Publications by authors named "Jeeyoun Kim"

This study aimed to investigate the effect of a 12-week accelerated rehabilitation exercise program on isokinetic strength and dynamic balance ability of thighs in 20 adult men who underwent anterior cruciate ligament reconstruction (ACLR) or posterior cruciate ligament reconstruction (PCLR) and to analyze intergroup differences in recovery patterns. In this study, we examined 10 patients who underwent ACLR and 10 who underwent PCLR. These patients participated in an accelerated rehabilitation exercise program 5 times weekly for 12 weeks.

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Purpose: Exercise is known to reduce proinflammatory cytokines production and apoptosis. We investigated the effect of treadmill running on spatial learning memory in terms of activation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathway in Alzheimer disease (AD) rats. We also evaluated the effect of treadmill running on proinflammatory cytokine production and apoptosis.

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Radiation therapy is the mainstay in the treatment of lung cancer, and lung fibrosis is a radiotherapy-related major side effect that can seriously reduce patient's quality of life. Nevertheless, effective strategies for protecting against radiation therapy-induced fibrosis have not been developed. Hence, we investigated the radioprotective effects and the underlying mechanism of the standardized herbal extract PM014 on radiation-induced lung fibrosis.

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To analyze the effects of 10-week combined training (aerobic and resistance exercise) in three groups that were divided according to the total exercise dose per week and elucidate its effects on insulin and leptin (lipid metabolic regulatory hormones) and metabolic syndrome index. We included 24 obese male college students with body mass index ≥25 kg/m. Each 8 subjects were randomly assigned according to the total exercise dose per week into the 150-, 270-, and 450-min/wk exercise groups, which performed 50-, 90-, and 90-min exercise per day for 3, 3, and 5 times a week, respectively.

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Purpose: Lung fibrosis is a major side effect experienced by patients after lung cancer radiotherapy. However, effective protection strategies and underlying treatment targets remain unclear. In an effort to improve clinical outcomes, pharmacologic treatment of fibrosis is becoming increasingly popular; however, no ideal therapeutic strategy is yet available.

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It remains controversial whether targeting tumour vasculature can improve radiotherapeutic efficacy. We report that radiation-induced endothelial-to-mesenchymal transition (EndMT) leads to tumour vasculature with abnormal SMANG2 pericyte recruitment during tumour regrowth after radiotherapy. Trp53 (but not Tgfbr2) deletion in endothelial cells (ECs) inhibited radiation-induced EndMT, reducing tumour regrowth and metastases with a high CD44v6 cancer-stem-cell (CSC) content after radiotherapy.

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NOP53 ribosome biogenesis factor (NOP53) is a nucleolar protein involved in oncogenesis/tumor suppression, cell cycle regulation, and cell death. Here, we investigated the role of NOP53 in the maintenance of normal nuclear shape and chromosomal stability. Depletion of NOP53 by shRNA caused abnormal nuclear morphology, including large nucleus, irregular nucleus, and multinucleated cells, and chromosomal instability resulting in micronucleus or nuclear bud formation.

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Background/aims: Radiation-induced skin fibrosis is a common side effect of clinical radiotherapy. Our previous next-generation sequencing (NGS) study demonstrated the reduced expression of the regulatory α subunit of phosphatidylinositol 3-kinase (PIK3r1) in irradiated murine skin. Metformin has been reported to target the PIK3-FOXO3 pathway.

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[Purpose] The aim was to investigate the effects of university students' smoking and aerobic exercise on metabolic syndrome risk factors. [Subjects and Methods] Twenty-three male students were randomly assigned to the following groups: exercise smoker (n=6), non-exercise smoker (n=6), exercise non-smoker (n=6), and non-exercise non-smoker (n=5). A basketball exercise program was conducted three times per week (70 minutes per session) for 8 weeks with exercise intensity set at 50-80% of heart rate reserve.

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Radiation therapy has been used to treat over 70% of thoracic cancer; however, the method usually causes radiation pneumonitis. In the current study, we investigated the radioprotective effects of HSP27 inhibitor (J2) on radiation-induced lung inflammation in comparison to amifostine. In gross and histological findings, J2 treatment significantly inhibited immune cell infiltration in lung tissue, revealing anti-inflammatory potential of J2.

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Radiation therapy is widely used for thoracic cancers. However, it occasionally causes radiation-induced lung injuries, including pneumonitis and fibrosis. Chung-Sang-Bo-Ha-Tang (CSBHT) has been traditionally used to treat chronic pulmonary disease in Korea.

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Although lung injury including fibrosis is a well-documented side effect of lung irradiation, the mechanisms underlying its pathology are poorly understood. X-rays are known to cause apoptosis in the alveolar epithelial cells of irradiated lungs, which results in fibrosis due to the proliferation and differentiation of fibroblasts and the deposition of collagen. Apoptosis and BH3-only pro-apoptotic proteins have been implicated in the pathogenesis of pulmonary fibrosis.

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The aim of this study was to investigate the effects of an 8-week Pilates exercise program on menopausal symptoms and lumbar strength and flexibility in postmenopausal women. In total, 74 postmenopausal women were recruited and randomly allocated to a Pilates exercise group (n=45) and a control group (n=29). Menopausal symptoms were measured through a questionnaire, while lumbar strength was measured through a lumbar extension machine, and lumbar flexibility was measured through sit-and-reach and trunk lift tests performed before and after the Pilates exercise program, respectively.

