In this paper, we systematically calculate two-body strong decays of newly observed D J ð3000Þ and D sJ ð3040Þ with 2Pð1 þ Þ and 2Pð1 þ0 Þ assignments in an instantaneous approximation of the Bethe-Salpeter equation method. Our results show that both resonances can be explained as the 2Pð1 þ 0 Þ with broad width . For D sJ ð3040Þ, the total width is 157.4 MeV in our calculation, close to the lower limit of experimental data, and the dominant channels are D Ã K and D Ã K Ã . These results are consistent with observed channels in experiments. Given the very little information that has been obtained from experiments and the large error bars of the total decay widths, we recommend the detection of dominant channels in our calculation.
We calculate the two-body strong decays of the orbitally excited scalar mesons D * 0 (2400) and D * J (3000) by using the relativistic Bethe-Salpeter (BS) method. D * J (3000) was observed recently by the LHCb Collaboration, the quantum number of which has not been determined yet. In this paper, we assume that it is the 0 + (2P) state and obtain the transition amplitude by using the PCAC relation, low-energy theorem and effective Lagrangian method. For the 1P state, the total widths of D * 0 (2400) 0 and D * 0 (2400) + are 226 and 246 MeV, respectively. With the assumption of 0 + (2P) state, the widths of D * J (3000) 0 and D * J (3000) + are both about 131 MeV, which is close to the present experimental data. Therefore, D * J (3000) is a strong candidate for the 2 3 P 0 state.
Background
Polycystic ovary syndrome (PCOS) is an endocrine-related follicular developmental disorder that affects 50 %-70 % of reproductive-aged women diagnosed with ovulation-related infertility. Abnormal proliferation and apoptosis of granulosa cells (GCs) are thought to be the critical factors leading to abnormal maturation of follicles. It has been shown that microRNAs (miRNAs) exert a significant influence in the pathogenesis of PCOS; however, the relationship between miRNA, PCOS, and GC apoptosis is not entirely understood.
Methods
To clarify the effect of miR-194 in PCOS, CCK-8, Ki67 staining, AO/EB, and flow cytometry assays were used to assess cell growth, proliferation, and apoptosis in KGN cells, which were artificially stimulated to overexpress miR-194. Luciferase reporter assays and rescue experiments were used to elucidate the mechanism underlying miR-194 in PCOS.
Results
miR-194 expression was significantly up-regulated in rat models of PCOS and the ovarian GCs of PCOS patients. miR-194 suppression promoted KGN cell growth and proliferation. miR-194 overexpression also induced cell apoptosis, while miR-194 downregulation had an opposite effect. Furthermore, up-regulating heparin-binding EGF-like growth factor (HB-EGF) expression rescued the pro-apoptotic effects of miR-194 upregulation on KGN cells.
Conclusions
miR-194 is increased in PCOS granulosa cell and may
function as a novel biomarker and therapeutic target for KGN cells via HB-EGF
regulation.
Spirodiclofen is one of the most widely used acaricides in China. The citrus red mite, Panonychus citri (McGregor) (Acari: Tetranychidae), is one of the most destructive citrus pests worldwide and has developed a high resistance to spirodiclofen. However, the molecular mechanism of spirodiclofen resistance in P. citri is still unknown. In this study, we identified a field spirodiclofen-resistant strain (DL-SC) that showed 712-fold resistance to spirodiclofen by egg bioassay compared to the susceptible strain. Target-site resistance was not detected as non-synonymous mutations were not found by amplification and sequencing of the ACCase gene of resistant and susceptible strains; in addition, the mRNA expression levels of ACCase were similar in both resistant and susceptible strains. The activity of detoxifying enzymes P450s and CCEs in the resistant strain was significantly higher than in the susceptible strain. The transcriptome expression data showed 19 xenobiotic metabolisms genes that were upregulated. Stage-specific expression profiling revealed that the most prominent upregulated gene, CYP385C10, in transcriptome data was significantly higher in resistant strains in all stages. Furthermore, functional analysis by RNAi indicated that the mortality caused by spirodiclofen was significantly increased by silencing the P450 gene CYP385C10. The current results suggest that overexpression of the P450 gene, CYP385C10, may be involved in spirodiclofen resistance in P. citri.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.