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Biomedical subjects

Byung-Woo Yoon

Publications and source records attributed to Byung-Woo Yoon.

At least 19 recordsLinked to original sources
PubMed2006

Retinopathy as an indicator of silent brain infarction in asymptomatic hypertensive subjects.

BACKGROUND AND PURPOSE: Silent brain infarction (SBI), which is cerebral target organ damage of hypertensive microangiopathies, is frequently seen in hypertensive patients. The purpose of this study is to investigate the relation between hypertensive retinopathy (HTR) and SBI in subjects without a history of stroke or transient ischemic attack. METHODS: Five hundred-fifty hypertensive subjects without history of stroke or transient ischemic attack had brain MRI and retinal photographs taken. The presence of SBI was assessed from the MRI scans, which was defined as a lesion of at least 3 mm in diameter with typical imaging characteristics. The presence HTR was defined from digitized retinal photographs. RESULTS: Seventy-seven subjects (14%) showed HTR (grade 1 in 46, grade 2 in 31 persons). A multivariate analysis showed that age (OR, 1.07; 95% CI, 1.03 to 1.10) and HTR (OR, 2.01 for grade 1; OR, 3.03 for grade 2) were the independent indicators for the presence of SBI. The higher the grade of HTR, the more prevalent SBI than persons with normal retina (by linear by linear association test, p=0.001). CONCLUSION: HTR is associated with the presence of SBI. This finding suggests that retinal photography may be useful for identifying hypertensive subjects at increased risk of having SBI regardless of current blood pressure status.

Aged↗
PubMed2006

Mild left ventricular dysfunction is associated with thrombogenicity in cardioembolic stroke.

BACKGROUND: Transesophageal echocardiography (TEE) has been recognized as a valuable tool for identifying the left cardiac thrombus (LCT) or spontaneous echocardiographic contrast (SEC). We aimed to identify risk groups where TEE should be performed in patients with suspected cardioembolic stroke according to magnetic resonance imaging analysis. METHODS: One hundred and forty-six patients (mean age 64.7 +/- 11.8 years, 101 males) with suspected cardioembolic stroke were analyzed. We used TEE for the presence of LCT and/or SEC as indication of thrombogenicity. We evaluated the association between thrombogenicity and demographic features, stroke risk factors and echocardiographic variables. RESULTS: The study included 40 patients (27.3%) who showed thrombogenicity (10 LCT and 30 SEC). The independent echocardiographic variables of thrombogenicity were atrial fibrillation (OR 7.14; 95% CI 2.62-19.48; p < 0.001) and left ventricular ejection fraction </=50% (OR 4.01; 95% CI 1.40-11.49; p = 0.01). CONCLUSION: We recommend that TEE should be considered in patients with mildly reduced left ventricular dysfunction (ejection fraction </=50%) after suspected cardioembolic stroke.

Atrial Fibrillation↗
PubMed2006

Symptomatic intracerebral hematomas in posterior circulation stroke patients anticoagulated with heparin.

BACKGROUND: A lot of clinicians use heparin in patients with posterior circulation stroke. Frequency and risk factors of symptomatic intracerebral hematoma (ICH) in posterior circulation infarct patients anticoagulated with unfractionated heparin are not known. METHODS: To determine the incidence and the risk factors of the heparin-related ICH in posterior circulation infarct patients, we retrospectively reviewed the clinical features of 37 patients who had acute posterior circulation infarct and received intravenous heparin after they underwent brain computed tomographic scans and diffusion-weighted imaging (DWI). Follow-up brain scans were obtained at any time if clinical symptoms worsened. Volumes of acute posterior circulation infarction were calculated on DWI. RESULTS: Of 37 patients, four (10.8%) developed symptomatic ICH during heparin infusion. The location of ICH was cerebellum in all the hemorrhagic worsening patients. We found that the size of an acute infarction calculated on DWI is the risk factor of symptomatic ICH during intravenous heparin therapy in patients with posterior circulation infarct. CONCLUSIONS: Until a large prospective study is performed, it may be prudent to avoid heparin infusion in patients with large posterior circulation infarct documented on DWI.

Aged↗
PubMed2005

Metabolic syndrome as an independent risk factor of silent brain infarction in healthy people.

