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.

This study aimed to determine if sampling of oropharyngeal secretions (OSs) helps improves detection of SARS-CoV-2 RNA by nucleic acid amplification testing of potential patients with COVID-19. The first prospective study consisted of 75 patients with COVID-19 who were ready for discharge and who had 2 consecutive negative results per nucleic acid amplification testing (NAAT) of viral samples retrieved with nasopharyngeal swabs (NPSs). Because of detection of potential false negatives in that cohort, the NAAT results of paired OS and NPS samples from 50 additional recruits with COVID-19 during their recovery stage were used in a second prospective study to compare the diagnostic values of the 2 viral RNA sampling methods. For identification of the frequency of inconsistency between the sampling methods, the McNemar’s test was used for difference analysis and the kappa statistic for consistency analysis. OSs obtained from 2 of the 75 participants in the first study yielded positive results for SARS-CoV-2 nucleic acid. Both were male and aged >60 y. Subsequent chemiluminescence enzyme immunoassays indicated that they were positive for the SARS-CoV-2 IgM and IgG antibodies. For parallel NAAT of OS and NPS samples in the second study, McNemar’s test indicated that the difference between the frequencies of inconsistent parts of OS and NPS was statistically significant ( P = 0.021). Cohen’s kappa coefficient for OS and NPS was 0.244, which is indicative of fair consistency. The NPS test has a risk of sending home more patients (59%) who still have the infection, while the OS test will make such an error in fewer patients (14%). Although OS sampling improves the accuracy of SARS-CoV-2 nucleic acid testing, it has to be emphasized that this conclusion is based on a very small sample size. Detection of viral RNA from a patient’s secretions is not confirmative of viral infectivity.

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.

Background: There has been an increasing number of COVID-19 patients around the world. Since some patients developed with gastrointestinal bleeding, our study focused on the clinical features and gastroscopic findings of these patients, and factors associated with occult gastrointestinal bleeding. Patients and Methods: In this retrospective, observational study, we collected 368 COVID-19 patients who performed fecal or gastric occult blood from Wuhan Tongji Hospital, Jin Yin-tan Hospital, and Wuhan Union Hospital between February 1, 2020 and March 6, 2020. Clinical features were compared between patients with or without occult gastrointestinal bleeding, and gastroscopic findings of seven patients were described. Logistic regression analyses were performed to explore the factors associated with occult gastrointestinal bleeding. Results: In total, 43 (11.7%) patients presented occult gastrointestinal bleeding, whereas 35 (81.4%) of severe cases. CRP level, prothrombin time and D-dimer were higher, while lymphocyte count and albumin levels were decreased in patients with occult gastrointestinal bleeding. Gastroscopy in seven COVID-19 patients showed mucosal congestion, erosion or scattered bleeding at different sites. Albumin levels (OR, 0.856 [95% CI 0.793-0.924]; p < 0.001), prothrombin time (OR,]; p = 0.002) on admission and severe disease (OR,]; p = 0.001) were independent factors associated with GIB in COVID-19 patients, while antiviral drugs and glucocorticoid therapy were not associated with it. Conclusion: COVID-19 patients with occult gastrointestinal bleeding suffered from worse prognosis. Patients with decreased serum albumin levels or prolonged prothrombin time, and severe cases were at higher risk of occult gastrointestinal bleeding.

BackgroundBAFF production is increased in IBD patients. However, the specific role of BAFF in IBD is still uncovered. This study aimed to investigate the expression and function of BAFF in experimental colitis and the potential mechanisms.MethodsBAFF levels in the serum and colon tissues were measured by ELISA in DSS-induced colitis mice. Mouse-derived BAFF antibody was administered in DSS mice. The changes of body weight, disease activity index (DAI) scores, colon length, spleen weight, histopathological damage, inflammatory indicators, NF-κB signaling, and NLRP3 inflammasome were assayed in DSS mice and control. LPS-primed RAW264.7 cells and bone marrow derived macrophages (BMDMs) were treated with BAFF blockage and recombinant mouse BAFF. Inflammatory associated cytokines, NLRP3 inflammasomes and NF-κB signaling were detected among groups.ResultsBAFF production was elevated systemically and locally in colitis mice. BAFF blockade improved the body weight loss, DAI scores, colon length, spleen weight, and histopathological damage in colitis mice. Immunoflurescence analysis revealed that elevated macrophages in mucosal lamina propria were the primary source of BAFF in the colon. NLRP3 inflammasome and NF-κB signaling pathway activation were dramatically inhibited in DSS mice treated with BAFF blockage. In LPS-primed RAW264.7 cells/BMDMs, BAFF blockade decreased the activation of NLRP3 inflammasome (NLPR3, ASC, cleaved IL-1β, cleaved caspase 1) via inhibiting NF-κB signaling pathway. Moreover, LPS synergizes with BAFF to promote inflammatory factor secretion and expression of NF-κB signaling pathway in RAW264.7 cells.ConclusionsThese results suggested that BAFF blockade protected against colitis partially by relieving inflammation, inhibiting intestinal NLRP3 inflammasome and NF-κB signaling pathway from macrophages. BAFF plays an important role in inflammation regulation in IBD, thus providing a novel idea for further research on colitis and experimental evidences for novel potential therapeutic target in IBD.