We profiled the serological responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleocapsid (N) protein and spike (S) glycoprotein. The majority of the patients developed robust antibody responses between 17 and 23 days after illness onset. Delayed, but stronger, antibody responses were observed in critical patients.
Background: Co-infections, secondary bacterial or fungal infections, are important risk factors for poor outcomes in viral infections. The prevalence of co-infection and secondary infection in patients infected with SARS-CoV-2 is not well understood. Aims: To investigate the role of co-infections and secondary infections in disease severity of hospitalized individuals with COVID-19. Materials and Methods: A retrospective study was carried out between 11 January 2020 and 1 March 2020 among 408 laboratory confirmed COVID-19 patients in China. These patients were divided into three groups based on disease severity: mild or moderate, severe, or critically ill. Microbiological pathogens in blood, urine, and respiratory tract specimens were detected by the combination of culture, serology, polymerase chain reaction, and metagenomic next-generation sequencing (mNGS). Results: The median age of participants was 48 years (IQR 34-60 years). Fifty-two patients (12.7%) had at least one additional pathogen, 8.1% were co-infected, and 5.1% had a secondary infection. There were 13 Mycoplasma pneumoniae cases, 8Haemophilus influenzae cases, 8 respiratory viruses, and 3 Streptococcus pneumoniae cases, primarily detected in mild and moderate COVID-19 patients. Hospitalacquired infection pathogens were more common in critically ill patients. Compared to those without additional pathogens, patients with co-infections and/or secondary infections were more likely to receive antibiotics (p < 0.001) and have elevated levels of d-dimer (p = 0.0012), interleukin-6 (p = 0.0027), and procalcitonin (p = 0.0002).The performance of conventional culture was comparable with that of mNGS in diagnosis of secondary infections. Conclusion: Co-infections and secondary infections existed in hospitalized COVID-19 patients and were relevant to the disease severity. Screening of common respiratory pathogens and hospital infection control should be strengthened.
Objective Abnormal liver function is a common form of extra‐pulmonary organ damage in patients with coronavirus disease 2019 (COVID‐19). Patients with severe COVID‐19 have a higher probability and progression of liver injury than those without severe disease. We aimed to evaluate the prognosis of liver injury in patients with COVID‐19. Methods We retrospectively included 502 patients with laboratory‐confirmed SARS‐CoV‐2 infection. Clinical features and survival of patients with and without liver injury were compared. Cox proportional hazards models were used to determine the variables that might have an effect on survival. Results Among the 502 patients enrolled, 301 patients had abnormal liver function with increased neutrophil count, C‐reactive protein, creatinine, troponin I (TnI), D‐dimer, lactose dehydrogenase and creatine kinase. Patients with abnormal liver functions had a higher mortality rate (28.9% vs 9.0%, P < 0.001), a higher ratio of male sex (65.1% vs 40.8%, P < 0.001) and a higher chance of developing systemic inflammatory response syndrome (53.5% vs 41.3%, P = 0.007). Among patients with abnormal liver functions, patients with grade 2 liver damage (with both abnormal alanine aminotransferase or aspartate aminotransferase levels and abnormal alkaline phosphatase or gamma‐glutamyl transpeptidase levels) had a higher ratio of male patients, elevated neutrophil count, procalcitonin, D‐dimer levels and mortality rate. Multivariate Cox regression analyses suggested that the grade of liver damage (hazard ratio: 1.377, 95% confidence interval: 1.000‐1.896, P = 0.049) was an independent predictor of death. Conclusions Patients with COVID‐19 and abnormal liver functions have a higher mortality than those with normal liver functions. Liver damage is an independent prognostic factor of COVID‐19.
Aim: Liguzinediol is a novel derivative of ligustrazine isolated from the traditional Chinese medicine Chuanxiong (Ligusticum wallichii Franch), and produces significant positive inotropic effect in isolated rat hearts. In this study we investigated the effects of liguzinediol on a rat model of heart failure. Methods: To induce heart failure, male SD rats were injected with doxorubicin (DOX, 2 mg/kg, ip) once a week for 4 weeks. Then the rats were administered with liguzinediol (5, 10, and 20 mg·kg -1 ·d -1 , po) for 2 weeks. Hemodynamic examination was conducted to evaluate heart function. Myocardial cell apoptosis was examined morphologically. The expression of related genes and proteins were analyzed using immunohistochemical staining and Western blot assays, respectively. Results: Oral administration of liguzinediol dose-dependently improved the heart function in DOX-treated rats. Electron microscopy revealed that liguzinediol (10 mg·kg -1 ·d -1 ) markedly attenuated DOX-induced injury of cardiomyocytes, and decreased the number of apoptotic bodies in cardiomyocytes. Furthermore, liguzinediol significantly decreased Bax protein level, and increased Bcl-2 protein level in cardiomyocytes of DOX-treated rats, led to an increase in the ratio of Bcl-2/Bax. Moreover, liguzinediol significantly decreased the expression of both cleaved caspase-3 and NF-κB in cardiomyocytes of DOX-treated rats. Administration of digitalis (0.0225 mg·kg -1 ·d -1 ) also markedly improved the heart function and the morphology of cardiomyocytes in DOX-treated rats. Conclusion: Liguzinediol improves the heart function and inhibits myocardial cell apoptosis in the rat model of heart failure, which is associated with regulating Bcl-2, Bax, caspase-3, and NF-κB expression.
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