Feedback Control of Flow Separation Using Plasma Actuator and FBG Sensor

A feedback control system for mitigating flow separation was developed by using a string-type dielectric-barrier-discharge (DBD) plasma actuator and a fiber Bragg grating (FBG) sensor. Tangential jets were induced from the string-type DBD plasma actuator, which was located at 5% chord from the leading edge of an NACA0024 airfoil. The FBG sensor was attached to the interior surface near the root of the cantilever beam modeled on the pressure surface of the airfoil. The strain at the cantilever root was reflected in the form of Bragg wavelengths (λB) detected by the FBG sensor when the cantilever tip was vibrated by the flow near the trailing edge of the airfoil. It was found that calculating running standard deviations in the Bragg wavelength (λB′) detected by the sensor was valuable for judging flow separation in real time. The feedback control of flow separation on the NACA0024 airfoil was successfully demonstrated by setting λB′=0.0028 with periodic flow separations generated in a wind tunnel by oscillating a side wall of the test section with frequency fw=0.42 Hz. It was confirmed that the appearance probability of flow separation tends to decrease with a decrease in the duration for calculating λB′ and with an increase in the duration of jet injection

Astrocytic dysfunction induced by ABCA1 deficiency causes optic neuropathy

Astrocyte abnormalities have received great attention for their association with various diseases in the brain but not so much in the eye. Recent independent genome-wide association studies of glaucoma, optic neuropathy characterized by retinal ganglion cell (RGC) degeneration, and vision loss found that single-nucleotide polymorphisms near the ABCA1 locus were common risk factors. Here, we show that Abca1 loss in retinal astrocytes causes glaucoma-like optic neuropathy in aged mice. ABCA1 was highly expressed in retinal astrocytes in mice. Thus, we generated macroglia-specific Abca1-deficient mice (Glia-KO) and found that aged Glia-KO mice had RGC degeneration and ocular dysfunction without affected intraocular pressure, a conventional risk factor for glaucoma. Single-cell RNA sequencing revealed that Abca1 deficiency in aged Glia-KO mice caused astrocyte-triggered inflammation and increased the susceptibility of certain RGC clusters to excitotoxicity. Together, astrocytes play a pivotal role in eye diseases, and loss of ABCA1 in astrocytes causes glaucoma-like neuropathy

Anterior cruciate ligament-derived cells have high chondrogenic potential

Anterior cruciate ligament (ACL)-derived cells have a character different from medial collateral ligament (MCL)-derived cells. However, the critical difference between ACL and MCL is still unclear in their healing potential and cellular response. The objective of this study was to investigate the mesenchymal differentiation property of each ligament-derived cell. Both ligament-derived cells differentiated into adipogenic, osteogenic, and chondrogenic lineages. In chondrogenesis, ACL-derived cells had the higher chondrogenic property than MCL-derived cells. The chondrogenic marker genes, Sox9 and α1(II) collagen (Col2a1), were induced faster in ACL-derived pellets than in MCL-derived pellets. Sox9 expression preceded the increase of Col2a1 in both pellet-cultured cells. However, the expression level of Sox9 and a ligament/tendon transcription factor Scleraxis did not parallel the increase of Col2a1 expression along with chondrogenic induction. The present study demonstrates that the balance between Sox9 and Scleraxis have an important role in the chondrogenic differentiation of ligament-derived cells

Transcriptional Regulation of CD4+ T Cell Differentiation in Experimentally Induced Arthritis and Rheumatoid Arthritis

Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation of the joint synovium and infiltration by activated inflammatory cells. CD4+ T cells form a large proportion of the inflammatory cells invading the synovial tissue, and are involved in the RA pathologic process. In general, CD4+ T cells differentiate into various T helper cell subsets and acquire the functional properties to respond to specific pathogens, and also mediate some autoimmune disorders such as RA. Because the differentiation of T helper cell subsets is determined by the expression of specific transcription factors in response to the cytokine environment, these transcription factors are considered to have a role in the pathology of RA. Treg cells control an excess of T cell–mediated immune response, and the transcription factor FoxP3 is critical for the differentiation and function of Treg cells. Treg cell dysfunction can result in the development of systemic autoimmunity. In this review, we summarize how the expression of transcription factors modulates T helper cell immune responses and the development of autoimmune diseases, especially in RA. Understanding the role of transcription factors in the pathogenesis of autoimmunity may lead to novel therapeutic strategies to control the differentiation and function of both T helper cells and Treg cells

