Publications by authors named "Seong-Ryong Lee"

43 Publications

Neuroprotective effects of N-acetylcysteine via inhibition of matrix metalloproteinase in a mouse model of transient global cerebral ischemia.

Brain Res Bull 2020 01 10;154:142-150. Epub 2019 Nov 10.

Department of Pharmacology and ODR center, Brain Research Institute, School of Medicine, Keimyung University, Daegu, 42601, South Korea. Electronic address:

N-acetylcysteine (NAC) is known to serve many biological functions including acting as an antioxidant, and electing antiinflammatory effects. Previous reports have revealed that NAC may have neuroprotective effects against the deleterious effects of brain ischemia. Despite of this, the mechanism by which NAC prevents neuronal damage after brain ischemia remains unclear. The current study aimed to investigate this mechanism in a mouse model of transient global brain ischemia. In the present study, mice were subjected to 20 min of transient global brain ischemia, proceeded by intraperitoneal administration of NAC (150 mg/kg) in one group. The mice were then euthanized 72 h after this ischemic insult for collection of experimental tissues. The effect of NAC on neuronal damage and matrix metalloproteinase (MMP)-9 activity were assessed and immunofluorescence, and hippocampal terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay experiments were conducted and results compared between NAC- and vehicle-treated groups. Neuronal damage was primarily observed in the hippocampal CA1 and CA2 regions. In NAC-treated mice, neuronal damage was significantly reduced after ischemia when compared to vehicle-treated animals. NAC also inhibited increased MMP-9 activity after global brain ischemia. NAC increased laminin and NeuN expression and inhibited increases in TUNEL-positive cells, all in the hippocampus. These results suggest that NAC reduces hippocampal neuronal damage following transient global ischemia, potentially via reductions in MMP-9 activity.
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http://dx.doi.org/10.1016/j.brainresbull.2019.10.004DOI Listing
January 2020

Deficiency of primary cilia in kidney epithelial cells induces epithelial to mesenchymal transition.

Biochem Biophys Res Commun 2018 02 11;496(2):450-454. Epub 2018 Jan 11.

Department of Molecular Medicine and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea. Electronic address:

Primary cilium is a microtubule-based non-motile organelle that plays critical roles in kidney pathophysiology. Our previous studies revealed that the lengths of primary cilia decreased upon renal ischemia/reperfusion injury and oxidative stress, and restored with recovery. Here, we tested the hypothesis that lack of primary cilium causes epithelial to mesenchymal transition (EMT) of kidney tubule cells. We investigated the alteration of length of primary cilia in TGF-β-induced EMT via visualization of primary cilia by fluorescence staining against acetylated α-tubulin. EMT was determined by measuring mesenchymal protein expression using quantitative PCR and indirect fluorescence staining. As a result, TGF-β treatment decreased ciliary length along with EMT. To test whether defect of primary cilia trigger onset of EMT, cilia formation was disturbed by knock down of ciliary protein using siRNA along with/without TGF-β treatment. Knock down of Arl13b and Ift20 reduced cilia elongation and increased expression of EMT markers such as fibronectin, α-SMA, and collagen III. TGF-β-induced EMT was greater as well in Arl13b and Ift20-knock down cells compared to control cells. Taken together, deficiency of primary cilia trigger EMT and exacerbates it under pro-fibrotic signals.
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http://dx.doi.org/10.1016/j.bbrc.2018.01.079DOI Listing
February 2018

Downregulation of exocyst Sec10 accelerates kidney tubule cell recovery through enhanced cell migration.

Biochem Biophys Res Commun 2018 02 8;496(2):309-315. Epub 2018 Jan 8.

Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea; Department of Molecular Medicine Keimyung University School of Medicine, Daegu, Republic of Korea. Electronic address:

Migration of surviving kidney tubule cells after sub-lethal injury, for example ischemia/reperfusion (I/R), plays a critical role in recovery. Exocytosis is known to be involved in cell migration, and a key component in exocytosis is the highly-conserved eight-protein exocyst complex. We investigated the expression of a central exocyst complex member, Sec10, in kidneys following I/R injury, as well as the role of Sec10 in wound healing following scratch injury of cultured Madin-Darby canine kidney (MDCK) cells. Sec10 overexpression and knockdown (KD) in MDCK cells were used to investigate the speed of wound healing and the mechanisms underlying recovery. In mice, Sec10 decreased after I/R injury, and increased during the recovery period. In cell culture, Sec10 OE inhibited ruffle formation and wound healing, while Sec10 KD accelerated it. Sec10 OE cells had higher amounts of diacylglycerol kinase (DGK) gamma at the leading edge than did control cells. A DGK inhibitor reversed the inhibition of wound healing and ruffle formation in Sec10 OE cells. Conclusively, downregulation of Sec10 following I/R injury appears to accelerate recovery of kidney tubule cells through activated ruffle formation and enhanced cell migration.
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http://dx.doi.org/10.1016/j.bbrc.2018.01.013DOI Listing
February 2018

Lupeol Isolated from Sorbus commixta Suppresses 1α,25-(OH)2D3-Mediated Osteoclast Differentiation and Bone Loss in Vitro and in Vivo.

J Nat Prod 2016 Feb 16;79(2):412-20. Epub 2016 Feb 16.

College of Pharmacy, Keimyung University , Daegu 704-701, Republic of Korea.

Lupeol is a lupane-type triterpene isolated from Sorbus commixta, an oriental medicine used to treat arthritis and inflammatory diseases. However, the antiosteoporotic effects of S. commixta or any of its constituents have not been studied yet. In the present study, we have examined the effect of lupeol (a major active triterpenoid isolated from S. commixta) on osteoclastogenesis and sought to elucidate its underlying molecular mechanisms. We evaluated whether lupeol antagonized osteoclast differentiation and bone resorption. Lupeol markedly inhibited osteoclast differentiation and bone resorption activity through its effects on MAP kinases and transcription factors (NF-κB, NFATc1, and c-Fos) downstream of the osteoclast differentiation factor receptor RANK. Furthermore, in vivo efficacy of lupeol was confirmed by using an animal model of hypercalcemic mediated bone loss. Taken together, lupeol showed strong inhibitory effects on osteoclastogenesis. Supplementation with S. commixta and lupeol could be beneficial for bone health or osteoclast-related diseases such as osteoporosis, Paget's disease, osteolysis associated with periodontal disease, and multiple myeloma.
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http://dx.doi.org/10.1021/acs.jnatprod.5b01088DOI Listing
February 2016

Protective effect of resveratrol against neuronal damage following transient global cerebral ischemia in mice.

