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1
Content available remote

Comparison of cerebrocortical microvascular effects of different hypoxic-ischemic insults in piglets: a LASER-speckle imaging study

100%
Domoki F., Zolei-Szenasi D., Olah O., Toth-Szuki V., Nemeth J., Hopp B., Bari F., Smausz T.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 4
2

Acidosis inhibits calcium accumulation in intrasynaptosomal mitochondria

100%
Fedorovich S. V., Aksentsev S. L., Konev S. V.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 3
3

Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

84%
Strosznajder J., Chalimoniuk M.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 1
4

Changes of Ca 2-calmodulin-dependent protein kinase-II after transient ischemia in gerbil hippocampus

84%
Zalewska T., Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 1
5

Calcium transients in brain ischemia : role in neuronal injury

84%
Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 1
6

Role of brain glutamic acid metabolism changes in neurodegenerative pathologies

67%
Kanunnikova N. P.
Journal of Biology and Earth Sciences
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2012
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tom 02
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nr 1
7

Intracerebral transplantation of human umbilical cord blood-derived neural stem cells (HUCB-NSC) in rats after focal brain ischemia ameliorates tissue expression of endogenous and exogenous neurotrophic factors

67%
Jablonska A., Drela K., Wojcik-Stanaszek L., Wanacka E., Zalewska T., Lukomska B.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
There is a great interest in the possibility of repairing the nervous system by transplantation new cells that can replace those lost through damage in neurological disorders. Key functions such as the replacement of neural cells have been recently challenged by intrinsic bystander capacities of undifferentiated donor cells to restore these cells. A comprehensive knowledge how transplanted stem cells exert their therapeutic achievements is still lacking. Here we investigated the effects of HUCB-NSC infused into the damaged rat brain at 72 h post ischemia on endogenous neurogenesis. The goal of our studies was to examine the proliferation and migration of host progenitor cells, analyze the substantial matrix remodeling of tissue and the presence of neurotrophic factors in rat brain after focal ischemia followed by HUCB-NSC transplantation. Methods: 2×104 HUCB-NSC were transplanted into corpus callosum of naive or focally injured rat brain 3 days after ischemic insult. At 1, 3, 7 and 14 days rat brains were removed. Endogenous cell proliferation was determined by BrdU incorporation. Then immunocytochemical analysis of doublecortin (DCX) and PSA-NCAM (markers expressed by immature migratory neuroblasts), and in situ zymography of MMPs activity was performed. Additionally, total RNA was isolated from rat brain tissue and RTPCR was performed using sets of primers of each of human and rat neurotrophic factor genes. Results: OUA-induced brain lesion resulted in increase of proliferating (BrdU+) and migrating (DCX+ and PSA-NCAM+) cells in subventricular zone (SVZ) and subgranular zone (SGZ) regions in comparison to intact rats. This response has been potentiated by HUCB-NSC transplantation. At 7th day after HUCB-NSC infusion the intense migration of DCX+cells from SVZ towards ischemic boundary regions of the striatum was observed. Moreover, the activation of MMPs in cells was visible in SVZ. Double-labeling showed co-localization of DCX marker with MMPs activity. The presence of MMPs appeared to be associated with cell nuclei and cytoplasm but interestingly it was also seen outside the cell bodies and in the neuronal protrusions. In OUAinduced lesion rat brain tissue, the expression pattern of rat-origin neurotrophic factors mRNA was higher than in intact rats. HUCBNSC transplantation into focal brain ischemic tissue significantly increased mRNA expression of several rat-origin growth factors, such as GDNF, CNTF responsible for regulation of proliferation and maturation of stem cells as well as IGF-1, HGF and presaposin functioning as anti-apoptotic mediators. The significant increment was observed 7 days after HUCB-NSC infusion. Using Real Time PCR method we were able to detect the presence of mRNA of BDNF, GDNF, NT3, IGF-1, HGF, semaphorin and presaposin of human-origin factors in the rat brain recipients of HUCB-NSC grafts. Conclusions: Transplantation of HUCB-NSC triggers early expansion of endogenous progenitor pool increasing fraction of proliferating cells in SVZ and SGZ of brain ischemic rats. Proteolytic activity of MMPs in extracellular compartment suggests its ability to remodel extracellular matrix and facilitate migration of neuroblasts to the damaged brain areas. The mechanism promoting recovery from ischemic injury remains to be clarified, although it is likely that it might be due to HUCB-NSC graft-induced release of neurotrophic factors by the host cells as well as the presence of human neural stem cells derived factors. Supported by MMRC statutory fund.
8
Content available remote

