RESUMO
We propose a homogeneous five-mode twelve-core fiber with a trench-assisted structure, combining a low refractive index circle and a high refractive index ring (LCHR). The 12-core fiber utilizes the triangular lattice arrangement. The properties of the proposed fiber are simulated by the finite element method. The numerical result shows that the worst inter-core crosstalk (ICXT) can achieve at -40.14â dB/100â km, which is lower than the target value (-30â dB/100â km). Since adding the LCHR structure, the effective refractive index difference between LP21 and LP02 mode is 2.8 × 10-3, which illustrates that the LP21 and LP02 modes can be separated. In contrast to without the LCHR, the dispersion of LP01 mode has an apparent dropping, which is 0.16 ps/(nm·km) at 1550â nm. Moreover, the relative core multiplicity factor can reach 62.17, which indicates a large core density. The proposed fiber can be applied to the space division multiplexing system to enhance the fiber transmission channels and capacity.
RESUMO
In order to understand the negative effects of bisphenol A (BPA) alternatives comprehensively, zebrafish embryos were used to assess the lethality, developmental effects, and estrogenic activity of bisphenol analogues. The in silico estrogenic activities of bisphenol analogues were assayed by binding simulation. According to our results, the lethality of bisphenol analogues decreased in order of bisphenol AF (BPAF) > BPA > bisphenol F (BPF) > bisphenol S (BPS). BPAF and BPF induced significant effects on zebrafish embryos, including decreased heart rate, hatching inhibition, and teratogenic effects. The binding potentials of bisphenol analogues toward zebrafish ERs (zfERS) decreased in the following order: BPAF > BPA > BPF > BPS. Among the three subtypes of zfERs, zfERß2 showed the highest binding activity toward the bisphenols, followed by zfERα and zfERß1. In vivo estrogenic activity tests showed that BPAF, BPA, and BPF significantly enhanced the protein levels of ERα along with the mRNA levels of esr1, esr2a, esr2b, and vtg1 in zebrafish embryos. Esr2b showed the strongest response to BPAF and BPA exposure among the three esrs. In contrast, BPS did not significantly regulate ER protein level or ER transcription. In conclusion, BPAF showed the highest lethality, developmental effects, and estrogenic activity (both in silico and in vivo) followed by BPA and BPF. BPS showed the weakest toxicity and estrogenic activity. zfERß2 might act as the main target among the three ER subtypes of zebrafish after exposure to BPAF and BPA.
Assuntos
Compostos Benzidrílicos , Peixe-Zebra , Animais , Bioensaio , Estrona , FenóisRESUMO
The potential risks of phthalates affecting human and animal health as well as the environment are emerging as serious concerns worldwide. However, the mechanism by which phthalates induce developmental effects is under debate. Herein, we found that embryonic exposure of zebrafish to di-(2-ethylhexyl) phthalate (DEHP) and di-butyl phthalate (DBP) increased the rate of heart defects including abnormal heart rate and pericardial edema. Changes in the transcriptional profile demonstrated that genes involved in the development of the heart, such as tbx5b, nppa, ctnt, my17, cmlc1, were significantly altered by DEHP and DBP at 50⯵g/L, which agreed with the abnormal cardiac outcomes. Methylated DNA immunoprecipitation sequencing (MeDIP-Seq) further showed that significant hypomethylation of nppa and ctnt was identified after DEHP and DBP exposure, which was consistent with the up-regulation of these genes. Notably, hypermethylation on the promoter region (<1â¯kb) of tbx5b was found after DEHP and DBP exposure, which might be responsible for its decrease in transcription. In conclusion, phthalates have the potential to induce cardiac birth defects, which might be associated with the transcriptional regulation of the involved developmental factors such as tbx5b. These findings would contribute to understand the molecular pathways that mediated the cardiac defects caused by phthalates.
Assuntos
Ácidos Ftálicos , Peixe-Zebra , Animais , Dibutilftalato , Coração , HumanosRESUMO
To investigate the developmental effects and corresponding molecular mechanism of diesel in freshwater organisms, zebrafish embryos were exposed to 0# diesel water-accommodated fraction (WAF) at different concentrations. Mortality, embryonic morphological endpoints, transcriptional profile and lipid profile were evaluated after exposure. Exposure to 0# diesel WAF had no significant effect on the survival of zebrafish embryos from 1.5 to 96 hpf. However, a significant increase in mortality was observed at 144 and 196 hpf in the groups of 20 and 40â¯mg/L 0# diesel WAF. RNA-Seq results demonstrated that 0# diesel WAF could induce significant alterations in transcription profile at concentrations of 0.05â¯mg/L (the limit for petroleum hydrocarbon concentration in surface water in China) and 5â¯mg/L. Gene Ontology enrichment and similarity analysis indicated that lipid metabolism, lipid synthesis, biological transport, drug metabolism and homeostatic processes were the most altered biological processes after exposure to 0# diesel WAF. Further, transcription levels of genes involved in cholesterol and fatty acid synthesis were significantly inhibited by diesel WAF according to qPCR results. Lipidomics results also indicated that several lipid species (cholesterol ester, fatty acid, diglyceride and triglyceride) decreased after 0# diesel WAF exposure. These results reflect the potential risk of diesel pollution in freshwater ecosystems especially on the alteration of lipid homeostasis and enable a better understanding of the molecular pathways underlying the action of diesel WAF in zebrafish embryos.
Assuntos
Embrião não Mamífero/efeitos dos fármacos , Petróleo/toxicidade , Poluentes Químicos da Água/toxicidade , Animais , China , Ecossistema , Homeostase , Hidrocarbonetos/análise , Metabolismo dos Lipídeos , Lipídeos , Petróleo/análise , Água/análise , Poluentes Químicos da Água/análise , Poluentes Químicos da Água/metabolismo , Peixe-Zebra/embriologia , Peixe-Zebra/metabolismo , Peixe-Zebra/fisiologiaRESUMO
To investigate the biological pathways involved in phthalate-induced developmental effects, zebrafish embryos were exposed to different concentrations of di-(2-ethylhexyl) (DEHP) and di-butyl phthalate (DBP) for 96â¯h. Embryonic exposure to DEHP and DBP induced body length decrease, yolk sac abnormities, and immune responses (up-regulation of immune proteins and genes). The lipidomic results showed that at a concentration of 50⯵g/L, DEHP and DBP significantly reduced the levels of fatty acids, triglycerides, diacylglycerol, and cholesterol. These effects are partly explained by biological pathway enrichment based on data from the transcriptional and proteomic profiles. Co-exposure to DBP and ER antagonist did not significantly relieve the toxic symptoms compared with exposure to DBP alone. This indicates that phthalate-induced developmental abnormities in zebrafish might not be mediated by the ER pathway. In conclusion, we identified the possible biological pathways that mediate phthalate-induced developmental effects and found that these effects may not be driven by estrogenic activation.