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>

사람 신경 간세포에서 도파민 신경세포 분화유도에 대한 Nurr 1 유전자의 역할 규명

김한집(Han Jip Kim),이학섭(Haksup Lee),김현창(Hyon Chang Kim),민철기(Churl Ki Min),이명애(Myung Ae Lee),김승업(Seung Up Kim),한진(Jin Han),염재범(Jae Boum Youm),김나리(Nari Kim),박원선(Won Sun Park),김태호(Taeho Kim),김의용(Euiyong Kim 한국생물공학회 2005 KSBB Journal Vol.20 No.5

Role of K<SUP>⁢</SUP> Channels to Resting Membrane Potential of Rabbit Middle Cerebral Arterial Smooth Muscle Cells

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.

Intracellular Ca<SUP>2+</SUP> modulation by Angiotensin Ⅱ in cerebral artery during cardiac hypertrophy

Hyunsuk Lee(이현숙),Nari Kim(김나리),Hyun Joo(주현),Jae Boum Youm(염재범),Won sun Park(박원선),Sunghyun Knag(강성현),Dang Van Cuong,Hyoungkyu Kim,Teaho Kim,Hyunju Kim,Hyejin Moon,Tran Min Khoa,Vu Thi Thu,Euiyong Kim,J 한국생물공학회 2005 한국생물공학회 학술대회 Vol.2005 No.10

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.

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.

Altered Delayed Rectifier K<SUP>⁢</SUP> Current of Rabbit Coronary Arterial Myocytes in Isoproterenol-Induced Hypertrophy

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.

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.

The Alteration of Ca<SUP>2⁢</SUP>-activated K<SUP>⁢</SUP> Channels in Coronary Arterial Smooth Muscle Cells Isolated from Isoproterenol-induced Cardiac Hypertrophy in Rabbit

Nari Kim,Jin Han,Euiyong Kim 대한생리학회-대한약리학회 2001 The Korean Journal of Physiology & Pharmacology Vol.5 No.2

<P> It has been proposed that Ca<SUP>2⁢</SUP>-activated K<SUP>⁢</SUP> (K<SUB>Ca</SUB>) channels play an essential role in vascular tone. The alterations of the properties of coronary K<SUB>Ca</SUB> channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present studies were carried out to determine the properties of coronary K<SUB>Ca</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 present study are as follows: (1) the unitary current amplitudes and the slope conductance of coronary K<SUB>Ca</SUB> channels were decreased without changes of the channel kinetics in isoproterenol-induced cardiac hypertrophy; (2) the sensitivity of coronary K<SUB>Ca</SUB> channels to the changes of intracellular concentration of Ca<SUP>2⁢</SUP> was reduced in isoproterenol-induced cardiac hypertrophy. From above results, we suggest for the first time that the alteration of K<SUB>Ca</SUB> channels are involved in impaired coronary reserve in isoproterenol-induced cardiac hypertrophy.

The Effects of Melatonin on Cisplatin-Induced Renal Cortical Cell Injury in Rabbits

Chunghui Kim,Jin Han,Nari Kim,Juhee Park,Youngchurl Yang,Euiyong Kim 대한생리학회-대한약리학회 2001 The Korean Journal of Physiology & Pharmacology Vol.5 No.3

<P> Melatonin, a pineal gland hormone, is believed to act as an antioxidant via the stimulation of radical detoxifying enzymes and scavenging of free radicals. In this study, effects of <I>in vitro </I>and<I> in vivo</I> treatments of melatonin on the cisplatin-induced lipid peroxidation, LDH release and plasma creatinine were determined in rabbit renal cortical cells. The level of malondialdehyde (MDA) was assayed as an index of lipid peroxidation and the level of LDH release as an indicator of cellular damage. In <I>in vitro</I> studies, cisplatin increased the levels of MDA and LDH release in a concentration-and time-dependent manner. Melatonin inhibited the cisplatin-induced lipid peroxidation and LDH release in a concentration-dependent manner. The minimal effective concentration of melatonin that significantly reduced the 300μM cisplatin- induced lipid peroxidation and LDH release was 1 mM. In <I>in vivo</I> studies, the levels of lipid peroxidation and LDH release in renal cortical cells increased significantly 24 or 48 hours after a single injection of cisplatin (6 mg/kg). When the cisplatin-injected rabbits were pretreated with 10 mg/kg of melatonin, a significant reduction in both lipid peroxidation and LDH release was observed. The plasma creatinine level increased from 0.87⁑0.07 mg/dl in control to 6.33⁑0.54 mg/dl in cisplatin-injected rabbits (P<0.05). Melatonin partially prevented the increase in serum creatinine level (1.98⁑0.11 mg/dl) by cisplatin (P<0.05). In the proximal tubules from cisplatin-treated group, tubular cells had microvilli of variable heights. Necrotic debris was seen in tubular lumens. In most of cells, the mitochondria and lysosomes were increased in frequency. The endocytic vacuoles were not prominent and distribution of the brush border was irregular and shortened. These cisplatin-induced morphological changes were moderate in the melatonin-pretreated group. These results suggest that the toxicity of cisplatin is associated with the generation of reactive oxygen free radicals and that melatonin is a powerful antioxidant, which prevents some of the adverse effects of cisplatin.