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Articles by Kai Cui
Total Records ( 3 ) for Kai Cui
  Pingyan Shi , Xiaofeng Tao , Jianchao Ji , Xiaohui Liu and Kai Cui
  Ultra Wideband (UWB) wireless communication has become the hot spot of the new generation ultra-high speed wireless communications in short-range. DS-UWB is one of the most important work patterns which can be applied to high speed wireless communications in dense indoor multipath environment. DS-UWB has various inherent advantages, one is that it can make full use of the radio frequency spectrum resources, but it also brings the problem of interference to existing radio systems. According to the particularity of confined spaces, it is needed a new analytical design method of UWB signal waveform which has the diffraction and penetration ability, so as to match the requirement. The UWB systems can coexist with other radio systems in confined spaces by using the specific waveform designed before. In this study, a waveform design method based on Soft Spectrum Adaptation (SSA) is proposed for UWB systems in confined spaces and it is evaluated through both theoretic analysis and computer simulation. In order to decrease or avoid the influence of spectrum aliasing on other narrowband radio systems, a design scheme for pulse waveform optimization based on Prolate Spheroidal Wave Functions (PSWF) has been investigated for producing the expected pulse waveform while matching with the required spectrum mask.
  Willis K. Samson , Jian V. Zhang , Orna Avsian-Kretchmer , Kai Cui , Gina L. C. Yosten , Cindy Klein , Rong-Ming Lyu , Yong Xiong Wang , Xiang Qun Chen , Jun Yang , Christopher J. Price , Ted D. Hoyda , Alastair V. Ferguson , Xiao-bin Yuan , Jaw Kang Chang and Aaron J. W. Hsueh
  Somatostatin is important in the regulation of diverse neuroendocrine functions. Based on bioinformatic analyses of evolutionarily conserved sequences, we predicted another peptide hormone in pro-somatostatin and named it neuronostatin. Immuno-affinity purification allowed the sequencing of an amidated neuronostatin peptide of 13 residues from porcine tissues. In vivo treatment with neuronostatin induced c-Fos expression in gastrointestinal tissues, anterior pituitary, cerebellum, and hippocampus. In vitro treatment with neuronostatin promoted the migration of cerebellar granule cells and elicited direct depolarizing actions on paraventricular neurons in hypothalamic slices. In a gastric tumor cell line, neuronostatin induced c-Fos expression, stimulated SRE reporter activity, and promoted cell proliferation. Furthermore, intracerebroventricular treatment with neuronostatin increased blood pressure but suppressed food intake and water drinking. Our findings demonstrate diverse neuronal, neuroendocrine, and cardiovascular actions of a somatostatin gene-encoded hormone and provide the basis to investigate the physiological roles of this endogenously produced brain/gut peptide.
  Yuxing Zhao , Jonathan L. Coloff , Emily C. Ferguson , Sarah R. Jacobs , Kai Cui and Jeffrey C. Rathmell
  Growth factor stimulation and oncogenic transformation lead to increased glucose metabolism that may provide resistance to cell death. We have previously demonstrated that elevated glucose metabolism characteristic of stimulated or cancerous cells can stabilize the anti-apoptotic Bcl-2 family protein Mcl-1 through inhibition of GSK-3. Here we show that the pro-apoptotic Bcl-2 family protein, Puma, is also metabolically regulated. Growth factor deprivation led to the loss of glucose uptake and induction of Puma. Maintenance of glucose uptake after growth factor withdrawal by expression of the glucose transporter, Glut1, however, suppressed Puma up-regulation and attenuated growth factor withdrawal-induced activation of Bax, DNA fragmentation, and cell death. Conversely, glucose deprivation led to Puma induction even in the presence of growth factor. This regulation of Puma expression was a central component in cell death as a consequence of growth factor or glucose deprivation because Puma deficiency suppressed both of these cell death pathways. Puma induction in growth factor or glucose withdrawal was dependent on p53 in cell lines and in activated primary T lymphocytes because p53 deficiency suppressed Puma induction and delayed Bax and caspase activation, DNA fragmentation, and loss of clonogenic survival. Importantly, although p53 levels did not change or were slightly reduced, p53 activity was suppressed by elevated glucose metabolism to inhibit Puma induction after growth factor withdrawal. These data show that p53 is metabolically regulated and that glucose metabolism initiates a signaling mechanism to inhibit p53 activation and suppress Puma induction, thus promoting an anti-apoptotic balance to Bcl-2 family protein expression that supports cell survival.
 
 
 
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