Objective To evaluate the diagnostic value of cardiac magnetic resonance (MR) for acute heart failure (AHF) with unknown cause. Methods A retrospective study was conducted, eleven patients with AHF with unknown cause admitted to Tianjin First Center Hospital from September 2017 to August 2018 were enrolled, and all the patients underwent complete cardiac MR imaging (plain MR and delayed enhancement imaging) with satisfactory image quality fulfilled the diagnostic requirement. Additionally, all of them had no history of heart disease and lack of diagnostic laboratory tests (routine blood test, blood biochemistry and myocardial enzyme), electrocardiogram (ECG) changes and echocardiography abnormality. Besides, 10 patients had completed invasive coronary angiography or coronary CT angiography (CCTA); the results of laboratory tests, ECG abnormality, echocardiography and cardiac MR were recorded, and the values of echocardiography and cardiac MR examination in the diagnosis and exploring the cause of patients with AHF with unknown cause were analyzed. Results Nine of 11 patients with AHF with unknown cause had positive finding on cardiac MR examination; there were 3 patients with chronic myocardial infarction, 3 with dilated cardiomyopathy, 2 with cardiac involvement of amyloidosis and 1 with myocarditis. The left ventricular end systolic volume (LVESV) measured on cardial MR was significantly higher than that on echocardiography (mL: 120.68±57.47 vs. 108.84±50.49, P < 0.05), the left ventricular ejection fraction (LVEF) and myocardial valvular regurgitation measured on MR were less than those on echocardiography (LVEF: 0.36±0.09 vs. 0.43±0.10; regurgitation: 11 vs. 22, both P < 0.05); while, the differences of the end diastolic volume (LVEDV) and the number of patients with pericardial effusions between MR and echocardiography had no statistical significant differences [LVEDV (mL): 183.37±65.26 vs. 182.26±70.44; pericardial effusion: 6 cases vs. 6 cases, all P > 0.05]. Conclusion Cardiac MR could synthetically evaluate the heart by its morphology, function as well as accompanied sign (pericardial effusion) and cardiac tissue characteristics; eventually, it may provide valuable information concerning the selection of proper clinical therapeutic strategies and improvement of AHF patients' prognose.

Objective: To understand the pathogenic spectrum characteristics of enteroviruses of non-enterovirus (EV) 71 and non-coxsackievirus (CV) A16 associated with hand, foot and mouth disease (HFMD) in Xinjiang. Methods: Specimens were collected from HFMD patients infected with non-EV-A71 non-CV-A16 enterovirus from 2011 to 2016 in Xinjiang. The virion protein (VP)1 gene sequence was amplified by reverse transcription polymerase chain reaction (RT-PCR) and sequenced. Sequencing and genotyping were performed through erterovirus genotyping tool. Results: A total of 119 sequences were obtained, 15 human enterovirus serotypes were identified including CV-A6, CV-A10, CV-A4, CV-A8, CV-B1, CV-B3 (4 strains), CV-B4, CV-B5, ECHO30, ECHO12, ECHO14, CV-A9, CV-A24, PV1 and PV3. The composition ratio of CV-A6 among non-EV-A71 non-CV-A16 enterovirus in 2013, 2015 and 2016 was 87.9%, 79.5% and 88.3% respectively. Conclusions The pathogens causing HFMD in Xinjiang included more than 17 kinds of human enterovirus serotypes. Since 2013, CV-A6 has become the main pathogen of HFMD simultaneously or alternately with EV-A71 and CV-A16.

Background::Sepsis, a serious condition with high mortality, usually causes sepsis associated encephalopathy (SAE) that involves neuronal cell death. However, the cell death programs involved and their underlying mechanisms are not clear. This study aimed to explore the regulatory mechanisms of different cell death programs in SAE.Methods::A neonatal rat model of SAE was established by cecal ligation and perforation. Survival rate and vital signs (mean arterial pressure and heart rate) were monitored, nerve reflexes were evaluated, and cortical pathological changes were observed by hematoxylin and eosin staining. The expression of pyroptosis, apoptosis, and necroptosis (PANoptosis)-related proteins, mitogen-activated protein kinase (MAPK), and its upstream regulator toll-like receptor 9 (TLR9) were detected. The expression of TLR9 in neurons was observed by immunofluorescence staining. The ultrastructure of neurons was observed by transmission electron microscope.Results::First, PANoptosis was found in cortical nerve cells of the SAE rats. Meanwhile, the subunits of MAPKs, p38 MAPK, Jun N-terminal kinase, and extracellular signal-regulated kinase (ERK) were activated. After pharmacologically inhibiting each of the subunits, only p38 MAPK was found to be associated with PANoptosis. Furthermore, blocking the p38 MAPK signaling pathway activated necroptosis but inhibited apoptosis and pyroptosis. When necroptosis was pharmacologically inhibited, apoptosis and pyroptosis were reactivated. Finally, we found that the expression of TLR9, a regulator of MAPKs, was significantly increased in this model. After down-regulation of TLR9, p38 MAPK, and ERK signaling pathways were inhibited, which led to the inhibition of PANoptosis. Further analysis found that down-regulation of TLR9 improved the survival rate and reduced the pathological changes in SAE rats.Conclusions::Our study showed that the programs comprising PANoptosis are activated simultaneously in SAE rats. TLR9 activated PANoptosis through the p38 MAPK signaling pathway. TLR9 may work as a potential target for SAE treatment.