Browsing by Author "Chen, Peng-Sheng"

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3D DEPTH MAP GENERATION FOR EMBEDDED STEREO APPLICATIONS
(2012)
Lee, Jui-Sheng
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Jian, Guo-An
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Chien, Cheng-An
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Chen, Peng-Sheng
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Guo, Jiun-In
This paper presents a low complexity 3D image depth map generation algorithm for embedded stereo applications. The proposed algorithm generates depth information based on a single view 2D image automatically. Owing to different scene characteristics of image, we propose a mechanism to classify images to "Scenery", "Normal" and "Close-up" types first and generate the associated depth map according to the proposed techniques. In addition, we propose a human detection method for strengthening the depth information in images with humans and post-processing for refining depth map. With good quality in the generated depth map, the proposed algorithm achieves about 93% in complexity reduction as compared to the traditional algorithm, which is suitable for realization in both the hardware and embedded systems for portable stereo applications.
A REAL-TIME PARALLEL SCALABLE VIDEO ENCODER FOR MULTIMEDIA STREAMING SYSTEMS
(2013)
Jian, Guo-An
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Lee, Jui-Sheng
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Tan, Kheng-Joo
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Chen, Peng-Sheng
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Guo, Jiun-In
Scalable video coding (SVC) is a video coding technique that mainly aims its target in resolving problems of multimedia communication between servers and various clients with different computational power, transmission bandwidths, and display resolutions. In this paper, we developed a parallel SVC encoding system to achieve the real-time coding performance of SVC. First, a GOP-level bit-stream structure that is fully compatible with the standard SVC decoder was proposed to eliminate the data dependencies of encoding among GOPs. Based on this bit-stream structure, we developed a parallel SVC encoding algorithm to exploit the parallelism on multicore systems. Finally, the proposed parallel SVC encoder was implemented and integrated into a multimedia streaming system for the evaluation. The experimental results showed that for CIF/QCIF and VGA/QVGA 2-layer SVC encoding, the proposed parallel SVC encoder can achieve 50.96 and 103.99 times speedup with negligible PSNR drop, respectively.
A Verification-Aware Design Methodology for Thread Pipelining Parallelization
(2012-10-01)
Jian, Guo-An
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Chien, Cheng-An
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Chen, Peng-Sheng
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Guo, Jiun-In
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電子工程學系及電子研究所
This paper proposes a verification-aware design methodology that provides developers with a systematic and reliable approach to performing thread-pipelining parallelization on sequential programs. In contrast to traditional design flow, a behavior-model program is constructed before parallelizing as a bridge to help developers gradually leverage the technique of thread-pipelining parallelization. The proposed methodology integrates verification mechanisms into the design flow. To demonstrate the practicality of the proposed methodology, we applied it to the parallelization of a 3D depth map generator with thread pipelining. The parallel 3D depth map generator was further integrated into a 3D video playing system for evaluation of the verification overheads of the proposed methodology and the system performance. The results show the parallel system can achieve 33.72 fps in D1 resolution and 12.22 fps in HD720 resolution through a five-stage pipeline. When verifying the parallel program, the proposed verification approach keeps the performance degradation within 23% and 21.1% in D1 and HD720 resolutions, respectively.
Acute reversal of phospholamban inhibition facilitates the rhythmic whole-cell propagating calcium waves in isolated ventricular myocytes
(2015-03-01)
Chan, Yi-Hsin
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Tsai, Wei-Chung
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Song, Zhen
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Ko, Christopher Y.
;
Qu, Zhilin
Phospholamban (PLB) inhibits the activity of cardiac sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a). Phosphorylation of PLB during sympathetic activation reverses SERCA2a inhibition, increasing SR Ca2+ uptake. However, sympathetic activation also modulates multiple other intracellular targets in ventricular myocytes (VMs), making it impossible to determine the specific effects of the reversal of PLB inhibition on the spontaneous SR Ca2+ release. Therefore, it remains unclear how PLB regulates rhythmic activity in VMs. Here, we used the Fab fragment of 2D12, a monoclonal anti-PLB antibody, to test how acute reversal of PLB inhibition affects the spontaneous SR Ca2+ release in normal VMs. Ca2+ sparks and spontaneous Ca2+ waves (SCWs) were recorded in the line-scan mode of confocal microscopy using the Ca2+ fluorescent dye Fluo-4 in isolated permeabilized mouse VMs. Fab, which reverses PLB inhibition, significantly increased the frequency, amplitude, and spatial/temporal spread of Ca2+ sparks in VMs exposed to 50 nM free [Ca2+]. At physiological diastolic free [Ca2+] (100-200 nM), Fab facilitated the formation of whole-cell propagating SCWs. At higher free [Ca2+], Fab increased the frequency and velocity, but decreased the decay time of the SCWs. cAMP had little additional effect on the frequency or morphology of Ca2+ sparks or SCWs after Fab addition. These findings were complemented by computer simulations. In conclusion, acute reversal of PLB inhibition alone significantly increased the spontaneous SR Ca2+ release, leading to the facilitation and organization of whole-cell propagating SCWs in normal VMs. PLB thus plays a key role in subcellular Ca2+ dynamics and rhythmic activity of VMs. (C) 2015 Elsevier Ltd. All rights reserved.
