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Towards a reduced order model of battery systems: Approximation of the cooling plate
Szardenings, Anna,Hoefer, Nathalie,Fassbender, Heike Techno-Press 2022 Coupled systems mechanics Vol.11 No.1
In order to analyse the thermal performance of battery systems in electric vehicles complex simulation models with high computational cost are necessary. Using reduced order methods, real-time applicable model can be developed and used for on-board monitoring. In this work a data driven model of the cooling plate as part of the battery system is built and derived from a computational fluid dynamics (CFD) model. The aim of this paper is to create a meta model of the cooling plate that estimates the temperature at the boundary for different heat flow rates, mass flows and inlet temperatures of the cooling fluid. In order to do so, the cooling plate is simulated in a CFD software (ANSYS Fluent ®). A data driven model is built using the design of experiment (DOE) and various approximation methods in Optimus ®. The model can later be combined with a reduced model of the thermal battery system. The assumption and simplification introduced in this paper enable an accurate representation of the cooling plate with a real-time applicable model.
강민구,김유나,이준형,Michael Szardenings,백희조,국훈,김혜란,신명근 대한진단검사의학회 2016 Annals of Laboratory Medicine Vol.36 No.2
Background: To the best of our knowledge, the association between pediatric AML and mitochondrial aberrations has not been studied. We investigated various mitochondrial aberrations in pediatric AML and evaluated their impact on clinical outcomes. Methods: Sequencing, mitochondrial DNA (mtDNA) copy number determination, mtDNA 4,977-bp large deletion assessments, and gene scan analyses were performed on the bone marrow mononuclear cells of 55 pediatric AML patients and on the peripheral blood mononuclear cells of 55 normal controls. Changes in the mitochondrial mass, mitochondrial membrane potential, and intracellular reactive oxygen species (ROS) levels were also examined. Results: mtDNA copy numbers were about two-fold higher in pediatric AML cells than in controls (P<0.0001). Furthermore, a close relationship was found between mtDNA copy number tertiles and the risk of pediatric AML. Intracellular ROS levels, mitochondrial mass, and mitochondrial membrane potentials were all elevated in pediatric AML. The frequency of the mtDNA 4,977-bp large deletion was significantly higher (P< 0.01) in pediatric AML cells, and pediatric AML patients harboring high amount of mtDNA 4,977-bp deletions showed shorter overall survival and event-free survival rates, albeit without statistical significance. Conclusions: The present findings demonstrate an association between mitochondrial genome alterations and the risk of pediatric AML.
김혜란,Stephanie Jane Won,Claire Fabian,강민구,Michael Szardenings,신명근 대한진단검사의학회 2015 Annals of Laboratory Medicine Vol.35 No.1
Mitochondria are important intracellular organelles that produce energy for cellular development, differentiation, and growth. Mitochondrial DNA (mtDNA) presents a 10- to 20-fold higher susceptibility to genetic mutations owing to the lack of introns and histone proteins. The mtDNA repair system is relatively inefficient, rendering it vulnerable to reactive oxygen species (ROS) produced during ATP synthesis within the mitochondria, which can then target the mtDNA. Under conditions of chronic inflammation and excess stress, increased ROS production can overwhelm the antioxidant system, resulting in mtDNA damage. This paper reviews recent literature describing the pathophysiological implications of oxidative stress, mitochondrial dysfunction, and mitochondrial genome aberrations in aging hematopoietic stem cells, bone marrow failure syndromes, hematological malignancies, solid organ cancers, chronic inflammatory diseases, and other diseases caused by exposure to environmental hazards.
Kim, TaeHyung,Tyndel, Marc S.,Zhang, Zhaolei,Ahn, Jaesook,Choi, Seunghyun,Szardenings, Michael,Lipton, Jeffrey H.,Kim, Hyeoung-Joon,Kim Dong Hwan, Dennis Elsevier 2017 Leukemia research Vol.59 No.-
<P><B>Abstract</B></P> <P><B>Objective</B></P> <P>The development of tyrosine kinase inhibitors (TKIs) has significantly improved the treatment of chronic myeloid leukemia (CML). However, approximately one third of patients are resistant to TKI and/or progress to advanced disease stages. TKI therapy failure has a well-known association with <I>ABL1</I> kinase domain (KD) mutations, but only around half of TKI non-responders have detectable <I>ABL1</I> KD mutations.</P> <P><B>Method</B></P> <P>We attempt to identify genetic markers associated with TKI therapy failure in 13 patients (5 resistant, 8 progressed) without <I>ABL1</I> KD mutations using whole-exome sequencing.</P> <P><B>Results</B></P> <P>In 6 patients, we detected mutations in 6 genes commonly mutated in other myeloid neoplasms: <I>ABL1</I>, <I>ASXL1</I>, <I>DNMT3A</I>, <I>IDH1</I>, <I>SETBP1</I>, and <I>TP63</I>. We then used targeted deep sequencing to validate our finding in an independent cohort consisting of 100 CML patients with varying drug responses (74 responsive, 18 resistant, and 8 progressed patients). Mutations in genes associated with epigenetic regulations such as <I>DNMT3A</I> and <I>ASXL1</I> seem to play an important role in the pathogenesis of CML progression and TKI-resistance independent of <I>ABL1</I> KD mutations.</P> <P><B>Conclusion</B></P> <P>This study suggests the involvement of other somatic mutations in the development of TKI resistant progression to advanced disease stages in CML, particularly in patients lacking <I>ABL1</I> KD mutations.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Acquisition of somatic mutation is associated with TKI therapy failure and progression in CML patients. </LI> <LI> Exome sequencing revealed mutations in 6 genes: <I>ABL1, ASXL1, DNMT3A, IDH1, SETBP1,</I> and <I>TP63.</I> </LI> <LI> Somatic mutations is responsible for TKI resistance esp. lacking <I>ABL1</I> KD mutations. </LI> </UL> </P>
Engineering of Bacteria for the Visualization of Targeted Delivery of a Cytolytic Anticancer Agent
Jiang, Sheng-Nan,Park, Seung-Hwan,Lee, Hee Jung,Zheng, Jin Hai,Kim, Hyung-Seok,Bom, Hee-Seung,Hong, Yeongjin,Szardenings, Michael,Shin, Myung Geun,Kim, Sun-Chang,Ntziachristos, Vasilis,Choy, Hyon E,Mi Elsevier 2013 Molecular therapy Vol.21 No.11