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Feature Transformation based Music Retrieval System
Jungim Heo,Jinmo Yang,Dong-hyun Kim,Kyoungro Yoon,Wonil Kim 한국지능시스템학회 2008 INTERNATIONAL JOURNAL of FUZZY LOGIC and INTELLIGE Vol.8 No.3
People have tendency of forgetting music title, though they easily remember particular part of music. If a music search system can find the title through a part of melody, this will provide very convenient interface to users. In this paper, we propose an algorithm that enables this type of search using feature transformation function. The original music is transformed to new feature information with sequential melodies. When a melody that is a part of search music is given to the system, the music retrieval system searches the music similar to the feature information of the melody. Moreover, this transformation function can be easily extended to various music recognition systems.
Ko, Byung Woong,Han, Jeongsu,Heo, Jun Young,Jang, Yunseon,Kim, Soo Jeong,Kim, Jungim,Lee, Min Joung,Ryu, Min Jeong,Song, Ik Chan,Jo, Young Suk,Kweon, Gi Ryang Informa UK (Informa Healthcare) 2016 Leukemia & lymphoma Vol.57 No.9
<P>Long-term imatinib treatment induces drug-resistant chronic myeloid leukemia (CML) cells harboring T315I gate keeper mutation of breakpoint cluster region (BCR)-ABL oncogenic kinase. However, although cell proliferation is coupled with cellular energy status in CML carcinogenesis, the metabolic characteristics of T315I-mutant CML cells have never been investigated. Here, we analyzed cell proliferation activities and metabolic phenotypes, including cell proliferation, oxygen consumption, lactate production, and redox state in the KBM5 (imatinib-sensitive) and KBM5-T315I (imatinib-resistant) CML cell lines. Interestingly, KBM5-T315I cells showed decreased cell proliferation, lactate production, fatty acid synthesis, ROS production, and down regulation of mRNA expression related to ROS scavengers, such as SOD2, catalase, GCLm, and GPx1. Taken together, our data demonstrate that the lower growth ability of KBM5-T315I CML cells might be related to the decreased expression of glycolysis-related genes and ROS levels, and this will be used to identify therapeutic targets for imatinib resistance in CML.</P>
Kim, Soo Jeong,Ryu, Min Jeong,Han, Jeongsu,Jang, Yunseon,Kim, Jungim,Lee, Min Joung,Ryu, Ilhwan,Ju, Xianshu,Oh, Eungseok,Chung, Woosuk,Kweon, Gi Ryang,Heo, Jun Young Academic Press 2017 Biochemical and biophysical research communication Vol. No.
<P><B>Abstract</B></P> <P>The derangement of tyrosine hydroxylase (TH) activity reduces dopamine synthesis and is implicated in the pathogenesis of Parkinson's disease. However, the extracellular modulator and intracellular regulatory mechanisms of TH have yet to be identified. Recently, high-mobility group box 1 (HMGB1) was reported to be actively secreted from glial cells and is regarded as a mediator of dopaminergic neuronal loss. However, the mechanism for how HMGB1 affects TH expression, particularly through the receptor for advanced glycation endproducts (RAGE), has not yet been investigated. We found that recombinant HMGB1 (rHMGB1) upregulates TH mRNA expression via simultaneous activation of JNK phosphorylation, and this induction of TH expression is blocked by inhibitors of RAGE and JNK. To investigate how TH expression levels change through the HMGB1-RAGE axis as a result of MPP<SUP>+</SUP> toxicity, we co-treated SN4741 dopaminergic cells with MPP<SUP>+</SUP> and rHMGB1. rHMGB1 blocked the reduction of TH mRNA following MPP<SUP>+</SUP> treatment without altering cell survival rates. Our results suggest that HMGB1 upregulates TH expression to maintain dopaminergic neuronal function via activating RAGE, which is dependent on JNK phosphorylation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Activation of HMGB1-RAGE stimulates the TH expression in dopaminergic neuron cells. </LI> <LI> HMGB1 regulates TH expression via phosphorylation of JNK. </LI> <LI> HMGB1 rescues the TH expression without alteration of cell viability in MPP<SUP>+</SUP> treated dopaminergic neuron cells. </LI> </UL> </P>