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Telomerase is essential for regulating telomeres, and its activation is a critical step in cellular immortalization and tumorigenesis. The transcriptional activation of human telomerase reverse transcriptase (hTERT) is critical for telomerase expression. Although several transcriptional activators have been identified, factors responsible for enhancing the hTERT promoter remain to be fully elucidated.

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The green tea component (-)-epigallocatechin-3-gallate (EGCG) has been shown to sensitize many different types of cancer cells to anticancer drug-induced apoptosis, although it protects against non-cancerous primary cells against toxicity from certain conditions such as exposure to arsenic (As) or ultraviolet irradiation. Here, we found that EGCG promotes As-induced toxicity of primary-cultured bovine aortic endothelial cells (BAEC) at doses in which treatment with each chemical alone had no such effect. Increased cell toxicity was accompanied by an increased condensed chromatin pattern and fragmented nuclei, cleaved poly(ADP-ribose) polymerase (PARP), activity of the pro-apoptotic enzymes caspases 3, 8 and 9, and Bax translocation into mitochondria, suggesting the involvement of an apoptotic signaling pathway.

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The transcriptional factor MYC and the nucleophosphoprotein nucleophosmin (NPM) act in concert to regulate the proliferation of both normal and cancer cells. MYC directly interacts with NPM to form an NPM-MYC binary complex, which is recruited to the promoter of MYC target genes to induce the transcription of proteins required for transformation, thus forming an oncogenic NPM-MYC axis. However, the regulatory molecules and mechanisms that control the transcription of MYC target genes by NPM remain to be determined.

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Nucleophosmin (NPM)/B23, a multifunctional nucleolar phosphoprotein, plays an important role in ribosome biogenesis, cell cycle regulation, apoptosis and cancer pathogenesis. The role of NPM in cells is determined by several factors, including total expression level, oligomerization or phosphorylation status, and subcellular localization. In the nucleolus, NPM participates in rRNA maturation to enhance ribosomal biogenesis.

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Glioma tumor-suppressor candidate region gene2 (GLTSCR2) is a recently identified nucleolus-localized protein participating in the regulation of cell cycle progression and apoptosis. Down-regulation of GLTSCR2 in several types of cancers and increased transforming activity in GLTSCR2-downregulated cancer cells indicated its tumor suppressive potential. The aim of this study was to evaluate GLTSCR2 expression in breast cancer and to investigate the question of whether reduced expression of GLTSCR2 may have any pathological significance in breast cancer development or progression.

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The most important cause of cutaneous squamous cell carcinomas (SCC) is DNA damage induced by exposure to solar UV irradiation. DNA damage induced by UV irradiation is sensed by early DNA damage response (DDR) proteins. Recently, GLTSCR2 has been suggested to play a role in UV light-induced DDR.

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GLTSCR2 is a nuclear/nucleolar protein that translocates to the nucleoplasm, suppressed and mutated in human cancers. Our aim in this study was to investigate whether downregulation or cytoplasmic expression of GLTSCR2 has any pathological significance in prostatic cancer development or progression. In this study we show that GLTSCR2 is suppressed in prostatic cancers and its expression is significantly associated with Gleason's scores.

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Adrenomedullin (ADM), initially identified in human pheochromocytoma, participates in a wide range of physiological and pathological processes, including vasorelaxation, angiogenesis and apoptosis. Recent studies have reported that ADM protected tumor cells against apoptotic cell death via the upregulation of Bcl-2 or the activation of the phosphatidylinositol 3-kinase/Akt pathway. Several studies have also provided evidence that ADM is involved in tumor initiation and progression.

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The Bcl-2 family proteins plays a central role in apoptosis. The pro- or anti-apoptotic activities of Bcl-2 family are dependent on the Bcl-2 homology (BH) regions. Bcl-rambo, a new pro-apoptotic member, is unusual in that its pro-apoptotic activity is independent of its BH domains.

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Tumor hypoxia may be an indicator of poor survival in cancer patients. Thus, an understanding of the molecular mechanism responsible for hypoxic tumor selection is essential to gain further insight into tumor biology. Our aim in this study was to investigate whether hypoxia-responsive GLTSCR2 contributes to death resistance and increased invasiveness of hypoxia-selected glioblastoma cells.

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The cellular DNA damage response (DDR) ensures genomic stability and protects against genotoxic stresses. Conversely, defects in the DDR contribute to genome instability, with the resulting accumulated genetic changes capable of inducing neoplastic transformation. Thus, DDR is central to both the mechanism of oncogenesis and cancer therapy.

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Objective: Hypoxia signals the release of cytochrome c from mitochondria as well as sequential activation of caspase-9 and caspase-3 in the pathway to apoptosis. In this report, we describe novel mechanisms governing the nuclear translocation of cytochrome c during hypoxia-induced apoptosis in neuroepithelioma, SK-N-MC cells.

Methods: This work focuses on an investigation of the mechanism of cytochrome c translocation by means of immunocytochemistry, cell fractionation, Western blot and caspase assay.

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