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Narcissin is a natural flavonoid from some edible and traditional medicinal plants. It has been proven to have multiple biological functions and exhibits potential therapeutic effects on hypertension, cancer, and Alzheimer's disease. However, the toxicity of narcissin is largely unknown. Here, we revealed that narcissin treatment led to reduced hatchability, increased malformation rate, shorter body length, and slowed blood flow in zebrafish. Furthermore, bradycardia, pericardial edema, increased SV‐BA distance, diminished stroke volume, ejection fraction, and ventricular short‐axis shortening rate were also found. A large accumulation of ROS, increased apoptotic cells, and histopathological changes were detected in the heart region. Moreover, the gene expression profiles and molecular docking analysis indicated that Nrf2/HO‐1 and calcium signaling pathways were involved in narcissin‐induced toxicity. In conclusion, here we provide the first evidence that demonstrates narcissin‐induced developmental toxicity and cardiotoxicity in zebrafish via Nrf2/HO‐1 and calcium signaling pathways for the first time. Narcissin is a natural flavonoid from some edible and traditional medicinal plants, while its toxicity is largely unknown. Here, we revealed that narcissin treatment led to reduced hatchability, increased malformation rate, shorter body length, slowed blood flow, and cardiodevelopmental toxicity in zebrafish. A large accumulation of ROS, increased apoptotic cells, and histopathological changes were detected in the heart region. Nrf2/HO‐1 and calcium signaling pathways were involved in narcissin‐induced toxicity. [ABSTRACT FROM AUTHOR]

Implementing and integrating spiking neurons for neuromorphic hardware realization conforming to spiking neural networks holds great promise in enabling efficient learning and decision‐making. The spiking neurons, however, may lack the spiking dynamics to encode the dynamical information in complex real‐world problems. Herein, using filamentary memristors from solution‐processed hexagonal boron nitride, this study assembles leaky integrate‐and‐fire spiking neurons and, particularly, harnesses the common switching stochasticity feature in the memristors to allow key neural dynamics, including Poisson‐like spiking and adaptation. The neurons, with the dynamics fitted via hardware‐algorithm codesign, suggest a potential in realizing spike‐based neuromorphic hardware capable of handling complex problems. Simulation of an autoencoder for anomaly detection of time‐series real analog and digital data from physical systems is demonstrated, underscoring its promising prospect in applications, especially, at the edges with limited computation resources, for instance, auto‐pilot, manufacturing, wearables, and Internet of things. [ABSTRACT FROM AUTHOR]

Single-nucleotide polymorphisms (SNPs) of microRNA (miRNA) (miRSNP) are SNPs located on miRNA genes or miRNA target sites, which have been supposed to be involved in the development of central nervous system diseases by interfering with miRNA-mediated regulatory functions. However, the association of miRSNP with post-stroke depression (PSD) has not been well-investigated. In this study, we collected 54 PSD risk genes via manual literature-mining and integrated PSD-related risk pathways based on multiple public databases. Furthermore, we systematically screened candidate functional miRSNPs for PSD and integrated a miRSNP-based PSD-associated pathway network, which included 99 miRNAs that target 12 PSD risk pathways. We also reviewed the association between three risk pathways and PSD pathogenetic mechanism thoroughly. Combining literature mining and network analysis, our results proposed an underlying mechanism of “miRSNP → miRNA → risk gene → pathway” axis effects on PSD pathogenesis, especially for rs28457673 (miR-15/16/195/424/497 family) → IGF1R → hsa04010 (MAPK signaling pathway). Our studies revealed a functional role in genetic modifier at the system level in the pathogenesis of PSD, which might provide further information for the miRSNP studies in PSD.