13 results about "Neuron death" patented technology

The invention belongs to the field of bioinformatics, and relates to an improved integrated deep learning cell communication ligand-receptor interaction prediction method. The method comprises the following steps: firstly, carrying out extraction and dimensionality reduction on biological sequence features of a ligand and a receptor, and constructing multi-modal feature input; secondly, constructing an improved deep neural network branch, introducing a batch normalization layer and a Leaky ReLU activation function, solving the problems of gradient disappearance and neuronal necrosis, and improving regularization strength to prevent overfitting; meanwhile, an enhanced heterogeneous graph auto-encoder branch is constructed, the graph embedding dimension is remarkably expanded to improve the feature capacity, and full convergence of the model is ensured by increasing training rounds; thirdly, fusing the improved deep network with the prediction probability of a heterogeneous graph auto-encoder by adopting a weighted integration strategy; and finally, outputting a potential interaction relationship based on the fusion probability. By optimizing the architecture and the strategy, the prediction accuracy and robustness are remarkably improved, and a reliable tool is provided for analyzing a complex cell communication network.

The application belongs to the field of control system design, and discloses a thrust estimation method based on a time domain convolution network, and proposes a thrust estimator based on a multilayer residual time domain convolution network. On the one hand, a Gaussian error linear unit activation function is used to replace the correction linear unit in the residual block to solve the neuron death problem. On the other hand, the overall structure of the multilayer convolution network is adjusted by using residual connection, so that the network training speed and the thrust estimation effect are further improved. The comparison results with the traditional seven methods show that the method has significant advantages in convergence speed and estimation accuracy. In addition, the application also applies the method to an actual control system of an aero-engine, and further verifies the real-time performance and feasibility of the control scheme through a micro turbojet engine test bed test.

This invention relates to the field of pharmaceutical technology for treating diseases related to heavy metal exposure, specifically to the application of a small molecule compound targeting the phosphorylated serine 43 site of ARMC10 in the preparation of drugs for treating neurological damage caused by tin exposure. This technical solution is the first to discover that trimethyltin chloride exposure can specifically induce abnormal phosphorylation of ARMC10, thereby causing neuronal death and cognitive impairment. Based on this mechanism, a small molecule compound targeting a specific phosphorylation site of ARMC10 is proposed, which effectively reverses neurological damage and protects neuronal structure and function by blocking its mediated abnormal mitochondrial division and dysfunction. This solution solves the problem of existing technologies lacking effective treatments for tin exposure-related neurological damage due to the lack of clear drug targets, and has ideal application prospects. This small molecule compound has a well-defined structure and a clear mechanism of action, is easy to further develop, and possesses good drug development and commercialization prospects.

Provided are compounds, methods, and pharmaceutical compositions for reducing the amount or activity of ATXN3 RNA in a cell or animal, and in certain embodiments reducing the amount of ATXN3 protein in a cell or animal. Such compounds, methods, and pharmaceutical compositions are useful to ameliorate at least one symptom or hallmark of a neurodegenerative disease. Such symptoms and hallmarks include motor dysfunction, aggregation formation, and neuron death. Such neurodegenerative diseases include spinocerebellar ataxia type 3 (SCA3).

Compositions consist essentially of trigonelline or consist of trigonelline. The compositions can be used in food or beverage applications, pharmaceutical formulations, or as a dietary supplement. The compositions can be administered to a mammal to treat or prevent a mitochondria-related disease or a condition associated with altered mitochondrial function in an individual in need thereof or at risk thereof. The mitochondria-related disease or condition is selected from the group consisting of deleterious effects of aging, stress (e.g., oxidative stress), obesity, overweight, reduced metabolic rate, metabolic syndrome, diabetes mellitus, complications from diabetes, hyperlipidemia, neurodegenerative disease, cognitive disorder, stress-induced or stress-related cognitive dysfunction, mood disorder, anxiety disorder, age-related neuronal death or dysfunction, chronic kidney disease, kidney failure, trauma, infection, cancer, hearing loss, macular degeneration, myopathies and dystrophies, and combinations thereof.

The invention relates to the field of neuroscience experiments, and discloses a method for increasing the survival rate of brain slice neurons through intrathecal injection of KN93, which comprises the following steps: intrathecal injection: carrying out intrathecal injection of an injection containing KN93 into an experimental animal, the concentration of KN93 in the injection being 5-20 [mu] M; preparing a brain slice: after injection is completed, anesthetizing the experimental animal, cutting the head, taking the brain, cooling the brain tissue, and cutting to form the brain slice; incubating the brain slice: incubating the brain slice in artificial cerebrospinal fluid; and survival rate evaluation: evaluating the neuron survival rate of the brain slice at a preset time point. KN93 directly enters cerebrospinal fluid circulation through intrathecal injection to target calcium / calmodulin dependent protein kinase II in central neurons and block excessive activation of the protein kinase II, so that neuronal death in the brain slice preparation and incubation process is reduced, the survival rate and functional integrity of neurons after long-time incubation are improved, and the brain slice has a good application prospect. And the survival time of brain slice neurons is effectively prolonged.

Provided are compounds, methods, and pharmaceutical compositions for reducing the amount or activity of ATXN3 RNA in a cell or animal, and in certain embodiments reducing the amount of ATXN3 protein in a cell or animal. Such compounds, methods, and pharmaceutical compositions are useful to ameliorate at least one symptom or hallmark of a neurodegenerative disease. Such symptoms and hallmarks include motor dysfunction, aggregation formation, and neuron death. Such neurodegenerative diseases include spinocerebellar ataxia type 3(SCA3).

