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The codling moth, Cydia pomonella (Lepidoptera: Tortricidae) is a major pest of pome fruit and walnuts worldwide. Although environmentally compatible integrated control strategies, such as mating disruption, attract-kill strategy, and sterile insect technique have been conducted for management of this notorious pest, effects to control of codling moth have mainly relied on insecticides. In consequence, different levels of insecticide resistance towards organophosphates, neonicotinoids, hydrazines, benzoylureas, pyrethroids, diamides, spinosyns, avermectins, JH mimics, carbamates, oxadiazines and C. pomonella granulovirus (CpGVs) have developed in codling moth in different countries and areas. Both metabolic and target-site mechanisms conferring resistance have been revealed in the codling moth. In this review, we summarize the current global status of insecticide resistance, the biochemical and molecular mechanisms involved, and the implications for resistance management.

Traumatic brain injury (TBI) is a major cause of mortality and disability worldwide. To date, therapies to treat any forms of TBI are still limited. Recent studies have demonstrated the potential neuroprotective effects of molecular hydrogen on TBI. Although it has been demonstrated that hydrogen inhalation (HI) for about 5 hrs immediately after TBI has a beneficial effect on brain injury, the most effective intervention procedure in the treatment of TBI remains unknown. The mechanism underlying the neuroprotective effects of HI on TBI also needs to be further investigated. Our results showed that inhalation of 4% hydrogen during the first day after TBI was the most effective hydrogen intervention procedure in the treatment of TBI. Pathological examination showed that HI could attenuate TBI-induced reactive astrocytosis and microglial activation. Nissl staining demonstrated a significant decrease in the number of nissl-stained dark neurons (N-DNs) in HI group compared to TBI group at 2 h post-TBI, and the TBI-induced neuronal loss was attenuated by HI at day 3 post-TBI. IHC staining showed that HI resulted a decrease in CD16-positive cells and a further increase in CD206-positive cells as compared to TBI group. Multiplex cytokine assay demonstrated the most profound regulatory effects induced by HI on the levels of IL-12, IFN-γ, and GM-CSF at 24 h post-TBI, which confirmed the inhibitory effect of hydrogen on microglia activation. We concluded that inhalation of 4% hydrogen during the first day after TBI was the most effective intervention procedure in the treatment of TBI. Our results also showed that hydrogen may exert its protective effects on TBI via inhibition of microglia activation and neuroinflammation.