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Moon-Ku Han

Publications and source records attributed to Moon-Ku Han.

4 recordsLinked to original sources

Fiber tracking by diffusion tensor imaging in corticospinal tract stroke: Topographical correlation with clinical symptoms.

Fiber tracking of the white matter using diffusion tensor imaging is a new imaging technique to visualize the integrity of the white matter. This study investigated the capability of this technique to localize the lacunar infarctions, particularly with respect to the body parts affected, by correlating the location of the lesion with the clinical symptoms topographically. Twenty-seven patients with capsular and pericapsular small acute infarctions underwent diffusion tensor imaging and subsequent fiber tracking of the corticospinal tract (CST). According to the lesion topography with regard to the CST, the infarctions were classified into four types: (1) the anterior type (n = 9) involving the anterior part of the CST, (2) the central type (n = 9) involving the middle or whole part of the CST, (3) the posterior type (n = 5) involving the posterior part of the CST and (4) the intact type (n = 4) not involving the CST. Motor weakness of the face, upper extremities and lower extremities was found at 100%, 67% and 44%, respectively in the anterior type, at 89%, 100% and 89%, respectively in the central type and at 20%, 80% and 100%, respectively in the posterior type. The intact type was not associated with motor weakness. In conclusion, the fiber tracking technique of the CST enables the specific localization of capsular and pericapsular infarctions with regard to the body parts affected. These results also confirm the topographical accuracy of the fiber tracking of the CST.

Aged↗

Ferrous and ferric iron accumulates in the brain of aged Long-Evans Cinnamon rats, an animal model of Wilson's disease.

The Long-Evans Cinnamon (LEC) rat, which accumulates excess copper (Cu) in its liver, is an animal model of Wilson's disease. We evaluated and compared the distributions of Cu, ferrous (Fe2+), and ferric (Fe3+) iron in four-brain regions, namely, in the cerebral cortex, cerebellum, substantia nigra (SN), and striatum of LEC and Long-Evans Agouti rats at 30 and 55 weeks. Cu levels were elevated in the striatum of LEC rats, and Fe2+ and Fe3+ were higher in the striatum and SN of LEC rats. Ratios of Fe2+ to Fe3+ were > 1 in four regions, and were highest in the striatum and SN of LEC rats. Cu and iron levels were found to be augmented during aging, and we suggest that these accumulations may exert deleterious effects in aged LEC rats. This study is the first report that demonstrates regional differences of Fe2+ and Fe3+ accumulation in the brain of aged LEC rats. Further studies are required to elucidate the mechanisms of Cu and iron accumulations and of their effects.

Aging↗

Aphasia following striatocapsular infarction may be explained by concomitant small cortical infarct on diffusion-weighted imaging.

BACKGROUND: The underlying mechanism of aphasia following striatocapsular infarction (SCI) remains controversial. We hypothesized that aphasia resulting from SCI might be associated with concomitant cortical lesions, which can be demonstrated by diffusion-weighted imaging (DWI). METHODS: We analyzed 24 patients with left SCI who underwent DWI and MR angiography within 2 days after the onset. Aphasia was assessed by the modified Korean version of the Boston Diagnostic Aphasia Examination test. RESULTS: DWI showed the presence of additional ischemic lesions involving the cortical areas in 13 of 24 SCI patients (54%). Ten patients (42%) showed aphasia. All 10 patients with aphasia had cortical lesions in addition to SCI (p = 0.0002), whereas 21% (3/14) of the nonaphasic patients had additional cortical lesions. Conventional MRI did not reveal the presence of corresponding acute cortical lesions in any of the aphasic patients. There was no difference between the patients with and without aphasia in terms of their stroke etiology. CONCLUSIONS: Our data suggest that aphasia due to SCI in the acute stage may be attributed to direct cortical injury, whose presence can be demonstrated by DWI, even though it might be invisible on conventional imaging.

Aged↗

VEGF protects human cerebral hybrid neurons from in vitro ischemia.

Vascular endothelial growth factor (VEGF), the most potent angiogenic peptide, protects the neurons against experimental ischemia. However, its neuroprotective effect on human brain is unknown. The present study attempted to determine whether VEGF can protect human cerebral neurons in vitro. A1 human hybrid clonal neurons (human cerebral neuron + neuroblastoma cell) were exposed to hypoxia with glucose deprivation. Pretreatment with VEGF reduced the A1 cell death, and VEGFR-2/Flk-1 and VEGF increased with a neuroprotective effect. However, the human neuroblastoma or neuroglioma cells failed to show these findings. Our results suggest that VEGF can protect human cerebral neurons from cell death after an ischemic insult in vitro, which is correlated to both increased expression of VEGFR-2/Flk-1 and VEGF within the cells.

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