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  1. Article ; Online: Phosphorylation of Lamin A/C at serine 22 modulates Na

    Olaopa, Michael A / Ai, Tomohiko / Chao, Bo / Xiao, Xiangshu / Vatta, Matteo / Habecker, Beth A

    Physiological reports

    2021  Volume 9, Issue 22, Page(s) e15121

    Abstract: Variants in the LMNA gene, which encodes for Lamin A/C, are associated with cardiac conduction disease (CCD). We previously reported that Lamin A/C variants p.R545H and p.A287Lfs*193, which were identified in CCD patients, decreased peak ... ...

    Abstract Variants in the LMNA gene, which encodes for Lamin A/C, are associated with cardiac conduction disease (CCD). We previously reported that Lamin A/C variants p.R545H and p.A287Lfs*193, which were identified in CCD patients, decreased peak I
    MeSH term(s) Cardiac Conduction System Disease/genetics ; Cardiac Conduction System Disease/metabolism ; HEK293 Cells ; Humans ; Lamin Type A/genetics ; Lamin Type A/metabolism ; Mutation ; Mutation, Missense ; NAV1.5 Voltage-Gated Sodium Channel/metabolism ; Patch-Clamp Techniques ; Phosphorylation
    Chemical Substances LMNA protein, human ; Lamin Type A ; NAV1.5 Voltage-Gated Sodium Channel ; SCN5A protein, human
    Language English
    Publishing date 2021-11-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15121
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Heterogeneous cardiac sympathetic innervation gradients promote arrhythmogenesis in murine dilated cardiomyopathy.

    Dajani, Al-Hassan J / Liu, Michael B / Olaopa, Michael A / Cao, Lucian / Valenzuela-Ripoll, Carla / Davis, Timothy J / Poston, Megan D / Smith, Elizabeth H / Contreras, Jaime / Pennino, Marissa / Waldmann, Christopher M / Hoover, Donald B / Lee, Jason T / Jay, Patrick Y / Javaheri, Ali / Slavik, Roger / Qu, Zhilin / Ajijola, Olujimi A

    JCI insight

    2023  Volume 8, Issue 22

    Abstract: Ventricular arrhythmias (VAs) in heart failure are enhanced by sympathoexcitation. However, radiotracer studies of catecholamine uptake in failing human hearts demonstrate a proclivity for VAs in patients with reduced cardiac sympathetic innervation. We ... ...

    Abstract Ventricular arrhythmias (VAs) in heart failure are enhanced by sympathoexcitation. However, radiotracer studies of catecholamine uptake in failing human hearts demonstrate a proclivity for VAs in patients with reduced cardiac sympathetic innervation. We hypothesized that this counterintuitive finding is explained by heterogeneous loss of sympathetic nerves in the failing heart. In a murine model of dilated cardiomyopathy (DCM), delayed PET imaging of sympathetic nerve density using the catecholamine analog [11C]meta-Hydroxyephedrine demonstrated global hypoinnervation in ventricular myocardium. Although reduced, sympathetic innervation in 2 distinct DCM models invariably exhibited transmural (epicardial to endocardial) gradients, with the endocardium being devoid of sympathetic nerve fibers versus controls. Further, the severity of transmural innervation gradients was correlated with VAs. Transmural innervation gradients were also identified in human left ventricular free wall samples from DCM versus controls. We investigated mechanisms underlying this relationship by in silico studies in 1D, 2D, and 3D models of failing and normal human hearts, finding that arrhythmogenesis increased as heterogeneity in sympathetic innervation worsened. Specifically, both DCM-induced myocyte electrical remodeling and spatially inhomogeneous innervation gradients synergistically worsened arrhythmogenesis. Thus, heterogeneous innervation gradients in DCM promoted arrhythmogenesis. Restoration of homogeneous sympathetic innervation in the failing heart may reduce VAs.
    MeSH term(s) Humans ; Mice ; Animals ; Cardiomyopathy, Dilated/diagnostic imaging ; Heart ; Myocardium ; Arrhythmias, Cardiac/diagnostic imaging ; Catecholamines
    Chemical Substances Catecholamines
    Language English
    Publishing date 2023-11-22
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.157956
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Complex Arrhythmia Syndrome in a Knock-In Mouse Model Carrier of the N98S

    Tsai, Wen-Chin / Guo, Shuai / Olaopa, Michael A / Field, Loren J / Yang, Jin / Shen, Changyu / Chang, Ching-Pin / Chen, Peng-Sheng / Rubart, Michael

    Circulation

    2020  Volume 142, Issue 20, Page(s) 1937–1955

    Abstract: Background: Calmodulin mutations are associated with arrhythmia syndromes in humans. Exome sequencing previously identified a de novo mutation in : Methods: Mouse lines heterozygous for the Calm1: Results: Two biologically independent knock-in ... ...

