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Monoidal categories associated with strata of flag manifolds
Kashiwara, Masaki,Kim, Myungho,Oh, Se-jin,Park, Euiyong Elsevier 2018 Advances in mathematics Vol.328 No.-
<P><B>Abstract</B></P> <P>We construct a monoidal category <SUB> C w , v </SUB> which categorifies the doubly-invariant algebra C <SUP> N ′ </SUP> ( w ) <SUP> [ N ] N ( v ) </SUP> associated with Weyl group elements <I>w</I> and <I>v</I>. It gives, after a localization, the coordinate algebra C [ <SUB> R w , v </SUB> ] of the open Richardson variety associated with <I>w</I> and <I>v</I>. The category <SUB> C w , v </SUB> is realized as a subcategory of the graded module category of a quiver Hecke algebra <I>R</I>. When v = id , <SUB> C w , v </SUB> is the same as the monoidal category which provides a monoidal categorification of the quantum unipotent coordinate algebra <SUB> A q </SUB> <SUB> ( n ( w ) ) Z [ q , <SUP> q − 1 </SUP> ] </SUB> given by Kang–Kashiwara–Kim–Oh. We show that the category <SUB> C w , v </SUB> contains special determinantial modules M ( <SUB> w ≤ k </SUB> Λ , <SUB> v ≤ k </SUB> Λ ) for k = 1 , … , ℓ ( w ) , which commute with each other. When the quiver Hecke algebra <I>R</I> is symmetric, we find a formula of the degree of <I>R</I>-matrices between the determinantial modules M ( <SUB> w ≤ k </SUB> Λ , <SUB> v ≤ k </SUB> Λ ) . When it is of finite <I>ADE</I> type, we further prove that there is an equivalence of categories between <SUB> C w , v </SUB> and <SUB> C u </SUB> for w , u , v ∈ W with w = v u and ℓ ( w ) = ℓ ( v ) + ℓ ( u ) .</P>
Nari Kim,Jin Han,Euiyong Kim,Yun-Hee Kim,Jae-Hong Sim,Soo-Cheon Kim 대한생리학회-대한약리학회 1999 The Korean Journal of Physiology & Pharmacology Vol.3 No.6
<P> The aim of the present study is to investigate the contribution of Ca<SUP>2</SUP>-activated K<SUP></SUP> (K<SUB>Ca</SUB>) channels and delayed rectifier K<SUP></SUP> (K<SUB>V</SUB>) channels to the resting membrane potential (RMP) in rabbit middle cerebral arterial smooth muscle cells. The RMP and membrane currents were recorded using the whole-cell patch configuration and single K<SUB>Ca</SUB> channel was recorded using the outside-out patch configuration. Using the pipette solution containing 0.05 mM EGTA, the RMP was 25.76⁑5.08 mV (n=12) and showed spontaneous transient hyperpolarizations (STHPs). The membrane currents showed time- and voltage-dependent outward currents with spontaneous transient outward currents (STOCs). When we recorded the membrane potential using the pipette solution containing 10 mM EGTA, the RMP was depolarized and did not show STHPs. The membrane currents showed no STOCs but only showed slowly inactivating outward currents. External TEA (1 mM) reversibly inhibited the STHPs, depolarized the RMP, reduced the membrane currents, abolished STOCs, and decreased the open probability of single K<SUB>Ca</SUB> channel. When K<SUB>V</SUB> currents were isolated, the application of 4-AP (5 mM) depolarized the RMP. The important aspect of our results is that K<SUB>Ca</SUB> channel is responsible for the generation of the STHPs in the membrane potential and plays an important role in the regulation of the RMP and K<SUB>V</SUB> channel is also responsible for the regulation of the RMP in rabbit middle cerebral arterial smooth muscle cells.
