• Journal of Korean Society of Transportation
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• v.20 no.6
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• pp.31-43
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• 2002

Traffic signal control methods are suggested to improve the operational effectiveness of COSMOS system in Seoul. First. a method that improves progression of the corridor traffic flow within a common sub-area was explored. Applying this method, both frequency and magnitude of offset transition were reduced as compared to the existing method. In addition, the level of connection among neighboring corridors increased by applying the method, thus the qualify of progression was also improved. Second, a practical guideline on signal phase design was proposed to improve the efficiency of actuated operations for the left-turn movement. Last, a method for estimating optimal queue length parameters was surveyed and evaluated. An evaluation study was performed for the suggested methods through both field and simulation studies. Results showed that the proposed methods gave better performance than the existing methods. It is expected that the use of proposed methods can improve operational performance of COSMOS.

• The Korea Journal of Herbology
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• v.25 no.1
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• pp.55-63
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• 2010

Objectives : The object of this study was to verify the inhibitory effect of a decoction of Eucommiae ulmides OLIVER (EU) and Dipsacus asperoides C. Y. Cheng et T.M.Ai (DA) on Collagen II-induced Arthritis Mice (CIA mice). Methods : DBA/1OlaHsd mice were immunized with bovine type II collagen. Boostnig same collagen 21 days later, arthritis was induced and then administrated orally the extract of EU+DA (200 or 50 mg/kg) once a day for 4 weeks and compared with that of methotrexate (MTX, 0.3 mg/kg) as a positive control. Results : Administration of EU+DA suppressed the inflammatory progression of CIA mice and the results were 1. Arthritis index of CIA mice was decreased. 2. EU+DA decreased the production of TNF-$\alpha$, IL-6, IL-$1{\beta}$ in the serum of CIA mice. 3. EU+DA decreased the level of IgM. 4. EU+DAincreasaed $CD3^+$, $CD4^+$, $CD4^+$/CD25 but decreased $CD19^+$, $CD3^+/CD49b^+$(NKT), $CD3^-/CD49b^+$(NK), $B220^+/CD23^+$ in PBMC of CIA mice. 5. EU+DA decreased $CD3^+$, $CD4^+$, $CD3^+/CD69^+$ of paw joint in CIA mice. 6. EU+DA decreased subsynovial inflammation. Conclusions : This results demonstrated that extract of EU+DA suppressed the inflammatory progression of CIA mice and supported further studies are required to clarify a mechanism of therapeutic role.

• Journal of Microbiology and Biotechnology
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• v.31 no.10
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• pp.1358-1365
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• 2021

To clarify the role of long intergenic nonprotein-coding RNA 1232 (LINC01232) in the progression of gastric cancer and the potential mechanism, we analyzed the expression of LINC01232 in TCGA database using the GEPIA online tool, and the LINC01232 level in gastric cancer cell lines was detected by quantitative real time-polymerase chain reaction (qRT-PCR) as well. Cell proliferation assay, colony formation assay, transwell assay and tumor formation experiment in nude mice were conducted to observe the biological behavior changes of gastric cancer cells through the influence of LINC01232 knockdown. LncATLAS database and subcellular isolation assay were used for subcellular distribution of LINC01232 in gastric cancer cells. The interaction among LINC01232, zeste homolog 2 (EZH2) and kruppel-like factor 2 (KLF2) was clarified by RNA-protein interaction prediction (RPISeq), RNA immunoprecipitation (RIP), qRT-PCR and chromatin immunoprecipitation (ChIP) assay. Rescue experiments were further conducted to elucidate the biological function of LINC01232/KLF2 axis in the progression of gastric cancer. LINC01232 was upregulated in stomach adenocarcinoma (STAD) tissues and gastric cancer lines. LINC01232 knockdown inhibited the proliferative capacities of gastric cancer cells in vitro, and impaired in vivo tumorigenicity. LINC01232 was mainly distributed in the cell nucleus where it epigenetically repressed KLF2 expression via binding to the enhancer of EZH2, which was capable of binding to promoter regions of KLF2 to induce histone H3 lysine 27 trimethylation (H3K27me3). LINC01232 exerts oncogenic activities in gastric cancer via inhibition of KLF2, and therefore, the knockdown of KLF2 could reverse the regulatory effect of LINC01232 in the proliferative ability of gastric cancer cells.