    Abstract Background: Calmodulin mutations are associated with arrhythmia syndromes in humans. Exome sequencing previously identified a de novo mutation in
    Methods: Mouse lines heterozygous for the Calm1
    Results: Two biologically independent knock-in mouse lines heterozygous for the Calm1
    Conclusions: Heterozygosity for the
    MeSH term(s) Amino Acid Substitution ; Animals ; Calmodulin/genetics ; Calmodulin/metabolism ; Disease Models, Animal ; Heart Ventricles/metabolism ; Heart Ventricles/physiopathology ; Humans ; Male ; Mice ; Mice, Transgenic ; Mutation, Missense ; Myocytes, Cardiac/metabolism ; Purkinje Fibers/metabolism ; Purkinje Fibers/physiopathology ; Sick Sinus Syndrome/congenital ; Sick Sinus Syndrome/genetics ; Sick Sinus Syndrome/metabolism ; Sick Sinus Syndrome/physiopathology
    Chemical Substances Calm1 protein, mouse ; Calmodulin
    Language English
    Publishing date 2020-09-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.120.046450
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui IV Zs.60: Show issues Location:
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  4. Article: Genetic Variation of SCN5A in Korean Patients with Sick Sinus Syndrome.

    Lee, Young Soo / Olaopa, Michael A / Jung, Byung Chun / Lee, Sang Hee / Shin, Dong Gu / Park, Hyoung Seob / Cho, Yongkeun / Han, Sang Mi / Lee, Myung Hoon / Kim, Yoon Nyun

    Korean circulation journal

    2016  Volume 46, Issue 1, Page(s) 63–71

    Abstract: Background and objectives: Due to recent studies that have shown an association between the genetic variation of SCN5A and sick sinus syndrome (SSS), we sought to determine if a similar correlation existed in Korean patients with SSS.: Subjects and ... ...

    Abstract Background and objectives: Due to recent studies that have shown an association between the genetic variation of SCN5A and sick sinus syndrome (SSS), we sought to determine if a similar correlation existed in Korean patients with SSS.
    Subjects and methods: We enrolled 30 patients with SSS who showed a sinus pause (longer than 3.0 s) in Holter monitoring, in addition to 80 controls. All exons including the putative splicing sites of the SCN5A gene were amplified by polymerase chain reaction and sequenced either directly or following subcloning. Wild-type and single nucleotide polymorphisms were expressed in human embryonic kidney cells, and the peak sodium current (INa ) was analyzed using the whole-cell patch-clamp technique.
    Results: A total of 9 genetic variations were identified: 7 variations (G87A-A29A, IVS9-3C>A, A1673G-H558R, G3823A-D1275N, T5457C-D1819D, T5963G-L1988R, and C5129T-S1710L) had been previously reported, and 2 variants (A3075T-E1025D and T4847A-F1616Y) were novel; the potential structural effects of F1616Y were analyzed in a three-dimensional model of the SCN5A domain. Patch-clamp studies at room temperature demonstrated that the peak INa was significantly increased by 140% in HEK cells transfected with F1616Y compared with wild-type (-335.13 pA/pF±24.04, n=8 vs. -139.95 pA/pF±23.76, n=7, respectively). Furthermore, the voltage dependency of the activation and steady-state inactivation of F1616Y were leftward-shifted compared with wild-type (Vh activation=-55.36 mv±0.22, n=8 vs. Vh activation=-44.21 mV±0.17, n=7; respectively; Vh inactivation=-104.47 mV±0.21, n=7 vs. Vh inactivation=-84.89 mV±0.09, n=12, respectively).
    Conclusion: F1616Y may be associated with SSS.
    Language English
    Publishing date 2016-01-14
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2557464-4
    ISSN 1738-5520
    ISSN 1738-5520
    DOI 10.4070/kcj.2016.46.1.63
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6894: Show issues Location:
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  5. Article ; Online: Small conductance calcium-activated potassium current and the mechanism of atrial arrhythmia in mice with dysfunctional melanocyte-like cells.

