Development of a 2-DOF Electrostatic Haptic Joystick for MRI/fMRI Applications

Abstract—This paper describes the development of a 2-DOF electrostatic haptic joystick designed for neuroscience studies in an MRI/fMRI. The joystick is fabricated using non-magnetic materials and actuated by two high-power electrostatic motor units which produce various force fields in the horizontal plane. The electrostatic motor is a synchronous drive and thus the positioning of the joystick is achieved in an open-loop control. As for force sensing, a 2-DOF force sensor is developed using non-magnetic materials and optical fibers so as to measure interaction force with a user; hence, the haptic rendering is based on the admittance control scheme that respects the rule of force-in and position-out. The operation of both the actuators and force sensor respects non-magnetic principles. Thus, the haptic joystick into which these components are integrated is expected to have high MR compatibility, although the evaluation of the MR compatibility is beyond the scope of this paper. In this paper, the device performance is evaluated in the normal environment, which verifies the operation of the unique electrostatic haptic device. T I

NADPH-oxidase 4 protects against kidney fibrosis during chronic renal injury

NADPH oxidases synthesize reactive oxygen species that may participate in fibrosis progression. NOX4 and NOX2 are NADPH oxidases expressed in the kidneys, with the former being the major renal isoform, but their contribution to renal disease is not well understood. Here, we used the unilateral urinary obstruction model of chronic renal injury to decipher the role of these enzymes using wild-type, NOX4-, NOX2-, and NOX4/NOX2-deficient mice. Compared with wild-type mice, NOX4-deficient mice exhibited more interstitial fibrosis and tubular apoptosis after obstruction, with lower interstitial capillary density and reduced expression of hypoxia-inducible factor-1α and vascular endothelial growth factor in obstructed kidneys. Furthermore, NOX4-deficient kidneys exhibited increased oxidative stress. With NOX4 deficiency, renal expression of other NOX isoforms was not altered but NRF2 protein expression was reduced under both basal and obstructed conditions. Concomitant deficiency of NOX2 did not modify the phenotype exhibited by NOX4-deficient mice after obstruction. NOX4 silencing in a mouse collecting duct (mCCD(cl1)) cell line increased TGF-β1-induced apoptosis and decreased NRF2 protein along with expression of its target genes. In addition, NOX4 silencing decreased hypoxia-inducible factor-1α and expression of its target genes in response to hypoxia. In summary, these results demonstrate that the absence of NOX4 promotes kidney fibrosis, independent of NOX2, through enhanced tubular cell apoptosis, decreased microvascularization, and enhanced oxidative stress. Thus, NOX4 is crucial for the survival of kidney tubular cells under injurious conditions