Assessing the risk of post-surgical mortality is a key component of pre-surgical planning. The Surgical Outcome Risk Tool (SORT) uses pre-operative variables to predict 30-day mortality. The aim of this study was to externally validate SORT in patients undergoing major abdominal surgery.
 
  Data were collected from patients treated in five independent hospitals in the UK. Individualised SORT scores were calculated, and area under the receiver operating characteristic (AUROC) and precision-recall curves (PRC) plus 95% confidence intervals (CI) were drawn to test the ability of SORT to identify in-hospital death. Outcomes of patients with a SORT predicted risk of mortality of ≥ 5% (high risk) were compared to those with a predicted risk of < 5% (standard risk).
 
  The study population comprised 3305 patients, mean age 51 years, 2783 (84.2%) underwent elective surgery most frequently involving the colon (24.6%), or liver, pancreas or gallbladder (18.2%). Overall, 1551 (46.9%) patients were admitted to ICU and 29 (0.88%) died. The AUROC of SORT for discriminating patients at risk of death in hospital was 0.899 (95% CI 0.849 to 0.949) and the PRC 0.247. In total, 72 (2.18%) patients were stratified as high risk. There were more unplanned ICU admissions and deaths in this group compared to the standard risk group (25.0% and 3.3%, versus 3.1% and 0.5%, respectively).
 
  We externally validated SORT in a large population of abdominal surgery patients. SORT performed well in patients with lower risk profiles, but underpredicted adverse outcomes in the higher risk group.
 We externally validated SORT in a large population of abdominal surgery patients.  https://www.selleckchem.com/products/l-glutamic-acid-monosodium-salt.html  SORT performed well in patients with lower risk profiles, but underpredicted adverse outcomes in the higher risk group.
  Systemic lupus erythematosus (SLE) is a complex and challenging autoimmune disease. Severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) is a novel viral agent that can cause a life-threatening respiratory disorder named coronavirus disease 2019 (COVID‑19). Association between SARS‑CoV‑2 and SLE is not clear. We reported the first case of SLE manifestation following COVID-19.
 
  A 39-year-old Iranian/Persian man with complaints of fever, scaling on the palms of the hands and feet, lower extremity edema, and ankle swelling was referred to Kashan Rheumatology Clinic in 2020. He was infected with SARS-CoV-2 2months ago. The patient had proteinuria and was positive for SLE laboratory tests. After one week of treatment with prednisolone (30mg daily) and hydroxychloroquine, paresthesia, proteinuria, and edema continued. The patient was treated with pulse methylprednisolone (1000 mg for three consecutive days), gabapentin, and vitamin B (300mg daily), which reduced paresthesia.
 
  This is the first case of SLE manifestation following COVID-19. SARS-CoV-2 may produce autoantibodies or develop the clinical features of subclinical SLE.
 This is the first case of SLE manifestation following COVID-19. SARS-CoV-2 may produce autoantibodies or develop the clinical features of subclinical SLE.
  Sepsis is a life-threatening condition accompanied by organ dysfunction subsequent to a dysregulated host response to infection. Up to 60% of patients with sepsis develop acute kidney injury (AKI), which is associated with a poor clinical outcome. The pathophysiology of sepsis-associated AKI (sepsis-AKI) remains incompletely understood, but mitochondria have emerged as key players in the pathogenesis. Therefore, our aim was to identify mitochondrial damage in patients with sepsis-AKI.
 
  We conducted a clinical laboratory study using "warm" postmortem biopsies from sepsis-associated AKI patients from a university teaching hospital. Biopsies were taken from adult patients (n = 14) who died of sepsis with AKI at the intensive care unit (ICU) and control patients (n = 12) undergoing tumor nephrectomy. To define the mechanisms of the mitochondrial contribution to the pathogenesis of sepsis-AKI, we explored mRNA and DNA expression of mitochondrial quality mechanism pathways, DNA oxidation and mitochondrial DNA (mitochondrial quality control mechanisms, which likely resulted in a reduction in mitochondrial mass.
 Sepsis-AKI induces mitochondrial DNA damage in the human kidney, without upregulation of mitochondrial quality control mechanisms, which likely resulted in a reduction in mitochondrial mass.
  MicroRNAs have been reported to participate in tumorigenesis, treatment resistance, and tumor metastasis. Novel microRNAs need to be identified and investigated to guide the clinical prognosis or therapy for breast cancer.
 
  The copy number variations (CNVs) of MIR3613 from Cancer Genome Atlas (TCGA) or Cancer Cell Line Encyclopedia (CCLE) were analyzed, and its correlation with breast cancer subtypes or prognosis was investigated. The expression level of miR-3613-3p in tumor tissues or serum of breast cancer patients was detected using in situ hybridization and qPCR. Gain-of-function studies were performed to determine the regulatory role of miR-3613-3p on proliferation, apoptosis, and tumor sphere formation of human breast cancer cells MDA-MB-231 or MCF-7. The effects of miR-3613-3p on tumor growth or metastasis in an immunocompromised mouse model of MDA-MB-231-luciferase were explored by intratumor injection of miR-3613-3p analogue. The target genes, interactive lncRNAs, and related signaling pathways of miR-3613-3p were identified by bioinformatic prediction and 3'-UTR assays.
 
  We found that MIR3613 was frequently deleted in breast cancer genome and its deletion was correlated with the molecular typing, and an unfavorable prognosis in estrogen receptor-positive patients. MiR-3613-3p level was also dramatically lower in tumor tissues or serum of breast cancer patients. Gain-of-function studies revealed that miR-3613-3p could suppress proliferation and sphere formation and promote apoptosis in vitro and impeded tumor growth and metastasis in vivo. Additionally, miR-3613-3p might regulate cell cycle by targeting SMS, PAFAH1B2, or PDK3 to restrain tumor progression.
 
  Our findings indicate a suppressive role of miR-3613-3p in breast cancer progression, which may provide an innovative marker or treatment for breast cancer patients.
 Our findings indicate a suppressive role of miR-3613-3p in breast cancer progression, which may provide an innovative marker or treatment for breast cancer patients.