Distribution and Kinematics of H I through Raman He II Spectroscopy of NGC 6302

The young planetary nebula NGC 6302 is known to exhibit Raman-scattered He II features at 6545 and 4851 Angstrom. These features are formed through inelastic scattering of He II$\lambda\lambda$ 1025 and 972 with hydrogen atoms in the ground state, for which the cross sections are $1.2 \times 10^{-21}$ and $1.4\times 10^{-22} {\rm\ cm^2}$, respectively. We investigate the spectrum of NGC 6302 archived in the ESO Science Portal. Our Gaussian line fitting analysis shows that the Raman-scattered He II features are broader and more redshifted than the hypothetical model Raman features that would be formed in a cold static H I medium. We adopt a simple scattering geometry consisting of a compact He II emission region surrounded by a H I medium to perform Monte Carlo simulations using the radiative transfer code ${\it STaRS}$. Our simulations show that the H I region is characterized by the H I column density $N_{\rm HI}=3\times 10^{21}{\rm\ cm^{-2}}$ with the random speed component $v_{\rm ran}=10{\rm\ km\ s^{-1}}$ expanding with a speed $v_{\rm exp}= 13{\rm\ km\ s^{-1}}$from the He II emission region. Based on our best fit parameters, we estimate the H I mass of the neutral medium$M_{\rm HI} \simeq 1.0\times 10^{-2}\ {\rm M_\odot}$, pointing out the usefulness of Raman He II spectroscopy as a tool to trace H I components.Comment: 12 pages, 8 figures, accepted for publication in Ap

Differences in the Fatty Acid Profile, Morphology, and Tetraacetylphytosphingosine-Forming Capability Between Wild-Type and Mutant Wickerhamomyces ciferrii

One tetraacetylphytosphingosine (TAPS)-producing Wickerhamomyces ciferrii mutant was obtained by exposing wild-type W. ciferrii to γ-ray irradiation. The mutant named 736 produced up to 9.1 g/L of TAPS (218.7 mg-TAPS/g-DCW) during batch fermentation in comparison with 1.7 g/L of TAPS (52.2 mg-TAPS/g-DCW) for the wild type. The highest production, 17.7 g/L of TAPS (259.6 mg-TAPS/g-DCW), was obtained during fed-batch fermentation by mutant 736. Fatty acid (FA) analysis revealed an altered cellular FA profile of mutant 736: decrease in C16:0 and C16:1 FA levels, and increase in C18:1 and C18:2 FA levels. Although a significant change in the cellular FA profile was observed, scanning electron micrographs showed that morphology of wild-type and mutant 736 cells was similar. Genetic alteration analysis of eight TAPS biosynthesis-related genes revealed that there are no mutations in these genes in mutant 736; however, mRNA expression analysis indicated 30% higher mRNA expression of TCS10 among the eight genes in mutant 736 than that in the wild-type. Collectively, these results imply that the enhancement of TAPS biosynthesis in mutant 736 may be a consequence of system-level genetic and physiological alterations of a complicated metabolic network. Reverse metabolic engineering based on system-level omics analysis of mutant 736 can make the mutant more suitable for commercial production of TAPS

A Case of Severe Anemia by Necator americanus Infection in Korea

This report describes clinical and parasitological findings of an 82-yr-old female patient who lived in a local rural village and suffered from severe chronic anemia for several years. She was transferred to the National Police Hospital in Seoul for management of severe dyspnea and dizziness. At admission, she showed symptoms or signs of severe anemia. Gastroduodenoscopy observed hyperemic mucosa of the duodenum and discovered numerous moving roundworms on the mucosa. Endoscopy isolated seven of them, which were identified as Necator americanus by characteristic morphology of cutting plates in the buccal cavity. The patient was treated with albendazole and supportive measures for anemia, and her physical condition much improved. This case suggests the possibility that hookworm N. americanus is still transmitted in a remote local mountainous area in Korea

