21 results about "Depolarization" patented technology

Techniques for determining whether a ventricular depolarization is a premature ventricular contraction (PVC) depolarization can include processing circuitry of a medical system that identifies an interval from a maximum slope point to a minimum slope point of each of a plurality of ventricular depolarizations and, for each of the plurality of ventricular depolarizations as a current ventricular depolarization, determines that an interval from a maximum slope point to a minimum slope point of the current ventricular depolarization, a previous adjacent ventricular depolarization of the plurality of ventricular depolarizations, and a subsequent adjacent ventricular depolarization of the plurality of ventricular depolarizations satisfies one or more slope criteria. The processing circuitry determines, based on the interval from the maximum slope point to the minimum slope point that satisfies the one or more slope criteria, that the current ventricular depolarization is a PVC depolarization.

A device for activating the mitochondrion, wherein negative charge and reactive oxygen are delivered from outside to the mitochondrion via a negative charge and reactive oxygen delivery unit to serve as material for the mitochondrial redox reaction; and, wherein a calcium ion channel stimulation unit can stimulate an in vivo calcium ion to transport a protein across a calcium ion on an inner membrane of the mitochondrion into a matrix space of the mitochondrion, whereby an influx of the calcium ion promotes the depolarization of the mitochondrion and increases the activity of mitochondrial oxidative phosphorylation.

Provided herein are depolarizing ion channel therapeutics and methods of using the same for treating retinal and neurodegenerative diseases.

The invention is suitable for the technical field of biological feedback, and provides a non-invasive feedback method, device, equipment and program product for pelvic floor muscle training. The method comprises the steps that in the pelvic floor muscle training process of a living body, a first electromyographic signal generated by pelvic floor muscle fiber depolarization when the pelvic floor muscle of the living body contracts is obtained through an active electrode arranged on the pelvic floor muscle of the living body; and according to the first electromyographic signal, determining whether pelvic floor muscle training performed by the living body meets a preset requirement or not. According to the method, the electromyographic signal for determining whether the pelvic floor muscle training carried out by the living body meets the preset requirement or not is obtained by the active electrode arranged on the pelvic floor muscle of the living body, and the active electrode can be directly attached to the skin, so that the pelvic floor muscle training effect can be determined without using a vaginal probe; therefore, the effect of pelvic floor muscle training performed by the living body can be determined noninvasively, and the safety and comfort of pelvic floor muscle training are improved.

A dual-chamber leadless pacemaker (LP) system includes a first leadless pacemaker (LP1) and a second leadless pacemaker (LP2), wherein LP1 is configured to be implanted in or on a first heart chamber and deliver pacing pulses to the first heart chamber, and LP2 is configured to be implanted in or on a second heart chamber and deliver pacing pulses to the second heart chamber. Information is obtained regarding the amplitude of the pacing pulses delivered by LP2 to the second heart chamber and / or the sensitivity of a sensing circuit of LP1, which is configured to be used by LP1 to detect the inherent depolarization of the first heart chamber. A crosstalk protection duration is determined based on at least some of this information, such that it is performed for an appropriate duration when crosstalk protection is executed.

Provided herein are depolarizing ion channel therapeutics and methods of using the same for boosting retinal neuronal function.

A non-invasive method for cardiac arrhythmia risk stratification may include identifying, based at least on an electrical recording of a patient, a cardiac depolarization simulation and a cardiac repolarization simulation corresponding to an electrical recording of a patient. One or more regions of increased spatial repolarization gradient in which a first area of a myocardium of the patient exhibits a first repolarization rate that differs from a second repolarization rate of a second area of the myocardium by an amount then divided by the spatial distance between the two regions, by a threshold value may be determined based on the cardiac depolarization simulation and the cardiac repolarization simulation. A risk of cardiac arrhythmia for the patient may be determined based a magnitude of the increased spatial repolarization gradient. Moreover, a treatment plan for the patient may be determined based on the magnitude and / or location of the increased spatial repolarization gradient.

The present disclosure provides a compound for specifically enhancing the spatial coupling degree of a TRPV4-KCa2.3 complex and use thereof, and belongs to the field of chemical medicine. The compound with a structure shown in a general formula (I) in the present disclosure is mainly used for re-coupling two uncoupled proteins and restoring the proteins to a normal state under uncoupling of TRPV4 and KCa2.3 in hypertensive patients. Under normal conditions of the TRPV4 and the KCa2.3, a signal of calcium ions is received by the TRPV4. As the calcium ions flow in, potassium ions in a KCa2.3 channel in the downstream are stimulated to flow out. Due to depolarization, vasodilation is caused, and therefore, the blood pressure of the hypertensive patients is returned to a normal level.

