heart rate variability version 3.1 software Search Results


90
BioSignal Group heart rate variability analysis software – kubios hrv version 2.0
Heart Rate Variability Analysis Software – Kubios Hrv Version 2.0, supplied by BioSignal Group, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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heart rate variability analysis software – kubios hrv version 2.0 - by Bioz Stars, 2026-09
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MindWare Technologies LTD heart rate variability software hrv 3.0.25
Heart Rate Variability Software Hrv 3.0.25, supplied by MindWare Technologies LTD, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/heart+rate+variability+version+3%2E1+software/heart+variability+3+2+1+software/pm31840839-85-5-12
Average 90 stars, based on 1 article reviews
heart rate variability software hrv 3.0.25 - by Bioz Stars, 2026-09
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MindWare Technologies LTD heart rate variability scoring module version 2.16
Heart Rate Variability Scoring Module Version 2.16, supplied by MindWare Technologies LTD, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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AtCor Medical sphygmocor software
Sphygmocor Software, supplied by AtCor Medical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sphygmocor software - by Bioz Stars, 2026-09
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BioCheck Inc equipment and software to analyze heart rate variability
Equipment And Software To Analyze Heart Rate Variability, supplied by BioCheck Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
equipment and software to analyze heart rate variability - by Bioz Stars, 2026-09
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POWERLAB INC powerlab® model ml870
Powerlab® Model Ml870, supplied by POWERLAB INC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ADInstruments heart rate
Heart Rate, supplied by ADInstruments, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MindWare Technologies LTD eda/hrv analysis software
Variable description of <t> HRV </t> data.
Eda/Hrv Analysis Software, supplied by MindWare Technologies LTD, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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ATCC h9c2 rat cardiomyocyte cells
(A) Schematic overview of CRISPR–Cas9–mediated knock-in (KI) of the BMR-derived ULK1 insertion into <t>H9c2</t> rat cardiomyocytes. Wild-type (WT) and ULK1-KI cells were subjected to hypoxia–reoxygenation (H/R) with or without pharmacological modulation of mitophagy prior to downstream analyses. (B) Cell viability of WT and ULK1-KI cells under normoxia and following H/R (24 h hypoxia followed by 24 h reoxygenation). (C) Representative fluorescence microscopy images showing intracellular reactive oxygen species (ROS) levels detected by H₂DCFDA staining in WT and ULK1-KI cells following H/R. H₂O₂-treated cells (100 µM) are shown as a positive control. Images were acquired at 10X magnification; representative images are shown from at least three independent biological replicates per condition. (D) Quantification of intracellular ROS levels measured by H₂DCFDA fluorescence and normalized to cell viability assessed by CCK-8 in WT and ULK1-KI cells under normoxic and H/R conditions. ROS values were normalized to the WT normoxia group. (E) Effects of mitophagy modulation on cell viability following H/R in ULK1-KI cells. Cells were treated with urolithin A (5 µM), Mdivi-1 (20 µM), or vehicle control during H/R. (F) Representative fluorescence micrographs of ULK1-KI cells stained with MitoTracker Green (mitochondria) and Hoechst 33342 (nuclei) under the indicated conditions. Images were initially acquired using a 20X objective. Selected regions of interest (ROIs) were digitally magnified (3X) using Fiji/ImageJ software to visualize mitochondrial details. A scale bar of 75 µm was applied to the representative images. (G–J) Quantitative morphometric analysis of mitochondrial networks in ULK1-KI cells following H/R, including mitochondrial area (G), circularity (H), aspect ratio (I), and form factor (J), under vehicle, Mdivi-1, or urolithin A treatment. (K) Conceptual model summarizing the effects of the BMR-specific ULK1 insertion on mitophagy-dependent protection during H/R. ULK1 knock-in promotes mitochondrial quality control, limits ROS accumulation, and preserves cell survival under H/R stress, whereas inhibition of mitophagy abrogates this protective phenotype. Data are presented as mean ± s.e.m. unless otherwise indicated. For viability and morphometric analyses, n = 3 independent biological replicates per condition. Statistical significance was determined using two-way ANOVA with multiple-comparisons correction or unpaired two-tailed t tests, as indicated. Exact P values are shown.
H9c2 Rat Cardiomyocyte Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/heart+rate+variability+version+3%2E1+software/H9c2(2-1)/bio_rxiv__64898__2026__03__13__711419-321-0-4
Average 99 stars, based on 1 article reviews
h9c2 rat cardiomyocyte cells - by Bioz Stars, 2026-09
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97
ADInstruments blood pressure
