A preparation process of 2-methylnaphthalene (2-MN) was proposed by isomerization , side-stream distillation and extractive distillation. The isomerization of alkyl naphthalene was catalyzed by acid-treated HBEA zeolites, and the 2-MN selectivity of isomerization was 92.70%. Side-stream distillation and extractive distillation were investigated by simulation, and effects of operation parameters on 2-MN were studied. Further, the simulated results were verified by experiment. Under the optimal condition, the mass fraction of 2-MN reached to 98.09% in the product, and the yield was 83.84% in refining process.
Hair cells in the inner ear and lateral lines are mechanosensitive receptor cells whose development and function are tightly regulated. Several transcription factors as well as splicing factors have been identified to play important roles in hair cell development, whereas the role of RNA stability in this process is poorly understood. In the present work, we report that RNA-binding motif protein 24a (Rbm24a) is indispensable for hair cell development in zebrafish. Rbm24a expression is detected in the inner ear as well as lateral line neuromasts. Albeit rbm24a deficient zebrafish do not survive beyond 9 days post fertilization (dpf) due to effects outside of the inner ear, rbm24a deficiency does not affect the early development of inner ear except for delayed otolith formation and semicircular canal fusion. However, hair cell development is severely affected and hair bundle is disorganized in rbm24a mutants. As a result, the auditory and vestibular function of rbm24a mutants are compromised. RNAseq analyses identified several Rbm24a-target mRNAs that are directly bound by Rbm24a and are dysregulated in rbm24a mutants. Among the identified Rbm24a-target genes, lrrc23, dfna5b, and smpx are particularly interesting as their dysregulation might contribute to the inner ear phenotypes in rbm24a mutants. In conclusion, our data suggest that Rbm24a affects hair cell development in zebrafish through regulating mRNA stability.
Min Xia,Xuedong Wang,Jiaqi Xu,Qiuhui Qian,Ming Gao,Huili Wang
The organophosphate flame retardant, tris (1-chloro-2-propyl) phosphate (TCPP), is ubiquitous in environmental matrices; however, there is a paucity of information concerning its systemic toxicity. Herein, we investigated the effects of TCPP exposure on zebrafish neurodevelopment and swimming behavior to elucidate the underlying molecular mechanisms of neurotoxicity. Under TCPP gradient concentration exposure, the hatching rates were declined by up to 33.3% in 72 hpf, and the malformation rates increased from 15% to 50%. Meanwhile, TCPP led to abnormal behaviors including decreased locomotive activity in the dark and slow/insensitive responses to sound and light stimulation of larvae. TCPP caused excessive apoptosis and ROS accumulation in early embryonic development, with hair cell defects and structural deformity of neuromast. Abnormal expression of neurodevelopment ( pax6a , nova1 , sox11b , syn2a , foxo3a and robo2 ) and apoptosis-related genes ( baxa , bcl2a and casp8 ) revealed molecular mechanisms regarding abnormal behavioral and phenotypic symptoms. Chronic TCPP exposure led to anxiety-like behavior and excessive panic, lower capacity for discrimination and risk avoidance, and conditioned place preference in adults. Social interaction tests demonstrated that long-term TCPP stress resulted in unsociable, eccentric, lonely and silent behaviors in adults. Zebrafish memory and cognitive function were severely reduced as concluded from T-maze tests. Potential mechanisms triggering behavioral abnormality were attributed to histopathological injury of diencephalon, abnormal changes in nerve-related genes at transcription and expression levels, and inhibited activity of AChE by TCPP stress. These findings provide an important reference for risk assessment and early warning to TCPP exposure, and offer insights for prevention/mitigation of pollutant-induced nervous system diseases.
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