32 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.

The invention relates to the technical field of biology, in particular to acoustoelectric Ba0. 85Ca0. 15Ti0. 9Yb0. 1O3 nanoparticles capable of triggering post-translational modification as well as a preparation method and application of the acoustoelectric Ba0. 85Ca0. 15Ti0. 9Yb0.1 O3 nanoparticles. Stirring and mixing the titanium tetrachloride solution and the mixed reagent solution to obtain a stirred mixed solution; mixing the stirred mixed solution with sodium hydroxide and polyvinylpyrrolidone, and performing heat treatment to obtain a heat-treated substance; and carrying out solid-liquid separation on the heat-treated substance to obtain a solid, washing the solid to be neutral, and drying. The nanoparticles provided by the invention consume H < + > near mitochondria under ultrasonic stimulation, so that mitochondrial membrane potential depolarization is caused. After mitochondrial membrane potential depolarization, E3 ubiquitin ligase Parkin is transferred from cytoplasm to a mitochondrial outer membrane, and is massively gathered and accumulated on the mitochondrial outer membrane, so that ubiquitination modification and cascade degradation of mitochondrial outer membrane anti-apoptosis protein MCL-1 are caused, and cell apoptosis is promoted.

Cardiac mapping catheters and methods for using the catheters are described. The catheter can detect the presence, direction and / or source of a depolarization wave front associated with cardiac arrhythmia. A mapping catheter includes a plurality of bipolar electrode pairs in which the members of each pair are opposed to one another across a perimeter, for instance in a circular pattern (compass mode). The spaced arrangement of the electrodes can be utilized to identify directional paths of moving electric fields or wave fronts in any direction passing across the endocardial surface. Double potential (DP) recordings in compass mode can provide a regional assessment for the existence of rotational activity. Simultaneous DP recordings in compass mode, narrow-adjacent bipolar, and unipolar recording provide an accurate assessment of the time, location, and path that a rotational mechanism breaches a perimeter of electrodes. Accurate time, location, and path of perimeter breaches can be used to electrically track rotational mechanisms during atrial fibrillation.

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.

Electrophysiologic biomarkers for prognostication of neurological outcome are described herein. An inverse correlation was found between timing of a cortical spreading depolarization (SD) wave and neurological outcome as tested at 24 hours post-CPR. Additionally, a minor image of this SD was identified as a “repolarization (RP) wave.” Quantifying features of SD and RP during cardiac arrest and cardiopulmonary resuscitation (CPR) provide important metrics for diagnosis and prognosis of neurological injury from hypoxia-ischemia and can serve as an early prognostication tool for predicting outcome at subsequent days after successful CPR. This discovery may also allow for novel therapeutic interventions to improve neurological recovery after hypoxia-ischemia insults.

The embodiment of the invention discloses a model deprejudice method and device based on a medical large model, equipment and a medium. A specific embodiment of the method comprises the following steps: carrying out multi-level prejudice removal correction on a multi-modal medical data set, and then carrying out data equalization grouping to obtain a multi-modal equalization medical training data set; performing resource detection on the server cluster; inputting the multi-modal equilibrium medical training data set into the medical large model to obtain a multi-modal medical diagnosis information set; inputting the multi-modal medical diagnosis information set and the multi-modal medical sample diagnosis information set into a multi-modal adversarial fair depolarization loss function to obtain a model loss value; and after model deprejudice processing is carried out on the multi-modal equilibrium medical test data set, model training is carried out on the drug recommendation model, and a drug delivery robot is controlled to carry out transportation. According to the embodiment, the resource load balance of the server cluster and the quality of the medical data after prejudice removal can be improved, the training speed of the model is improved, and the robot is accurately controlled to convey medicines.

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.