A method for localizing the source of an arrhythmia within a heart wall is disclosed. The method involves accessing an indication of the source location of the arrhythmia within the endocardium. A normal vector is generated that is normal to the endocardium at the source location in the direction of the epicardium layer. An activation vector indicating the direction of electrical force of the heart during an initial stage of depolarization is determined. The depth angle between the normal vector and the activation vector is determined, and the depth of the source location within the heart wall is indicated based on a depth angle.

The invention belongs to the technical field of biological medicine, and particularly relates to application of lactic acid in preparation of a neuron protective agent. Results of the invention show that the exogenous lactic acid can improve late-stage injury caused by HIE injury of newborn rats, and the neuroprotective effect of the exogenous lactic acid plays a role through a plurality of mechanisms; comprising the following steps: reducing excessive hyperplasia of microglial cells and astrocytes, regulating phenotypic polarization of the neuroglial cells, inhibiting neuroinflammatory response, reducing excessive synaptic phagocytosis mediated by the microglial cells and reducing a depolarization state of the astrocytes AQP4, so that neuron damage and behavioral defects of HIE newborn rats are relieved.

Patient treatment systems and methods for sensing cardiac depolarization and / or stimulating the carotid sinus nerve are disclosed herein. Exemplary patient treatment systems can include a neuromodulator and an implantable signal delivery device electrically coupleable to the neuromodulator. The signal delivery device comprises a lead body including a first region, a second region positionable over the first region, and lead electrodes. The patient treatment system further comprises computer-readable media having instructions that cause the patient treatment system to perform operations comprising: (i) obtaining a physiological parameter of the patient, (ii) generating neuromodulation pulses based on the obtained physiological parameter, and (iii) delivering the neuromodulation pulses to the CSN afferent fibers via one or more of the lead electrodes. The physiological parameter can include at least one of blood pressure, heart rate, bioimpedance, or activity level of the patient.

The application relates to the technical field of biology, and particularly relates to a sound electricity Ba that triggers post-translational modification 0.85 Ca 0.15 Ti 0.9 Yb 0.1 O3 nanoparticles, a preparation method and application thereof. A titanium tetrachloride solution and a mixed reagent solution are stirred and mixed to obtain a stirring mixed solution; the stirring mixed solution is mixed with sodium hydroxide and polyvinylpyrrolidone and then subjected to heat treatment to obtain a heat-treated product; the heat-treated product is subjected to solid-liquid separation to obtain a solid, and the solid is washed to be neutral and dried. + The nanoparticles provided by the application consume H + around mitochondria under ultrasonic stimulation, leading to depolarization of a mitochondrial membrane potential. After the mitochondrial membrane potential is depolarized, E3 ubiquitin ligase Parkin is transferred from a cytoplasm to a mitochondrial outer membrane, and is massively aggregated and accumulated on the mitochondrial outer membrane, leading to ubiquitination modification and cascade degradation of an anti-apoptotic protein MCL-1 of the mitochondrial outer membrane, so that cell apoptosis is promoted.

A clinical evaluation system and method are disclosed that facilitate the use of one or more morphologic atrial depolarization waveform-based features or parameters determined from biophysical signals such as cardiac or biopotential signals that are acquired, in preferred embodiments, non-invasively from surface sensors placed on a patient while the patient is at rest. Morphologic atrial depolarization waveform-based features or parameters can be used in a model or classifier to estimate metrics associated with the physiological state of a patient, including the presence or non-presence of a disease, medical condition, or an indication of either. The estimated metric may be used to assist a physician or other healthcare provider in diagnosing the presence or non-presence and / or severity and / or localization of diseases or conditions or in the treatment of said diseases or conditions.

A therapy system includes an implantable medical device including one or more implantable electrodes (40, 42, 48, 50, 94), and a computing apparatus (24) including processing circuitry and operably coupled to the one or more implantable electrodes (40, 42, 48, 50, 94). The one or more implantable electrodes (40, 42, 48, 50, 94) include a left bundle branch (LBB) electrode positionable adjacent a portion of a patient's LBB, and a right bundle branch (RBB) electrode positionable adjacent a portion of the patient's RBB. The computing apparatus (24) is configured to monitor electrical activity using the LBB and RBB electrodes, detect electrical activity based on the monitored electrical activity indicative of left ventricle (LV) depolarization and indicative of right ventricle (RV) depolarization, determine a temporal difference based on the detected electrical activity indicative of LV depolarization and the detected electrical activity indicative of RV depolarization, and determine whether there is a cardiac physiological condition based on the determined difference.

