Previous neuropathologic studies of Enterovirus 71 encephalomyelitis have not investigated the anatomic distribution of inflammation and viral localization in the central nervous system (CNS) in detail. We analyzed CNS and non-CNS tissues from 7 autopsy cases from Malaysia and found CNS inflammation patterns to be distinct and stereotyped. Inflammation was most marked in spinal cord gray matter, brainstem, hypothalamus, and subthalamic and dentate nuclei; it was focal in the cerebrum, mainly in the motor cortex, and was rare in dorsal root ganglia. Inflammation was absent in the cerebellar cortex, thalamus, basal ganglia, peripheral nerves, and autonomic ganglia. The parenchymal inflammatory response consisted of perivascular cuffs, variable edema, neuronophagia, and microglial nodules. Inflammatory cells were predominantly CD68-positive macrophage/microglia, but there were a few CD8-positive lymphocytes. There were no viral inclusions; viral antigens and RNA were localized only in the somata and processes of small numbers of neurons and in phagocytic cells. There was no evidence of virus in other CNS cells, peripheral nerves, dorsal root autonomic ganglia, or non-CNS organs. The results indicate that Enterovirus 71 is neuronotropic, and that, although hematogenous spread cannot be excluded, viral spread into the CNS could be via neural pathways, likely the motor but not peripheral sensory or autonomic pathways. Viral spread within the CNS seems to involve motor and possibly other pathways.
The case of acute Hendra virus infection demonstrated evidence of systemic infection and acute encephalitis. The case of relapsing Hendra virus encephalitis showed no signs of extraneural infection but in the brain, extensive inflammation and infected neurones were observed. Hendra virus can cause acute and relapsing encephalitis and the findings suggest that the pathology and pathogenesis are similar to Nipah virus infection.
Silver nanoparticles (AgNPs) were synthesized in aqueous solutions by reduction of silver nitrate (AgNO3) assisted by a helium dc microplasma jet at atmospheric pressure without additional chemical reducing agents. Surfactant-free AgNPs were obtained at low initial AgNO3 precursor concentrations ≤0.5 mM. A surface plasmon resonance peak at approximately 400 nm confirmed the presence of AgNPs. At higher concentrations, sucrose was used to prevent agglomeration and cap the growth of nanoparticles. The effects of the molar ratio of sucrose/AgNO3 on the size distribution and morphologies of AgNPs were investigated. The average sizes of AgNPs synthesized at molar ratios of 20, 50, and 60% were 11.2 ± 0.4, 10.0 ± 0.2, and 6.2 ± 0.1 nm, respectively.
The
potential of titanium dioxide (TiO2) nanofibers in antibacterial
applications has received wide attention. This interest is further
enhanced by the possible incorporation of silver (Ag) to form a double-antibacterial
composite agent. In this study, Ag-doped TiO2 (AgTiO2) nanofibers were synthesized with various Ag concentrations
using electrospinning and calcination. The obtained fibers were then
assessed for its antibacterial performance against a gamut of common
Gram-positive and Gram-negative bacteria cells. The results showed
a deterioration in the fiber surface area and pore volume at increasing
Ag concentration, which is attributed to pore blocking by the Ag nanoparticles.
The fiber diameter is also affected by the addition of Ag, with a
minimum fiber diameter of 88.9 ± 22.8 nm achieved at 1% Ag loading.
The change in the TiO2 fiber crystallinity is relatively
minor, with highly crystalline anatase observed for all samples with
small differences in the anatase crystallite sizes. In antibacterial
tests, AgTiO2 nanofibers are found to have a performance
superior to that of intrinsic TiO2 nanofibers because of
the synergistic combination of Ag and photocatalytic TiO2. Maximum log reductions of 5.92 ± 0 and 1.38 ± 0.07 colony-forming
units for Salmonella Albany and Staphylococcus
aureus bacteria samples, respectively, are reported for AgTiO2 nanofibers with 2% Ag loading.
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