[The effect of catastrophic health expenditure on the transition to poverty and the persistence of poverty in South Korea].

Objectives: The low benefit coverage rate of South Korea's health security system has been continually pointed out. A low benefit coverage rate inevitably causes catastrophic health expenditure, which can be the cause of the transition to poverty and the persistence of poverty. This study was conducted to ascertain the effect of catastrophic health expenditure on the transition to poverty and the persistence of poverty in South Korea.

Region-specific plasticity in the epileptic rat brain: a hippocampal and extrahippocampal analysis.

Purpose: Recent evidence suggests that aberrant neuro/gliogenesis and/or inflammation play critical roles in epileptogenesis. Although the plastic and inflammatory changes have been described in the postseizure hippocampus, little data is available concerning extrahippocampal regions, notably in the piriform and entorhinal cortices, amygdala, and parts of the thalamus. In this study, we examined histological changes in whole epileptic rat brain, with respect to cell death, cell genesis, and inflammation.

Spinal subdural hematoma following tissue plasminogen activator treatment for acute ischemic stroke.

A 49-year-old woman with an acute ischemic stroke was treated by the intravenous administration of tissue plasminogen activator within 2 h of symptom onset. She complained of severe upper thoracic back pain the following day. Progressive paraparesis was detected on the third admission day.

Circulating endothelial progenitor cells as a pathogenetic marker of moyamoya disease.

Moyamoya disease (MMD) is an unusual form of chronic cerebrovascular occlusive disease that involves the formation of characteristically abnormal vessels. Recent studies have reported that colony-forming unit (CFU) and outgrowth cells represent a subpopulation of endothelial progenitor cells (EPCs). Here, we attempted to determine the significance of CFU number and outgrowth cell yield in MMD.

Transplantation of human neural stem cells protect against ischemia in a preventive mode via hypoxia-inducible factor-1alpha stabilization in the host brain.

Hypoxia-inducible factor-1 (HIF-1) plays important roles in the prevention of cerebral ischemia. Deferoxamine (DFX), an iron chelator stabilizes the HIF-1alpha and activates target genes involved in compensation for ischemia. In this study, we are to investigate whether HIF-1alpha can be stabilized in human neural stem cells (NSCs) by DFX, and pre-transplantation of NSCs with HIF-1alpha stabilization can induce prolonged ischemic tolerance.

Circulating endothelial progenitor cells as a new marker of endothelial dysfunction or repair in acute stroke.

Background And Purpose: Understanding on distinct subsets of endothelial progenitor cells may provide insights of endothelial dysfunction or repair in the acute ischemic event. Recent in vitro data have reported the colony-forming unit (CFU) and outgrowth cell population as a subset of endothelial progenitor cells. In this study, we undertook to validate the significance of CFU number and outgrowth cell yield in acute stroke.

Identification of neuronal outgrowth cells from peripheral blood of stroke patients.

Objective: Recent studies have identified a subset of outgrowth cell population with endothelial phenotype in long-term cultures of peripheral blood mononuclear cells. The concept that peripheral blood-derived cells participate in neuronal regeneration remains highly controversial, and no specific cell type has been identified. In this study, we undertook to characterize outgrowth cells in the peripheral blood culture from stroke patients.

Systemic transplantation of human adipose stem cells attenuated cerebral inflammation and degeneration in a hemorrhagic stroke model.

Adipose-derived stem cells (ASCs) are readily accessible multipotent mesenchymal stem cells and are known to secrete multiple growth factors, and thereby to have cytoprotective effects in various injury models. In the present study, the authors investigated the neuroprotective effect of ASCs in an intracerebral hemorrhage (ICH) model. ICH was induced via the stereotaxic infusion of collagenase, and human ASCs (three million cells per animal) isolated from human fresh fat tissue, were intravenously administered at 24 h post-ICH induction.

Neurotoxic syndrome developed after taking sertraline and risperidone.

Neuroleptic malignant syndrome and serotonin syndrome share many common clinical features, and the term "Neurotoxic syndrome" can be used when a clear distinction cannot be made between the two. Here we present a case of 19-year-old man who experienced serotonin syndrome caused by sertraline intake, and consecutive neuroleptic malignant syndrome by risperidone. This case suggests that these two syndromes can be concomitantly induced in some patients who are susceptible to these drugs.

Blockade of AT1 receptor reduces apoptosis, inflammation, and oxidative stress in normotensive rats with intracerebral hemorrhage.