Antiarrhythmic effects of stimulating the left dorsal branch of the thoracic nerve in a canine model of paroxysmal atrial tachyarrhythmias
(2018-08-01)
Zhao, Ye
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Yuan, Yuan
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Tsai, Wei-Chung
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Jiang, Zhaolei
;
Tian, Zhi-peng
BACKGROUND Stellate ganglion nerve activity (SGNA) precedes paroxysmal atrial tachyarrhythmia (PAT) episodes in dogs with intermittent rapid left atrial (LA) pacing. The left dorsal branch of the thoracic nerve (LDTN) contains sympathetic nerves originating from the stellate ganglia. OBJECTIVE The purpose of this study was to test the hypothesis that high-frequency electrical stimulation of the LDTN can cause stellate ganglia damage and suppress PATs. METHODS We performed long-term LDTN stimulation in 6 dogs with and 2 dogs without intermittent rapid LA pacing while monitoring SGNA. RESULTS LDTN stimulation reduced average SGNA from 4.36 mu V (95% confidence interval [CI] 4.10-4.62 mu V) at baseline to 3.22 mu V (95% CI 3.04-3.40 mu V) after 2 weeks (P5.028) and completely suppressed all PAT episodes in all dogs studied. Tyrosine hydroxylase staining showed large damaged regions in both stellate ganglia, with increased percentages of tyrosine hydroxylase-negative cells. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed that 23.36% (95% CI 18.74%-27.98%) of ganglion cells in the left stellate ganglia and 11.15% (95% CI 9.34%-12.96%) ganglion cells in the right stellate ganglia were positive, indicating extensive cell death. A reduction of both SGNA and heart rate was also observed in dogs with LDTN stimulation but without rapid LA pacing. Histological studies in the 2 dogs without intermittent rapid LA pacing confirmed the presence of extensive stellate ganglia damage, along with a high percentage of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. CONCLUSION LDTN stimulation damages both left and right stellate ganglia, reduces left SGNA, and is antiarrhythmic in this canine model of PAT.
Apamin induces early afterdepolarizations and torsades de pointes ventricular arrhythmia from failing rabbit ventricles exhibiting secondary rises in intracellular calcium
(2013-10-01)
Chang, Po-Cheng
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Hsieh, Yu-Cheng
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Hsueh, Chia-Hsiang
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Weiss, James N.
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Lin, Shien-Fong
BACKGROUND A secondary rise of intracellular Ca2+ (Ca) and an upregulation of apamin-sensitive K+ current (I-KAs) are characteristic findings of failing ventricular myocytes. We hypothesize that apamin, a specific IKAs Mocker, may induce torsades de pointes (TdP) ventricular arrhythmia from failing ventricles exhibiting secondary rises of Ca,. OBJECTIVE To test the hypothesis that small conductance Ca2+ activated Los maintains repolarization reserve and prevents ventricular arrhythmia in a rabbit model of heart failure (HF). METHODS We performed Langendorff perfusion and optical mapping studies in 7 hearts with pacing-induced HF and in 5 normal control rabbit hearts. Atrioventricular block was created by cryoablation to allow pacing at slow rates. RESULTS The left ventricular ejection fraction reduced from 69.1% [95% confidence interval 62.3%-76.0%] before pacing to 30.4% [26.8%-34.0%] (N = 7; P <.001) after pacing. The corrected QT interval in failing ventricles was 337 [313-360] ms at baseline and 410 [381-439] ms after applying 100 nmol/L of apamin (P = .01). Apamin induced early afterdepolarizations (EADs) in 6 ventricles, premature ventricular beats (PVBs) in 7 ventricles, and polymorphic ventricular tachycardia consistent with TdP in 4 ventricles. The earliest activation site of EADs and PVBs always occurred at the site with long action potential duration and large amplitude of the secondary rises of Ca,. Apamin induced secondary rises of Ca, in 1 nonfailing ventricle, but no EAD or TdP were observed. CONCLUSIONS In HF ventricles, apamin induces EADs, PVBs, and TdP from areas with secondary rises of Ca,. IKAs is important in maintaining repolarization reserve and preventing TdP in HF ventricles.
