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The clinical application of lung ultrasound (LUS) in the assessment of coronavirus disease 2019 (COVID-19) pneumonia severity remains limited. Herein, we investigated the role of LUS imaging in COVID-19 pneumonia patients and the relationship between LUS findings and disease severity. This was a retrospective, observational study at Tongji Hospital in Wuhan, on 48 recruited patients with COVID-19 pneumonia, including 32 non-critically ill patients and 16 critically ill patients. LUS was performed and the respiratory rate oxygenation (ROX) index, disease severity, and confusion, urea nitrogen, respiratory rate, blood pressure and age (CURB-65) score were recorded on days 0–7, 8–14, and 15–21 after symptom onset. Lung images were divided into 12 regions, and the LUS score (0–36 points) was calculated. Chest computed tomography (CT) scores (0–20 points) were also recorded on days 0–7. Correlations between the LUS score, ROX index, and CURB-65 scores were examined. LUS detected COVID-19 pneumonia in 38 patients. LUS signs included B line (34/38, 89.5%), consolidation (6/38, 15.8%), and pleural effusion (2/41, 5.3%). Most cases showed more than one lesion (32/38, 84.2%) and involved both lungs (28/38, 73.7%). Compared with non-critically ill patients, the LUS scores of critically ill patients were higher (12 (10–18) vs 2 (0–5), p < 0.001). The LUS score showed significant negative correlations with the ROX index on days 0–7 ( r = –0.85, p < 0.001), days 8–14 ( r = –0.71, p < 0.001), and days 15–21 ( r = –0.76, p < 0.001) after symptom onset. However, the LUS score was positively correlated with the CT score ( r = 0.82, p < 0.001). The number of patients with LUS-detected lesions decreased from 27 cases (81.8%) to 20 cases (46.5%), and the LUS scores significantly decreased from 4 (2–10) to 0 (0–5) ( p < 0.001) from days 0–7 to 17–21. We conclude that LUS can detect lung lesions in COVID-19 pneumonia patients in a portable, real-time, and safe manner. Thus, LUS is helpful in assessing COVID-19 pneumonia severity in critically ill patients.

SynopsisMicro-inflammation plays an important role in the pathogenesis of spontaneously hypertensive rat (SHR). In the present study, we investigated the therapeutic potential of resveratrol (RSV), a polyphenol with anti-fibrosis activity in hypertensive renal damage model. In SHR renal damage model, RSV treatment blunted the increase in urine albumin excretion, urinary β 2 -microglobulin (β 2 -MG), attenuated the decrease in creatinine clearance rate (CCR). The glomerular sclerosis index (1.54 + − 0.33 compared with 0.36 + − 0.07) and tubulointerstitial fibrosis (1.57 + − 0.31 compared with 0.19 + − 0.04) were significantly higher in SHRs compared with Wistar Kyoto rats (WKYs), which were significantly lower by RSV treatment. The increases in mesangium accumulation and the expression of renal collagen type I (Col I), fibronectin (Fn), plasminogen activator inhibitor-1 (PAI-1) and transforming growth factor-β1 (TGF-β1) in SHR were also reduced by RSV treatment. Nuclear factor κB (NF-κB) expression was increased in the cytoplasm and nuclei of the SHR kidneys, which was significantly decreased by RSV treatment. Furthermore, the protein level of IκB-α significantly decreased in the kidneys of the SHR when compared with the WKYs. RSV treatment partially restored the decreased IκB-α level. In SHR kidney, increased expression of interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein 1 (MCP-1) were observed. These changes were attenuated by RSV treatment. No changes in blood pressure were detected between SHR group and SHR + RSV group. Taken together, the present study demonstrated that RSV treatment may significantly attenuate renal damage in the SHR model of chronic kidney disease (CKD). The renal protective effect is associated with inhibition of IL-6, ICAM-1 and MCP-1 expression via the regulation of the nuclear translocation of NF-κB, which suggesting that micro-inflammation may be a potential therapeutic target of hypertensive renal damage.Key words: inflammation, intercellular adhesion molecule-1 (ICAM-1), interleukin-6 (IL-6), monocyte chemoattractant protein 1 (MCP-1), nuclear factor κB (NF-κB), resveratrol (RSV), spontaneously hypertensive rat (SHR).

No abstract

Salidroside is a major phenylethanoid glycoside in Rhodiola rosea L., a traditional Chinese medicine, with multiple biological activities. It has been shown that salidroside possesses protective effects for alleviating diabetic renal dysfunction, contrast‐induced‐nephropathy and other kidney diseases. However, the involved molecular mechanism was still not understood well. Herein, we examined the protective effects of salidroside in mice with Adriamycin (ADR)‐induced nephropathy and the underlying molecular mechanism. The results showed that salidroside treatment ameliorates proteinuria; improves expressions of nephrin and podocin; and reduces kidney fibrosis and glomerulosclerosis induced by ADR. Mechanistically, ADR induces a robust accumulation of β‐catenin in the nucleus and stimulates its downstream target gene expression. The application of salidroside largely abolishes the nuclear translocation of β‐catenin and thus inhibits its activity. Furthermore, the activation of β‐catenin almost completely counteracts the protective roles of salidroside in ADR‐injured podocytes. Taken together, our data indicate that salidroside ameliorates proteinuria, renal fibrosis and podocyte injury in ADR nephropathy, which may rely on inhibition of β‐catenin signalling pathway.