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Articles by D. H Kim
Total Records ( 6 ) for D. H Kim
  J Groenendyk , P. K Sreenivasaiah , D. H Kim , L. B Agellon and M. Michalak

The endoplasmic reticulum (ER) is a multifunctional intracellular organelle supporting many processes required by virtually every mammalian cell, including cardiomyocytes. It performs diverse functions, including protein synthesis, translocation across the membrane, integration into the membrane, folding, posttranslational modification including N-linked glycosylation, and synthesis of phospholipids and steroids on the cytoplasmic side of the ER membrane, and regulation of Ca2+ homeostasis. Perturbation of ER-associated functions results in ER stress via the activation of complex cytoplasmic and nuclear signaling pathways, collectively termed the unfolded protein response (UPR) (also known as misfolded protein response), leading to upregulation of expression of ER resident chaperones, inhibition of protein synthesis and activation of protein degradation. The UPR has been associated with numerous human pathologies, and it may play an important role in the pathophysiology of the heart. ER stress responses, ER Ca2+ buffering, and protein and lipid turnover impact many cardiac functions, including energy metabolism, cardiogenesis, ischemic/reperfusion, cardiomyopathies, and heart failure. ER proteins and ER stress-associated pathways may play a role in the development of novel UPR-targeted therapies for cardiovascular diseases.

  D. H Kim and H. J. Lee

This paper proposes a new register allocation technique in which register allocation is performed at every reference of a variable. For each reference, the costs of various possible register allocations are estimated by tracing a possible instruction sequence. A cost model is formulated to reduce the scope of tracing. With an extension of the cost model to the estimation of instruction execution time, a new technique for the integration of instruction scheduling and register allocation is also proposed. Experiments show that the proposed register allocation and the integration techniques achieve significant improvements when compared with widely used existing techniques.

  J. A Lee , M. S Kim , J. S Koh , D. H Kim , J. S Lim , C. B Kong , W. S Song , W. H Cho , S. Y Lee and D. G. Jeon

We aimed to understand the biology of osteosarcoma of the flat bone, which is a rare tumor entity.


Cases with osteosarcoma of the flat bone were compared with those of the extremity in order to evaluate their clinicopathologic characteristics. And the influences of heterogeneous treatment modalities on outcome were analyzed.


Tumors of the flat bone comprised 91 (11.3%) of 806 osteosarcoma cases. Eight cases were secondary osteosarcoma associated with previous radiotherapy. Patients with a flat bone tumor were significantly older and more likely to present with metastases at diagnosis than extremity tumor. The proportions of female sex and chondroblastic subtype were higher among flat bone tumors than among extremity tumors. The 5-year overall survival and event-free survival rates were 35.2 ± 5.4% and 24.7 ± 5.5%, respectively. Although age and histologic response to pre-operative chemotherapy were not related to outcome of flat bone tumors, treatment modality influenced the survival. Patients treated surgically had better outcomes than those treated by another means. Radiation therapy did not appear to be an effective local control measure as surgery.


Treatment outcome of the tumor of the flat bone was worse than extremity tumors. Further studies are needed to identify effective local control measures that can substitute for surgery and to determine the biologic characteristics of osteosarcoma of the flat bone.

  J. A Lee , D. H Kim , J. S Lim , J. S Koh , M. S Kim , C. B Kong , W. S Song , W. H Cho , S. Y Lee and D. G. Jeon

Due to the low incidence, treatments for Korean soft tissue Ewing sarcoma patients have been heterogeneous, and reported data are limited. In this study, we retrospectively analyzed soft tissue Ewing cases treated at our institution.


We analyzed the clinicopathologic characteristics and treatment outcome of soft tissue Ewing sarcoma patients and compared with those of skeletal cases.


