Take home message: The median time from symptoms onset to viral RNA shedding was 19 days. Patients with CHD comorbidity or decreased albumin levels experienced delays in clearance of SARS-CoV-2 RNA.
In December 2019, an outbreak of coronavirus disease 2019 (COVID‐19) emerged in Wuhan, China. Although it has been reported that some COVID‐19 patients showed elevated liver biochemistries, there are few studies regarding clinical features and prognosis of these patients. In this multicenter, retrospective study, we collected data on laboratory‐confirmed COVID‐19 patients from three hospitals in Wuhan, China, who died or were discharged between February 1, 2020, and February 20, 2020. The data on demographics, comorbidities, clinical symptoms, laboratory examinations on admission, complications, treatment, and outcome were collected. A total of 482 patients were enrolled in this study. Of those, 142 (29.5%) patients showed abnormal liver biochemistries on admission, and patients with elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBIL) accounted for 67.6%, 69.0%, and 16.2%, respectively. Those with abnormal liver biochemistries showed higher percentages of severe cases and comorbidities and were more likely to have dyspnea, chest distress or pain, and increased hemoglobin (Hb) on admission. Higher rates of complications and mortality and worse recovery when discharged were observed in patients with abnormal AST or TBIL. The multivariable regression analysis showed that chest distress or pain (odds ratio [OR], 1.765; P = 0.018), dyspnea (OR, 2.495; P = 0.001), elevated C‐reactive protein [CRP] level (OR, 1.007; P = 0.008), elevated white blood count (WBC) (OR, 1.139; P = 0.013), and elevated Hb concentration (OR, 1.024; P = 0.001) were independent factors associated with elevated liver biochemistries in COVID‐19 patients. Conclusion: Elevated liver biochemistries were common in COVID‐19 patients. Patients with hypoxia or severe inflammation are more likely to experience increased liver biochemistries on admission. Those with abnormal AST or TBIL on admission are more likely to suffer from severe complications and death.
Background: Hypoalbuminemia has been reported in COVID-19 patients. Exploring the influencing factors and possible adverse consequences of albumin reduction may provide some guidance for the treatment of COVID-19 patients. Methods: In this multicentre retrospective study, we collected information including demographics, comorbidities, clinical symptoms, complications, laboratory tests, treatment, and outcomes of patients diagnosed with COVID-19 from three hospitals in Wuhan, China. We compared the indexes between patients with hypoalbuminemia and normal albumin. Regression model was used to evaluate various influencing factors of patients with hypoalbuminemia and their relationship with clinical outcomes. We also compared the changes of particular laboratory indexes in patients with hypoalbuminemia before and after enteral nutrition therapy. Results: A total of 482 patients were enrolled in the study. About 53.7% patients developed hypoalbuminemia during admission. Patients with hypoalbuminemia were older, had a higher proportion of combined diabetes mellitus, fever, dyspnea, and natriuresis, and had a relatively poorer prognosis than patients with normal albumin. Patients with hypoalbuminemia had higher levels of CRP, leukocytes, ALT, AST, total bilirubin, ALP, GGT, LDH, creatine kinase, D-dimer, globulin, and lower levels of lymphocytes and eosinophils. Severe, older, anorexia, elevated CRP, and decreased lymphocytes were the independent predictors for decreased albumin in COVID-19 patients. In addition, decreased albumin is correlated with adverse outcomes. Nutritional support therapy to correct serum albumin may improve patient outcomes. Conclusion: COVID-19 patients with hypoalbuminemia tend to have more severe clinical manifestations and more abnormal biochemical tests, which may result in poorer clinical outcomes. Nutritional support therapy may improve the clinical outcome of these patients.
Nearest neighbor (NN) search is inherently computationally expensive in high-dimensional spaces due to the curse of dimensionality. As a well-known solution, locality-sensitive hashing (LSH) is able to answer c-approximate NN (c-ANN) queries in sublinear time with constant probability. Existing LSH methods focus mainly on building hash bucket-based indexing such that the candidate points can be retrieved quickly. However, existing coarse-grained structures fail to offer accurate distance estimation for candidate points, which translates into additional computational overhead when having to examine unnecessary points. This in turn reduces the performance of query processing. In contrast, we propose a fast and accurate in-memory LSH framework, called PM-LSH, that aims to compute c-ANN queries on large-scale, high-dimensional datasets. First, we adopt a simple yet effective PM-tree to index the data points. Second, we develop a tunable confidence interval to achieve accurate distance estimation and guarantee high result quality. Third, we propose an efficient algorithm on top of the PM-tree to improve the performance of computing c-ANN queries.
B cell-activating factor (BAFF) production is increased in septic patients. However, the specific role of BAFF in sepsis remains unknown. This study was designed to investigate the expression and function of BAFF in an experimental endotoxemia model and to identify the potential mechanisms. We established an endotoxemia mouse (6–8 weeks, 20–22 g) model by administering 30 mg/kg lipopolysaccharide (LPS). BAFF levels in the circulating system and organ tissues were measured 4 and 8 h after LPS injection. Survival rates in the endotoxemia mice were monitored for 72 h after BAFF blockade. The effects of BAFF blockade on systemic and local inflammation, organ injuries, and intestinal barrier function were also evaluated 4 h after LPS treatment. BAFF production was systemically and locally elevated after LPS challenge. BAFF blockade improved the survival rate, systemic inflammation, and multi-organ injuries. Moreover, BAFF blockade attenuated both intestinal inflammation and impaired intestinal permeability. BAFF blockade upregulated ZO-1 and occludin protein levels via the NF-κB/MLCK/MLC signaling pathway. These results suggested that BAFF blockade protects against lethal endotoxemia at least partially by alleviating inflammation, multi-organ injuries, and improving intestinal barrier function and provides a novel focus for further research on sepsis and experimental evidence for clinical therapy.
This study found that VNP, which could elevate the tissue blood perfusion and mitigate the tissue damage and inflammatory reaction, is associated with a higher percentage of survival random pattern skin flap area.
Atrial Natriuretic Peptide (ANP) has known anti-inflammatory effects. However, the role of ANP in Ulcerative colitis (UC) remains unclear. This study aimed to explore the expression and function of ANP in UC, and its potential regulatory role in the stimulator of interferon genes (STING) pathway. Human colon biopsy and serum samples were collected between September 2018 and December 2019 at Wuhan Union Hospital. Levels of ANP and its receptors and STING pathway components were detected in people with UC and mice with dextran sulfate sodium (DSS)-induced colitis. These mice and HT-29 cells were treated with ANP and an agonist of the STING pathway. The level of inflammation, STING pathway, gut barrier, and endoplasmic reticulum (ER) stress-induced autophagy were measured. We found that the levels of ANP and its receptor decreased and the STING pathway activated statistically in people with UC and the mouse model of colitis. ANP treatment attenuated DSS-induced colitis and inhibited STING pathway phosphorylation in colonic tissue and epithelial cells. An interaction between cGAS and NPR-A was verified. ANP repaired the gut barrier and inhibited ER stress-induced autophagy via the STING pathway. ANP may thus alter colonic barrier function and regulate ER stress-induced autophagy as a promising therapy for UC.
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