Factors affecting recurrent positive RT-PCR results in clinically cured COVID-19 patients: a multicenter study.

The aim of this study was to evaluate factors affecting the recurrence of positive RT-PCR results. By performing a retrospective analysis, we evaluated the clinical data of recurrent positive coronavirus disease 2019 (COVID-19) patients in multiple medical institutions in Wuhan. We recruited COVID-19 patients who were hospitalized from January 1 to March 10, 2020, in three tertiary hospitals in Wuhan, met the discharge criteria and received at least one additional nucleic acid test before leaving the hospital. According to the RT-PCR results, patients were split into a recurrent positive group (RPos group) and a nonrecurrent positive group (non-RPos group). Clinical characteristics, therapeutic schedules and antibody titers were compared between the two groups. AI-assisted chest high-resolution computed tomography (HRCT) technology was applied to investigate pulmonary inflammatory exudation and compare the extent of lung areas with different densities. This study involved 122 COVID-19 patients. There were no significant differences in age, sex, preexisting diseases, clinical symptoms, clinical classification, course of disease, therapeutic schedules or serum-specific antibodies between the two groups. A higher proportion of patients who showed pulmonary inflammatory exudation on HRCT scans were recurrent positive at the time of discharge than other patients (81.6% vs 13.7%, P < 0.01). In addition, the degree of pulmonary fibrosis was higher in the RPos group than in the non-RPos group (P < 0.05). Subpleural exudation at the peripheral edge of the lung and extensive pulmonary fibrosis at the time of discharge represent risk factors for the recurrence of COVID-19.

The Protective Role of the Long Pentraxin PTX3 in Spontaneously Hypertensive Rats with Heart Failure.

Pentraxin 3 (PTX3) is synthesized locally and released into the circulation, reflecting local inflammation in the cardiovascular system. Therefore, we conducted a study to explore the effect of PTX3 in spontaneously hypertensive heart failure (SHHF) rats. Sprague Dawley (SD) and SHHF rats were treated with recombinant PTX3 protein, and the blood pressure (BP) and echocardiographic parameters were collected. Radioimmunoassay, enzyme immunoassay and enzyme-linked immunosorbent assay (ELISA) were applied to detect plasma levels of atrial/B-type natriuretic peptide (ANP/BNP) and PTX3. The pathological changes in the myocardial tissues were observed by hematoxylin and eosin (HE) and Masson stainings. The mRNA and protein expressions were detected by quantitative real-time reverse-transcription polymerase chain reaction (qPCR) and western blotting. Cardiomyocyte apoptosis was evaluated by TUNEL staining and DNA fragmentation test. Increased plasma concentrations of PTX3 were found in SHHF rats compared with SD rats, which was further enhanced by recombinant PTX3 protein. After injection with recombinant PTX3 protein, the heart function was improved in SHHF rats with the decreased systolic and diastolic BP, and the reduced plasma levels of ANP and BNP. Moreover, PTX3 improved the myocardial damage and interstitial fibrosis in SHHF rats with reduced cardiomyocyte apoptosis and decreased mRNA expressions of pro-inflammatory factors in myocardial tissues. PTX3 could decrease the BP and plasma levels of ANP and BNP in SHHF rats, as well as improve the inflammation, cardiomyocyte apoptosis, and pathological changes of myocardial tissues, suggesting it may be a useful intervention in the treatment of SHHF.

MicroRNA-27a mediates the Wnt/ß-catenin pathway to affect the myocardial fibrosis in rats with chronic heart failure.

OBJECTIVE: To clarify the influence of MicroRNA-27a (miR-27a)-mediated Wnt/ß-catenin pathway on the myocardial fibrosis in rats with chronic heart failure (CHF). METHODS: The CHF rat models were constructed and randomly divided into four groups (Sham, Model, AntagomiR-27a, and NC antagomiR-27a groups). Echocardiography was used to test the cardiac function indexes, HE (haematoxylin-eosin) staining to observe the pathological injury of myocardium, Masson staining to analyze the collagen volume fraction (CVF), and qRT-PCR (quantitative real-time PCR) and Western blotting to detect the expressions of miR-27a and Wnt/ß-catenin pathway-related proteins. Besides, cardiomyocytes were isolated and transfected with miR-27a mimic or miR-27a inhibitor to detect the expressions of Wnt/ß-catenin pathway. RESULTS: The CHF rats were significantly increased in LVESD (left ventricular end systolic diameter) and LVEDD (left ventricular end diastolic diameter), and clearly reduced in FS (fractional shortening) and EF (left ventricular ejection fraction) (all P < 0.05). Moreover, LVWI (left ventricular mass index) and CVF (Collagen Volume Fraction), type I and type III collagen, and the ratio of type I/III collagen, as well as the expression of miR-27a, TGF-ß1 and p-Smad2/3, ß-catenin, p-GSK-3ß and α-SMA were also elevated (all P < 0.05). Additionally, the CHF rats treated with AntagomiR-27a were improved in these indexes, and the expression of miR-27a and Wnt/ß-catenin pathway was significantly inhibited (all P < 0.05). Furthermore, cardiomyocytes transfected with miR-27a inhibitor significantly decreased the levels of miR-27a and Wnt/ß-catenin pathway (all P < 0.05). CONCLUSION: Down-regulation of miR-27a may inhibit the Wnt/ß-catenin pathway to reduce the deposition of myocardial collagen, prevent myocardial fibrosis and improve cardiac function. This article is protected by copyright. All rights reserved.