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Disruption of ecdysis in Leptinotarsa decemlineata by knockdown of chitin deacetylase 1
Jian-Jian Wu,Li-Li Mu,Zhong-Chao Chen,Kai-Yun Fu,Wen-Chao Guo,Chao Li,Guo-Qing Li 한국응용곤충학회 2019 Journal of Asia-Pacific Entomology Vol.22 No.2
Chitin deacetylases (CDAs) catalyze N-deacetylation of chitin, a crucial process for chitin modification. In the present paper, LdCDA1 was identified in Leptinotarsa decemlineata. It was copiously expressed in larval foregut, hindgut and epidermis. Just before the molt in the first, second and third larval instars, the mRNA levels of LdCDA1 were high. In the fourth (final)-instar larvae, a peak occurred 4 days after ecdysis. In vivo results revealed that LdCDA1 transcriptionally responded, positively and negatively respectively, to 20-hydroxyecdysone and juvenile hormone titers. Moreover, knockdown of LdCDA1 significantly reduced foliage consumption, lengthened developing period and prevented growth in the final instar larvae. Three distinct lethal phenotypes were noted in the LdCDA1 RNAi larvae. About 30% of the RNAi larvae became moribund and finally died; approximately 50% of deformed pupae died as pharate adults; and around 20% of LdCDA1 depleted pupae finally emerged as abnormal adults and eventually died within 1 week after emergence. Furthermore, chitin content was low and the mRNA levels of five chitin biosynthesis transcripts (LdUAP1, LdUAP2, LdChSAa, LdChSAb and LdChSB) were significantly declined in the LdCDA1 RNAi larvae. In addition, glucose, trehalose and glycogen contents were increased in the LdCDA1 depleted hypomorphs, along with highly expressed genes coding for trehalose and glycogen synthesis enzymes. The findings provide a compelling piece of evidence that CDA1 is critical for chitin deposition in L. decemlineata. Moreover, LdCDA1 may be a potential target for control of the larvae.
Primary-Side Control for Flyback Converter with Wide Range Operation
Bin-Kun Huang,Tsorng-Juu Liang,Wei-Jing Tseng,Kai-Hui Chen,Qing-Mu Chen 전력전자학회 2019 ICPE(ISPE)논문집 Vol.2019 No.5
Most of current primary side regulation (PSR) control methods are implemented in either discontinuous conduction mode (DCM) or continuous conduction mode (CCM). Because of the difficulty in sensing the output voltage, no algorithm is suitable for both DCM and CCM, and the power range of the system is limited. The proposed controller is suitable for both DCM and CCM with wide power range operation. The “TSMC 0.25 μm CMOS high voltage mixed signal process” is adopted to implement the proposed IC. A flyback converter with 400 V input and 20 V/150 W output is built to verify the feasibility of proposed control IC.
Dou, Xue,Wang, Ren-Ben,Meng, Xiang-Jiao,Yan, Hong-Jiang,Jiang, Shu-Mei,Zhu, Kun-Li,Xu, Xiao-Qing,Chen, Dong,Song, Xian-Rang,Mu, Dian-Bin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.2
Objective: The purpose of this study was to examine the role of programmed cell death 4 (PDCD4) expression in predicting tumor response to neoadjuvant chemoradiotherapy and outcomes for patients with locally advanced rectal cancer. Methods: Clinicopathological factors and expression of PDCD4 were evaluated in 92 patients with LARC treated with nCRT. After the completion of therapy, 4 cases achieved clinical complete response (cCR), and thus the remaining 88 patients underwent a standardized total mesorectal excision procedure. There were 38 patients (41.3%) with a good response (TRG 3-4) and 54 (58.7%) with a poor one (TRG 0-2). Results: Immunohistochemical staining analyses showed that patients with high expression of PDCD4 were more sensitive to nCRT than those with low PDCD4 expression (P=0.02). High PDCD4 expression before nCRT and good response (TRG3-4) were significantly associated with improved 5-year disease-free survival and 5-year overall survival (P<0.05). Multivariate analysis demonstrated that the pretreatment PDCD4 expression was an independent prognostic factor. Conclusion: Our study demonstrated that high expression of PDCD4 protein is a useful predictive factor for good tumor response to nCRT and good outcomes in patients with LARC.