Locusts aggregate into bands of nymphs and swarms of adults that can pose a major threat to crop. Previous studies have shown that infection by the microsporidian parasite Paranosema locustae prevents locust aggregation behavior and we show that gut bacteria, which produce components of locust aggregation pheromones, are substantially reduced in locusts infected with P. locustae. We found that P. locustae could reduce the diversity, abundance and community composition of Locusta migratoria’s gut bacteria. The parasite infection was also shown to interrupt the peroxidase activity of locust hindgut. Genome-wide expression analysis showed that the parasite infection suppressed peroxidase mRNA relative expression of locust hindgut, but had no effects on attacin expression and superoxide dismutase at 16 d post-inoculation with 20,000 P. locustae spores. Our findings reveal the mechanisms by which P. locustae impairs bacterial diversity and community structure of Locusta migratoria’s gut bacteria.

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This thesis is aimed at shedding light on the effects of the Zhenwu decoction (ZWD) on the activities and mRNA expressions of seven CYP450 isoenzymes. In the first step, we determined the main chemical compounds of ZWD by high-performance liquid chromatography (HPLC). Next, 48 male (SD) rats were randomly divided into the normal saline (NS) group and the ZWD low- (2.1875 g/kg), medium- (4.375 g/kg), and high- (8.75 g/kg) dose groups (12 per group). All rats were gavaged once daily for 28 consecutive days. A mixed solution of seven probe drugs was injected into 24 rats through the caudal vein after the last intragastric administration. Lastly, a validated cocktail method and real-time quantitative reverse-transcription polymerase chain reaction (RT-qPCR) were used to detect pharmacokinetic parameters and mRNA expressions, respectively. Compared with the NS group, ZWD at medium- and high-dose groups could significantly induce CYP2C6 (P<0.05) activity, while the mRNA expression (P<0.05) increased only in the high-dose group. Additionally, CYP2C11 activity was induced and consistent with mRNA expression (P<0.05). Moreover, ZWD could induce the activity of CYP3A1 (P<0.05), but the mRNA expression showed no significant differences except in high-dose groups. Additionally, ZWD has no effects on CYP1A2, CYP2B1, CYP2C7, and CYP2D2. In conclusion, the significant inductive effects of ZWD on three CYP450 isoenzymes indicated that when ZWD was coadministrated with drugs mediated by these enzymes, not only should the potential herb-drug interactions (HDIs) be observed, but the dosage adjustment and tissue drug concentration should also be considered. Furthermore, the approach described in this article can be applied to study the importance of gender, age, and disease factors to HDI prediction.

Transforming growth factor-beta (TGF-beta) is a multifunctional growth and differentiation factor that affects almost all cells. Although equipotent in many cases, the three isoforms of TGF-beta (-beta1, -beta2, -beta3) have several important isoform specific activities. For example, TGF-beta2 binds with higher affinity to a 60 kDa cell-surface glycosyl phosphatidylinositol (GPI)-linked protein, expressed on vascular endothelial cells. We used chimeric TGF-beta proteins, in which selected regions of TGF-beta1 had been exchanged for the corresponding region of TGF-beta2, to demonstrate that amino acids 67 and 68 regulate binding of TGF-beta to this protein. Exchange of amino acids 67 and 68 of TGF-beta1 into TGF-beta2 resulted in a protein similar in affinity to TGF-beta1 for binding to the GPI-linked protein. In contrast, exchange of only amino acid 67 of TGF-beta1 into TGF-beta2, or exchange of only amino acid 68 of TGF-beta1 into TGF-beta2, resulted in a protein with affinity similar to that of TGF-beta2. This suggests that the coordinated change of Gln and His of TGF-beta1 to Thr and Ile at positions 67 and 68 alters the specificity of TGF-beta. Amino acids 67 and 68 are part of a surface-exposed alpha-helix that forms a projection away from the center of the TGF-beta molecule and is accessible for receptor binding.

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