47 results about "Depolarization" patented technology

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. In some embodiments, a method of implanting a signal delivery device to deliver an electrical signal to a patient includes identifying a target region of a blood vessel of the patient; forming an opening on a side of the target region to partially separate periadventitial tissue surrounding the blood vessel, including fibers associated with baroreceptors and / or the carotid sinus nerve of the patient, from the underlying the blood vessel; positioning a first region of the signal delivery device at least partially through the opening between the blood vessel and the periadventitial tissue; and positioning a second region of the signal delivery device at least partially over the first region such that the periadventitial tissue is between the first region and the second region.

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.

Patient treatment systems and methods for sensing cardiac depolarization and / or stimulating the carotid sinus nerve are disclosed herein. In some embodiments, a method of implanting a signal delivery device to deliver an electrical signal to a patient includes identifying a target region of a blood vessel of the patient; forming an opening on a side of the target region to partially separate periadventitial tissue surrounding the blood vessel, including fibers associated with baroreceptors and / or the carotid sinus nerve of the patient, from the underlying the blood vessel; positioning a first region of the signal delivery device at least partially through the opening between the blood vessel and the periadventitial tissue; and positioning a second region of the signal delivery device at least partially over the first region such that the periadventitial tissue is between the first region and the second region.

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

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 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.

The ventricular electrical depolarization may be represented with a vector heart diagram (QRS) ring present in the 3D space. By knowing that the QRS ring is typically a closed trajectory on a plane (2D), a single-channel QRS can be changed (e.g., by rotation, projection, etc.) to different viewing angles along the plane to provide a viewpoint that is more favorable for morphological interpretation. Any single-phase or dual-phase single-channel QRS (time series) waveform can be decomposed into the form x (alpha, t) = sin (alpha t) u (t), t spanning [0, 2pi], where u (t) is an invariant intrinsic component, typically upright and single-phase, and sin (alpha t) is a variable component of the waveform. In this way, x (alpha, t) may be changed by replacing one parameter of the original variable component sin (alpha t) with a second parameter (e.g., upright single phase sin (0.5 t)) associated with the target view of the waveform. Meanwhile, the inherent component remains unchanged in the changing process.

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.

Techniques that include applying machine learning models to episode data, including a cardiac electrogram, stored by a medical device are disclosed. In some examples, based on the application of one or more machine learning models to the episode data, processing circuitry derives, for each of a plurality of arrhythmia type classifications, class activation data indicating varying likelihoods of the classification over a period of time associated with the episode. The processing circuitry may display a graph of the varying likelihoods of the arrhythmia type classifications over the period of time. In some examples, processing circuitry may use arrhythmia type likelihoods and depolarization likelihoods to identify depolarizations, e.g., QRS complexes, during the episode.

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.

Systems and methods for expression and delivery of proteinaceous species are described. Generally, a system can comprise biological cells within a porous membrane. The biological cells can be utilized to produce proteinaceous species. The biological cells can further store proteinaceous species within secretory granules such that the species can be controllably released upon depolarization of the cell. A secondary force can be provided to release proteinaceous species out of the porous membrane. Proteinaceous species can be expressed from an expression cassette configured to provide controllable release.

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.

A system and method for the safe delivery of treatment energy to a patient, which includes verification of system integrity before, during, or after the delivery of treatment energy and provides several mechanisms for rapid termination of the delivery of potentially harmful energy to the patient when a fault condition in the device and / or system is identified. The system may include an energy generator having processing circuitry to determine if there is a fault condition in the system and to automatically terminate a delivery of treatment energy when the processing circuitry determines there is a fault condition. The method may generally include performing a series of pre-checks, synchronizing a treatment energy delivery to the proper segment of the heart's depolarization pattern, configuring the system for treatment energy delivery, delivering the treatment energy, and performing post-treatment evaluation.

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.

Conventionally, invasive techniques are used to localize Atrial Fibrillation sources, but they are inconvenient, technically complex, and expensive. Non-invasive methods such as ECGI are prone to errors due to small volume and wall thickness of the atria. Thus, embodiments of present disclosure provide a method and system for source localization of AF utilizing a modified dominant frequency approach and atrium depolarization time. The method initially obtains heart and torso scan images and extracts atrial and torso meshes from them. Then, Body Surface Potential (BSP) signals are sampled from the atrial meshes and torso meshes. Cardiac potential is reconstructed from BSP. Further, AF-DF probability and probable rotor regions are determined from the cardiac potential. AF sources are then localized by combining AF-DF probability and probable rotor regions. Thus, the disclosed method which is non-invasive can be used for patient stratification for AF treatment plan, personalize procedure planning, and reduce ablation time.

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 present invention discloses an automatic detection method of a pacing threshold of a cardiac pacemaker and a pacemaker, comprising: when the pacing threshold is automatically detected, the cardiac pacemaker issues pacing pulses according to the current pacing output voltage, and at the end of the pacing pulse issuance, the sensing time and the sensing circuit are turned on to detect the myocardial depolarization wave, wherein the sensing time is set to the time required to detect the myocardial depolarization wave, and depolarization discharge is performed at the end of the sensing time, and the cardiac pacemaker determines whether capture is successful according to the detection result of the myocardial depolarization wave; when capture is successful, backup pacing is not issued, and the current pacing output voltage is updated by reducing one level, and the above pacing threshold automatic detection process is repeated until it is determined that the capture is unsuccessful, and the previous level pacing output voltage corresponding to the unsuccessful capture is used as the detected pacing threshold; when capture is unsuccessful, backup pacing is performed after the last discharge. In this way, automatic and accurate detection of the pacing threshold can be achieved at a low cost.