Relationship Diagnosis between Sciences and Arts - STEAM Power of 19th Century and STEAM education in 21st Century -

David Worley,조청원 한국전시산업융합연구원 2015 한국과학예술융합학회 Vol.19 No.-

The Keyword of human development in the 19thcentury was industrial revolution and its originstems from steam power. The stem power engineinvented in England using steam brought bigchange of social development New type of ships,trains equipped with steam power engine wereintroduced. These new transportation tool wakedinnovation of speed and communication methods inhuman life. In the 20th century, the keyword ofhuman development was information revolution, ofwhich the source of revolution was the connectionthrough internet. Enormous flow of informationaround the globe broke the walls of geologicalbarrier, then the global community has appeared inhuman society. This new Informationcommunication Tool completely changed the scopeand speed of human thinking. Then, the keyword of21st century is the convergence revolution. Its majorlocomotive is the fusion of science and art. TheSTEAM(Science, Technology, Engineering, Art andMathematics) education based upon coowork inbetween science and art at schools will make theflexibility in creative mind and fluentcommunication. It surely bring forth new vision ofhuman life. This article discussed the steam powerin the case of 19th century case study of England. The future study will be the bonding analysis ofscience and art in various cases alonf with theirrelationship explorations.

KNOWLEDGE DISCOVERY FROM DYNAMIC, DISPARATE DATA

Brian A. Worley 한국산업응용수학회 2012 한국산업응용수학회 학술대회 논문집 Vol.7 No.1

Data has now become the fourth pillar of the discovery process, joining experimentation, theory, and simulations. Examples can be found in many fields of application such as healthcare, medicine, economics, science, disaster recovery, national security, and others. Today the data landscape is very rich. Data can be generated from experiments (e.g. science facilities), output from simulations (e.g. high performance computers), provided by humans (e.g. social media), or collected from sensors (e.g. satellite data). Bringing all types of disparate data to bear on a particular discovery process or mission outcome is one of the new frontiers of science and technology. In this paper, we provide an overview of our approach to putting together a knowledge discovery portfolio and provide a few recent and current examples across applications of national interest.

Native Store-operated Ca2+ Influx Requires the Channel Function of Orai1 and TRPC1.

Kim, Min Seuk,Zeng, Weizhong,Yuan, Joseph P,Shin, Dong Min,Worley, Paul F,Muallem, Shmuel American Society for Biochemistry and Molecular Bi 2009 The Journal of biological chemistry Vol.284 No.15

<P>With the discovery of STIM1 and Orai1 and gating of both TRPC and Orai1 channels by STIM1, a central question is the role of each of the channels in the native store-operated Ca(2+) influx (SOCs). Here, we used a strategy of knockdown of Orai1 and of TRPC1 alone and in combination and rescue by small interfering RNA-protected mutants (sm) of smOrai1 and smTRPC1 to demonstrate that in human embryonic kidney (HEK) cells, rescue of SOCs required co-transfection of low levels of both smOrai1 and smTRPC1. The pore mutant Orai1(E106Q) failed to rescue the SOCs in the presence or absence of TRPC1 and, surprisingly, the pore mutant TRPC1(F562A) failed to rescue the SOCs in the presence or absence of Orai1. TRPC1 is gated by electrostatic interaction between TRPC1(D639D,D640D) with STIM1(K684K, K685K). Strikingly, the channel-dead TRPC1(D639K,D640K) that can be rescued only by the STIM1(K684E,K685E) mutant could restore SOCs only when expressed with Orai1 and STIM1(K684E,K685E). Accordingly, we found a mutual requirement of Orai1 and TRPC1 for their interaction with the native STIM1 in HEK cells. By contrast, SOC and the CRAC current in Jurkat cells were inhibited by knockdown of Orai1 but were not influenced by knockdown on TRPC1 or TRPC3. These findings define the molecular makeup of the native SOCs in HEK cells and the role of a STIM1-Orai1-TRPC1 complex in SOC activity.</P>

Molecular determinants of fast Ca2+-dependent inactivation and gating of the Orai channels.

