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김용준,Guillaume Jourdain,손채훈,윤영빈 대한기계학회 2017 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.31 No.9
The acoustic tuning of a swirl coaxial jet injector mounted upstream a combustion chamber is investigated in the aspect of stabilization of unstable combustion. The injector, which has a primary function to mix the oxidizer injected through the central passage and the fuel injected through the peripheral holes, is designed to be used as a half-wave resonator. The least damped modes are extracted by applying Dynamic mode decomposition (DMD) and the injector length is tuned to damp the second longitudinal mode. Then, the sensitivity of the heat release perturbation to the velocity perturbation at the frequency of the second longitudinal mode is evaluated by flame transfer function calculated by DMD. The relation between these two quantities is achieved by combining two equations, that is, the Crocco’s model and the inhomogeneous wave equation, and enables us to compute Flame transfer function (FTF) at a specific mode. The gain field of FTF shows that the sensitivity of the heat release fluctuation to the inlet velocity fluctuation is minimal with the optimal injector length. The proposed approach for application of dynamic mode decomposition would be a valuable tool in tuning a resonator acoustically, computing efficiently flame transfer function, and quantifying the relative stability of a combustion chamber.
Wilson, William C.,Hornig-Do, Hue-Tran,Bruni, Francesco,Chang, Jeong Ho,Jourdain, Alexis A.,Martinou, Jean-Claude,Falkenberg, Maria,Spå,hr, Henrik,Larsson, Nils-Gö,ran,Lewis, Richard J.,Hewit Oxford University Press 2014 Human Molecular Genetics Vol.23 No.23
<P>The p.N478D missense mutation in human mitochondrial poly(A) polymerase (mtPAP) has previously been implicated in a form of spastic ataxia with optic atrophy. In this study, we have investigated fibroblast cell lines established from family members. The homozygous mutation resulted in the loss of polyadenylation of all mitochondrial transcripts assessed; however, oligoadenylation was retained. Interestingly, this had differential effects on transcript stability that were dependent on the particular species of transcript. These changes were accompanied by a severe loss of oxidative phosphorylation complexes I and IV, and perturbation of <I>de novo</I> mitochondrial protein synthesis. Decreases in transcript polyadenylation and in respiratory chain complexes were effectively rescued by overexpression of wild-type mtPAP. Both mutated and wild-type mtPAP localized to the mitochondrial RNA-processing granules thereby eliminating mislocalization as a cause of defective polyadenylation. <I>In vitro</I> polyadenylation assays revealed severely compromised activity by the mutated protein, which generated only short oligo(A) extensions on RNA substrates, irrespective of RNA secondary structure. The addition of LRPPRC/SLIRP, a mitochondrial RNA-binding complex, enhanced activity of the wild-type mtPAP resulting in increased overall tail length. The LRPPRC/SLIRP effect although present was less marked with mutated mtPAP, independent of RNA secondary structure. We conclude that (i) the polymerase activity of mtPAP can be modulated by the presence of LRPPRC/SLIRP, (ii) N478D mtPAP mutation decreases polymerase activity and (iii) the alteration in poly(A) length is sufficient to cause dysregulation of post-transcriptional expression and the pathogenic lack of respiratory chain complexes.</P>