J Nutr Biochem 2016 Jan 3;27:146-52. Epub 2015 Sep 3.

Department of Pharmacology and Obesity-mediated Disease Research Center School of Medicine, Keimyung University, Daegu, 42601, Korea; Brain Research Institute, Keimyung University, Daegu, 42601, Korea. Electronic address:

Resveratrol (3,5,4'-trihydroxystilbene) is a natural polyphenol which is rich in grape seeds and skin. Several studies have revealed that resveratrol possesses neuroprotective effects. In the case of global brain ischemia, there are few reports regarding the protective effect of resveratrol. Therefore, the influence of resveratrol on neuronal damage after transient global brain ischemia remains to be clarified. In the current study, C57BL/6 black mice were subjected to 20 min of transient global brain ischemia and followed by 72 h of reperfusion. Resveratrol (20 or 40 mg/kg, once daily, dissolved in 0.5% carboxymethylcellulose) was administered orally for 7 days before ischemia and daily until the mice were euthanized. The effect of lower or higher dose of resveratrol on neuronal damage, matrix metalloproteinase (MMP) activity and in situ DNA fragmentation (TUNEL) assay in the hippocampus after global ischemia was examined. Neuronal damages were remarkable in CA1 and CA2 pyramidal cell layers after global ischemia. In resveratrol-treated mice (40 mg/kg), neuronal damage was significantly reduced compared with vehicle-treated mice. Mice treated with resveratrol showed reduced MMP-9 activity. Resveratrol also inhibited TUNEL staining. These data suggest that resveratrol, a natural polyphenol, reduces hippocampal neuronal cell damage following transient global ischemia by reducing MMP-9 activity.
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http://dx.doi.org/10.1016/j.jnutbio.2015.08.029DOI Listing
January 2016

Protective effect of melatonin against transient global cerebral ischemia-induced neuronal cell damage via inhibition of matrix metalloproteinase-9.

Life Sci 2014 Jan 22;94(1):8-16. Epub 2013 Nov 22.

Department of Pharmacology, School of Medicine and Brain Research Institute, Keimyung University, Daegu 704-701, South Korea. Electronic address:

Aims: Melatonin possesses various pharmacological effects including neuroprotective effects against brain ischemia. Post-ischemic increases in matrix metalloproteinase-9 (MMP-9) expression and activity mainly contribute to neuronal damage by degradation of the extracellular matrix. This study was designed to examine whether melatonin has a neuroprotective effect and an influence on MMP-9 in transient global brain ischemia.

Main Methods: Mice were subjected to 20 min of global brain ischemia and sacrificed 72h later. Melatonin (30 mg/kg) was administered 30 min before and 2h after ischemia as well as once daily until sacrifice.

Key Findings: Hippocampal pyramidal cell damage after ischemia was significantly decreased by melatonin. As observed by zymography, melatonin inhibited the increase of MMP-9 activity after ischemia. In the brain sections, the increased gelatinase activity was mainly observed in the hippocampus after ischemia and melatonin also reduced gelatinase activity. The laminin and NeuN expression levels were reduced in the hippocampal CA1 and CA2 regions after ischemia, and melatonin reduced laminin degradation and neuronal loss. A TUNEL assay demonstrated that there were TUNEL-positive cells in the hippocampus and the number of TUNEL-positive cells was significantly decreased by melatonin. There was no difference in the ischemia-induced hippocampal neuronal damage between the vehicle- and melatonin-treated groups of MMP-9 knock-out mice.

Significance: These data demonstrate that melatonin suppressed the occurrence of neuronal injury, which might be partly due to its inhibitory effects on MMP-9 in addition to its anti-oxidative effects. MMP-9 may be an important key target of melatonin in neuroprotection against global ischemia.
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http://dx.doi.org/10.1016/j.lfs.2013.11.013DOI Listing
January 2014

Attenuation of β-amyloid-induced oxidative cell death by sulforaphane via activation of NF-E2-related factor 2.

Oxid Med Cell Longev 2013 20;2013:313510. Epub 2013 Jun 20.

Department of Pharmacology, School of Medicine, Keimyung University, Daegu 704-701, Republic of Korea.

β-amyloid peptide (Aβ), a major component of senile plaques, plays important roles in neuropathology of Alzheimer's disease (AD). An array of in vitro and in vivo data indicates that Aβ-induced neuronal death is mediated by oxidative stress. In this study, we aimed to investigate effects of sulforaphane (SUL), an isothiocyanate in cruciferous vegetables, on Aβ-induced oxidative cell death in SH-SY5Y cells. Cells treated with Aβ(25-35) exhibited decreased cell viability and underwent apoptosis as determined by MTT assay and TUNEL, respectively. Aβ(25-35)-induced cytotoxicity and apoptotic characteristics such as activation of c-JNK, dissipation of mitochondrial membrane potential, altered expression of Bcl-2 family proteins, and DNA fragmentation were effectively attenuated by SUL pretreatment. The antiapoptotic activity of SUL seemed to be mediated by inhibition of intracellular accumulation of reactive oxygen species and oxidative damages. SUL exerted antioxidant potential by upregulating expression of antioxidant enzymes including γ-glutamylcysteine ligase, NAD(P)H:quinone oxidoreductase-1, and heme oxygenase-1 via activation of NF-E2-related factor 2(Nrf2). The protective effect of SUL against Aβ(25-35)-induced apoptotic cell death was abolished by siRNA of Nrf2. Taken together, the results suggest that pharmacologic activation of Nrf2 signaling pathway by SUL might be a practical prevention and/or protective treatment for the management of AD.
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http://dx.doi.org/10.1155/2013/313510DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705986PMC
August 2014

Effects of single treatment of anti-dementia drugs on sleep-wake patterns in rats.

