Fundamental Bounds in Measurements for Estimating Quantum States

Quantum measurement unavoidably disturbs the state of a quantum system if any information about the system is extracted. Recently, the concept of reversing quantum measurement has been introduced and has attracted much attention. Numerous efforts have thus been devoted to understanding the fundamental relation of the amount of information obtained by measurement to either state disturbance or reversibility. Here, we experimentally prove the trade-off relations in quantum measurement with respect to both state disturbance and reversibility. By demonstrating the quantitative bound of the trade-off relations, we realize an optimal measurement for estimating quantum systems with minimum disturbance and maximum reversibility. Our results offer fundamental insights on quantum measurement and practical guidelines for implementing various quantum information protocols

Targeting Mannitol Metabolism as an Alternative Antimicrobial Strategy Based on the Structure-Function Study of Mannitol-1-Phosphate Dehydrogenase in Staphylococcus aureus

Mannitol-1-phosphate dehydrogenase (M1PDH) is a key enzyme in Staphylococcus aureus mannitol metabolism, but its roles in pathophysiological settings have not been established. We performed comprehensive structure-function analysis of M1PDH from S. aureus USA300, a strain of community-associated methicillin-resistant S. aureus, to evaluate its roles in cell viability and virulence under pathophysiological conditions. On the basis of our results, we propose M1PDH as a potential antibacterial target. In vitro cell viability assessment of ΔmtlD knockout and complemented strains confirmed that M1PDH is essential to endure pH, high-salt, and oxidative stress and thus that M1PDH is required for preventing osmotic burst by regulating pressure potential imposed by mannitol. The mouse infection model also verified that M1PDH is essential for bacterial survival during infection. To further support the use of M1PDH as an antibacterial target, we identified dihydrocelastrol (DHCL) as a competitive inhibitor of S. aureus M1PDH (SaM1PDH) and confirmed that DHCL effectively reduces bacterial cell viability during host infection. To explain physiological functions of SaM1PDH at the atomic level, the crystal structure of SaM1PDH was determined at 1.7-Å resolution. Structure-based mutation analyses and DHCL molecular docking to the SaM1PDH active site followed by functional assay identified key residues in the active site and provided the action mechanism of DHCL. Collectively, we propose SaM1PDH as a target for antibiotic development based on its physiological roles with the goals of expanding the repertory of antibiotic targets to fight antimicrobial resistance and providing essential knowledge for developing potent inhibitors of SaM1PDH based on structure-function studies.IMPORTANCE Due to the shortage of effective antibiotics against drug-resistant Staphylococcus aureus, new targets are urgently required to develop next-generation antibiotics. We investigated mannitol-1-phosphate dehydrogenase of S. aureus USA300 (SaM1PDH), a key enzyme regulating intracellular mannitol levels, and explored the possibility of using SaM1PDH as a target for developing antibiotic. Since mannitol is necessary for maintaining the cellular redox and osmotic potential, the homeostatic imbalance caused by treatment with a SaM1PDH inhibitor or knockout of the gene encoding SaM1PDH results in bacterial cell death through oxidative and/or mannitol-dependent cytolysis. We elucidated the molecular mechanism of SaM1PDH and the structural basis of substrate and inhibitor recognition by enzymatic and structural analyses of SaM1PDH. Our results strongly support the concept that targeting of SaM1PDH represents an alternative strategy for developing a new class of antibiotics that cause bacterial cell death not by blocking key cellular machinery but by inducing cytolysis and reducing stress tolerance through inhibition of the mannitol pathway

AKARI Detection of the Infrared-Bright Supernova Remnant B0104-72.3 in the Small Magellanic Cloud

We present a serendipitous detection of the infrared-bright supernova remnant (SNR) B0104-72.3 in the Small Magellanic Cloud by the Infrared Camera (IRC) onboard AKARI. An elongated, partially complete shell is detected in all four observed IRC bands covering 2.6-15 um. The infrared shell surrounds radio, optical, and X-ray emission associated with the SNR and is probably a radiative SNR shell. This is the first detection of a SNR shell in this near/mid-infrared waveband in the Small Magellanic Cloud. The IRC color indicates that the infrared emission might be from shocked H2 molecules with some possible contributions from ionic lines. We conclude that B0104-72.3 is a middle-aged SNR interacting with molecular clouds, similar to the Galactic SNR IC 443. Our results highlight the potential of AKARI IRC observations in studying SNRs, especially for diagnosing SNR shocks.Comment: 12 pages with 3 figures, accepted for publication in AKARI PASJ special issu

Metals in Particulate Pollutants Affect Peak Expiratory Flow of Schoolchildren

BACKGROUND: The contribution of the metal components of particulate pollutants to acute respiratory effects has not been adequately evaluated. Moreover, little is known about the effects of genetic polymorphisms of xenobiotic metabolism on pulmonary function. OBJECTIVES: This study was conducted to assess lung function decrement associated with metal components in particulate pollutants and genetic polymorphisms of glutathione S-transferase M1 and T1. METHODS: We studied 43 schoolchildren who were in the 3rd to 6th grades. Each student measured peak expiratory flow rate three times a day for 42 days. Particulate air concentrations were monitored every day, and the concentrations of iron, manganese, lead, zinc, and aluminum in the particles were measured. Glutathione S-transferase M1 and T1 genetic polymorphisms were determined using DNA extracted from participant buccal washings. We used a mixed linear regression model to estimate the association between peak expiratory flow rate and particulate air pollutants. RESULTS: We found significant reduction in the peak expiratory flow rate after the children’s exposure to particulate pollutants. The effect was shown most significantly 1 day after exposure to the ambient particles. Manganese and lead in the particles also reduced the peak expiratory flow rate. Genetic polymorphisms of glutathione S-transferase M1 and T1 did not significantly affect peak expiratory flow rate. CONCLUSIONS: This study demonstrated that particulate pollutants and metals such as manganese and lead in the particles are associated with a decrement of peak expiratory flow rate. These effects were robust even with consideration of genetic polymorphisms of glutathione S-transferase