[en] The RBS technique and ¹⁹F(p, αγ)¹⁶O resonance nuclear reaction at 872.1 keV, with Γ=4.2 keV, were used to measure the depth profiles of implanted ⁷⁹Br, ¹³²Xe and ¹⁹F in silicon samples. A special convolution procedure was used to extract the depth profiles from the RBS spectra and the experimental excitation yield curves. The range parameters, R_p and ΔR_p obtained in this experiment were compared with theoretical calculations. (orig.)

[en] Electronic stopping cross sections for ¹⁹F⁺ in Pb_1-xSn_xTe and ¹⁹F⁺, ⁴⁰Ar⁺, ⁷⁵As⁺, ⁷⁹Br⁺ and ¹³²Xe⁺ in silicon were obtained by range measurements. Depth profiles of F in Pb_1-xSn_xTe and Si were measured by ¹⁹F(p,αγ)¹⁶O resonance nuclear reaction and those of Ar, As, Br and Xe were determined by RBS. In order to obtain the true range distribution from the measured NRA excitation curves or RBS spectra, a deconvolution program was developed using a reference function, the Edgeworth distribution function, and parameter optimization process. By forcing a fit between the experimentally determined projected range and that calculated with the range statistics program the total stopping power was obtained. After subtracting the nuclear stopping power the electronic stopping power was derived. The electronic stopping power can be described by a four-parameter formula. (author)

[en] Depth profiles of fluorine in ¹⁹F⁺ implanted LiNbO₃ have been accurately measured using the ¹⁹F(p, αγ)¹⁶O resonant nuclear reaction at E_R = 872.1 keV, with Γ = 4.2 keV. A proper convolution calculation method was used to extract the true distribution of fluorine from the experimental excitation yield curves. The experimental range distribution parameters, R_p and ΔR_p, were compared with those obtained by Monte Carlo simulation using a computer code developed recently in this group and with results obtained using the TRIM90 code. It shows that the experimental R_p values agree with the Monte Carlo simulation values very well, while the experimental ΔR_p values are larger than those obtained from the simulations. The simulation with our computer code improves the agreement between the experimental and calculated range straggling, ΔR_p. (orig.)

[en] LncRNA embryonic stem cells expressed 1 (Lncenc1), named after its high expression in naïve embryonic stem cells (nESCs), has been rarely studied in almost all pathological processes. Evidences suggest that Lncenc1 is likely to work in the form of RNA-protein complex. Here, we found that Lncenc1 in dorsal root ganglion (DRG) was significantly upregulated in response to mouse nerve injury caused by partial sciatic nerve ligation (pSNL). Overexpression of Lncenc1 mediated by adenoviral expression vector promoted the activation of microglia and the production of inflammatory cytokines including TNF-α, IL-1β and MCP-1. In contrast, knockdown of Lncenc1 suppressed activation of microglia and production of inflammatory cytokines. In the mechanism exploration, we found that Lncenc1 could bind with the RNA binding protein (RBP) enhancer of zeste homologue 2 (EZH2), an identified contributor in microglial activation and neuropathic pain. Lncenc1 interacted with EZH2 and downregulated the expression of brain-specific angiogenesis inhibitor 1 (BAI1). Either inhibition of EZH2 or overexpression of BAI1 could reverse the effects of Lncenc1 overexpression on microglial activation and neuroinflammation. Finally, the Lncenc1-siRNA was intrathecally injected into pSNL mice, and its effects on neuropathic pain were evaluated. Knockdown of Lncenc1 attenuated the development and maintenance of mechanical and thermal hyperalgesia of pSNL mice, accompanied by an increase in BAI1 expression and decrease in inflammatory cytokines. In conclusion, Lncenc1 contributes to neuropathic pain by interacting with EZH2 and downregulating the BAI1 gene in mouse microglia.