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

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 present invention discloses a compound with endoplasmic reticulum targeting and its application. The compound has the following chemical formula: #imgabs0# The compound provided by the present invention has good endoplasmic reticulum targeting and the ability to induce the production of type I reactive oxygen species. In addition, the compound can induce time-dependent depletion of endoplasmic reticulum calcium in cancer cells under light conditions. More importantly, the existing anti-diabetic drug glibenclamide closes the ATP-dependent potassium ion channel (K) on the endoplasmic reticulum membrane. + ATP ), the compound-induced loss of endoplasmic reticulum calcium into the cytoplasm will lead to severe depolarization of the endoplasmic reticulum membrane potential, and ultimately activate the downstream endoplasmic reticulum and mitochondria-dependent apoptosis pathways, leading to cancer cell death, while also embodying the new use of glibenclamide.

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.

A method for the automated detection of sites of latest electrical activation of the human heart, envisages: constructing a number of isopotential maps associated with the electrical potential distribution on the surface of the heart in respective times within a processing period occurring near the end of the ventricular or atrial depolarization; processing the isopotential maps to identify regions of maximal positive electrical potential; determining the barycenters of the identified regions; and localizing the site of latest heart electrical activation based on, in particular as an average of, the determined barycenters.

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.

The present application relates to the technical field of cardiovascular disease recognition, in particular to a cardiovascular disease recognition system, device and medium based on electrocardiogram fusion, the system segments the preprocessed electrocardiogram time domain signal to obtain electrocardiogram depolarization / recovery time domain signal; the electrocardiogram depolarization / recovery time domain signal is subjected to dynamic modeling to obtain depolarization / recovery dynamic domain signal; based on the electrocardiogram depolarization time domain signal, the depolarization time domain non-threshold recurrent graph is determined; based on the electrocardiogram depolarization dynamic domain signal, the depolarization dynamic domain non-threshold recurrent graph is determined; based on the electrocardiogram recovery time domain signal, the recovery time domain non-threshold recurrent graph is determined; based on the electrocardiogram recovery dynamic domain signal, the recovery dynamic domain non-threshold recurrent graph is determined; based on the depolarization / recovery non-threshold recurrent graph, the non-threshold joint recurrent graph is determined; the upper / lower triangular matrix of the non-threshold joint recurrent graph is used to determine the fusion recurrent graph; based on the fusion recurrent graph, the recognition result of the cardiovascular disease category is obtained, and the accuracy of cardiovascular disease recognition is improved.

The invention relates to the technical field of cardiovascular disease recognition, in particular to a cardiovascular disease recognition system and device based on electrocardio fusion and a medium. The system divides preprocessed electrocardio time-domain signals to obtain electrocardio depolarization / repolarization time-domain signals; performing dynamic modeling on the electrocardio depolarization / repolarization time domain signal to obtain a depolarization / repolarization dynamic domain signal; determining a depolarization time domain non-threshold recurrence plot based on the electrocardio depolarization time domain signal; based on the ECG depolarization dynamic domain signal, determining a depolarization dynamic domain non-threshold recurrence plot; based on the electrocardio repolarization time-domain signal, determining a repolarization time-domain non-threshold recurrence plot; determining a repolarization dynamic domain non-threshold recurrence plot based on the electrocardio repolarization dynamic domain signal; determining a non-threshold joint recurrence plot based on the depolarized / repolarized non-threshold recurrence plot; determining a fusion recurrence plot based on the upper / lower triangular matrix of the non-threshold joint recurrence plot; the recognition result of the cardiovascular disease category is obtained based on the fused recurrence plot, and the accuracy of cardiovascular disease recognition is improved.

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.

Disclosed are deuterated glycoluril tetramer compounds having aryl groups incorporated at both ends represented by formula (1), pharmaceutical compositions containing the compounds. The deuterated compounds are useful for antagonizing clinically used non-depolarizing muscle relaxants, and have significantly superior antagonistic activity against rocuronium and vecuronium to sugammadex at the same dose, and significantly superior antagonistic activity against cisatracurium and rocuronium to a non-deuterated control molecule.

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.