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Regulation of $Ca^{2+}$ Signaling in Pulmonary Hypertension
Firth, Amy L.,Won, Jun Yeon,Park, Won Sun The Korean Society of Pharmacology 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.1
Understanding the cellular and molecular mechanisms involved in the development and progression of pulmonary hypertension (PH) remains imperative if we are to successfully improve the quality of life and life span of patients with the disease. A whole plethora of mechanisms are associated with the development and progression of PH. Such complexity makes it difficult to isolate one particular pathway to target clinically. Changes in intracellular free calcium concentration, the most common intracellular second messenger, can have significant impact in defining the pathogenic mechanisms leading to its development and persistence. Signaling pathways leading to the elevation of $[Ca^{2+}]_{cyt}$ contribute to pulmonary vasoconstriction, excessive proliferation of smooth muscle cells and ultimately pulmonary vascular remodeling. This current review serves to summarize the some of the most recent advances in the regulation of calcium during pulmonary hypertension.
Tourism as a Tool for Urban Cultural Heritage Conservation
Tracey Firth,Hongyan Jia 세계문화관광학회 2009 Conference Proceedings Vol.10 No.0
This paper presents a comparison study of tourism at two urban heritage sites, Woolloomooloo Finger Wharf in Sydney Australia and The Residence of Ganxi in Nanjing China. Both sites are evaluated according to the criteria for successful tourism at heritage places outlined in a report published by The Australian Heritage Commission (AHC) (2001). Through case analysis the role of tourism as a tool for urban cultural heritage conservation is discussed. Data were collected through interviews and a survey with the key stakeholders associated with each heritage site including residents, visitors, business owners and government. The findings of both cases indicate that tourism has notable efficacy on tangible-heritage conservation and has limitations on intangible-heritage conservation because the historical connection between the original inhabitants and the heritage site is weakened. Several lessons can be learned from the development of tourism at these heritage sites. The effectiveness of tourism as a tool for heritage conservation and management can be improved when tourism adheres to certain development principles. Firstly that the original character of the heritage site is maintained and secondly that the historical ties that local residents and original inhabitants have to the site are respected so as to create a rich heritage context for both local residents and tourists.
Regulation of Ca2+ Signaling in Pulmonary Hypertension
Amy L Firth,원준연,박원선 대한약리학회 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.1
Understanding the cellular and molecular mechanisms involved in the development and progression of pulmonary hypertension (PH) remains imperative if we are to successfully improve the quality of life and life span of patients with the disease. A whole plethora of mechanisms are associated with the development and progression of PH. Such complexity makes it difficult to isolate one particular pathway to target clinically. Changes in intracellular free calcium concentration, the most common intracellular second messenger, can have significant impact in defining the pathogenic mechanisms leading to its development and persistence. Signaling pathways leading to the elevation of [Ca2+]cyt contribute to pulmonary vasoconstriction, excessive proliferation of smooth muscle cells and ultimately pulmonary vascular remodeling. This current review serves to summarize the some of the most recent advances in the regulation of calcium during pulmonary hypertension.
Regulation of Ca<SUP>2+</SUP> Signaling in Pulmonary Hypertension
Amy L. Firth,Jun Yeon Won,Won Sun Park* 대한생리학회-대한약리학회 2013 The Korean Journal of Physiology & Pharmacology Vol.17 No.1
Understanding the cellular and molecular mechanisms involved in the development and progression of pulmonary hypertension (PH) remains imperative if we are to successfully improve the quality of life and life span of patients with the disease. A whole plethora of mechanisms are associated with the development and progression of PH. Such complexity makes it difficult to isolate one particular pathway to target clinically. Changes in intracellular free calcium concentration, the most common intracellular second messenger, can have significant impact in defining the pathogenic mechanisms leading to its development and persistence. Signaling pathways leading to the elevation of [Ca<sup>2+</sup>]<sub>cyt</sub> contribute to pulmonary vasoconstriction, excessive proliferation of smooth muscle cells and ultimately pulmonary vascular remodeling. This current review serves to summarize the some of the most recent advances in the regulation of calcium during pulmonary hypertension.
( Yahya Al Abed ),( Mohammed Elsherif ),( John Firth ),( Rudi Borgstein ),( Fiona Myint ) 대한내과학회 2012 The Korean Journal of Internal Medicine Vol.27 No.3
There have been reports of the coexistence of abdominal aortic aneurysm (AAA) with intra-abdominal malignancy including gastric, colonic, pancreatic, and renal. We herein report a case of a previously undiagnosed AAA and a presenting complaint consistent with acute cholecystitis. Following cholecystectomy, this was noted to be a rare form of chronic cholecystitis: xanthogranulomatous cholecystitis. There is a known possible association of this uncommon condition with gallbladder cancer. The management of concomitant pathologies can present a real challenge to the multidisciplinary team, especially with large aneurysms.
