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Bae, Hyemi,Choi, Jeongyoon,Kim, Young-Won,Lee, Donghee,Kim, Jung-Ha,Ko, Jae-Hong,Bang, Hyoweon,Kim, Taeho,Lim, Inja MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.3
<P>This study investigated the expression of voltage-gated K<SUP>+</SUP> (K<SUB>V</SUB>) channels in human cardiac fibroblasts (HCFs), and the effect of nitric oxide (NO) on the K<SUB>V</SUB> currents, and the underlying phosphorylation mechanisms. In reverse transcription polymerase chain reaction, two types of K<SUB>V</SUB> channels were detected in HCFs: delayed rectifier K<SUP>+</SUP> channel and transient outward K<SUP>+</SUP> channel. In whole-cell patch-clamp technique, delayed rectifier K<SUP>+</SUP> current (I<SUB>K</SUB>) exhibited fast activation and slow inactivation, while transient outward K<SUP>+</SUP> current (I<SUB>to</SUB>) showed fast activation and inactivation kinetics. Both currents were blocked by 4-aminopyridine. An NO donor, <I>S</I>-nitroso-<I>N</I>-acetylpenicillamine (SNAP), increased the amplitude of I<SUB>K</SUB> in a concentration-dependent manner with an EC<SUB>50</SUB> value of 26.4 µM, but did not affect I<SUB>to</SUB>. The stimulating effect of SNAP on I<SUB>K</SUB> was blocked by pretreatment with 1H-(1,2,4)oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or by KT5823. 8-bromo-cyclic GMP stimulated the I<SUB>K</SUB>. The stimulating effect of SNAP on I<SUB>K</SUB> was also blocked by pretreatment with KT5720 or by SQ22536. Forskolin and 8-bromo-cyclic AMP each stimulated I<SUB>K</SUB>. On the other hand, the stimulating effect of SNAP on I<SUB>K</SUB> was not blocked by pretreatment of <I>N</I>-ethylmaleimide or by DL-dithiothreitol. Our data suggest that NO enhances I<SUB>K</SUB>, but not I<SUB>to</SUB>, among K<SUB>V</SUB> currents of HCFs, and the stimulating effect of NO on I<SUB>K</SUB> is through the PKG and PKA pathways, not through <I>S</I>-nitrosylation.</P>
Bae, Hyemi,Lee, Donghee,Kim, Young-Won,Choi, Jeongyoon,Lee, Hong Jun,Kim, Sang-Wook,Kim, Taeho,Noh, Yun-Hee,Ko, Jae-Hong,Bang, Hyoweon,Lim, Inja The Korean Society of Pharmacology 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.3
Human cardiac fibroblasts (HCFs) have various voltage-dependent $K^+$ channels (VDKCs) that can induce apoptosis. Hydrogen peroxide ($H_2O_2$) modulates VDKCs and induces oxidative stress, which is the main contributor to cardiac injury and cardiac remodeling. We investigated whether $H_2O_2$ could modulate VDKCs in HCFs and induce cell injury through this process. In whole-cell mode patch-clamp recordings, application of $H_2O_2$ stimulated $Ca^{2+}-activated$ $K^+$ ($K_{Ca}$) currents but not delayed rectifier $K^+$ or transient outward $K^+$ currents, all of which are VDKCs. $H_2O_2-stimulated$ $K_{Ca}$ currents were blocked by iberiotoxin (IbTX, a large conductance $K_{Ca}$ blocker). The $H_2O_2-stimulating$ effect on large-conductance $K_{Ca}$ ($BK_{Ca}$) currents was also blocked by KT5823 (a protein kinase G inhibitor) and 1 H-[1, 2, 4] oxadiazolo-[4, 3-a] quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor). In addition, 8-bromo-cyclic guanosine 3', 5'-monophosphate (8-Br-cGMP) stimulated $BK_{Ca}$ currents. In contrast, KT5720 and H-89 (protein kinase A inhibitors) did not block the $H_2O_2-stimulating$ effect on $BK_{Ca}$ currents. Using RT-PCR and western blot analysis, three subtypes of $K_{Ca}$ channels were detected in HCFs: $BK_{Ca}$ channels, small-conductance $K_{Ca}$ ($SK_{Ca}$) channels, and intermediate-conductance $K_{Ca}$ ($IK_{Ca}$) channels. In the annexin V/propidium iodide assay, apoptotic changes in HCFs increased in response to $H_2O_2$, but IbTX decreased $H_2O_2$-induced apoptosis. These data suggest that among the VDKCs of HCFs, $H_2O_2$ only enhances $BK_{Ca}$ currents through the protein kinase G pathway but not the protein kinase A pathway, and is involved in cell injury through $BK_{Ca}$ channels.
