Ming-Hsien Chiang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Ming-Hsien Chiang has a total of 73 co-authors. Here are the top co-authors by number of shared publications:
- Yung-Hsiang Chen
Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung 404, Taiwan
5 shared publications - Jen-Jie Chieh
Institute of Electro-Optical Engineering, National Taiwan Normal University, Taipei 116, Taiwan
4 shared publications Chen-Wei Liu
Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan
3 shared publicationsChan-Jung Liang
Lipid Science and Aging Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan; Center for Lipid Biosciences, Kaohsiung Medical University Hospital, Taiwan
2 shared publications- Chiang-Wen Lee
Department of Respiratory Care and Chronic Diseases and Health Promotion Research Center Chang Gung University of Science and Technology Chiayi Taiwan
2 shared publications Hsin-Ching Sung
Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan; Department of Anatomy, College of Medicine, Chang Gung University, Taoyuan, Taiwan
2 shared publications
Latest Publications
- Open Access
- 27 September 2022
- Published by MDPI AG in Micromachines
- Vol. 13 (10) , 1605
Synthesised Conductive/Magnetic Composite Particles for Magnetic Ablations of Tumours
Ablation is a clinical cancer treatment, but some demands are still unsatisfied, such as electromagnetic interferences amongst multiple ablation needles during large tumour treatments. This work proposes a physical synthesis for composite particles of biocompatible iron oxide particles and liquid metal gallium (Ga) with different alternative-current (AC)-magnetic-field-induced heat mechanisms of magnetic particle hyperthermia and superior resistance heat. By some imaging, X-ray diffraction, and vibrating sample magnetometer, utilised composite particles were clearly identified as the cluster of few iron oxides using the small weight ratio of high-viscosity liquid metal Ga as conjugation materials without surfactants for physical targeting of limited fluidity. Hence, well penetration inside the tissue and the promotion rate of heat generation to fit the ablation requirement of at least 60 °C in a few seconds are achieved. For the injection and the post-injection magnetic ablations, the volume variation ratios of mice dorsal tumours on Day 12 were expressed at around one without tumour growth. Its future powerful potentiality is expected through a percutaneous injection.
- 27 September 2022
- Published by MDPI AG in Micromachines
- Vol. 13 (10) , 1605
Open AccessSynthesised Conductive/Magnetic Composite Particles for Magnetic Ablations of Tumours
Ablation is a clinical cancer treatment, but some demands are still unsatisfied, such as electromagnetic interferences amongst multiple ablation needles during large tumour treatments. This work proposes a physical synthesis for composite particles of biocompatible iron oxide particles and liquid metal gallium (Ga) with different alternative-current (AC)-magnetic-field-induced heat mechanisms of magnetic particle hyperthermia and superior resistance heat. By some imaging, X-ray diffraction, and vibrating sample magnetometer, utilised composite particles were clearly identified as the cluster of few iron oxides using the small weight ratio of high-viscosity liquid metal Ga as conjugation materials without surfactants for physical targeting of limited fluidity. Hence, well penetration inside the tissue and the promotion rate of heat generation to fit the ablation requirement of at least 60 °C in a few seconds are achieved. For the injection and the post-injection magnetic ablations, the volume variation ratios of mice dorsal tumours on Day 12 were expressed at around one without tumour growth. Its future powerful potentiality is expected through a percutaneous injection.
- Open Access
- 30 September 2021
- Published by MDPI AG in Biosensors
- Vol. 11 (10) , 363
An Optical Smartphone-Based Inspection Platform for Identification of Diseased Orchids
Infections of orchids by the Odontoglossum ringspot virus or Cymbidium mosaic virus cause orchid disfiguration and are a substantial source of economic loss for orchid farms. Although immunoassays can identify these infections, immunoassays are expensive, time consuming, and labor consuming and limited to sampling-based testing methods. This study proposes a noncontact inspection platform that uses a spectrometer and Android smartphone. When orchid leaves are illuminated with a handheld optical probe, the Android app based on the Internet of Things and artificial intelligence can display the measured florescence spectrum and determine the infection status within 3 s by using an algorithm hosted on a remote server. The algorithm was trained on optical data and the results of polymerase chain reaction assays. The testing accuracy of the algorithm was 89%. The area under the receiver operating characteristic curve was 91%; thus, the platform with the algorithm was accurate and convenient for infection screening in orchids.
