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surface ecg recordings  (ADInstruments)


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    Structured Review

    ADInstruments surface ecg recordings
    A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. <t>ECG</t> and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).
    Surface Ecg Recordings, supplied by ADInstruments, used in various techniques. Bioz Stars score: 96/100, based on 214 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/surface ecg recordings/product/ADInstruments
    Average 96 stars, based on 214 article reviews
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    Images

    1) Product Images from "STIM1-Ca 2+ signaling in coronary sinus cardiomyocytes contributes to interatrial conduction"

    Article Title: STIM1-Ca 2+ signaling in coronary sinus cardiomyocytes contributes to interatrial conduction

    Journal: Cell calcium

    doi: 10.1016/j.ceca.2020.102163

    A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. ECG and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).
    Figure Legend Snippet: A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. ECG and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).

    Techniques Used: Injection



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    ADInstruments surface ecg recordings
    A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. <t>ECG</t> and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).
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    ADInstruments surface ecg recording
    A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. <t>ECG</t> and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).
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    A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. <t>ECG</t> and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).
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    A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. <t>ECG</t> and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).
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    ADInstruments standard surface ecg recordings
    a, GCaMP3+ hESC-CM graft in a cryoinjured heart immunostained for GFP (green) and βMHC (red). Small graft nests were located in host muscle within the border zone, but most of the graft was in scar. b, Percentage of visible GCaMP3+ hESC-CM graft in each cryoinjured heart that showed 1:1 host-graft coupling at 14- and 28-days post-transplantation (n=7 and n=15 animals, respectively). c, Representative 28-day-old GCaMP3+ hESC-CM graft in a cryoinjured heart imaged ex vivo during mechanical arrest with blebbistatin and pacing at 3 Hz. Upper: Traces of mean fluorescent intensity versus time for graft regions located within host muscle (‘1’, blue) and the cryoinjury zone (‘2’, red). Both were activated in a 1:1 correlation with the host <t>ECG</t> (black). Lower: Corresponding activation map showing the interval (in ms) between the stimulus pulse and the local rise in GCaMP3 fluorescence. Graft in host muscle (1) showed uniformly rapid activation, while graft in scar (2) activated first in central scar and then gradually progressed toward the border zone. In other instances, graft activation started at the border zone and radiated into the scar. d , GCaMP3 fluorescence and EGG traces (upper) as well as the activation map (lower) for a representative GCaMP3+ hESC-CM graft in a blebbistatin-arrested uninjured heart. This graft showed 1:1 host-graft coupling and a brief interval between stimulus and GCaMP3 transient upstroke.
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    Image Search Results


    A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. ECG and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).

    Journal: Cell calcium

    Article Title: STIM1-Ca 2+ signaling in coronary sinus cardiomyocytes contributes to interatrial conduction

    doi: 10.1016/j.ceca.2020.102163

    Figure Lengend Snippet: A. Surface ECGs recorded from cSTIM1−/− mice with (blue trace, middle panel) or without (red trace, top panel) intraperitoneal injection of 100 ng/g CCh. Bottom panel showed superimposed P waves from cSTIM1−/− mice at baseline and with CCh, indicating that CCh induced a wider and biphasic P wave from cSTIM1−/− mice. B. no significant difference in P wave duration from STIM1fl/fl and cSTIM1−/− mice (top panel). P wave duration significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5, bottom panel). C. No significant difference in PR interval from STIM1fl/fl and cSTIM1−/− mice (top panel) at baseline. PR interval significantly increased in cStim1−/− mice (n = 5) with CCh compared to STIM1fl/fl mice (n = 5) (bottom panel). D. ECG and intracardiac potentials following rapid atrial pacing reveal induction of atrial fibrillation in cSTIM1−/− mice treated with CCh. A greater number of cSTIM1−/− mice were induced into AF compared to STIM1fl/fl mice (left). In addition the duration of AF was sustained for a greater period of time in the cSTIM1−/− mice (right).

    Article Snippet: Surface ECG recordings were obtained with subcutaneously placed 29-gauge needle electrodes connected to a ML138 Octal Bioamp (ADInstruments Colorado Springs, CO) and a Powerlab 16/30 acquisition system (ADInstruments) in both forelimbs and hindlimbs to create a Lead I and Lead II configuration.

    Techniques: Injection

    a, GCaMP3+ hESC-CM graft in a cryoinjured heart immunostained for GFP (green) and βMHC (red). Small graft nests were located in host muscle within the border zone, but most of the graft was in scar. b, Percentage of visible GCaMP3+ hESC-CM graft in each cryoinjured heart that showed 1:1 host-graft coupling at 14- and 28-days post-transplantation (n=7 and n=15 animals, respectively). c, Representative 28-day-old GCaMP3+ hESC-CM graft in a cryoinjured heart imaged ex vivo during mechanical arrest with blebbistatin and pacing at 3 Hz. Upper: Traces of mean fluorescent intensity versus time for graft regions located within host muscle (‘1’, blue) and the cryoinjury zone (‘2’, red). Both were activated in a 1:1 correlation with the host ECG (black). Lower: Corresponding activation map showing the interval (in ms) between the stimulus pulse and the local rise in GCaMP3 fluorescence. Graft in host muscle (1) showed uniformly rapid activation, while graft in scar (2) activated first in central scar and then gradually progressed toward the border zone. In other instances, graft activation started at the border zone and radiated into the scar. d , GCaMP3 fluorescence and EGG traces (upper) as well as the activation map (lower) for a representative GCaMP3+ hESC-CM graft in a blebbistatin-arrested uninjured heart. This graft showed 1:1 host-graft coupling and a brief interval between stimulus and GCaMP3 transient upstroke.

    Journal: Nature

    Article Title: hESC-Derived Cardiomyocytes Electrically Couple and Suppress Arrhythmias in Injured Hearts

    doi: 10.1038/nature11317

    Figure Lengend Snippet: a, GCaMP3+ hESC-CM graft in a cryoinjured heart immunostained for GFP (green) and βMHC (red). Small graft nests were located in host muscle within the border zone, but most of the graft was in scar. b, Percentage of visible GCaMP3+ hESC-CM graft in each cryoinjured heart that showed 1:1 host-graft coupling at 14- and 28-days post-transplantation (n=7 and n=15 animals, respectively). c, Representative 28-day-old GCaMP3+ hESC-CM graft in a cryoinjured heart imaged ex vivo during mechanical arrest with blebbistatin and pacing at 3 Hz. Upper: Traces of mean fluorescent intensity versus time for graft regions located within host muscle (‘1’, blue) and the cryoinjury zone (‘2’, red). Both were activated in a 1:1 correlation with the host ECG (black). Lower: Corresponding activation map showing the interval (in ms) between the stimulus pulse and the local rise in GCaMP3 fluorescence. Graft in host muscle (1) showed uniformly rapid activation, while graft in scar (2) activated first in central scar and then gradually progressed toward the border zone. In other instances, graft activation started at the border zone and radiated into the scar. d , GCaMP3 fluorescence and EGG traces (upper) as well as the activation map (lower) for a representative GCaMP3+ hESC-CM graft in a blebbistatin-arrested uninjured heart. This graft showed 1:1 host-graft coupling and a brief interval between stimulus and GCaMP3 transient upstroke.

    Article Snippet: In brief, each animal was mechanically ventilated, anesthetized with 2% isoflurane, and outfitted for standard surface ECG recordings (ADInstruments).

    Techniques: Transplantation Assay, Ex Vivo, Activation Assay, Fluorescence