Reduction techniques of the back gate effect in the SOI Pixel Detector

We have fabricated monolithic pixel sensors in 0.2 μm Silicon-On-Insulator (SOI) CMOS technology, consisting of a thick sensor layer and a thin circuit layer with an insulating buried-oxide, which has many advantages. However, it has been found that the applied electric field in the sensor layer also affects the transistor operation in the adjacent circuit layer. This limits the applicable sensor bias well below the full depletion voltage. To overcome this, we performed a TCAD simulation and added an additional p-well (buried pwell) in the SOI process. Designs and preliminary results are presented

Periodontitis induced by bacterial infection exacerbates features of Alzheimer\u27s disease in transgenic mice.

Periodontitis is a localized infectious disease caused by periodontopathic bacteria,such as Porphyromonas gingivalis. Recently, it has been suggested that bacterial infections may contribute to the onset and the progression of Alzheimer’s disease (AD). However, we do not have any evidence about a causative relationship between periodontitis and AD. In this study, we investigated by using a transgenic mouse model of AD whether periodontitis evoked by P. gingivalis modulates the pathological features of AD. Cognitive function was significantly impaired in periodontitis-induced APP-Tg mice, compared to that in control APP-Tg mice. Levels of Amiloid β (Aβ) deposition, Aβ40, and Aβ42 in both the hippocampus and cortex were higher in inoculated APP-Tg mice than in control APP-Tg mice. Furthermore, levels of IL-1β and TNF-α in the brain were higher in inoculated mice than in control mice. The levels of LPS were increased in the serum and brain of P. gingivalis-inoculated mice. P. gingivalis LPS-induced production of Aβ40 and Aβ42 in neural cell cultures and strongly enhanced TNF-α and IL-1β production in a culture of microglial cells primed with Aβ. Periodontitis evoked by P. gingivalismay exacerbate brain Aβ deposition, leading to enhanced cognitive impairments, by a mechanism that involves triggering brain inflammation