Virulent Salmonella enterica infections can be exacerbated by concomitant infection of the host with a live attenuated S. enterica vaccine via Toll-like receptor 4-dependent interleukin-10 production with the involvement of both TRIF and MyD88.

During systemic disease in mice, Salmonella enterica grows intracellularly within discrete foci of infection in the spleen and liver. In concomitant infections, foci containing different S. enterica strains are spatially separated. We have investigated whether functional interactions between bacterial populations within the same host can occur despite the known spatial separation of the foci and independence of growth of salmonellae residing in different foci. In this study we have demonstrated that bacterial numbers of virulent S. enterica serovar Typhimurium C5 strain in mouse tissues can be increased by the presence of the attenuated aroA S. Typhimurium SL3261 vaccine strain in the same tissue. Disease exacerbation does not require simultaneous coinjection of the attenuated bacteria. SL3261 can be administered up to 48 hr after or 24 hr before the administration of C5 and still determine higher tissue numbers of the virulent bacteria. This indicates that intravenous administration of a S. enterica vaccine strain could potentially exacerbate an established infection with wild-type bacteria. These data also suggest that the severity of an infection with a virulent S. enterica strain can be increased by the prior administration of a live attenuated vaccine strain if infection occurs within 48 hr of vaccination. Exacerbation of the growth of C5 requires Toll-like receptor 4-dependent interleukin-10 production with the involvement of both Toll/interleukin-1 receptor-domain-containing adaptor inducing interferon-beta and myeloid differentiation factor 88.

Multi-field simulations and characterization of CMOS-MEMS high-temperature smart gas sensors based on SOI technology

This paper describes multiple field-coupled simulations and device characterization of fully CMOS-MEMS-compatible smart gas sensors. The sensor structure is designated for gas/vapour detection at high temperatures (>300 °C) with low power consumption, high sensitivity and competent mechanic robustness employing the silicon-on-insulator (SOI) wafer technology, CMOS process and micromachining techniques. The smart gas sensor features micro-heaters using p-type MOSFETs or polysilicon resistors and differentially transducing circuits for in situ temperature measurement. Physical models and 3D electro-thermo-mechanical simulations of the SOI micro-hotplate induced by Joule, self-heating, mechanic stress and piezoresistive effects are provided. The electro-thermal effect initiates and thus affects electronic and mechanical characteristics of the sensor devices at high temperatures. Experiments on variation and characterization of micro-heater resistance, power consumption, thermal imaging, deformation interferometry and dynamic thermal response of the SOI micro-hotplate have been presented and discussed. The full integration of the smart gas sensor with automatically temperature-reading ICs demonstrates the lowest power consumption of 57 mW at 300 °C and fast thermal response of 10 ms. © 2008 IOP Publishing Ltd.

First human hNT neurons patterned on parylene-C/silicon dioxide substrates: Combining an accessible cell line and robust patterning technology for the study of the pathological adult human brain

In this communication, we describe a new method which has enabled the first patterning of human neurons (derived from the human teratocarcinoma cell line (hNT)) on parylene-C/silicon dioxide substrates. We reveal the details of the nanofabrication processes, cell differentiation and culturing protocols necessary to successfully pattern hNT neurons which are each key aspects of this new method. The benefits in patterning human neurons on silicon chip using an accessible cell line and robust patterning technology are of widespread value. Thus, using a combined technology such as this will facilitate the detailed study of the pathological human brain at both the single cell and network level. © 2010 Elsevier B.V.