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A population of Aedes (Stegomyia) albopictus (Skuse) (Diptera: Culicidae), a vector of chikungunya, dengue, yellow fever, and Zika and West Nile viruses, has been detected in Windsor, Ontario, Canada from 2016 onwards. Here, we describe its seasonal distribution, as well as the various aquatic habitats from which this species was collected and its larval co-habitation. We collected immatures from tires, treeholes, extruded polystyrene foam containers, discarded plastic cups, old recycling bins and oviposition traps. Aedes albopictus larvae were collected with Aedes japonicus (Theobald), Anopheles punctipennis (Say), Culex pipiens Linnaeus, Ochlerotatus hendersoni (Cockerell), Ochlerotatus triseriatus (Say) and Orthopodomyia signifera (Coquillett). Adult female and male specimens were collected from Biogents sentinel traps (Biogents AG, Regensburg, Germany), as well as Centers for Disease Control and Prevention miniature light traps (CDC, Atlanta, GA, U.S.A.), and also as they alighted on the investigators. Peak adult collections occurred in September during epidemiological week 37. We also collected Aedes (Stegomyia) aegypti (Linnaeus), a new record for Canada, in 2016 and from two new collection sites in 2017. The 2017 collections were 3.5 km north and 19.4 km south of the index site. The present study adds to the increasing number of studies reporting range expansions of these mosquito species.

L1 retrotransposons can pose a threat to genome integrity. The host has evolved to restrict L1 replication. However, mechanisms underlying L1 propagation out of the host surveillance remains unclear. Here, we propose a novel survival strategy of L1, which exploits RNA m6A modification. We discover that m6A ‘writer’ METTL3 facilitates L1 retrotransposition, whereas m6A ‘eraser’ ALKBH5 suppresses it. The essential m6A cluster that is located on L1 5′ UTR serves as a docking site for eukaryotic initiation factor 3 (eIF3), enhances translational efficiency and promotes the formation of L1 ribonucleoprotein. Furthermore, through the comparative analysis of human- and primate-specific L1 lineages, we find that the most functional m6A motif-containing L1s have been positively selected and became a distinctive feature of evolutionarily young L1s. Thus, our findings demonstrate that L1 retrotransposons hijack RNA m6A modification system for its successful replication.

PurposeTo explore the clinical and radiological differences between urachal carcinoma and urachal infection.MethodsClinical and imaging information for 13 cases of urachal carcinoma and 14 cases of urachal infection confirmed by pathology were retrospectively analyzed. The size, location, shape, margin, lesion composition, calcification, T1 and T2 signal intensity, peripheral lymph nodes, degree of enhancement, adjacent bladder wall, and apparent diffusion coefficient (ADC) value were examined in both groups, and distinguish features were determined. The student t-test or Mann-Whitney U test was used for quantitative data, and Fisher’s exact test was used for qualitative data. Kappa coefficient consistency test was used to evaluate the interobserver agreement.ResultsSex, hematuria, abdominal pain, calcification, and thickening of adjacent bladder wall can distinguish between urachal carcinoma and urachal infection (p < 0.05). There were no statistical differences in age (p = 0.076), size (p = 0.797), location (p = 0.440), shape (p = 0.449), margin (p = 0.449), lesion composition (p = 0.459), T1 signal intensity (p = 0.196), T2 signal intensity (p = 0.555), peripheral lymph nodes (p = 0.236), degree of enhancements (p = 0.184) and ADC value (p = 0.780) between two groups.ConclusionThe following clinical and imaging features help distinguish urachal carcinoma from urachal infection: sex, hematuria, abdominal pain, calcification, and thickening of the adjacent bladder wall.