9 results about "Synapse structure" patented technology

The application relates to a synapse structure for storing positive and negative weights of a single non-volatile device, which comprises a first non-volatile memory (NVM) column, a second NVM column, a current-voltage converter (IVC), an activation function circuit, a common-mode signal calculation circuit and a common-mode signal extraction circuit; the input ends of the first NVM column and the second NVM column are directly connected with an input signal group, the output end of the first NVM column is connected with the input end of the IVC, the output end of the IVC is connected with the input end of the activation function circuit, the output end of the second NVM column is connected with the input end of the common-mode signal calculation circuit, the output end of the common-mode signal calculation circuit is connected with the input end of the common-mode signal extraction circuit, and the output end of the common-mode signal extraction circuit is connected with the output end of the first NVM column. The application reduces the device resource consumption in a neural network circuit by sharing a common-mode conductance NVM column and a simple peripheral circuit.

The invention discloses a construction method of a mouse autism intervention model, and belongs to the technical field of neurobiology and animal model construction. Comprising the following steps: S1, selecting a pregnant C57BL / 6J female mouse, performing VPA induction on the 12th to 13th embryo to form an experimental group, and injecting normal saline into another mouse to form a control group; s2, performing AAV-shRNA targeted mGluR5 virus injection on the mice in the experimental group, and retaining the injection for 15 minutes after the injection so as to avoid backflow; s3, recovering the postoperative mouse for 3 weeks, performing behavioral detection on the mouse at the age of 7 weeks, and performing protein and morphological analysis on the hippocampal tissue after an experiment; s4, carrying out behavioral experiments to evaluate ASD sample behavioral characteristics, detecting mGluR5 and PSD95 protein expression levels in the hippocampus tissues by using Western blot, and analyzing changes of synaptic structures by adopting Golgi staining. The VPA model provided by the invention can be used for wider autism research, and a model platform which is low in toxicity, easy to operate and repeatable is provided.

The invention relates to an application of L-glutamine in prevention of offspring neurodysplasia caused by prenatal air pollutant exposure. Currently, prenatal exposure to air contaminants has been widely confirmed to be associated with offspring neurodysplasia, while existing preventive strategies lack sufficient effects and coverage. In order to solve the problem, a mouse model of offspring neurodevelopment abnormality caused by prenatal PM2.5 exposure is constructed, and the prevention potential of L-glutamine is explored. Researches show that L-glutamine can significantly improve neurological behavior phenotypes such as filial generation anxiety, memory decline, social behavior defects and the like caused by prenatal PM2.5 exposure, and also can improve brain synaptic structure and related protein expression. Due to the advantages and low side effect of the natural amino acid, the L-glutamine not only shows a remarkable potential of protecting the health of a fetal nervous system, but also has a wide application prospect and economic benefits.

The application provides an attenuated, replication-controllable forward HSV tracing system and a construction method and application thereof. Specifically disclosed is a recombinant herpes simplex virus type 1 crossing a nerve synapse, which is obtained by knocking out two copies of a nerve virulence factor coding gene gamma 34.5 in a H129 strain genome, then back-supplementing an expression-controllable gamma 34.5 self-degradation recombination gene into the original gene site of gamma 34.5, and the expression-controllable gamma 34.5 self-degradation recombination gene contains the gamma 34.5 gene with a function domain participating in the cell autophagy process knocked out and a degradation sequence PEST. The herpes simplex virus provided by the application can be used as a gene transduction carrier for long-term high expression of a target gene, long-term, anterograde crossing multi-level synapse structure tracing of a nerve circuit, functional nerve circuit analysis and the like, and has wide application value in nervous system targeted gene therapy, oncolytic virus therapy, virus replication and pathogenic mechanism analysis, animal infection model establishment and the like.

The invention provides a neuroprotective effect of DIRAS1 on Alzheimer's disease (AD), and belongs to the technical field of biological medicine. The invention provides application of a reagent for overexpressing a DIRAS1 gene in preparation of a medicine for preventing and / or treating AD by taking the DIRAS1 gene as a therapeutic target of AD. The treatment of a model mouse in the embodiment finds that the DIRAS1 gene is over-expressed in the brain of the AD mouse, and the cognitive function detection finds that the recognition memory, the working memory and the long-term spatial learning memory of the AD mouse can be remarkably improved; morphological and molecular biological detection finds that deposition of A beta and excessive phosphorylation of Tau protein are reduced, and Golgi staining and western blot detection finds that damage to a synaptic structure is reduced and expression of synaptic related protein is increased. Therefore, the cognitive function, pathological characteristics and synaptic plasticity of AD mice can be improved by a method of overexpressing the DIRAS1 gene.

This invention discloses the application of ZBTB7A as a target in the preparation of products for the diagnosis or treatment of sepsis-associated encephalopathy (SAE), belonging to the field of biomedical technology. This invention confirms that ZBTB7A can serve as a diagnostic biomarker and therapeutic target for SAE, providing strong technical support for the early diagnosis and treatment of SAE. Clinical sample validation shows that the expression level of ZBTB7A in peripheral blood astrocyte-derived exosomes of SAE patients is significantly downregulated, enabling early, non-invasive auxiliary diagnosis of SAE with high clinical diagnostic efficacy. This invention clarifies that high expression of ZBTB7A can effectively inhibit the release of pro-inflammatory factors, reduce lipid peroxidation and iron overload, improve the structural and functional integrity of mitochondria, protect neuronal and synaptic structures, and significantly reverse cognitive impairment.

The circuit structure includes a first ferroelectric field effect transistor (FeFET) having a first gate electrode, a first source electrode, and a first drain electrode, and a second FeFET having a second gate electrode, a second source electrode, and a second drain electrode. The first gate electrode is connected to a word line, and the first source electrode and the second source electrode are connected to a bit line. The first drain electrode is connected to the second gate electrode and the second drain electrode is connected to a bias line. A weight synapse structure is constructed by combining the two circuit structures. A plurality of weight synapse structures are incorporated into a crossbar array.

This invention discloses a method for monitoring catering fume emissions based on edge computing, comprising the following steps: collecting catering kitchen fume sensor data, operational behavior data, and environmental parameter data; generating fume emission pulse sequences and operational stimulus pulse sequences; establishing propagation correlations to form a fume emission synaptic network; generating emission behavior neural coding sequences based on the relationship between the operational stimulus pulse sequences and the fume emission pulse sequences; marking synaptic connections as synaptic locked states when stability criteria are met; performing propagation calculations to obtain counterfactual pulse propagation paths and identifying key pollution triggering behaviors; updating synaptic connection weights to obtain a dynamic synaptic structure; and combining key pollution triggering behaviors with the dynamic synaptic structure to generate abnormal fume emission warning information. This invention utilizes counterfactual propagation and dynamic synaptic control methods to achieve causal identification of fume emissions, possessing advantages of high accuracy and robustness.

The application provides a printed circuit board defect detection method based on a pulse neural network, and comprises the following steps: S1, modeling a pulse neuron based on a biological synapse structure, encoding information to be transmitted, and setting a response function of the pulse neuron, so as to combine the pulse neurons to form a pulse neural network; S2, training the pulse neural network by using an unsupervised learning algorithm; S3, adjusting a synapse weight to obtain a desired pulse neural network; S4, acquiring image data of a printed circuit board to be detected by using an image acquisition device, processing the data, inputting the processed image data to be detected into the desired pulse neural network, judging whether the printed circuit board has defects according to the pulse neural network, and outputting a detection result. The application can detect defects of the printed circuit board with high precision and high efficiency.