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Imidacloprid has been used for many years to control planthopper Nilaparvata lugens (Stål) (Homoptera: Delphacidae) in China. To provide resistance assessment for the national insecticide resistance management program, we collected a total of 42 samples of the planthoppers from 27 locations covering eight provinces to monitor their dose responses and susceptibility changes to imidacloprid over an 11-yr period (1996-2006). Results showed that most field populations maintained susceptibility from 1996 to 2003 except for a population from Guilin, Guangxi, in 1997, which showed a low level of resistance to imidacloprid. However, surveys conducted in 2005 indicated that 16 populations from six provinces quickly developed resistance with resistance ratios ranging from 79 to 811. The data collected in 2006 revealed that the resistance levels in 12 populations collected from seven different provinces decreased slightly (RR = 107-316), except the Tongzhou population (Jiangsu Province), which developed 625-fold resistance. Dominant and intensive use of imidacloprid in a wide range of rice, Oryza savita L., growing areas might be a driving force for the resistance development. Migration of the insect also significantly boosted the resistance levels due to extensive and intensive use of imidacloprid in emigrating areas and continuous postmigration sprays of the chemical. In addition, laboratory resistance selection using imidacloprid showed that resistance ratio increased to 14-fold after 27 generations, suggesting that quick resistance development might be associated with more frequent applications of the insecticide in recent years.

Extensive use of imidacloprid for suppressing the brown planthopper, Nilaparvata lugens (Stål) (Homoptera: Delphacidae), has placed heavy selection pressure on the target insect. A systematic study was carried out to determine imidacloprid resistance dynamics and cross‐resistance. Data collected from a 3‐year study (2005–2007) showed that in 2005, the resistance levels in Nanning (Guangxi), Haiyan (Zhejiang), and Nanjing and Tongzhou (Jiangsu) populations ranged from 200‐ to 799‐fold compared with the susceptible strain. However, the resistance levels decreased to 135‐ to 233‐fold in 2007, after reduced application of the chemical. A laboratory population was challenged with imidacloprid in successive generations. After 23 generations, the resistance ratio had increased from 200‐ to 1 298‐fold. Continuous selection with imidacloprid could increase the resistance level even more than has already been developed in the population. Stopping selection with imidacloprid led to a rapid decrease of resistance from 759‐ to 114‐fold after 17 generations. Resistance levels then became stable without decreasing any further. A similar result was also obtained from a study involving a field population (resistance ratio = 625‐fold) collected from Tongzhou. At first, the population showed a rapid decrease in resistance right after imidacloprid selection was stopped, and then the resistance stabilized at a level of 105–129‐fold. More interestingly, resistance increased again when selection was resumed. In addition, the resistant strain selected with imidacloprid showed substantial cross‐resistance to imidaclothiz, thiacloprid, and acetamiprid, and slight levels of cross‐resistance to dinotefuran and thiamethoxam, but no obvious cross‐resistance to nitenpyram, buprofezin, and fipronil. The information from this study is valuable for formulating resistance‐management strategies against N. lugens.

Acute myocardial infarction (AMI), the leading cause of mortality worldwide, is a rapidly developing and irreversible disease. Therefore, proper prompt intervention at the early stage of AMI is crucial for its treatment. However, the molecular features in the early stage have not been clarified. Here, we constructed mouse AMI model and profiled transcriptomes and proteomes at the early stages of AMI progress. Immune system was extensively activated at 6-h AMI. Then, pyroptosis was activated at 24-h AMI. VX-765 treatment, a pyroptosis inhibitor, significantly reduced the infarct size and improved the function of cardiomyocytes. Besides, we identified that WIPI1, specifically expressed in heart, was significantly upregulated at 1 h after AMI. Moreover, WIPI1 expression is significantly higher in the peripheral blood of patients with AMI than healthy control. WIPI1 can serve as a potential early diagnostic biomarker for AMI. It likely decelerates AMI progress by activating autophagy pathways. These findings shed new light on gene expression dynamics in AMI progress, and present a potential early diagnostic marker and a candidate drug for clinical pre-treatment to prolong the optimal cure time.