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In this letter, reconfigurable intelligent surface (RIS) is studied from an electronic device reliability perspective. Runtimes and lifetimes of the RIS are introduced for the first time as impairment factors that degrade the system performance. In particular, Weibull distributions are used to model the runtime‐related hardware aging (HA) effect on the RIS at first. Then, a practical RIS‐assisted system model with phase‐dependent amplitude variations, residual hardware impairments, and HA effects, is obtained. Besides, closed‐form expressions of the received signal power and spectral efficiency for the proposed system are also derived. Analytical and numerical evaluations reveal that the HA effect on the RIS is the major impairment factor when the runtime is beyond the lifetime of the RIS. [ABSTRACT FROM AUTHOR]

The formation of myelin is dependent on a reciprocal and intimate relationship between neurons and the myelin-forming glia. Recently, the neurotrophin family of growth factors has been shown to regulate the complex cell–cell interactions that control myelination. Neurotrophins and their receptors influence myelin formation via two distinct mechanisms, either by acting on the neurons, changing the axonal signals that control myelination, or by acting directly on the myelin-forming glia. In this review, we will discuss research highlighting the ability of neurotrophins to both promote and inhibit the myelination process. As reflected in the work presented here, these effects are dependent on a delicate balance of which neurotrophins are expressed, and what receptors are activated. Additionally, we examine an emerging model in which the growth factors that promote the early survival and differentiation of particular sets of neurons later play important roles as key regulators in glial development. Characterizing the temporal expression and the cellular targets of neurotrophins, both during development and after injury, represents a pivotal step in developing a greater understanding of the myelination process, contributing to the development of effective treatments for demyelinating conditions. We conclude this review by discussing the potential for neurotrophins as therapeutics in the quest for remyelination. [ABSTRACT FROM AUTHOR]

Fluorescence digital imaging microscopy was used to develop a method that allows the continuous monitoring and quantitative measurement of a single myelin internode throughout its development. Using this technique, steroid hormones such as progesterone and dexamethasone were shown to reduce the time required for the initiation and to regulate the rate of myelin synthesis. Progesterone was capable of increasing the rate of myelin synthesis in Schwann cell/neuronal co-cultures in a dose-dependent manner. RT-PCR and in situ hydridization studies revealed that the mRNAs for P450scc and 3&#03B2;-hydroxysteroid dehydrogenase, the enzymes involved in progesterone biosynthesis, were induced at the onset of myelin synthesis. The progesterone receptor protein translocated into the nucleus of the neurons during myelin synthesis, suggesting that progesterone could also be affecting neuronal gene expression. Changes in gene expression caused by progesterone are being examined to identify additional factors that may control myelin formation. [ABSTRACT FROM AUTHOR]