Publications by authors named "Shinobu Kuratomi"

Background: First-degree atrioventricular block (AVB) may lead to complete AVB. Herein, we present a case of a complete AVB under thoracic epidural catheter infusion of ropivacaine with fentanyl in a patient with first-degree AVB and myasthenia gravis.

Case Presentation: A 74-year-old woman with first-degree AVB underwent thymectomy for myasthenia gravis.

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Aims: Hcn4, which encodes the hyperpolarization-activated, cyclic nucleotide-sensitive channel (I(h)), is a well-established marker of the cardiac sino-atrial node. We aimed to identify cis-elements in the genomic locus of the Hcn4 gene that regulate the transcription of Hcn4.

Methods And Results: We screened evolutionarily conserved non-coding sequences (CNSs) that are often involved in the regulation of gene expression.

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The HCN4 channel shows differential expression patterns during the embryonic development and hypertrophy of hearts. Briefly, HCN4 expression is maximally activated in embryonic hearts and quickly diminishes after birth. However, it is reactivated during cardiac hypertrophy.

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The matrix metalloproteinase (MMP) family (approximately 25 members in mammals) has been implicated in extracellular matrix remodeling associated with embryonic development, cancer formation and progression, and various other physiological and pathological events. Inactivating mutations in individual matrix metalloproteinase genes in mice described so far, however, are nonlethal at least up to the first few weeks after birth, suggesting functional redundancy among MMP family members. Here, we report that mice lacking two MMPs, MMP-2 (nonmembrane type) and MT1-MMP (membrane type), die immediately after birth with respiratory failure, abnormal blood vessels, and immature muscle fibers reminiscent of central core disease.

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Article Synopsis
  • The fetal cardiac gene program is activated in hypertrophied and failing hearts, impacting heart function and prognosis.
  • NRSF (neuron-restrictive silencer factor) is identified as a key regulator of multiple fetal cardiac genes, influencing their expression in heart cells.
  • Mice with a mutated version of NRSF exhibit severe heart issues, including dilated cardiomyopathy and increased risk of arrhythmias, highlighting NRSF's crucial role in cardiac health.
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This paper discusses the development of a cardiac sinoatrial (SA) node pacemaker model. The model successfully reconstructs the experimental action potentials at various concentrations of external Ca2+ and K+. Increasing the amplitude of L-type Ca2+ current (I(CaL)) prolongs the duration of the action potential and thereby slightly decreases the spontaneous rate.

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Individual ion channels or exchangers are described with a common set of equations for both the sinoatrial node pacemaker and ventricular cells. New experimental data are included, such as the new kinetics of the inward rectifier K+ channel, delayed rectifier K+ channel, and sustained inward current. The gating model of Shirokov et al.

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Types and distributions of inwardly rectifying potassium (Kir) channels are one of the major determinants of the electrophysiological properties of cardiac myocytes. Kir2.1 (classical inward rectifier K(+) channel), Kir6.

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