- 30 September 2021
- Published by MDPI AG in Biosensors
- Vol. 11 (10) , 363
Open AccessAn Optical Smartphone-Based Inspection Platform for Identification of Diseased Orchids
Infections of orchids by the Odontoglossum ringspot virus or Cymbidium mosaic virus cause orchid disfiguration and are a substantial source of economic loss for orchid farms. Although immunoassays can identify these infections, immunoassays are expensive, time consuming, and labor consuming and limited to sampling-based testing methods. This study proposes a noncontact inspection platform that uses a spectrometer and Android smartphone. When orchid leaves are illuminated with a handheld optical probe, the Android app based on the Internet of Things and artificial intelligence can display the measured florescence spectrum and determine the infection status within 3 s by using an algorithm hosted on a remote server. The algorithm was trained on optical data and the results of polymerase chain reaction assays. The testing accuracy of the algorithm was 89%. The area under the receiver operating characteristic curve was 91%; thus, the platform with the algorithm was accurate and convenient for infection screening in orchids.
- 28 January 2020
- Published by Wiley in Journal of Cellular Physiology
- Vol. 235 (9) , 6085-6102
miR‐26a attenuates cardiac apoptosis and fibrosis by targeting ataxia–telangiectasia mutated in myocardial infarction
Apoptosis and fibrosis play a vital role in myocardial infarction (MI) induced tissue injury. Although microRNAs have been the focus of many studies on cardiac apoptosis and fibrosis in MI, the detailed effects of miR‐26a is needed to further understood. The present study demonstrated that miR‐26a was downregulated in ST‐elevation MI (STEMI) patients and oxygen‐glucose deprivation (OGD)‐treated H9c2 cells. Downregulation of miR‐26a was closely correlated with the increased expression of creatine kinase, creatine kinase‐MB and troponin I in STEMI patients. Further analysis identified that ataxia–telangiectasia mutated (ATM) was a target gene for miR‐26a based on a bioinformatics analysis. miR‐26a overexpression effectively reduced ATM expression, apoptosis, and apoptosis‐related proteins in OGD‐treated H9c2 cells. In a mouse model of MI, the expression of miR‐26a was significantly decreased in the infarct zone of the heart, whereas apoptosis and ATM expression were increased. miR‐26a overexpression effectively reduced ATM expression and cardiac apoptosis at Day 1 after MI. Furthermore, we demonstrated that overexpression of miR‐26a improved cardiac function and reduced cardiac fibrosis by the reduced expression of collagen type I and connective tissue growth factor (CTGF) in mice at Day 14 after MI. Overexpression of miR‐26a or ATM knockdown decreased collagen I and CTGF expression in cultured OGD‐treated cardiomyocytes. Taken together, these data demonstrate a prominent role for miR‐26a in linking ATM expression to ischemia‐induced apoptosis and fibrosis, key features of MI progression. miR‐26a reduced MI development by affecting ATM expression and could be targeted in the treatment of MI.
- 28 January 2020
- Published by Wiley in Journal of Cellular Physiology
- Vol. 235 (9) , 6085-6102
miR‐26a attenuates cardiac apoptosis and fibrosis by targeting ataxia–telangiectasia mutated in myocardial infarction
Apoptosis and fibrosis play a vital role in myocardial infarction (MI) induced tissue injury. Although microRNAs have been the focus of many studies on cardiac apoptosis and fibrosis in MI, the detailed effects of miR‐26a is needed to further understood. The present study demonstrated that miR‐26a was downregulated in ST‐elevation MI (STEMI) patients and oxygen‐glucose deprivation (OGD)‐treated H9c2 cells. Downregulation of miR‐26a was closely correlated with the increased expression of creatine kinase, creatine kinase‐MB and troponin I in STEMI patients. Further analysis identified that ataxia–telangiectasia mutated (ATM) was a target gene for miR‐26a based on a bioinformatics analysis. miR‐26a overexpression effectively reduced ATM expression, apoptosis, and apoptosis‐related proteins in OGD‐treated H9c2 cells. In a mouse model of MI, the expression of miR‐26a was significantly decreased in the infarct zone of the heart, whereas apoptosis and ATM expression were increased. miR‐26a overexpression effectively reduced ATM expression and cardiac apoptosis at Day 1 after MI. Furthermore, we demonstrated that overexpression of miR‐26a improved cardiac function and reduced cardiac fibrosis by the reduced expression of collagen type I and connective tissue growth factor (CTGF) in mice at Day 14 after MI. Overexpression of miR‐26a or ATM knockdown decreased collagen I and CTGF expression in cultured OGD‐treated cardiomyocytes. Taken together, these data demonstrate a prominent role for miR‐26a in linking ATM expression to ischemia‐induced apoptosis and fibrosis, key features of MI progression. miR‐26a reduced MI development by affecting ATM expression and could be targeted in the treatment of MI.
