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김대웅(Kim, Dae-woong),이상옥(Lee, Sang-ok) 한국어문학회 2016 語文學 Vol.0 No.133
This essay purposes to explain the consciousness on time in Lee Sang’s poems, focusing specifically on his poem, Strange Reversible Reaction. The argument will start from the obvious fact that the poet"s literature was based on the discovery of the material condition, called, the colony Gyeongsung. Through this discussion, what caused rejection and distrust for the time, which appear repeatedly in his literary texts, will be explained. Once, the modernist Lee Sang was dreaming of the perfect world of modernity. But the modern world he experienced was nothing but a cruel civilization with no vitality. As a result, he gave the death sentence to the world and tried to build up a new civilization. His literary texts will answer to the question, “Did the straight line kill the circle?”
Kim, Hee Kyung,Kim, Sun Young,Lee, Su Jin,Kang, Mihyeon,Kim, Seung Tae,Jang, Jiryeon,Rath, Oliver,Schueler, Julia,Lee, Dong Woo,Park, Woong Yang,Kim, Sung Joo,Park, Se Hoon,Lee, Jeeyun Neoplasia Press 2016 Translational oncology Vol.9 No.3
<P><I>BACKGROUND:</I> Although pazopanib treatment has become the standard chemotherapy in salvage setting for metastatic sarcoma patients, most patients progress after pazopanib treatment in 4 to 6 months. After failure to pazopanib, patients have limited options for treatment. Therefore, subsequent therapy in patients who failed to pazopanib is urgently needed and the use of patient derived cells or patient derived tumors for accompanying testing with various pharmacological inhibitors could offer additional treatment options for these patients. <I>METHODS:</I> Patient derived tumor cells were collected from ascites at the time of progression to pazopanib and a 13-drug panel was tested for drug sensitivity. We confirmed the results using <I>in vitro</I> cell viability assay and immunoblot assay. We also performed the genomic profiling of PDX model. <I>RESULTS:</I> The growth of patient derived tumor cells was significantly reduced by exposure to 1.0 μM AZD2014 compared with control (control versus AZD2014, mean growth = 100.0% vs 16.04%, difference = 83.96%, 95% CI = 70.01% to 97.92%, <I>P</I> = .0435). Similarly, 1.0 μM BEZ235 profoundly inhibited tumor cell growth <I>in vitro</I> when compared to control (control versus BEZ235, mean growth = 100.0% vs 7.308%, difference = 92.69%, 95% CI = 78.87% to 106.5%, <I>P</I> < .0001). Despite the presence of CDK4 amplification in the patient-derived tumor cells, LEE011 did not considerably inhibit cell proliferation when compared with control (control vs LEE011, mean growth = 100.0% vs 80.23%, difference = 19.77%, 95% CI = 1.828% to 37.72%, <I>P</I> = .0377). The immunoblot analysis showed that BEZ235 treatment decreased pAKT, pmTOR and pERK whereas AZD2014 decreased only pmTOR. <I>CONCLUSION:</I> Taken together, upregulation of mTOR/AKT pathway in sarcoma patient derived cells was considerably inhibited by the treatment of AZD2014 and BEZ235 with downregulation of AKT pathway (greater extent for BEZ235). These molecules may be considered as treatment option in STS patient who have failed to pazopanib in the context of clinical trials.</P>
( Hee Yeon Kim ),( Jong Young Choi ),( Dong Goo Kim ),( Myoung Soo Kim ),( Soon Il Kim ),( Shin Hwang ),( Sung Gyu Lee ),( Kwang Woong Lee ),( Kyung Suk Suh ),( Young Seok Han ),( Dong Lak Choi ),( Se 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.-
Background: The outcome of hepatitis B virus (HBV) infection after liver transplantation (LT) was improved by hepatitis B immunoglobulin (HBIG) and nucles(t)ide analogue (NUA). However, HBV recurrence after LT is critical because the recurrence is occasionally accompanied by a progressive destruction of graft and poor survival. The aims of this study were to investigate the significance HBV recurrence and identity factors associated with HBV recurrence. Methods: From October 1999 to February 2011, a total of 2684 consecutive LT recipients who underwent HBV-associated LT were retrospectively enrolled from 7 transplantation centers in Korea. Results: