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The RS775 DC motor was chosen to analyze its performance of temperature field by finite element analysis software of ANSYS workbench. The result indicates that the temperature of carbon brush and the coil rises sharply in the process of the motor coil sliding against carbon brush when the machine works in rated voltage. The main cause of the motor damage is the abrasion wear and oxidative wear due to temperature rise of contact couple. Moreover, the temperature rise of carbon brush is higher than that of the coil. The carbon brush of motor is the most vulnerable parts. The replacing carbon brush and regular maintenance should be applied to reduce the wear due to high temperature in order to extend the service life of the motor.

Necroptosis is an essential pathophysiological process in cerebral ischemia-related diseases. Therefore, targeting necroptosis may prevent cell death and provide a much-needed therapy. Ansiomycin is an inhibitor of protein synthesis which can also activate c-Jun N-terminal kinases. The present study demonstrated that anisomycin attenuated necroptosis by upregulating CHIP (carboxyl terminus of Hsc70-interacting protein) leading to the reduced levels of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3) proteins in two in vitro models of cerebral ischemia. Further exploration in this research revealed that losing neither the co-chaperone nor the ubiquitin E3 ligase function of CHIP could abolish its ability to reduce necroptosis. Collectively, this study identifies a novel means of preventing necroptosis in two in vitro models of cerebral ischemia injury through activating the expression of CHIP, and it may provide a potential target for the further study of the disease.

This paper presents the stability and bifurcation of a continuum rotor with transverse electromagnetic and bearing excitations. The rotor system is modeled as continuous beam which is excited by uniformly distributed electromagnetic force and two oil-film forces. Using the Galerkin’s method, the partial differential equation of nonlinear motion is discretized as second order ordinary differential equations. The harmonic balance method is used to determine the approximate periodic solution, then the Floquet multipliers are obtained and the stability of periodic solution can be judged. The Andronov-Hopf bifurcation is presented when the leading Floquet multiplier continually changing with rotation speed passes the unit circle on the complex plane. Bifurcation diagrams of displacement with varying rotation speed are obtained using the Runge-Kutta method. Periodic motion and quasi-periodic motions appear alternately with the rotation speed showing inherent interaction between electromagnetic force and oil-film forces.

Neurodegenerative diseases are a group of chronic progressive disorders characterized by neuronal loss. Necroptosis, a recently discovered form of programmed cell death, is a cell death mechanism that has necrosis-like morphological characteristics. Necroptosis activation relies on the receptor-interacting protein (RIP) homology interaction motif (RHIM). A variety of RHIM-containing proteins transduce necroptotic signals from the cell trigger to the cell death mediators RIP3 and mixed lineage kinase domain-like protein (MLKL). RIP1 plays a particularly important and complex role in necroptotic cell death regulation ranging from cell death activation to inhibition, and these functions are often cell type and context dependent. Increasing evidence suggests that necroptosis plays an important role in the pathogenesis of neurodegenerative diseases. Moreover, small molecules such as necrostatin-1 are thought inhibit necroptotic signaling pathway. Understanding the precise mechanisms underlying necroptosis and its interactions with other cell death pathways in neurodegenerative diseases could provide significant therapeutic insights. The present review is aimed at summarizing the molecular mechanisms of necroptosis and highlighting the emerging evidence on necroptosis as a major driver of neuron cell death in neurodegenerative diseases.

Hereditary motor and sensory neuropathy (HMSN), also known as Charcot-Marie-Tooth disease (CMT), is a genetically heterogeneous disorder that affects both sensory and motor peripheral nerves. HMSN is characterized by distal and symmetric muscle atrophy in the lower limbs and hands, foot abnormalities, and distal sensory loss. It is associated with more than 50 causative genes or loci; however, the genetic cause remains undetermined in almost 50% of HMSN cases.1,2 Acknowledgment: The authors thank the family for their participation in this study.