- Open Access
- 1 August 2019
- Published by Elsevier in EBioMedicine
- Vol. 46, 236-247
MicroRNA let-7-TGFBR3 signalling regulates cardiomyocyte apoptosis after infarction
- 1 August 2019
- Published by Elsevier in EBioMedicine
- Vol. 46, 236-247
Open AccessMicroRNA let-7-TGFBR3 signalling regulates cardiomyocyte apoptosis after infarction
- Open Access
Eight-Channel AC Magnetosusceptometer of Magnetic Nanoparticles for High-Throughput and Ultra-High-Sensitivity Immunoassay
An alternating-current magnetosusceptometer of antibody-functionalized magnetic nanoparticles (MNPs) was developed for immunomagnetic reduction (IMR). A high-sensitivity, high-critical-temperature superconducting quantum interference device was used in the magnetosusceptometer. Minute levels of biomarkers of early-stage neurodegeneration diseases were detectable in serum, but measuring each biomarker required approximately 4 h. Hence, an eight-channel platform was developed in this study to fit minimal screening requirements for Alzheimer’s disease. Two consistent results were measured for three biomarkers, namely Aβ40, Aβ42, and tau protein, per human specimen. This paper presents the instrument configuration as well as critical characteristics, such as the low noise level variations among channels, a high signal-to-noise ratio, and the coefficient of variation for the biomarkers’ IMR values. The instrument’s ultrahigh sensitivity levels for the three biomarkers and the substantially shorter total measurement time in comparison with the previous single- and four-channels platforms were also demonstrated in this study. Thus, the eight-channel instrument may serve as a powerful tool for clinical high-throughput screening of Alzheimer’s disease.
Open AccessEight-Channel AC Magnetosusceptometer of Magnetic Nanoparticles for High-Throughput and Ultra-High-Sensitivity Immunoassay
An alternating-current magnetosusceptometer of antibody-functionalized magnetic nanoparticles (MNPs) was developed for immunomagnetic reduction (IMR). A high-sensitivity, high-critical-temperature superconducting quantum interference device was used in the magnetosusceptometer. Minute levels of biomarkers of early-stage neurodegeneration diseases were detectable in serum, but measuring each biomarker required approximately 4 h. Hence, an eight-channel platform was developed in this study to fit minimal screening requirements for Alzheimer’s disease. Two consistent results were measured for three biomarkers, namely Aβ40, Aβ42, and tau protein, per human specimen. This paper presents the instrument configuration as well as critical characteristics, such as the low noise level variations among channels, a high signal-to-noise ratio, and the coefficient of variation for the biomarkers’ IMR values. The instrument’s ultrahigh sensitivity levels for the three biomarkers and the substantially shorter total measurement time in comparison with the previous single- and four-channels platforms were also demonstrated in this study. Thus, the eight-channel instrument may serve as a powerful tool for clinical high-throughput screening of Alzheimer’s disease.
- Open Access
- 14 November 2017
- Published by Frontiers Media SA in Frontiers in Pharmacology
- Vol. 8, 819
Aliskiren Improves Ischemia- and Oxygen Glucose Deprivation-Induced Cardiac Injury through Activation of Autophagy and AMP-Activated Protein Kinase
Aliskiren is a direct renin inhibitor that has been effective in anti-hypertension. We investigated whether aliskiren could improve the ischemia-induced cardiac injury and whether the autophagy was involved in this effect. A myocardial infarction (MI) model was created by the ligation of the left anterior coronary artery in C57J/BL6 mice. They were treated for 1, 3, 7, and 14 days with vehicle or aliskiren (25 mg/kg/day via subcutaneous injection). In vivo, the MI mice exhibited worse cardiac function by echocardiographic assessment and showed larger myocardial scarring by light microscopy, whereas aliskiren treatment reversed these effects, which were also associated with the changes in caspase-3 and Bcl-2 expression as well as in the number of apoptotic cells. Aliskiren increased autophagy, as demonstrated by LC3B-II expression and transmission electron microscopy. Furthermore, H9c2 cardiomyocytes were employed as an in vitro model to examine the effects of aliskiren on apoptosis and autophagy under oxygen glucose deprivation (OGD)-induced injury. Aliskiren significantly increased cell viability in a dose-dependent manner. The beneficial effects of aliskiren were associated with decreased apoptosis and mitochondrial membrane potential as well as increased autophagy via increased autophagosome formation. We also found that aliskiren-induced cardiomyocyte survival occurred via AMP-activated protein kinase (AMPK)-dependent autophagy. Taken together, these results indicated that aliskiren increased cardiomyocyte survival through increased autophagosomal formation and decreased apoptosis and necrosis via modulating AMPK expression. AMPK-dependent autophagy may represent a novel mechanism for aliskiren in ischemic cardiac disease therapy.
