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3%) patients died including 4467 (60.1%) with a history of MI and 1880 (52.1%) with a history of revascularization. Prior MI (adjusted HR 1.12, p=0.001) and prior revascularization without MI (adjusted HR 1.15, p less then 0.001) were independently associated with increased all-cause mortality. Previous MI (adjusted HR 1.27, p less then 0.001) and previous revascularization without MI (adjusted HR 1.21, p less then 0.001) were significantly associated with increased all-cause mortality only in patients without ischemia. CONCLUSIONS In this large cohort of patients undergoing SPECT MPI, previous MI and previous revascularization without MI were independent predictors of all-cause mortality, with no significant difference in associated risk. History of CAD may be particularly important for risk stratification in patients without ischemia. V.PURPOSE Atherosclerosis is the leading cause of cardiovascular diseases (CVD) with high incidence rate and mortality rate. Long non-coding RNAs (lncRNAs) are important functional molecules in atherosclerosis. Present study aimed to explore the functional role and underlying mechanism of ZFAS1 in atherosclerosis. METHODS The in-vitro cell model of atherosclerosis was established by using oxidized low-density lipoprotein (ox-LDL) to induce THP-1 macrophage-derived foam cells. qRT-PCR measured the mRNA levels of ZFAS1, miR-654-3p, ADAM10 and RAB22A. Western blot detected the protein levels of ADAM10 and RAB22A. The levels of IL-1β, IL-6 and TNF-ɑ (inflammatory biomarkers) were tested with ELISA assay. Detection of cholesterol efflux rate was experimented. The interaction between RNAs was affirmed with luciferase reporter and RNA pull-down experiments. RESULTS The expression of ZFAS1 was significantly up-regulated in in-vitro cell model of atherosclerosis at a dose- and time-dependent manner. Knockdown of ZFAS1 impaired inflammatory responses and promoted cholesterol efflux rate. Overexpression of ZFAS1 accelerated inflammatory responses and hampered cholesterol efflux rate. Then, the cytoplasmic role of ZFAS1 was revealed. By bio-informatics analysis and mechanism assays, miR-654-3p was identified to bind with ZFAS1. Moreover, ADAM10 and RAB22A were targeted and suppressed by miR-654-3p. ZFAS1 served as a ceRNA to positively regulate ADAM10 and RAB22A expression through endogenously sponging miR-654-3p. CONCLUSION In conclusion, ZFAS1 elevated ADAM10/RAB22A expression to reduce cholesterol efflux rate and facilitate inflammatory responses in atherosclerosis at a miR-654-3p-dependent way, suggesting a prospective treatment method for amelioration of atherosclerosis. read more The current World Health Organization guidance is not to start corticosteroids, but there is no robust evidence of risk in patients with cancer and coronavirus disease 2019. A risk-benefit analysis should be performed for each patient on the use of steroids in cancer care. Disparity between genome-wide mutations in bladder and other cancers where smoking is a risk factor raises questions about carcinogenesis in different epithelia. To develop an experimental model of bladder carcinogenesis, we clonally expanded in vitro differentiated normal human urothelial (NHU) cells following exposure to an exemplar procarcinogen and used whole-genome DNA sequencing to derive mutational signatures. Benzo[a]pyrene (BaP) was activated by endogenous cytochrome P450 (cytochrome P450 family 1 subfamily A member 1 [CYP1A1]) to create genomically modified NHU cells. Comparison with the Catalogue of Somatic Mutations in Cancer (COSMIC) showed that mutations induced by BaP in NHU cells were similar to smoking-associated signatures in bladder and other cancers, including single- and doublet-base substitution signatures characterised by C > A transversions (COSMIC_SBS4 and COSMIC_DBS2, respectively), and an insertion/deletion signature of C deletions in homopolymer regions (ID3). Our study provides the is another unknown mutational process in bladder cancer that is not the direct result of smoke carcinogens, and this will require further investigation. V.Non-muscle-invasive bladder cancer patients with COVID-19 are more likely to develop acute respiratory distress syndrome. Thus, several adjustments to the use of intravesical instillations of bacillus Calmette-Guérin should be made during the current pandemic to limit the risk of contamination. V.INTRODUCTION Neoadjuvant chemotherapy with docetaxel and estramustine (DE) significantly improved relapse-free survival in patients with high-risk localized prostate cancer treated with androgen deprivation therapy (ADT) for 3 years and a local treatment in the GETUG-12 phase III trial. We sought to explore whether the addition of DE impacts long-term treatment-related side effects. PATIENTS AND METHODS Patients randomized within the UNICANCER GETUG-12 trial at Gustave Roussy who were alive when ADT was discontinued were followed-up prospectively. Serum testosterone levels and clinical data regarding body weight, libido, erection, and cardio-vascular events were collected. RESULTS Seventy-eight patients were included 36 patients had been treated with ADT plus a local treatment and 42 with ADT+DE plus a local treatment. With a median follow-up of 5.9 years after ADT discontinuation, serum testosterone levels returned to normal values (> 200 ng/mL) for 57 (78%) of 72 evaluable patients, and 29 (43%) of 68 evaluable patients reported erections allowing intercourse without medical assistance. No impact of DE on testosterone level recovery, libido, quality of erections, and changes in body weight after ADT discontinuation was detected. The incidence of cardiovascular events was low and similar in both treatment arms. CONCLUSION Treatment with DE was not associated with excess long-term castration-related toxicity in men with high-risk localized prostate cancer. The relapse-free survival improvement seen with DE in GETUG-12 is likely not related to differed testosterone recovery. Unlike the situation for humans and microbes, the active multiprotein assemblies of plants have not been systematically defined. A recent report by McWhite et al. remedies this by analyzing the protein complexes of 13 plant species, thereby defining core assemblies and providing an essential resource for interpreting the genotype-phenotype space of plants.