Methods and compositions are provided for the treatment of Parkinson's Disease. Aspects of the methods include administering Miro1 reducer. Also provided are reagents and kits for practicing the subject methods. In some embodiments, a method is provided for reducing undesirable levels of Miro1 in a cell having depolarized or otherwise damaged mitochondria. In some embodiments the cell is in vivo, e.g. in an animal model for PD, in an individual diagnosed with PD, in a clinical trial for treatment of PD, and the like.

The invention discloses application of a luteolin-zinc composite material in multi-target inhibition of valsa mali, and the luteolin-zinc composite material can cause the membrane potential change of a hypha cell membrane of the valsa mali to generate depolarization and destroy the integrity of the cell membrane to cause the leakage of intracellular nucleic acid and protein, so that the valsa mali is inhibited. An inhibiting effect and a killing effect are achieved on apple rot fungi; the ATP level in cells of valsa mali can be remarkably reduced, the activity of alkaline phosphatase is improved, and the content of malondialdehyde and the level of active oxygen are improved, so that bacteriostasis is realized through multiple ways of interfering energy metabolism, inducing membrane lipid peroxidation, oxidative stress and the like; in drug research and development and practical application, people can more scientifically and efficiently use the composite material to resist the apple rot fungi through the clear key concentration value, namely, the minimum inhibitory concentration of 4mM, and the composite material has important significance for guaranteeing healthy development of the apple industry and is expected to bring a new solution to prevention and treatment of the apple rot.

The invention provides a method for activating granulate bodies, which mainly comprises the following steps of: supplying negative charges and active oxygen to the granulate bodies from the outside through a negative charge and active oxygen supply unit so as to serve as raw materials for redox of the granulate bodies; the calcium ion channel promoting unit promotes the calcium ions in the body to enter the matrix space of the granulonema through calcium transport proteins on the granulonema inner membrane, so that the internal flow of the calcium ions can promote the depolarization of the granulonema, and the oxidative phosphorylation activity of the granulonema is improved. Thus, granulocyte activation and ATP production are enhanced.

Embodiments of the present invention disclose a method and system for visualizing the depolarization of a heart as a wave across the surface of the heart while at the same time showing the underlying electrograms associated with the depolarization. Controls are provided to: start and pause the propagation (depolarization) animation, fast forward or rewind, reduce the speed from 1× to slower speeds, and select a subset of the signal for viewing.

Patient treatment systems and methods for sensing cardiac depolarization and / or stimulating the carotid sinus nerve are disclosed herein. Exemplary patient treatment systems can include a neuromodulator and an implantable signal delivery device electrically coupleable to the neuromodulator. The signal delivery device comprises a lead body including a first region, a second region positionable over the first region, and lead electrodes. The patient treatment system further comprises computer-readable media having instructions that cause the patient treatment system to perform operations comprising: (i) obtaining a physiological parameter of the patient, (ii) generating neuromodulation pulses based on the obtained physiological parameter, and (iii) delivering the neuromodulation pulses to the CSN afferent fibers via one or more of the lead electrodes. The physiological parameter can include at least one of blood pressure, heart rate, bioimpedance, or activity level of the patient.

The application provides a kind of magnetic nanometer medium magnetoacoustic multi-field coupling nerve regulation method and device, magnetic field is generated by coil, magnetic nanometer medium located in brain function area is excited, magnetic field excitation acts on magnetic nanometer medium, causes thermal expansion, magnetoacoustic or magnetic force, through the potential change of ultrasound, magnetic force and further generation caused by magnetoacoustic and electromagnetic excitation, the regulation of neuron is realized;The magnetic, thermal, force, acoustic, electric coupling physical effects generated by electromagnetic nanometer medium of biological target are used, membrane depolarization is triggered, the biological effects of intracellular calcium ion inflow of neuron are induced, the intracellular calcium signal conduction is regulated to affect synaptic plasticity and control neural behavior, and then precise controllable regulation of excitability of brain area neuron subgroup is realized.The magnetic nanometer medium magnetoacoustic multi-field coupling nerve regulation device using the method of the application is composed of multi-mode electromagnetic excitation unit, coil unit with focusable electromagnetic field distribution, coupling conversion unit and test unit.