Yong Jik Lee

Ulsan University Hospital, Urusan, Ulsan, South Korea

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Publications (16)26.25 Total impact

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    ABSTRACT: A 37-year-old woman was referred to our institution for further management of a mass lesion located in the thoracic cavity. The mass had grown by more than 10 cm over the course of a year and was initially considered to be a scar from previous pulmonary tuberculosis at another hospital. The patient had complained of left-sided flank pain for a year and experienced dyspnea for one month. Chest radiography and chest computed tomography revealed an irregular-shaped mass in the left mid to lower pleural cavity. The mass was widely excised through left thoracotomy. Pathologic examination of the biopsy specimen revealed a malignant spindle cell tumor, which consisted of components of osteosarcoma, pleomorphic sarcoma, and leiomyosarcoma. The patient underwent adjuvant chemotherapy and has been doing well without any evidence of recurrence for 14 months.
    06/2014; 47(3):320-4. DOI:10.5090/kjtcs.2014.47.3.320
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    ABSTRACT: The standard regimen in elderly patients with non-small-cell lung cancer (NSCLC) is still uncertain. Gemcitabine is one of the most widely used drugs for the treatment of NSCLC, and several phase II trials specifically designed for elderly patients with advanced NSCLC have confirmed the role of gemcitabine in this setting. In addition, oral uracil-tegafur (UFT) was associated with a survival advantage in the adjuvant setting. Therefore, we performed a phase II study using the combination of gemcitabine and UFT as first-line therapy in elderly patients with advanced NSCLC.
    Lung cancer (Amsterdam, Netherlands) 12/2011; 76(3):368-72. DOI:10.1016/j.lungcan.2011.11.021 · 3.74 Impact Factor
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    ABSTRACT: Type 2 diabetes mellitus is thought to be partially associated with endoplasmic reticulum (ER) stress toxicity on pancreatic beta cells and the result of decreased insulin synthesis and secretion. In this study, we showed that a well-known insulin sensitizer, metformin, directly protects against dysfunction and death of ER stress-induced NIT-1 cells (a mouse pancreatic beta cell line) via AMP-activated protein kinase (AMPK) and phosphatidylinositol-3 (PI3) kinase activation. We also showed that exposure of NIT-1 cells to metformin (5mM) increases cellular resistance against ER stress-induced NIT-1 cell dysfunction and death. AMPK and PI3 kinase inhibitors abolished the effect of metformin on cell function and death. Metformin-mediated protective effects on ER stress-induced apoptosis were not a result of an unfolded protein response or the induced inhibitors of apoptotic proteins. In addition, we showed that exposure of ER stressed-induced NIT-1 cells to metformin decreases the phosphorylation of c-Jun NH(2) terminal kinase (JNK). These data suggest that metformin is an important determinant of ER stress-induced apoptosis in NIT-1 cells and may have implications for ER stress-mediated pancreatic beta cell destruction via regulation of the AMPK-PI3 kinase-JNK pathway.
    Biochemical and Biophysical Research Communications 11/2011; 417(1):147-52. DOI:10.1016/j.bbrc.2011.11.073 · 2.28 Impact Factor
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    ABSTRACT: Hemangiomas that arise in cervical esophagus are extremely rare, representing 3.3% of all benign esophageal tumors. Although endoscopic mucosal resection (EMR) and potassium titanyl phosphate/yttrium aluminum garnet (KTP/YAG) laser therapy have been used with success for small tumors, the safety and efficacy in the case of large tumors remains uncertain. We report the successful resection of cervical esophageal hemangioma through a cervical esophagotomy in a patient with thyroid cancer who needed a cervical collar incision.
    08/2011; 44(4):311-3. DOI:10.5090/kjtcs.2011.44.4.311
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    ABSTRACT: Acupuncture-related hemopericardium is a rare but potentially fatal complication. We describe a hemopericardium that occurred shortly after acupuncture in a 55-year-old woman. A chest CT scan and echocardiography revealed a hemopericardium, and pericardiocentesis was then immediately and successfully performed. Subsequently, her clinical course improved. This case increases the attention of emergency physicians for acupuncture-related complications, especially hemopericardium, and the necessity of rapid diagnosis and management.
