peroxidation initiated by free radicals. The cell membranes and cellular organelles are the main targets for free radicals attack. Peroxidation of cell membrane increases with decreasing dose rate (Petkau effect). The aim of this study was to establish if chronic occupational exposure to low-dose ionizing radiation could induce cell membrane damage. METHODS: Our investigation comprised 77 medical workers: 44 occupationally exposed to ionizing radiation (E), divided in two subgroups-exposed to x-rays (Ex) or gamma rays (En), and 33 controls (C). Informed consent and questionnaire containing dietary, habits, medical factors and exposure history were taken. Groups were matched in gender, age, dietary habits, alcohol consumption, smoking habit, and specific exposure time. Radiation dose accumulated by occupationally exposed over years was calculated on the basis of individual TL-dose records. Besides regular biochemical and cytogenetic tests, lipid peroxidation index, expressed as malondyaldehyde production was performed. RESULTS: Significantly higher lipid peroxidation index was found in workers occupationally exposed to low-dose of ionizing radiation (p>0.000028), which is correlated with age, smoking habit, and significantly correlated with doses. After blood samples in vitro irradiation by 2 Gy of gamma-radiation malondyaldehyde production significantly increased in each group, but were not significantly different between groups. CONCLUSION: Lipid peroxidation index could be considered as triage parameter for further cytogenetic studies in workers chronically exposed to low-dose radiation.
N-Methyl-3,4-methylenedioxyamphetamine-induced hepatotoxicity in rats: Oxidative stress after acute and chronic administration
Ninkovi? Milica,Mali?evi? ?ivorad,SelakoviVesna M.,Simi? Ivan
Vojnosanitetski Pregled , 2004, DOI: 10.2298/vsp0402125n
Abstract: Background. The underlying mechanisms of N-Methyl-3,4-methylenedioxyamphetamine-MDMA-induced hepatotoxicity are still unknown. The aim of this study was to evaluate hepatic oxido-reductive status in the rats liver after the single and repeated administration of MDMA. Methods. MDMA was dissolved in distilled water and administered in the doses of 5 mg, 10 mg, 20 mg, and 40 mg/kg. The animals from the acute experiment were treated per os with the single dose of the appropriate solution, through the orogastric tube. The animals from the chronic experiment were treated per os, with the doses of 5, 10, or 20 mg/kg of MDMA every day during 14 days. The control groups were treated with water only. Eight hours after the last dose, the animals were sacrificed, dissected their livers were rapidly removed, frozen and stored at -70°C until the moment of analysis. The parameters of oxidative stress in the crude mitochondrial fractions of the livers were analyzed. Results. Superoxide dismutase (SOD) activity increased in the livers of the animals that were treated with single doses of MDMA. Chronically treated animals showed the increased SOD activity only after the highest dose (20 mg/kg). The content of reduced glutathione decreased in both groups, but the depletion was much more expressed after the single administration. Lipid peroxidation index increased in dose-dependent manner in both groups, being much higher after the single administration. Conclusion. The increased index of lipid peroxidation and the decreased reduced glutathione levels suggested that MDMA application induced the state of oxidative stress in the liver. These changes were much more expressed after the single administration of MDMA.