Lee, Kyu Pil,Yuan, Joseph P,Zeng, Weizhong,So, Insuk,Worley, Paul F,Muallem, Shmuel National Academy of Sciences 2009 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.106 No.34

<P>Ca(2+) influx by store-operated Ca(2+) influx channels (SOCs) mediates many cellular functions regulated by Ca(2+), and excessive SOC-mediated Ca(2+) influx is cytotoxic and associated with disease. One form of SOC is the CRAC current that is mediated by Orai channels activated by STIM1. A fundamental property of the native CRAC and of the Orais is fast Ca(2+)-dependent inactivation, which limits Ca(2+) influx to guard against cellular damage. The molecular mechanism of this essential regulatory mechanism is unknown. We report here the fast Ca(2+)-dependent inactivation is mediated by three conserved glutamates in the C termini (CT) of Orai2 and Orai3, which show prominent fast Ca(2+)-dependent inactivation compared with Orai1. Transfer of the CT between the Orais transfers both the extent of channel opening and the mode of fast Ca(2+)-dependent inactivation. Fast Ca(2+)-dependent inactivation of the Orais also requires a domain of STIM1; fragments of STIM1 that efficiently open Orai channels do not evoke fast inactivation unless they include an anionic sequence that is C-terminal to the STIM1-Orai activating region (SOAR). Our studies suggest that Orai CT are necessary and sufficient to control pore opening and uncover the molecular mechanism of fast Ca(2+)-dependent inactivation that has implications for Ca(2+) influx by SOC in physiological and pathological states.</P>

Electro-spun Antimicrobial Acrylic Fiber

Jaewoong Lee,Xuehong Ren,R. M. Broughton,Jie Liang,S. D. Worley,T. S. Huang 한국염색가공학회 2007 韓國染色加工學會誌 Vol.19 No.2

Preparation and Application of an s-Triazine-Based Novel N-Halamine Biocide for Antimicrobial Fibers

Lee, Jae-Woong,Broughton, Royall M.,Akdag, Akin,Worley, S.D.,Huang, Tung S. The Korean Fiber Society 2007 Fibers and polymers Vol.8 No.2

N-halamines serve as important antimicrobial agents. Development of this class of compounds has been shown to provide benefits especially from a biocidal point of view. A novel s-triazine-based N-heterocycle, dichloro-m-aminophenylhydantoinyl-s-triazine (DAPHT), which could be rendered antimicrobial through exposure to diluted chlorine bleach; was synthesized and characterized by $^1H\;NMR$, $^{13}C$ NMR, and FT-IR. A finishing method was used to apply the N-halamine precursor onto cotton fabric, and the optimum conditions for finishing were investigated. The DAPHT-treated cotton fabric had durable antimicrobial properties up to 50 standard washing cycles and was rechargeable under normal laundry/bleaching conditions. The antimicrobial efficacy against Gram-positive and Gram-negative bacteria was demonstrated.

Transient upregulation of postsynaptic IP3-gated Ca release underlies short-term potentiation of metabotropic glutamate receptor 1 signaling in cerebellar Purkinje cells.

Kim, Sang Jeong,Jin, Yunju,Kim, Jun,Shin, Jung Hoon,Worley, Paul F,Linden, David J The Society 2008 The Journal of neuroscience Vol.28 No.17

<P>Synaptic plasticity lasting approximately 100 s has been suggested to function as a temporary buffer for neural information. One example of this was reported by Batchelor and Garthwaite (1997), who found that a slow metabotropic glutamate receptor 1 (mGluR1)-evoked EPSP produced by burst stimulation of cerebellar parallel fiber-Purkinje cell synapses could be potentiated by a conditioning stimulus consisting of prior activation of climbing fiber synapses (or injection of depolarizing current) with a delay of up to 90 s. What is the molecular basis of the signal that spans this temporal gap? Here, we show that mGluR1-evoked slow EPSCs evoked by parallel fiber burst test stimuli show a similar form of short-term potentiation (mGluR1-STP) and that this phenomenon is also observed when parallel fiber bursts are replaced by pressure pulses of an exogenous mGluR1 agonist. Ca imaging experiments revealed that cytosolic Ca levels returned to baseline within several seconds after conditioning depolarization, indicating that this cannot underlie mGluR1-STP. To test the hypothesis that transient upregulation of inositol-1,4,5-trisphosphate (IP(3))-gated Ca release underlies this phenomenon, we used local photolytic uncaging of IP(3) to deplete IP(3)-gated Ca stores. IP(3) uncaging in the interval between conditioning depolarization and the test pulse produced a complete blockade of mGluR1-STP, as did blockade of IP(3) receptors with heparin. When Ca transients evoked by IP(3) uncaging were used as a test stimulus, conditioning depolarization produced a large STP of Ca response amplitudes. These data suggest that transient upregulation of postsynaptic IP(3)-gated Ca signaling constitutes a novel form of short-term synaptic plasticity.</P>