Korean J Physiol Pharmacol 2012 Aug 10;16(4):231-6. Epub 2012 Aug 10.

Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Korea.

We studied the effects of acetylcholinesterase inhibitors, donepezil and galantamine, and an N-methyl-D-aspartate (NMDA) receptor blocker, memantine, on sleep-wake architecture in rats. Screw electrodes were chronically implanted into the frontal and parietal cortex for the electroencephalography (EEG). EEG was recorded with a bio-potential amplifier for 8 h from 09:30 to 17:30. Vibration was recorded to monitor animal activity with a vibration measuring device. Sleep-wake states such as wake (W), slow-wave sleep (S) and paradoxical or rapid eye movement sleep (P), were scored every 10 sec by an experimenter. We measured mean episode duration and number of episode to determine which factor sleep disturbance was attributed to. Donepezil and memantine showed a significant increase in total W duration and decreases in total S and P duration and delta activity. Memantine showed increases in sleep latency and motor activity. Changes of S and P duration in memantine were attributed from changes of mean episode duration. Galantamine had little effect on sleep architecture. From these results, it is showed that galantamine may be an anti-dementia drug that does not cause sleep disturbances and memantine may be a drug that causes severe sleep disturbance.
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http://dx.doi.org/10.4196/kjpp.2012.16.4.231DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419757PMC
August 2012

The effect of Baicalein on hippocampal neuronal damage and metalloproteinase activity following transient global cerebral ischaemia.

Phytother Res 2012 Nov 17;26(11):1614-9. Epub 2012 Feb 17.

Department of Pharmacology, School of Medicine, Keimyung University, Taegu, 704-701, South Korea.

Baicalein, a flavonoid derived from Scutellaria baicalensis Georgi, is known to protect neural tissue from damage. Several studies have found that baicalein reduces brain infarction following focal brain ischaemia. However, there are few reports on the protective effects of baicalein following global brain ischaemia. Therefore, the current study was designed to address the effects of baicalein on neuronal damage and matrix metalloproteinase (MMP; gelatinase) activity in the hippocampus after transient global ischaemia. C57BL/6 mice were subjected to transient global brain ischaemia for 20 min and sacrificed 72 h after ischaemic insult. Baicalein (200 mg/kg, once daily, as a suspension in 0.5% carboxymethylcellulose) or an equal volume of vehicle was orally administered to the mice from 7 days prior to the ischaemic insult until sacrifice. After global ischaemia neuronal damage was significant in CA1 and CA2 pyramidal cell layers. In baicalein-treated mice, neuronal damage from the ischaemic insult was significantly less than that in vehicle-treated mice. Baicalein administration also inhibited MMP-9 activity in the hippocampus. These data demonstrate that baicalein reduces hippocampal neuronal damage after transient global ischaemia. Besides its possible protective mechanisms, the protective role of baicalein against global ischaemia may operate, at least in part, through the inhibition of MMP-9 activity.
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http://dx.doi.org/10.1002/ptr.4644DOI Listing
November 2012

Effects of berberine on hippocampal neuronal damage and matrix metalloproteinase-9 activity following transient global cerebral ischemia.

J Neurosci Res 2012 Feb 3;90(2):489-97. Epub 2011 Nov 3.

Department of Pharmacology, and Brain Research Institute, School of Medicine, Keimyung University, Taegu, Korea.

Berberine, an isoquinoline alkaloid with a long history of use in Chinese medicine, has several important pharmacological effects. Several studies have revealed that berberine has neuroprotective and neuropsychiatric effects. However, there are few reports regarding the protective effect of berberine against neuronal damage following transient global cerebral ischemia. In this study, mice were subjected to 20 min of global brain ischemia and sacrificed 72 hr later. Berberine was administered for 7 days prior to ischemia and daily until sacrifice. Mice treated with berberine showed reduced matrix metalloproteinase-9 (MMP-9) activity. Berberine inhibited gelatinase activity directly in in situ zymography and reduced neuronal damage following global ischemia. Laminin expression and NeuN expression were markedly reduced in CA1 and CA2 areas after ischemia, and berberine reduced the laminin degradation and neuronal loss. In the TUNEL assay, damaged neurons were also apparent in the CA1 and CA2 areas, and berberine reduced TUNEL-positive cells. These data demonstrate that berberine, a plant alkaloid, may protect from hippocampal neuronal damage following transient global ischemia by reducing MMP-9 activity.
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http://dx.doi.org/10.1002/jnr.22756DOI Listing
February 2012

Synergistic memory impairment through the interaction of chronic cerebral hypoperfusion and amlyloid toxicity in a rat model.

Stroke 2011 Sep 7;42(9):2595-604. Epub 2011 Jul 7.

Department of Neurology, Konkuk University School of Medicine, Center for Geriatric Neuroscience Research, Institute of Biomedical Science and Technology, 4-12 Hwayang-dong Gwangjin-gu, Seoul, 143-729 Republic of Korea.

Background And Purpose: Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (Aβ) toxicity.

Methods: In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular Aβ (Aβ toxicity) using a nonphysiological Aβ peptide (Aβ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (Aβ toxicity or BCCAo), and combined injury (BCCAo-Aβ toxicity) groups (n=7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed.

Results: Spatial memory impairment was synergistically exacerbated in the BCCAo-Aβ toxicity group as compared to the BCCAo or Aβ toxicity groups (P<0.05). Compared to the sham group, neuroinflammation with microglial or astroglial activation was increased both in multiple white matter lesions and the hippocampus in other experimental groups. AD-related pathology was enhanced in the BCCAo-Aβ toxicity group compared to the Aβ toxicity group.