Modulation by Melatonin of the Cardiotoxic and Antitumor Activities of Adriamycin
Kim, Chunghui,Kim, Nari,Joo, Hyun,Youm, Jae Boum,Park, Won Sun,Cuong, Dang Van,Park, Young Shik,Kim, Euiyong,Min, Churl-Ki,Han, Jin Lippincott Williams Wilkins, Inc. 2005 Journal of cardiovascular pharmacology Vol.46 No.2
In this study, we investigated the effects of melatonin on adriamycin-induced cardiotoxicity both in vivo in rats and in vitro, and on the antitumor activities of adriamycin on MDA-231 and NCI breast cancer cells. Rats that received a single intraperitoneal injection of 25 mg/kg adriamycin showed a mortality rate of 86%, which was reduced to 20% by melatonin treatment (10 mg/kg, SC for 6 days). Melatonin attenuated adriamycin-induced body-weight loss, hemodynamic dysfunction, and the morphologic and biochemical alterations caused by adriamycin. Melatonin also reduced adriamycin-induced nuclear DNA fragmentation, as assessed by the comet assay. In addition, the antitumor activity of adriamycin could be maintained using lower doses of this drug in combination with melatonin. Melatonin treatment in the concentration range of 0.1-2.5 mM inhibited the growth of human breast cancer cells. In terms of oncolytic activity, the combination of adriamycin and melatonin improved the antitumor activity of adriamycin, as indicated by an increase in the number of long-term survivors as well as decreases in body-weight losses resulting from adriamycin treatment. These results indicate that melatonin not only protects against adriamycin-induced cardiotoxicity but also enhances its antitumor activity. This combination of melatonin and adriamycin represents a potentially useful regimen for the treatment of human neoplasms because it allows the use of lower doses of adriamycin, thereby avoiding the toxic side effects associated with this drug.
Effects of Histamine on Cultured Interstitial Cells of Cajal in Murine Small Intestine
Kim, Byung Joo,Kwon, Young Kyu,Kim, Euiyong,So, Insuk The Korean Society of Pharmacology 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.2
Interstitial cells of Cajal (ICCs) are the pacemaker cells in the gastrointestinal tract, and histamine is known to regulate neuronal activity, control vascular tone, alter endothelial permeability, and modulate gastric acid secretion. However, the action mechanisms of histamine in mouse small intestinal ICCs have not been previously investigated, and thus, in the present study, we investigated the effects of histamine on mouse small intestinal ICCs, and sought to identify the receptors involved. Enzymatic digestions were used to dissociate ICCs from small intestines, and the whole-cell patch-clamp configuration was used to record potentials (in current clamp mode) from cultured ICCs. Histamine was found to depolarize resting membrane potentials concentration dependently, and whereas 2-PEA (a selective H1 receptor agonist) induced membrane depolarizations, Dimaprit (a selective H2-agonist), R-alpha-methylhistamine (R-alpha-MeHa; a selective H3-agonist), and 4-methylhistamine (4-MH; a selective H4-agonist) did not. Pretreatment with $Ca^{2+}$-free solution or thapsigargin (a $Ca^{2+}$-ATPase inhibitor in endoplasmic reticulum) abolished the generation of pacemaker potentials and suppressed histamine-induced membrane depolarization. Furthermore, treatments with U-73122 (a phospholipase C inhibitor) or 5-fluoro-2-indolyl des-chlorohalopemide (FIPI; a phospholipase D inhibitor) blocked histamine-induced membrane depolarizations in ICCs. On the other hand, KT5720 (a protein kinase A inhibitor) did not block histamine-induced membrane depolarization. These results suggest that histamine modulates pacemaker potentials through H1 receptor-mediated pathways via external $Ca^{2+}$ influx and $Ca^{2+}$ release from internal stores in a PLC and PLD dependent manner.
Nari Kim,Jin Han,Euiyong Kim 대한생리학회-대한약리학회 2001 The Korean Journal of Physiology & Pharmacology Vol.14 No.5
<P> An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of K<SUP></SUP> channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured Ca<SUP>2</SUP>-activated K (K<SUB>Ca</SUB>) currents and delayed rectifier K (K<SUB>dr</SUB>) currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of K<SUB>Ca</SUB> channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of K<SUB>Ca</SUB> channel to Ca<SUP>2</SUP> is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of K<SUB>Ca</SUB> channel by TEA were more sensitive in hypertrophy. K<SUB>dr</SUB> current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of K<SUB>dr</SUB> current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of K<SUB>Ca</SUB> channels and K<SUB>dr</SUB> channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.
