ZigBee(2.4G) Wireless Sensor Network Application on Indoor Intrusion Detection

[[sponsorship]]IEEE[[conferencetype]]國際[[conferencedate]]20150606~20150608[[booktype]]電子版[[iscallforpapers]]Y[[conferencelocation]]台灣/台北 國立臺灣科技大

Eliminating Motion Artifacts in PPG

[[conferencetype]]國際[[conferencedate]]20150606~20150608[[booktype]]電子版[[iscallforpapers]]Y[[conferencelocation]]台灣/台北 國立臺灣科技大

Analysis of Noncontact Heartbeat Detection

[[sponsorship]]IEEE[[conferencetype]]國際[[conferencedate]]20150606~20150608[[booktype]]電子版[[iscallforpapers]]Y[[conferencelocation]]台灣/台北 國立臺灣科技大

System Performance Analysis for 4G Mobile Wireless Communication System

[[sponsorship]]IEEE[[conferencetype]]國際[[conferencedate]]20150606~20150608[[booktype]]電子版[[iscallforpapers]]Y[[conferencelocation]]台灣/台北 國立臺灣科技大

Detection and Analysis of the D esigned Circuit for Ambulatory ECG Electrical Characteristic Points

[[sponsorship]]IEEE[[conferencetype]]國際[[conferencedate]]20150606~20150608[[booktype]]電子版[[iscallforpapers]]Y[[conferencelocation]]台灣/台北 國立臺灣科技大

Episodic and electrical nervous system disorders caused by nonchannel genes.

As noted in the separate introduction to this special topic section, episodic and electrical disorders can appear quite different clinically and yet share many overlapping features, including attack precipitants, therapeutic responses, natural history, and the types of genes that cause many of the genetic forms (i.e., ion channel genes). Thus, as we mapped and attempted to clone genes causing other episodic disorders, ion channels were always outstanding candidates when they mapped to the critical region of linkage in such a family. However, some of these disorders do not result from mutations in channels. This realization has opened up large and exciting new areas for the pathogenesis of these disorders. In some cases, the mutations occur in genes of unknown function or without understanding of molecular pathogenesis. Recently, emerging insights into a fascinating group of episodic movement disorders, the paroxysmal dyskinesias, and study of the causative genes and proteins are leading to the emerging concept of episodic electric disorders resulting from synaptic dysfunction. Much work remains to be done, but the field is evolving rapidly. As it does, we have come to realize that the molecular pathogenesis of electrical and episodic disorders is more complex than a scenario in which such disorders are simply due to mutations in the primary determinants of membrane excitability (channels)

Applying Genetic Algorithms to the Data Traffic Scheduling and Performance Analysis of a Long-Term Evolution System

[[abstract]]In this study it develops a superior transmission resource allocation method by using genetic algorithm. The convergence properties of genetic algorithm are employed to increase the transmission resource use efficiency of a base (station) to allow users to access wider bandwidth and to improve the system throughput and packet service rate. In this paper, it also studies the genetic algorithm convergent phenomena. The calculated system convergent time is significantly less than that of a long term evolution (LTE) frame duration. Finally, the system performances with and without implementing the genetic algorithm in resource allocations are simulated; their performances are compared to study the effectiveness of using the genetic algorithm in resource allocation.[[notice]]補正完畢[[booktype]]電子

The measurement and analysis of WiMAX base station signal coverage

[[abstract]]This paper presents the field trial measurement data of WiMAX base station; it includes the system coverage, signal strength and available transmission rate. Data consisting of real time images, VoIP internet telephone are transmitted through Skype software by using WiMAX, HSDPA (3.5G) and EDGE (2G) transmission techniques, and these data are connected to centrally equipped wireless monitoring servers to perform data monitoring and analysis. Finally, we make comparisons, analysis and discussions of these three transmission techniques from the measured and characterized data.[[incitationindex]]EI[[booktype]]線上

Deposition of F-doped ZnO transparent thin films using ZnF2-doped ZnO target under different sputtering substrate temperatures

Highly transparent and conducting fluorine-doped ZnO (FZO) thin films were deposited onto glass substrates by radio-frequency (RF) magnetron sputtering, using 1.5 wt% zinc fluoride (ZnF2)-doped ZnO as sputtering target. Structural, electrical, and optical properties of the FZO thin films were investigated as a function of substrate temperature ranging from room temperature (RT) to 300°C. The cross-sectional scanning electron microscopy (SEM) observation and X-ray diffraction analyses showed that the FZO thin films were of polycrystalline nature with a preferential growth along (002) plane perpendicular to the surface of the glass substrate. Secondary ion mass spectrometry (SIMS) analyses of the FZO thin films showed that there was incorporation of F atoms in the FZO thin films, even if the substrate temperature was 300°C. Finally, the effect of substrate temperature on the transmittance ratio, optical energy gap, Hall mobility, carrier concentration, and resistivity of the FZO thin films was also investigated

Mutations in PNKD causing paroxysmal dyskinesia alters protein cleavage and stability.

Paroxysmal non-kinesigenic dyskinesia (PNKD) is a rare autosomal dominant movement disorder triggered by stress, fatigue or consumption of either alcohol or caffeine. Attacks last 1-4 h and consist of dramatic dystonia and choreoathetosis in the limbs, trunk and face. The disease is associated with single amino acid changes (A7V or A9V) in PNKD, a protein of unknown function. Here we studied the stability, cellular localization and enzymatic activity of the PNKD protein in cultured cells and transgenic animals. The N-terminus of the wild-type (WT) long PNKD isoform (PNKD-L) undergoes a cleavage event in vitro, resistance to which is conferred by disease-associated mutations. Mutant PNKD-L protein is degraded faster than the WT protein. These results suggest that the disease mutations underlying PNKD may disrupt protein processing in vivo, a hypothesis supported by our observation of decreased cortical Pnkd-L levels in mutant transgenic mice. Pnkd is homologous to a superfamily of enzymes with conserved β-lactamase domains. It shares highest homology with glyoxalase II but does not catalyze the same reaction. Lower glutathione levels were found in cortex lysates from Pnkd knockout mice versus WT littermates. Taken together, our results suggest an important role for the Pnkd protein in maintaining cellular redox status