The neuroprotective effect of 2-oxoglutarate in the experimental ischemia of hippocampus

67%
Kovalenko T. N., Ushakova G. A., Osadchenko I., Skibo G. G., Pierzynowski S. G.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 2
In this study we investigated the potential neuroprotective effect of 2-oxoglutarate (2-OG) on the hippocampus in the transient vessel occlusion ischemia model in the Mongolian gerbil. The morphological and biochemical studies were performed at 7 days after occlusion of carotid arteries. The acute reduction of NeuN-positive neurons in the CA1 pyramidal layer of the hippocampus was accompanied by increased staining intensity for GFAP-positive astrocytes, indicative of glial reaction. The neuron death in the CA1 area coincided with a strong 2.4 fold decrease in the membrane forms of neuronal cell adhesion molecules and elevated levels of astrocyte-specific proteins (soluble GFAP to 2,6 times; filament GFAP to 1,5 times; calcium-binding protein S-100b to 1,6 times). Treatment with 2-oxoglutarate (2.28 g/l drinking water) for between 7 and 21 days attenuated the neuronal death and reactive astrogliosis in this model of experimental ischemia by 20-50%. Our results suggest that 2-OG may prevent the disturbances of neural cells that usually take place during ischemic pathology.
9
Content available remote

The importance of selected markers of inflammation and blood-brain barrier damage for short-term ischemic stroke prognosis

67%
Lasek-Bal A., Jedrzejowska-Szypulka H., Student S., Warsz-Wianecka A., Zareba K., Puz P., Bal W., Pawletko K., Lewin-Kowalik J.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 2
10

Oxygen-glucose deprivation (OGD) promotes microglia activation and gliogenesis but not neurogenesis in organotypic hippocampal slice culture (OHC)

67%
Ziemka-Nalecz M., Wojcik-Stanaszek L., Zajac H., Zalewska T.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr 1
Organotypic hippocampal cultures are used as an alternative model for studying molecular mechanism(s) of neurogenesis after combined oxygen-glucose deprivation (OGD) mimicking ischemic conditions. The aim of the present work was to investigate the effect of OGD on stem/progenitor cells proliferation and/or differentiation in the hippocampus. Our attention was primarily focused on the relationship between neurogenesis-associated processes and activity of matrix metalloproteinases (MMPs). Cell proliferation was detected by using BrdU incorporation. Newly generated BrdU (+) cells were identified by labeling with specific cell markers. In order to check the activity and localization of MMPs we conducted in situ zymography in conjunction with immunohistochemistry. In our experimental conditions OGD-insult followed by 24 h of recovery caused the damage of neuronal cells in CA1. At 1 week cell death appears all over the hippocampus. We found that expected stimulation of endogenous neurogenesis fails as a source of compensation for the lost neurons in OGD-treated cultures. The modulation of culture microenvironment after ischemia favors the dominant proliferation of glial cells expressed by the enhancement of newly-generated oligodendrocyte progenitors. In addition, during our study we also detected some BrdU labeled nuclei encapsulated by GFAP positive processes. However, the majority of BrdU positive cells expressed microglial specific stain, particularly pronounced in CAlarea. The OGD-promoted responses involved activation of metalloproteinases, which matches the progression of gliogenesis. On the other hand, the high activity of MMPs associated with microglial cells implicate their involvement in the mechanism participating in OGD-induced cell damage.
11

Protein serine-threonine kinases [PKA, PKC and CaMKII] involved in ischemic brain pathology

67%
Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 2
12

Gene expression in neuronal apoptosis - looking for a therapeutic window

67%
Figiel I., Filipkowski R. K., Hetman M., Kaminska B., Kaczmarek L.
Biotechnologia
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1996
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nr 4
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