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Adaptive Maximum Power Point Tracking Algorithm for Photovoltaic Power Systems
AHN, Chang Wook,CHOI, Ju Yeop,LEE, Dong-Ha,AN, Jinung The Institute of Electronics, Information and Comm 2010 IEICE TRANSACTIONS ON COMMUNICATIONS - Vol.93 No.5
<P>This paper presents an adaptive maximum power point tracking (MPPT) algorithm. The aim is to dynamically adjust the step length for updating duty ratio (or operating voltage) so as to make full utilization of the output power of photovoltaic (PV) systems, even under the rapidly changing atmospheric conditions. To this end, the average slope in terms of voltage and power is exploited for reducing the harmful effect of noise and error (incurred in measurement or quantization) on the slope. Also, a statistical decision-making scheme is employed for reliably deciding the time instant at which atmospheric conditions actually change. Empirical study has adduced grounds for its dominance over existing references.</P>
Chang, Dong-Yeop,Song, Sang Hoon,You, Sooseong,Lee, Jino,Kim, Jihye,Racanelli, Vito,Son, Hwancheol,Shin, Eui-Cheol Springer-Verlag Italia 2014 Clinical and experimental medicine Vol.14 No.3
<P>Genital papilloma is caused by human papilloma virus (HPV) infection and recurs frequently. Although T cells are known to play a critical role in the control of HPV infection and papilloma development, the function and phenotype of these cells in the lesion remain to be elucidated. In the present study, we examined the function and phenotype of CD4(+) T cells isolated from the lesions of primary (n = 9) and recurrent (n = 11) genital papillomas. In recurrent papillomas, the frequency of proliferating (Ki-67(+)) CD4(+) T cells was significantly reduced compared with primary papillomas. Cytokine production was evaluated by intracellular cytokine staining in anti-CD3/anti-CD28-stimulated CD4(+) T cells. CD4(+) T cells from recurrent lesions showed impaired production of IL-2, IFN-γ, and TNF-α. Of interest, the frequency of cytokine-producing CD4(+) T cells significantly correlated with the frequency of Ki-67(+)CD4(+) T cells. We also studied expression of programmed death-1 (PD-1), a T-cell exhaustion marker. The frequency of PD-1(+)CD4(+) T cells was significantly increased in recurrent lesions and inversely correlated with the frequency of cytokine-producing CD4(+) T cells. The functional significance of PD-1 expression was determined in blocking assays with anti-PD-L1, which restored cytokine production of CD4(+) T cells from recurrent lesions. Taken together, in recurrent genital papilloma lesions, proliferation, and cytokine production by CD4(+) T cells are impaired and the PD-1/PD-L1 interaction is responsible for the functional impairment of CD4(+) T cells.</P>
( Dong Yeop Chang ),( Hyun Woong Lee ),( Won Seok Kang ),( Young Jun Koh ),( Jino Lee ),( So Youn Shin ),( Soo Seong You ),( Yoon Seok Choi ),( Ji Hye Kim ),( In Soo Oh ),( Dong Ho Lee ),( Kyung Suk S 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.1
Background/Aims: During viral infection, tissue damage is caused not only by direct cytopathic effects of virus but also by host immune responses. We investigated activation status and functions of CD8+ T cells and the mechanism of CD8+ T cell-mediated host injury in acute hepatitis A (AHA), which is caused by hepatitis A virus (HAV) infection and manifested by severe liver injury in adults. Methods: The study population was AHA-diagnosed 56 patients, hospitalized in Chung-Ang University Hospital. All patients were seropositive for anti-HAV IgM and had clinical and laboratory features of acute hepatitis. The whole blood and serum were obtained, and peripheral blood mononuclear cells were isolated by Ficoll density-gradient centrifugation and cryopreserved. Direct ex vivo IFN-γ ELISpot assay of peripheral blood lymphocytes was performed by stimulating them with overlapping peptides for HAV VP2 and 3C proteins in order to assess comprehensively HAV-specific IFN-γ response. Results: Total IFN-γ response against VP2 and 3C did not show positive correlation to serum ALT level, corroborating that the liver injury of AHA is not associated with HAV-specific T cell response. Activation of unrelated virus-specific CD8+ T cells significantly correlated with the percentage of CD38+HLA-DR+ cells in total CD8+ T cells, which was a correlate of the liver injury. In a prospective analysis, the percentage of CD38+ HLA-DR+ cells in total CD8+ T cells or that in unrelated virusspecific CD8+ T cells decreased along with the decrease in serum ALT level at the time of discharge, but that in HAVspecific CD8+ T cell population did not. Conclusions: We demonstrate that unrelated virus-specific CD8+ T cells, which are not specific to HAV, are activated and proliferating in AHA, the severity of liver injury correlates with the activation of non-HAV-specific CD8+ T cells, not to that of HAV-specific T cells.