    Yonsei medical journal 01/2011; 52(1):207-9. DOI:10.3349/ymj.2011.52.1.207 · 1.26 Impact Factor
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    08/2010; 43(4). DOI:10.5090/kjtcs.2010.43.4.454
  • Yong Jik Lee, Shigeru Kitani, Takuya Nihira
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    ABSTRACT: Virginiae butanolide (VB) is a gamma-butyrolactone autoregulator that triggers production of the streptogramin antibiotic virginiamycin in Streptomyces virginiae. Our previous studies suggested that the barX gene, an afsA-family gene, is likely to participate in the regulatory pathway for the production of VB, rather than in the biosynthetic pathway of VB itself, in contrast to the function of other afsA-family genes. Mutation analysis now shows that BarX at least plays an enzymic role in the VB biosynthetic pathway. Heterologous expression of the afsA gene from Streptomyces griseus into the barX mutant partially restored the deficiency of virginiamycin production, suggesting that afsA-family genes have a common ability to synthesize the gamma-butyrolactone autoregulators. Taken together with previous works relating to the function of an afsA-family gene, these results support the idea that streptomycetes have two biosynthetic pathways for the gamma-butyrolactone autoregulators.
    Microbiology 09/2009; 156(Pt 1):206-10. DOI:10.1099/mic.0.032003-0 · 2.84 Impact Factor
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    ABSTRACT: Adiponectin receptors mediate the antidiabetic effects of adiponectin. Although suggested to be mainly expressed in muscle, liver, and adipocyte cells, the expression of adiponectin receptors in beta cells is unclear. Given the primary involvement of this cell type in diabetes mellitus, we presently examined the expression level of adiponectin receptor 2 (AdiR2) in beta cells. Expression was significantly increased under acute hyperlipidemic conditions but impaired under chronic conditions. The impaired AdiR2 expression may play a role in worsened beta cell function. Clofibrate, an agonist of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) delayed the palmitate-induced impairment of AdiR2 expression and PPAR-alpha; this delay was abolished by PPAR-alpha targeted small interfering RNA. The results suggest that AdiR2 expression is regulated by palmitate via PPAR-alpha.
    Endocrine Journal 05/2009; 56(3):377-82. · 2.02 Impact Factor
  • Endocrine Journal 01/2009; 56(3):377-382. DOI:10.1507/endocrj.K08E-354 · 2.02 Impact Factor
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    ABSTRACT: The human leukocyte antigen (HLA) system is an integral component of immune response. Highly polymorphic HLA genes may play a pivotal role in the response of antiviral therapy. We investigated the effects of HLA gene polymorphism on the clinical outcome of chronic hepatitis B patients who received lamivudine treatment. Depending on their clinical response to lamivudine therapy, a total of sixty one patients were divided into following groups; non-responders, viral breakthroughers, relapsers, and seroconverters. HLA-A, -B, -Cw, -DRB and HLA-DRB1 alleles typing was performed on each group through the polymerase chain reaction and the sequence-specific oligonucleotide hybridization method. The distribution patterns of HLA-A, HLA-B, HLA-Cw, HLA-DRB, and HLA-DRB1 were then analysed. When non-responders were compared to the other groups, high frequencies in HLA-Cw1, HLA-DRB14 and HLA-DRB4 (p=0.015, 0.033 and 0.004 respectively) were evident. When seroconverters were compared to viral breakthroughers, high frequencies in HLA-A2 and HLA-DRB4 (p=0.048, 0.025 respectively) were evident. Our data suggests that HLA-A2, HLA-Cw1, HLA-DRB14 genes are related to the clinical outcomes of lamivudine treatment in chronic hepatitis B patients. These genes may be used in the prediction of the clinical outcome of lamivudine therapy in chronic hepatitis B patients.
    The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi 01/2009; 52(6):368-75.
  • Archives of Physical Medicine and Rehabilitation 11/2008; 89(11):e9. DOI:10.1016/j.apmr.2008.09.012 · 2.44 Impact Factor