• Molecules and Cells
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• v.44 no.2
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• pp.101-115
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• 2021

The INO80 chromatin remodeling complex has roles in many essential cellular processes, including DNA replication. However, the mechanisms that regulate INO80 in these processes remain largely unknown. We previously reported that the stability of Ino80, the catalytic ATPase subunit of INO80, is regulated by the ubiquitin proteasome system and that BRCA1-associated protein-1 (BAP1), a nuclear deubiquitinase with tumor suppressor activity, stabilizes Ino80 via deubiquitination and promotes replication fork progression. However, the E3 ubiquitin ligase that targets Ino80 for proteasomal degradation was unknown. Here, we identified the C-terminus of Hsp70-interacting protein (CHIP), the E3 ubiquitin ligase that functions in cooperation with Hsp70, as an Ino80-interacting protein. CHIP polyubiquitinates Ino80 in a manner dependent on Hsp70. Contrary to our expectation that CHIP degrades Ino80, CHIP instead stabilizes Ino80 by extending its half-life. The data suggest that CHIP stabilizes Ino80 by inhibiting degradative ubiquitination. We also show that CHIP works together with BAP1 to enhance the stabilization of Ino80, leading to its chromatin binding. Interestingly, both depletion and overexpression of CHIP compromise replication fork progression with little effect on fork stalling, as similarly observed for BAP1 and Ino80, indicating that an optimal cellular level of Ino80 is important for replication fork speed but not for replication stress suppression. This work therefore idenitifes CHIP as an E3 ubiquitin ligase that stabilizes Ino80 via nondegradative ubiquitination and suggests that CHIP and BAP1 act in concert to regulate Ino80 ubiquitination to fine-tune its stability for efficient DNA replication.

• Journal of Genetic Medicine
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• v.19 no.1
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• pp.22-26
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• 2022

Cerebrotendinous xanthomatosis (CTX) is a rare genetic disease caused by a deficiency of enzymes for the synthesis of bile acid, resulting in the accumulation of cholestanol with reduced chenodeoxycholic acid (CDCA) production and causing various symptoms such as chronic diarrhea in infancy, juvenile cataracts in childhood, tendon xanthomas in adolescence and young adulthood, and progressive neurologic dysfunction in adulthood. Because oral CDCA replacement therapy can effectively prevent disease progression, early diagnosis and treatment are critical in CTX. This study reports the case of CTX in a 10-year-old male who presented with Achilles tendon xanthoma and mild intellectual disability. Biochemical testing showed normal cholesterol and sitosterol levels but elevated cholestanol levels. Genetic testing showed compound heterozygous variants of CYP27A1, c.379C>T (p.Arg127Trp), and c.1214G>A (p.Arg405Gln), which confirmed the diagnosis of CTX. The patient had neither cataracts nor other focal neurologic deficits and showed no abnormalities on brain imaging. The patient received oral CDCA replacement therapy without any adverse effects; thereafter, the cholestanol level decreased and no disease progression was noted. The diagnostic possibility of CTX should be considered in patients with tendon xanthoma and normolipidemic conditions to prevent neurological deterioration.

• Journal of Conservation Science
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• v.38 no.4
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• pp.265-276
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• 2022

A long-term monitoring investigation at Sarushima Battery (Kanagawa, Japan), which is one of the modernization heritages was conducted from 2017.06 to 2020.12. The investigation of the temperature and relative humidity (RH), measurement of the amount of brick decay, and X-ray diffraction analysis of the brick decay was conducted to understand in detail the environment in which the historical brick structure, the state of deterioration, identify the factors of deterioration. Furthermore, it was discussed whether the suitability of these investigation methods for assessing the status, identifying the level of deterioration and the factors that led to deterioration at the historical brick heritages. It was found that the brick deterioration at the site progressed especially in two periods: in April, and from June to August. These periods coincided with the period when the RH inside the structure decreased, and the Toyo-gumi bricks were in the process of absorbing moisture. Several different types of salts were detected in brick decay, especially thenardite, which is considered highly hazardous and destructive during periods when the amount of brick decay increased. Therefore, the RH in the structure and the salts present in the bricks were identified as one of the factors in the deterioration of the bricks at the site. The methods used in this study are appropriate as the initial survey methods for investigating the current conditions and identifying the causes of deterioration because it is possible to understand the environment within the modernization heritages, grasp the details of deterioration progression, and identify the characteristics of deterioration progression and its factors through long-term investigation using the simple methods.