Concomitant SK current activation and sodium current inhibition cause J wave syndrome
(2018-11-15)
Chen, Mu
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Xu, Dong-Zhu
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Wu, Adonis Z.
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Guo, Shuai
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Wan, Juyi
The mechanisms of J wave syndrome (JWS) are incompletely understood. Here, we showed that the concomitant activation of small-conductance calcium-activated potassium (SK) current (I-KAS) and inhibition of sodium current by cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA) recapitulate the phenotypes of JWS in Langendorff-perfused rabbit hearts. CyPPA induced significant J wave elevation and frequent spontaneous ventricular fibrillation (SVF), as well as sinus bradycardia, atrioventricular block, and intraventricular conduction delay. I-KAS activation by CyPPA resulted in heterogeneous shortening of action potential (AP) duration (APD) and repolarization alternans. CyPPA inhibited cardiac sodium current (I-Na) and decelerated AP upstroke and intracellular calcium transient. SVFs were typically triggered by short-coupled premature ventricular contractions, initiated with phase 2 reentry and originated more frequently from the right than the left ventricles. Subsequent I-KAS blockade by apamin reduced J wave elevation and eliminated SVF. beta-Adrenergic stimulation was antiarrhythmic in CyPPA-induced electrical storm. Like CyPPA, hypothermia (32.0 degrees C) also induced J wave elevation and SVF. It facilitated negative calcium-voltage coupling and phase 2 repolarization alternans with spatial and electromechanical discordance, which were ameliorated by apamin. These findings suggest that I-KAS activation contributes to the development of JWS in rabbit ventricles.
Differential effects of SKCa blockade on arrhythmogenesis in normal and remodeled hearts
(2015-01-01)
Hsueh, Chia-Hsiang
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Chen, Peng-Sheng
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Lin, Shien-Fong
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分子醫學與生物工程研究所
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Institute of Molecular Medicine and Bioengineering
Effects of ondansetron on apamin-sensitive small conductance calcium-activated potassium currents in pacing-induced failing rabbit hearts
(2020-02-01)
Yin, Dechun
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Yang, Na
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Tian, Zhipeng
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Wu, Adonis Z.
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Xu, Dongzhu
BACKGROUND Ondansetron, a widely prescribed antiemetic, has been implicated in drug-induced long QT syndrome. Recent patch clamp experiments have shown that ondansetron inhibits the apamin-sensitive small conductance calcium-activated potassium current (I-KAS). OBJECTIVE The purpose of this study was to determine whether ondansetron causes action potential duration (APD) prolongation by I-KAS inhibition. METHODS Optical mapping was performed in rabbit hearts with pacing-induced heart failure (HF) and in normal hearts before and after ondansetron (100 nM) infusion. APD at 80% repolarization (APD(80)) and arrhythmia inducibility were determined. Additional studies with ondansetron were performed in normal hearts perfused with hypokalemic Tyrode's (2.4 mM) solution before or after apamin administration. RESULTS The corrected QT interval in HF was 326 ms (95% confidence interval [CI] 306-347 ms) at baseline and 364 ms (95% CI 351-378 ms) after ondansetron infusion (P < .001). Ondansetron significantly prolonged APD(80) in the HF group and promoted early afterdepolarizations, steepened the APD restitution curve, and increased ventricular vulnerability. Ventricular fibrillation was not inducible in HF ventricles at baseline, but after ondansetron infusion, ventricular fibrillation was induced in 5 of the 7 ventricles (P = .021). In hypokalemia, apamin prolonged APD(80) from 163 ms (95% CI 146-180 ms) to 180 ms (95% CI 156-204 ms) (P = .018). Subsequent administration of ondansetron failed to further prolong APD(80) (180 ms [95% CI 156-204 ms] vs 179 ms [95% CI 165-194 ms]; P = .789). The results were similar when ondansetron was administered first, followed by apamin. CONCLUSION Ondansetron is a specific I-KAS blocker at therapeutic concentrations. Ondansetron may prolong the QT interval in HF by inhibiting small conductance calcium-activated potassium channels, which increases the vulnerability to ventricular arrhythmias.
