Stability, detonation properties and pyrolysis mechanisms of polynitrotriprismanes C6H6−n(NO2)n (n=1−6)

Abstract

To further test whether polynitriprismanes are capable of being potential high energy density materials (HEDMs), extensive theoretical calculations were carried out to investigate on a series of polynitrotriprismanes (PNNPs): C 6 H 6−n (NO 2 ) n (n=1−6). Heats of formation (HOFs), strain energies (SE), and disproportionation energy (DE) were obtained using B3LYP/6-311+G(2df, 2p)//B3LYP/6-31G* method by designing different isodesmic reactions, respectively. Detonation properties of PNNPs were obtained by the well-known KAMLET-JACOBS equations, using the predicted densities () obtained by Monte Carlo method and HOFs. It is found that they increase as the number of nitro groups n varies from 1 to 6, and PNNPs with n4 have excellent detonation properties. The relative stability and the pyrolysis mechanism of PNNPs were evaluated by the calculated bond dissociation energy (BDE). The comparison of BDE suggests that rupturing the C-C bond is the trigger for thermolysis of PNNPs. The computed BDE for cleavage of C-C bond (88.5 kJ/mol) further demonstrates that only the hexa-nitrotriprismane can be considered to be the target of HEDMs.

Cognitive Dysfunction and Postoperative Cognitive Dysfunction — A System Review

“…Inflammation: Central nervous system inflammation response is one of the recognized mechanisms of POCD occurrence. The mechanism by which central nervous system inflammation promotes the formation of POCD is that the pro-inflammatory factors (such as interleukin-6 and tumor necrosis factor-α) induced by invasive operations or drugs in the perioperative period, pass through the damaged blood-brain barrier into the central nervous system through direct or indirect pathways, activate neurons and microglia in the central nervous system, and produce a series of inflammatory mediators in the central nervous system (hippocampal brain region), mediating mitochondrial damage and decreased cell energy metabolism function, ultimately resulting in damage to the patient's memory and learning functions (Tang Y & Ouyang W, 2017).…”