ABSTRACT
It is well known that the rheological properties of magnetorheological (MR) material change under a magnetic field. So far, most works on MR materials have been oriented toward actuating characteristics instead of sensing functions. In this work, to realize dynamic tactile motion, a spherical MR structure was designed as a sensor, incorporating a magnetic circuit core to provide maximum dynamic motion. After manufacturing a prototype (sample), a sinusoidal magnetic field of varying exciting frequency and magnitude was applied to the sample, and the dynamic contraction and relaxation motion depending on the exciting magnetic field was observed. Among the test results, when 10% deformation occurred, the instantaneous force generated was from 2.8 N to 8.8 N, and the force when relaxed was from 1.2 N to 3.5 N. It is also shown that the repulsive force within this range can be implemented using an acceptable input current. The special tactile sensing structure proposed in this work can be used as a sensor to measure the field-dependent viscoelastic properties of human tissues such as stomach, liver, and overall body. In addition, it could be usefully applied to robot surgery, because it can mimic the dynamic motions of various human organs under various surgical conditions.
ABSTRACT
Aquaporins (AQPs) are water channels in the cell membrane that regulate osmosis in response to rapid changes in intracellular and extracellular fluid concentration caused by extrinsic factors. While there are so many studies on the association of AQPs with muscular atrophy, sarcopenia, and Duchenne muscular dystrophy (DMD), the expression of AQP has not been verified in naturally aging mice or humans. Notably, due to the characteristics of AQPs, the difference in function cannot be evaluated without extrinsic factors such as acute water restriction. The purpose of this study was to investigate the changes in AQPs expression and function due to natural aging under acute water restriction conditions in aging mice. The expression of AQP4 was shown to decrease with aging similar to previous studies. However, for the first time, this study results confirmed that AQP1 expression increased in aging mice. In addition, the expression of Aqp1 decreased in the acute water restricted group compared to the control group after acute water restriction in aging mice. These results suggest that although the expression of AQP1 increases with aging, its function is reduced. We also confirmed that overexpression of Aqp1 can inhibit myotube differentiation and that knockdown can promote myotube differentiation through in vitro experiments. In conclusion, based on our results, we suggest that the AQP1 is an important factor in sarcopenia caused by natural aging accompanied by chronic dehydration. (AU)
Subject(s)
Animals , Aquaporin 1 , Sarcopenia/metabolism , Aquaporins/metabolism , Muscular Atrophy , Cell MembraneABSTRACT
Aquaporins (AQPs) are water channels in the cell membrane that regulate osmosis in response to rapid changes in intracellular and extracellular fluid concentration caused by extrinsic factors. While there are so many studies on the association of AQPs with muscular atrophy, sarcopenia, and Duchenne muscular dystrophy (DMD), the expression of AQP has not been verified in naturally aging mice or humans. Notably, due to the characteristics of AQPs, the difference in function cannot be evaluated without extrinsic factors such as acute water restriction. The purpose of this study was to investigate the changes in AQPs expression and function due to natural aging under acute water restriction conditions in aging mice. The expression of AQP4 was shown to decrease with aging similar to previous studies. However, for the first time, this study results confirmed that AQP1 expression increased in aging mice. In addition, the expression of Aqp1 decreased in the acute water restricted group compared to the control group after acute water restriction in aging mice. These results suggest that although the expression of AQP1 increases with aging, its function is reduced. We also confirmed that overexpression of Aqp1 can inhibit myotube differentiation and that knockdown can promote myotube differentiation through in vitro experiments. In conclusion, based on our results, we suggest that the AQP1 is an important factor in sarcopenia caused by natural aging accompanied by chronic dehydration.
Subject(s)
Aquaporins , Sarcopenia , Animals , Humans , Mice , Aquaporins/metabolism , Cell Membrane/metabolism , Sarcopenia/metabolism , WaterABSTRACT
There has been an increasing awareness of sarcopenia, which is characterized by a concomitant decrease in skeletal muscle mass and quality due to aging. Resistance exercise is considered more effective than aerobic exercise in terms of therapeutic exercise. To confirm the effect of long-term aerobic exercise in preventing sarcopenia, we evaluated the skeletal muscle mass, quality, and angiogenic capacity of super-aged mice that had undergone lifelong spontaneous exercise (LSE) through various experiments. Our findings show that LSE could maintain skeletal muscle mass, quality, and fitness levels in super-aged mice. In addition, ex vivo experiments showed that the angiogenic capacity was maintained at a high level. However, these results were not consistent with the related changes in the expression of genes and/or proteins involved in protein synthesis or angiogenesis. Based on the results of previous studies, it seems certain that the expression at the molecular level does not represent the phenotypes of skeletal muscle and angiogenesis. This is because aging and long-term exercise are variables that can affect both protein synthesis and the expression patterns of angiogenesis-related genes and proteins. Therefore, in aging and exercise-related research, various physical fitness and angiogenesis variables and phenotypes should be analyzed. In conclusion, LSE appears to maintain the potential of angiogenesis and slow the aging process to maintain skeletal muscle mass and quality. Aerobic exercise may thus be effective for the prevention of sarcopenia.
