Effects of consecutive culture of Penaeus vannamei on phosphorus transformation and microbial community in sediment.

Phosphorus (P) is highly related to water quality during shrimp culture. Recognizing P transformation in pond-based cultures is crucial for sustainable and healthy aquaculture. However, P transformation remains unclear in the sediment of Penaeus vannamei cultures, although commercial species have been pervasive worldwide. To determine P transformation, samples with different culture years were collected from Zhejiang province, China. Sequential chemical extraction was applied to reveal the composition of inorganic P, while phosphatase activity was used to evaluate the biomineralization of organic P. The results indicated that the consecutive culture of Penaeus vannamei promoted the dissolution potential of sedimentary P. This was attributed to anoxic iron reduction that increased the formation of loosely bound P and Fe (II)-P. However, this phenomenon was dominated by biomineralization, which transformed the organic P to inorganic P. The results suggested that consecutive culture changed the microbial community structure in the sediment as well as the gene functions. The Shannon Wiener index showed that increasing the culture duration significantly decreased the stability of the microbial community. Overall, this study suggests that long-term consecutive culture of Penaeus vannamei may increase the P release potential of the sediment, which increases the risk of pond eutrophication.

The Multifaceted Roles of RCC1 in Tumorigenesis.

RCC1 (regulator of chromosome condensation 1) is the only known guanine nucleotide exchange factor of Ran, a nuclear Ras-like G protein. RCC1 combines with chromatin and Ran to establish a concentration gradient of RanGTP, thereby participating in a series of cell physiological activities. In this review, we discuss the structure of RCC1 and describe how RCC1 affects the formation and function of the nuclear envelope, spindle formation, and nuclear transport. We mainly focus on the effect of RCC1 on the cell cycle during tumorigenesis and the recent research progress that has been made in relation to different tumor types.

Properties of CaO2 for H2O2 release and phosphate removal and its feasibility in controlling Microcystis blooms.

Calcium peroxide (CP) has been widely applied in environmental remediation, but few studies have reported its application in controlling Microcystis blooms. To recognize its feasibility for mitigating Microcystis blooms, the properties of CP in terms of hydrogen peroxide (HP) release and phosphate removal were investigated at different CP doses, temperatures, and initial pH values. HP release kinetics followed the Higuchi model. Batch experiments conducted in this study suggested that the HP yield and release rate were positively correlated with the CP dose. Increasing temperature decreased the HP yield but accelerated the HP release rate. The phosphate removal kinetics were well simulated by the pseudo-second-order model. The batch experiments suggested that an increased CP dose enhanced the phosphate removal capacity, but it did not affect the phosphate removal rate. Moreover, increased temperature accelerated both phosphate removal capacity and rate. However, the initial pH of low-buffer-capacity solutions did not notably affect HP release and phosphate removal. According to laboratory experiments, HP released from CP could impair photosynthetic activity, resulting in Microcystis mortality. Furthermore, the reduced phosphate concentration in the solutions suggested that CP could facilitate the control of eutrophication, which directly reduced bloom formation. Hence, our results confirmed CP as a promising algicide for Microcystis bloom control, and it is worthwhile to develop novel methods for bloom mitigation based on CP. Graphic abstract.

Tanshinone IIA induced cell death via miR30b-p53-PTPN11/SHP2 signaling pathway in human hepatocellular carcinoma cells.

Tanshinone IIA, a multi-pharmaceutical compound from traditional Chinese herb, has been reported to have anti-hepatocarcinomic (HCC) properties through cell death induction. Apart from the typical p53-dependent pathway, mechanisms of the anti-carcinogenic role of Tanshinone remain scarce. In an effort to explore the mechanism behind Tanshinone IIA, we detected the upstream of the p53 and the potential novel pathway. Tanshinone IIA dose-dependently initiated HepG2 cell apoptosis and cell cycle arrest at the G1 checkpoint. In the miR30 family, only the transcription of miR30b was downregulated by Tanshinone IIA, which subsequently upregulated both the genomic and protein levels of p53. Further, we screened that PTPN11 and Tp53 are the two critical genomes involved in the pharmacology of Tanshinone IIA. Building upon LASAGNA-search and kinetics binding assay, p53 was found to be a potential transcription factor for PTPN11. Concomitant with the expression of p53, Tanshinone IIA stimulated both PTPN11 and its encoded protein SHP2. Inhibition miR30b attenuated the Tanshinone IIA-induced cytotoxicity, level of p53 and PTPN11 in HepG2 cells. Finally, the apoptotic molecules such as Bax/Bcl2, cleavage caspase 3 and the cell cycle regulation factors including p21, cyclin D1, and CDK6 were changed by Tanshinone IIA. Several cytotoxic endpoints induced by Tanshinone IIA were also checked in Hep3B cells. This study confirmed that Tanshinone IIA may induce hepatoma cell death through the miR30b-p53- PTPN11/SHP2 pathway. With regard to the complicated tumorigenesis of HCC and the multi-targets of Tanshinone IIA, our results propose developing Tanshinone IIA for clinic therapy and the interference of HCC.