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Weiguang Gu,Hua Zhang,Yiyu Lu,Minjing Li,Shuang Yang,Jianmiao Liang,Zhijian Ye,Zhihua Li,Minhong He,Xiaoliang Shi,Fei Wang,Dong You,Weiquan Gu,Weineng Feng 대한암학회 2023 Cancer Research and Treatment Vol.55 No.3
Purpose We aimed to evaluate whether the addition of pemetrexed is effective in improving progression-free survival (PFS) in epidermal growth factor receptor (EGFR)–mutated patients with or without concomitant alterations. Materials and Methods This multicenter clinical trial was conducted in China from June 15, 2018, to May 31, 2019. A total of 92 non–small cell lung cancer (NSCLC) patients harboring EGFR-sensitive mutations were included and divided into concomitant and non-concomitant groups. Patients in each group were randomly treated with EGFR–tyrosine kinase inhibitor (TKI) monotherapy or EGFR-TKI combined with pemetrexed in a ratio of 1:1. PFS was recorded as the primary endpoint. Results The overall median PFS of this cohort was 10.1 months. There were no significant differences in PFS between patients with and without concomitant and between patients received TKI monotherapy and TKI combined with pemetrexed (p=0.210 and p=0.085, respectively). Stratification analysis indicated that patients received TKI monotherapy had a significantly longer PFS in non-concomitant group than that in concomitant group (p=0.002). In concomitant group, patients received TKI combined with pemetrexed had a significantly longer PFS than patients received TKI monotherapy (p=0.013). Molecular dynamic analysis showed rapidly emerging EGFR T790M in patients received TKI monotherapy. EGFR mutation abundance decreased in patients received TKI combined chemotherapy, which supports better efficacy for a TKI combined chemotherapy as compared to TKI monotherapy. A good correlation between therapeutic efficacy and a change in circulating tumor DNA (ctDNA) status was found in 66% of patients, supporting the guiding role of ctDNA minimal residual disease (MRD) in NSCLC treatment. Conclusion EGFR-TKI monotherapy is applicable to EGFR-sensitive patients without concomitant alterations, while a TKI combined chemotherapy is applicable to EGFR-sensitive patients with concomitant alterations. CtDNA MRD may be a potential biomarker for predicting therapeutic efficacy.
시각장애인을 위한 ICT융합 자율주행 서비스 로봇 설계 및 구현
구예찬 ( Ye-chan Gu ),권세진 ( Se-jin Kwon ),남가빈 ( Ga-bin Nam ),이웅기 ( Woong-ki Lee ) 한국정보처리학회 2022 한국정보처리학회 학술대회논문집 Vol.29 No.2
코로나-19의 여파와 기술의 발전으로 비대면 거래가 증가하고 있는 추세다. 비대면 거래가 증가하면서 무인점포도 늘어나고 있고, 늘어남에 따라서 시각장애인들은 무인점포를 이용하는데 어려움을 겪고 있다. 본 논문에서는 자율주행 로봇에 음성인식 기술과 딥러닝 기술을 적용하여 시각장애인에게 도움을 줄 수 있도록 ICT융합 로봇을 구현하였다. 무인점포 뿐만이 아니라 안내가 필요한 다양한 장소에서도 적용될 수 있을 것으로 기대한다.
논문 : 고객관계관리를 위한 내부마케팅에서의 시스템 지원에 관한 연구
이예구 ( Ye Gu Lee ),윤재희 ( Jae Hee Yoon ) 안양대학교 복지행정연구소 2011 福祉行政硏究 Vol.27 No.-
본 연구는 초기 디지털 환경 하에서의 증권회사의 시스템 지원이 증권회사 외부와의 접점에서 외부고객을 상대로 하는 내부직원이 고객 관계 내부 품질 개선을 어떻게 인식 하는지 연구하였다. 연구모형은 시스템을 개발하는데 필요한 전문인력 확보. 시스템 특성과 지속적 투자를 독립변수로 하고. 이 변수들에 의해 영향을 받는 내부 업무절차 개선과 고객관계 내부품질 개선을 설정하였다. 분석에 이용된 설문자료는 수도권 지역의 증권회사 본사 및 지점의 고객관련직원을 대상으로 설문조사를 하였다. 이와 같이 수집된 설문지를 기본으로 통계패키지 SPSS 12.0 K를 이용하여 통계분석을 하였다. 우선 조사된 설문지의 인구통계학적 분석을 하였으며. 사용된 변수들에 대한 신뢰도와 타당도를 알아보기 위하여 베리멕스법에 의한 요인분석과 Cronbach’ α 계수에 의한 신뢰도를 검증한 결과 원래의 의도대로 변수들이 추출되었고. 상관관계분석을 실시하였다. 그리고 가설의 검증을 위하여 요인추출값에 의한 선형희귀분석을 하였다. 그 결과, 요인추출값에 의한 가설검증은 모두 채택되었으며, 다음과 같은 결과를 도출하였다. 첫째, 고객관계관리를 위한 시스템 지원이 IT 인력이 주를 이루고 있고. 효율적인 커스터마이징을 위한시스템 지원을 위해서는 시스템 개발 단계에서 각 실무부서별 실무자의 참여가 필요하다. 둘째, 디지털 환경 하의 증권회사 고객관계관리 시스템 지원이 이루어지고 있고, 이에 따라 성능 및 정보가 바뀌고 있다. 그러나 정보화 환경 하에서 증권회사의 고객에게 제공하는 기업정보가 디지털 환경 하에서도 계속 사용이 가능하며, 앞으로 증권회사의 고객관계관리 시스템개발을 위해서는 디지털 환경하의 H/W. S/W 및 다양한 기능의 Contents개발. 교육적인 부분을 중요시하여야 한다. 셋째, 증권회사의 고객관계관리 시스템 지원에 대하여 외부환경 인프라는 형성되었고, 내부환경적으로는 인프라에 따른 투자 및 지원을 중요시하고 있다. 그러나 변화에 따른 인력 및 기간 지원에는 단기 효과에 치중하고 있으며, 이와 같은 현상은 IT 기술의 빠른 현상에도 기인할수 있으나. 생산적 고객관계관리를 위하여는 충분한 인력 및 기간 투입이 필요하다. 넷째, 업무절차 중 고객관계 내부품질 개선에 미친 영향인 의사소통은 고객과의 의사소통에서 증권회사의 영업지원이 디지털 환경 하에서 장소와 시간에 구애받지 않고, 고객과 의사소통이 이루어지고 있음을 나타내었다. 그러나 효율적인 고객관계 내부품질 개선을 위해서는 Data 통합을 통한 영업 정보의 적시제공이 필요하며, 개발된 CRM를 전 직원들이 장소와 시간에 구애받지 않고 활용 및 전파 할 수 있는 교육 방안이 필요하다.