Effects of renal sympathetic denervation on the stellate ganglion and brain stem in dogs
(2017-02-01)
Tsai, Wei-Chung
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Chan, Yi-Hsin
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Chinda, Kroekkiat
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Chen, Zhenhui
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Patel, Jheel
BACKGROUND Renal sympathetic denervation (RD) is a promising method of neuromodulation for the management of cardiac arrhythmia. OBJECTIVE We tested the hypothesis that RD is antiarrhythmic in ambulatory dogs because it reduces the stellate ganglion nerve activity (SGNA) by remodeling the stellate ganglion (SG) and brain stem. METHODS We implanted a radiotransmitter to record SGNA and electrocardiogram in 9 ambulatory dogs for 2 weeks, followed by a second surgery for RD and 2 months SGNA recording. Cell death was probed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. RESULTS Integrated SGNA at baseline and 1 and 2 months after RD were 14.0 +/- 4.0, 9.3 +/- 2.8, and 9.6 +/- 2.0 mu V, respectively (P = .042). The SG from RD but not normal control dogs (n = 5) showed confluent damage. An average of 41% +/- 10% and 40% +/- 16% of ganglion cells in the left and right SG, respectively, were TUNEL positive in RD dogs compared with 0% in controls dogs (P = .005 for both). The left and right SG from RD dogs had more tyrosine hydroxylase-negative ganglion cells than did the left SG of control dogs (P = .028 and P = .047, respectively). Extensive TUNEL-positive neurons and glial cells were also noted in the medulla, associated with strongly positive glial fibrillary acidic protein staining. The distribution was heterogeneous, with more cell death in the medial than lateral aspects of the medulla. CONCLUSION Bilateral RD caused significant central and peripheral sympathetic nerve remodeling and reduced SGNA in ambulatory dogs. These findings may in part explain the antiarrhythmic effects of RD.
Estimating Sympathetic Tone by Recording Subcutaneous Nerve Activity in Ambulatory Dogs
(2015-01-01)
Robinson, Eric A.
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Rhee, Kyoung-Suk
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Doytchinova, Anisiia
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Kumar, Mohineesh
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Shelton, Richard
Subcutaneous Nerve Activity IntroductionWe tested the hypothesis that subcutaneous nerve activity (SCNA) of the thorax correlates with the stellate ganglion nerve activity (SGNA) and can be used to estimate the sympathetic tone. Methods and ResultsWe implanted radio transmitters in 11 ambulatory dogs to record left SGNA, left thoracic vagal nerve activity (VNA), and left thoracic SCNA, including 3 with simultaneous video monitoring and nerve recording. Two additional dogs were studied under general anesthesia with apamin injected into the right stellate ganglion while the right SGNA and the right SCNA were recorded. There was a significant positive correlation between integrated SGNA (iSGNA) and integrated SCNA (iSCNA) in the first 7 ambulatory dogs, with correlation coefficient of 0.70 (95% confidence interval [CI] 0.61-0.84, P < 0.05 for each dog). Tachycardia episodes (heart rate exceeding 150 bpm for 3 seconds) were invariably preceded by SGNA and SCNA. There was circadian variation of both SCNA and SGNA. Crosstalk was ruled out because SGNA, VNA, and SCNA bursts had different timing and activation patterns. In an eighth dog, closely spaced bipolar subcutaneous electrodes also recorded SCNA, but with reduced signal to noise ratio. Video monitoring in additional 3 dogs showed that movement was not a cause of high frequency SCNA. The right SGNA correlated strongly with right SCNA and heart rate in 2 anesthetized dogs after apamin injection into the right stellate ganglion. ConclusionsSCNA recorded by bipolar subcutaneous electrodes correlates with the SGNA and can be used to estimate the sympathetic tone.
