Advances in deep learning technology have enabled complex task solutions. The accuracy of image classification tasks has improved owing to the establishment of convolutional neural networks (CNN). Cellular senescence is a hallmark of ageing and is important for the pathogenesis of ageing-related diseases. Furthermore, it is a potential therapeutic target. Specific molecular markers are used to identify senescent cells. Moreover senescent cells show unique morphology, which can be identified. We develop a successful morphology-based CNN system to identify senescent cells and a quantitative scoring system to evaluate the state of endothelial cells by senescence probability output from pre-trained CNN optimised for the classification of cellular senescence, Deep Learning-Based Senescence Scoring System by Morphology (Deep-SeSMo). Deep-SeSMo correctly evaluates the effects of well-known anti-senescent reagents. We screen for drugs that control cellular senescence using a kinase inhibitor library by Deep-SeSMo-based drug screening and identify four anti-senescent drugs. RNA sequence analysis reveals that these compounds commonly suppress senescent phenotypes through inhibition of the inflammatory response pathway. Thus, morphology-based CNN system can be a powerful tool for anti-senescent drug screening.

SummaryA 69-year-old woman without any past disease history was hospitalized for heart failure. After hospitalization, she showed myocardial infarction, atrioventricular dissociation, and cardiac dysfunction, and finally she passed away despite intensive care. Autopsy revealed that the cardiac abnormalities were due to bacterial myocarditis possibly resulting from urinary tract infection by E. coli. Although bacterial myocarditis is rare in developed countries, we should consider its possibility when patients show various cardiac abnormalities with bacterial infection.(Int Heart J 2018; 59: 229-232) Key words: Heart failure, Myocardial infarction, Atrioventricular dissociation M yocarditis induces various cardiac abnormalities including systolic dysfunction and arrhythmia. The most common cause of myocarditis in developed countries is the infection of viruses such as coxsackievirus, adenovirus, enterovirus, parvovirus B-19, parainfluenza viruses and human herpesvirus-6. 1,2) Although bacterial myocarditis was has been very rare in developed countries, 3) the number of patients with bacterial myocarditis has recently been increasing because of an increase in immunocompromised hosts. In most cases, bacterial myocarditis is suspected based on clinical test results, but few cases have been diagnosed while alive. We here present a patient who suddenly developed myocardial infarction, atrioventricular dissociation, and heart failure without any past disease history. Morbid anatomy revealed that the diagnosis was bacterial myocarditis. Here we describe the various clinical and pathological findings of this case and with some also discussions about bacterial myocarditis in general. Case ReportA 69-year-old woman visited our hospital because of death of her brother's death. While she was plunged in grief, she suddenly felt dyspnea. Approximately 2 weeks before, she had visited a local doctor because of wheezing and insomnia. Pleural effusion had been found by chest X-ray examination, and a diuretic had been prescribed. In our hospital, she had slight tachycardia (106/minute) but other physical findings, including blood pressure (118/64 mmHg) and body temperature (35.5 ), were normal (35.5 ). X-ray examination revealed bilateral pleural effusion and pulmonary congestion, and the electrocardiogram showed a negative T wave in I, aVL, and V3-6 leads. Routine blood examination revealed the elevation of C-reactive protein levels (4.8 mg 8 mg/dL) and white blood cell counts (13.9 × 10 3 /μL). Ultrasound echocardiography showed dilatation of the left ventricle (left ventricular dimension diastolic/systolic 60/51 mm), systolic dysfunction (ejection fraction 31%), mild aortic regurgitation, and moderate mitral regurgitation. The wall motion was diffusely reduced, and in particular, the wall motions of the inferior apex wall and the anterolateral wall were severely impaired. We diagnosed her as acute decompensated heart failure with unknown etiology and administered furosemide, carperitide and dobutamine. Since she had no fever a...

Background: The concept of Clinical Scenario (CS) classification has been widely utilized to aid in choosing appropriate management strategies for acute decompensated heart failure (ADHF). Methods and Results: The West Tokyo-Heart Failure (WET-HF) Registry is a multicenter, prospective cohort registry enrolling consecutive hospitalized ADHF patients. Based on systolic blood pressure (SBP) at admission, 4,000 patients enrolled between 2006 and 2017 were classified into 3 groups: CS1, SBP ≥140 mmHg; CS2, 100≤SBP<140 mmHg; and CS3, SBP <100 mmHg. The CS1 group had a high rate of fluid retention such as leg edema, and the largest reduction in body weight at discharge. In-hospital diuretics use was the most frequent in CS1. Although the primary endpoint of long-term all-cause death and/or ADHF re-hospitalization was more common in more advanced CS, there was no significant difference between the 3 CS groups in patients with HF with preserved ejection fraction (HFpEF; P=0.10). Although more advanced CS was associated with larger left ventricular (LV) chamber size in HF with reduced EF (HFrEF), it was associated with smaller LV size in HFpEF. Conclusions: The long-term prognostic value of CS classification was limited in HFpEF. Whereas CS was closely associated with degree of LV remodeling in HFrEF, a smaller LV chamber might be associated with a lower cardiovascular functional reserve in HFpEF.

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Failure of the right ventricle plays a critical role in any type of heart failure. However, the mechanism remains unclear, and there is no specific therapy. Here, we show that the right ventricle predominantly expresses alternative complement pathway-related genes, including Cfd and C3aR1. Complement 3 (C3)-knockout attenuates right ventricular dysfunction and fibrosis in a mouse model of right ventricular failure. C3a is produced from C3 by the C3 convertase complex, which includes the essential component complement factor D (Cfd). Cfd-knockout mice also show attenuation of right ventricular failure. Moreover, the plasma concentration of CFD correlates with the severity of right ventricular failure in patients with chronic right ventricular failure. A C3a receptor (C3aR) antagonist dramatically improves right ventricular dysfunction in mice. In summary, we demonstrate the crucial role of the C3-Cfd-C3aR axis in right ventricular failure and highlight potential therapeutic targets for right ventricular failure.