Real-Time Imaging Reveals Properties of Glutamate-Induced Arc/Arg 3.1 Translation in Neuronal Dendrites

Na, Y.,Park, S.,Lee, C.,Kim, D.K.,Park, J.M.,Sockanathan, S.,Huganir, R.L.,Worley, P.F. Cell Press 2016 Neuron Vol.91 No.3

<P>The immediate early gene Arc (also Arg3.1) produces rapid changes in synaptic properties that are linked to de novo translation. Here we develop a novel translation reporter that exploits the rapid maturation and 'flash' kinetics of Gaussia luciferase (Gluc) to visualize Arc translation. Following glutamate stimulation, discrete Arc-Gluc bioluminescent flashes representing sites of de novo translation are detected within 15 s at distributed sites in dendrites, but not spines. Flashes are episodic, lasting similar to 20 s, and may be unitary or repeated at similar to minute intervals at the same sites. Analysis of flash amplitudes suggests they represent the quantal product of one or more polyribosomes, while inter-flash intervals appear random, suggesting they arise from a stochastic process. Surprisingly, glutamate-induced translation is dependent on Arc open reading frame. Combined observations support a model in which stalled ribosomes are reactivated to rapidly generate Arc protein.</P>

TRPC channels as STIM1-regulated SOCs.

Yuan, Joseph P,Kim, Min Seuk,Zeng, Weizhong,Shin, Dong Min,Huang, Guo,Worley, Paul F,Muallem, Shmuel Landes Bioscience 2009 Channels Vol.3 No.4

<P>Store-operated Ca(2+) channels (SOCs) are Ca(2+) influx channels at the plasma membrane whose opening is determined by the level of Ca(2+) stored in the endoplasmic reticulum lumen. SOCs are activated in response to receptor-mediated or passive depletion of ER Ca(2+) to regulate many Ca(2+)-dependent cellular functions. Early work implicated the TRPC channels as SOCs. More recently, it was found that the Orai channels mediate the CRAC current and that the Ca(2+) binding protein STIM1 functions as the ER Ca(2+) sensor that mediates activation of the SOCs in response to depletion of ER Ca(2+). Key questions are whether both TRPC and Orai channels are opened by STIM1 and the molecular mechanism by which STIM1 opens the SOCs. Ample biochemical and functional evidence indicate interaction of the TRPC channels with STIM1. Furthermore, it was found that STIM1 gates TRPC channels by electrostatic interaction of STIM1(K684,K685) in the polybasic domain of STIM1 with two negative charges (aspartates or glutamates) that are conserved in all TRPC channels. Charge mutants of STIM1(K684,K685) and TRPC1(D639,D640) and TRPC3(D697,D698) were used to develop further direct evidence for the function of TRPC channels as SOCs. The evidence in favor of TRPC channels as SOCs are discussed.</P>

STIM1 Regulates Somatic Ca²⁺ Signals and Intrinsic Firing Properties of Cerebellar Purkinje Neurons

Ryu, Changhyeon,Jang, Dong Cheol,Jung, Dayoon,Kim, Yong Gyu,Shim, Hyun Geun,Ryu, Hyun-Hee,Lee, Yong-Seok,Linden, David J.,Worley, Paul F.,Kim, Sang Jeong Society for Neuroscience 2017 The Journal of neuroscience Vol.37 No.37

<P>Control of Ca2+ flux between the cytosol and intracellular Ca2+ stores is essential for maintaining normal cellular function. It has been well established in both neuronal and non-neuronal cells that stromal interaction molecule 1 (STIM1) initiates and regulates refilling Ca2+ into the ER. Here, we describe a novel, additional role for STIM1, the regulation of free cytosolic Ca2+, and the consequent control of spike firing in neurons. Among central neurons, cerebellar Purkinje neurons express the highest level of STIM1, and they fire continuously in the absence of stimulation, making somatic Ca2+ homeostasis of particular importance. By using Purkinje neuron-specific STIM1 knock-out (STIM1(PKO)) male mice, we found that the deletion of STIM1 delayed clearance of cytosolic Ca2+ in the soma during ongoing neuronal firing. Deletion of STIM1 also reduced the Purkinje neuronal excitability and impaired intrinsic plasticity without affecting long-term synaptic plasticity. In vestibulo-ocular reflex learning, STIM1(PKO) male mice showed severe deficits in memory consolidation, whereas they were normal in memory acquisition. Our results suggest that STIM1 is critically involved in the regulation of the neuronal excitability and the intrinsic plasticity of the Purkinje neurons as well as cerebellar memory consolidation.</P>