Angiotensin II exerts its central nervous system effects primarily via its receptors AT1 and AT2, and it participates in the pathogenesis of ischemia via AT1. The selective AT1 receptor blocker (ARB) is used in the hypertension treatment, and it exerts a variety of pleiotropic effects, including antioxidative, antiapoptotic, and anti-inflammatory effects. In this study, we investigated the therapeutic effect of the ARB telmisartan in experimental intracerebral hemorrhage (ICH) in normotensive rats.

[Management of stroke in Korea, now].

Korea is a rapidly growing aging society and stroke is still the second cause of death, comprised of about 15% of the total death in Korea. But the mortality of stroke is slightly decreasing despite increase of stroke incidence, probably due to improvement of management of stroke and related risk factors. The advent of DWI/ MRA enables us to make more accurate patho-etiological diagnoses of ischemic strokes.

Valproic acid-mediated neuroprotection in intracerebral hemorrhage via histone deacetylase inhibition and transcriptional activation.

The modification of histone N-terminal tails by acetylation or deacetylation can alter the interaction between histones and DNA, and thus regulate gene expression. Recent experiments have demonstrated that valproic acid (VPA), a well-known anti-epileptic drug, can directly inhibit histone deacetylase (HDAC) activity and cause the hyperacetylation of histones. Moreover, VPA has been shown to mediate neuronal protection by activating signal transduction pathways and by inhibiting proapoptotic factors.

Proteasomal inhibition in intracerebral hemorrhage: neuroprotective and anti-inflammatory effects of bortezomib.

Inflammation is an important pathophysiologic mechanism of injury induced by intracerebral hemorrhage (ICH). The ubiquitin-proteasome system (UPS) regulates the inflammatory responses via the up-regulation of several pro-inflammatory molecules. In this study, we determined that a potent proteasome inhibitor, bortezomib, exerted therapeutic effects in experimental model of ICH.

Pharmacological induction of heat shock protein exerts neuroprotective effects in experimental intracerebral hemorrhage.

Heat shock proteins (HSPs) are reported to reduce inflammation and apoptosis in a variety of brain insults. Geranylgeranylacetone (GGA), developed as an antiulcer in Japan, has been known to induce HSP70 and to exert cytoprotective effects. In this study, we investigated whether GGA, as a specific HSP inducer, exerts therapeutic effects in experimentally induced intracerebral hemorrhage (ICH).

Combined neuroprotective effects of celecoxib and memantine in experimental intracerebral hemorrhage.

Memantine, a N-methyl-D-aspartate (NMDA) receptor antagonist, inhibits hematoma expansion and celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, reduces perihematomal inflammation in intracerebral hemorrhage. We examined whether the combination treatment has additive effects in experimental intracerebral hemorrhage (ICH). ICH was induced using stereotaxic infusion of collagenase into brains of adult rats.

Pharmacological Induction of Ischemic Tolerance by Glutamate Transporter-1 (EAAT2) Upregulation.

Background And Purpose: Astrocytic glutamate transporter protein, GLT-1 (EAAT2), recovers extracellular glutamate and ensures that neurons are protected from excess stimulation. Recently, beta-lactam antibiotics, like ceftriaxone (CTX), were reported to induce the upregulation of GLT-1. Here, we investigated ischemic tolerance induction by CTX in an experimental model of focal cerebral ischemia.

Early intravenous infusion of sodium nitrite protects brain against in vivo ischemia-reperfusion injury.

Background And Purpose: The rate of nitric oxide (NO) generation from nitrite is linearly dependent on reductions in oxygen and pH levels. Recently, nitrite-derived NO has been reported to exert a profound protection against liver and heart ischemia-reperfusion injury. In this study, we hypothesized that nitrite would be reduced to NO in the ischemic brain and exert NO-dependent neuroprotective effects.

Musical training-induced functional reorganization of the adult brain: functional magnetic resonance imaging and transcranial magnetic stimulation study on amateur string players.

We used the combined technique of functional magnetic resonance imaging (fMRI) and transcranial magnetic stimulation (TMS) to observe changes that occur in adult brains after the practice of stringed musical instruments. We carried out fMRI on eight volunteers (aged 20-22 years): five novices and three individuals who had discontinued practice for more than 5 years. The motor paradigm contained a repetitive lift-abduction/fall-adduction movement of the left/right little finger, carried out with maximum efforts without pacing.