Changes of cortisol levels and index of lipid peroxidation in cerebrospinal fluid of patients in the acute phase of completed stroke
SelakoviVesna M.,Jovanovi? Marina D.,Jovi?i? Aco
Vojnosanitetski Pregled , 2002, DOI: 10.2298/vsp0205485s
Abstract: Background. Brain ischemia initiates series of biochemical reactions that could, directly or indirectly, induce and extend processes that damage numerous cellular and subcellular structures. One of the reactions of organism to ischemia is the increased release of glucocorticoid hormones, included in regulation of effects of numerous mediators/modulators that could be released in the acute phase of brain ischemia. Considering that brain infarction induced systemic response of organism to stress, we presumed that it reflected the contents of cortisol in the cerebrospinal fluid (CSF) during the acute phase of the disease, and that cortisol influenced damaging processes of lipid peroxidation in CNS initiated by ischemia. The aim of our investigation was to define temporal dynamics and manner correlation of cortisol concentration and index of lipid peroxidation (ILP) in the CSF patients in the acute phase of completed stroke. Methods. In this investigation we followed changes of cortisol concentration and ILP in the CSF of 53 patients in the acute phase of completed stroke. Control group included 14 age and sex matched patients, subjected to diagnostic lumbar radiculography because of the sudden motor deficiency onset, without disturbances in the CSF passage and without pain and the consequences of anti-pain and anti-inflammatory therapy. From the perspective of the duration of period after an ischemic episode patients were divided into four groups: group A: 0-6 hours (n=12), group B: 7-12 hours (n=14), group C: 13-24 hours (n=14), and group D: 24-48 hours of postischemic period (n=13). Concentration of cortisol in the CSF was measured by quantitative RIA method (Cortisol Bridge kit, Biodata). The ILP was determined according to the spectrophotometric method. Results. Concentration of cortisol in the CSF of patients with completed stroke was of amount 69 ± 6.7 pmol/ml CSF and was significantly increased (p<0.001) compared to the values of the control group (2.49 ± 0.29 pmol/ml CSF). From 0 to 6 hours after the ischemic insults concentration of cortisol in the CSF the amount was 15.9 ± 2.4 pmol/ml CSF (p<0.001), then was progressively increasing and was maximal from 13 to 24 hours after insults (123.2 ± 7.1 pmol/ml CSF), (p<0.001). In patients with completed stroke ILP in the CSF was twice increased in the course of 48 hours compared to controls (0.54 ± 0.08 nmolMDA/ml CSF), (p<0.05). By comparing the observed parameters we found significant negative correlation between this two indicators in period from 7 to 24 hours (r=-0.77), (p<0.001). Conclusion. The mai
Biochemical, pharmacological, and toxic effects of n-metil 3,4-methylenedioxyamphetamine - "ecstasy"
Mali?evi? ?ivorad,Ninkovi? Milica,Vasiljevi? Ivana,SelakoviVesna
Vojnosanitetski Pregled , 2005, DOI: 10.2298/vsp0506467m
Abstract:
Inflamatorna reakcija i athezijski molekuli u ishemiji mozga
SelakoviVesna M.,?oli? Miodrag J.,Milosavljevi? Petar
Vojnosanitetski Pregled , 2002, DOI: 10.2298/vsp0206661s
Abstract:
Neuroprotectionby MK-801 following cerebral ischemia in Mongolian gerbils
Radenovi? Lidija,SelakoviVesna,An?us P.R.
Archives of Biological Sciences , 2008, DOI: 10.2298/abs0803341r
Abstract: Global cerebral ischemia in Mongolian gerbils is an established model in experimental research on cerebral ischemia, which is characterized morphologically by selective neuronal damage in the hippocampus, striatum, and cortex. Elevated glutamate levels are thought to be a primary cause of neuronal death after global cerebral ischemia. The purpose of this study was to investigate the potential neuroprotective effects of dizocilpine malate (MK-801), a non-competitive glutamate antagonist, in the model of 10-min gerbil cerebral ischemia. Gerbils were given MK-801(3 mg/kg i.p.)or saline immediately after the occlusion. On day 4 after reperfusion, neuronal damage was examined in the hippocampus (30 μm)and striatum slices (5 μm)stained with hematoxylin/eosin, fluorescent Nissl staining and membrane tracer DiI. The striatum and C3 regions of the hippocampus were analyzed by confocal microscopy. Neuroprotection was determined by quantifying the degree of cell loss, reduction of morphologically damaged cells, and the degree of preservation of recog-nizable neuroanatomical pathways after the ischemic insult. Our results demonstrate that the neuronal damage induced by sustained ischemia is related to abnormalities in glutamatergic function associated with NMDA receptors. MK-801significantly prevented neuronal loss in the tested brain structures. All of this contributes to a better understanding of the given pathophysiological process causing ischemic neuronal damage.
Page 1 /1278
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.