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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Electroconvulsive seizure (ECS) is an experimental animal model of electroconvulsive therapy, the most effective treatment for severe depression. ECS ...

University of Illinois at Urbana-Champaign

We present a 70-year-old woman with nonconvulsive status epilepticus (NCSE) with thalamic hyperintensity on diffusion-weighted MRI (DWI). She had no previous history of epilepsy. Her altered mentality was not normalized though we successfully controlled the ictal activity by standard treatment. Initial DWI showed diffuse hyperintensity in the right thalamus, which raised the possibility of seizure-related change. At the follow-up DWI, more localized high signal intensity lesion was present in the right pulvinar area. There was no apparent cause of her NCSE despite our extensive work-ups. The authors suggest that transient ischemia is a possible causative pathomechanism in this case.

Thalamic hyperintensity on diffusion-weighted MRI in a patient with nonconvulsive status epilepticus.

Positional occlusion of the internal carotid artery by thrombus plugging causing transient ischemic attack.

Early neurological deterioration (END) occurs in ≥20% of single small subcortical infarctions (SSSIs; axial diameter ≤20 mm in the perforator territories) and deters functional recovery. Both microvasculopathies and atherosclerosis have been proposed to independently contribute to the occurrence of END in SSSI cases. We hypothesized that the occurrence of END in SSSIs differs according to the pathological process.

Neuroimaging markers for early neurologic deterioration in single small subcortical infarction.

Reversible right heart failure after medullary stroke.

Sustained changes in network activity cause homeostatic synaptic plasticity in part by altering the postsynaptic accumulation of N-methyl-D-aspartate receptors (NMDAR) and α-amino-3-hydroxyle-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), which are primary mediators of excitatory synaptic transmission. A key trafficking modulator of NMDAR and AMPAR is STriatal-Enriched protein tyrosine Phosphatase (STEP61) that opposes synaptic strengthening through dephosphorylation of NMDAR subunit GluN2B and AMPAR subunit GluA2. However, the role of STEP61 in homeostatic synaptic plasticity is unknown.

Regulation of STEP61 and tyrosine-phosphorylation of NMDA and AMPA receptors during homeostatic synaptic plasticity.

Fimasartan is a newly developed angiotensin receptor blocker, which may have protective effects during myocardial infarction or atherosclerosis. In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in brain by transient intraluminal occlusion of middle cerebral artery (MCA) and administered low-dose (0.5 mg/kg) or regular doses (1 or 3 mg/kg) of fimasartan via intravenous routes. After the administration of low-dose (0.5 mg/kg) fimasartan, blood pressure did not decrease compared to the phosphate-buffered saline- (PBS-) control with MCA occlusion (MCAO) group. The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41 mm(3) for 0.5 mg/kg and 153 ± 47 mm(3) for PBS-control with MCAO; P < 0.01) but not in the regular-dose groups. Low-dose fimasartan treatment improved functional recovery after ischemia and significantly decreased mortality. In our study, fimasartan reduced the degradation of IκB and the formation of an inflammatory end-product, COX-2. As a result, the recruitment of inflammatory cells in the peri-infarct area decreased in fimasartan-treated group. We have demonstrated that long-term, low-dose fimasartan treatment improved outcomes after focal ischemia in the brain via a reduction of inflammation.

Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain.

Stroke unit care is associated with decrease in mortality and improvement in neurological outcome in patients with acute stroke. Heart rate is a commonly monitored variable in the stroke unit. However, little is known about tachycardia burden in the stroke unit and its association with outcome.

Tachycardia burden in stroke unit is associated with functional outcome after ischemic stroke.

Obesity has a significant contribution to the risk of intracerebral hemorrhage (ICH). However, little is known about the association between central obesity and the presence of cerebral microbleeds (CMBs), a precursor of ICH. We sought to assess whether visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) are associated with the presence of CMB.

Visceral Fat Is an Independent Predictor of Cerebral Microbleeds in Neurologically Healthy People.

Wake-up stroke (WUS) represents a quarter of all ischemic strokes and may be a specific subgroup. Nocturnal desaturation secondary to sleep-disordered breathing is an independent risk factor for stroke, but the association between nocturnal desaturation and WUS remains unclear. We investigated the relationship between nocturnal desaturation using oxygen desaturation index and WUS in patients with acute stroke in the stroke unit.

Nocturnal Desaturation in the Stroke Unit Is Associated With Wake-Up Ischemic Stroke.

To compare clinical outcomes of patients who received early initiation (<24 hours) of antithrombotics with those who received standard management (antithrombotics administered ≥24 hours).

Stroke outcomes with use of antithrombotics within 24 hours after recanalization treatment.

The susceptibility vessel sign (SVS) is a hypointense signal visualized because of the susceptibility effect of thrombi, sensitively detected on susceptibility-weighted magnetic resonance imaging. The relationship of SVS parameters with the stroke subtype and recanalization status after endovascular treatment remains uncertain.

Prediction of Stroke Subtype and Recanalization Using Susceptibility Vessel Sign on Susceptibility-Weighted Magnetic Resonance Imaging.

The two oxidation states of ceria nanoparticles, Ce(3+) and Ce(4+) , play a pivotal role in scavenging reactive oxygen species (ROS). In particular, Ce(3+) is largely responsible for removing O2(-) and (.) OH that are associated with inflammatory response and cell death. The synthesis is reported of 2 nm ceria-zirconia nanoparticles (CZ NPs) that possess a higher Ce(3+) /Ce(4+) ratio and faster conversion from Ce(4+) to Ce(3+) than those exhibited by ceria nanoparticles. The obtained Ce0.7 Zr0.3 O2 (7CZ) NPs greatly improve ROS scavenging performance, thus regulating inflammatory cells in a very low dose. Moreover, 7CZ NPs are demonstrated to be effective in reducing mortality and systemic inflammation in two representative sepsis models. These findings suggest that 7CZ NPs have the potential as a therapeutic nanomedicine for treating ROS-related inflammatory diseases.

Han Gil Jeong

Department of Molecular and Integrative Physiology

University of Illinois at Urbana-Champaign

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Han Gil Jeong

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Molecular and Integrative Physiology

University of Illinois at Urbana-Champaign

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Department of Molecular and Integrative Physiology