Neutrophil-microglia interaction drives reversible motor dysfunction in neuromyelitis optica model induced by subarachnoid AQP4-IgG.

Unlabelled: Neutrophils and neutrophil extracellular traps (NETs) contribute to early neuromyelitis optica (NMO) histopathology initiated by IgG targeting astrocytic aquaporin-4 water (AQP4) channels. Yet, the mechanisms recruiting neutrophils and their pathogenic roles in disease progression remain unclear. To investigate molecular-cellular events preceding classical complement cascade activation in a mouse NMO model, we continuously infused, via spinal subarachnoid route, a non-complement-activating monoclonal AQP4-IgG.

Trajectory Tracking Using Cumulative Risk-Sensitive Finite Impulse Response Filters.

Trajectory tracking is a critical component of autonomous driving and robotic motion control. This paper proposes a novel robust finite impulse response (FIR) filter for linear time-invariant systems, aimed at enhancing the accuracy and robustness of trajectory tracking. To address the limitations of infinite impulse response (IIR) filters in complex environments, we integrate a cumulative risk-sensitive criterion with an FIR structure.

Level-Ground and Stair Adaptation for Hip Exoskeletons Based on Continuous Locomotion Mode Perception.

Hip exoskeleton can provide assistance to users to augment movements in different scenarios. The assistive control for hip exoskeleton involves the interactions among exoskeleton, user, and environment, which depends on the environment perception (to predict locomotion) to design control strategy combined with gait mode and so on. Current exoskeleton control still needs to be improved in adaptation to continuous locomotion mode and different users.

Bayesian Transfer Filtering Using Pseudo Marginal Measurement Likelihood.

Integrating the advantage of the unbiased finite impulse response (UFIR) filter into the Kalman filter (KF) is a practical yet challenging issue, where how to effectively borrow knowledge across domains is a core issue. Existing methods often fall short in addressing performance degradation arising from noise uncertainties. In this article, we delve into a Bayesian transfer filter (BTF) that seamlessly integrates the UFIR filter into the KF through a knowledge-constrained mechanism.

Chemogenetic activation of microglial Gi signaling decreases microglial surveillance and impairs neuronal synchronization.

Microglia actively survey the brain and dynamically interact with neurons to maintain brain homeostasis. Microglial Gi protein-coupled receptors (Gi-GPCRs) play a critical role in microglia-neuron communications. However, the impact of temporally activating microglial Gi signaling on microglial dynamics and neuronal activity in the homeostatic brain remains largely unknown.

Rod-shaped microglia interact with neuronal dendrites to regulate cortical excitability in TDP-43 related neurodegeneration.

Motor cortical hyperexcitability is well-documented in the presymptomatic stage of amyotrophic lateral sclerosis (ALS). However, the mechanisms underlying this early dysregulation are not fully understood. Microglia, as the principal immune cells of the central nervous system, have emerged as important players in sensing and regulating neuronal activity.

Log-Euclidean metric based covariance propagation on SPD manifold for continuous-discrete extended Kalman filtering.

For nonlinear systems with continuous dynamic and discrete measurements, a Log-Euclidean metric (LEM) based novel scheme is proposed to refine the covariance integration steps of continuous-discrete Extended Kalman filter (CDEKF). In CDEKF, the covariance differential equation is usually integrated with regular Euclidean matrix operations, which actually ignores the Riemannian structure of underlying space and poses a limit on the further improvement of estimation accuracy. To overcome this drawback, this work proposes to define the covariance variable on the manifold of symmetric positive definite (SPD) matrices and propagate it using the Log-Euclidean metric.

CCR2 monocytes replenish border-associated macrophages in the diseased mouse brain.

Border-associated macrophages (BAMs) are tissue-resident macrophages that reside at the border of the central nervous system (CNS). Since BAMs originate from yolk sac progenitors that do not persist after birth, the means by which this population of cells is maintained is not well understood. Using two-photon microscopy and multiple lineage-tracing strategies, we determine that CCR2 monocytes are significant contributors to BAM populations following disruptions of CNS homeostasis in adult mice.

Microglial P2Y calcium signaling promotes phagocytosis and shapes neuroimmune responses in epileptogenesis.

Microglial calcium signaling is rare in a baseline state but strongly engaged during early epilepsy development. The mechanism(s) governing microglial calcium signaling are not known. By developing an in vivo uridine diphosphate (UDP) fluorescent sensor, GRAB, we discovered that UDP release is a conserved response to seizures and excitotoxicity across brain regions.

Chemogenetic activation of microglial Gi signaling decreases microglial surveillance and impairs neuronal synchronization.

Microglia actively survey the brain and dynamically interact with neurons to maintain brain homeostasis. Microglial Gi-protein coupled receptors (Gi-GPCRs) play a critical role in microglia-neuron communications. However, the impact of temporally activating microglial Gi signaling on microglial dynamics and neuronal activity in the homeostatic brain remains largely unknown.

Impaired microglial phagocytosis promotes seizure development.

In the central nervous system, triggering receptor expressed on myeloid cells 2 (TREM2) is exclusively expressed by microglia and is critical for microglial proliferation, migration, and phagocytosis. TREM2 plays an important role in neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis. However, little is known about the role TREM2 plays in epileptogenesis.

Tuning neural circuits and behaviors by microglia in the adult brain.

Microglia are the primary immune cells of the CNS, contributing to both inflammatory damage and tissue repair in neurological disorder. In addition, emerging evidence highlights the role of homeostatic microglia in regulating neuronal activity, interacting with synapses, tuning neural circuits, and modulating behaviors. Herein, we review how microglia sense and regulate neuronal activity through synaptic interactions, thereby directly engaging with neural networks and behaviors.