BACKGROUND AND PURPOSE: Metabolic syndrome (MetS) is associated with an increased risk of the subsequent development of cardiovascular disease or stroke. Moreover, a silent brain infarction (SBI) can predict clinical overt stroke or dementia. We examined the associations between SBI and MetS in apparently healthy individuals. METHODS: We evaluated 1588 neurologically healthy subjects (927 males and 661 females) who underwent brain MRI at Seoul National University Hospital Healthcare System Gangnam Center. MetS was defined using the criteria of the National Cholesterol Education Program Adult Treatment Panel III. We examined associations between full syndrome (> or =3 of the 5 conditions) as well as its components and SBI by controlling possible confounders. RESULTS: Eighty-eight (5.5%) were found to have > or =1 SBI on MRI. Age was found to be significantly related to SBI prevalence (odds ratio [OR], 1.06; 95% CI, 1.04 to 1.09). A history of coronary artery disease was associated with an elevated odds ratio of SBI (OR, 2.83; 95% CI, 1.38 to 5.82), and MetS was significantly associated with SBI (OR, 2.18; 95% CI, 1.38 to 3.44). The components model of MetS showed a strong significance between an elevated blood pressure (OR, 3.75; 95% CI, 2.05 to 6.85) and an impaired fasting glucose (OR, 1.74; 95% CI, 1.08 to 2.80) and the risk of SBI. CONCLUSIONS: MetS was found to be significantly associated with SBI. This finding has clinical utility in terms of identifying healthy people at increased risk of developing SBI.

Adult↗
PubMed2005

Correlation of coronary and cerebral atherosclerosis: difference between extracranial and intracranial arteries.

BACKGROUND: A difference with regard to the correlation with coronary atherosclerosis (CAS) between extracranial carotid atherosclerosis (ECAS) and intracranial cerebral atherosclerosis (ICAS) has been assumed but not proven clearly by direct comparison within the same population. METHODS: A consecutive series of 246 patients undergoing coronary artery bypass graft surgery were reviewed. The severity of CAS was estimated as a CAS score based on coronary angiography. The presence of ECAS and ICAS was screened by transcranial Doppler and carotid duplex sonography, and confirmed by magnetic resonance angiography. RESULTS: The CAS scores in patients with ECAS were observed to be higher than those in patients without ECAS (10.62+/- 4.80 vs. 9.45+/- 4.25; p=0.054 on the Mann-Whitney U test). The difference in CAS scores was smaller between patients with and without ICAS (10.41+/- 4.44 vs. 9.66+/- 4.49; p=0.201). Similar patterns were observed on comparing the correlation of ECAS and ICAS with a quartile of the CAS score. An advanced CAS, which was generated by collapsing the quartiles of the CAS score into 75th percentile or less and more than the 75th percentile, was significantly associated with ECAS, but not with ICAS. These associations remained unchanged after adjustments had been made for age, sex, hypertension, diabetes mellitus, hyperlipidemia, smoking and a history of stroke or transient ischemic attack. CONCLUSIONS: This study suggests that the correlation of CAS with ECAS is stronger than that of CAS with ICAS, and this difference is independent of the classic risk factors for atherosclerosis.

Aged↗
PubMed2005

Exercise increased BDNF and trkB in the contralateral hemisphere of the ischemic rat brain.

Previous studies have suggested that brain-derived neurotrophic factor (BDNF) and trkB both have a role in plasticity following brain insults and exercise increases BDNF and trkB mRNA levels in the normal brain. We attempted to determine whether treadmill exercise improves motor function following experimental cerebral ischemia, and whether motor outcome is associated with BDNF and trkB expression. We subjected adult male Sprague-Dawley rats to a permanent ischemia, followed by either 12 days of treadmill exercise or non-exercise. In the exercise group, improvements in the motor behavior index were found and BDNF and trkB proteins in contralateral hemisphere were increased. This study suggests that after permanent brain ischemia, exercise improves motor performance and elevates BDNF and trkB proteins in the contralateral hemisphere.

Animals↗
PubMed2005

Expression of Cu/Zn SOD protein is suppressed in hsp 70.1 knockout mice.

