Browsing by Author "Huang, Po-Hsun"

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A NOVEL INDEX OF PHOTOPLETHYSMOGRAPHY BY USING INSTANTANEOUS PULSE RATE VARIABILITY DURING NON-STATIONARY CONDITION
(2015)
Lin, Pei-Chen
;
Huang, Po-Hsun
;
Chang, Chia-Chi
;
Hsu, Hung-Yi
;
Hsiao, Tzu-Chien
Heart rate variability (HRV) and pulse rate variability (PRV) have been widely used as an automatic nervous system (ANS) activities observation. Based on the timescale limitation of heart beat (for HRV) and pulse waveform (for PRV), one method of instantaneous pulse rate variability (iPRV) with photoplethysmography (PPG) had been proposed as a HRV and PRV surrogate during non-stationary condition in frequency domain. In this paper, the examination in time-domain PPG during passive leg raise (PLR) trial was studied. The 24 subjects pre-experiment resulted that iPRV and HRV are positive correlation (r-value = 0.680 +/- 0.099 in baseline; r-value = 0.688 +/- 0.096 in PLR). Furthermore, the iPRV containing much complex intrinsic components on higher frequency bands provides more intrinsic cardiovascular information for further assessment. This proposed examination in time-domain PPG is the possible leading way to more useful indicator for healthcare application.
MicroRNA-92a Mediates Endothelial Dysfunction in CKD
(2017-11-01)
Shang, Fenqing
;
Wang, Shen-Chih
;
Hsu, Chien-Yi
;
Miao, Yifei
;
Martin, Marcy
CKD is an independent risk factor for cardiovascular disease (CVD). The accumulation of uremic toxins in CKD induces oxidative stress and endothelial dysfunction. MicroRNA-92a (miR-92a) is induced by oxidative stress in endothelial cells (ECs) and involved in angiogenesis and atherosclerosis. We investigated a role for oxidative stress responsive miR-92a in CKD. Our study of patients at three clinical sites showed increased serum miR-92a level with decreased kidney function. In cultured ECs, human CKD serum or uremic toxins (such as indoxyl sulfate), compared with non-CKD serum, induced the levels of miR-92a and suppressed the expression of miR-92a targets, including key endothelial-protective molecules. The antioxidant N-acetylcysteine inhibited these vasculopathic properties. In rats, adenine-induced CKD associated with increased levels of miR-92a in aortas, serum, and CD144(+) endothelial microparticles. Furthermore, CD144(+) microparticles from human uremic serum contained more miR-92a than those from control serum. Additional analysis showed a positive correlation between serum levels of miR-92a and indoxyl sulfate in a cohort of patients with ESRD undergoing hemodialysis. Collectively, our findings suggest that the uremic toxins accumulated in CKD can upregulate miR-92a in ECs, which impairs EC function and predisposes patients to CVD.
Oxidative Stress Activates Endothelial Innate Immunity via Sterol Regulatory Element Binding Protein 2 (SREBP2) Transactivation of MicroRNA-92a
(2015-03-03)
Chen, Zhen
;
Wen, Liang
;
Martin, Marcy
;
Hsu, Chien-Yi
;
Fang, Longhou
Background-Oxidative stress activates endothelial innate immunity and disrupts endothelial functions, including endothelial nitric oxide synthase-derived nitric oxide bioavailability. Here, we postulated that oxidative stress induces sterol regulatory element-binding protein 2 (SREBP2) and microRNA-92a (miR-92a), which in turn activate endothelial innate immune response, leading to dysfunctional endothelium. Methods and Results-Using cultured endothelial cells challenged by diverse oxidative stresses, hypercholesterolemic zebrafish, and angiotensin II-infused or aged mice, we demonstrated that SREBP2 transactivation of microRNA-92a (miR-92a) is oxidative stress inducible. The SREBP2-induced miR-92a targets key molecules in endothelial homeostasis, including sirtuin 1, Kruppel-like factor 2, and Kruppel-like factor 4, leading to NOD-like receptor family pyrin domain-containing 3 inflammasome activation and endothelial nitric oxide synthase inhibition. In endothelial cell-specific SREBP2 transgenic mice, locked nucleic acid-modified antisense miR-92a attenuates inflammasome, improves vasodilation, and ameliorates angiotensin II-induced and aging-related atherogenesis. In patients with coronary artery disease, the level of circulating miR-92a is inversely correlated with endothelial cell-dependent, flow-mediated vasodilation and is positively correlated with serum level of interleukin-1 beta. Conclusions-Our findings suggest that SREBP2-miR-92a-inflammasome exacerbates endothelial dysfunction during oxidative stress. Identification of this mechanism may help in the diagnosis or treatment of disorders associated with oxidative stress, innate immune activation, and endothelial dysfunction.
Pleiotropic Effects of Myocardial MMP-9 Inhibition to Prevent Ventricular Arrhythmia
(2016-12-14)
Weng, Ching-Hui
;
Chung, Fa-Po
;
Chen, Yao-Chang
;
Lin, Shien-Fong
;
Huang, Po-Hsun
Observational studies have established a strong association between matrix metalloproteinase-9 (MMP-9) and ventricular arrhythmia. However, whether MMP-9 has a causal link to ventricular arrhythmia, as well as the underlying mechanism, remains unclear. Here, we investigated the mechanistic involvement of myocardial MMP-9 in the pathophysiology of ventricular arrhythmia. Increased levels of myocardial MMP-9 are linked to ventricular arrhythmia attacks after angiotensin II (Ang II) treatment. MMP-9-deficient mice were protected from ventricular arrhythmia. Increased expressions of protein kinase A (PKA) and ryanodine receptor phosphorylation at serine 2808 (pS2808) were correlated with inducible ventricular arrhythmia. MMP-9 deficiency consistently prevented PKA and pS2808 increases after Ang II treatment and reduced ventricular arrhythmia. Calcium dynamics were examined via confocal imaging in isolated murine cardiomyocytes. MMP-9 inhibition prevents calcium leakage from the sarcoplasmic reticulum and reduces arrhythmia-like irregular calcium transients via protein kinase A and ryanodine receptor phosphorylation. Human induced pluripotent stem cell-derived cardiomyocytes similarly show that MMP-9 inhibition prevents abnormal calcium leakage. Myocardial MMP-9 inhibition prevents ventricular arrhythmia through pleiotropic effects, including the modulation of calcium homeostasis and reduced calcium leakage.
Towards instantaneous phase difference on the COPD pre-discrimination
(2018-01-01)
Huang, Po-Hsun
;
Yeh, Chun-Fu
;
Luo, Yi-Fei
;
Hsiao, Tzu-Chien
;
分子醫學與生物工程研究所
Chronic Obstructive Pulmonary Disease (COPD) is a common lung disease in Taiwan. People with COPD usually accompany dyspnea. When taking a spirometry test, they feel tired with measuring the tidal volume (VT). Some research estimated the VT by using respiratory inductive plethysmography (RIP), however, the movement between thoracic wall (TWM) and abdominal wall (AWM) might be distinct due to the different symptoms of COPD. Instantaneous phase difference (IPD) method was proposed for synchrony estimation between TWM and AWM continuity for healthy people. In this study, 26 subjects with COPD were recruited. The IPD was applied as a pre-discrimination of COPD symptoms and the prediction model for each type was further constructed. The error between real VT value and prediction VT value is calculated for validation. The results showed that three classes are classified and the errors are 20% 34% and 25% for each class in comparison with 36% for all. Based on this achievement, the IPD would be a useful index for assessing the progressive condition of COPD patient.