103 research outputs found

    An Evaluation of Relative Damage to the Powertrain System in Tracked Vehicles

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    The objective of this study was to improve the reliability of the endurance test for the powertrain system of military tracked vehicles. The measurement system that measures the driving duty applied to the powertrain system caused by mobility on roads consists of eight analog channels and two pulse channels, including the propeller shaft output torques for the left and right sides. The data obtained from this measurement system can be used to introduce a new technology that produces the output torque of a torque converter and that can be applied to analyze the revolution counting for the endurance and road mobility in the front unit and represent the relative fatigue damages analysis technique and its results according to the driven roads through a cumulative fatigue method

    A New Method for Investigation of the Hair Shaft: Hard X-Ray Microscopy with a 90-nm Spatial Resolution

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    Various methods have been used to investigate the hair shaft. In the ultrastructural hair field, scanning and transmission electron microscopies are widely used investigative methods, but they have some technical limitations. Recently, X-ray microscopes with sub-micron spatial resolution have emerged as useful instruments because they offer a unique opportunity to observe the interior of an undamaged sample in greater detail. In this report, we examined damaged hair shaft tips using hard X-ray microscopy with a 90 nm spatial resolution. The results of this study suggest that hard X-ray microscopy is an alternative investigative method for hair morphology studies

    Factors Associated with HIV-1 Proviral DNA Loads in Patients with Undetectable Plasma RNA Load

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    To evaluate factors associated with human immunodeficiency virus type 1 (HIV-1) proviral DNA load, we conducted a cross-sectional study of 36 chronically HIV-1-infected individuals with undetectable plasma viral RNA. We used real-time polymerase chain reaction to determine the number of HIV-1 proviral DNA copies per 106 peripheral blood mononuclear cells. The mean level of plasma viral RNA when the CD4+ T cell count was above 500 cells/µL without highly active antiretroviral therapy (HAART) was significantly associated with proviral DNA load at the time of undetectable plasma HIV RNA with HAART. Strategies to reduce the level of plasma viral RNA when patients' CD4+ T cell counts are above 500 cells/µL without HAART could help reduce HIV-1 proviral DNA load

    Characteristics of greenhouse gas concentrations derived from ground-based FTS spectra at Anmyeondo, South Korea

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    Since the late 1990s, the meteorological observatory established in Anmyeondo (36.5382° N, 126.3311° E, and 30 m above mean sea level) has been monitoring several greenhouse gases such as CO_2, CH_4, N_2O, CFCs, and SF_6 as a part of the Global Atmosphere Watch (GAW) Program. A high resolution ground-based (g-b) Fourier transform spectrometer (FTS) was installed at this observation site in 2013 and has been operated within the frame work of the Total Carbon Column Observing Network (TCCON) since August 2014. The solar spectra recorded by the g-b FTS cover the spectral range 3800 to 16 000 cm^(−1) at a resolution of 0.02 cm^(−1). In this work, the GGG2014 version of the TCCON standard retrieval algorithm was used to retrieve total column average CO_2 and CH_4 dry mole fractions (XCO_2, XCH_4) and from the FTS spectra. Spectral bands of CO_2 (at 6220.0 and 6339.5 cm^(−1) center wavenumbers, CH_4 at 6002 cm^(−1) wavenumber, and O_2 near 7880 cm^(−1)) were used to derive the XCO_2 and XCH_4. In this paper, we provide comparisons of XCO_2 and XCH_4 between the aircraft observations and g-b FTS over Anmyeondo station. A comparison of 13 coincident observations of XCO_2 between g-b FTS and OCO-2 (Orbiting Carbon Observatory) satellite measurements are also presented for the measurement period between February 2014 and November 2017. OCO-2 observations are highly correlated with the g-b FTS measurements (r^2 = 0.884) and exhibited a small positive bias (0.189 ppm). Both data set capture seasonal variations of the target species with maximum and minimum values in spring and late summer, respectively. In the future, it is planned to further utilize the FTS measurements for the evaluation of satellite observations such as Greenhouse Gases Observing Satellite (GOSAT, GOSAT-2). This is the first report of the g-b FTS observations of XCO_2 species over the Anmyeondo station

    Cystic Fibrosis in Korean Children: A Case Report Identified by a Quantitative Pilocarpine Iontophoresis Sweat Test and Genetic Analysis

