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Goyang, South Korea

Choi Y.J.,Yonsei University | Lim H.,Clinical Research Management Team | Chung C.J.,Yonsei University | Park K.H.,Yonsei University | Kim K.-H.,Yonsei University
International Journal of Oral and Maxillofacial Surgery | Year: 2014

This study was performed to examine the longitudinal changes in bite force and occlusal contact area after mandibular setback surgery via intraoral vertical ramus osteotomy (IVRO). Patients with mandibular prognathism who underwent IVRO (surgical group: 39 men and 39 women) were compared with subjects with class I skeletal and dental relationships (control group; 32 men and 35 women). The surgical group was divided into two subgroups: 1-jaw surgery (n = 30) and 2-jaw surgery (n = 48). Bite force and contact area were measured in maximum intercuspation with the Dental Prescale System before treatment, within 1 month before surgery, and at 1, 3, 6, 9, 12, and 24 months postsurgery. A linear mixed model was used to investigate the time-dependent changes and associated factors. Bite force and contact area decreased during presurgical orthodontic treatment, were minimal at 1 month postsurgery, and increased gradually thereafter. The 1-jaw and 2-jaw subgroups showed no significant differences in bite force. The time-dependent changes in bite force were significantly different according to the contact area (P < 0.05). The results of this study suggest that bite force and occlusal contact area gradually increase throughout the postsurgical evaluation period. Increasing the occlusal contact area may be essential for improving bite force after surgery. © 2014 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Kim J.H.,Dementia Center | Song P.,Inje University | Lim H.,Clinical Research Management Team | Lee J.-H.,Kyung Hee University | And 2 more authors.
PLoS ONE | Year: 2014

Alzheimer's disease (AD) has a strong propensity to run in families. However, the known risk genes excluding APOE are not clinically useful. In various complex diseases, gene studies have targeted rare alleles for unsolved heritability. Our study aims to elucidate previously unknown risk genes for AD by targeting rare alleles. We used data from five publicly available genetic studies from the Alzheimer's Disease Neuroimaging Initiative (ADNI) and the database of Genotypes and Phenotypes (dbGaP). A total of 4,171 cases and 9,358 controls were included. The genotype information of rare alleles was imputed using 1,000 genomes. We performed gene-based analysis of rare alleles (minor allele frequency≤3%). The genome-wide significance level was defined as meta P<1.8×10-6 (0.05/number of genes in human genome = 0.05/28,517). ZNF628, which is located at chromosome 19q13.42, showed a genome-wide significant association with AD. The association of ZNF628 with AD was not dependent on APOE ε4. APOE and TREM2 were also significantly associated with AD, although not at genome-wide significance levels. Other genes identified by targeting common alleles could not be replicated in our gene-based rare allele analysis. We identified that rare variants in ZNF628 are associated with AD. The protein encoded by ZNF628 is known as a transcription factor. Furthermore, the associations of APOE and TREM2 with AD were highly significant, even in gene-based rare allele analysis, which implies that further deep sequencing of these genes is required in AD heritability studies. Copyright: © 2014 Kim et al.

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