Notes

Transformed cortical activation related to hand mirror overflow powered by non-dominant hand activity throughout attention-deficit/hyperactivity disorder.
Medical imaging and pathological approaches aimed at exploring the associations between COVID-19 and its VOC, with cranial nerve and abnormal nerve discharge will shed light on the rehabilitation process of brain microstructural changes related to SARS-CoV-2, and aid future research in our understanding of the treatment and prognosis of COVID-19 encephalopathy.In response to external threatening signals, animals evolve a series of defensive behaviors that depend on heightened arousal. It is believed that arousal and defensive behaviors are coordinately regulated by specific neurocircuits in the central nervous system. The ventral tegmental area (VTA) is a key structure located in the ventral midbrain of mice. The activity of VTA glutamatergic neurons has recently been shown to be closely related to sleep-wake behavior. However, the specific role of VTA glutamatergic neurons in sleep-wake regulation, associated physiological functions, and underlying neural circuits remain unclear. In the current study, using an optogenetic approach and synchronous polysomnographic recording, we demonstrated that selective activation of VTA glutamatergic neurons induced immediate transition from sleep to wakefulness and obviously increased the amount of wakefulness in mice. Furthermore, optogenetic activation of VTA glutamatergic neurons induced multiple defensive behaviors, including burrowing, fleeing, avoidance and hiding. Finally, viral-mediated anterograde activation revealed that projections from the VTA to the central nucleus of the amygdala (CeA) mediated the wake- and defense-promoting effects of VTA glutamatergic neurons. Collectively, our results illustrate that the glutamatergic VTA is a key neural substrate regulating wakefulness and defensive behaviors that controls these behaviors through its projection into the CeA. We further discuss the possibility that the glutamatergic VTA-CeA pathway may be involved in psychiatric diseases featuring with excessive defense.Working memory is a fundamental feature of biological brains for perception, cognition, and learning. In addition, learning with working memory, which has been show in conventional artificial intelligence systems through recurrent neural networks, is instrumental to advanced cognitive intelligence. However, it is hard to endow a simple neuron model with working memory, and to understand the biological mechanisms that have resulted in such a powerful ability at the neuronal level. This article presents a novel self-adaptive multicompartment spiking neuron model, referred to as SAM, for spike-based learning with working memory. SAM integrates four major biological principles including sparse coding, dendritic non-linearity, intrinsic self-adaptive dynamics, and spike-driven learning. We first describe SAM's design and explore the impacts of critical parameters on its biological dynamics. We then use SAM to build spiking networks to accomplish several different tasks including supervised learning of the MNIST dataset using sequential spatiotemporal encoding, noisy spike pattern classification, sparse coding during pattern classification, spatiotemporal feature detection, meta-learning with working memory applied to a navigation task and the MNIST classification task, and working memory for spatiotemporal learning. Our experimental results highlight the energy efficiency and robustness of SAM in these wide range of challenging tasks. The effects of SAM model variations on its working memory are also explored, hoping to offer insight into the biological mechanisms underlying working memory in the brain. The SAM model is the first attempt to integrate the capabilities of spike-driven learning and working memory in a unified single neuron with multiple timescale dynamics. The competitive performance of SAM could potentially contribute to the development of efficient adaptive neuromorphic computing systems for various applications from robotics to edge computing.
Rehabilitation of post-stroke dysphagia is an urgent clinical problem, and repetitive transcranial magnetic stimulation (rTMS) has been widely used in the study of post-stroke function. However, there is no reliable evidence-based medicine to support the effect of rTMS on post-stroke dysphagia. This review aims to evaluate the effectiveness and safety of rTMS on post-stroke dysphagia.

English-language literature published before December 20, 2021, were searched in six electronic databases. Identified articles were screened, data were extracted, and the methodological quality of included trials was assessed. Meta-analysis was performed using RevMan 5.3 software. The GRADE method was used to assess the quality of the evidence.

A total of 10 studies with 246 patients were included. Meta-analysis showed that rTMS significantly improved overall swallowing function (standardized mean difference [SMD]-0.76, 95% confidence interval (CI)-1.07 to-0.46,
< 0.0001,
= 206; moderate-quality evidence), Penetralowing function and activity of daily living ability and reduced aspiration in post-stroke patients with good acceptability and mild adverse effects.(R,S)-ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist that was originally developed as an anesthetic. Most recently, (R,S)-ketamine has been used as a rapid-acting antidepressant, and we have reported that (R,S)-ketamine can also be a prophylactic against stress in adult mice. However, most pre-clinical studies have been performed in adult mice. It is still unknown how an acute (R,S)-ketamine injection influences behavior across the lifespan (e.g., to adolescent or aged populations). Here, we administered saline or (R,S)-ketamine at varying doses to adolescent (5-week-old) and aged (24-month-old) 129S6/SvEv mice of both sexes. One hour later, behavioral despair, avoidance, locomotion, perseverative behavior, or contextual fear discrimination (CFD) was assessed. A separate cohort of mice was sacrificed 1 h following saline or (R,S)-ketamine administration. Brains were processed to quantify the marker of inflammation Cyclooxygenase 2 (Cox-2) expression to determine whether the acute effects of (R,S)-ketamine were partially mediated by changes in brain inflammation. Our findings show that (R,S)-ketamine reduced behavioral despair and perseverative behavior in adolescent female, but not male, mice and facilitated CFD in both sexes at specific doses. (R,S)-ketamine reduced Cox-2 expression specifically in ventral CA3 (vCA3) of male mice. Notably, (R,S)-ketamine was not effective in aged mice. These results underscore the need for sex- and age-specific approaches to test (R,S)-ketamine efficacy across the lifespan.
We present a novel approach that allows the estimation of morphological features of axonal fibers from data acquired
in humans. This approach allows the assessment of white matter microscopic properties non-invasively with improved specificity.