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    Cystic fibrosis (CF) is inherited as an autosomal recessive trait, and the mutations in cystic fibrosis transmembrane conductance regulator (CFTR) gene contributes to the CF syndrome. Although CF is common in Caucasians, it is known to be rare in Asians. Recently, we experienced two cases of CF in Korean children. The patients were girls with chronic productive cough since early infancy. Chest computed tomography showed the diffuse bronchiectasis in both lungs, and their diagnosis was confirmed by the repeated analysis of a quantitative pilocarpine iontophoresis test (QPIT). The sweat chloride concentrations of the first patient were 108.1 mM/L and 96.7 mM/L. The genetic analysis revealed that she was the compound heterozygote of Q1291X and IVS8 T5-M470V. In the second case, the sweat chloride concentrations were 95.0 mM/L and 77.5 mM/L. Although we performed a comprehensive search for the coding regions and exon-intron splicing junctions of CFTR gene, no obvious disease-related mutations were detected in the second case. To our knowledge, this is the first report of CF in Korean children identified by a QPIT and genetic analysis. The possibility of CF should be suspected in those patients with chronic respiratory symptoms even in Korea

    CUGBP2 directly interacts with U2 17S snRNP components and promotes U2 snRNA binding to cardiac troponin T pre-mRNA

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    CUGBP2 (ETR-3/NAPOR/BRUNOL3) promotes inclusion of cardiac troponin T (cTNT) exon 5 via binding between positions 21 and 74 of the downstream intron. The molecular mechanism by which CUGBP2 activates cTNT exon 5 inclusion is unknown. Our results suggest that CUGBP2 promotes exon inclusion by a novel mechanism in which CUGBP2 directly interacts with components of the activated U2 snRNP and enhances binding of U2 snRNP to the branch site located upstream of the exon. Using an in vitro splicing assay, we show that recombinant CUGBP2 enhances complex A formation of a cTNT pre-mRNA. Enhanced complex A assembly requires both the upstream and downstream introns consistent with dual requirements for the downstream CUGBP2-binding site and an upstream branch site for U2 snRNP binding. We also show that CUGBP2 enhances binding of U2 snRNA to the cTNT pre-mRNA consistent with enhanced complex A assembly. Purification of CUGBP2-interacting proteins using tandem affinity purification leads to the demonstration that the core 17S U2 snRNP components, SF3b145 and SF3b49 bind directly to CUGBP2. We conclude that CUGBP2 activates exon inclusion by forming direct interactions with components of the 17S snRNP complex and recruits and/or stabilizes binding of U2 snRNP

    Identification of MBNL1 and MBNL3 domains required for splicing activation and repression

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    Muscleblind-like 1 (MBNL1) is a splicing regulator that controls developmentally regulated alternative splicing of a large number of exons including exon 11 of the Insulin Receptor (IR) gene and exon 5 of the cardiac Troponin T (cTNT) gene. There are three paralogs of MBNL in humans, all of which promote IR exon 11 inclusion and cTNT exon 5 skipping. Here, we identify a cluster of three binding sequences located downstream of IR exon 11 that constitute the MBNL1 response element and a weaker response element in the upstream intron. In addition, we used sequential deletions to define the functional domains of MBNL1 and MBNL3. We demonstrate that the regions required for splicing regulation are separate from the two pairs of zinc-finger RNA-binding domains. MBNL1 and MBNL3 contain core regulatory regions for both activation and repression located within an 80-amino-acid segment located downstream of the N-terminal zinc-finger pair. Deletions of these regions abolished regulation without preventing RNA binding. These domains have common features with the CUG-BP and ETR3-like Factor (CELF) family of splicing regulators. These results have identified protein domains required for splicing repression and activation and provide insight into the mechanism of splicing regulation by MBNL proteins

    Perilipin 2 (PLIN2)-Deficiency Does Not Increase Cholesterol-Induced Toxicity in Macrophages

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    Interventions on macrophages/foam cells to redirect intracellular cholesterol towards efflux pathways could become a very valuable addition to our therapeutic arsenal against atherosclerosis. However, certain manipulations of the cholesteryl ester cycle, such as the inhibition of ACAT1, an ER-resident enzyme that re-esterifies cholesterol, are not well tolerated. Previously we showed that targeting perilipin-2 (PLIN2), a major lipid droplet (LD)-associated protein in macrophages, prevents foam cell formation and protects against atherosclerosis. Here we have assessed the tolerance of PLIN2-deficient bone marrow derived macrophages (BMM) to several lipid loading conditions similar to the found during atherosclerosis development, including exposure to modified low-density lipoprotein (mLDL) and 7-ketocholesterol (7-KC), a free cholesterol (FC) metabolite, in media with or without cholesterol acceptors. BMM isolated from mice that do or do not express PLIN2 were tested for apoptosis (TUNEL and cleaved caspase-3), ER stress (CHOP induction and XBP-1 splicing), and inflammation (TNF-α and IL-6 mRNA levels). Like in other cell types, PLIN2 deficiency impairs LD buildup in BMM. However, while most stress parameters were elevated in macrophages under ACAT inhibition and 7-KC loading, PLIN2 inactivation was well tolerated. The data support the safety of targeting PLIN2 to prevent foam cell formation and atherosclerosis
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