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Additional file 1: Table S1. The component of different media used for basic medium screening. Table S2. List of levels and factors in the Plackett–Burman design experiments. Table S3. Strains and plasmids used in this study. Table S4. PCR primers used in this study.

Analyses of frequency domain characteristics of transformer noises are beneficial for the research of active noise control technology in substations. In this paper, all-phase FFT spectrum analysis is used to study the collected transformer noise signals. As shown in the frequency spectrograms, the fundamental frequency of the noise signals is 100Hz; the noise signals reach their peaks in 100Hz and 200Hz. A comparison of all-phase filtering and traditional segment filtering techniques is also conducted in this paper to extract the fundamental frequency components of the noise signals. It has shown that all-phase filtering can ensure phase linearity. Frequency leakages and latency can also be improved due to its continuous nature. Finally It is concluded that frequency domain characteristics can be better analyzed and extracted by applying all-phase FFT spectrum analysis and all-phase filtering techniques to the active noise control of transformers.

The molecular mechanisms underlying vascular inflammation and associated inflammatory vascular diseases are not well defined. Here we show that endothelial intracellular adenosine and its key regulator adenosine kinase (ADK) play important roles in vascular inflammation. Pro-inflammatory stimuli lead to endothelial inflammation by increasing endothelial ADK expression, reducing the level of intracellular adenosine in endothelial cells, and activating the transmethylation pathway through increasing the association of ADK with S-adenosylhomocysteine (SAH) hydrolase (SAHH). Increasing intracellular adenosine by genetic ADK knockdown or exogenous adenosine reduces activation of the transmethylation pathway and attenuates the endothelial inflammatory response. In addition, loss of endothelial ADK in mice leads to reduced atherosclerosis and affords protection against ischemia/reperfusion injury of the cerebral cortex. Taken together, these results demonstrate that intracellular adenosine, which is controlled by the key molecular regulator ADK, influences endothelial inflammation and vascular inflammatory diseases.The molecular mechanisms underlying vascular inflammation are unclear. Here the authors show that pro-inflammatory stimuli lead to endothelial inflammation by increasing adenosine kinase expression, and that its knockdown in endothelial cells inhibits atherosclerosis and cerebral ischemic injury in mice.