Direct training high-performance deep spiking neural networks: a review of theories and methods.

Spiking neural networks (SNNs) offer a promising energy-efficient alternative to artificial neural networks (ANNs), in virtue of their high biological plausibility, rich spatial-temporal dynamics, and event-driven computation. The direct training algorithms based on the surrogate gradient method provide sufficient flexibility to design novel SNN architectures and explore the spatial-temporal dynamics of SNNs. According to previous studies, the performance of models is highly dependent on their sizes.

SGLFormer: Spiking Global-Local-Fusion Transformer with high performance.

Introduction: Spiking Neural Networks (SNNs), inspired by brain science, offer low energy consumption and high biological plausibility with their event-driven nature. However, the current SNNs are still suffering from insufficient performance.

Methods: Recognizing the brain's adeptness at information processing for various scenarios with complex neuronal connections within and across regions, as well as specialized neuronal architectures for specific functions, we propose a Spiking Global-Local-Fusion Transformer (SGLFormer), that significantly improves the performance of SNNs.

DCAF1 regulates Treg senescence via the ROS axis during immunological aging.

As a hallmark of immunological aging, low-grade, chronic inflammation with accumulation of effector memory T cells contributes to increased susceptibility to many aging-related diseases. While the proinflammatory state of aged T cells indicates a dysregulation of immune homeostasis, whether and how aging drives regulatory T cell (Treg) aging and alters Treg function are not fully understood owing to a lack of specific aging markers. Here, by a combination of cellular, molecular, and bioinformatic approaches, we discovered that Tregs senesce more severely than conventional T (Tconv) cells during aging.

PHB Associates with the HIRA Complex to Control an Epigenetic-Metabolic Circuit in Human ESCs.

The chromatin landscape and cellular metabolism both contribute to cell fate determination, but their interplay remains poorly understood. Using genome-wide siRNA screening, we have identified prohibitin (PHB) as an essential factor in self-renewal of human embryonic stem cells (hESCs). Mechanistically, PHB forms protein complexes with HIRA, a histone H3.

Comprehensive profiling reveals mechanisms of SOX2-mediated cell fate specification in human ESCs and NPCs.

SOX2 is a key regulator of multiple types of stem cells, especially embryonic stem cells (ESCs) and neural progenitor cells (NPCs). Understanding the mechanism underlying the function of SOX2 is of great importance for realizing the full potential of ESCs and NPCs. Here, through genome-wide comparative studies, we show that SOX2 executes its distinct functions in human ESCs (hESCs) and hESC-derived NPCs (hNPCs) through cell type- and stage-dependent transcription programs.

Stk40 represses adipogenesis through translational control of CCAAT/enhancer-binding proteins.

A better understanding of molecular regulation in adipogenesis might help the development of efficient strategies to cope with obesity-related diseases. Here, we report that CCAAT/enhancer-binding protein (C/EBP) β and C/EBPδ, two crucial pro-adipogenic transcription factors, are controlled at a translational level by serine/threonine kinase 40 (Stk40). Genetic knockout (KO) or knockdown (KD) of Stk40 leads to increased protein levels of C/EBP proteins and adipocyte differentiation in mouse embryonic fibroblasts (MEFs), fetal liver stromal cells, and mesenchymal stem cells (MSCs).

Nucleolin maintains embryonic stem cell self-renewal by suppression of p53 protein-dependent pathway.

Embryonic stem cells (ESCs) can undergo unlimited self-renewal and retain pluripotent developmental potential. The unique characteristics of ESCs, including a distinct transcriptional network, a poised epigenetic state, and a specific cell cycle profile, distinguish them from somatic cells. However, the molecular mechanisms underlying these special properties of ESCs are not fully understood.