Conclusions: Our experimental results support a clinical hypothesis of the deleterious interaction between chronic cerebral hypoperfusion and Aβ toxicity. Chronic cerebral hypoperfusion-induced perturbation in the equilibrium of AD-related pathology may exacerbate cognitive impairment in a rat model of combined injury.
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http://dx.doi.org/10.1161/STROKEAHA.111.620179DOI Listing
September 2011

Long-term outcome of canal paresis of a vascular cause.

J Neurol Neurosurg Psychiatry 2011 Jan 28;82(1):105-9. Epub 2010 Jun 28.

Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea.

There have been several reports on the progress of the caloric response of vestibular neuritis, but little is known about the recovery of canal paresis (CP) of a vascular cause. This study found that the caloric response normalised in 20 (67%) of 30 patients with CP associated with posterior circulation ischaemic stroke who were followed for at least 1 year (mean, 42.5 months; range, 14-85 months). The most commonly infarcted territory on brain MRI associated with CP was in the distribution of the anterior inferior cerebellar artery (26/30, 87%). None of the patients who were followed for >5 years after the onset of vertigo showed persistent CP. Residual dizziness did not differ significantly between patients with or without CP at the final follow-up. These findings suggest that CP associated with posterior circulation ischaemic stroke often has a good long-term outcome. Following patients for at least 5 years increases the likelihood of normalisation of the vestibular response to caloric stimulation.
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http://dx.doi.org/10.1136/jnnp.2009.180497DOI Listing
January 2011

Onion extract and quercetin induce matrix metalloproteinase-1 in vitro and in vivo.

Int J Mol Med 2010 Mar;25(3):347-52

Department of Dermatology, School of Medicine, Daegu 700-712, Korea.

A scar is usually developed by an imbalance of collagen synthesis and degradation. It is believed that the flavonoids (quercetin and kaempferol) in onion extract play a role in reducing scar formation through inhibition of fibroblast activities. Even though several commercial products are composed of onion extract, the precise molecular mechanisms of onion extract in reduction of scar formation in skin are still largely unknown. In this study we investigated the effect both of onion extract and quercetin on the proliferation of fibroblasts, expression of type I collagen and matrix metalloproteinase-1 (MMP-1). Our data show that proliferation rates of fibroblasts were decreased in a dose-dependent manner of the onion extract and quercetin. The expression of type I collagen was not markedly changed by the onion extract and quercetin. Interestingly, the expression of MMP-1 was markedly increased by both onion extract and quercetin in vitro and in vivo. Thus, our data indicate that onion extract and quercetin play a role in the anti-scar effect in skin through up-regulation of MMP-1 expression, implying this agent is a promising material for reducing scar formation.
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March 2010

Green tea polyphenol (-)-epigallocatechin gallate reduces matrix metalloproteinase-9 activity following transient focal cerebral ischemia.

J Nutr Biochem 2010 Nov 4;21(11):1038-44. Epub 2009 Dec 4.

Chronic Disease Research Center and Institute for Medical Science, School of Medicine, Keimyung University, Taegu 700-712, South Korea.

Green tea polyphenol (-)-epigallocatechin gallate (EGCG) has been reported to reduce neuronal damage after cerebral ischemic insult. EGCG is known to reduce matrix metalloproteinase (MMP) activity. MMP can play an important role in the pathophysiology of neurological disorders including cerebral ischemia. The purpose of the current study was to investigate whether EGCG shows an inhibitory effect on MMP activity and neural tissue damage following transient focal cerebral ischemia. In the present study, C57BL/6 mice were subjected to 80 min of focal ischemia induced by middle cerebral artery occlusion (MCAO). Animals were killed 24 h after ischemia. EGCG (50 mg/kg) was administered intraperitoneally immediately after ischemia. Gelatin gel zymography showed an increase in the active form of MMP-9 after ischemia. EGCG reduced ischemia-induced up-regulation of the active form of MMP-9. In in situ zymography, EGCG reduced up-regulation of gelatinase activity induced by cerebral ischemia. Co-incubation with EGCG reduced gelatinase activity directly in postischemic brain section. In 2,3,5-triphenyltetrazolium chloride (TTC) assay, brain infarction was remarkable in the middle cerebral artery territory after focal cerebral ischemia. In EGCG-treated mice, infarct volume was significantly reduced compared with vehicle-treated mice. These results demonstrate that EGCG, a green tea polyphenol, may reduce up-regulation of MMP-9 activity and neuronal damage following transient focal cerebral ischemia. In addition to its antioxidant effect, MMP-9 inhibition might be a possible mechanism potentially involved in the neuroprotective effect of a green tea polyphenol, EGCG.
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http://dx.doi.org/10.1016/j.jnutbio.2009.08.009DOI Listing
November 2010

Infarction in the territory of anterior inferior cerebellar artery: spectrum of audiovestibular loss.

Stroke 2009 Dec 24;40(12):3745-51. Epub 2009 Sep 24.

Department of Neurology, Keimyung University School of Medicine, 194 Dongsan dong, Daegu, 700-712 South Korea.

Background And Purpose: To define the detailed spectrum of audiovestibular dysfunction in anterior inferior cerebellar artery territory infarction.

Methods: Over 8.5 years, we prospectively identified 82 consecutive patients with anterior inferior cerebellar artery territory infarction diagnosed by MRI. Each patient completed a standardized audiovestibular questionnaire and underwent a neuro-otologic evaluation, including bithermal caloric tests and pure tone audiogram.

Results: All but 2 (80 of 82 [98%]) patients had acute prolonged vertigo and vestibular dysfunction of peripheral, central, or combined origin. The most common pattern of audiovestibular dysfunction was the combined loss of auditory and vestibular function (n=49 [60%]). A selective loss of vestibular (n=4 [5%]) or cochlear (n=3 [4%]) function was rarely observed. We could classify anterior inferior cerebellar artery territory infarction into 7 subgroups according to the patterns of neuro-otological presentations: (1) acute prolonged vertigo with audiovestibular loss (n=35); (2) acute prolonged vertigo with audiovestibular loss preceded by an episode(s) of transient vertigo/auditory disturbance within 1 month before the infarction (n=13); (3) acute prolonged vertigo and isolated auditory loss without vestibular loss (n=3); (4) acute prolonged vertigo and isolated vestibular loss without auditory loss (n=4); (5) acute prolonged vertigo but without documented audiovestibular loss (n=24); (6) acute prolonged vertigo and isolated audiovestibular loss without any other neurological symptoms/signs (n=1); and (7) nonvestibular symptoms with normal audiovestibular function (n=2).

