Viera Danielisová

TL;DR: It is confirmed that postconditioning if used at right time and with optimal intensity can prevent process of delayed neuronal death, and protective impact of post conditioning in less-sensitive neuronal populations is very good after such a damaging insult like 15 min ischemia.

TL;DR: These findings are consistent with a potential role for eif4E, 4E-BP1 and eIF4G in the down-regulation of translation during ischaemia, and suggest eIF 4F complex formation is likely to contribute to the persistent inhibition of translation observed at longer reperfusion times.

TL;DR: Use of many modern therapeutical methods and the incorporation of several substances into the diet of patients is possible to stimulate the endogenous protective mechanisms and improve the life quality.

TL;DR: It seems that the mechanisms of ischemic tolerance‐delayed postconditioning could be used not only after ischemia but also in some other processes leading to apoptosis, since pre‐ or post‐conditioners can be used plenty of harmful stimuli and some physiological compounds, such as norepinephrine, bradykinin.

TL;DR: The results suggest that endogenous antioxidants SOD and CAT could play considerable neuroprotective role after postconditioning and it is interesting that the greatest changes were established in selectively vulnerable hippocampus and striatum.