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•Single Material was used to fabricate the sensing and connection parts of the flexible strain sensor with one-step printing.•Theoretical model and experiments show that the ...dimensions of the sensor have a negligible effect on the gauge factor.•Novel fabric strain sensor fabricated using a simple manufacturing process exhibited excellent mechanical stability and fatigue life.•Good response of the fabric strain sensor for detecting human motion verifies its prospective wearable applications.
The manufacturing of flexible strain sensors for wearable electronics usually requires different conductive materials for the sensing part and the connection part. This increases the complexity, cost, and performance issues due to the mismatch of the thermo-electro-mechanical properties of the materials. Herein, a new design scheme using a single conductive material is presented for a low-cost mass-producible fabric strain sensor, where a carbon/silicone nanocomposite is screen-printed to make both parts. By exploring the dimension effect and modelling of the conductive tracks, and adopting a large difference of over 100 times in aspect ratio, this research makes the electrical response of the fabric strain sensor depend almost exclusively on the sensing part, while its connection part has a low resistance. The sensor exhibits outstanding performance with a wide working range (60% strain), adequate linearity, long fatigue life (∼50,000 cycles), and mechanical robustness, rendering it suitable for human body movement detection. Moreover, the manufacturing process is simple and low-cost ($11 per m2). Thus, the new design scheme overcomes the mismatch issue and provides an important reference value for the design of flexible resistive sensors working in a high resistance range, from ∼ 100 KΩ to several MΩ.
This paper presents a biologically-inspired saliency prediction method to imitate two main characteristics of the human perception process: focalization and orienting. The proposed network, named ...ACNet is composed of two modules. The first one is an essential concentrated module (CM), which assists the network to “see” images with appropriate receptive fields by perceiving rich multi-scale multi-receptive-field contexts of high-level features. The second is a parallel attention module (PAM), which explicitly guides the network to learn “what” and “where” is salient by simultaneously capturing global and local information with channel-wise and spatial attention mechanisms. These two modules compose the core component of the proposed method, named ACBlock, which is cascaded to progressively refine the inference of saliency estimation in a manner similar to that humans zoom in their lens to focus on the saliency. Experimental results on seven public datasets demonstrate that the proposed ACNet outperforms the state-of-the-art models without any prior knowledge or post-processing.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with growing major health impacts, particularly in countries with aging populations. The examination of neural circuit mechanisms ...in AD mouse models is a recent focus for identifying new AD treatment strategies. We hypothesize that age-progressive changes of both long-range and local hippocampal neural circuit connectivity occur in AD. Recent advancements in viral-genetic technologies provide new opportunities for semi-quantitative mapping of cell-type-specific neural circuit connections in AD mouse models. We applied a recently developed monosynaptic rabies tracing method to hippocampal neural circuit mapping studies in AD model mice to determine how local and global circuit connectivity to hippocampal CA1 excitatory neurons may be altered in the single APP knock-in (APP-KI) AD mouse model. To determine age-related AD progression, we measured circuit connectivity in age-matched littermate control and AD model mice at two different ages (3–4 vs. 10–11 months old). We quantitatively mapped the connectivity strengths of neural circuit inputs to hippocampal CA1 excitatory neurons from brain regions including hippocampal subregions, medial septum, subiculum and entorhinal cortex, comparing different age groups and genotypes. We focused on hippocampal CA1 because of its clear relationship with learning and memory and that the hippocampal formation shows clear neuropathological changes in human AD. Our results reveal alterations in circuit connectivity of hippocampal CA1 in AD model mice. Overall, we find weaker extrinsic CA1 input connectivity strengths in AD model mice compared with control mice, including sex differences of reduced subiculum to CA1 inputs in aged female AD mice compared with aged male AD mice. Unexpectedly, we find a connectivity pattern shift with an increased proportion of inputs from the CA3 region to CA1 excitatory neurons when comparing young and old AD model mice, as well as old wild-type mice and old AD model mice. These unexpected shifts in CA3-CA1 input proportions in this AD mouse model suggest the possibility that compensatory circuit increases may occur in response to connectivity losses in other parts of the hippocampal circuits. We expect that this work provides new insights into the neural circuit mechanisms of AD pathogenesis.
•Our study is the first to apply monosynaptic rabies tracing to an AD mouse model.•AD mice exhibit age-progressive and reduced hippocampal CA1 connectivity.•CA1 excitatory neuron inputs shift with hippocampal regions in AD mice.•Aged female AD mice show significantly reduced subiculum to CA1 projections.
The high fall rate of the elderly brings enormous challenges to families and the medical system; therefore, early risk assessment and intervention are quite necessary. Compared to other sensor-based ...technologies, in-shoe plantar pressure sensors, effectiveness and low obtrusiveness are widely used for long-term fall risk assessments because of their portability. While frequently-used bipedal center-of-pressure (COP) features are derived from a pressure sensing platform, they are not suitable for the shoe system or pressure insole owing to the lack of relative position information. Therefore, in this study, a definition of "weak foot" was proposed to solve the sensitivity problem of single foot features and facilitate the extraction of temporal consistency related features. Forty-four multi-dimensional weak foot features based on single foot COP were correspondingly extracted; notably, the relationship between the fall risk and temporal inconsistency in the weak foot were discussed in this study, and probability distribution method was used to analyze the symmetry and temporal consistency of gait lines. Though experiments, foot pressure data were collected from 48 subjects with 24 high risk (HR) and 24 low risk (LR) ones obtained by the smart footwear system. The final models with 87.5% accuracy and 100% sensitivity on test data outperformed the base line models using bipedal COP. The results and feature space shown the novel features of wearable plantar pressure could comprehensively evaluate the difference between HR and LR groups. Our fall risk assessment models based on these features had good generalization performance, and showed practicability and reliability in real-life monitoring situations.