Conclusions: Infarction in the anterior inferior cerebellar artery territory can present with a broad spectrum of audiovestibular dysfunctions. Unlike a viral cause, labyrinthine dysfunction of a vascular cause usually leads to combined loss of both auditory and vestibular functions.
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http://dx.doi.org/10.1161/STROKEAHA.109.564682DOI Listing
December 2009

Silibinin inhibits expression of HIF-1alpha through suppression of protein translation in prostate cancer cells.

Biochem Biophys Res Commun 2009 Dec 22;390(1):71-6. Epub 2009 Sep 22.

Chronic Disease Research Center, School of Medicine, Keimyung University, Daegu 700-712, Republic of Korea.

Silibinin is a polyphenolic flavonoid isolated from the milk thistle (Silybum marianum) and is reported to exhibit anticancer properties. Recently, it has been reported that silibinin inhibits hypoxia-inducible factor-1alpha (HIF-1alpha) expression in cancer cells. However, the precise mechanism by which silibinin decreases HIF-1 expression is not fully understood. In this study, silibinin inhibited basal and hypoxia induced expression levels of HIF-1alpha protein in LNCaP and PC-3 prostate cancer cells, while the rate of HIF-1alpha protein degradation and mRNA levels were not affected. We found that the decrease in HIF-1 protein by silibinin correlated with suppression of de novo synthesis of HIF-1alpha protein. Silibinin inhibited global protein synthesis coincided with reduction of eIF4F complex formation and induction of phosphorylation of the translation initiation factor 2alpha (eIF-2alpha) which can cause inhibition of general protein synthesis. These results suggest that silibinin's activity to inhibit HIF-1alpha protein expression is associated with the suppression of global protein translation.
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http://dx.doi.org/10.1016/j.bbrc.2009.09.068DOI Listing
December 2009

Anticancer activity and differentially expressed genes in head and neck cancer cells treated with a novel cyclin-dependent kinase inhibitor.

Chemotherapy 2009 5;55(5):353-62. Epub 2009 Aug 5.

Department of Otolaryngology, Keimyung University, Daegu, South Korea.

Background: Cyclin-dependent kinases (CDKs) are involved in the regulation of the cell cycle and the growth of tumor cells. In this study, we investigated the antitumor effect and differentially expressed genes (DEGs) in head and neck cancer cells treated by a novel CDK inhibitor, 2-[1,1'-biphenyl]- 4-yl-N-[5-(1,1-dioxo-1lambda(6)-isothiazolidin-2-yl)-1H-indazol-3-yl] acetamide (BAI).

Methods: Cell growth was measured by XTT assay. Cell cycle and apoptosis were determined using flow cytometry. GeneFishing PCR was utilized to identify DEGs. Protein expression was analyzed by Western blot.

Results: Exposure to BAI of 2 different head and neck cancer cell lines, AMC-HN4 and AMC-HN6, induced apoptosis in association with growth inhibition, cell cycle arrest, caspase-3 activation and cytochrome c release. Significantly, data from GeneFishing PCR experiments demonstrated 10 DEGs in AMC-HN6 cells treated with BAI. Some of these DEGs turned out to encode proteins with functions related to key cellular processes.

Conclusions: These results indicate that BAI has strong anticancer activities on head and neck cancer cells, and the DEGs induced by BAI may become involved in BAI-induced cancer cell death.
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http://dx.doi.org/10.1159/000232450DOI Listing
December 2009

Pattern of otolith dysfunction in posterior inferior cerebellar artery territory cerebellar infarction.

J Neurol Sci 2009 May 27;280(1-2):65-70. Epub 2009 Feb 27.

Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea.

Objectives: To document otolith dysfunction in patients with posterior inferior cerebellar artery (PICA) territory cerebellar infarction.

Methods: From March to October 2006, 14 consecutive patients with PICA territory cerebellar infarctions (brainstem spared) diagnosed by brain MRI from the acute stroke registry at the Keimyung University Dongsan Medical Center were enrolled within 12 days of onset (mean 4.0 days). Otolith function tests included ocular torsion (OT), skew deviation, and subjective visual vertical (SVV) were performed. The extent of the cerebellar infarction was determined by previously validated MR anatomical templates.

Results: All patients had an abnormal posture as a result of otolithic dysfunction. Eleven patients (79%) had at least one otolith-related test abnormality: abnormal tilt of SVV (79%), abnormal OT (29%), or skew deviation (21%). Two common patterns of otolith dysfunction were identified based on whether or not the nodulus was infarcted: 1) ipsilesional SVV tilt (mean 5.0 degrees at binocular viewing) without accompanying abnormal OT or skew deviation (nodulus spared); 2) contralesional SVV tilt (mean 11.3 degrees at binocular viewing) with concomitant abnormal OT and skew deviation (nodulus infarcted). Patients with type 1 infarcts (i.e., nodulus spared) fell toward the side of lesion while patients with type 2 infarcts (i.e., nodulus infracted) fell toward the opposite side.

Conclusion: Isolated PICA territory cerebellar infarction usually produces two distinct patterns of otolith dysfunction - Ipsilesional SVV tilt and falling without accompanying OT or skew deviation if the nodulus is spared and contralesional SVV tilt and falling with OT and skew deviation if nodulus is infarcted.
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http://dx.doi.org/10.1016/j.jns.2009.02.002DOI Listing
May 2009

Doxycycline inhibits matrix metalloproteinase-9 and laminin degradation after transient global cerebral ischemia.

Neurobiol Dis 2009 May 6;34(2):189-98. Epub 2009 Jan 6.

Brain Research Institute, Keimyung University, South Korea.

