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C language를 위한 Concurrent Programming 환경의 개발
윤용익(Y I Yoon),조주현(J H Cho),정영조(Y C Chung),강석열(S Y. Kang) 한국정보과학회 1988 한국정보과학회 학술발표논문집 Vol.15 No.1
Multiprocessor system이 널리 보급되고 사용됨에 따라 concurrent programming은 더욱 더 중요한 feature가 되어가고 있다. 기존의 C 언어는 concurrent programming을 위한 feature들을 가지고 있지 못하나, 본 논문에서는 concurrent processing이 가능한 Concurrent-C 언어를 설계, 구현하였다. Concurrent feature들을 첨가하는 방법으로는 여러 종류의 runtime library routine들을 제공하여 C program 내에서 이 routine들을 call하는 방식을 사용하였다. Concurrent-C는 UNIX 환경하에서 구현되었으며, 실제로 C compiler를 제공하는 어떠한 OS 상에서도 host machine의 종류에 관계없이 구현될 수 있다.
Yu, S.J.,Bae, S.,Kang, J.S.,Yoon, J.H.,Cho, E.J.,Lee, J.H.,Kim, Y.J.,Lee, W.J.,Kim, C.Y.,Lee, H.S. North-Holland ; Elsevier Science Ltd 2015 european journal of pharmacology Vol.762 No.-
<P>Prevention and restoration of hepatic fibrosis from chronic liver injury is essential for the treatment of patients with chronic liver diseases. Vitamin C is known to have hepatoprotective effects, but their underlying mechanisms are unclear, especially those associated with hepatic fibrosis. Here, we analyzed the impact of vitamin Con bile acid induced hepatocyte apoptosis in vitro and lithocholic acid (LCA) induced liver injury in vitamin C-insufficient Gulo(-/-) mice, which cannot synthesize vitamin C similarly to humans. When Huh BAT cells were treated with bile acid, apoptosis was induced by endoplasmic retiiculum stress related JNK activation but vitamin C attenuated bile acid induced hepatocyte apoprosis in vitro. In our in vivo experiments. LCA feeding increased plasma marker of cholestasis and resulted in more extensive liver damage and hepatic fibrosis by more prominent apoptotic cell death and recruiting more intrahepatic inflammatory CD11b(+) cells in the liver of vitamin C-insufficient Gulo(-/-) mice compared to wild type mice which have minimal hepatic fibrosis. However, when vitamin C was supplemented to vitamin C-insufficient Gulo(-/-) mice, hepatic fibrosis was significantly attenuated in the liver of vitamin C-sufficient Gulo(-/-) mice like in wild type mice and this hepatoprotective effect of vitamin C was thought to be associated with both decreased hepatic apoptosis and necrosis. These results suggested that vitamin C had hepatoprotective effect against cholestatic liver injury. (C) 2015 Elsevier B.V. All rights reserved.</P>
방사성동위원소심혈관조영술상 관찰된 주폐동맥유와 동맥관개존증이 병발된 1예
조보연,이명철,고창순,한만청,손인,윤용수,홍창의,노준량,연경모 대한핵의학회 1981 핵의학 분자영상 Vol.15 No.2
A Case of main pulmonary artery aneurysm in a 9-year-old boy with patent ductus arteriosus is presented. In this case presented with a huge mass density on the chest X-ray, radionuclide cardiac angiography showed a vascular lesion, which was confirmed as an aneurysm of the main pulmonary artery at roentgenologic angiogram. The aneurysm appeared following an episode of bacterial endocarditis and pulmonary hypertension. A successfu1 aneurysmectomy with multiple ligation of ductus arteriosus was performed.
Yoon, J.H.,Kim, H.J.,Park, S.S.,Jeon, Y.W.,Lee, S.E.,Cho, B.S.,Eom, K.S.,Kim, Y.J.,Lee, S.,Min, C.K.,Cho, S.G.,Kim, D.W.,Lee, J.W.,Min, W.S. AMERICAN SOCIETY FOR BLOOD AND MARROW 2017 BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION Vol.23 No.4
The role of autologous hematopoietic cell transplantation (auto-HCT) for postremission therapy of acute myeloid leukemia is yet to be elucidated. We retrospectively analyzed 240 patients treated with auto-HCT in first remission. All patients were treated with standard induction chemotherapy, and CD34<SUP>+</SUP>@?stem cells were collected at each cycle of consolidation. Stem cells were infused after total body irradiation (1200 cGy), cytarabine (9 g/m<SUP>2</SUP>), and melphalan (100@?mg/m<SUP>2</SUP>). Estimated 5-year overall survival, disease-free survival (DFS), cumulative incidence of relapse (CIR), and nonrelapse mortality were 58.4%, 55.3%, 38.8%, and 5.9%, respectively. We identified that poor-risk karyotype showed very poor outcome after auto-HCT, and then analyzed 85 patients with good to intermediate-risk molecular cytogenetics with available molecular study results and markers for minimal residual disease (MRD) such as WT1 and core-binding factor (CBF) associated MRD (ie, AML1/ETO and CBFβ/MYH11). Our data identified that old age, pre-HCT markers for MRD, and high post-HCT WT1, high dose of CD34<SUP>+</SUP>@?stem cell (≥4.5 x 10<SUP>6</SUP>/kg) infusion, and c-kit or FLT3-ITD mutations were associated with higher relapse rate and poor DFS. Using pre-HCT parameters, except for post-HCT WT1, multivariate analysis revealed that patients with young age (<40 years old), no adverse mutations, and limited dose of CD34<SUP>+</SUP>@?stem cells might be good candidate for auto-HCT (3-year DFS and CIR were 83.4% and 16.6%, respectively). Young patients with good- to intermediate-risk molecular cytogenetics may benefit from auto-HCT if stem cell dose is limited.