Ganglionated plexi and ligament of Marshall ablation reduces atrial vulnerability and causes stellate ganglion remodeling in ambulatory dogs
(2016-10)
Zhao, Ye
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Jiang, Zhaolei
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Tsai, Wei-Chung
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Yuan, Yuan
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Chinda, Kroekkiat
BACKGROUND Simultaneous activation of the stellate ganglion (SG), the ligament of Marshall (LOM), and the ganglionated plexi often precedes the onset of paroxysmal atrial tachyarrhythmia (PAT). OBJECTIVE The purpose of this study was to test the hypothesis that ablation of the LOM and the superior left ganglionated plexi (SLGP) reduces atrial vulnerability and results in remodeling of the SG. METHODS Nerve activity was correlated to PAT and ventricular rate (VR) at baseline, after ablation of the LOM and SLGP, and after atrial fibrillation. Neuronal cell death was assessed with tyrosine hydroxylase and terminal deoxynucleotidyl transferase dUTP nick end label (TUNEL) staining. RESULTS There were 4 2 PAT episodes per day in controls. None were observed in the ablation group, even though SG nerve activity and VR increased from 2.2 mu V (95% confidence interval [CI] 1.2-3.3 mu V) and 80 bpm (95% CI 68-92 bpm) at baseline, to 3.0 mu V (95% CI 2.6-3.4 mu V, P = .046) and 90 bpm (95% CI 75-108 bpm, P = .026) after ablation, and to 3.1 mu V (95% CI 1.7-4.5 mu V, P = .116) and 95 bpm (95% CI 79-110 bpm, P = .075) after atrial fibrillation. There was an increase in tyrosine hydroxylase negative cells in the ablation group and 19.7% (95% CI 8.6%-30.8%) TUN EL-positive staining in both the left and right SG. None were observed in the control group. CONCLUSION LOM and SLGP ablation caused left SG remodeling and cell death. There was reduced correlation of the VR response and PAT to SG nerve activity. These findings support the importance of SLGP and LOM in atrial arrhythmogenesis.
Intermittent left cervical vagal nerve stimulation damages the stellate ganglia and reduces the ventricular rate during sustained atrial fibrillation in ambulatory dogs
(2016-03)
Chinda, Kroekkiat
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Tsai, Wei-Chung
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Chan, Yi-Hsin
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Lin, Andrew Y-T
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Patel, Jheel
BACKGROUND The effects of intermittent open-loop vagal nerve stimulation (VNS) on the ventricular rate (VR) during atrial fibrillation (AF) remain unclear. OBJECTIVE The purpose of this study was to test the hypothesis that VNS damages the stellate ganglion (SG) and improves VR control during persistent AF. METHODS We performed left cervical VNS in ambulatory dogs while recording the left SG nerve activity (SGNA) and vagal nerve activity. Tyrosine hydroxylase (TH) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were used to assess neuronal cell death in the SG. RESULTS We induced persistent AF by atrial pacing in 6 dogs, followed by intermittent VNS with short ON-time (14 seconds) and long OFF-time (66 seconds). The integrated SGNA and VR during AF were 4.84 mV . s (95% confidence interval [CI] 3.08-6.60 mV . s) and 142 beats/min (95% CI 116-168 beats/min), respectively. During AF, VNS reduced the integrated SGNA and VR, respectively, to 3.74 mV . s (95% CI 2.27-5.20 mV . s; P =.021) and 115 beats/ min (95% CI 96-134 beats/min; P =.016) during 66-second OFF-time and to 4.07 mV . s (95% CI 2.42-5.72 mV . s; P =.037) and 114 beats/min (95% CI 83-146 beats/min; P =.039) during 3-minute OFF-time. VNS increased the frequencies of prolonged (>3 seconds) pauses during AF. TH staining showed large confluent areas of damage in the left SG, characterized by pyknotic nuclei, reduced TH staining, increased percentage of TH-negative ganglion cells, and positive TUNEL staining. Occasional TUN EL-positive ganglion cells were also observed in the right SG. CONCLUSION VNS damaged the SG, leading to reduced SGNA and better rate control during persistent AF.
Left cervical vagal nerve stimulation reduces skin sympathetic nerve activity in patients with drug resistant epilepsy
(2017-12-01)
Yuan, Yuan
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Hassel, Jonathan L.
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Doytchinova, Anisiia
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Adams, David
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Wright, Keith C.