The application provides a kind of vehicle CAN bus anomaly detection method based on lightweight network MobileViT, it is related to network and information security field. By data cleaning and dimension transformation to the original data set, obtain the behavior sample picture data set;An improved lightweight network model MobileViT is constructed and trained to realize the classification of generated behavior sample pictures, so as to convert the vehicle CAN bus anomaly detection problem into a picture classification problem. Use GELU as the activation function of MV2 module in lightweight MobileViT network model, effectively solve the neuron death problem, improve the model convergence speed;In the training process of the model, the learning rate is automatically updated using exponential decay, which prevents the model from falling into local optimum and reduces the training time. The application first applies lightweight network MobileViT to vehicle CAN bus anomaly detection, which can efficiently detect vehicle CAN bus anomalies under the condition of consuming less hardware resources.

The invention discloses fingolimod-modified selenium nanoparticles as well as a preparation method and application thereof, and fingolimod containing amino and hydroxyl is added in the process of preparing the selenium nanoparticles by reducing selenium-containing salt with a reducing agent, so that the fingolimod-modified selenium nanoparticles are obtained. The fingolimod-modified selenium nanoparticles prepared by the invention can be used as a nano-scale drug to carry out intracerebral anti-oxidation and anti-inflammatory treatment in vivo level, alleviate the tau protein phosphorylation process in neurons, inhibit neuronal death, regulate microglial cell polarization in the brain and play a neuroinflammation protection function, and can be used for preparing a drug for treating neuroinflammation. Neuroprotection and selenium nanoparticles are combined, and the treatment effect of the Alzheimer's disease is enhanced through a synergistic mechanism, so that a more effective strategy is possibly provided for treatment of the Alzheimer's disease.

The application discloses a kind of polypeptides for treating Parkinson's disease.In the application, it is first found that transient receptor potential M2 type (TRPM2) channel is more expressed in fragile DA neuron subgroup, and its expression amount is positively correlated with age in Parkinson's disease (PD) patient, and the mechanism of action is determined through rigorous experiment, i.e.TRPM2 channel is preferentially activated in ADE neuron through PARP-1 / PARG / ADPR axis, drives Mfn2 / Bcl-2 complex dependent mitochondrial superfusion, causes ADE neuron death.In addition, TRPM2 channel also drives MPTP treatment mouse SNc DA neuron susceptibility through Mfn2 / Bcl-2 mediation.Firstly, it is found that blocking PARP-1 / PARG / ADPR and Mfn2 / Bcl-2 mediated DA neuron death pathway can prevent the death of induced pluripotent stem cell (iPSC) derived DA neuron specific to spontaneous Parkinson's disease (SPD) patient.As susceptible SNc DA neuron loss is the main symptom of PD, therefore, PARP-1 / PARG / ADPR and Mfn2 / Bcl-2 pathway can become a new therapeutic target for PD.

The present disclosure relates to a pharmaceutical composition for preventing or treating a brain disease, comprising a stem cell-derived exosome surface-modified with a compound capable of binding to dopamine receptors or L-amino acid transporters as an active ingredient. The stem cell-derived exosome according to the present disclosure selectively binds to dopamine receptors (D2) overexpressed as autoreceptors in dopaminergic neurons in the substantia nigra through surface modification. Thereby, local accumulation in dopaminergic neurons is possible. In addition, it was identified that the stem cell-derived exosome exhibited an excellent neuron protective effect and neuron death inhibitory effect. Accordingly, the surface-modified stem cell-derived exosome according to the present disclosure is expected to be usefully used as a composition for preventing or treating a brain disease including Parkinson's disease and Alzheimer's disease.

The invention relates to the technical field of drugs for treating diseases related to heavy metal exposure, in particular to application of a small molecule compound of a targeted phosphorylated ARMC10 serine 43 site in preparation of drugs for treating nervous system injury caused by tin exposure. According to the technical scheme, it is found for the first time that exposure of trimethyltin chloride can specifically induce abnormal phosphorylation of ARMC10, and then neuronal death and cognitive impairment are caused. On the basis of the mechanism, a small molecule compound targeting a specific phosphorylation site of ARMC10 is provided, and by blocking mitochondrial abnormal division and dysfunction mediated by the small molecule compound, nerve injury is effectively reversed, and the structure and function of neurons are protected. The scheme solves the problem that in the prior art, due to the lack of definite drug targets, no effective therapeutic drug is provided for tin exposure related nervous system injury, and has ideal application prospects. The small molecule compound is clear in structure, clear in action mechanism and easy to carry out subsequent development, and has good druggability and commercialization prospects.

Proposed is a gene-therapy DNA vector, based on gene-therapy DNA vector GDTT1.8NAS12, for treating diseases characterized by progressive pathological changes in the nerve tissue structure and neuron function, including neuron death, which are associated with genetic factors, including mutations in genes coding for proteins critical to the normal functioning of the neurons, inter alia Huntington's disease and hereditary forms of amyotrophic lateral sclerosis, as well as with misfolding of the tertiary structure of proteins, inter alia Parkinson's disease and Alzheimer's disease, damage to the central nervous system, disruption of the oxygen supply to the brain or spinal cord, defective neuronal energy metabolism and axonal transport, or autoimmune demyelinating processes, inter alia multiple sclerosis. As a result of the limited size of the vector part GDTT1.8NAS12, which is not greater than 2600 bp, each of the proposed gene-therapy DNA vectors is capable of effectively penetrating into human and animal cells and expressing the target gene cloned within it.