Twenty-seven soft tissue Ewing sarcoma cases were evaluated. Patients with soft tissue Ewing sarcoma were older than patients with skeletal tumors (P = 0.03), and tended to have metastasis at diagnosis (P = 0.12). However, sex ratios, pathologies, tumor volumes, and histologic response to preoperative chemotherapy were not different in the two groups. The 5-year overall survival (49.0%) and event-free survival (45.6%) of soft tissue Ewing sarcoma patients were similar to those of skeletal tumor patients (51.8% and 46.0%, respectively). Presence of metastasis at diagnosis and poor histologic response to preoperative chemotherapy were associated with an adverse outcome for both groups. Similar to skeletal tumors, central tumor location, pathology and tumor volume tended to be related to the survival of soft tissue Ewing sarcoma. However, age and the use of a modality other than surgery to achieve local control did not influence the survival of soft tissue Ewing sarcoma patients.


Our data could provide a basis to design a collaborative or multinational study targeting Ewing sarcoma family tumors.

  S. J Peterson , D. H Kim , M Li , V Positano , L Vanella , L. F Rodella , F Piccolomini , N Puri , A Gastaldelli , C Kusmic , A L'Abbate and N. G. Abraham

We examined mechanisms by which L-4F reduces obesity and diabetes in obese (ob) diabetic mice. We hypothesized that L-4F reduces adiposity via increased pAMPK, pAKT, HO-1, and increased insulin receptor phosphorylation in ob mice. Obese and lean mice were divided into five groups: lean, lean-L-4F-treated, ob, ob-L-4F-treated, and ob-L-4F-LY294002. Food intake, insulin, glucose adipocyte stem cells, pAMPK, pAKT, CB1, and insulin receptor phosphorylation were determined. Subcutaneous (SAT) and visceral adipose tissue (VAT) were determined by MRI and hepatic lipid content by magnetic resonance spectroscopy. SAT and VAT volumes decreased in ob-L-4F-treated animals compared with control. L-4F treatment decreased hepatic lipid content and increased the numbers of small adipocytes (P < 0.05) and phosphorylation of insulin receptors. L-4F decreased CB1 in SAT and VAT and increased pAKT and pAMPK in endothelium. L-4F-mediated improvement in endothelium was prevented by LY294002. Inhibition of pAKT and pAMPK by LY294002 was associated with an increase in glucose levels. Upregulation of HO-1 by L-4F produced adipose remodeling and increased the number of small differentiated adipocytes. The anti-obesity effects of L-4F are manifested by a decrease in visceral fat content with reciprocal increases in adiponectin, pAMPK, pAKT, and phosphorylation of insulin receptors with improved insulin sensitivity.

  D. H Kim , J Lee , B Lee and J. W. Lee

Activating signal cointegrator-2 (ASC-2), a coactivator of multiple nuclear receptors and transcription factors, belongs to a steady-state complex named ASCOM (for ASC-2 complex), which contains histone H3 lysine 4 (H3K4) methyltransferase MLL3 or its paralog MLL4. ASC-2 binds to many nuclear receptors in a ligand-dependent manner through its two LxxLL motifs. Here we show that the first LxxLL motif of ASC-2 shows relatively weak but specific interaction with the nuclear receptor farnesoid X receptor (FXR) and that ASCOM plays crucial roles in FXR transactivation. Our results reveal that ASC-2, MLL3, and MLL4 are recruited to FXR target genes in a ligand-dependent manner. We further show that the recruitment of MLL3 requires ASC-2 and that FXR ligand induces not only expression of FXR-target genes but also their H3K4 trimethylation in a manner dependent on the presence of ASC-2, MLL3, and MLL4. In addition, MLL3 and MLL4 function redundantly with FXR transactivation. Correspondingly, expression of FXR target genes is partially impaired in mice expressing an enzymatically inactivated mutant form of MLL3, and these mice show disrupted bile acid homeostasis. Overall, these results suggest that ASCOM-MLL3 and ASCOM-MLL4 play redundant but essential roles in FXR transactivation via their H3K4 trimethylation activity.

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