ABSTRACT
Controlling the selectivity of detonation initiation reaction to reduce the explosive sensitivity has been a Holy Grail in the field of energetic materials. The effects of the external electric fields on the homolysis of the N-NO2 bond and initiation reaction dynamics of NH2NO2âââH2O (i.e., intermolecular and 1,3-intramolecular hydrogen transfers) were investigated at the MP2/6-311++G(2d,p) and CCSD/6-311++G(2d,p)//MP2/6-311++G(2d,p) levels. The results show that the N-NO2 bond is not the "trigger linkage." The notable transiliences of the activation energy of the intermolecular hydrogen transfer are found with the field strength of - 0.012 a.u. along the -x-direction, leading to the conversion of the main reaction between the intermolecular and 1,3-intramolecular hydrogen transference. The activation energies of two kinds of the hydrogen transferences are increased under the external electric fields along the -y-direction. In particular, due to the conversion of the main reaction, the activation energies of the overall reaction are increased significantly along the -x-direction, leading to the significant reduced explosive sensitivities. Therefore, by controlling the field strengths and orientations between the "reaction axis" and external electric field along the y- and x-directions, the selectivity of the initiation reaction could be controlled and the explosive sensitivity could be reduced. Employing AIM (atoms in molecules) and surface electrostatic potentials, the origin of the control of reaction selectivity and the reduction of sensitivity is revealed. This work is of great significance to the improvement of the technology that the external electric fields are added safely into the energetic material system to enhance the explosive performance. Graphical abstract.
ABSTRACT
BACKGROUND AND AIMS: The pathogenesis of inflammatory bowel disease (IBD) has not been fully understood yet. Eosinophils (Eo) are one type of the major proinflammatory cells of the chronic inflammation in the intestine. CD98 is involved in the pathogenesis of a number of inflammations. This study aims to elucidate the role of CD98(+) Eos in the initiation of intestinal inflammation. METHODS: The colon biopsies were collected from 60 patients with IBD. The expression of CD98 in the biopsies was examined by immunohistochemistry. The serum levels of the flagellin (FGN) antibody and Eo-derived mediators in the culture supernatants were assessed by enzyme-linked immunosorbent assay. The role of FGN on Eo activation was examined in a cell culture model. The role of FGN in the induction of colitis was observed in a mouse model. RESULTS: Compared to normal controls, the frequency of CD98(+) Eos was markedly increased in the IBD colon mucosa. FGN were detected in the colon biopsies and in the sera of IBD patients. Exposure to FGN induced the expression of galectin 3 (the ligand of CD98) in dendritic cells. The exposure to galectin 3 activated the CD98(+) Eos. After treatment with FGN intrarectally, mice with eosinophilia showed severe inflammation in the colon. CONCLUSIONS: The interaction of galectin 3 and CD98 can induce Eos to release chemical mediators that contributes to the initiation of the intestinal inflammation.