Subject(s)
Physical Conditioning, Animal , Sarcopenia , Aging/physiology , Animals , Cardiovascular Physiological Phenomena , Mice , Muscle, Skeletal/physiology , Physical Conditioning, Animal/physiology , Sarcopenia/pathologyABSTRACT
Dimerized translationally controlled tumor protein (dTCTP) initiates a variety of allergic responses in mouse models and that dTCTP-binding peptide 2 (dTBP2) attenuates the allergic inflammation by targeting dTCTP. However, the usefulness of peptide-based drugs is often limited due to their short half-lives, rapid degradation, and high levels of clearance after systemic administration. In this study, we chemically conjugated dTBP2 with 10 kDa polyethylene glycol (PEG) to improve its therapeutic potential. N-terminal mono-PEGylated dTBP2 (PEG-dTBP2) was characterized by in vitro bioactivity assay, pharmacokinetics study, and in vivo efficacy. When compared to the unmodified dTBP2, PEG-dTBP2 reduced proinflammatory cytokine IL-8 secretion in human bronchial cells by 10 to 15% and increased plasma half-life by approximately 2.5-fold in mice. This study specifically demonstrated that PEG-dTBP2 shows higher inhibitory action against ovalbumin (OVA)-induced airway inflammation in mice compared to dTBP2. Importantly, PEG-dTBP2, when administered once at 1 mg/kg, significantly reduced the migration of inflammatory cells and the levels of cytokines in the bronchoalveolar lavage fluids as well as OVA-specific IgE levels in serum. In addition, the degree of goblet cell hyperplasia and mucus secretion were significantly attenuated in the PEG-dTBP2 group compared with the control group. These results suggest that PEG-dTBP2 can be considered a potential candidate drug for regulating allergic inflammation.
Subject(s)
Inflammation , Tumor Protein, Translationally-Controlled 1 , Animals , Bronchoalveolar Lavage Fluid/chemistry , Disease Models, Animal , Humans , Inflammation/drug therapy , Inflammation/metabolism , Mice , Mice, Inbred BALB C , Ovalbumin/adverse effects , Peptides/therapeutic useABSTRACT
In this study, we experimentally demonstrate fabrication of ultra-smooth and crystalline barium titanate (BTO) films on magnesium oxide (MgO) substrates by engineering lattice strain and crystal structure via thermal treatment. We observe that oxygen-depleted deposition allows growth of highly strained BTO films on MgO substrates with crack-free surface. In addition, post-thermal treatment relaxes strain, resulting in an enhancement of ferroelectricity. Surface roughening of the BTO films caused by recrystallization during post-thermal treatment is controlled by chemical-mechanical polishing (CMP) to retain their initial ultra-smooth surfaces. From Raman spectroscopy, reciprocal space map (RSM), and capacitance-voltage (C-V) curve measurements, we confirm that the ferroelectricity of BTO films strongly depend on the relaxation of lattice strain and the phase transition from a-axis to c-axis oriented crystal structure.
ABSTRACT
We report the temperature dependence of the dielectric function ε = ε1 + iε2 and critical point (CP) energies of biaxial α-SnS in the spectral energy region from 0.74 to 6.42 eV and temperatures from 27 to 350 K using spectroscopic ellipsometry. Bulk SnS was grown by temperature gradient method. Dielectric response functions were obtained using multilayer calculations to remove artifacts due to surface roughness. We observe sharpening and blue-shifting of CPs with decreasing temperature. A strong exciton effect is detected only in the armchair direction at low temperature. New CPs are observed at low temperature that cannot be detected at room temperature. The temperature dependences of the CP energies were determined by fitting the data to the phenomenological expression that contains the Bose-Einstein statistical factor and the temperature coefficient for describing the electron-phonon interaction.