• Journal of Gastric Cancer
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• v.22 no.4
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• pp.319-338
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• 2022

Purpose: Gastric cancer (GC) has high morbidity and mortality, the cure rate of surgical treatment and drug chemotherapy is not ideal. Therefore, development of new treatment strategies is necessary. We aimed to identify the mechanism underlying Sp1 regulation of GC progression. Methods and Methods: The levels of Sp1, β-catenin, SET domain bifurcated 1 (SETDB1), and 15-hydroxyprostaglandin dehydrogenase (HPGD) were detected by quantitative reverse transcription polymerase chain reaction and western blot analysis. The targets of SETDB1 were predicted by AnimalTFDB, and dual-luciferase reporter assay was used for confirming the combination of Sp1, β-catenin, and SETDB1. HGC27 or AGS cells (1×10⁶ cells/mouse) were injected into mice via the caudal vein for GC model establishment. The level of Ki67 was detected using immunohistochemistry, and hematoxylin and eosin staining was performed for evaluating tumor metastasis in mice with GC. Results: HPGD was inhibited, while the protein levels of Sp1, β-catenin, and SETDB1 were up-regulated in GC tissues and cell lines. HPGD overexpression or SETDB1 silencing inhibited the proliferation, invasion, and migration of GC cells, and Sp1 regulated the proliferation, invasion, and migration of GC cells in a β-catenin-dependent manner. Furthermore, HPGD served as a target of SETDB1, and it was negatively regulated by SETDB1; additionally, Sp1 and β-catenin bound to the SETDB1 promoter and negatively regulated HPGD expression. We proved that Sp1 regulated GC progression via the SETDB1/HPGD axis. Conclusions: Our findings revealed that Sp1 transcriptionally inhibited HPGD via SETDB1 in a β-catenin-dependent manner and promoted the proliferation and metastasis of GC cells.

• Journal of Microbiology and Biotechnology
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• v.34 no.2
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• pp.249-261
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• 2024

New anti-lung cancer therapies are urgently required to improve clinical outcomes. Since ganodermanontriol (GDNT) has been identified as a potential antineoplastic agent, its role in lung adenocarcinoma (LUAD) is investigated in this study. Concretely, lung cancer cells were treated with GDNT and/or mycophenolate mofetil (MMF), after which MTT assay, flow cytometry and Western blot were conducted. Following bioinformatics analysis, carboxylesterase 2 (CES2) was knocked down and rescue assays were carried out in vitro. Xenograft experiment was performed on mice, followed by drug administration, measurement of tumor growth and determination of CES2, IMPDH1 and IMPDH2 expressions. As a result, the viability of lung cancer cells was reduced by GDNT or MMF. GDNT enhanced the effects of MMF on suppressing viability, promoting apoptosis and inducing cell cycle arrest in lung cancer cells. GDNT up-regulated CES2 level, and strengthened the effects of MMF on down-regulating IMPDH1 and IMPDH2 levels in the cells. IMPDH1 and IMPDH2 were highly expressed in LUAD samples. CES2 was a potential target for GDNT. CES2 knockdown reversed the synergistic effect of GDNT and MMF against lung cancer in vitro. GDNT potentiated the role of MMF in inhibiting tumor growth and expressions of CES2 and IMPDH1/2 in lung cancer in vivo. Collectively, GDNT suppresses the progression of LUAD by activating CES2 to enhance the metabolism of MMF.

• BMB Reports
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• v.57 no.7
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• pp.336-341
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• 2024

Lung cancer is one of the most significant malignancies, with both high morbidity and mortality. CDK10 is closely related to cancer progression and metastasis. However, its role in lung cancer radioresistance demands further clarification. In this study, we demonstrated that CDK10 was downregulated in lung cancer tissues, and CDK10 expression level was associated with the clinical prognosis in lung cancer patients. We also found that silencing CDK10 promoted lung cancer cell proliferation, migration, and radioresistance. We further verified that silencing CDK10 facilitated the activation of JNK/c-Jun signaling, and c-Jun depletion could reverse the effects of CDK10 knockdown in lung cancer cells. Our findings revealed that CDK10 plays an important role in cell growth and radioresistance by inhibiting JNK/c-Jun signaling pathway in lung cancer. Therefore, CDK10 might be a promising therapeutic target in lung cancer.

• Steel and Composite Structures
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• v.16 no.2
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• pp.135-156
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• 2014

In this research the effect of seismic design level as a practical approach for progressive collapse mitigation and reaching desired structural safety against it in seismically designed concentric braced frame buildings was investigated. It was achieved by performing preliminary and advanced progressive collapse analysis of several split-X braced frame buildings, designed for each seismic zone according to UBC 97 and by applying various Seismic Load Factors (SLFs). The outer frames of such structures were studied for collapse progression while losing one column and connected brace in the first story. Preliminary analysis results showed the necessity of performing advanced element loss analysis, consisting of Vertical Incremental Dynamic Analysis (VIDA) and Performance-Based Analysis (PBA), in order to compute the progressive collapse safety of the structures while increasing SLF for each seismic zone. In addition, by sensitivity analysis it became possible to introduce the equation of structural safety against progressive collapse for concentrically braced frames as a function of SLF for each seismic zone. Finally, the equation of progressive collapse safety as a function of bracing member capacity was presented.