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56 results for “Action potentials”
Safe cardiac action potential test (www.scaptest.com) : a database describing the in silico cardiac safety profile of drugs and their propensity to induce early afterdepolarization - Part II : description of 50 additional drugs
<p><span>This file describes the<em> in silico</em> cardiac safety profile of 50 additional drugs (in addition to the 150 drugs already described in the zenodo file 7541554) in order to complete the “scaptest” database.<span> </span>The aim of this database is to describe the <em>in silico</em> cardiac safety profile of drugss and their propensity to induce early afterdepolarization.<span> </span>This is based on the study of the effects of drugs on the non-failing human ventricular myocyte action potential (endo-, mid- and epicardial subtypes) reconstructed by computational simulation (O’Hara-Rudy dynamic algorithm) in order to identify cardiac action potential abnormalities such as high variations and/or occurrence of resting membrane potential, action potential amplitude, maximal rate of action potential rise, action potential duration, triangulation, early afterdepolarization, transmural dispersion of repolarization, reverse use dependence, qNet or minimal rate of action potential decrease at early afterdepolarization take-off voltage. These various parameters are useful in order to assume a more accurate predictability of pro-arrhythmic liabilities of new drug candidate in the cardiac safety pharmacology screening process, which is the aim of the comprehensive in vitro pro-arrhythmia assay (CiPA) initiative. The <em>in silico</em> cardiac safety profile of each drug is illustrated by a separate page describing the effects induced by each compound on these various parameters. The results are summarized regarding the expected pro-arrhythmia profile of the various compounds as described by the CredibleMeds classification evaluating their propensity to induce torsade de pointes.</span></p>
The role of action potential changes in depolarization-induced failure of excitation contraction coupling in mouse skeletal muscle
<p>Excitation-contraction coupling (ECC) is the process by which electrical excitation of muscle is converted into force generation. Depolarization of skeletal muscle resting potential contributes to failure of ECC in diseases such as periodic paralysis, intensive care unit acquired weakness and possibly fatigue of muscle during vigorous exercise. When extracellular K<sup>+</sup> is raised to depolarize the resting potential, failure of ECC occurs suddenly, over a narrow range of resting potentials. Intracellular recordings of action potentials (APs) in individual mouse skeletal muscle fibers during depolarization of the resting potential revealed small APs are still generated at resting potentials at which force production has failed. Simultaneous imaging of Ca<sup>2+ </sup>transients and recording of APs demonstrated failure to generate Ca<sup>2+ </sup>transients when APs peaked at potentials more negative than -30 mV. An AP property that closely correlated with failure of the Ca<sup>2+</sup> transient was the integral of AP voltage with respect to time. Simultaneous recording of Ca<sup>2+ </sup>transients and APs with electrodes separated by 1.6 mm revealed AP conduction fails when APs peak below -21 mV. We hypothesize propagation of APs and generation of Ca<sup>2+</sup> transients are governed by distinct AP properties: AP conduction is governed by AP peak, whereas Ca<sup>2+</sup> release from the sarcoplasmic reticulum is governed by AP integral of voltage with respect to time. The reason distinct AP properties may govern separate steps of ECC is the kinetics of the ion channels involved in the different steps of ECC. Na channels, which govern propagation, have rapid kinetics such that propagation is insensitive to AP width (and integral) whereas Ca<sup>2+</sup> release is governed by movement of gating charges in Cav1.1 channels, which have slower kinetics such that Ca<sup>2+ </sup>release is sensitive to AP width (and integral). The quantitative relationships established between resting potential, AP properties, AP conduction and Ca<sup>2+</sup> transients provide the foundation for future studies of failure of ECC induced by depolarization of the resting potential.</p>
Safe cardiac action potential test (www.scaptest.com): a database describing the in silico cardiac safety profile of drugs and their propensity to induce early afterdepolarization
<p>The aim of the present database is to describe the <em>in silico</em> cardiac safety profile of drugs and their propensity to induce early afterdepolarization. This is based on the study of the effects of drugs on the non-failing human ventricular myocyte action potential (endo-, mid- and epicardial subtypes) reconstructed by computational simulation (O’Hara-Rudy dynamic algorithm) in order to identify cardiac action potential abnormalities such as high variations and/or occurrence of resting membrane potential, action potential amplitude, maximal rate of action potential rise, action potential duration, triangulation, early afterdepolarization, transmural dispersion of repolarization, reverse use dependence, qNet or minimal rate of action potential decrease at early afterdepolarization take-off voltage. These various parameters are useful in order to assume a more accurate predictability of pro-arrhythmic liabilities of new drug candidate in the cardiac safety pharmacology screening process, which is the aim of the comprehensive in vitro pro-arrhythmia assay (CiPA) initiative. The <em>in silico</em> cardiac safety profile of each drug (150 drugs described in this first version) is illustrated by a separate page describing the effects induced by each compound on these various parameters. The results are summarized regarding the expected pro-arrhythmia profile of the various compounds as described by the CredibleMeds classification evaluating their propensity to induce torsade de pointes.</p>
Fig. 6 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 6. The antiapoptotic effect of saponins in neurological diseases. They activate the PI3K/Akt survival pathway, promote the phosphorylationdependent inactivation of Bad, which leads to a decrease in caspasedependent neuronal apoptosis. Also, they maintain mitochondria integrity through modulation of p38 and mitogen-activated protein kinase (MEK) signalling pathways, which reduces the cytochrome c release and inhibits caspasedependent apoptosis (Wu et al., 2015).