Unleashing the full potential of Hsp90 inhibitors as cancer therapeutics through simultaneous inactivation of Hsp90, Grp94, and TRAP1

Cancer therapeutics: Extending a drug's reach A new drug that blocks heat shock proteins (HSPs), helper proteins that are co-opted by cancer cells to promote tumor growth, shows promise for cancer treatment. Several drugs have targeted HSPs, since cancer cells are known to hijack these helper proteins to shield themselves from destruction by the body. However, the drugs have had limited success. Hye-Kyung Park and Byoung Heon Kang at Ulsan National Institutes of Science and Technology in South Korea and coworkers noticed that the drugs were not absorbed into mitochondria, a key cellular compartment, and HSPs in this compartment were therefore not being blocked. They identified a new HSP inhibitor that can reach every cellular compartment and inhibit all HSPs. Testing in mice showed that this inhibitor effectively triggered death of tumor cells, and therefore shows promise for anti-cancer therapy. The Hsp90 family proteins Hsp90, Grp94, and TRAP1 are present in the cell cytoplasm, endoplasmic reticulum, and mitochondria, respectively; all play important roles in tumorigenesis by regulating protein homeostasis in response to stress. Thus, simultaneous inhibition of all Hsp90 paralogs is a reasonable strategy for cancer therapy. However, since the existing pan-Hsp90 inhibitor does not accumulate in mitochondria, the potential anticancer activity of pan-Hsp90 inhibition has not yet been fully examined in vivo. Analysis of The Cancer Genome Atlas database revealed that all Hsp90 paralogs were upregulated in prostate cancer. Inactivation of all Hsp90 paralogs induced mitochondrial dysfunction, increased cytosolic calcium, and activated calcineurin. Active calcineurin blocked prosurvival heat shock responses upon Hsp90 inhibition by preventing nuclear translocation of HSF1. The purine scaffold derivative DN401 inhibited all Hsp90 paralogs simultaneously and showed stronger anticancer activity than other Hsp90 inhibitors. Pan-Hsp90 inhibition increased cytotoxicity and suppressed mechanisms that protect cancer cells, suggesting that it is a feasible strategy for the development of potent anticancer drugs. The mitochondria-permeable drug DN401 is a newly identified in vivo pan-Hsp90 inhibitor with potent anticancer activity

Long-term trends in smoking prevalence and its socioeconomic inequalities in Korea, 1992–2016

Background The aim of this study was to investigate long-term trends in smoking prevalence and its socioeconomic inequalities in Korea. Methods Data were collected from 10 rounds of the Social Survey of Statistics Korea between 1992 and 2016. A total of 524,866 men and women aged 19 or over were analyzed. Age-adjusted smoking prevalence was calculated according to three major socioeconomic position indicators: education, occupational class, and income. The prevalence difference, prevalence ratio, slope index of inequality (SII), and relative index of inequality (RII) were calculated to examine the magnitude of inequality in smoking. Results Smoking prevalence among men decreased from 71.7% in 1992 to 39.7% in 2016, while smoking prevalence among women decreased from 6.5% in 1992 to 3.3% in 2016. Socioeconomic inequalities in smoking prevalence according to the three socioeconomic position indicators were found in both men and women throughout the study period. In general, absolute and relative socioeconomic inequalities in smoking, measured by prevalence difference and prevalence ratio for education and occupational class, widened during the study period among Korean men and women. In men, the SII for income increased from 7.6% in 1999 to 10.8% in 2016 and the RII for income also increased from 1.11 in 1999 to 1.31 in 2016. In women, the SII for income increased from 0.1% in 1999 to 2.4% in 2016 and the RII for income increased from 1.39 in 1999 to 2.25 in 2016. Conclusion Pro-rich socioeconomic inequalities in smoking prevalence were found in men and women. Socioeconomic inequalities in smoking have increased in parallel with the implementation of tobacco control policies. Tobacco control policies should be developed to decrease socioeconomic inequalities in cigarette use in Korea.This paper has been adapted and developed from a research report, titled A Simulation Study on the Impact of Changes in Smoking Inequalities according to Tobacco Control Policies, which was supported by the Korea Health Promotion Institute. This study was also supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) funded by the Ministry of Health & Welfare (Grant No. HI18C0446) and the Mid-career Researcher Program of the National Research Foundation (NRF) funded by the Ministry of Science & ICT (2017R1A2A2A05069746)

In vitro activity of gemifloxacin against recent clinical isolates of bacteria in Korea.