Doxycycline, a tetracycline antibiotic inhibits matrix metalloproteinase (MMP) and reduces neuronal damage in focal brain ischemia. This study was undertaken to assess if doxycycline reduces delayed neuronal damage following transient global cerebral ischemia through MMP inhibition. C57BL/6 mice were subjected to 20 min global cerebral ischemia. Doxycycline was administered to mice 30 min before and 2 h after ischemia. In TUNEL assay, damaged neurons were also apparent in the CA1 and CA2 areas and doxycycline reduced TUNEL-positive neurons. Gelatin gel and in situ zymography showed upregulation of gelatinase activity after ischemia. Doxycycline significantly inhibited MMP-9 activity in gel zymography and also suppressed in situ gelatinase activity. Laminin degradation was remarkable in CA1 and CA2 areas after ischemia and doxycycline reduced the laminin degradation and neuronal loss. Our data suggest that doxycycline may provide a neuroprotection against global cerebral ischemia since it reduces perineuronal laminin degradation by inhibiting MMP-9 activity.
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http://dx.doi.org/10.1016/j.nbd.2008.12.012DOI Listing
May 2009

PPARgamma agonist pioglitazone reduces matrix metalloproteinase-9 activity and neuronal damage after focal cerebral ischemia.

Biochem Biophys Res Commun 2009 Feb 9;380(1):17-21. Epub 2009 Jan 9.

Department of Pharmacology, School of Medicine and Brain Research Institute, Keimyung University, Taegu, South Korea.

Pioglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, has shown protective effects against ischemic insult in various tissues. Pioglitazone is also reported to reduce matrix metalloproteinase (MMP) activity. MMPs can remodel extracellular matrix components in many pathological conditions. The current study was designed to investigate whether the neuroprotection of pioglitazone is related to its MMP inhibition in focal cerebral ischemia. Mice were subjected to 90 min focal ischemia and reperfusion. In gel zymography, pioglitazone reduced the upregulation of active form of MMP-9 after ischemia. In in situ zymograms, pioglitazone also reduced the gelatinase activity induced by ischemia. After co-incubation with pioglitazone, in situ gelatinase activity was directly reduced. Pioglitazone reduced the infarct volume significantly compared with controls. These results demonstrate that pioglitazone may reduce MMP-9 activity and neuronal damage following focal ischemia. The reduction of MMP-9 activity may have a possible therapeutic effect for the management of brain injury after focal ischemia.
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http://dx.doi.org/10.1016/j.bbrc.2008.12.181DOI Listing
February 2009

Green tea polyphenol (-)-epigallocatechin gallate reduces neuronal cell damage and up-regulation of MMP-9 activity in hippocampal CA1 and CA2 areas following transient global cerebral ischemia.

J Neurosci Res 2009 Feb;87(2):567-75

Department of Pharmacology, School of Medicine, Keimyung University, Taegu, South Korea.

Previous studies have demonstrated that (-)-epigallocatechin gallate (EGCG), a green tea polyphenol, protects against ischemia and reperfusion-induced injury in many organ systems. Here, we test the hypothesis that part of EGCG's neuroprotective effects may involve a modulation of matrix metalloproteinases (MMPs) after cerebral ischemia. C57BL/6 mice were subjected to 20 min of transient global cerebral ischemia. EGCG (50 mg/kg) or vehicle (saline) was administered i.p. immediately after ischemia. Brains were examined 3 days after ischemia. The effects of EGCG on MMP (gelatinase) activity and neuronal damage in the hippocampus were assessed. Gelatin gel zymography showed induction of active forms of MMP-9 protein after transient global cerebral ischemia. In situ zymography showed that ischemic gelatinase activity occurred primarily in pyramidal neuronal areas after brain ischemia. Mice treated with EGCG showed significantly reduced gelatinase levels. Neuronal damage was evident in CA1 and CA2 pyramidal sectors, corresponding to TUNEL-positive signals. In EGCG-treated mice, delayed neuronal damage was significantly reduced compared with vehicle-treated mice. These results demonstrate that the green tea polyphenol EGCG suppresses MMP-9 activation and reduces the development of delayed neuronal death after transient global cerebral ischemia in mouse brain.
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http://dx.doi.org/10.1002/jnr.21847DOI Listing
February 2009

PPARgamma agonist pioglitazone reduces [corrected] neuronal cell damage after transient global cerebral ischemia through matrix metalloproteinase inhibition.

Eur J Neurosci 2008 Jan;27(2):334-42

Department of Pharmacology, School of Medicine, Keimyung University, Taegu 700-712, South Korea.

Previous studies have demonstrated that pioglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, inhibits ischemia-induced injury in various tissues including neural tissue. Pioglitazone has also been shown to reduce matrix metalloproteinase (MMP) activity. Because MMP is known to play a major role in the pathophysiology of brain ischemia, the present study was undertaken to test whether pioglitazone attenuates ischemic neuronal damage through MMP inhibition. C57BL/6 mice were subjected to global brain ischemia for 20 min. Animals were killed 72 h after ischemia. Oral pioglitazone (40 mg/kg/day, as a suspension in 0.5% carboxymethylcellulose) was administered to mice twice daily for 3 days before ischemia and twice daily after ischemia until the animals were killed. We investigated gelatinase activity by zymography and laminin immunohistochemistry. Histological analysis was also performed to test the protective effect of pioglitazone on neuronal damage. Mice treated with pioglitazone had attenuated gelatinase activity. Gelatin gel and in situ zymography showed up-regulation of gelatinase activity after ischemia. Pioglitazone significantly inhibited ischemia-induced elevation of the active form of MMP-9. Pioglitazone also reduced up-regulation of in situ gelatinase activity and laminin breakdown induced by ischemia in the hippocampus. There was marked neuronal damage in the CA1 and CA2 areas after ischemia. Neuronal damage in mice was significantly decreased by pioglitazone treatment, compared with vehicle-treated mice. Pioglitazone also inhibited TdT-mediated dUTP nick end labeling staining in CA1 and CA2 areas. Pioglitazone, a PPARgamma agonist, reduces delayed neuronal damage induced by global ischemia through inhibition of MMP-9 activity.
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http://dx.doi.org/10.1111/j.1460-9568.2007.06007.xDOI Listing
January 2008

Ocular torsion associated with infarction in the territory of the anterior inferior cerebellar artery: frequency, pattern, and a major determinant.

