Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add more filters










Database
Type of study
Publication year range
1.
World J Clin Cases ; 11(19): 4648-4654, 2023 Jul 06.
Article in English | MEDLINE | ID: mdl-37469729

ABSTRACT

BACKGROUND: Edaravone is a widely used treatment for patients with cerebral infarction and, in most cases, edaravone-induced side effects are mild. However, edaravone-related adverse reactions have been receiving increasing attention. CASE SUMMARY: We treated three patients with acute cerebral infarction who died following treatment with edaravone. Edaravone is a widely used treatment for patients with cerebral infarction and, in most cases, edaravone-induced side effects are mild. However, edaravone-related adverse reactions have been receiving increasing attention. CONCLUSION: Our cases highlight the importance of educating clinicians regarding the new edaravone-induced clinical syndromes of cerebral infarction as potentially fatal adverse drug reactions. Considering that no laboratory or confirmatory test exists to diagnose edaravone-induced death from cerebral infarction, clinicians' knowledge is the key element in recognizing this phenomenon.

2.
Seizure ; 18(10): 680-5, 2009 Dec.
Article in English | MEDLINE | ID: mdl-19819736

ABSTRACT

Extracellular signal-regulated protein kinase, ERK1/2 is activated by phosphorylation (p-ERK1/2) during environmental stress such as epileptiform discharge. We investigated the role of ERK1/2 in abnormal axon growth and synapse reorganization in cultured neurons displaying epileptiform activity. The cultured neurons displaying epileptiform activity were treated with magnesium-free extracellular fluid for 3h and monitored epileptiform discharges using whole-cell patch clamp. Two study groups, neurons displaying epileptiform activity and the same neurons treated with ERK1/2 inhibitor U0126, were studied at six time points, 0 min, 30 min, 2h, 6h, 12h, and 24h following discharge. The expressions of p-ERK1/2, C-fos, growth-associated protein 43 (GAP-43) and synaptophysin (SYP), as markers of axon growth and synapse reorganization, were investigated by double-label immunofluorescence and western blotting. In the neurons displaying epileptiform activity, p-ERK1/2 was detected immediately following discharge, and expression peaked at 30 min. The expression of C-fos, GAP-43 and SYP followed the same pattern as p-ERK1/2. In the treated group, p-ERK1/2 was inhibited completely, and C-fos, GAP-43 and SYP were reduced. These findings indicate that epileptiform discharge activates ERK1/2 which regulates C-fos in cultured neurons displaying epileptiform activity, and this cascade may upregulate GAP-43 and SYP to contribute to axon growth and synapse reorganization to potentiate epileptic activities.


Subject(s)
Extracellular Signal-Regulated MAP Kinases/metabolism , GAP-43 Protein/metabolism , Hippocampus/cytology , Neurons/drug effects , Synaptophysin/metabolism , Up-Regulation/physiology , Action Potentials/drug effects , Action Potentials/physiology , Animals , Animals, Newborn , Cells, Cultured , Enzyme Inhibitors/pharmacology , Magnesium/metabolism , Rats , Rats, Wistar , Time Factors , Up-Regulation/drug effects
SELECTION OF CITATIONS
SEARCH DETAIL
...