RESUMEN
In this report, we propose a novel framework for toughening brittle oxide glass originated from enhanced ductility by implanting a secondary material comprising different mechanical properties. To do so, copper-metal nanoparticles are implanted into the subsurface layer of commercial soda-lime silica glass by using the electrofloat method. The crack initiation load of the implanted glass is found to be comparable to the glass chemically strengthened in ordinary tempering conditions. By observing crack propagation and stress distribution from cross-section, it is found that the crack propagation stops within the metal nanoparticle implanted layer, due to the stress dissipation or relaxation. The copper-implanted glass shows improved toughness with decreased hardness. The toughening mechanism of the composite glass is theoretically studied using molecular dynamics calculations on an amorphous silica model with copper nanoparticles embedded, and Peridynamics fracture simulations for indentation on a glass sheet model whose surface was implicitly modeled as the copper-implanted oxide glass. The experimentally observed phenomena of intrinsic toughening were well explained by the series of the conducted simulations.
RESUMEN
BACKGROUND: Hepatitis E virus (HEV) transmitted via the oral route through the consumption of contaminated water or uncooked or undercooked contaminated meat has been implicated in major outbreaks. Rats may play a critical role in HEV outbreaks, considering their negative effects on environmental hygiene and food sanitation. Although the serological evidence of HEV infection in wild rodents has been reported worldwide, the infectivity and propagation of HEV in wild rats remain unknown. To investigate if rats are a possible carrier of HEV, we studied wild Norway rats (Rattus norvegicus) that were caught near a pig farm, where HEV was prevalent among the pigs. METHODS: We examined 56 Norway rats for HEV. RNA from internal organs was examined for RT-PCR and positive samples were sequenced. Positive tissue samples were incubated with A549 cell line to isolate HEV. Anti-HEV antibodies were detected by ELISA. RESULTS: Sixteen rats were seropositive, and the HEV RNA was detected in 10 of the 56 rats. Sequencing of the partial ORF1 gene from 7 samples resulted in partially sequenced HEV, belonging to genotype 3, which was genetically identical to the HEV prevalent in the swine from the source farm. The infectious HEVs were isolated from the Norway rats by using the human A549 cell line. CONCLUSIONS: There was a relatively high prevalence (17.9%) of the HEV genome in wild Norway rats. The virus was mainly detected in the liver and spleen. The results indicate that these animals might be possible carrier of swine HEV in endemic regions. The HEV contamination risk due to rats needs to be examined in human habitats.