BACKGROUND We recently reported that skin sympathetic nerve activity (SKNA) can be used to estimate sympathetic tone in humans. In animal models, vagal nerve stimulation (VNS) can damage the stellate ganglion, reduce stellate ganglion nerve activity, and suppress cardiac arrhythmia. Whether VNS can suppress sympathetic tone in humans remains unclear. OBJECTIVE The purpose of this study was to test the hypothesis that VNS suppresses SKNA in patients with drug-resistant epilepsy. METHODS ECG patch electrodes were used to continuously record SKNA in 26 patients with drug-resistant epilepsy who were admitted for video electroencephalographic monitoring. Among them, 6 (2 men, age 40 +/- 11 years) were previously treated with VNS and 20 (7 men, age 37 +/- 8 years) were not. The signals from ECG leads I and II were filtered to detect SKNA. RESULTS VNS had an on-time of 30 seconds and off-time of 158672 seconds, with output of 1.9260.42 mA at 24.17 +/- 2.01 Hz. Average SKNA during VNS off-time was 1.06 mV (95% confidence interval [CI] 0.93-1.18) in lead I and 1.13 mV (95% CI 0.99-1.27) in lead II, which was significantly lower than 1.38 mV (95% CI 1.01-1.75; P = .036) and 1.38 mV (95% CI 0.98-1.78; P = .035) in the control group, respectively. Heart rate was 65 bpm (95% CI 59-71) in the VNS group, which was significantly lower than 77 bpm (95% CI 71-83) in the control group. CONCLUSION Patients with VNS had significantly lower SKNA than those without VNS.
Long-term intermittent high-amplitude subcutaneous nerve stimulation reduces sympathetic tone in ambulatory dogs
(2018-03-01)
Yuan, Yuan
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Jiang, Zhaolei
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Zhao, Ye
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Tsai, Wei-Chung
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Patel, Jheel
BACKGROUND Reducing sympathetic efferent outflow from the stellate ganglia (SG) may be antiarrhythmic. OBJECTIVE The purpose of this study was to test the hypothesis that chronic thoracic subcutaneous nerve stimulation (ScNS) could reduce SG nerve activity (SGNA) and control paroxysmal atrial tachycardia (PAT). METHODS Thoracic ScNS was performed in 8 dogs while SGNA, vagal nerve activity (VNA), and subcutaneous nerve activity (ScNA) were monitored. An additional 3 dogs were used for sham stimulation as controls. RESULTS Xinshu ScNS and left lateral thoracic nerve ScNS reduced heart rate (HR). Xinshu ScNS at 3.5 mA for 2 weeks reduced mean average SGNA from 5.32 mV (95% confidence interval [ CI] 3.89-6.75) at baseline to 3.24 mV (95% CI 2.16-4.31; P = .015) and mean HR from 89 bpm (95% CI 80-98) at baseline to 83 bpm (95% CI 76-90; P = .007). Bilateral SG showed regions of decreased tyrosine hydroxylase staining with increased terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive nuclei in 18.47% (95% CI 9.68-46.62) of all ganglion cells, indicating cell death. Spontaneous PAT episodes were reduced from 9.83 per day (95% CI 5.77-13.89) in controls to 3.00 per day (95% CI 0.11-5.89) after ScNS (P = .027). Left lateral thoracic nerve ScNS also led to significant bilateral SG neuronal death and significantly reduced average SGNA and HR in dogs. CONCLUSION ScNS at 2 different sites in the thorax led to SG cell death, reduced SGNA, and suppressed PAT in ambulatory dogs.
Method for detection and quantification of non-invasive skin sympathetic nerve activity
(2018-01-01)
Liu, Chun
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Wong, Johnson
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Doytchinova, Anisiia
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Chen, Peng-Sheng
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Lin, Shien-Fong
Sympathetic nerve activity is an important trigger of cardiac arrhythmia. Our laboratory recently developed a new method for non-invasive recording of the skin sympathetic nerve activity (SKNA) using conventional electrocardiography (ECG) patch electrodes. Recent studies showed that SKNA can adequately estimate sympathetic tone in humans. In order to improve the analysis of SKNA, we developed automatic standard assessment system based on the concept of microneurography and applied to non-invasive SKNA recording via 4 steps of signal processing. Every parameters in procedures can be manually selected by users in order to meet requirements. After using these signal processing, the results obtained by this system show improved nerve burst morphology and trend. Intuitive nerve discharge pattern and occurrence frequency can be automatically generated. Verification of the method with the cold water pressor test data further established the reliability and usefulness of the system. This new method offered a convenient tool to evaluate SKNA for comprehensive and detailed application in neurocardiology. The analysis system may facilitate the study between SKNA and cardiac arrhythmia, thus advance the field of neurocardiology research.