Fig. 1 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 1. Chemical structures of the major constituents of triterpenoid saponins identified in Astragalus radix extract (Chu et al., 2010).
Fig. 5 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 5. Pathways through which Astragalus polysaccharides (APS) mediates anti-inflammatory effect (Zheng et al., 2020).
Fig. 3 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 3. Astragalus membranaceus: (A) Aerial parts, (B) Roots, (C) Root extract (Cited at https://www.cambridge.org).
The Effect of Prior Muscle Activation on the Compound Muscle Action Potential (CMAP)
ClinicalTrials.gov study NCT01182558. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Changes in the Threshold of Electrically Evoked Compound Action Potential in Children Following Cochlear Implantation
ClinicalTrials.gov study NCT03500718. IPD Sharing: NO. Countries: 1. Publications: 2.
Alemtuzumab in Autoimmune Inflammatory Neurodegeneration: Mechanisms of Action and Neuroprotective Potential
ClinicalTrials.gov study NCT02419378. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Data from: Collision and annihilation of nonlinear sound waves and action potentials at interfaces
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Medium spiny neuron electrophysiological properties across male rats and female rats in different estrous cycle phases in the nucleus accumbens core: Excitatory synaptic input, action potential, and intrinsic properties
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The role of action potential changes in depolarization-induced failure of excitation contraction coupling in mouse skeletal muscle
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Data from: The adhesion function of the sodium channel beta subunit (β1) contributes to cardiac action potential propagation
Computational modeling indicates that cardiac conduction may involve ephaptic coupling - intercellular communication involving electrochemical signaling across narrow extracellular clefts between cardiomyocytes. We hypothesized that β1(SCN1B) -mediated adhesion scaffolds trans-activating NaV1.5 (SCN5A) channels within narrow (V1.5. Smart patch clamp (SPC) indicated greater sodium current density (INa) at perinexi, relative to non-junctional sites. A novel, rationally designed peptide, βadp1, potently and selectively inhibited β1-mediated adhesion, in electric cell-substrate impedance sensing studies. βadp1 significantly widened perinexi in guinea pig ventricles, and selectively reduced perinexal INa, but not whol e cell INa, in myocyte monolayers. In optical mapping studies, βadp1 precipitated arrhythmogenic conduction slowing. In summary, β1-mediated adhesion at the perinexus facilitates action potential propagation between cardiomyocytes and may represent a novel target for anti-arrhythmic therapies.
Fig. 2 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 2. Chemical structure of Astragalus polysaccharide (Liu et al., 2020).
Fig. 4 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 4. Astragalus spinosus (Alsirhan, 2002).
Electrically Evoked Compound Action Potentials Human Observation Medtronic Algorithm Comparison Study
ClinicalTrials.gov study NCT04765735. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Data from: The adhesion function of the sodium channel beta subunit (β1) contributes to cardiac action potential propagation
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Data from: A four-component model of the action potential in mouse detrusor smooth muscle cell
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Genome-wide chromatin-immunoprecipitation studies of sympathetic neurons reveals critical direct targets of ISL1 and suggests potential co-factor families for ISL1 action in sympathetic neurons
GEO Series GSE93304. Mus musculus. 2 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.