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1

Biochemical aspects of damage of cardiomyocytes during ischemia and reperfusion

100%
Sklodowska M.
Postępy Higieny i Medycyny Doświadczalnej
|
1995
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vol. 49
|
issue 2
287-296
2

Calcium accumulation in synapses of the rat hippocampus after cerebral ischemia

100%
Gajkowska B., Mossakowski M. J.
Neuropatologia Polska
|
1992
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vol. 30
|
issue 2
111-126
EN
The ultrastructural localization of calcium deposits in the synapses of rat hippocampus after 10 min global cerebral ischemia was evaluated. Oxalate-pyroantimonate technique was applied. After 24 hours of postischemic recirculation enhancement of intracellular (pre- and postsynaptic parts) and extracellular (synaptic clefts) calcium deposits was found in great proportion of synapses in CA1 sector. Abundant Ca-precipitates appeared specially in synaptics clefts and in the postsynaptic parts near synaptic densities. Increased calcium deposits in some changed mitochondria were also observed, The results presented in this paper suggest synaptic modulation of calcium homeostasis, disturbed after ischemic incident. Presence of Ca-precipitates in synaptic clefts and postsynaptic parts seems to be a sensitive indicator of increased calcium influx from the extracellular to the intracellular compartments.
3

Changes in endogenous prostacyclin in the rat brain during clinical death and after resuscitation

100%
Kapuscinski A.
Neuropatologia Polska
|
1992
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vol. 30
|
issue 2
127-132
EN
By means of the radioimmunologic method changes of concentration of 6-keto prostaglandin F1alpha(PGF1alpha) - the stable metabolite of prostacyclin in the rat brain have been evaluated during 5-min clinical death and up to 2 hrs after resuscitation Ischemia did not produce significant changes of 6-keto-PGF1 in the and 7-fold control values. Later the concentration of 6-keto-PGF1alpha in the brain decreased reaching in 30 min a 3-fold the control level, and in 60 and 120 min after resuscitation control values. The reasons of unsuccessful therapy of ischemic stroke with prostacyclin are discussed.
4
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Involvement of in various cellular systems transducting evoked signal

88%
Zablocka B., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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1993
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vol. 53
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issue 1
25-29
EN
(1) We favour a hypothesis that the delayed in is iniated by the increase of intracellular concentration, activating transiently Ca-dependent .(2) The secondary effects of the , short-lasting PKC translocation/activation could involve:an activation of cAMP signaling pathway; an activation of early response like .
5
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Brain injury: prolonged induction of transcription factors

88%
Pennypacker K. R., Kassed K. C. A., Kassed C. A., Eidizadeh E. S., Eidizadeh S., O. C. J. P., O?Callaghan J. P., O?Callaghan J. P.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 4
515-528
EN
A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kB transcription factors, two of the most studied DNA binding regulatory proteins. Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kB p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult. Fos-related antigen-2 is induced in neurons in several models of injury and its elevated expression lasts days to months, corresponding to the severity. The time-course of FRA-2 induction is abbreviated with less severe insult (terminal damage) relative to the cell death, but the induction occurs during the period of regeneration and repair in both models. NF-kB p65 is basally expressed in hippocampal and cortical neurons, but is elevated in reactive astrocytes in hippocampus and entorhinal cortex starting at two days and lasting at least two weeks after kainate treatment. Neurons of the hippocampus surviving ischemic or neurotoxic injury increase expression of NF-kB p50 for at least a week after injury, suggesting a function for p50 in neuronal survival and/or repair. The extended expression of these transcription factors implies a role in the activation of genes related to repair and regeneration, such as growth factors and synaptic proteins, after injury to the CNS.
6

Nitric oxide (NO) in pathology of hypoxia/ischemia ? the ally or the enemy

75%
Justyna R.
Postępy Higieny i Medycyny Doświadczalnej
|
2000
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vol. 54
|
issue 5
669-686
EN
Nitric oxide (NO) has been found to play an important role as a signal molecule in many parts of the organism. However, under certain conditions, like hypoxia or ischemia, it acts as a cytotoxic effector molecule. It appears paradoxical that NO on the one hand acts as a physiological intercellular messenger and on the other can have damaging effects to cells. To make things even more complicated cytoprotective properties of NO are also described. Whether NO is useful or harmful depends on the rate and location of its production.
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