( Dong Yeop Chang ),( Hyun Woong Lee ),( Won Seok Kang ),( Young Jun Koh ),( Jino Lee ),( So Youn Shin ),( Soo Seong You ),( Yoon Seok Choi ),( Ji Hye Kim ),( In Soo Oh ),( Dong Ho Lee ),( Kyung Suk S 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.-
Background/Aims: During viral infection, tissue damage is caused not only by direct cytopathic effects of virus but also by host immune responses. We investigated activation status and functions of CD8+ T cells and the mechanism of CD8+ T cell-mediated host injury in acute hepatitis A (AHA), which is caused by hepatitis A virus (HAV) infection and manifested by severe liver injury in adults. Methods: The study population was AHA-diagnosed 56 patients, hospitalized in Chung-Ang University Hospital. All patients were seropositive for anti-HAV IgM and had clinical and laboratory features of acute hepatitis. The whole blood and serum were obtained, and peripheral blood mononuclear cells were isolated by Ficoll density-gradient centrifugation and cryopreserved. Direct ex vivo IFN-γ ELISpot assay of peripheral blood lymphocytes was performed by stimulating them with overlapping peptides for HAV VP2 and 3C proteins in order to assess comprehensively HAV-specific IFN-γ response. Results: Total IFN-γ response against VP2 and 3C did not show positive correlation to serum ALT level, corroborating that the liver injury of AHA is not associated with HAV-specific T cell response. Activation of unrelated virus-specific CD8+ T cells significantly correlated with the percentage of CD38+HLA-DR+ cells in total CD8+ T cells, which was a correlate of the liver injury. In a prospective analysis, the percentage of CD38+ HLA-DR+ cells in total CD8+ T cells or that in unrelated virusspecific CD8+ T cells decreased along with the decrease in serum ALT level at the time of discharge, but that in HAVspecific CD8+ T cell population did not. Conclusions: We demonstrate that unrelated virus-specific CD8+ T cells, which are not specific to HAV, are activated and proliferating in AHA, the severity of liver injury correlates with the activation of non-HAV-specific CD8+ T cells, not to that of HAV-specific T cells.
Immune-based therapy for chronic hepatitis C.