Hyemi Bae,Donghee Lee,Young-Won Kim,Jeongyoon Choi,Hong Jun Lee,Sang-Wook Kim,Taeho Kim,Yun-Hee Noh,Jae-Hong Ko,Hyoweon Bang,Inja Lim 대한생리학회-대한약리학회 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.3
Human cardiac fibroblasts (HCFs) have various voltage-dependent K<sup>+</sup> channels (VDKCs) that can induce apoptosis. Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) modulates VDKCs and induces oxidative stress, which is the main contributor to cardiac injury and cardiac remodeling. We investigated whether H<sub>2</sub>O<sub>2</sub> could modulate VDKCs in HCFs and induce cell injury through this process. In whole-cell mode patch-clamp recordings, application of H<sub>2</sub>O<sub>2</sub> stimulated Ca<sup>2+</sup>-activated K<sup>+</sup> (K<sub>Ca</sub>) currents but not delayed rectifier K<sup>+</sup> or transient outward K<sup>+</sup> currents, all of which are VDKCs. H<sub>2</sub>O<sub>2</sub>-stimulated K<sub>Ca</sub> currents were blocked by iberiotoxin (IbTX, a large conductance K<sub>Ca</sub> blocker). The H<sub>2</sub>O<sub>2</sub>-stimulating effect on large-conductance K<sub>Ca</sub> (BK<sub>Ca</sub>) currents was also blocked by KT5823 (a protein kinase G inhibitor) and 1 H-[1, 2, 4] oxadiazolo-[4, 3-a] quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor). In addition, 8-bromo-cyclic guanosine 3’, 5’-monophosphate (8-Br-cGMP) stimulated BK<sub>Ca</sub> currents. In contrast, KT5720 and H-89 (protein kinase A inhibitors) did not block the H<sub>2</sub>O<sub>2</sub>-stimulating effect on BK<sub>Ca</sub> currents. Using RT-PCR and western blot analysis, three subtypes of K<sub>Ca</sub> channels were detected in HCFs: BK<sub>Ca</sub> channels, small-conductance K<sub>Ca</sub> (SK<sub>Ca</sub>) channels, and intermediate-conductance K<sub>Ca</sub> (IK<sub>Ca</sub>) channels. In the annexin V/propidium iodide assay, apoptotic changes in HCFs increased in response to H<sub>2</sub>O<sub>2</sub>, but IbTX decreased H<sub>2</sub>O<sub>2</sub>-induced apoptosis. These data suggest that among the VDKCs of HCFs, H<sub>2</sub>O<sub>2 </sub>only enhances BK<sub>Ca</sub> currents through the protein kinase G pathway but not the protein kinase A pathway, and is involved in cell injury through BK<sub>Ca</sub> channels.
Hyemi Bae,Taeho Kim,Inja Lim 대한생리학회-대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.1
To identify the effect and mechanism of carbon monoxide (CO) on delayed rectifier K+ currents (I K) of human cardiac fibroblasts (HCFs), we used the wholecell mode patch-clamp technique. Application of CO delivered by carbon monoxidereleasing molecule-3 (CORM3) increased the amplitude of outward K+ currents, and diphenyl phosphine oxide-1 (a specific I K blocker) inhibited the currents. CORM3- induced augmentation was blocked by pretreatment with nitric oxide synthase blockers (L-NG-monomethyl arginine citrate and L-NG-nitro arginine methyl ester). Pretreatment with KT5823 (a protein kinas G blocker), 1H-[1,-2,-4] oxadiazolo-[4,-3-a] quinoxalin-1-on (ODQ, a soluble guanylate cyclase blocker), KT5720 (a protein kinase A blocker), and SQ22536 (an adenylate cyclase blocker) blocked the CORM3 stimulating effect on I K. In addition, pretreatment with SB239063 (a p38 mitogen-activated protein kinase [MAPK] blocker) and PD98059 (a p44/42 MAPK blocker) also blocked the CORM3’s effect on the currents. When testing the involvement of S-nitrosylation, pretreatment of N-ethylmaleimide (a thiol-alkylating reagent) blocked CO-induced I K activation and DL-dithiothreitol (a reducing agent) reversed this effect. Pretreatment with 5,10,15,20-tetrakis(1-methylpyridinium-4-yl)-21H,23H porphyrin manganese (III) pentachloride and manganese (III) tetrakis (4-benzoic acid) porphyrin chloride (superoxide dismutase mimetics), diphenyleneiodonium chloride (an NADPH oxidase blocker), or allopurinol (a xanthine oxidase blocker) also inhibited CO-induced I K activation. These results suggest that CO enhances I K in HCFs through the nitric oxide, phosphorylation by protein kinase G, protein kinase A, and MAPK, S-nitrosylation and reduction/oxidation (redox) signaling pathways.