Heat shock proteins (HSPs) are known to protect cells from oxidative stress and other types of injuries. We previously reported the neuroprotective effect of HSP70 following cerebral ischemia and reperfusion using hsp 70.1 knockout (KO) mice. However, the precise role of HSP70 in neuroprotection has not been established yet. The purpose of this study was to investigate the relationship between HSP70 and antioxidant enzymes using hsp 70.1 KO mice. The activities of both SOD-1 and SOD-2 were significantly decreased in hsp 70.1 KO mice than in the wild type (WT) littermates. SOD-1 protein level in the hsp 70.1 KO mice was lower than that of WT. We speculate that HSP70 might be involved in regulation of expression of SOD-1 at the level of transcription or by post-transcriptional modification.

Animals↗
PubMed2005

Down-regulation of MHC class I expression in human neuronal stem cells using viral stealth mechanism.

Due to their unique capacity for self-renewal in addition to their ability to differentiate into cells of all neuronal lineages, neuronal stem cells (NSCs) are promising candidates for cell replacement therapy in neuronal injury and neurodegenerative diseases. However, there are few studies on immune rejection, which is one of the main problems facing successful stem cell therapy. In order to determine if human NSC might be rejected after transplantation the MHC expression level was examined in the HB1.F3 cell line, which has previously been shown to exhibit NSC properties. The results showed low expression levels of the MHC class I molecules on the surfaces of these cells. A dramatic increase in the MHC class I expression level was observed when the cells were treated with IFN-gamma, TNF-alpha, and IL-1beta, alone or in combination. The maximum induction of MHC class I protein expression was observed at above 20ng/ml IFN-gamma 48h after the treatment. The apparent additive effects of TNF-alpha and IL-1beta in combination on the maximum induction of MHC class I expression exerted by IFN-gamma treatment were not observed. The MHC class I levels elevated by IFN-gamma were sustained for 72h after withdrawing the IFN-gamma. Therefore, this study introduced human cytomegalovirus (hCMV) US genes, which are known to be able to reduce the MHC class I expression level on the cell surface after infection, into HB1.F3 cells. The cells transfected with the hCMV US2, US3, US6 or US11 genes showed 20-50% reduction in the MHC class I expression level compared with the mock-transfected cells. These results suggest that NSC expresses high levels of the MHC class I proteins, and unless they are modified, might be rejected upon transplantation. In addition, the various viral stealth mechanisms can be exploited for stem cell transplantation.

Cell Line↗
PubMed2005

Ipsilateral hemiparesis caused by a corona radiata infarct after a previous stroke on the opposite side.

Ipsilateral hemiparesis after a supratentorial stroke is rare. However, the role of the reorganization of the unaffected hemisphere in recovery after a stroke is poorly understood. Two patients developed ipsilateral hemiparesis after a left corona radiata infarct. Both of these patients had previously experienced contralateral hemiparesis after a right-sided supratentorial stroke. Functional magnetic resonance imaging demonstrated bilateral motor area activation during paretic left hand movement. This finding suggests that the ipsilateral hemiparesis was caused by a new stroke in the ipsilateral motor system that was functionally reorganized after the previous stroke.

Adult↗
PubMed2005

Effects of microbleeds on hemorrhage development in leukoaraiosis patients.

The possible influences of cerebral microbleeds (CMBs) on the development of intracerebral hemorrhage (ICH) in patients with leukoaraiosis (LA) have rarely been examined. We aimed to determine whether CMBs might be a risk factor for ICH in hypertensive patients with leukoaraiosis. We studied 70 hypertensive patients with acute ICH and LA (the ICH group) by brain MRI, including T2*-weighted gradient-echo sequences. The control group was composed of 73 hypertensive LA patients without ICH. CMBs and old lacunae were counted in the group of patients with ICH and in the control subjects and compared. The ICH group contained more patients with CMBs (68 patients; control group, 41; p < 0.01), and showed a higher mean number of lesions (19.9 +/- 31.1; control group, 7.4 +/- 19.6; p < 0.01). The negative predictive value for ICH was highest among the ICH patients without CMB (94.1%), and the positive predictive value was highest among the ICH patients with 6 or more CMBs (75.4%). Old lacunae were observed more frequently in the ICH group (65 patients; control group, 58; p = 0.02), but their predictive value for ICH was not high (positive, 52.3%; negative, 75.0%). Our results indicated that CMBs may be used to predict the risk of ICH in hypertensive patients with advanced LA.

