28 research outputs found

    Enhanced second-harmonic generation in strained germanium-on-insulator microdisks for integrated quantum photonic technologies

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    Quantum photonic circuits have recently attracted much attention owing to the potential to achieve exceptional performance improvements over conventional classical electronic circuits. Second-order χ(2) nonlinear processes play an important role in the realization of several key quantum photonic components. However, owing to their centrosymmetric nature, CMOS-compatible materials including silicon (Si) and germanium (Ge) traditionally do not possess the χ(2) response. Recently, second-harmonic generation (SHG) that requires the χ(2) response was reported in Ge, but no attempts at enhancing the SHG signal have been conducted and proven experimentally. Herein, we demonstrate the effect of strain on SHG from Ge by depositing a silicon nitride (Si3N4) stressor layer on Ge-on-insulator (GOI) microdisks. This approach allows the deformation of the centrosymmetric unit cell structure of Ge, which can further enhance the χ(2) nonlinear susceptibility for SHG emission. The experimental observation of SHG under femtosecond optical pumping indicates a clear trend of enhancement in SHG signals with increasing strain. Such improvements boost conversion efficiencies by 300% when compared to the control counterpart. This technique paves the way toward realizing a CMOS-compatible material with nonlinear characteristics, presenting unforeseen opportunities for its integration in the semiconductor industry.Agency for Science, Technology and Research (A*STAR)Ministry of Education (MOE)National Research Foundation (NRF)Ministry of Education - Singapore (AcRF TIER 1 (RG115/21)); iGrant of Singapore (A*STAR AME IRG (A2083c0053)); National Research Foundation Singapore (Competitive Research Program (NRF-CRP19-2017-01)); NRF-A*STAR Joint Grant (Quantum Engineering Program (NRF2022-QEP2-02-P13))

    Targeted Transgenic Overexpression of Mitochondrial Thymidine Kinase (TK2) Alters Mitochondrial DNA (mtDNA) and Mitochondrial Polypeptide Abundance : Transgenic TK2, mtDNA, and Antiretrovirals

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    Mitochondrial toxicity limits nucleoside reverse transcriptase inhibitors (NRTIs) for acquired immune deficiency syndrome. NRTI triphosphates, the active moieties, inhibit human immunodeficiency virus reverse transcriptase and eukaryotic mitochondrial DNA polymerase pol-Îł. NRTI phosphorylation seems to correlate with mitochondrial toxicity, but experimental evidence is lacking. Transgenic mice (TGs) with cardiac overexpression of thymidine kinase isoforms (mitochondrial TK2 and cytoplasmic TK1) were used to study NRTI mitochondrial toxicity. Echocardiography and nuclear magnetic resonance imaging defined cardiac performance and structure. TK gene copy and enzyme activity, mitochondrial (mt) DNA and polypeptide abundance, succinate dehydrogenase and cytochrome oxidase histochemistry, and electron microscopy correlated with transgenesis, mitochondrial structure, and biogenesis. Antiretroviral combinations simulated therapy. Untreated hTK1 or TK2 TGs exhibited normal left ventricle mass. In TK2 TGs, cardiac TK2 gene copy doubled, activity increased 300-fold, and mtDNA abundance doubled. Abundance of the 17-kd subunit of complex I, succinate dehydrogenase histochemical activity, and cristae density increased. NRTIs increased left ventricle mass 20% in TK2 TGs. TK activity increased 3 logs in hTK1 TGs, but no cardiac phenotype resulted. NRTIs abrogated functional effects of transgenically increased TK2 activity but had no effect on TK2 mtDNA abundance. Thus, NRTI mitochondrial phosphorylation by TK2 is integral to clinical NRTI mitochondrial toxicity
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