• Journal of Life Science
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• v.17 no.1 s.81
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• pp.150-161
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• 2007

Acori graminei Rhizomn (AGR) is a perennial herb which has been used clinically as a traditional oriental medicine against stroke, Alzheimer's disease, and vascular dementia. We investigated the effect of AGR on the modulation of gene expression profile in a hypoxic model of cultured rat cortical cells. Rat cerebrocortical cells were grown in Neurobasal medium. On DIV12, cells were treated with AGR $(10ug/m\ell)$, given a hypoxic shock (2% $O_2$, 3 hr) on DIV14, and total RNAs were prepared one day after shock. Microarray analyses indicated that the expression levels of most genes were altered within the global M values +0.5 and -0.5, i.e., 40% increase or decrease. There were 750 genes which were upregulated by < global M +0,2, while 700 genes were downregulated by > global M -0.2. The overall profile of gene expression suggests that AGR suppresses apoptosis (upregulation of anti-apopotic genes such as TEGT, TIEG, Dad, p53, and downregulation of pro-apopotic genes such as DAPK, caspase 2, pdcd8), ROS (upregulation of RARa, AhR), and that AGR has neurotrophic effects (upregulation of Aktl, Akt2). These results provide a platform for investigation of the molecular mechanism of the effect of AGR in neuroprotection.

• Journal of Audiology & Otology
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• v.25 no.3
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• pp.163-170
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• 2021

Cortical deafness is a clinical rarity whereby a patient is unresponsive to all types of sounds despite the preserved integrity of the peripheral hearing organs. In this study, we present a patient who suddenly lost his hearing following ischaemic infarcts in both temporal lobes with no other neurological deficits. The CT confirmed damage to the primary auditory cortex (Heschl's gyrus) of both hemispheres. Initially, the patient was unresponsive to all sounds, however, he regained some of the auditory abilities during 10 months follow up. Pure tone threshold improvement from complete deafness to the level of moderate hearing loss in the right ear and severe in the left was observed in pure tone audiometry. Otoacoustic emissions, auditory brainstem responses, and acoustic reflex findings showed normal results. The middle and late latency potential results confirmed objectively the improvement of the patient's hearing, however, after 10 months still, they were somewhat compromised on both sides. In speech audiometry, there was no comprehension of spoken words neither at 3 nor at 10 months. The absent mismatch negativity confirmed above mentioned comprehension deficit. The extensive auditory electrophysiological testing presented in this study contributes to the understanding of the neural and functional changes in cortical deafness. It presents the evolution of changes after ischaemic cerebrovascular event expressed as auditory evoked potentials starting from short through middle and long latency and ending with event-related potentials and supported by neuroimaging.

• Korean Journal of Audiology
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• v.25 no.3
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• pp.163-170
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• 2021

Cortical deafness is a clinical rarity whereby a patient is unresponsive to all types of sounds despite the preserved integrity of the peripheral hearing organs. In this study, we present a patient who suddenly lost his hearing following ischaemic infarcts in both temporal lobes with no other neurological deficits. The CT confirmed damage to the primary auditory cortex (Heschl's gyrus) of both hemispheres. Initially, the patient was unresponsive to all sounds, however, he regained some of the auditory abilities during 10 months follow up. Pure tone threshold improvement from complete deafness to the level of moderate hearing loss in the right ear and severe in the left was observed in pure tone audiometry. Otoacoustic emissions, auditory brainstem responses, and acoustic reflex findings showed normal results. The middle and late latency potential results confirmed objectively the improvement of the patient's hearing, however, after 10 months still, they were somewhat compromised on both sides. In speech audiometry, there was no comprehension of spoken words neither at 3 nor at 10 months. The absent mismatch negativity confirmed above mentioned comprehension deficit. The extensive auditory electrophysiological testing presented in this study contributes to the understanding of the neural and functional changes in cortical deafness. It presents the evolution of changes after ischaemic cerebrovascular event expressed as auditory evoked potentials starting from short through middle and long latency and ending with event-related potentials and supported by neuroimaging.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.6
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• pp.435-440
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• 2010