Gemifloxacin is an enhanced-affinity fluoroquinolone with broad-spectrum antibacterial activity. In Korea, resistant bacteria are relatively more prevalent than in other industrialized countries. In this study, we studied the in vitro activities of gemifloxacin, gatifloxacin, moxifloxacin, levofloxacin, ciprofloxacin, and other commonly used antimicrobial agents against 1,689 bacterial strains isolated at four Korean university hospitals during 1999-2000. Minimum inhibitory concentrations (MICs) were determined using the agar dilution method of National Committee for Clinical Laboratory Standards. Gemifloxacin had the lowest MICs for the respiratory pathogens: 90% of Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae were inhibited by 0.06, 0.03, and 0.03 mg/L, respectively. Gemifloxacin was more active than the other fluoroquinolones against methicillin-susceptible Staphylococcus aureus, coagulase-negative staphylococci, streptococci, and Enterococcus faecalis. The MIC90s of gemifloxacin for Klebsiella oxytoca, Proteus vulgaris, and non-typhoidal Salmonella spp. were 0.25, 1.0, and 0.12 mg/L, respectively, while those for other Gram-negative bacilli were 4-64 mg/L. In conclusion, gemifloxacin was the most active among the comparative agents against Gram-positive species, including respiratory pathogens isolated in Korea

Role of Hydrogen in Active Layer of Oxide-Semiconductor-Based Thin Film Transistors

Hydrogen in oxide systems plays a very important role in determining the major physical characteristics of such systems. In this study, we investigated the effect of hydrogen in oxide host systems for various oxygen environments that acted as amorphous oxide semiconductors. The oxygen environment in the sample was controlled by the oxygen gas partial pressure in the radio-frequency-sputtering process. It was confirmed that the hydrogen introduced by the passivation layer not only acted as a “killer” of oxygen deficiencies but also as the “creator” of the defects depending on the density of oxide states. Even if hydrogen is not injected, its role can change owing to unintentionally injected hydrogen, which leads to conflicting results. We discuss herein the correlation with hydrogen in the oxide semiconductor with excess or lack of oxygen through device simulation and elemental analysis. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.1

Activation of PERK Signaling Attenuates Aβ-Mediated ER Stress

Alzheimer's disease (AD) is characterized by the deposition of aggregated beta-amyloid (Aβ), which triggers a cellular stress response called the unfolded protein response (UPR). The UPR signaling pathway is a cellular defense system for dealing with the accumulation of misfolded proteins but switches to apoptosis when endoplasmic reticulum (ER) stress is prolonged. ER stress is involved in neurodegenerative diseases including AD, but the molecular mechanisms of ER stress-mediated Aβ neurotoxicity still remain unknown. Here, we show that treatment of Aβ triggers the UPR in the SK-N-SH human neuroblastoma cells. Aβ mediated UPR pathway accompanies the activation of protective pathways such as Grp78/Bip and PERK-eIF2α pathway, as well as the apoptotic pathways of the UPR such as CHOP and caspase-4. Knockdown of PERK enhances Aβ neurotoxicity through reducing the activation of eIF2α and Grp8/Bip in neurons. Salubrinal, an activator of the eIF2α pathway, significantly increased the Grp78/Bip ER chaperone resulted in attenuating caspase-4 dependent apoptosis in Aβ treated neurons. These results indicate that PERK-eIF2α pathway is a potential target for therapeutic applications in neurodegenerative diseases including AD