(A) Schematic overview of CRISPR–Cas9–mediated knock-in (KI) of the BMR-derived ULK1 insertion into <t>H9c2</t> rat cardiomyocytes. Wild-type (WT) and ULK1-KI cells were subjected to hypoxia–reoxygenation (H/R) with or without pharmacological modulation of mitophagy prior to downstream analyses. (B) Cell viability of WT and ULK1-KI cells under normoxia and following H/R (24 h hypoxia followed by 24 h reoxygenation). (C) Representative fluorescence microscopy images showing intracellular reactive oxygen species (ROS) levels detected by H₂DCFDA staining in WT and ULK1-KI cells following H/R. H₂O₂-treated cells (100 µM) are shown as a positive control. Images were acquired at 10X magnification; representative images are shown from at least three independent biological replicates per condition. (D) Quantification of intracellular ROS levels measured by H₂DCFDA fluorescence and normalized to cell viability assessed by CCK-8 in WT and ULK1-KI cells under normoxic and H/R conditions. ROS values were normalized to the WT normoxia group. (E) Effects of mitophagy modulation on cell viability following H/R in ULK1-KI cells. Cells were treated with urolithin A (5 µM), Mdivi-1 (20 µM), or vehicle control during H/R. (F) Representative fluorescence micrographs of ULK1-KI cells stained with MitoTracker Green (mitochondria) and Hoechst 33342 (nuclei) under the indicated conditions. Images were initially acquired using a 20X objective. Selected regions of interest (ROIs) were digitally magnified (3X) using Fiji/ImageJ software to visualize mitochondrial details. A scale bar of 75 µm was applied to the representative images. (G–J) Quantitative morphometric analysis of mitochondrial networks in ULK1-KI cells following H/R, including mitochondrial area (G), circularity (H), aspect ratio (I), and form factor (J), under vehicle, Mdivi-1, or urolithin A treatment. (K) Conceptual model summarizing the effects of the BMR-specific ULK1 insertion on mitophagy-dependent protection during H/R. ULK1 knock-in promotes mitochondrial quality control, limits ROS accumulation, and preserves cell survival under H/R stress, whereas inhibition of mitophagy abrogates this protective phenotype. Data are presented as mean ± s.e.m. unless otherwise indicated. For viability and morphometric analyses, n = 3 independent biological replicates per condition. Statistical significance was determined using two-way ANOVA with multiple-comparisons correction or unpaired two-tailed t tests, as indicated. Exact P values are shown.
Blood Pressure, supplied by ADInstruments, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/heart+rate+variability+version+3%2E1+software/Blood+Pressure/pm40597238-61-6-18
Average 97 stars, based on 1 article reviews
blood pressure - by Bioz Stars, 2026-09
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90
Ergoline GmbH software ers.2
(A) Schematic overview of CRISPR–Cas9–mediated knock-in (KI) of the BMR-derived ULK1 insertion into <t>H9c2</t> rat cardiomyocytes. Wild-type (WT) and ULK1-KI cells were subjected to hypoxia–reoxygenation (H/R) with or without pharmacological modulation of mitophagy prior to downstream analyses. (B) Cell viability of WT and ULK1-KI cells under normoxia and following H/R (24 h hypoxia followed by 24 h reoxygenation). (C) Representative fluorescence microscopy images showing intracellular reactive oxygen species (ROS) levels detected by H₂DCFDA staining in WT and ULK1-KI cells following H/R. H₂O₂-treated cells (100 µM) are shown as a positive control. Images were acquired at 10X magnification; representative images are shown from at least three independent biological replicates per condition. (D) Quantification of intracellular ROS levels measured by H₂DCFDA fluorescence and normalized to cell viability assessed by CCK-8 in WT and ULK1-KI cells under normoxic and H/R conditions. ROS values were normalized to the WT normoxia group. (E) Effects of mitophagy modulation on cell viability following H/R in ULK1-KI cells. Cells were treated with urolithin A (5 µM), Mdivi-1 (20 µM), or vehicle control during H/R. (F) Representative fluorescence micrographs of ULK1-KI cells stained with MitoTracker Green (mitochondria) and Hoechst 33342 (nuclei) under the indicated conditions. Images were initially acquired using a 20X objective. Selected regions of interest (ROIs) were digitally magnified (3X) using Fiji/ImageJ software to visualize mitochondrial details. A scale bar of 75 µm was applied to the representative images. (G–J) Quantitative morphometric analysis of mitochondrial networks in ULK1-KI cells following H/R, including mitochondrial area (G), circularity (H), aspect ratio (I), and form factor (J), under vehicle, Mdivi-1, or urolithin A treatment. (K) Conceptual model summarizing the effects of the BMR-specific ULK1 insertion on mitophagy-dependent protection during H/R. ULK1 knock-in promotes mitochondrial quality control, limits ROS accumulation, and preserves cell survival under H/R stress, whereas inhibition of mitophagy abrogates this protective phenotype. Data are presented as mean ± s.e.m. unless otherwise indicated. For viability and morphometric analyses, n = 3 independent biological replicates per condition. Statistical significance was determined using two-way ANOVA with multiple-comparisons correction or unpaired two-tailed t tests, as indicated. Exact P values are shown.
Software Ers.2, supplied by Ergoline GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Miltenyi Biotec neonatal heart dissociation kit

Neonatal Heart Dissociation Kit, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Variable description of  HRV  data.