Ondansetron blocks wild-type and p.F503L variant small conductance C2+-activated K+ channels
(2018-08-01)
Ko, Jum-Suk
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Guo, Shuai
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Hassel, Jonathan
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Celestino-Soper, Patricia
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Lynnes, Ty C.
Apamin-sensitive small-conductance Ca2+ activated K+ (SK) current (I-KAS) is encoded by Ca2+ -activated K+ channel subfamily N (KCNN) genes. I-KAS importantly contributes to cardiac repolarization in conditions associated with reduced repolarization reserve. To test the hypothesis that I-KAS inhibition contributes to drug-induced long QT syndrome (diLQTS), we screened for KCNN variants among patients with diLQTS, determined the properties of heterologously expressed wild-type (WI) and variant KCNN channels. and determined if the 5-HT3 receptor antagonist ondansetron blocks I-KAS. We searched 2,306.335 records in the Indiana Network for Patient Care and found 11 patients with diLQTS who had DNA available in the Indiana Biobank. DNA sequencing discovered a heterozygous KCNN2 variant (p.F503L) in a 52-yr-old woman presenting with corrected QT interval prolongation at baseline (473 ms) and further corrected QT interval lengthening (601 ms) after oral administration of ondansetron. That patient was also heterozygous for the p.S38G and p.P2835S variants of the QT-controlling genes KCNEI and ankyrin 2, respectively. Patch-clamp experiments revealed that the p.F503L KCNN2 valiant heterologously expressed in human embryonic kidney (HEK)-293 cells augmented Ca2+ sensitivity, increasing I KAS density. The fraction of total F503L-KCNN2 protein retained in the membrane was higher than that of WT KCNN2 protein. Ondansetron at nanomolar concentrations inhibited WI and p.F503L SK2 channels expressed in HEK-293 cells as well as native SK channels in ventricular cardiomyocytes. Ondansetron-induced I-KAS inhibition was also demonstrated in Langendorff-perfused murine hearts. In conclusion, the heterozygous p.F5031. KCNN2 variant increases Ca2+ sensitivity and I-KAS density in transfected HEK-293 cells. Ondansetron at therapeutic (i.e., nanomolar) concentrations is a potent I-KAS blocker. NEW & NOTEWORTHY We showed that ondansetron, a 5-HT3 receptor antagonist, blocks small-conductance Ca2+-activated K+ (SK) current. Ondansetron may be useful in controlling arrhythmias in which increased SK current is a likely contributor. However, its SK-blocking effects may also facilitate the development of druginduced long QT syndrome.
Phospholamban is concentrated in the nuclear envelope of cardiomyocytes and involved in perinuclear/nuclear calcium handling
(2016-11)
Wu, Adonis Z.
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Xu, Dongzhu
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Yang, Na
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Lin, Shien-Fong
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Chen, Peng-Sheng
Aims: Phospholamban (PLB) regulates the cardiac Ca2+-ATPase (SERCA2a) in sarcoplasmic reticulum (SR). However, the localization of PLB at subcellular sites outside the SR and possible contributions to Ca2+ cycling remain unknown. We examined the intracellular distribution of PLB and tested whether a pool of PLB exists in the nuclear envelope (NE) that might regulate perinuclear/nuclear Ca2+ (nCa(2+)) handling in cardiomyocytes (CMs). Methods and results: Using confocal immunofluorescence microscopy and immunoblot analyses of CMs and CM nuclei, we discovered that PLB was highly concentrated in NE. Moreover, the ratio of PLB levels to SERCA levels was greater in NE than in SR. The increased levels of PLB in NE were a consistent finding using a range of antibodies, tissue samples, and species. To address a possible role in affecting Ca2+ handling, we used Fluo-4 based con focal Ca2+ imaging, with scan-lines across cytosol and nuclei, and evaluated the effects of PLB on cytosolic and nCa(2+) uptake and release in mouse CMs. In intact CMs, isoproterenol increased amplitude and decreased the decay time of Ca2+ transients not only in cytosol but also in nuclear regions. In saponin-permeabilized mouse CMs ([Ca2+]; = 400 nM), we measured spontaneous Ca2+ waves after specific reversal of PLB activity by addition of the Fab fragment of an anti-PLB monoclonal antibody (100 mu g/ml).This highly selective immunological reagent enhanced Ca2+ uptake (faster decay times) and Ca2+ release (greater intensity) in both cytosol and across the nuclear regions. Conclusions: Besides SR, PLB is concentrated in NE of CMs, and may be involved in modulation of nCa(2+) dynamics. (C) 2016 Elsevier Ltd. All rights reserved.