Prophylaxis regimens were HBIG monotherapy (67.7%) or a combination of HBIG with NUA (22.3%). The recurrence rate of HBV was 6.1% (164 recipients) during mean follow-up duration of 10.9 years. The median time from transplantation to recurrence was 2.1 years (0.1-7.9 years). Of the 1,071 patients with hepatocellular carcinoma (HCC) prior to LT, 155 patients (14.5%) had HCC recurrence after transplantation, and 48 patients (31.0%) had HBV recurrence. Of the 48 patients with recurrence of both HBV and HCC, 25 patients (52.1%) experienced HBV recurrence after HCC recurrence. In the multivariate analysis, pretransplant HCC, pretransplant HBV DNA above 5.5 log copies/mL was independent clinical factors influencing HBV recurrence after LT. The mortality rate among the recipients with HBV recurrence was 34.1% (56 recipients). Mean overall survival was 6.4 years in the HBV-recurrence group and 9.9 years in the HBV-nonrecurrence group (p<0.001). HBV recurrence was not an independent prognostic factor for overall survival. HCC recurrence was the most important factor for overall survival. Conclusions: The overall outcome of LT in HBV-related liver disease was excellent with the current prophylaxis regimen Choon Hyuck David Kwon,8 Suk-Koo Lee8 Pretransplant HBV DNA and HCC were important factors for HBV recurrence. HBV recurrence after LT did not significantly influence on the overall survival without combining of HCC recurrence.
Simultaneous Bilateral Patellar Tendon Ruptures Associated with Osteogenesis Imperfecta
Woong Hee Kim(김웅희),Sang Ho Ha(하상호),Hyeon Jun Lee(이현준) 대한정형외과학회 2016 대한정형외과학회지 Vol.51 No.5
골 형성 부전증 환자에서의 양측 슬개건 파열은 매우 드물며, 이는 골의 파쇄성에 기인한다. 저자들은 이에 대한 증례 보고 및 슬개건 실질의 파열인 경우, 일차적 봉합 및 추가적 환형 강선 봉합을 적절한 치료법으로 제시하는 바이다. Bilateral patella tendon rupture is rare, particulary when associated with osteogenesis imperfecta. Brittleness of the bone in osteogenenesis imperfect patients may cause this rupture. We report on this rare case and suggest the direct repair with the additional wire loop as a proper treatment option for patients with the substantial rupture of patella tendon.
Clinical Relevance of Genomic Changes in Recurrent Pediatric Solid Tumors
Lee, Boram,Lee, Ji Won,Shim, Joon Ho,Joung, Je-Gun,Yun, Jae Won,Bae, Joon Seol,Shin, Hyun-Tae,Sung, Ki Woong,Park, Woong-Yang Neoplasia Press 2018 Translational oncology Vol.11 No.6
<P><I>PURPOSE:</I> Relapsed/refractory pediatric cancers show poor prognosis; however, their genomic patterns remain unknown. To investigate the genetic mechanisms of tumor relapse and therapy resistance, we characterized genomic alterations in diagnostic and relapsed lesions in patients with relapsed/refractory pediatric solid tumors using targeted deep sequencing. <I>PATIENTS AND METHODS:</I> A targeted sequencing panel covering the exons of 381 cancer genes was used to characterize 19 paired diagnostic and relapsed samples from patients with relapsed/refractory pediatric solid tumors. <I>RESULTS:</I> The mean coverage for all samples was 930.6× (SD = 213.8). Among the 381 genes, 173 single nucleotide variations (SNVs)/insertion-deletions (InDels), 100 copy number alterations, and 1 structural variation were detected. A total of 72.6% of SNVs in primary tumors were also found in recurrent lesions, and 27.2% of SNVs in recurrent tumors had newly occurred. Among SNVs/InDels detected only in recurrent lesions, 71% had a low variant allele fraction (<10%). Patients were classified into three categories based on the mutation patterns after cancer treatment. A significant association between the major mutation patterns and clinical outcome was observed. Patients whose relapsed tumor had fewer mutations than the diagnostic sample tended to be older, had longer progression-free survival, and achieved complete remission after relapse. Contrastingly, patients whose genetic profile only had concordant mutations without any change had the worst outcome. <I>CONCLUSIONS:</I> We characterized genomic changes in recurrent pediatric solid tumors. These findings could help to understand the biology of relapsed childhood cancer and to develop personalized treatment based on their genetic profile.</P>