Microglia enhance post-anesthesia neuronal activity by shielding inhibitory synapses.

Microglia are resident immune cells of the central nervous system and play key roles in brain homeostasis. During anesthesia, microglia increase their dynamic process surveillance and interact more closely with neurons. However, the functional significance of microglial process dynamics and neuronal interaction under anesthesia is largely unknown.

Sprouting of afferent and efferent inputs to pelvic organs after spinal cord injury.

Neural plasticity occurs within the central and peripheral nervous systems after spinal cord injury (SCI). Although central alterations have extensively been studied, it is largely unknown whether afferent and efferent fibers in pelvic viscera undergo similar morphological changes. Using a rat spinal cord transection model, we conducted immunohistochemistry to investigate afferent and efferent innervations to the kidney, colon, and bladder.

TREM2 mediates MHCII-associated CD4+ T-cell response against gliomas.

Background: Myeloid cells comprise up to 50% of the total tumor mass in glioblastoma (GBM) and have been implicated in promoting tumor progression and immunosuppression. Modulating the response of myeloid cells to the tumor has emerged as a promising new approach for cancer treatment. In this regard, we focus on the Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), which has recently emerged as a novel immune modulator in peripheral tumors.

Chemogenetic approaches reveal dual functions of microglia in seizures.

Microglia are key players in maintaining brain homeostasis and exhibit phenotypic alterations in response to epileptic stimuli. However, it is still relatively unknown if these alterations are pro- or anti-epileptic. To unravel this dilemma, we employed chemogenetic manipulation of microglia using the artificial Gi-Dreadd receptor within a kainic acid (KA) induced murine seizure model.

A Learning-Free Method for Locomotion Mode Prediction by Terrain Reconstruction and Visual-Inertial Odometry.

This research introduces a novel, highly precise, and learning-free approach to locomotion mode prediction, a technique with potential for broad applications in the field of lower-limb wearable robotics. This study represents the pioneering effort to amalgamate 3D reconstruction and Visual-Inertial Odometry (VIO) into a locomotion mode prediction method, which yields robust prediction performance across diverse subjects and terrains, and resilience against various factors including camera view, walking direction, step size, and disturbances from moving obstacles without the need of parameter adjustments. The proposed Depth-enhanced Visual-Inertial Odometry (D-VIO) has been meticulously designed to operate within computational constraints of wearable configurations while demonstrating resilience against unpredictable human movements and sparse features.

Microglial P2Y calcium signaling promotes phagocytosis and shapes neuroimmune responses in epileptogenesis.

Microglial calcium signaling is rare in a baseline state but shows strong engagement during early epilepsy development. The mechanism and purpose behind microglial calcium signaling is not known. By developing an UDP fluorescent sensor, GRAB, we discovered that UDP release is a conserved response to seizures and excitotoxicity across brain regions.

Chemogenetic manipulation of CX3CR1 cells transiently induces hypolocomotion independent of microglia.

Chemogenetic approaches using Designer Receptors Exclusively Activated by Designer Drugs (DREADD, a family of engineered GPCRs) were recently employed in microglia. Here, we used Cx3cr1:R26 mice to express Gi-DREADD (hM4Di) on CX3CR1 cells, comprising microglia and some peripheral immune cells, and found that activation of hM4Di on long-lived CX3CR1 cells induced hypolocomotion. Unexpectedly, Gi-DREADD-induced hypolocomotion was preserved when microglia were depleted.

TREM2 mediates MHCII-associated CD4 T cell response against gliomas.

Triggering receptor expressed on myeloid cells 2 (TREM2) was recently highlighted as a novel immune suppressive marker in peripheral tumors. The aim of this study was to characterize expression in gliomas and investigate its contribution in glioma progression by using mouse line. Our results showed that higher expression was correlated with poor prognosis in glioma patients.

Variational Bayesian Student's-t Mixture Model With Closed-Form Missing Value Imputation for Robust Process Monitoring of Low-Quality Data.

Due to record errors, transmission interruptions, etc., low-quality process data, including outliers and missing data, commonly exist in real industrial processes, challenging the accurate modeling and reliable monitoring of the operating statuses. In this study, a novel variational Bayesian Student's-t mixture model (VBSMM) with a closed-form missing value imputation method is proposed to develop a robust process monitoring scheme for low-quality data.

Bayesian Inference for State-Space Models With Student-t Mixture Distributions.

This article proposes a robust Bayesian inference approach for linear state-space models with nonstationary and heavy-tailed noise for robust state estimation. The predicted distribution is modeled as the hierarchical Student- t distribution, while the likelihood function is modified to the Student- t mixture distribution. By learning the corresponding parameters online, informative components of the Student- t mixture distribution are adapted to approximate the statistics of potential uncertainties.

TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration.

Triggering receptor expressed on myeloid cell 2 (TREM2) is linked to risk of neurodegenerative disease. However, the function of TREM2 in neurodegeneration is still not fully understood. Here, we investigated the role of microglial TREM2 in TAR DNA-binding protein 43 (TDP-43)-related neurodegeneration using virus-mediated and transgenic mouse models.

Microglial TREM2 in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is an aggressive motor neuron degenerative disease characterized by selective loss of both upper and lower motor neurons. The mechanisms underlying disease initiation and progression are poorly understood. The involvement of nonmotor neuraxis emphasizes the contribution of glial cells in disease progress.