Aged↗
PubMed2005

Cerebellopontomandibular vascular malformation: a rare type of cerebrofacial arteriovenous metameric syndrome. Case report.

The concept of a cerebrofacial arteriovenous metameric syndrome (CAMS) recently has been posited. A 22-year-old woman presented with gait ataxia. She had unilateral angiomatous lesions involving the lower face, the auricle, and the retromastoid area, as well as the tongue on the right side. Angiography revealed the presence of extensive arteriovenous malformations (AVMs) in the ipsilateral cerebellum and pons, in addition to those located in the facial region. The authors report a case of multiple AVMs of the face, cerebellum, and pons, corresponding to CAMS Type 3, and include a review of the literature.

Adult↗
PubMed2004

Metronidazole-induced encephalopathy.

We report the clinical, neuropsychological, and neuroimaging findings of two patients of diffuse encephalopathy associated with the use of metronidazole. Both patients showed characteristic abnormalities on magnetic resonance imaging (MRI) with diffusion weighted imaging (DWI) and recovered incompletely after the discontinuation of metronidazole. We also suggest that MRI with DWI may be useful in the diagnosis of metronidazole-induced encephalopathy, and that they have a role in the prediction of prognosis.

Adult↗
PubMed2004

Effects of hsp70.1 gene knockout on the mitochondrial apoptotic pathway after focal cerebral ischemia.

BACKGROUND AND PURPOSE: Murine heat-shock protein 70 (HSP70) protein, which is produced from 2 genes, hsp70.1 and hsp70.3, is known to protect the brain against ischemic injury. However, little information is available on the antiapoptotic mechanism of HSP70.1 protein after cerebral ischemia. To evaluate the role of HSP70.1 protein in ischemia, we analyzed the mitochondrial apoptotic pathway using hsp70.1 knockout (KO) mice and their wild-type (WT) mice. METHODS: hsp70.1 KO and WT mice underwent focal ischemia for 120 minutes. DNA fragmentation was evaluated by TUNEL staining. Cytochrome c release and the activation of caspase-3 were analyzed by Western blotting and immunohistochemistry. RESULTS: hsp70.1 mRNA was not detected in hsp70.1 KO mice after ischemia, and HSP70 protein expression was markedly suppressed versus WT mice. KO mice showed a significantly greater infarction volume and DNA fragmentation in the cortex than WT mice at 24 hours after ischemia. At 8 hours, cytochrome c release into the cytoplasm was markedly higher in KO mice than in WT mice. Caspase-3 activation was also significantly enhanced in KO mice versus WT mice, as evidenced by higher levels of activated caspase-3 and cleaved gelsolin. CONCLUSIONS: These findings suggest that the deletion of the hsp70.1 gene increases cytochrome c release into the cytoplasm and subsequent caspase-3 activation, thereby exacerbating apoptosis after focal cerebral ischemia.

Animals↗
PubMed2004

Cerebral microbleeds in patients with hypertensive stroke. Topographical distribution in the supratentorial area.

OBJECTIVE: To analyse the topography of cerebral microbleeds (CMBs) visualized by T2*-weighted gradient-echo MR imaging in the supratentorial brain area, based on the anatomical classification of the regions and the arterial territories. BACKGROUND: CMBs are associated with hypertension and the risk of intracerebral hemorrhage; however, little is known about the cerebral topography of CMBs. METHODS: We examined 164 consecutive patients with hypertensive stroke who underwent T2*-weighted gradient-echo MRI. The anatomical locations and the vascular territories of the CMBs were determined in the subcortical white matter, basal ganglia/internal capsule and thalamus along the standard axial slices. RESULTS: We detected 2,193 CMBs in 98 patients (13.4+/-39.0 per patient). The CMBs showed a significant predilection for the temporo-occipital area of the subcortical white matter, the posterolateral part of the upper putamen, and the lateral nuclei of the mid-level thalamus. The most common arterial territories were those of the middle-posterior cerebral artery in the white matter, the middle cerebral artery in the basal ganglia, and the thalamogeniculate artery in the thalamus. CONCLUSIONS: These findings were quite similar to the cerebral topography of intracerebral hemorrhage described in the literature. Our results suggest that CMBs are regionally associated with intracerebral hemorrhage.

