Ventricular arrhythmias are difficult to study in man. The current experimental models are arrhythmias induced by electrical stimulation, coronary artery ligation or by subsequent reperfusion. An electrophysiological model will be useful for exploring the cellular mechanism of arrhythmias and for studying the mechanism of action of new anti-arrhythmic drugs. This project seeks to establish automaticity as a model for studying ventricular arrhythmias. Objectives 1. To review the literature on the mechanism of ventricular arrhythmias. 2. To explore ventricular automaticity induced by "reperfusion" after O₂ and substrate deprivation. 3 . To explore beta-adrenoceptor mediated ventricular automaticity. 4 . To evaluate possible new anti-arrhythmic drugs, carminomycin and ketanserin.

Wnt/β-catenin signaling is activated in the heart after myocardial infarction (MI). This study aims to investigate if β-catenin deletion affects post-MI ion channel gene alterations and ventricular tachycardias (VT). MI was induced by permanent ligation of left anterior descending artery in wild-type (WT) and cardiomyocyte-specific β-catenin knockout (KO) mice. KO mice showed reduced susceptibility to VT (18% vs. 77% in WT) at 8 weeks after MI, associated with reduced scar size and attenuated chamber dilation. qPCR analyses of both myocardial tissues and purified cardiomyocytes demonstrated upregulation of Wnt pathway genes in border and infarct regions after MI, including Wnt ligands (such as Wnt4) and receptors (such as Fzd1 and Fzd2). At 1 week after MI, cardiac sodium channel gene (Scn5a) transcript was reduced in WT but not in KO hearts, consistent with previous studies showing Scn5a inhibition by Wnt/β-catenin signaling. At 8 weeks after MI when Wnt genes have declined, Scn5a returned to near sham levels and K⁺ channel gene downregulations were not different between WT and KO mice. This study demonstrated that VT susceptibility in the chronic phase after MI is reduced in mice with cardiomyocyte-specific β-catenin deletion primarily through attenuated structural remodeling, but not ion channel gene alterations.

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京都大学 / 新制・課程博士 / 博士(医学) / 甲第24802号 / 医博第4994号 / 新制||医||1067(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 石見 拓, 教授 近藤 尚己, 教授 湊谷 謙司 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

An ECG (electrocardiogram) simulator is an electronic tool that plays an essential role in the testing, design, and development of ECG monitors and other ECG equipment. Principally an ECG simulator provides ECG monitors with an electrical signal that emulates the human heart's electrical signal so that the monitor can be tested for reliability and important diagnostic capabilities. However, the current portable commercially available ECG simulators are lacking in their ability to fully test ECG monitors. Specifically, the portable simulators presently on the market do not produce authentic ECG signals but rather they endeavor to create the ECG signals mathematically. They even attempt to mathematically create arrhythmias (irregular heartbeats of which there are many different types). Arrhythmia detection is an important capability for any modern ECG monitor because arrhythmias are often the critical link to the diagnosis of heart conditions or cardiovascular disease. The focus of this thesis is the design and implementation of a portable ECG simulator. The important innovation of this prototype simulator is that it will not create its ECG signals mathematically, but rather it will store ECG data files on a memory module and use this data to produce an authentic ECG signal. The data files will consist of different types of ECG signals including different types of arrhythmias. The data files are obtained via the internet and require formatting and storing onto a memory chip. These files are then processed by a digital to analog converter and output on a four lead network to produce an authentic ECG signal. The system is built around the ultra-low power Texas Instruments MSP430 microcontroller.

Although we have several therapeutic interventions for depression, we lack an understanding of the mechanisms that underlie these interventions. To gain a better understanding of the mental health conditions we treat, diagnoses we make, and interventions we use, mechanistic understandings are necessary. There is evidence that exposure to depressive emotion and cognitions can yield therapeutic outcome. The current study examines the physiology associated with an intervention, expressive writing (EW), which other research has shown to produce therapeutic outcomes because it increases exposure to negative feelings. The current study tests the hypothesis that EW increases depressive emotion, cognition, and physiology. Depression has been associated with decreased respiratory sinus arrhythmia (RSA) and increased heart rate (HR). RSA and HR were measured while participants did either EW or a control writing (CW) task. Because measures of RSA can be confounded by respiratory rate (RR), RR was also measured and statistically controlled for. Results revealed that EW does not alter RSA or HR. Interestingly, exploratory regression analyses between HR and RR during EW suggest that EW might trigger exposure to a depressive physiological state. Further investigation into the relationship between HR and RR during EW is warranted. / Thesis / Master of Science (MSc) / The current study examines the emotion, cognition, and physiology associated with an intervention, expressive writing (EW), which is commonly used as a treatment for anxiety and depression. Research has suggested that EW produces therapeutic outcome because it increases exposure to negative feelings. The current study tests the hypothesis that EW increases depressive emotion, cognition, and physiology. Results suggest that EW increases depressive emotion and cognition but does not alter some of the physiological parameters that have been associated with depression in prior research. An unpredicted exploratory result was that EW affected the relationship between heart rate and respiratory rate. Further investigation into the relationship between heart rate and respiratory rate during EW is warranted.

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