Phospholamban regulates nuclear Ca2+ stores and inositol 1,4,5-trisphosphate mediated nuclear Ca2+ cycling in cardiomyocytes
(2018-10-01)
Chen, Mu
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Xu, Dongzhu
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Wu, Adonis Z.
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Kranias, Evangelia
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Lin, Shien-Fong
Aims: Phospholamban (PLB) is the key regulator of the cardiac Ca(2+ )pump (SERCA2a)-mediated sarcoplasmic reticulum Ca2+ stores. We recently reported that PLB is highly concentrated in the nuclear envelope (NE) from where it can modulate perinuclear Ca2+ handling of the cardiomyocytes (CMs). Since inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) mediates nuclear Ca2+ release, we examined whether the nuclear pool of PLB regulates IP3-induced nuclear Ca2+ handling. Methods and results: Fluo-4 based confocal Ca2+ imaging was performed to measure Ca2+ dynamics across both nucleus and cytosol in saponin-permeabilized CMs isolated from wild-type (WT) or PLB-knockout (PLB-KO) mice. At diastolic intracellular Ca2+ ([Ca2+](i) = 100 nM), the Fab fragment of the monoclonal PLB antibody (anti-PLB Fab) facilitated the formation and increased the length of spontaneous Ca2+ waves (SCWs) originating from the nuclear region in CMs from WT but not from PLB-KO mice. We next examined nuclear Ca2+ activities at basal condition and after sequential addition of IP3, anti-PLB Fab, and the IP3R inhibitor 2-aminoethoxydiphenyl borate (2-APB) at a series of [Ca2+](i). In WT mice, at 10 nM [Ca2+](i) where ryanodine receptor (RyR2) based spontaneous Ca2+ sparks rarely occurred, IP(3 )increased fluorescence amplitude (F/F-0) of overall nuclear region to 1.19 +/- 0.02. Subsequent addition of anti-PLB Fab significantly decreased F/F-0 to 1.09 +/- 0.02. At 50 nM [Ca2+](i), anti-PLB Fab not only decreased the overall nuclear F/F-0 previously elevated by IP3, but also increased the amplitude and duration of spark-like nuclear Ca2+ release events. These nuclear Ca2+ releases were blocked by 2-APB. At 100 nM [Ca2+](i), IP3 induced short SCWs originating from nucleus. Anti-PLB Fab transformed those short waves into long SCWs with propagation from the nucleus into the cytosol. In contrast, neither nuclear nor cytosolic Ca2+ dynamics was affected by anti-PLB Fab in CMs from PLB-KO mice in all these conditions. Furthermore, in WT CMs pretreated with RyR2 blocker tetracaine, IP3 and anti-PLB Fab still increased the magnitude of nuclear Ca2+ release but failed to regenerate SCWs. Finally, anti-PLB Fab increased low Ca2+ affinity mag-fluo 4 fluorescence intensity in the lumen of NE of nuclei isolated from WT but not in PLB-KO mice. Conclusion: PLB regulates nuclear Ca(2+ )handling. By increasing Ca2+ uptake into lumen of the NE and perhaps other perinuclear membranes, the acute reversal of PLB inhibition decreases global Ca2+ concentration at rest in the nucleoplasm, and increases Ca2+ release into the nucleus, through mechanisms involving IP3R and RyR2 in the vicinity.
Real-Time 3D Depth Generation for Stereoscopic Video Applications with Thread-Level Superscalar-Pipeline Parallelization
(2013-07-01)
Jian, Guo-An
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Chien, Cheng-An
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Chen, Peng-Sheng
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Guo, Jiun-In
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電子工程學系及電子研究所
We propose a low-complexity algorithm for stereoscopic video applications that generates a high-quality 3D image depth map from a single 2D image. Based on their characteristics, 2D images are classified into one of three categories before being processed by the proposed low-complexity algorithm to generate corresponding depth maps. We also extend the 3D depth algorithm to construct a parallel 3D video system. A thread-level superscalar-pipelining approach is developed to parallelize the 3D video system. Experimental results for HD1080 resolution images demonstrate that the algorithm can generate high-quality depth maps with an average reduction in the computational complexity of 98.2 % compared with a conventional algorithm. The parallel 3D video system can achieve a processing speed of 63.66 fps for HD720 resolution video.