Ye Ryoung Jang,Hye Rin Yoon,Mi Hyoung Kim,Hong Gu Joo 한국예방수의학회 2018 예방수의학회지 Vol.42 No.2
Doxorubicin has been used to treating cancers, including breast cancer, bladder cancer, and acute lymphocytic leukemia, however, few studies have investigated its anti-inflammatory activity. In this study, we used mouse spleen cells treated with lipopolysaccharide (LPS), a representative inflammatory agent to investigate the effects of doxorubicin. Specially, we investigated the effects of doxorubicin on metabolic activity, cell size, cell death, and cytokine production of LPS-treated spleen cells. Doxorubicin significantly decreased the metabolic activity, even when applied at relatively low concentrations (1.6-8 ng/mL). To investigate the potential mechanism, we measured the mitochondrial membrane potential (MMP) of the LPS-treated spleen cells using Rhodamine 123. Doxorubicin decreased MMP and cell size, and induced cell death. Furthermore, doxorubicin suppressed the production of tumor necrosis factor (TNF)-alpha, a representative cytokine, in LPS-treated spleen cells. Taken together, doxorubicin decreased metabolic activity and the production of inflammatory cytokines, while increasing the death of LPS-induced hyperactivated spleen cells. This results will enable broader application of doxorubicin, as an anti-inflammatory agent, in clinical and research fields.
Ye Jee Byun,Hyun-Jeong Do,Seong-Hee Oh,Chong Jai Kim,Beom Hee Lee,Gu Hwan Kim,Byoung Sop Lee,Ki-Soo Kim,Ai-Rhan Kim 대한신생아학회 2015 Neonatal medicine Vol.22 No.4
Autosomal recessive polycystic kidney disease is among the most common inherited ciliopathies and is caused by mutations in the polycystic kidney and hepatic disease 1 (PKHD1) gene. Despite its great phenotypic variability, this condition is usually diagnosed during the neonatal and early infantile periods. We report a 37+3-gestational-week neonate presenting with fatal autosomal recessive polycystic kidney disease who died at 28 hours of life from severe respiratory failure. The familial history is significant because a previous sibling died in utero at 24+2 weeks of gestational age and was diagnosed with polycystic kidney disease based on prenatal ultrasonography and autopsy. Our patient’s autopsy revealed findings compatible with polycystic kidney disease. In addition, a PKHD1 gene study of peripheral blood leukocytes identified the compound heterozygote mutation c.274C>T(p.Arg92Trp), as well as the novel heterozygous nonsense mutation c.2770C>T(p.Gln924*).
NUP210 and MicroRNA-22 Modulate Fas to Elicit HeLa Cell Cycle Arrest
Qiao Gu,Wenjie Hou,Huan Liu,Lijuan Shi,Zonghao Zhu,Wenfeng Ye,Xiaoyuan Ni 연세대학교의과대학 2020 Yonsei medical journal Vol.61 No.5
Purpose: Cervical cancer is one of the most fatal diseases among women in under-developed countries. To improve cervical cancer treatment, discovery of new targets is needed. In this study, we investigated the expression of NUP210, miR-22, and Fas in cervical cancer tissues and their functions in cell cycle regulation. Materials and Methods: We detected and compared the expression levels of NUP210, miR-22, and Fas in cervical cancer tissues with paired normal tissues using immunohistochemistry, Western blot, and real-time quantitative polymerase chain reaction. NUP210 was knocked down in HeLa cells via lentivirus, followed by cell cycle and proliferation analysis. Using a luciferase reporter assay, we explored the link between miR-22 and NUP210. We overexpressed miR-22 in HeLa cells and analyzed cell cycle and proliferation function. We then overexpressed miR-22 in NUP210 knockdown cells to explore the connection between Fas and miR-22-NUP210 signaling. Results: We found that NUP210 was overexpressed in cervical cancer patients. Knocking down NUP210 restored cell apoptosis and proliferation. We confirmed miR-22 as a regulator of NUP210 and verified that miR-22 was inhibited in cervical cancer development. We also found that restoring miR-22 expression could induce cell apoptosis. Finally, we found that miR-22-regulated expression of NUP210 could alter Fas expression and, in turn, elicit cell cycle arrest and proliferation. Conclusion: miR-22 in cervical cancer is downregulated, resulting in NUP210 overexpression and inhibition of Fas-induced cell apoptosis.