    Tsai, Wei-Chung / Chan, Yi-Hsin / Hsueh, Chia-Hsiang / Everett, Thomas H / Chang, Po-Cheng / Choi, Eue-Keun / Olaopa, Michael A / Lin, Shien-Fong / Shen, Changyu / Kudela, Maria Aleksandra / Rubart-von der Lohe, Michael / Chen, Zhenhui / Jadiya, Pooja / Tomar, Dhanendra / Luvison, Emily / Anzalone, Nicholas / Patel, Vickas V / Chen, Peng-Sheng

    Heart rhythm

    2016  Volume 13, Issue 7, Page(s) 1527–1535

    Abstract: Background: The melanin synthesis enzyme dopachrome tautomerase (Dct) regulates intracellular Ca(2+) in melanocytes. Homozygous Dct knockout (Dct(-/-)) adult mice are vulnerable to atrial arrhythmias (AA).: Objective: The purpose of this study was to ...

    Abstract Background: The melanin synthesis enzyme dopachrome tautomerase (Dct) regulates intracellular Ca(2+) in melanocytes. Homozygous Dct knockout (Dct(-/-)) adult mice are vulnerable to atrial arrhythmias (AA).
    Objective: The purpose of this study was to determine whether apamin-sensitive small conductance Ca(2+)-activated K(+) (SK) currents are upregulated in Dct(-/-) mice and contribute to AA.
    Methods: Optical mapping was used to study the membrane potential of the right atrium in Langendorff perfused Dct(-/-) (n = 9) and Dct(+/-) (n = 9) mice.
    Results: Apamin prolonged action potential duration (APD) by 18.8 ms (95% confidence interval [CI] 13.4-24.1 ms) in Dct(-/-) mice and by 11.5 ms (95% CI 5.4-17.6 ms) in Dct(+/-) mice at a pacing cycle length of 150 ms (P = .047). The pacing cycle length threshold to induce APD alternans was 48 ms (95% CI 34-62 ms) for Dct(-/-) mice and 21 ms (95% CI 12-29 ms) for Dct(+/-) mice (P = .002) at baseline, and it was 35 ms (95% CI 21-49 ms) for Dct(-/-) mice and 22 ms (95% CI 11-32 ms) for Dct(+/-) mice (P = .025) after apamin administration. Apamin prolonged post-burst pacing APD by 8.9 ms (95% CI 3.9-14.0 ms) in Dct(-/-) mice and by 1.5 ms (95% CI 0.7-2.3 ms) in Dct(+/-) mice (P = .005). Immunoblot and quantitative polymerase chain reaction analyses showed that protein and transcripts levels of SK1 and SK3 were increased in the right atrium of Dct(-/-) mice. AA inducibility (89% vs 11%; P = .003) and duration (281 seconds vs 66 seconds; P = .008) were greater in Dct(-/-) mice than in Dct(+/-) mice at baseline, but not different (22% vs 11%; P = 1.00) after apamin administration. Five of 8 (63%) induced atrial fibrillation episodes in Dct(-/-) mice had focal drivers.
    Conclusion: Apamin-sensitive SK current upregulation in Dct(-/-) mice plays an important role in the mechanism of AA.
    MeSH term(s) Animals ; Atrial Fibrillation/metabolism ; Atrial Fibrillation/pathology ; Atrial Fibrillation/physiopathology ; Heart Atria/metabolism ; Heart Atria/physiopathology ; Heart Conduction System/metabolism ; Heart Conduction System/physiopathology ; Intramolecular Oxidoreductases/metabolism ; Melanins/metabolism ; Membrane Potentials/physiology ; Mice ; Small-Conductance Calcium-Activated Potassium Channels/physiology ; Statistics as Topic ; Up-Regulation ; Voltage-Sensitive Dye Imaging/methods
    Chemical Substances Melanins ; Small-Conductance Calcium-Activated Potassium Channels ; Intramolecular Oxidoreductases (EC 5.3.-) ; dopachrome isomerase (EC 5.3.3.12)
    Language English
    Publishing date 2016-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2016.03.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6278: Show issues Location:
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