Bradysia odoriphaga Yang et Zhang is a destructive insect pest of Chinese chives. To understand the current status of insecticide resistance of B. odoriphaga in China, the sensitivity variation of eight field populations to six commonly used insecticides, including chlorpyrifos, phoxim, imidacloprid, thiamethoxam, clothianidin and beta-cypermethrin were evaluated. The results showed that almost all the tested B. odoriphaga populations had developed moderate to high resistance to chlorpyrifos and phoxim. There were different resistance levels found in the eight field populations among the three neonicotinoids, imidacloprid, thiamethoxam and clothianidin. Imidacloprid was very effective against B. odoriphaga in most tested populations except those from Yangzhou (10.35-fold) and Tangshan (14.56-fold). While four populations kept susceptible to thiamethoxam, the other four populations showed decreased susceptibility or low resistance. To clothianidin, five populations displayed moderate resistance, two populations displayed low resistance, and one population exhibited susceptibility, respectively. All the tested populations were resistance to beta-cypermethrin, the highest resistance was found in the Tangshan population with a resistance ratio of 172.56-fold. The results of this study provided valuable information for choosing insecticides for control and integrated resistance management of B. odoriphaga.
The COVID-19 pandemic caused by the SARS-CoV-2 virus, overlaps with the ongoing epidemics of cigarette smoking and electronic cigarette (e-cig) vaping. However, there is scarce data relating COVID-19 risks and outcome with cigarette or e-cig use. In this study, we mined three independent RNA expression datasets from smokers and vapers to understand the potential relationship between vaping/smoking and the dysregulation of key genes and pathways related to COVID-19. We found that smoking, but not vaping, upregulates ACE2, the cellular receptor that SARS-CoV-2 requires for infection. Both smoking and use of nicotine and flavor-containing e-cigs led to upregulation of pro-inflammatory cytokines and inflammasome-related genes. Specifically, chemokines including CCL20 and CXCL8 are upregulated in smokers, and CCL5 and CCR1 are upregulated in flavor/nicotine-containing e-cig users. We also found genes implicated in inflammasomes, such as CXCL1, CXCL2, NOD2, and ASC, to be upregulated in smokers and these e-cig users. Vaping flavor and nicotine-less e-cigs, however, did not lead to significant cytokine dysregulation and inflammasome activation. Release of inflammasome products, such as IL-1B, and cytokine storms are hallmarks of COVID-19 infection, especially in severe cases. Therefore, our findings demonstrated that smoking or vaping may critically exacerbate COVID-19-related inflammation or increase susceptibility to COVID-19.
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