Adult↗
PubMed2004

Distribution and in situ proliferation patterns of intravenously injected immortalized human neural stem-like cells in rats with focal cerebral ischemia.

Neural stem cells are considered as a candidate for cell replacement therapy in various neurological diseases. To investigate whether human neural stem cells can migrate into the adult ischemic rat brain, we transplanted immortalized human neural 'tem-like' cells intravenously 24 h after focal cerebral ischemia. The intravenously injected human neural stem-like cells were found around the infarcted area, differentiated into neurons and astrocytes in the lesioned areas, and survive up to 56 days after transplantation. The number of the injected cells increased between 7 and 14 days after transplantation with incorporating BrdU. Our findings show that intravenously injected human neural stem-like cells may incorporate into the ischemic brain, and undergo proliferation responding to the endogenous mitotic signal during the acute period of focal ischemia.

Animals↗
PubMed2004

Topographical distribution of pontocerebellar microbleeds.

BACKGROUND AND PURPOSE: Microbleeds (MBs) visualized by use of T2*-weighted gradient-echo MR imaging are pathologic blood-breakdown products after tiny cerebral hemorrhages. The topographic distribution of the lesions has not been compared with that of symptomatic intracerebral hemorrhage (ICH). The purpose of this study was to evaluate the distribution of MBs in the pontocerebellar region and to compare it with the distribution of ICHs reported in the literature. METHODS: We examined 164 consecutive hypertensive patients with ischemic infarction or spontaneous ICH over a 1-year period. Two experienced neuroradiologists assessed cerebral localization of MBs without prior knowledge of the clinical information and in consensus. After obtaining 16 standard axial brain images, we analyzed the anatomic locations and the vascular territories of the MBs in the pontocerebellar area. RESULTS: We detected 374 pontocerebellar MBs in 40 patients (8.1 +/- 12.7). Pontine MBs showed a significant predilection for the central portion (middle part along the axial plane, 3.4 +/- 4.9 [P < .01]; medial part along the coronal plane, 3.4 +/- 4.1 [P < .01]) and mostly belonged to the territory of the anteromedial group arising from the basilar artery. Cerebellar MBs had a frequent distribution around the dentate nucleus, occurring significantly more in the lower half, in the medial part (3.4 +/- 4.6; P < .01), and in the middle part along the axial plane (4.8 +/- 7.0; P < .01). CONCLUSION: These findings were similar to the topography of ICH described in the literature. Our results suggest that MBs may be a lesional marker for ICH.

Aged↗
PubMed2003

Hyperglycemia exacerbates brain edema and perihematomal cell death after intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Hyperglycemia has a deleterious effect on brain ischemia. However, the effect of hyperglycemia in intracerebral hemorrhage (ICH) is not well known. We investigated the effect of hyperglycemia on the development of brain edema and perihematomal cell death in ICH. METHODS: Hyperglycemia was induced by intraperitoneal injection of streptozotocin (60 mg/kg) in adult Sprague-Dawley male rats. ICH was induced by stereotaxic infusion of 0.23 U of collagenase into the left striatum. Seventy-two hours after ICH, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining was performed for perihematomal cell death. We also measured brain water content to evaluate edema formation. RESULTS: The serum glucose level of the hyperglycemic group was 394.0+/-180.3 mg/dL (n=31), and that of the normoglycemic group was 97.5+/-27.4 mg/dL (n=31). The size of hemorrhage was similar between groups, without any significant difference (n=8 in each group). The brain water content of hyperglycemic rats (n=17) increased in both lesioned (81.0+/-0.5%) and nonlesioned hemispheres (78.7+/-0.6%) compared with the normoglycemic group (n=17; lesioned: 78.9+/-0.8%; nonlesioned: 77.3+/-1.1%). In the hyperglycemic group, more TUNEL-positive cells were found in the perihematomal regions (n=6). CONCLUSIONS: Hyperglycemia caused more profound brain edema and perihematomal cell death in experimental ICH.

Animals↗