519 research outputs found
An Evaluation of Relative Damage to the Powertrain System in Tracked Vehicles
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
High-Isolation 5G Repeater Antenna Using a Novel DGS and an EBG
Repeaters have been widely used to improve communication quality and extend the coverage areas of wireless communication systems. However, mutual coupling between the Tx and Rx antennas significantly deteriorates the performance of repeater systems. This work presents a high-isolation repeater antenna operating in a frequency range of 3.6–3.7 GHz in a 5G communication system. Perpendicularly arranged microstrip patch antennas are used because this arrangement can lead to greater isolation than a parallel arrangement. However, the perpendicular arrangement results in radiation pattern distortion due to the ground mode. A novel defected ground structure (DGS) is developed to suppress the ground mode and simultaneously reduce the mutual coupling between the Tx and Rx antennas. An electromagnetic bandgap (EBG) is additionally employed to further increase isolation. The measurement results of a fabricated repeater antenna show no radiation pattern deformation and an isolation improvement of 28 dB over the repeater antenna without the DGS and EBG
Effects of 4-Week Intervention with Ulmus macrocarpa
Ulmus macrocarpa extract has been shown to have immune-related effects in animals, but no studies have yet been performed in humans. This randomized, double-blind, placebo-controlled trial was conducted to determine the effect of short-term administration of Ulmus macrocarpa Hance extract (UME) on immune function biomarkers and its safety in human subjects. Fifty-eight subjects were randomly assigned to a UME group or a placebo group. Subjects in the UME group were given 500 mg per day of UME orally for 4 weeks. Mean fluorescence intensity (MFI) of tumor necrotic factor-α increased only in the UME group at 1 week (P=0.027). The MFI of interleukin-2 decreased less significantly in the UME group than in the placebo group at 1 week (P=0.028). However, unfortunately, at 4 weeks, no intergroup differences were detected in MFIs of cytokine. In conclusion, administration of UME for 1 week increased serum TNF-α and sustains IL-2 in human, which suggests that UME increases Th1-related immune function in the short term in healthy people. However, additional studies are needed to confirm the results of this first-stage study and further trials are required to decide on optimal dosage and duration of administration. This trial is registered with ClinicalTrials.gov Identifier: NCT02414412
5-Deoxy-Δ 12,14 -Prostaglandin J 2 Down-Regulates Activin-Induced Activin Receptor, Smad, and Cytokines Expression via Suppression of NF-B and MAPK Signaling in HepG2 Cells
15-Deoxy-Δ 12,14 -prostaglandin J 2 (15d-PGJ 2 ) and activin are implicated in the control of apoptosis, cell proliferation, and inflammation in cells. We examined both the mechanism by which 15d-PGJ 2 regulates the transcription of activin-induced activin receptors (ActR) and Smads in HepG2 cells and the involvement of the nuclear factor-B (NF-B) and mitogen-activated protein kinase (MAPK) pathways in this regulation. Activin A (25 ng/mL) inhibited HepG2 cell proliferation, whereas 15d-PGJ 2 (2 M and 5 M) had no effect. Activin A and 15d-PGJ 2 showed different regulatory effects on ActR and Smad expression, NF-B p65 activity and MEK/ERK phosphorylation, whereas they both decreased IL-6 production and increased IL-8 production. When costimulated with 15d-PGJ 2 and activin, 15d-PGJ 2 inhibited the activin-induced increases in ActR and Smad expression, and decreased activin-induced IL-6 production. However, it increased activin-induced IL-8 production. In addition, 15d-PGJ 2 inhibited activininduced NF-B p65 activity and activin-induced MEK/ERK phosphorylation. These results suggest that 15d-PGJ 2 suppresses activin-induced ActR and Smad expression, down-regulates IL-6 production, and up-regulates IL-8 production via suppression of NF-B and MAPK signaling pathway in HepG2 cells. Regulation of ActR and Smad transcript expression and cytokine production involves NF-B and the MAPK pathway via interaction with 15d-PGJ 2 /activin/Smad signaling
Zur and zinc increase expression of E. coli ribosomal protein L31 through RNA-mediated repression of the repressor L31p
Bacteria can adapt in response to numerous stress conditions. One such stress condition is zinc depletion. The zinc-sensing transcription factor Zur regulates the way numerous bacterial species respond to severe changes in zinc availability. Under zinc sufficient conditions, Zn-loaded Zur (Zn2-Zur) is well-known to repress transcription of genes encoding zinc uptake transporters and paralogues of a few ribosomal proteins. Here, we report the discovery and mechanistic basis for the ability of Zur to up-regulate expression of the ribosomal protein L31 in response to zinc in E. coli. Through genetic mutations and reporter gene assays, we find that Zur achieves the up-regulation of L31 through a double repression cascade by which Zur first represses the transcription of L31p, a zinc-lacking paralogue of L31, which in turn represses the translation of L31. Mutational analyses show that translational repression by L31p requires an RNA hairpin structure within the l31 mRNA and involves the N-terminus of the L31p protein. This work uncovers a new genetic network that allows bacteria to respond to host-induced nutrient limiting conditions through a sophisticated ribosomal protein switching mechanism
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