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.

Colorectal cancer (CRC) is a leading cause of cancer deaths worldwide. Although polypectomy at early stage reduces CRC incidence, 90% of the polyps are small and diminutive, where removal of them poses risks to patients that may outweigh the benefits. Correctly detecting and predicting polyp type during colonoscopy allows endoscopists to resect and discard the tissue without submitting it for histology, saving time, and costs. Nevertheless, human visual observation of early stage polyps varies. Therefore, this paper aims at developing a fully automatic algorithm to detect and classify hyperplastic and adenomatous colorectal polyps. Adenomatous polyps should be removed, whereas distal diminutive hyperplastic polyps are considered clinically insignificant and may be left in situ . A novel transfer learning application is proposed utilizing features learned from big nonmedical datasets with 1.4-2.5 million images using deep convolutional neural network. The endoscopic images we collected for experiment were taken under random lighting conditions, zooming and optical magnification, including 1104 endoscopic nonpolyp images taken under both white-light and narrowband imaging (NBI) endoscopy and 826 NBI endoscopic polyp images, of which 263 images were hyperplasia and 563 were adenoma as confirmed by histology. The proposed method identified polyp images from nonpolyp images in the beginning followed by predicting the polyp histology. When compared with visual inspection by endoscopists, the results of this study show that the proposed method has similar precision (87.3% versus 86.4%) but a higher recall rate (87.6% versus 77.0%) and a higher accuracy (85.9% versus 74.3%). In conclusion, automatic algorithms can assist endoscopists in identifying polyps that are adenomatous but have been incorrectly judged as hyperplasia and, therefore, enable timely resection of these polyps at an early stage before they develop into invasive cancer.

Purpose: This review provides an update on the current clinical, epidemiological and pathophysiological evidence alongside the diagnostic, prevention and treatment approach to chemotherapy-induced peripheral neuropathy (CIPN). Findings: The incidence of cancer and longterm survival after treatment is increasing. CIPN affects sensory, motor and autonomic nerves and is one of the most common adverse events caused by chemotherapeutic agents, which in severe cases leads to dose reduction or

BackgroundPatients with colorectal cancer (CRC) have a high incidence of regional and distant metastases. Although metastasis is the main cause of CRC-related death, its molecular mechanisms remain largely unknown.MethodsUsing array-CGH and expression microarray analyses, changes in DNA copy number and mRNA expression levels were investigated in human CRC samples. The mRNA expression level of RASAL2 was validated by qRT-PCR, and the protein expression was evaluated by western blot as well as immunohistochemistry in CRC cell lines and primary tumors. The functional role of RASAL2 in CRC was determined by MTT proliferation assay, monolayer and soft agar colony formation assays, cell cycle analysis, cell invasion and migration and in vivo study through siRNA/shRNA mediated knockdown and overexpression assays. Identification of RASAL2 involved in hippo pathway was achieved by expression microarray screening, double immunofluorescence staining and co-immunoprecipitation assays.ResultsIntegrated genomic analysis identified copy number gains and upregulation of RASAL2 in metastatic CRC. RASAL2 encodes a RAS-GTPase-activating protein (RAS-GAP) and showed increased expression in CRC cell lines and clinical specimens. Higher RASAL2 expression was significantly correlated with lymph node involvement and distant metastasis in CRC patients. Moreover, we found that RASAL2 serves as an independent prognostic marker of overall survival in CRC patients. In vitro and in vivo functional studies revealed that RASAL2 promoted tumor progression in both KRAS/NRAS mutant and wild-type CRC cells. Knockdown of RASAL2 promoted YAP1 phosphorylation, cytoplasm retention and ubiquitination, therefore activating the hippo pathway through the LATS2/YAP1 axis.ConclusionsOur findings demonstrated the roles of RASAL2 in CRC tumorigenesis as well as metastasis, and RASAL2 exerts its oncogenic property through LATS2/YAP1 axis of hippo signaling pathway in CRC.Electronic supplementary materialThe online version of this article (10.1186/s12943-018-0853-6) contains supplementary material, which is available to authorized users.