Chang, Dong-Yeop,Shin, Eui-Cheol Liss 2009 Journal of Leukocyte Biology Vol.86 No.1
<P>Chronic, persistent HCV infection is a public health issue. It often progresses to life-threatening complications, including liver cirrhosis and hepatocellular carcinoma. The current standard therapy is a combination of pegylated IFN-alpha and ribavirin. This therapy results in a sustained virologic response in only 50% of patients infected with HCV genotype 1 and is often accompanied with substantial side-effects. Therefore, it is imperative to develop novel therapies with higher efficacy and less substantial side-effects. Impaired immune responses to HCV are key features of chronic HCV infection; thus, intervention strategies typically involve boosting the immune responses against HCV. These immune-based therapies for chronic HCV infection include therapeutic vaccines, antagonists of T cell inhibitory factors, anti-HCV neutralizing antibodies, cytokines, and agonists for TLRs. Currently, various types of immune-based therapies are under development that might be used as a monotherapy or in combination with other antiviral drugs for the treatment of chronic HCV infection.</P>
Ho Yeop Lee,Byeong Chang Sim,Ha Thi Nga,Ji Sun Moon,Jingwen Tian,Nguyen Thi Linh,Sang Hyeon Ju,Dong Wook Choi,Daiki Setoyama,이현승 대한내분비학회 2022 Endocrinology and metabolism Vol.37 No.6
Background: An excess of thyroid hormones in Graves’ disease (GD) has profound effects on systemic energy metabolism that are currently partially understood. In this study, we aimed to provide a comprehensive understanding of the metabolite changes that occur when patients with GD transition from hyperthyroidism to euthyroidism with methimazole treatment. Methods: Eighteen patients (mean age, 38.6±14.7 years; 66.7% female) with newly diagnosed or relapsed GD attending the endocrinology outpatient clinics in a single institution were recruited between January 2019 and July 2020. All subjects were treated with methimazole to achieve euthyroidism. We explored metabolomics by performing liquid chromatography-mass spectrometry analysis of plasma samples of these patients and then performed multivariate statistical analysis of the metabolomics data. Results: Two hundred metabolites were measured before and after 12 weeks of methimazole treatment in patients with GD. The levels of 61 metabolites, including palmitic acid (C16:0) and oleic acid (C18:1), were elevated in methimazole-naïve patients with GD, and these levels were decreased by methimazole treatment. The levels of another 15 metabolites, including glycine and creatinine,were increased after recovery of euthyroidism upon methimazole treatment in patients with GD. Pathway analysis of metabolomics data showed that hyperthyroidism was closely related to aminoacyl-transfer ribonucleic acid biosynthesis and branched-chain aminoacid biosynthesis pathways. Conclusion: In this study, significant variations of plasma metabolomic patterns that occur during the transition from hyperthyroidism to euthyroidism were detected in patients with GD via untargeted metabolomics analysis.
Shin, Dong-Yeop,Park, Jin Kyun,Li, Chih Chiao,Park, Hee Sue,Moon, Soo Young,Kim, Sung-Min,Im, Kyongok,Chang, Yoon Hwan,Yoon, Sung-Soo,Lee, Dong-Soon Elsevier 2019 Leukemia research Vol.79 No.-
<P><B>Abstract</B></P> <P>We hypothesized that a subset of idiopathic cytopenia of undetermined significance (ICUS) is associated with an increased autonomous proliferation with exhaustion of hematopoiesis. The aim of this study was to investigate the cell turnover rate and replicative history of the bone marrow cells of ICUS patients. To this end, we examined telomere length (TL), proliferation, and apoptosis of the bone marrow cells of ICUS patients and healthy controls (HCs) using telomere quantitative fluorescence <I>in situ</I> hybridization and immunohistochemical staining for Ki-67 and cleaved caspase-3. We also performed targeted sequencing of 88 myeloid-associated genes. A total of 37 patients with ICUS were enrolled in this study, with a median age of 66 years (range: 31–83). TLs were significantly shorter in patients with ICUS than in the HCs (8.8, interquartile range [IQR] 6.8–12.1 vs 18.4, IQR 14.4–22.0, p < 0.0001). Proliferation (Ki-67-positive) and apoptosis (cleaved caspase-3-positive) were significantly increased in patients with ICUS compared to HCs (median = 20.0% vs 5.0%, <I>p</I> = 0.0003; 45.0% vs 22.5%, <I>p</I> = 0.0005, respectively). The shortening of TL and the increased proliferation and apoptotic activity was also prominent in patients with ICUS without mutation and dysplasia than in HCs (p < 0.0001, p < 0.0001, and p = 0.0093, respectively). TL was not associated with mutational profile and clinical characteristics as well in patients with ICUS. To our knowledge, this is the first study to show that ICUS is associated with premature replicative senescence with increased proliferation and apoptosis of bone marrow cells. Further study is needed to address the cause of replicative exhaustion in ICUS patients.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Telomere is shortened in idiopathic cytopenia of undetermined significance (ICUS). </LI> <LI> Proliferation (Ki-67) and apoptosis activity (caspase-9) are increased in ICUS. </LI> <LI> Telomere shortening and increased Ki-67/caspase-9 is consistent in non-mutated ICUS. </LI> <LI> ICUS can be associated with premature replicative senescence. </LI> </UL> </P>