J Neurol Sci 2008 Jun 11;269(1-2):18-23. Epub 2008 Jan 11.

Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea.

Background: Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) can cause the vestibular dysfunction in the roll plane of the vestibuloocular reflex with abnormal ocular torsion (OT). There has been no systemic study that carefully investigates the nature of OT that occurs with AICA infarction.

Objectives: To investigate the frequency, the characteristic patterns of OT associated with AICA territory infarction, and the crucial site for determining the direction of OT in AICA territory infarction.

Methods: We studied 12 consecutive cases of infarction in the territory of the AICA diagnosed by brain MRI. Fundus photography, prism cover test, and subjective visual vertical tilting test were performed to evaluate the function of the otolith system. Pure tone audiogram was also performed to evaluate the function of the auditory system.

Results: Nine (75%) of 12 patients exhibited pathological ocular torsion (OT). Two types of pathological OT were found: ipsiversive OT accompanying skew deviation (n=6), and contraversive OT only (n=3). Six patients with ipsiversive OT with skew deviation showed an audiovestibular loss with canal paresis and hearing loss ipsilaterally whereas three patients with contraversive OT without skew deviation had a normal audiovestibular response. In all cases with pathological OT, the direction of the subjective visual vertical tilt corresponded to the direction of the OT.

Conclusions: Our findings emphasize that the peripheral vestibular structure with inner ear probably plays a crucial role in determining the direction of OT associated with AICA territory infarction.
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http://dx.doi.org/10.1016/j.jns.2007.12.009DOI Listing
June 2008

Protective effects of several components of Gastrodia elata on lipid peroxidation in gerbil brain homogenates.

Phytother Res 2007 Oct;21(10):960-4

Department of Microbiology, School of Medicine, Keimyung University, Taegu, 700-712 South Korea.

Gastrodia elata (GE) Blume, a traditional herbal agent, has been used mainly in anticonvulsive treatment in Asia. Recently, extracts of GE were evaluated for their potential as neuroprotectives and antioxidants. This study was designed to examine the antioxidant effect of the ether fraction of the methanol extract (EFME) of GE along with its major constituents vanillin, vanillyl alcohol, hydroxybenzaldehyde and hydroxybenzyl alcohol. In experiment 1, gerbils were treated with EFME of GE at a dosage of 500 mg/kg/day for 2 weeks. Oxidative stress was induced with H(2)O(2) or ferrous ion, and lipid peroxidation was measured. In experiment 2, oxidative stress was induced with various concentrations of H(2)O(2) or ferrous ammonium sulfate, and lipid peroxidation was measured. To compare the antioxidant potency, the inhibitory concentration 50% (IC(50)) was determined. EFME of GE reduced auto-peroxidation and H(2)O(2)-induced lipid peroxidation. However, it did not significantly reduce ferrous ammonium sulfate-induced lipid peroxidation. The order of antioxidation potency was as follows: hydroxybenzyl alcohol > vanillyl alcohol > vanillin > hydroxybenzaldehyde. In the case of hydroxybenzaldehyde, its antioxidant effect was more potent than that of melatonin. The excellent antioxidant effects of GE and its main constituents may have potential in the treatment of lipid peroxidation-associated neurological disease.
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http://dx.doi.org/10.1002/ptr.2193DOI Listing
October 2007

Acute peripheral vestibular syndrome of a vascular cause.

J Neurol Sci 2007 Mar 24;254(1-2):99-101. Epub 2007 Jan 24.

Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea.

Background: Acute peripheral vestibular syndrome (APVS) is an idiopathic peripheral vestibulopathy characterized by prolonged vertigo (over 24 h), nausea, vomiting, and postural instability. There has been no previous report of APVS presumably of a vascular cause.

Objectives: To describe APVS presumably resulting from a vascular disturbance with embolic cerebral infarction.

Patient: A 67-year-old woman developed sudden onset of severe isolated vertigo, nausea, and vomiting, which lasted for 3 days. Ten days earlier, she had had 4 episodes of transient vertigo lasting a few minutes. She had a spontaneous right-beating horizontal nystagmus with a torsional component, in the primary position and on gaze to the right or left. Caloric test showed a decreased response on the left side. Diffusion-weighted brain MRI showed 2 tiny acute infarcts in the left hippocampus and basal ganglia. Magnetic resonance angiogram showed no abnormalities. Continuous electrocardiographic monitoring for 24 h showed paroxysmal atrial fibrillation.

Conclusion: In this patient, clinical and laboratory findings were consistent with APVS. Considering the simultaneous onset of acute silent infarcts on brain MRI, the definite cardioembolic source with atrial fibrillation, and the episodic transient vertigo attacks before APVS, we speculate that small emboli arising from the heart may have lodged selectively in the anterior vestibular artery, producing APVS.
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http://dx.doi.org/10.1016/j.jns.2006.12.015DOI Listing
March 2007

Baicalein and 12/15-lipoxygenase in the ischemic brain.

Stroke 2006 Dec 19;37(12):3014-8. Epub 2006 Oct 19.

Stroke and Neurovascular Research Group, Department of Radiology, Massachusetts General Hospital, 149 13th St., R. 2401, Charlestown, MA 02129, USA.

Background And Purpose: The natural product baicalein is a specific inhibitor of 12/15-lipoxygenase, but it also has antioxidant properties. The current study was designed to test if the neuroprotective properties of baicalein are related to its lipoxygenase inhibition.

Methods: The presence of 12/15-lipoxygenase in the ischemic mouse brain was demonstrated by immunohistochemistry. A mouse model of transient middle cerebral artery occlusion was used to study lipoxygenase-dependent protection of the ischemic brain by baicalein. Rat primary neurons were subjected to oxidative stress in the presence or absence of baicalein.