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    ABSTRACT: Virginiae butanolide (VB) is a member of the gamma-butyrolactone autoregulators and triggers the production of streptogramin antibiotics virginiamycin M1 and S in Streptomyces virginiae. A VB biosynthetic gene (barS2) was localized in a 10-kb regulatory island which controls the virginiamycin biosynthesis/resistance of S. virginiae, and analyzed by gene disruption/complementation. The barS2 gene is flanked by barS1, another VB biosynthetic gene catalyzing stereospecific reduction of an A-factor-type precursor into a VB-type compound, and barX encoding a pleiotropic regulator for virginiamycin biosynthesis. The deduced product of barS2 possessed moderate similarity to a putative dehydrogenase of Streptomyces venezuelae, encoded by jadW2 located in similar gene arrangement to that in the regulatory island of S. virginiae. A barS2-disruptant (strain IC152), created by means of homologous recombination, showed no differences in growth in liquid medium or morphology on solid medium compared to a wild-type strain, suggesting that BarS2 does not play any role in primary metabolism or morphological differentiation of S. virginiae. In contrast, no initiation of virginiamycin production or VB production was detected with the strain IC152 until 18 h of cultivation, at which time full production of virginiamycin occurs in the wild-type strain. The delayed virginiamycin production of the strain IC152 was fully restored to the level of the wild-type strain either by the exogenous addition of VB or by complementation of the intact barS2 gene, indicating that the lack of VB production at the initiation phase of virginiamycin production is the sole reason for the defect of virginiamycin production, and the barS2 gene is of primary importance for VB biosynthesis in S. virginiae.
    Archives of Microbiology 05/2008; 189(4):367-74. DOI:10.1007/s00203-007-0327-5 · 1.86 Impact Factor
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    ABSTRACT: To investigate the effects of pioglitazone and metformin treatment during pre-diabetic period for the prevention of diabetes in a rat model. OLETF rats aged 18-weeks, were treated with pioglitazone (10 mg/kg/day) and metformin (300 mg/kg/day) for 10 weeks from their pre-diabetic period. We measured weight, lipid profiles, fat distribution, glucose tolerance, and pancreatic insulin content. Prominent weight gain (mostly subcutaneous fat area) was observed in the pioglitazone-treated OLETF (O-P) rats versus significant weight loss was observed in the metformin-treated OLETF (O-M) rats. Pioglitazone reversed the serum triglyceride (TG) and FFAs levels to normal (TG 0.46 +/- 0.04 vs 0.88 +/- 0.05 mmol/l in LETO). At the age of 28 weeks, the O-P rats showed completely normal glucose tolerance, and the glucose disposal rate (GDR) was markedly improved (25.6 +/- 0.4 vs 20.6 +/- 0.5 mg/min/kg in O-C, p < 0.05). The O-M rats also showed an improved fasting glucose and GDR level, but not as much as those with O-P rats. The pancreas insulin contents were much improved in the O-P rats (22.9 +/- 1.2 vs 18.8 +/- 1.3 nmol/pancreas in O-M rats, p < 0.05) with histological improvement. The pre-diabetic treatment with pioglitazone, despite significant weight gain, completely prevents to develop diabetes and enhances beta cell function with preservation of islet cell changes. Metformin treatment was also effective, but mainly by ameliorating the insulin resistance with marked reduction in body weight. The reversal of dyslipidaemia and the fat redistribution might contribute to the greater improvement of pioglitazone treatment compared to metformin in OLETF rats.
    Diabetes/Metabolism Research and Reviews 07/2007; 23(5):411-8. DOI:10.1002/dmrr.756 · 2.97 Impact Factor
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    ABSTRACT: Studies for the regulation of fatty acid metabolism are deficient relatively in skeletal muscle and heart. The investigations in pathological conditions for malonyl-CoA decarboxylase (MCD) and for the relation of MCD and PPAR-α·-γ agonists are insufficient in particular.
    01/2006; 30(5). DOI:10.4093/jkda.2006.30.5.324