Japanese glaciological activities at NEEM, Greenland

第2回極域科学シンポジウム　氷床コアセッション 11月16日（水） 国立極地研究所 2階大会議室前フロ

Effects of Input Voltage on Flow Separation Control for Low-Pressure Turbine at Low Reynolds Number by Plasma Actuators

Active flow control using dielectric barrier discharge (DBD) plasma actuators was investigated to reattach the simulated boundary layer separation on the suction surface of a turbine blade at low Reynolds number, Re = 1.7 × 104. The flow separation is induced on a curved plate installed in the test section of a low-speed wind tunnel. Particle image velocimetry (PIV) was used to obtain instantaneous and time-averaged two-dimensional velocity measurements. The amplitude of input voltage for the plasma actuator was varied from ±2.0 kV to ±2.8 kV. The separated flow reattached on the curved wall when the input voltage was ±2.4 kV and above. The displacement thickness of the boundary layer near the trailing edge decreased by 20% at ±2.0 kV. The displacement thickness was suddenly reduced as much as 56% at ±2.2 kV, and it was reduced gradually from ±2.4 kV to ±2.8 kV (77% reduction). The total pressure loss coefficient, estimated from the boundary layer displacement thickness and momentum thickness, was 0.172 at the baseline (actuator off) condition. The total pressure loss was reduced to 0.107 (38% reduction) at ±2.2 kV and 0.078 (55% reduction) at ±2.8 kV

Effects of Input Voltage and Freestream Velocity on Active Flow Control of Passage Vortex in a Linear Turbine Cascade Using Dielectric Barrier Discharge Plasma Actuator

Passage vortex exists as one of the typical secondary flows in turbomachines and generates a significant total pressure loss and degrades the aerodynamic performance. Herein, a dielectric barrier discharge (DBD) plasma actuator was utilized for an active flow control of the passage vortex in a linear turbine cascade. The plasma actuator was installed on the endwall, 10 mm upstream from the leading edge of the turbine cascade. The freestream velocity at the outlet of the linear turbine cascade was set to range from UFS,out = 2.4 m/s to 25.2 m/s, which corresponded to the Reynolds number ranging from Reout = 1.0 × 104 to 9.9 × 104. The two-dimensional velocity field at the outlet of the linear turbine cascade was experimentally analyzed by particle image velocimetry (PIV). At lower freestream velocity conditions, the passage vortex was almost negligible as a result of the plasma actuator operation (UPA,max/UFS,out = 1.17). Although the effect of the jet induced by the plasma actuator weakened as the freestream velocity increased, the magnitude of the peak vorticity was reduced under all freestream velocity conditions. Even at the highest freestream velocity condition of UFS,out = 25.2 m/s, the peak value of the vorticity was reduced approximately 17% by the plasma actuator operation at VAC = 15 kVp-p (UPA,max/UFS,out = 0.18)

How many electron traps are formed in persistent phosphors?

Persistent luminescence is caused by a charge carrier detrapping process from the carrier traps filled by excitation light. Thus, the carrier storage capacity is an important factor in determining the persistent luminescence intensity. Here, the electron storage capacity was investigated in the YAGG:Ce³⁺-Yb³⁺ transparent ceramic persistent phosphor, in which the Ce³⁺ ion is the luminescence center and the Yb³⁺ ion acts as the electron trap. The number density of the Yb²⁺ electron trapping center was estimated to be approximately 1.6 × 10¹⁸ ions cm⁻³ from the absorption coefficient spectrum of Yb²⁺:4f–5d photochromic absorption center and the Yb-LIII edge XANES spectrum, which means that approximately 12% of the Yb³⁺ ions in the sample were changed to the divalent state after charging. Although the maximum energy density of 0.61 J cm⁻³ was calculated as a storage property of persistent phosphors from the Yb²⁺ number density and the photon energy of Ce³⁺:5d₁−4f luminescence at 520 nm, the actual energy density which was detected as persistent luminescence was 0.011 J cm⁻³. It is suggested that the recombination efficiency of the detrapped electrons from the Yb²⁺ ions with the hole-trapped Ce³⁺ ions is approximately a few percent