Journal: Data in Brief

Article Title: Dataset of physiological, behavioral, and self-report measures from a group decision-making lab study

doi: 10.1016/j.dib.2022.108630

Figure Lengend Snippet: Variable description of HRV data.

Article Snippet: How the data were acquired: , Physiological data were acquired using MindWare Impedance Cardiograph mobile recorders connected to each individual in the group via electrodes at 500 Hz. (MindWare Technologies, Gahanna, OH). Electrocardiogram data (ECG) were obtained using a modified lead II configuration and the respiratory data for the analysis of IBI were obtained using the standard tetrapolar electrode system for impedance recording . Electrodermal Activity (EDA) was collected using two disposable Ag-AgCl electrodes, placed on the palm of participants’ nondominant hand. EDA and heart rate values were later outputted from the MindWare EDA/HRV analysis software. Upon arrival at the lab, participants filled out questionnaires about their level of anxiety and social phobia, and each group was recorded for later coding of positive affective behavior. .

Techniques: Standard Deviation, Derivative Assay, Transformation Assay

Variable description of  EDA  data.

Journal: Data in Brief

Article Title: Dataset of physiological, behavioral, and self-report measures from a group decision-making lab study

doi: 10.1016/j.dib.2022.108630

Figure Lengend Snippet: Variable description of EDA data.

Article Snippet: How the data were acquired: , Physiological data were acquired using MindWare Impedance Cardiograph mobile recorders connected to each individual in the group via electrodes at 500 Hz. (MindWare Technologies, Gahanna, OH). Electrocardiogram data (ECG) were obtained using a modified lead II configuration and the respiratory data for the analysis of IBI were obtained using the standard tetrapolar electrode system for impedance recording . Electrodermal Activity (EDA) was collected using two disposable Ag-AgCl electrodes, placed on the palm of participants’ nondominant hand. EDA and heart rate values were later outputted from the MindWare EDA/HRV analysis software. Upon arrival at the lab, participants filled out questionnaires about their level of anxiety and social phobia, and each group was recorded for later coding of positive affective behavior. .

Techniques:

Journal: Data in Brief

Article Title: Dataset of physiological, behavioral, and self-report measures from a group decision-making lab study

doi: 10.1016/j.dib.2022.108630

Figure Lengend Snippet:

Article Snippet: How the data were acquired: , Physiological data were acquired using MindWare Impedance Cardiograph mobile recorders connected to each individual in the group via electrodes at 500 Hz. (MindWare Technologies, Gahanna, OH). Electrocardiogram data (ECG) were obtained using a modified lead II configuration and the respiratory data for the analysis of IBI were obtained using the standard tetrapolar electrode system for impedance recording . Electrodermal Activity (EDA) was collected using two disposable Ag-AgCl electrodes, placed on the palm of participants’ nondominant hand. EDA and heart rate values were later outputted from the MindWare EDA/HRV analysis software. Upon arrival at the lab, participants filled out questionnaires about their level of anxiety and social phobia, and each group was recorded for later coding of positive affective behavior. .

Techniques: Modification

(A) Schematic overview of CRISPR–Cas9–mediated knock-in (KI) of the BMR-derived ULK1 insertion into H9c2 rat cardiomyocytes. Wild-type (WT) and ULK1-KI cells were subjected to hypoxia–reoxygenation (H/R) with or without pharmacological modulation of mitophagy prior to downstream analyses. (B) Cell viability of WT and ULK1-KI cells under normoxia and following H/R (24 h hypoxia followed by 24 h reoxygenation). (C) Representative fluorescence microscopy images showing intracellular reactive oxygen species (ROS) levels detected by H₂DCFDA staining in WT and ULK1-KI cells following H/R. H₂O₂-treated cells (100 µM) are shown as a positive control. Images were acquired at 10X magnification; representative images are shown from at least three independent biological replicates per condition. (D) Quantification of intracellular ROS levels measured by H₂DCFDA fluorescence and normalized to cell viability assessed by CCK-8 in WT and ULK1-KI cells under normoxic and H/R conditions. ROS values were normalized to the WT normoxia group. (E) Effects of mitophagy modulation on cell viability following H/R in ULK1-KI cells. Cells were treated with urolithin A (5 µM), Mdivi-1 (20 µM), or vehicle control during H/R. (F) Representative fluorescence micrographs of ULK1-KI cells stained with MitoTracker Green (mitochondria) and Hoechst 33342 (nuclei) under the indicated conditions. Images were initially acquired using a 20X objective. Selected regions of interest (ROIs) were digitally magnified (3X) using Fiji/ImageJ software to visualize mitochondrial details. A scale bar of 75 µm was applied to the representative images. (G–J) Quantitative morphometric analysis of mitochondrial networks in ULK1-KI cells following H/R, including mitochondrial area (G), circularity (H), aspect ratio (I), and form factor (J), under vehicle, Mdivi-1, or urolithin A treatment. (K) Conceptual model summarizing the effects of the BMR-specific ULK1 insertion on mitophagy-dependent protection during H/R. ULK1 knock-in promotes mitochondrial quality control, limits ROS accumulation, and preserves cell survival under H/R stress, whereas inhibition of mitophagy abrogates this protective phenotype. Data are presented as mean ± s.e.m. unless otherwise indicated. For viability and morphometric analyses, n = 3 independent biological replicates per condition. Statistical significance was determined using two-way ANOVA with multiple-comparisons correction or unpaired two-tailed t tests, as indicated. Exact P values are shown.

