国立情報学研究所で電子化したコンテンツを使用している。

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 6 uppsatser.

Freiburg i. Br., Univ., Diss., 2008.

Thesis (M.Sc.). / Written for the Dept. of Biology. Title from title page of PDF (viewed 2008/01/14). Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 152-168).

Techn. Universiẗat, Diss., 2005--München.

Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 143-159).

Background-In cardiomyocytes from patients with hypertrophic cardiomyopathy, mechanical dysfunction and arrhythmogenicity are caused by mutation-driven changes in myofilament function combined with excitation-contraction (E-C) coupling abnormalities related to adverse remodeling. Whether myofilament or E-C coupling alterations are more relevant in disease development is unknown. Here, we aim to investigate whether the relative roles of myofilament dysfunction and E-C coupling remodeling in determining the hypertrophic cardiomyopathy phenotype are mutation specific. Methods and Results-Two hypertrophic cardiomyopathy mouse models carrying the R92Q and the E163R TNNT2 mutations were investigated. Echocardiography showed left ventricular hypertrophy, enhanced contractility, and diastolic dysfunction in both models; however, these phenotypes were more pronounced in the R92Q mice. Both E163R and R92Q trabeculae showed prolonged twitch relaxation and increased occurrence of premature beats. In E163R ventricular myofibrils or skinned trabeculae, relaxation following Ca2+ removal was prolonged; resting tension and resting ATPase were higher; and isometric ATPase at maximal Ca2+ activation, the energy cost of tension generation, and myofilament Ca2+ sensitivity were increased compared with that in wildtype mice. No sarcomeric changes were observed in R92Q versus wild-type mice, except for a large increase in myofilament Ca2+ sensitivity. In R92Q myocardium, we found a blunted response to inotropic interventions, slower decay of Ca2+ transients, reduced SERCA function, and increased Ca2+/calmodulin kinase II activity. Contrarily, secondary alterations of E-C coupling and signaling were minimal in E163R myocardium. Conclusions-In E163R models, mutation-driven myofilament abnormalities directly cause myocardial dysfunction. In R92Q, diastolic dysfunction and arrhythmogenicity are mediated by profound cardiomyocytesignaling and E-C coupling changes. Similar hypertrophic cardiomyopathy phenotypes can be generated through different pathways, implying different strategies for a precision medicine approach to treatment.

No description available.

Background: Early post-percutaneous coronary intervention chest pain (EPPCP) appears to be a common clinical phenomenon. EPPCP has not been fully explained or studied in the literature despite the abundance of clinical trials on percutaneous coronary intervention (PCI). The objective of this questionnaire-based survey is to assess the current perception of EPPCP among practicing interventional cardiologists nationwide. Methods: A survey questionnaire was designed utilizing the Survey Monkey tool to address the perceptions and current practices regarding key aspects of EPPCP among interventional cardiologists. The survey was sent to the interventional cardiologists via email. Results: The survey questionnaire regarding EPPCP was provided to 2615 practicing interventional cardiologists and resulted in 623 total survey responses, with 503 of those respondents completing all eight survey questions. A total of 50.2% of the interventional cardiologists perceive that the incidence of EPPCP is 5–10%, and 57.5% consider that repeat angiography or PCI is rarely needed (1 in 1000 cases). A total of 47.1% of the participants think that EPPCP is due to transient microvascular dysfunction, while 39% perceive it as a different entity requiring a different approach. When asked about developing a standardized labeling for the phenomenon of EPPCP, 34.8% of responders indicated that they believe EPPCP should be labeled as a benign form of chest pain/angina, and 28% preferred to describe EPPCP in non-standardized terms. Among interventional cardiologists, 80% thought that the treatment of this entity is a combination of reassurance and vasodilators and, without ischemic ECG changes, medical management is appropriate. Conclusion: A total of 72% of interventional cardiologists in our survey preferred to label EPPCP as standard nomenclature to facilitate communication between healthcare providers, patients and families in a consistent way. There is a diversity of opinion regarding EPPCP, no standard nomenclature, and no guideline to standardize practice. Further large-scale prospective studies are needed to better understand the pathophysiological mechanisms, optimal management strategies, prognostic implications, and clinical reporting of EPPCP.