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Jong-Hoon Kim, Young-Jin Jung, and Chul-Hoon Chang


The optimal treatment for underlying intracranial atherosclerosis (ICAS) in patients with emergent large-vessel occlusion (ELVO) remains unclear. Reocclusion during endovascular treatment (EVT) occurs frequently (57.1%–77.3%) after initial recanalization with stent retriever (SR) thrombectomy in ICAS-related ELVO. This study aimed to compare treatment outcomes of the strategy of first stenting without retrieval (FRESH) using the Solitaire FR versus SR thrombectomy in patients with ICAS-related ELVO.


The authors retrospectively reviewed consecutive patients with acute ischemic stroke and intracranial ELVO of the anterior circulation who underwent EVT between January 2017 and December 2019 at Yeungnam University Medical Center. Large-vessel occlusion (LVO) of the anterior circulation was classified by etiology as follows: 1) no significant stenosis after recanalization (embolic group) and 2) remnant stenosis > 70% or lesser degree of stenosis with a tendency toward reocclusion and/or flow impairment during EVT (ICAS group). The ICAS group was divided into the SR thrombectomy group (SR thrombectomy) and the FRESH group.


A total of 105 patients (62 men and 43 women; median age 71 years, IQR 62.5–79 years) were included. The embolic, SR thrombectomy, and FRESH groups comprised 66 (62.9%), 26 (24.7%), and 13 (12.4%) patients, respectively. There were no significant differences between the SR thrombectomy and FRESH groups in symptom onset–to-door time, but puncture-to-recanalization time was significantly shorter in the latter group (39 vs 54 minutes, p = 0.032). There were fewer stent retrieval passes but more first-pass recanalizations in the FRESH group (p < 0.001). Favorable functional outcomes were significantly more frequent in the FRESH group (84.6% vs 42.3%, p = 0.017).


This study’s findings suggest that FRESH, rather than rescue stenting, could be a treatment option for ICAS-related ELVO.

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Myung-Jin Park, In-Chul Park, Jin-Heang Hur, Mi-Suk Kim, Hyung-Chan Lee, Sang-Hyeok Woo, Kyung-Hee Lee, Chang-Hun Rhee, Seok-Il Hong, and Seung-Hoon Lee

Object. Expression of matrix metalloproteinases (MMPs) has been postulated to play a central role in brain tumor invasion; however, its underlying mechanism is not yet fully understood. In the present study, by assessing the effect of a specific p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, on the secretion of MMPs and in vitro invasion of various glioma cells, the authors attempt to define the role of the p38 MAPK pathway in the regulation of MMPs and tissue inhibitors of metalloproteinases (TIMPs) activated by phorbol ester (phorbol-12-myristate-13-acetate [PMA]) in the D54 human glioblastoma cell line.

Methods. The activation of MAPKs was determined using Western blot analysis after addition of phospho-specific antibodies against these kinases, the status of MMPs and TIMPs was analyzed using gelatin zymography and Western blot analysis, and the invasion rate of D54 cells and other glioma cells was analyzed using a modified Boyden chamber assay. Treatment of D54 cells with PMA activated two distinct MAPKs, extracellular signal-regulated kinase (ERK) 1/2 and p38 MAPK, but not c-Jun N-terminal kinase/stress-activated protein kinase. Induction of MMP-9 production and MMP-2 activation by PMA were blocked by SB203580, a specific inhibitor of p38 MAPK, but not by PD98059, a specific inhibitor of ERK 1/2. In addition, PMA-induced downregulation of TIMP-1 and TIMP-2 secretion and upregulation of the membrane type 1 MMP, a major activator of MMP-2 on the cell surface, were reversed by SB203580 in these cells; the PMA-induced increase of invasion in vitro decreased when SB203580 was added to the top compartment of a modified Boyden chamber; and the inhibitor also reduced the MMP secretion and PMA-induced in vitro invasion in various glioma cell lines.

Conclusions. These results indicate that activation of p38 MAPK by PMA plays a central role in the regulation of MMPs and TIMPs in D54 cells, which has a major influence in tumor invasion and metastasis. Furthermore, inhibition of p38 MAPK by SB203580 blocked the secretion of MMPs and in vitro invasion of various glioma cells, underscoring a possible role of p38 MAPK inhibitors as antiinvasive and/or antimetastatic agents of malignant gliomas.

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Ji Hoon Phi, Seung-Ki Kim, Joongyub Lee, Chul-Kee Park, Il Han Kim, Hyo Seop Ahn, Hee Young Shin, In-One Kim, Hee-Won Jung, Dong Gyu Kim, Sun Ha Paek, and Kyu-Chang Wang


Intracranial germ cell tumors (GCTs) frequently present with bifocal lesions in both the suprasellar and pineal areas. The pathogenesis of these bifocal GCTs has been the subject of controversy. Bifocal GCTs may be caused by synchronous tumors or by metastatic spread of tumor cells from one site to the other. The prognosis associated with bifocal GCTs has also been a cause of concern.


The authors constructed a single-institution patient cohort comprising 181 patients with intracranial GCTs. The clinical characteristics of bifocal GCTs were compared with those of suprasellar and pineal GCTs.


Bifocal GCTs were observed in 23 patients (12.8%). Eighteen patients presented with bifocal GCTs that were diagnosed as germinomas, but 5 patients exhibited mixed GCTs. Analyses of age distributions and comparisons of tumor sizes were compatible with a model of a metastatic origin of bifocal GCTs. Eleven patients (47.8%) presenting with bifocal GCTs exhibited tumor seeding at presentation. Tumor seeding was significantly associated with bifocal lesions (p < 0.001). Patients with bifocal germinomas showed significantly shorter event-free survival and overall survival than did those presenting with germinomas from a single site of origin.


Bifocal GCTs are not restricted to germinomas, as had been previously reported, but do include mixed GCTs. The authors hypothesize that bifocal GCTs may result from the metastatic spread of suprasellar or pineal GCTs. The bifocal presentation of germinomas may be a poor prognostic sign and should alert clinicians to the possibility of a disseminated disease.