Valproic acid (VPA) is a well-known anti-epileptic and mood stabilizing drug. A growing number of reports demonstrate that VPA is neuroprotective against various insults. Despite intensive efforts to develop new therapeutics for stroke over the past two decades, all treatments have thus far failed to show clinical effect because of treatment-limiting side effects of the drugs. Therefore, a safety-validated drug like VPA would be an attractive candidate if it has neuroprotective effects against ischemic insults. The present study was undertaken to examine whether pre- and post-insult treatments with VPA protect against brain infarct and neurological deficits in mouse transient (tMCAO) and permanent middle cerebral artery occlusion (pMCAO) models. In the tMCAO (2 hr MCAO and 22 hr reperfusion) model, intraperitoneal injection of VPA (300 mg/kg, Lp.) 30 min prior to MCAO significantly reduced the infarct size and the neurological deficit. VPA treatment immediately after reperfusion significantly reduced the infarct size. The administration of VPA at 4 hr after reperfusion failed to reduce the infarct size and the neurological deficit. In the pM CAO model, treatment with VPA (300 mg/kg, i.p.) 30 min prior to MCAO significantly attenuated the infarct size, but did not affect the neurological deficit. Western blot analysis of acetylated H3 and H4 protein levels in extracts from the ischemic cortical area showed that treatment with VPA increased the expression of acetylated H3 and H4 at 2 hrs after MCAO. These results demonstrated that treatment with VPA prior to ischemia attenuated ischemic brain damage in both mice tMCAO and pMCAO models and treatment with VPA immediately after reperfusion reduced the infarct area in the tMCAO model. VPA could therefore be evaluated for clinical use in stroke patients.

• Korean Journal of Veterinary Research
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• v.63 no.1
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• pp.6.1-6.9
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• 2023

Stroke is a major cause of death and long-term disability. Chlorogenic acid is a phenolic compound with a potent neuroprotective effect. γ-enolase is a phosphopyruvate hydratase found in mature neurons and plays an important role in neuronal survival. This study investigated whether chlorogenic acid regulates the expression of γ-enolase during cerebral ischemia. Middle cerebral artery occlusion (MCAO) was performed to induce cerebral ischemia. Adult male rats were used and chlorogenic acid (30 mg/kg) or phosphate buffered saline (PBS) was injected intraperitoneally 2 hours after MCAO surgery. Cerebral cortical tissues were collected 24 hours after MCAO surgery. Our proteomic approach identified the reduction of γ-enolase caused by MCAO damage and the mitigation of this reduction by chlorogenic acid treatment. Results of reverse transcription-polymerase chain reaction and Western blot analyses showed a decrease in γ-enolase expression in the PBS-treated MCAO group. However, chlorogenic acid treatment attenuated this decrease. Results of immunofluorescence staining showed the change of γ-enolase by chlorogenic acid treatment. These results demonstrated that chlorogenic acid regulates the γ-enolase expression during MCAO-induced ischemia. Therefore, we suggest that chlorogenic acid mediates the neuroprotective function by regulating the γ-enolase expression in cerebral ischemia and may be used as a therapeutic agent for brain diseases including stroke.

