We report on our experience at the highly interactive special session "General Cardiology Hangout" at the 63rd Annual Scientific Session of the Japanese College of Cardiology, in which the e-portfolio system of Tokyo Medical University and a personal response system (PRS) were used to collect real-time free comments and feedback from the audience.

　In order to effectively manage an interactive session at an academic meeting by collecting feedback from the audience through a PRS and free comments, it is necessary to train facilitators who have the ability to organically extract and integrate the opinions and feedback from the audience in a relevant matter, and to develop tools that are both more user-friendly and secure.

No abstract available.
Angioplasty* ; Hypertension, Pulmonary*

No abstract available.
Mitral Valve Insufficiency

No abstract available.
Acute Disease ; Aneurysm, Dissecting/complications/*diagnosis/physiopathology ; Aortic Aneurysm/complications/*diagnosis/physiopathology ; Aortic Valve Insufficiency/*diagnosis/etiology/physiopathology ; Fingers/*blood supply ; Humans ; Light/*diagnostic use ; Male ; Middle Aged ; Predictive Value of Tests ; *Pulse

A 36-year-old female with a high-grade fever and epigastric abdominal pain was prescribed antibiotics, but developed hypoxia and dyspnea. An echocardiography revealed diffuse hypokinesis and massive pericardial effusion, after which diagnostic cardiac catheterization and an endomyocardial biopsy (EMB) were peformed to reveal fibrosis and infiltration of inflammation cells composed primarily of neutrophils. Clinical manifestation of a spiking fever, leukocytosis, elevated ferritin levels, skin rash and EMB findings led to a diagnosis of adult-onset Still's disease (AOSD) with acute myocarditis. Pulse therapy of intravenous methylprednisolone was performed for three days, followed by a daily dose of prednisone (60 mg). After a course of steroid therapy for fever and pericardial effusion, and conducting a left ventricular ejection fraction, the patient showed improvement and was discharged asymptomatic within 32 days of admission. This study is the first to report on a case of myocarditis in AOSD diagnosed by neutrophil infiltration in the myocardium.
Abdominal Pain ; Adult ; Anoxia ; Anti-Bacterial Agents ; Biopsy* ; Cardiac Catheterization ; Cardiac Catheters ; Diagnosis ; Dyspnea ; Echocardiography ; Exanthema ; Female ; Ferritins ; Fever ; Fibrosis ; Heart Failure ; Humans ; Inflammation ; Leukocytosis ; Magnetic Resonance Imaging* ; Methylprednisolone ; Myocarditis* ; Myocardium ; Neutrophil Infiltration ; Neutrophils ; Pericardial Effusion ; Prednisone ; Still's Disease, Adult-Onset* ; Stroke Volume

BACKGROUND/OBJECTIVES: Patients with chronic kidney disease (CKD) have a high concentration of uremic toxins in their blood and often experience muscle atrophy. Indoxyl sulfate (IS) is a uremic toxin produced by tryptophan metabolism. Although an elevated IS level may induce muscle dysfunction, the effect of IS on physiological concentration has not been elucidated. Additionally, the effects of ursolic acid (UA) on muscle hypertrophy have been reported in healthy models; however, it is unclear whether UA ameliorates muscle dysfunction associated with chronic diseases, such as CKD. Thus, this study aimed to investigate whether UA can improve the IS-induced impairment of mitochondrial biogenesis.MATERIALS/METHODS: C2C12 cells were incubated with or without IS (0.1 mM) and UA (1 or 2 µM) to elucidate the physiological effect of UA on CKD-related mitochondrial dysfunction and its related mechanisms using real-time reverse transcription-polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay. RESULTS: IS suppressed the expression of differentiation marker genes without decreasing cell viability. IS decreased the mitochondrial DNA copy number and ATP levels by downregulating the genes pertaining to mitochondrial biogenesis (Ppargc1a, Nrf1, Tfam, Sirt1, and Mef2c), fusion (Mfn1 and Mfn2), oxidative phosphorylation (Cycs and Atp5b), and fatty acid oxidation (Pdk4, Acadm, Cpt1b, and Cd36). Furthermore, IS increased the intracellular mRNA and secretory protein levels of interleukin (IL)-6. Finally, UA ameliorated the IS-induced impairment in C2C12 cells. CONCLUSIONS Our results indicated that UA improves the IS-induced impairment of mitochondrial biogenesis by affecting differentiation, ATP levels, and IL-6 secretion in C2C12 cells. Therefore, UA could be a novel therapeutic agent for CKD-induced muscle dysfunction.