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Zhang Ziyi,Ding Honglei,Zhou Qi,Pan Weiguo,Qiu Kaina,Mu Xiaotian,Ma Junchi,Zhang Kai,Zhao Yuetong 한국탄소학회 2023 Carbon Letters Vol.33 No.4
In recent years, people are increasingly interested in CO2 hydrogenation to produce value-added chemicals and fuels (CH4, CH3OH, etc.). In the quest for an efficient treatment in CO2 methanation and methanolization, several technologies have been practiced, and DBD plasma technology gain attention due to its easily handling, mild operating conditions, strong activation ability, and high product selectivity. In addition, its reaction mechanism and the effect of packing materials and reaction parameters are still controversial. To address these problems efficiently, a summary of the reaction mechanism is presented. A discussion on plasma-catalyzed CO2 hydrogenation including packing materials, reaction parameters, and optimizing methods is addressed. In this review, the overall status and recent findings in DBD plasma-catalyzed CO2 hydrogenation are presented, and the possible directions of future development are discussed.
Incomplete autophagy promotes the replication of Mycoplasma hyopneumoniae
Wang Zhaodi,Wen Yukang,Zhou Bingqian,Tian Yaqin,Ning Yaru,Ding Honglei 한국미생물학회 2021 The journal of microbiology Vol.59 No.8
Autophagy is an important cellular homeostatic mechanism for recycling of degradative proteins and damaged organelles. Autophagy has been shown to play an important role in cellular responses to bacteria and bacterial replication. However, the role of autophagy in Mycoplasma hyopneumoniae infection and the pathogenic mechanism is not well characterized. In this study, we showed that M. hyopneumoniae infection significantly increases the number of autophagic vacuoles in host cells. Further, we found significantly enhanced expressions of autophagy marker proteins (LC3-II, ATG5, and Beclin 1) in M. hyopneumoniae-infected cells. Moreover, immunofluorescence analysis showed colocalization of P97 protein with LC3 during M. hyopneumoniae infection. Interestingly, autophagic flux marker, p62, accumulated with the induction of infection. Conversely, the levels of p62 and LC3-II were decreased after treatment with 3-MA, inhibiting the formation of autophagosomes, during infection. In addition, accumulation of autophagosomes promoted the expression of P97 protein and the survival of M. hyopneumoniae in PK- 15 cells, as the replication of M. hyopneumoniae was downregulated by adding 3-MA. Collectively, these findings provide strong evidence that M. hyopneumoniae induces incomplete autophagy, which in turn enhances its reproduction in host cells. These findings provide novel insights into the interaction of M. hyopneumoniae and host.