• Animal cells and systems
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• v.10 no.2
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• pp.79-83
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• 2006

Tissue plasminogen activator (tPA) is used to lyse clots and reperfuse brain in ischemic stroke. However, sideeffects of intracerebral hemorrhage (ICH) and edema limit their clinical application. In part, these phenomena has been linked with elevations in matrix metalloproteinase-9 (MMP-9) in neurovascular unit. However little is known about their regulatory signaling pathways in brain cells. Here, I examine the role of MAP kinase pathways in tPA-induced MMP-9 regulation in rat cortical astrocytes. tPA $(1-10\;{\mu}g/ml)$ induced dose-dependent elevations in MMP-9 and MMP-2 in conditioned media. Although tPA increased phosphorylation in two MAP kinases (ERK, JNK), only inhibition of the JNK pathway by the JNK inhibitor SP600126 significantly reduced MMP-9 upregulation. Neither ERK inhibition with U0126 nor p38 inhibition with SB203580 had any significant effects. Taken together, these results suggest that c-jun N-terminal kinase (JNK) plays an essential role for tPA-induced MMP-9 upregulation.

• Journal of the Korean Magnetic Resonance Society
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• v.6 no.2
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• pp.89-93
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• 2002

We report a preliminary fMRI evidence of modulation of somatomotor areas by acupuncture in GB34 acupoint. GB34, located in the back of the knee, is known to be effective in recovering motor function after stroke. Using 3T MR scanner, functional MR imaging was performed in five normal volunteers in two stimulation paradigms; acupuncture manipulation on GB34 and sham points. Group analysis form five individuals showed that bilateral sensorimotor areas (BA 3,4,6 and 7) showed stimulation related BOLD signal contrast of approximately 6% whereas very few areas were activated when sham stimulation is given. Our results suggest that acupuncture fMRI study can be safely conducted in 3T environment and stimulation in GB34 modulate the cortical activities of the somatomotor area in human.

• Proceedings of the Korean Magnetic Resonance Society Conference
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• 2002.08a
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• pp.21-25
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• 2002

We report a preliminary fMRI evidence of modulation of somatomotor areas by acupuncture in GB34 acupoint. GB34, located in the back of the knee, is known to be effective in recovering motor function after stroke. Using 3T MR scanner, functional MR imaging was performed in five normal volunteers in two stimulation paradigms; acupuncture manipulation on GB34 and sham points. Group analysis from five individuals showed that bilateral sensorimotor areas (BA 3,4,6 and 7) showed stimulation related BOLD signal contrast of approximately 6％ whereas very few areas were activated when sham stimulation is given. Our results suggest that acupuncture fMRI study can be safely conducted in 3T environment, and stimulation in GB34 modulate the cortical activities of the somatomotor area in human.

• Annals of Clinical Neurophysiology
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• v.24 no.2
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• pp.84-89
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• 2022

Vestibular dysfunction has rarely been reported in MELAS syndrome. A 40-year-old male with long-term diabetes and hearing loss experienced a stroke-like episode with hemisensory disturbance and lactic acidosis. Brain MRI showed temporo-parieto-occipital cortical lesions, and a final diagnosis was made of MELAS syndrome with the mitochondrial 3243A>G mutation. Neuro-otologic evaluations revealed anterior-canal-sparing bilateral impairments of the vestibulo-ocular reflex in the video head impulse test and no caloric paresis. This unique pattern of vestibular dysfunction may aid in diagnosing MELAS syndrome.

• Therapeutic Science for Rehabilitation
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• v.7 no.3
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• pp.23-33
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• 2018

Objective : This systematic review aimed to investigate the effect of focal muscle vibration in patients with post-stroke spastic hemiplegia. Methods : We searched literature published between April 2009 and October 2017 using PubMed and RISS databases. The main search terms were Vibration therapy, Focal vibration, Somatosensory, Upper limb, and Spasticity after stroke. Based on inclusion/exclusion criteria, 6 articles were selected. Results : Articles on focal muscle vibration intervention ranged from evaluation of application-only vibration to muscle vibration with task-oriented activity. Intervention effects on upper extremity spasticity and function and activities of daily living were assessed. There were significant effects on upper extremity spasticity, function, and cortical excitability. Conclusions : This study can provide information on focal muscle vibration for use by clinical therapists. However, further studies are needed to identify the optimal stimulation site and frequency/amplitude of application to maximize the effects of focal muscle vibration.