The proposed approach is based on a biophysical model of Magnetic Resonance Imaging (MRI) data and of axonal conduction velocity estimates obtained with Electroencephalography (EEG). In a white matter tract of interest, these data depend on (1) the distribution of axonal radius [
(
)] and (2) the g-ratio of the individual axons that compose this tract [
(
)].
(
) is assumed to follow a Gamma distribution with mode and scale parameters,
and θ, and
(
) is described by a power law with parameters α and β.

MRI and EEG data were recorded from 14 healthy volunteers. MRI data were collected with a 3T scanner. MRI-measured g-ratio maps were computed and sampled along the visual transcallosal tract. EEG data were recorded using a 128-lead system with a visvenues for the combined study of brain structure and function, and for
histological studies of the human brain.
The estimates of axonal radius and myelination are consistent with histological findings, illustrating the feasibility of this approach. The proposed method allows the measurement of the distribution of axonal radius and myelination within a white matter tract, opening new avenues for the combined study of brain structure and function, and for in vivo histological studies of the human brain.
Tumor-related hyperintensities in high
-value diffusion-weighted imaging (DWI) are radiologically important in the workup of gliomas. However, the white matter may also appear as hyperintense, which may conflate interpretation.

To investigate whether DWI with spherical b-tensor encoding (STE) can be used to suppress white matter and enhance the conspicuity of glioma hyperintensities unrelated to white matter.

Twenty-five patients with a glioma tumor and at least one pathology-related hyperintensity on DWI underwent conventional MRI at 3 T. The DWI was performed both with linear and spherical tensor encoding (LTE-DWI and STE-DWI). The LTE-DWI here refers to the DWI obtained with conventional diffusion encoding and averaged across diffusion-encoding directions. Retrospectively, the differences in contrast between LTE-DWI and STE-DWI, obtained at a
-value of 2,000 s/mm
, were evaluated by comparing hyperintensities and contralateral normal-appearing white matter (NAWM) both visually and quantitativelyve been missed out if only LTE-DWI was inspected.

The contrast mechanism of high
-value STE-DWI results in a stronger suppression of white matter than conventional LTE-DWI, and may, therefore, be more sensitive and specific for assessment of glioma tumors and DWI-hyperintensities.
The contrast mechanism of high b-value STE-DWI results in a stronger suppression of white matter than conventional LTE-DWI, and may, therefore, be more sensitive and specific for assessment of glioma tumors and DWI-hyperintensities.Although plenty of evidences from preclinical studies have led to potential treatments for patients with spinal cord injury (SCI), the failure to translate promising preclinical findings into clinical advances has long puzzled researchers. Thus, a more reliable combination of anatomical assessment and behavioral testing is urgently needed to improve the translational worth of preclinical studies. To address this issue, the present study was designed to relate magnetic resonance imaging (MRI)-based anatomical assessment to behavioral outcome in a rat contusion model. Rats underwent contusion with three different heights to simulate various severities of SCI, and their locomotive functions were evaluated by the grid-walking test, Louisville swim scale (LSS), especially catwalk gait analysis system and basic testing, and Basso, Beattie, Bresnahan (BBB) score. The results showed that the lesion area (LA) is a better indicator for damage assessment compared with other parameters in sagittal T2-weighted MRI (T2WI). H3B-120 research buy Although two samples are marked as outliers by the box plot analysis, LA correlated closely with all of the behavioral testing without ceiling effect and floor effect. Moreover, with a moderate severity of SCI in a contusion height of 25 mm, the smaller the LA of the spinal cord measured on sagittal T2WI the better the functional performance, the smaller the cavity region and glial scar, the more spared the myelin, the higher the volatility, and the thicker the bladder wall. We found that LA significantly related with behavior outcomes, which indicated that LA could be a proxy of damage assessment. The combination of sagittal T2WI and four types of behavioral testing can be used as a reliable scheme to evaluate the prognosis for preclinical studies of SCI.
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