Dynamical electron diffraction simulation for non-orthogonal crystal system by a revised real space method.

In the transmission electron microscopy, a revised real space (RRS) method has been confirmed to be a more accurate dynamical electron diffraction simulation method for low-energy electron diffraction than the conventional multislice method (CMS). However, the RRS method can be only used to calculate the dynamical electron diffraction of orthogonal crystal system. In this work, the expression of the RRS method for non-orthogonal crystal system is derived. By taking Na2 Ti3 O7 and Si as examples, the correctness of the derived RRS formula for non-orthogonal crystal system is confirmed by testing the coincidence of numerical results of both sides of Schrödinger equation; moreover, the difference between the RRS method and the CMS for non-orthogonal crystal system is compared at the accelerating voltage range from 40 to 10 kV. Our results show that the CMS method is almost the same as the RRS method for the accelerating voltage above 40 kV. However, when the accelerating voltage is further lowered to 20 kV or below, the CMS method introduces significant errors, not only for the higher-order Laue zone diffractions, but also for zero-order Laue zone. These indicate that the RRS method for non-orthogonal crystal system is necessary to be used for more accurate dynamical simulation when the accelerating voltage is low. Furthermore, the reason for the increase of differences between those diffraction patterns calculated by the RRS method and the CMS method with the decrease of the accelerating voltage is discussed.

MiR-543-3p promotes locomotor function recovery after spinal cord injury by inhibiting the expression of tumor necrosis factor superfamily member 15 in rats.

OBJECTIVE: To explore the effect of miR-543-3p on the recovery of locomotor function after spinal cord injury (SCI) by regulating tumor necrosis factor superfamily member 15 (TNFSF15) mediated inflammation and apoptosis. MATERIALS AND METHODS: Macrophages were isolated from the abdominal cavity of 2-3 months old Sprague-Dawley (SD) rats and cultured. The levels of miR-543-3p, tumor necrosis factor superfamily member 15 (TNFSF15), TNF-like molecule 1A (TL1A) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) after transfection of miR-92b-5p into activated macrophages were detected by quantitative Real-time polymerase chain reaction (qRT-PCR). Moreover, the mRNA expressions of miR-543-3p, TNFSF15, TL1A and NF-κB after SCI in rats were detected by qRT-PCR. Meanwhile, the protein expressions of tumor necrosis factor (TNF-α), interleukin-1 ß (IL-1ß) and Caspase8 were detected by Western blot. After intrathecal injection of miR-543-3p mimics, the mRNA expressions of miR-543-3p, TNFSF15, TL1A and NF-κB and the protein expressions of TNF-α, IL-1ß and Caspase8 in spinal cord injured area of mice were measured by qRT-PCR and Western blot, respectively. Basso Beattie Bresnahan (BBB) locomotor rating scale was used to determine the recovery of locomotor function after spinal cord injury and injection of miR-543-3p mimics. RESULTS: Compared with inactivated cells, the expression of miR-543-3p in activated macrophages was significantly declined. However, the levels of TNFSF15, TL1A and NF-κB were significantly elevated. The expressions of TNFSF15, TL1A and NF-κB were remarkably downregulated after transfection of miR-543-3p. In addition, the level of miR-543-3p was significantly downregulated, accompanied by an increase in TNFSF15, TL1A and NF-κB in SCI rats. Accordingly, the protein levels of TNF-α and IL-1ß and Caspase8 were also significantly increased. However, the expressions of TNFSF15, TL1A and NF-κB were significantly down-regulated in rats injected with miR-543-3p mimics, whereas the protein levels of TNF-α and IL-1ß and Caspase8 were significantly suppressed. Finally, compared with SCI group, the recovery of locomotor function in miR-543-3p mimics administration group was significantly improved. CONCLUSIONS: After SCI, miR-543-3p can inhibit the activity of NF-κB by suppressing the inflammatory aggravation of TNFSF15 and decreasing its product TL1A. MiR-543-3p leads to the improvement of neuron protection and locomotor function via attenuating inflammatory reaction and cell apoptosis.

MicroRNA-448 inhibits the regeneration of spinal cord injury through PI3K/AKT/Bcl-2 axis.

OBJECTIVE: This study aims to elucidate the potential role of microRNA-448 in the recovery of spinal cord injury (SCI), and to explore the underlying mechanism. MATERIALS AND METHODS: MicroRNA-448 expression was determined by microarray and the established SCI model in mice. The target gene of microRNA-448 was predicted using bioinformatics. The functional binding of the target gene to microRNA-448 was verified by Dual-Luciferase reporter gene assay. The regulatory effects of microRNA-448 and Bcl-2 on apoptosis, motor neuron number and grip strength were evaluated. After injection of microRNA-448 mimics, microRNA-448 inhibitor or Bcl-2 siRNA in mice, expression levels of PI3K/AKT and Caspase3 were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. RESULTS: Grip strength of SCI mice significantly decreased compared with mice in the sham group. The microRNA-448 expression gradually increased with the progression of SCI, whereas the Bcl-2 expression decreased. Dual-Luciferase reporter gene assay showed the binding condition between microRNA-448 and Bcl-2. Furthermore, the Bcl-2 expression was negatively regulated by microRNA-448 at both mRNA and protein levels. The injection of microRNA-448 inhibitor into the injured spinal cord of SCI mice significantly upregulated the expressions of p-PI3K, p-AKT and Caspase3, as well as motor neuron regeneration and grip strength. However, the promotive effects of microRNA-448 inhibitor were blocked by Bcl-2 siRNA transfection. CONCLUSIONS: MicroRNA-448 is upregulated after SCI, which may be involved in the regenerative process of spinal motor nerves by regulating PI3K/AKT/Bcl-2 axis.