Yoon, C.H.,Chung, W.Y.,Suh, J.W.,Cho, Y.S.,Youn, T.J.,Chun, E.J.,Choi, S.I.,Chae, I.H.,Choi, D.J. Elsevier/North-Holland Biomedical Press 2013 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.167 No.5
Background: Protection of distal embolization by balloon occlusion and thrombus aspiration has not improved microvascular circulation nor decreased myocardial injury during primary percutaneous intervention (PCI) for ST-elevation myocardial infarction (STEMI) in randomized trials. In a prospective randomized trial, we investigated the mechanism of the poor effect of distal protection and thrombus aspiration (DP-TA) in 126 patients with STEMI. Methods: Patients with first-diagnosed STEMI were randomly assigned to DP-TA pretreatment or conventional PCI (c-PCI). Primary endpoint was reduced left ventricular end-diastolic volume (LVEDV) measured by MRI at post-PCI and 6months after PCI. Secondary end points were infarct ratio (infarct size to entire LV size) by delayed enhancement (DE), area at risk (AAR) ratio (AAR to entire LV size) by T2 high signal, microvascular occlusion index (MVO) ratio (MVO to entire LV size) by DE, and myocardial salvage index (MSI: (AAR-infarct size)*100/AAR) using cardiac magnetic resonance imaging (MRI) within 3days after PCI. Results: Baseline characteristics of the patients including cardiovascular risk factors and lesion characteristics were similar between the two groups. DT-PA failed to improve LV remodeling at 6months (LVEDV 140+/-39 vs 133+/-37 in c-PCI group, p=0.418). Infarct ratio, AAR ratio and MSI were not statistically different between DP-TA group and c-PCI group. However, MVO ratio was significantly larger in DP-TA group than in c-PCI group (2.4+/-2.7 vs 1.1+/-1.9, p=0.045). Conclusion: DP-TA was potentially hazardous in primary PCI for STEMI by increasing MVO. DP-TA should not be used in STEMI.
A new <i>HLA‐C*07:244</i> allele identified by sequence‐based typing in a Korean individual
Cho, D.,Jang, M. J.,Yoon, C. E.,Kwon, O. J.,Shin, M. G. Blackwell Publishing Ltd 2012 Tissue antigens Vol.80 No.4
<P>The <I>C*07:244</I> changes single nucleotide of <I>C*07:02:01</I> at codon 75 (CGA → CAA), Arg to Gln.</P>
Yeo, C.E.,Kang, W.Y.,Seong, S.J.,Cho, S.,Lee, H.W.,Yoon, Y.R.,Kim, H.J. Academic Press 2017 Experimental cell research Vol.359 No.1
Neuromedin B (NMB), a mammalian bombesin-like peptide, regulates diverse physiological processes, such as energy metabolism, memory and fear behavior, and cellular growth, through its cognate receptor, NMBR. In this study, we report that NMB expression was upregulated during osteoclast development and that silencing NMB or NMBR attenuated osteoclast generation mediated by macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL). We found that knockdown of NMB or NMBR using a small hairpin RNA suppressed M-CSF-induced proliferation of osteoclast precursor cells without altering osteoclast differentiation. Interestingly, NMB or NMBR knockdown reduced the expression of the M-CSF receptor, c-Fms, which is an important modulator of osteoclast development. Consequently, NMB or NMBR silencing inhibited M-CSF/c-Fms-mediated downstream signaling pathways like activation of ERK and Akt and induction of D-type cyclins, cyclin D1 and D2. Moreover, knockdown of NMB or NMBR accelerated apoptosis in osteoclast lineage cells by inducing caspase-3, caspase-9, and Bim expression. In summary, our study demonstrates that the NMB/NMBR axis plays a pivotal role in osteoclast generation by modulating the proliferation and survival of osteoclast lineage cells.