Bae, Hyemi,Kim, Taeho,Lim, Inja The Korean Society of Pharmacology 2021 The Korean Journal of Physiology & Pharmacology Vol.25 No.3
Carbon monoxide (CO) is a cardioprotectant and potential cardiovascular therapeutic agent. Human cardiac fibroblasts (HCFs) are important determinants of myocardial structure and function. Large-conductance Ca2+-activated K+ (BK) channel is a potential therapeutic target for cardiovascular disease. We investigated whether CO modulates BK channels and the signaling pathways in HCFs using whole-cell mode patch-clamp recordings. CO-releasing molecules (CORMs; CORM-2 and CORM-3) significantly increased the amplitudes of BK currents (IBK). The CO-induced stimulating effects on IBK were blocked by pre-treatment with specific nitric oxide synthase (NOS) blockers (L-NG-monomethyl arginine citrate and L-NG-nitroarginine methyl ester). 8-bromo-cyclic GMP increased IBK. KT5823 (inhibits PKG) or ODQ (inhibits soluble guanylate cyclase) blocked the CO-stimulating effect on IBK. Moreover, 8-bromo-cyclic AMP also increased IBK, and pre-treatment with KT5720 (inhibits PKA) or SQ22536 (inhibits adenylate cyclase) blocked the CO effect. Pre-treatment with N-ethylmaleimide (a thiol-alkylating reagent) also blocked the CO effect on IBK, and DL-dithiothreitol (a reducing agent) reversed the CO effect. These data suggest that CO activates IBK through NO via the NOS and through the PKG, PKA, and S-nitrosylation pathways.
Simulation study of a novel target oriented SPECT design using a variable pinhole collimator
Bae, Seungbin,Chun, Jaehee,Cha, Hyemi,Yeom, Jung Yeol,Lee, Kisung,Lee, Hakjae Published for the American Association of Physicis 2017 Medical physics Vol.44 No.2
<P>Conclusions: In this study, we designed a novel pinhole collimator for SPECT and presented preliminary results of target oriented imaging with a simulation study. Currently, we are pursuing strategies to realize the proposed system, with the goal to apply the technology into a high-sensitivity and high-resolution preclinical SPECT. Should VP SPECT be applied to the clinical setting, we anticipate a high-sensitivity, high-resolution system for applications such as heart dedicated SPECT or related fields. (C) 2016 American Association of Physicists in Medicine</P>
Auto-Tuning CNNs for Coarse-Grained Reconfigurable Array-Based Accelerators
Bae, Inpyo,Harris, Barend,Min, Hyemi,Egger, Bernhard IEEE 2018 IEEE transactions on computer-aided design of inte Vol.37 No.11
<P>As more and more deep learning tasks are pushed to mobile devices, accelerators for running these networks efficiently gain in importance. We show a that an existing class of general purpose accelerators, modulo-scheduled coarse-grained reconfigurable array (CGRA) processors typically used to accelerate multimedia workloads, can be a viable alternative to dedicated deep neural network processing hardware. To this end, an auto-tuning compiler is presented that maps convolutional neural networks (CNNs) efficiently on such architectures. The auto-tuner analyzes the structure of the CNN and the features of the CGRA, then explores the large optimization space to generate code that allows for an efficient mapping of the network. Evaluated with various CNNs, the auto-tuned code achieves an 11-fold speedup over the initial mapping. Comparing the energy per interference, the CGRA outperforms other general-purpose accelerators and an ARMv8 processor by a significant margin.</P>
Kwon, Hyemi,Jeon, Min Ji,Kim, Won Gu,Park, Suyeon,Kim, Mijin,Song, Dong Eun,Sung, Tae-Yon,Yoon, Jong Ho,Hong, Suck Joon,Kim, Tae Yong,Shong, Young Kee,Kim, Won Bae Bioscientifica 2017 European journal of endocrinology Vol.176 No.4
<B>Objective</B><P>Papillary thyroid microcarcinoma (PTMC) accounts for most of the increase in thyroid cancer in recent decades. We compared clinical outcomes and surgical complications of lobectomy and total thyroidectomy (TT) in PTMC patients.</P><B>Design and methods</B><P>In this retrospective individual risk factor-matched cohort study, 2031 patients with PTMC were initially included. Patients who underwent lobectomy or TT were one-to-one matched according to individual risk factors, including age, sex, primary tumor size, extrathyroidal extension, multifocality and cervical lymph node (LN) metastasis.</P><B>Results</B><P>In total, 688 patients were assigned to each group. During the median 8.5 years of follow-up, 26 patients (3.8%) in the lobectomy group and 11 patients (1.6%) in the TT group had recurrences. The relative risk of recurrence was significantly less in the TT than that in the lobectomy group (hazard ratio (HR) 0.41; 95% confidence interval (CI) 0.21-0.81; <I>P</I> = 0.01). Most recurrences (84.6%) in the lobectomy group occurred in the contralateral lobe, and all patients were disease-free after completion of thyroidectomy. There were no significant differences in recurrence-free survival between the two groups after exclusion of contralateral lobe recurrences (HR, 2.75; 95% CI, 0.08-8.79; <I>P</I> = 0.08). There were significantly more patients with transient and permanent hypoparathyroidism in the TT than that in the lobectomy group (<I>P</I> < 0.001).</P><B>Conclusions</B><P>Lobectomy could be appropriate for most patients with PTMC when there is no evidence of extrathyroidal disease in the preoperative work-up. Preoperative and postoperative imaging studies are important for patients who undergo lobectomy for PTMC, because most recurrences are in the contralateral lobe.</P>