A 37-year-old male patient was admitted to hospital on 14 January 2020, with chest pain and dyspnoea for 3 days, accompanied by diarrhoea. His blood pressure decreased to 80/50 mmHg. X-ray chest film showed significant enlargement of the heart (Panel A: cardiothoracic ratio 0.70). Chest computed tomography (CT) examination indicated pulmonary infection, enlarged heart, and pleural effusion (Panels B and C). The electrocardiogram suspected ST-segment elevation acute myocardial infarction (III, AVF STsegment elevation, Panels D and E), an emergency CT coronary angiography revealed no coronary stenosis. Markers of myocardial injury were significantly elevated. Troponin T was more than 10 000 ng/L. Creatine kinase isoenzyme CKMB 112.9 ng/L. Natriuretic peptide BNP was up to 21 025 ng/L. Echocardiography revealed an enlarged heart and a marked decrease in ventricular systolic function [left ventricle (end diastolic) dimension (LV) 58 mm, left atrium dimension (LA) 39 mm, right ventricle dimension (RV) 25 mm, right atrium dimension (RA) 48 mm, left ventricular ejection fraction (LVEF) 27%, trace 2 mm pericardial effusion]. Sputum was examined for 13 viral nucleic acids related to respiratory tract. Only the coronavirus nucleic acid test was positive. All of the other 12 nucleic acid tests were negative, including influenza A virus, adenovirus, bocavirus, rhinovirus, influenza A(H1N1) 2009, parainfluenza, chlamydia, partial pulmonary virus, influenza B virus, mycoplasma pneumoniae, influenza A virus H3N2, and respiratory syncytial virus. The diagnosis of this patient is coronavirus fulminant myocarditis with cardiogenic shock and pulmonary infection.Treatments include methylprednisolone to suppress inflammation (200 mg/day, 4 days), and immunoglobulin to regulate immune status (20 g/day, 4 days), norepinephrine to raise blood pressure, diuretic (toracemide and furosemide) to reduce cardiac load, milrinone to increase myocardial contractility, piperacillin sulbactam for anti-infection, pantoprazole, to inhibit gastric acid. After treatment, the patient's symptoms improved significantly. One week later, X-ray chest film showed heart size normal (Panel F cardiothoracic ratio 0.49). Echocardiography showed that the size and function of the heart had returned to normal (LV 42 mm, LA 34 mm, RV 24 mm, RA 33 mm, LVEF 66%). Markers of myocardial injury dropped significantly after 1 week of treatment. Troponin T was 220.5 ng/L. Creatine kinase isoenzyme CKMB 9.14 ng/L. Natriuretic peptide BNP was 1587 ng/L. After 3 weeks, the myocardial injury markers had fully recovered to the normal range. Troponin T was 21.4 ng/L. Creatine kinase isoenzyme CKMB was 2.25 ng/L. Natriuretic peptide BNP was 139 ng/L.In 2020, there was a major outbreak of coronavirus infection. Unlike other coronavirus infections, which mainly cause pulmonary infections, this case of coronavirus infection was characterized by heart damage. The heart grew rapidly in a short period of time and quickly returns to normal after treatment. This type of clinical presentat...

Background: Coronavirus disease 2019 (COVID-19) is posing a huge threat to human health worldwide. We aim to investigate the immune status of CD8 + T and NK cells in COVID-19 patients. Methods: The count and immune status of lymphocytes were detected by flow cytometry in 32 COVID-19 patients and 18 healthy individuals. Results: As the disease progression in COVID-19 patients, CD8 + T and NK cells were significantly decreased in absolute number but highly activated. After patients' condition improved, the count and immune status of CD8 + T and NK cells restored to some extent. GrA + CD8 + T and perforin + NK cells had good sensitivity and specificity for assisting diagnosis of COVID-19. Conclusions: As the disease progression, the declined lymphocytes in COVID-19 patients might lead to compensatory activation of CD8 + T and NK cells. GrA + CD8 + T and perforin + NK cells might be used as meaningful indicators for assisting diagnosis of COVID-19.

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COVID-19 patients with preexisting cardiovascular diseases or with cardiovascular complications have showed a higher risk of mortality. The main cardiovascular complications of COVID-19 include acute cardiac injury, acute myocardial infarction, myocarditis, arrhythmia, heart failure, shock, and venous thromboembolism/pulmonary embolism. COVID-19 could cause cardiovascular complications or deterioration of coexisting cardiovascular diseases through direct or indirect mechanisms, including viral toxicity, dysregulation of the renin–angiotensin–aldosterone system, endothelial cell damage and thromboinflammation, cytokine storm, and demand-supply mismatch of oxygen. This study systematically reviews cardiovascular manifestations, histopathology, and mechanisms of COVID-19, to help formulate future research goals and facilitate the development of therapeutic management strategies.

Background5-Fluorouracil (5-FU) has been widely applied to treat various types of cancers, including hepatocellular carcinoma (HCC). However, primary or acquired 5-FU resistance prevents the clinical application of this drug in cancer therapy. Herein, our study is the first to demonstrate that lower expression of KRAL, a long non-coding RNA (lncRNA), mediates 5-FU resistance in HCC via the miR-141/Keap1 axis.MethodsCell proliferation assays, western blot analysis, qRT-PCR, the dual-luciferase reporter assay and RNA immunoprecipitation were performed to investigate the mechanisms by which KRAL mediates 5-fluorouracil resistance in HCC cell lines.ResultsThe quantitative analysis indicated that KRAL and Keap1 were significantly decreased and that Nrf2 was increased in HepG2/5-FU and SMMC-7721/5-FU cells compared with the corresponding expression levels in the respective parental cells. Overexpression of KRAL increased Keap1 expression, and inactivating the Nrf2-dependent antioxidant pathway could reverse the resistance of HepG2/5-FU and SMMC-7721/5-FU cells to 5-FU. Moreover, KRAL functioned as a competitive endogenous RNA (ceRNA) by effectively binding to the common miR-141 and then restoring Keap1 expression. These findings demonstrated that KRAL is an important regulator of Keap1; furthermore, the ceRNA network involving KRAL may serve as a treatment strategy against 5-FU resistance in hepatocellular carcinoma cells.ConclusionsKRAL/miR-141/Keap1 axis mediates 5-fluorouracil resistance in HCC cell lines.