Corticotropin‐releasing hormone (CRH) is an essential, evolutionarily‐conserved stress neuropeptide. In addition to hypothalamus, CRH is expressed in brain regions including amygdala and hippocampus ...where it plays crucial roles in modulating the function of circuits underlying emotion and cognition. CRH+ fibers are found in nucleus accumbens (NAc), where CRH modulates reward/motivation behaviors. CRH actions in NAc may vary by the individual's stress history, suggesting roles for CRH in neuroplasticity and adaptation of the reward circuitry. However, the origin and extent of CRH+ inputs to NAc are incompletely understood. We employed viral genetic approaches to map both global and CRH+ projection sources to NAc in mice. We injected into NAc variants of a new designer adeno‐associated virus that permits robust retrograde access to NAc‐afferent projection neurons. Cre‐dependent viruses injected into CRH‐Cre mice enabled selective mapping of CRH+ afferents. We employed anterograde AAV1‐directed axonal tracing to verify NAc CRH+ fiber projections and established the identity of genetic reporter‐labeled cells via validated antisera against native CRH. We quantified the relative contribution of CRH+ neurons to total NAc‐directed projections. Combined retrograde and anterograde tracing identified the paraventricular nucleus of the thalamus, bed nucleus of stria terminalis, basolateral amygdala, and medial prefrontal cortex as principal sources of CRH+ projections to NAc. CRH+ NAc afferents were selectively enriched in NAc‐projecting brain regions involved in diverse aspects of the sensing, processing and memory of emotionally salient events. These findings suggest multiple, complex potential roles for the molecularly‐defined, CRH‐dependent circuit in modulation of reward and motivation behaviors.
Novel viral genetic studies employing retrograde and anterograde tracing demonstrate corticotropin releasing hormone‐expressing afferent projection to the nucleus accumbens (NAc). A novel basolateral amygdala to NAc projection is identified as well as a surprising enrichment of projections from brain regions involved in stress, anxiety and emotional memory (e.g., paraventricular thalamus).
Mutations that cause intellectual disability (ID) and autism spectrum disorder (ASD) are commonly found in genes that encode for synaptic proteins. However, it remains unclear how mutations that ...disrupt synapse function impact intellectual ability. In the SYNGAP1 mouse model of ID/ASD, we found that dendritic spine synapses develop prematurely during the early postnatal period. Premature spine maturation dramatically enhanced excitability in the developing hippocampus, which corresponded with the emergence of behavioral abnormalities. Inducing SYNGAP1 mutations after critical developmental windows closed had minimal impact on spine synapse function, whereas repairing these pathogenic mutations in adulthood did not improve behavior and cognition. These data demonstrate that SynGAP protein acts as a critical developmental repressor of neural excitability that promotes the development of life-long cognitive abilities. We propose that the pace of dendritic spine synapse maturation in early life is a critical determinant of normal intellectual development.
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► Pathogenic SYNGAP1 mutations promote early maturation of hippocampal spine synapses ► Mutations lead to neonatal hyperactivity of the hippocampal trisynaptic circuit ► Mutations have greatest impact during the first 3 weeks of development ► Reversal of mutations in adults does not improve behavior and cognition
A monogenic mouse model connects premature development of hippocampal dendritic spine synapses to life-long disruptions in cognition and memory. These findings indicate that the pace of synapse maturation in early life is a critical determinant of normal intellectual development.
Until recently our approach to analyzing human genetic diseases has been to accurately phenotype patients and sequence the genes known to be associated with those phenotypes; for example, in ...thalassemia, the globin loci are analyzed. Sequencing has become increasingly accessible, and thus a larger panel of genes can be analyzed and whole exome and/or whole genome sequencing can be used when no variants are found in the candidate genes. By using such approaches in patients with unexplained anemias, we have discovered that a broad range of hitherto unrelated human red cell disorders are caused by variants in KLF1, a master regulator of erythropoiesis, which were previously considered to be extremely rare causes of human genetic disease.
Adaptive fear responses to external threats rely upon efficient relay of computations underlying contextual encoding to subcortical circuits. Brain-wide analysis of highly coactivated ensembles ...following contextual fear discrimination identified the dorsolateral septum (DLS) as a relay of the dentate gyrus-CA3 circuit. Retrograde monosynaptic tracing and electrophysiological whole-cell recordings demonstrated that DLS somatostatin-expressing interneurons (SST-INs) receive direct CA3 inputs. Longitudinal in vivo calcium imaging of DLS SST-INs in awake, behaving mice identified a stable population of footshock-responsive SST-INs during contextual conditioning whose activity tracked and predicted non-freezing epochs during subsequent recall in the training context but not in a similar, neutral context or open field. Optogenetic attenuation or stimulation of DLS SST-INs bidirectionally modulated conditioned fear responses and recruited proximal and distal subcortical targets. Together, these observations suggest a role for a potentially hard-wired DLS SST-IN subpopulation as arbiters of mobility that calibrate context-appropriate behavioral fear responses.
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