Results: In a mouse model of transient middle cerebral artery occlusion, 12/15-lipoxygenase is increased in the peri-infarct area surrounding the primary infarction, predominantly in neurons. Oxidative toxicity in primary rat neurons is reduced by baicalein. C57Bl6J mice are protected against transient focal ischemia by intraperitoneal injection of baicalein, and a similar degree of protection is seen in 12/15-lipoxygenase knockout mice compared with wild-type mice. In contrast, the 12/15-LOX knockout mice are not further protected by baicalein.

Conclusions: Baicalein protects against ischemia/reperfusion injury by inhibiting the 12/15-lipoxygenase pathway to neuronal cell death.
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http://dx.doi.org/10.1161/01.STR.0000249004.25444.a5DOI Listing
December 2006

Protective effect of quercetin, a natural flavonoid against neuronal damage after transient global cerebral ischemia.

Neurosci Lett 2006 Sep 27;404(3):330-5. Epub 2006 Jun 27.

Department of Anesthesiology, School of Medicine, Keimyung University, Taegu, South Korea.

Previous studies have demonstrated that quercetin, a bioflavonoid shows the inhibitory effect against ischemia and reperfusion-induced injury in various tissues including neural tissue. Quercetin is also reported to have an inhibitory effect against matrix metalloproteinases (MMPs). Because MMPs are known to play a main role in the pathophysiology of brain ischemic insult, their mechanisms of possible protective effect of quercetin against brain ischemia remain to be clarified. In the present study, C57BL/6 mice were subjected to 20 min transient global brain ischemia. Cerebral blood flow was monitored by laser doppler flowmeter. Animals were sacrificed 72 h after ischemia. Quercetin (50 mg/kg, dissolved in saline) was intraperitoneally administered to mice at 30 min before and immediately after ischemia and from the second day, quercetin was then administered once daily until sacrifice. The present study was undertaken to test the effect of quercetin on neuronal damage after transient cerebral ischemia. Neuronal damages were remarkable in the medial portion of CA1 and CA2 areas after ischemic insult. In quercetin-treated mice, delayed neuronal damage was significantly decreased compared with vehicle-treated mice. Mice treated with quercetin showed attenuated brain MMP-9 activity. Gelatin gel zymography showed an induction of MMP-9 protein after ischemia. Quercetin significantly inhibited ischemia-induced elevation of MMP-9. In situ zymography showed elevations in gelatinase activities after brain ischemia. Quercetin also inhibited TdT-mediated dUTP nick end labeling (TUNEL) staining in CA1 and CA2 areas. These results demonstrate that quercetin, a natural flavonoid reduces global ischemia-induced neuronal damage through inhibition of MMP-9 activity.
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http://dx.doi.org/10.1016/j.neulet.2006.06.010DOI Listing
September 2006

Involvement of matrix metalloproteinase in neuroblast cell migration from the subventricular zone after stroke.

J Neurosci 2006 Mar;26(13):3491-5

Department of Neurology and Radiology, Massachusetts General Hospital, Boston, Massachusetts 02129, USA.

After brain injury, neuroblast cells from the subventricular zone (SVZ) expand and migrate toward damaged tissue. The mechanisms that mediate these neurogenic and migratory responses remain to be fully dissected. Here, we show that bromodeoxyuridine-labeled and doublecortin-positive cells from the SVZ colocalize with the extracellular protease matrix metalloproteinase-9 (MMP-9) during the 2 week recovery period after transient focal cerebral ischemia in mice. Treatment with the broad spectrum MMP inhibitor GM6001 significantly decreases the migration of doublecortin-positive cells that extend from the SVZ into the striatum. These data suggest that MMPs are involved in endogenous mechanisms of neurogenic migration as the brain seeks to heal itself after injury.
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http://dx.doi.org/10.1523/JNEUROSCI.4085-05.2006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6673870PMC
March 2006

Bilateral infarcts in the territory of the superior cerebellar artery: clinical presentation, presumed cause, and outcome.

J Neurol Sci 2006 Jul 29;246(1-2):103-9. Epub 2006 Mar 29.

Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea.

Backgrounds And Purpose: The aim of this study was to document the clinical presentation, vascular topographic patterns, stroke mechanism, and outcome of bilateral infarcts in the territory of the superior cerebellar artery (SCA) based on data collected from a prospective acute stroke registry.

Methods: We studied the clinical and radiological features of 11 patients with bilateral infarctions in the territory of the SCA diagnosed by brain MRI.

Results: Bilateral SCA infarcts represented 23.4% (11/47) of all SCA territory infarction. Bilateral SCA infarcts mostly associated with brainstem (n = 5), cerebral (n = 5), or non-SCA cerebellar lesions (n = 4). The most common clinical presentation at onset was sudden fall with axial lateropulsion and dysarthria (n = 6). In five patients with a coexisting infarct(s) in the brainstem, limb weakness and/or mental change were prominent and often masked the signs of cerebellar dysfunction. Six patients showed no stenosis or occlusion in the vertebrobasilar system on brain MRA. Five had an obvious cardiac source of emboli. Eight patients showed favorable outcomes with complete recovery or minimal disability, but three patients with additional extensive brainstem infarcts died within 1 week.

Conclusions: Bilateral SCA territory infarcts show variable clinical, vascular topographic, and prognostic features. They usually result from cardiac emboli.
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http://dx.doi.org/10.1016/j.jns.2006.02.013DOI Listing
July 2006

Cerebellar infarction in the territory of the medial branch of the superior cerebellar artery.

Neurology 2006 Jan;66(1):115-7

Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea.

The authors studied 14 patients with an isolated cerebellar infarct in the territory of the medial branch of the superior cerebellar artery (MSCA). The most common clinical finding was severe gait ataxia with sudden falling (n = 9) or severe veering (n = 2). Cerebellar dysarthria was found in 8 patients. Eight patients had a mild unilateral limb ataxia. These findings emphasize that MSCA territory cerebellar infarction presented with the prominent gait ataxia and cerebellar dysarthria.
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http://dx.doi.org/10.1212/01.wnl.0000191389.81651.deDOI Listing
January 2006