Protein Kinase C Activates ATP-sensitive Potassium Channels in Rabbit Ventricular Myocytes
Nari Kim,Jae Boum Youm,Hyun Joo,Hyungkyu Kim,Euiyong Kim,Jin Han 대한생리학회-대한약리학회 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.4
Several signal transduction pathways have been implicated in ischemic preconditioning induced by the activation of ATP-sensitive K<SUP></SUP> (K<SUB>ATP</SUB>) channels. We examined whether protein kinase C (PKC) modulated the activity of K<SUB>ATP</SUB> channels by recording K<SUB>ATP</SUB> channel currents in rabbit ventricular myocytes using patch-clamp technique and found that phorbol 12,13-didecanoate (PDD) enhanced pinacidil-induced K<SUB>ATP</SUB> channel activity in the cell-attached configuration; and this effect was prevented by bisindolylmaleimide (BIM). K<SUB>ATP</SUB> channel activity was not increased by 4α-PDD. In excised inside- out patches, PKC stimulated K<SUB>ATP</SUB> channels in the presence of 1 mM ATP, and this effect was abolished in the presence of BIM. Heat-inactivated PKC had no effect on channel activity. PKC-induced activation of K<SUB>ATP</SUB> channels was reversed by PP2A, and this effect was not detected in the presence of okadaic acid. These results suggest that PKC activates K<SUB>ATP</SUB> channels in rabbit ventricular myocytes.
Nari Kim,Jin Han,Euiyong Kim 대한생리학회-대한약리학회 2001 The Korean Journal of Physiology & Pharmacology Vol.5 No.1
<P> The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier K<SUP></SUP> (K<SUB>DR</SUB>) channel function in isoproterenol-induced hypertrophy. It has been proposed that K<SUB>DR</SUB> channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary K<SUB>DR</SUB> channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present study was carried out to compare the properties of coronary K<SUB>DR</SUB> channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the study are as follows: (1) the K<SUB>DR</SUB> current density was decreased without changes of the channel kinetics in isoproterenol-induced hypertrophy; (2) the sensitivity of coronary K<SUB>DR</SUB> channels to 4-AP was increased in isoproterenol-induced hypertrophy. From the above results, we suggest for the first time that the alteration of K<SUB>DR</SUB> channels may limit vasodilating responses to several stimuli and may be involved in impaired coronary reserve in isoproterenol-induced hypertrophy.
Nari Kim,Jin Han,Won Gue Kim,Euiyong Kim 대한생리학회-대한약리학회 2000 The Korean Journal of Physiology & Pharmacology Vol.4 No.4
<P> The purpose of our investigation was to examine the effects of prostaglandin F<SUB>2</SUB><SUB>α</SUB> (PGF<SUB>2</SUB><SUB>α</SUB>) on membrane potentials, Ca<SUP>2</SUP>-activated K<SUP></SUP> (K<SUB>Ca</SUB>) channels, and delayed rectifier K<SUP></SUP> (K<SUB>V</SUB>) channels using the patch-clamp technique in single rabbit middle cerebral arterial smooth muscle cells. PGF<SUB>2</SUB><SUB>α</SUB> significantly hyperpolarized membrane potentials and increased outward whole-cell K<SUP></SUP> currents. PGF<SUB>2</SUB><SUB>α</SUB> increased open-state probability of K<SUB>Ca</SUB> channels without the change of the open and closed kinetics. PGF<SUB>2</SUB><SUB>α</SUB> increased the amplitudes of K<SUB>V</SUB> currents with a leftward shift of activation and inactivation curves and a decrease of activation time constant. Our results suggest that the activation of K<SUB>Ca</SUB> and K<SUB>V</SUB> channels, at least in part, may lead to attenuate or counteract vasoconstriction by PGF<SUB>2</SUB><SUB>α</SUB> in middle cerebral artery.