cerebral infarction/tyrosine

A 76-year-old man, diagnosed with chronic myeloid leukemia in 2010, had been on nilotinib for 7 years. He presented with right hemiparesis in September 2017. He had no history of hypertension, diabetes, hyperlipidemia, heart disease, or smoking. Brain MRI revealed a border-zone infarction of the

Cerebral ischemia induces rapid efflux of glutamate into the extracellular space contributing to excessive activation of glutamate receptors in postsynaptic cells, particularly N-methyl-D-aspartate (NMDA) receptors, which triggers the neuron lesion through calcium overload. Our studies indicated

The determinations were carried out in the blood and cerebrospinal fluid of 40 patients with recent cerebral infarction and 30 controls. Tryptophan concentration was determined by the fluorimetric method of Denckla and Dewey, and tyrosine concentration by the method of Waalkes and Udenfried. A

Activation of trophic factor receptors stimulates tyrosine phosphorylation on proteins and supports neuronal survival. We report that in the recovery phase following reversible cerebral ischemia, tyrosine phosphorylation increases in the membrane fraction of the resistant hippocampal CA3/dentate

OBJECTIVE Extracellular signal-regulated kinases (ERKs) can be activated by calcium signals. In this study, we investigated whether calcium-dependent kinases were involved in ERKs cascade activation after global cerebral ischemia. METHODS Cerebral ischemia was induced by four-vessel occlusion, and

To explore the new mechanism of neuroprtection of monosialotetrahexosylganglioside and providing reliable theoretical foundation and experimental evidence for the emergency treatment and rehabilitation of cerebral ischemia/reperfusion injury. A rat model of cerebral ischemia/reperfusion injury was

A brief period of sublethal cerebral ischemia, followed by several days of recovery, renders the brain resistant to a subsequent lethal ischemic insult, a phenomenon termed ischemic preconditioning or tolerance. Ischemic tolerance was established in the rat two-vessel occlusion model of ischemia,

Striatal enriched protein tyrosine phosphatase (STEP) acts in the central nervous system to dephosphorylate a number of important proteins involved in synaptic function including ERK and NMDA receptor subunits. These proteins are also linked to stroke, in which cerebral ischemia triggers a complex

OBJECTIVE Electroacupuncture effect on neurological behavior and the expression of tyrosine kinase Janus kinase 2 (JAK 2) of ischemic cortex in rats with the focal cerebral ischemia were investigated in this study. METHODS The model of focal cerebral ischemia was established by the heat-coagulation

Neuron damage contributes to ischemic brain injury. Although FMS-like tyrosine kinase-3 (FLT3) plays a critical role in neuron survival, its function and molecular mechanism in cerebral ischemia/reperfusion injury is unclear. In the present study, we exposed SH-SY5Y cells to oxygen and glucose

Changes in the dynamic interactions of macromolecules in cell membranes appear to underlie the robust neuroprotective effect of hypothermia against selective neuronal degeneration in the CA1 region of the rat hippocampus after transient cerebral ischemia, but the detailed mechanisms are still

We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia. A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, tyrosine kinase receptor B, phosphorylated cAMP response element binding protein,

Cerebral ischemia results in activation of the mitogen-activated protein kinase pathway and increased tyrosine phosphorylation of proteins associated with postsynaptic densities (PSDs). The authors investigated the possible relation between these events by determining the effect of ischemia on

OBJECTIVE To study the mechanisms of the regulation of the tyrosine phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunit 2B(NR2B) in the gerbil hippocampal synaptosomes following ischemia/reperfusion (I/R). METHODS Transient (15 min) cerebral ischemia was produced by bilateral carotid

The contribution of metabotropic glutamate receptors to brain injury after in vivo cerebral ischemia remains to be determined. We investigated the effects of the metabotropic glutamate receptor 1 (mGluR1) antagonist LY367385 on brain injury after transient (90 min) middle cerebral artery occlusion