Peri-operative SARS-CoV-2 infection increases postoperative mortality. The aim of this study was to determine the optimal duration of planned delay before surgery in patients who have had SARS-CoV-2 infection. This international, multicentre, prospective cohort study included patients undergoing elective or emergency surgery during October 2020. Surgical patients with pre-operative SARS-CoV-2 infection were compared with those without previous SARS-CoV-2 infection. The primary outcome measure was 30-day postoperative mortality. Logistic regression models were used to calculate adjusted 30-day mortality rates stratified by time from diagnosis of SARS-CoV-2 infection to surgery. Among 140,231 patients (116 countries), 3127 patients (2.2%) had a pre-operative SARS-CoV-2 diagnosis. Adjusted 30-day mortality in patients without SARS-CoV-2 infection was 1.5% (95%CI 1.4-1.5). In patients with a pre-operative SARS-CoV-2 diagnosis, mortality was increased in patients having surgery within 0-2 weeks, 3-4 weeks and 5-6 weeks of the diagnosis (odds ratio (95%CI) 4.1 (3.3-4.8), 3.9 (2.6-5.1) and 3.6 (2.0-5.2), respectively). Surgery performed ≥ 7 weeks after SARS-CoV-2 diagnosis was associated with a similar mortality risk to baseline (odds ratio (95%CI) 1.5 (0.9-2.1)). After a ≥ 7 week delay in undertaking surgery following SARS-CoV-2 infection, patients with ongoing symptoms had a higher mortality than patients whose symptoms had resolved or who had been asymptomatic (6.0% (95%CI 3.2-8.7) vs. 2.4% (95%CI 1.4-3.4) vs. 1.3% (95%CI 0.6-2.0), respectively). Where possible, surgery should be delayed for at least 7 weeks following SARS-CoV-2 infection. Patients with ongoing symptoms ≥ 7 weeks from diagnosis may benefit from further delay.

Highlights We assess the performance of the LUMIPULSE antigen test compared to RT-qPCR The antigen level was significantly higher in PCR-positive samples than in negative samples The antigen test determined all samples (>100 viral copies) to be positive Likewise, it determined 85% of samples (>10 viral copies) to be positive The kinetics of viral loads and antigen levels showed a similar declining trend

No abstract

A sensitive enzyme immunoassay (EIA) specific for hepatitis B virus core antigen (HBcAg) and hepatitis B e antigen (HBeAg) was developed. We designated the precore/core gene products as hepatitis B virus (HBV) core-related antigens (HBcrAg). In order to detect HBcrAg even in anti-HBc/e antibody-positive specimens, the specimens were pretreated in detergents. The antibodies are inactivated by this pretreatment and, simultaneously, the antigens are released and the epitopes are exposed. The assay demonstrated 71 to 112% recovery using HBcrAg-positive sera. We observed no interference from the tested anticoagulants or blood components. When the cutoff value was tentatively set at 10 3 U/ml, all healthy control (HBsAg/HBV-DNA negative; n ‫؍‬ 108) and anti-HCV antibody-positive (n ‫؍‬ 59) sera were identified as negative. The assay showed a detection limit of 4 ؋ 10 2 U/ml using recombinant antigen. Detection limits were compared in four serially diluted HBV high-titer sera. The HBcrAg assay demonstrated higher sensitivity than HBV-DNA transcription-mediated amplification ( Many hepatitis B virus (HBV) markers are used for diagnosing and monitoring hepatitis B patients. HBV-DNA tests, such as the branched-chain DNA (b-DNA) signal amplification assay (7, 31), and transcription-mediated amplification (TMA)-based (11) or PCR-based (12,14,20) assays are used to diagnose and monitor the efficacy of treatment. However, these methods require cumbersome procedures and expensive equipment, thus requiring considerable skill and high costs. These gene amplification assays also present some limitations (22,23,35). The b-DNA assay provides quantitative results but requires a long incubation time and lacks adequate sensitivity. Amplification assays have adequate sensitivity but are less quantitative.Immunoassays are generally easy and inexpensive. There have been a few reports of serum HBcAg assays with specimen pretreatment (4, 32). The concentration of HBcAg in these assays correlated with levels of HBV-associated DNA polymerase (4). Thus, HBcAg could be a marker for virus load. However, the use of these assays is limited because of relatively low sensitivity and complex procedures.Serum HBeAg concentration reflects virus replication and hepatitis activity and is closely correlated with virus load in anti-HBe antibody-negative patients (8). Seroconversion of HBeAg to anti-HBe antibody reveals the inactive phase of infection (17,25). However, after seroconversion, many patients may exhibit reactivation and high viral load (3,10,18). In these cases, HBeAg is usually negative due to masking by anti-HBe antibody (24), although the HBeAg/anti-HBe immune complex can be indirectly detected according to the levels of alanine aminotransferase (ALT) and HBV-DNA (6). Therefore, HBcAg and HBeAg could be expected to be efficient markers of virus load if antibodies were inactivated and the antigens released.In the present study, for the purpose of developing a simple, sensitive, and inexpensive assay for determining HBV virus load, we targete...

DNA methylation constitutes an important epigenetic regulation mechanism in many eukaryotes, although the extent of DNA methylation in the regulation of gene expression in the mammalian genome is poorly understood. We developed D-REAM, a genome-wide DNA methylation analysis method for tissue-dependent and differentially methylated region (T-DMR) profiling with restriction tag-mediated amplification in mouse tissues and cells. Using a mouse promoter tiling array covering a region from −6 to 2.5 kb (∼30,000 transcription start sites), we found that over 3000 T-DMRs are hypomethylated in liver compared to cerebrum. The DNA methylation profile of liver was distinct from that of kidney and spleen. This hypomethylation profile marked genes that are specifically expressed in liver, including key transcription factors such as Hnf1a and Hnf4a. Genes with T-DMRs, especially those lacking CpG islands and those with HNF-1A binding motifis in their promoters, showed good correlation between their tissue-specific expression and liver hypomethylation status. T-DMRs located downstream from their transcription start sites also showed tissue-specific gene expression. These data indicate that multilayered regulation of tissue-specific gene function could be elucidated by DNA methylation tissue profiling.