An indium nitride (InN) gas sensor of 10 nm in thickness has achieved detection limit of 0.4 ppm acetone. The sensor has a size of 1 mm by 2.5 mm, while its sensing area is 0.25 mm by 2 mm. Detection of such a low acetone concentration in exhaled breath could enable early diagnosis of diabetes for portable physiological applications. The ultrathin InN epilayer extensively enhances sensing sensitivity due to its strong electron accumulation on roughly 5–10 nm deep layers from the surface. Platinum as catalyst can increase output current signals by 2.5-fold (94 vs. 37.5 μA) as well as reduce response time by 8.4-fold (150 vs. 1,260 s) in comparison with bare InN. More, the effect of 3% oxygen consumption due to breath inhalation and exhalation on 2.4 ppm acetone gas detection was investigated, indicating that such an acetone concentration can be analyzed in air.
TNF-alpha induces CCL2 transcription in NPFs. B-Raf/MEK/ERK signaling cascade and to a less extent the p38 pathway are responsible for c-Fos activation and the subsequent AP-1/DNA interaction leading to CCL2 expression.
A 63-year-old man developed acute transverse myelitis (ATM) with a rapid progression of sensory and motor deficits and autonomic dysfunction 2 days after chest surgery. Thoracic epidural anesthesia/analgesia (TEA) had been administered in this case. Since the temporal and spatial relationships between TEA and ATM are so close, one may easily mistake the TEA as the cause. Therefore, we discuss here the differential diagnoses for cord damage after TEA and the characteristics of ATM, and suggest that it is unlikely that TEA is the cause of ATM in this case.
These data suggest that NPFs may contribute to NP development by synthesizing CCL2 to promote macrophage recruitment. Furthermore, COX-2 facilitates CCL2 transcription in NPFs via a c-Fos and AP-1 signaling pathway.
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