12 results about "Cells heart" patented technology

The present disclosure provides recombinant adeno-associated virus (rAAV) virions with an engineered capsid protein identified using a high-throughput sequencing screen or rational design. In particular, the disclosure provides AAV5 virions and capsid proteins with increased transduction efficiency in cardiac cells, increased cell-type selectivity, and / or other desirable properties.

A computational system and method for digital modeling of cardiac cell membrane electrophysiology is disclosed. The system generates a digital model representing the cell membrane as a dielectric lipid bilayer comprising a capacitor element and a resistor element, where the resistor element is emulated by a plurality of ion channels. The system calculates cell membrane potential based on intracellular and extracellular concentrations of key ions, such as Na+, K+, Ca2+, and Cl-, using the Goldman-Hodgkin-Katz equation. Generation of cellular membrane action potentials is simulated by modeling the opening and closing of voltage-gated ion channels in response to triggering events. The model provides dynamic visualizations of the distinct phases of the action potential, including depolarization and repolarization, offering a high-fidelity tool for research and for enhancing the realism of training simulations in electrophysiology procedures.

The present disclosure provides recombinant adeno-associated virus (rAAV) virions with an engineered capsid protein. In particular, the disclosure provides AAV9 virions with engineered AAV9 capsid, AAV5 / 9 chimeric capsid or combinatory capsid that achieves increased transduction efficiency in cardiac cells, increased cell-type selectivity, and / or other desirable properties.

A computational system and method for digital modeling of biochemical reactions within cardiac cells are disclosed. The system comprises processors and a computer-readable storage device with instructions to maintain biological data related to cardiac cell reactions and receive user selections via a user interface to configure a simulation. The user can select a cardiac cell class, and functions to load cellular components, generate enzyme activity, load specific enzymes, and perform enzymatic reactions. The system performs in silico experiments, predicts new biological data, and compiles this into configuration data. An enzyme activity model is generated and simulated under various conditions, including user-defined enzymatic dysregulation, to replicate and study cardiac physiology and pathology. The results, such as changes in energy metabolism parameters like glucose consumption and ATP usage, are outputted. The system provides a detailed and interactive platform for research and education in cardiac electrophysiology and disease.

The present application relates to a novel micropeptide MP29 and a use thereof and relates to a use of the micropeptide in the preparation of a reagent or drug for preventing, treating, or alleviating diseases related to abnormal mitochondrial energy metabolism in cells, wherein the diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, schizophrenia, aging, photoaging, fatty liver disease, liver fibrosis, liver cirrhosis, liver cancer, diabetic nephropathy, cardiovascular diseases such as heart failure, etc. By means of endogenous overexpression or exogenous synthesis, the reducing equivalents NADH in the tricarboxylic acid cycle are up-regulated to promote intracellular ATP production, thereby significantly enhancing the proliferation of high-energy-demanding cardiac cells and brain tissue cells, or suppressing oxidative damage and apoptosis of cells in Alzheimer's disease models and Parkinsonism, or alleviating hypertrophy and aging of myocardial cells in heart failure models, or ameliorating the photodamage of cells in photoaging models. These results indicate that the micropeptide MP29 has an application value in preventing or treating diseases related to abnormal mitochondrial energy metabolism.

Provided herein are composition and methods for gene therapy of LEM domain-containing protein 2 (LEMD2) cardiomyopathy. Viral vectors are used to deliver LEMD2 reading frame for gene augmentation in cardiac cells that harbor loss-of-function LEMD2 mutations. A murine model for LEMD2 cardiomyopathy is also described.

This disclosure relates generally to methods of screening and preparing high purity cardiac cell therapies and related cell preparations.

The present invention provides a heart tissue model of at least 60% cardiac cells, wherein the cardiac cells surround an inner cavity, wherein the cardiac cells are selected from cardiomyocytes, endocardial cells and epicardial cells; method for the generation of such a tissue model and uses thereof.

This invention discloses a method for extracting interstitial fluid from cardiac tissue, belonging to the field of biomedical technology. Based on the unique characteristics of the heart, a organ closely related to blood circulation, and its differences in tissue physical properties compared to other organs, this invention designs and develops this extraction method, which specifically includes: rinsing isolated cardiac tissue with pre-cooled physiological saline; low-speed centrifugation to remove residual rinsing fluid from the heart; and centrifugation again to obtain interstitial fluid from the cardiac tissue. Comparison of the obtained interstitial fluid with cardiac cell fluid and serum confirms the accuracy and specificity of the extraction scheme of this invention. The centrifugation process of this invention does not damage cells, preserving its unique differences from serum and cardiac cell fluid. The extracted interstitial fluid has a high protein concentration, which can better reflect changes in the cardiac microenvironment, facilitating subsequent related medical and basic research.

A method of increasing sodium current in a cardiac cell generally includes introducing into the cardiac cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription, thereby increasing sodium current in the cardiac cell. A method of increasing translation of SCN5A mRNA in a cell generally includes introducing into the cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription. A method of decreasing arrythmia in a cardiac cell generally includes introducing into the cardiac cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription. A method of treating arrythmia in a patient having, or at risk of having, arrythmia generally includes administering to the patient an miR-448 inhibitor in an amount effective to decrease the likelihood or extent of arrythmia in the patient. In some embodiments of all methods, the miR-448 inhibitor can be an miR-448 antagomir or an miR-448 sponge.