Journal: bioRxiv

Article Title: ULK1-linked mitophagy promotes cardiac hypoxia tolerance in the blind mole-rat

doi: 10.64898/2026.03.13.711419

Figure Lengend Snippet: (A) Schematic overview of CRISPR–Cas9–mediated knock-in (KI) of the BMR-derived ULK1 insertion into H9c2 rat cardiomyocytes. Wild-type (WT) and ULK1-KI cells were subjected to hypoxia–reoxygenation (H/R) with or without pharmacological modulation of mitophagy prior to downstream analyses. (B) Cell viability of WT and ULK1-KI cells under normoxia and following H/R (24 h hypoxia followed by 24 h reoxygenation). (C) Representative fluorescence microscopy images showing intracellular reactive oxygen species (ROS) levels detected by H₂DCFDA staining in WT and ULK1-KI cells following H/R. H₂O₂-treated cells (100 µM) are shown as a positive control. Images were acquired at 10X magnification; representative images are shown from at least three independent biological replicates per condition. (D) Quantification of intracellular ROS levels measured by H₂DCFDA fluorescence and normalized to cell viability assessed by CCK-8 in WT and ULK1-KI cells under normoxic and H/R conditions. ROS values were normalized to the WT normoxia group. (E) Effects of mitophagy modulation on cell viability following H/R in ULK1-KI cells. Cells were treated with urolithin A (5 µM), Mdivi-1 (20 µM), or vehicle control during H/R. (F) Representative fluorescence micrographs of ULK1-KI cells stained with MitoTracker Green (mitochondria) and Hoechst 33342 (nuclei) under the indicated conditions. Images were initially acquired using a 20X objective. Selected regions of interest (ROIs) were digitally magnified (3X) using Fiji/ImageJ software to visualize mitochondrial details. A scale bar of 75 µm was applied to the representative images. (G–J) Quantitative morphometric analysis of mitochondrial networks in ULK1-KI cells following H/R, including mitochondrial area (G), circularity (H), aspect ratio (I), and form factor (J), under vehicle, Mdivi-1, or urolithin A treatment. (K) Conceptual model summarizing the effects of the BMR-specific ULK1 insertion on mitophagy-dependent protection during H/R. ULK1 knock-in promotes mitochondrial quality control, limits ROS accumulation, and preserves cell survival under H/R stress, whereas inhibition of mitophagy abrogates this protective phenotype. Data are presented as mean ± s.e.m. unless otherwise indicated. For viability and morphometric analyses, n = 3 independent biological replicates per condition. Statistical significance was determined using two-way ANOVA with multiple-comparisons correction or unpaired two-tailed t tests, as indicated. Exact P values are shown.

Article Snippet: H9c2 rat cardiomyocyte cells (ATCC, CRL-1446) were maintained in Dulbecco’s Modified Eagle Medium (DMEM, Gibco) supplemented with 10% fetal bovine serum (FBS, Sigma-Aldrich) and 0.5% penicillin-streptomycin (Gibco) at 37°C in 5% CO2.

Techniques: CRISPR, Knock-In, Derivative Assay, Fluorescence, Microscopy, Staining, Positive Control, CCK-8 Assay, Control, Software, Inhibition, Two Tailed Test

Journal: STAR Protocols

Article Title: Analysis of epicardial genes in embryonic mouse hearts with flow cytometry

doi: 10.1016/j.xpro.2021.100359

Figure Lengend Snippet:

Article Snippet: Reconstitute components of the Neonatal Heart Dissociation Kit (Miltenyi Biotec) before start of experiment.

Techniques: Recombinant, Staining, Red Blood Cell Lysis, Software, Microscopy, Fluorescence, Light Microscopy, Dissection, Control, Flow Cytometry