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    ABSTRACT: With primers designed for the conserved region of the gamma-butyrolactone autoregulator receptor proteins from Streptomyces species, PCR using the Streptomyces clavuligerus genome DNA as a template gave a clear band of 100 bp, the sequence of which revealed high similarity to the expected region of a receptor gene. By Southern blot and colony hybridization with the 100-bp insert as a probe, plasmid pSCA, harboring a 4.2 kb- SalI fragment, was obtained. Sequence analysis on the insert revealed a 702-bp ORF encoding a protein with a moderate similarity (identity, 33-43%; similarity, 51-62%) to known gamma-butyrolactone autoregulator receptor proteins from Streptomyces sp. The ORF was named scaR ( S. clavuligerus autoregulator receptor). The scaR/pET-3d plasmid was constructed for overexpression of the recombinant ScaR protein (rScaR) in Escherichia coli, and the rScaR protein was purified to homogeneity by DEAE-ion-exchange HPLC. The molecular mass of the purified rScaR protein was determined to be 27 kDa as determined by SDS-PAGE, and 54 kDa by gel filtration HPLC under nondenatured conditions at a low protein concentration, indicating that the majority of the native ScaR is present in the form of a dimer, although rScaR tended to aggregate into a higher molecular form of 230 kDa at a high protein concentration. A binding assay with tritium-labeled autoregulators indicated that IM-2 type compounds with a long C2 side chain were the most effective ligands for rScaR, demonstrating for the first time that the beta-lactam producer S. clavuligerus contains a gene for the gamma-butyrolactone autoregulator receptor.
    Archives of Microbiology 10/2004; 182(1):44-50. DOI:10.1007/s00203-004-0697-x · 1.86 Impact Factor
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    ABSTRACT: The aim of this study was to determine whether the peroxisome proliferator-activated receptor (PPAR) ligands could prevent left-ventricular diastolic dysfunction (LVDD) in rats with advanced diabetes. In addition, this study examined whether the activity of malonyl-CoA decarboxylase (MCD), which is an enzyme related to the degradation of malonyl-CoA that is known to regulate the fatty acid metabolism, is changed by the diabetic state itself or by treatment with the PPAR ligands. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes, aged 28 weeks, were divided into 3 groups: the untreated, pioglitazone-treated (10 mg/kg/d), and fenofibrate-treated (150 mg/kg/d) groups. The rats were treated for 10 weeks. Male Long-Evans Tokushima Otsuka (LETO) rats were used as nondiabetic control. Doppler echocardiography and measurements of the MCD activity at the myocardium were performed. At the age of 38 weeks, the OLETF rats treated with either pioglitazone or fenofibrate showed an improvement in the plasma glucose levels after glucose loading as well as an improvement in the fasting plasma insulin, triglyceride, and FFA levels compared to the untreated OLETF rats. The untreated OLETF rats showed a prolonged deceleration time of the E-wave (DTE) (74.3 +/- 3.7 vs LETO, 56.3 +/- 3.8 ms, P < 0.05) and a reduced ratio of the peak early diastolic velocity wave to the late diastolic wave (E/A ratio) (1.25 +/- 0.06 vs LETO 1.54 +/- 0.08, P < 0.05). Pioglitazone treatment in the OLETF rats improved the DTE (51.6 +/- 1.7 ms, P < 0.05), and the fenofibrate treatment also improved the DTE (61.4 +/- 4.3 ms, P < 0.05) and E/A ratio (1.57 +/- 0.05, P < 0.05) compared to the untreated OLETF rats. The parameters related to the systolic function did not change among the groups at both pre- and post-treatments. The MCD activity of the myocardium was remarkably lower in the OLETF rats compared to the LETO rats (3.26 +/- 0.38 vs 7.76 +/- 0.84 nmol/min/mg protein, P < 0.05). The pioglitazone and fenofibrate treatments resulted in an increase in the MCD activity compared to that in the untreated rats (7.20 +/- 0.74 and 8.33 +/- 0.83 nmol/min/mg protein, P < 0.05, respectively). The PPAR-alpha or -gamma agonists prevented LVDD in the advanced diabetic rat hearts, possibly through an improvement in the fatty acid metabolism in the myocardium or a correction of the hyperglycemia and/or hyperlipidemia.
    Diabetes/Metabolism Research and Reviews 11/2003; 19(6):487-93. DOI:10.1002/dmrr.410 · 2.97 Impact Factor

Publication Stats

91 Citations
26.25 Total Impact Points

Institutions

  • 2011–2014
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
    • University of Ulsan
      Urusan, Ulsan, South Korea
  • 2008–2011
    • Seoul Medical Center
      Sŏul, Seoul, South Korea
  • 2008–2009
    • Osaka University
      • International Center for Biotechnology
      Ōsaka-shi, Osaka-fu, Japan
  • 2007
    • Yonsei University
      • Department of Internal Medicine
      Sŏul, Seoul, South Korea
  • 2004
    • Keimyung University
      • Department of Microbiology
      Sŏul, Seoul, South Korea
  • 2003
    • Yonsei University Hospital
      • Department of Internal Medicine
      Sŏul, Seoul, South Korea