Direct effect of protein kinase C inhibitors on cardiovascular ion channels
( Youn Kyoung Son ),( Da Hye Hong ),( Dae Joong Kim ),( Amy L Firth ),( Won Sun Park ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.9
Protein kinase C (PKC) is a central enzyme that modulates numerous biological functions. For this reason, specific PKC inhibitors/activators are required to study PKC-related signaling mechanisms. To date, although many PKC inhibitors have been developed, they are limited by poor selectivity and nonspecificity. In this review, we focus on the nonspecific actions of PKC inhibitors on cardiovascular ion channels in addition to their PKC-inhibiting functions. The aim of this paper is to urge caution when using PKC inhibitors to block PKC function. This information may help to better understand PKC-related physiological/biochemical studies. [BMB reports 2011; 44(9): 559-565]
신성은,Hongliang Li,김한솔,김혜원,서미선,하권수,한은택,홍석호,Amy L. Firth,최일환,배영민,박원선 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.2
We demonstrated the effect of nortriptyline, a tricyclic antidepressant drug and serotonin reuptake inhibitor, on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Nortriptyline inhibited Kv currents in a concentration-dependent manner, with an apparent IC50 value of 2.86±0.52 µM and a Hill coefficient of 0.77±0.1. Although application of nortriptyline did not change the activation curve, nortriptyline shifted the inactivation current toward a more negative potential. Application of train pulses (1 or 2 Hz) did not change the nortriptyline-induced Kv channel inhibition, suggesting that the effects of nortiprtyline were not usedependent. Preincubation with the Kv1.5 and Kv2.1/2.2 inhibitors, DPO-1 and guangxitoxin did not affect nortriptyline inhibition of Kv channels. From these results, we concluded that nortriptyline inhibited Kv channels in a concentrationdependent and state-independent manner independently of serotonin reuptake.
The anti-diabetic drug dapagliflozin induces vasodilation via activation of PKG and Kv channels
Li, Hongliang,Shin, Sung Eun,Seo, Mi Seon,An, Jin Ryeol,Choi, Il-Whan,Jung, Won-Kyo,Firth, Amy L.,Lee, Dae-Sung,Yim, Mi-Jin,Choi, Grace,Lee, Jeong Min,Na, Sung Hun,Park, Won Sun Elsevier 2018 Life sciences Vol.197 No.-
<P><B>Abstract</B></P> <P><B>Aim</B></P> <P>Considering the clinical efficacy of dapagliflozin in patients with type 2 DM and the pathophysiological relevance of Kv channels for vascular reactivity. We investigate the vasodilatory effect of dapagliflozin and related mechanisms using phenylephrine (Phe)-induced contracted aortic rings.</P> <P><B>Material and methods</B></P> <P>Arterial tone measurement was performed in aortic smooth muscle.</P> <P><B>Key findings</B></P> <P>Application of dapagliflozin induced vasodilation in a concentration-dependent manner. Pre-treatment with the BK<SUB>Ca</SUB> channel inhibitor paxilline, the K<SUB>ATP</SUB> channel inhibitor glibenclamide, and the Kir channel inhibitor Ba<SUP>2+</SUP> did not change dapagliflozin-induced vasodilation. However, application of the Kv channels inhibitor 4-AP effectively inhibited dapagliflozin-induced vasodilation. Application of the Ca<SUP>2+</SUP> channel inhibitor nifedipine and the sarcoplasmic/endoplasmic reticulum Ca<SUP>2+</SUP>-ATPase (SERCA) pump inhibitor thapsigargin did not alter the vasodilatory effect of dapagliflozin. Moreover, the adenylyl cyclase inhibitor SQ 22536 and the protein kinase A (PKA) inhibitor KT 5720 had no effect on dapagliflozin-induced vasodilation. Although guanylyl cyclase inhibitors, NS 2028 and ODQ, did not reduce the vasodilatory effect of dapagliflozin, the protein kinase G (PKG) inhibitor KT 5823 effectively inhibited dapagliflozin-induced vasodilation. The vasodilatory effect of dapagliflozin was not affected by elimination of the endothelium. Furthermore, pretreatment with the nitric oxide synthase inhibitor L-NAME or the small-conductance Ca<SUP>2+</SUP>-activated K (SKCa) channel inhibitor apamin did not change the vasodilatory effect of dapagliflozin.</P> <P><B>Significance</B></P> <P>We concluded that dapagliflozin induced vasodilation via the activation of Kv channels and PKG, and was independent of other K<SUP>+</SUP> channels, Ca<SUP>2+</SUP> channels, intracellular Ca<SUP>2+</SUP>, and the endothelium.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>