- 14 November 2017
- Published by Frontiers Media SA in Frontiers in Pharmacology
- Vol. 8, 819
Open AccessAliskiren Improves Ischemia- and Oxygen Glucose Deprivation-Induced Cardiac Injury through Activation of Autophagy and AMP-Activated Protein Kinase
Aliskiren is a direct renin inhibitor that has been effective in anti-hypertension. We investigated whether aliskiren could improve the ischemia-induced cardiac injury and whether the autophagy was involved in this effect. A myocardial infarction (MI) model was created by the ligation of the left anterior coronary artery in C57J/BL6 mice. They were treated for 1, 3, 7, and 14 days with vehicle or aliskiren (25 mg/kg/day via subcutaneous injection). In vivo, the MI mice exhibited worse cardiac function by echocardiographic assessment and showed larger myocardial scarring by light microscopy, whereas aliskiren treatment reversed these effects, which were also associated with the changes in caspase-3 and Bcl-2 expression as well as in the number of apoptotic cells. Aliskiren increased autophagy, as demonstrated by LC3B-II expression and transmission electron microscopy. Furthermore, H9c2 cardiomyocytes were employed as an in vitro model to examine the effects of aliskiren on apoptosis and autophagy under oxygen glucose deprivation (OGD)-induced injury. Aliskiren significantly increased cell viability in a dose-dependent manner. The beneficial effects of aliskiren were associated with decreased apoptosis and mitochondrial membrane potential as well as increased autophagy via increased autophagosome formation. We also found that aliskiren-induced cardiomyocyte survival occurred via AMP-activated protein kinase (AMPK)-dependent autophagy. Taken together, these results indicated that aliskiren increased cardiomyocyte survival through increased autophagosomal formation and decreased apoptosis and necrosis via modulating AMPK expression. AMPK-dependent autophagy may represent a novel mechanism for aliskiren in ischemic cardiac disease therapy.
- Open Access
- 24 March 2017
- Published by Springer Nature in Scientific Reports
- Vol. 7 (1) , srep44689
Resveratrol attenuates ICAM-1 expression and monocyte adhesiveness to TNF-α-treated endothelial cells: evidence for an anti-inflammatory cascade mediated by the miR-221/222/AMPK/p38/NF-κB pathway
Resveratrol, an edible polyphenolic phytoalexin, improves endothelial dysfunction and attenuates inflammation. However, the mechanisms have not been thoroughly elucidated. Therefore, we investigated the molecular basis of the effects of resveratrol on TNF-α-induced ICAM-1 expression in HUVECs. The resveratrol treatment significantly attenuated the TNF-α-induced ICAM-1 expression. The inhibition of p38 phosphorylation mediated the reduction in ICAM-1 expression caused by resveratrol. Resveratrol also decreased TNF-α-induced IκB phosphorylation and the phosphorylation, acetylation, and translocation of NF-κB p65. Moreover, resveratrol induced the AMPK phosphorylation and the SIRT1 expression in TNF-α-treated HUVECs. Furthermore, TNF-α significantly suppressed miR-221/-222 expression, which was reversed by resveratrol. miR-221/-222 overexpression decreased p38/NF-κB and ICAM-1 expression, which resulted in reduced monocyte adhesion to TNF-α-treated ECs. In a mouse model of acute TNF-α-induced inflammation, resveratrol effectively attenuated ICAM-1 expression in the aortic ECs of TNF-α-treated wild-type mice. These beneficial effects of resveratrol were lost in miR-221/222 knockout mice. Our data showed that resveratrol counteracted the TNF-α-mediated reduction in miR-221/222 expression and decreased the TNF-α-induced activation of p38 MAPK and NF-κB, thereby suppressing ICAM-1 expression and monocyte adhesion. Collectively, our results show that resveratrol attenuates endothelial inflammation by reducing ICAM-1 expression and that the protective effect was mediated partly through the miR-221/222/AMPK/p38/NF-κB pathway.
- 24 March 2017
- Published by Springer Nature in Scientific Reports
- Vol. 7 (1) , srep44689
Open AccessResveratrol attenuates ICAM-1 expression and monocyte adhesiveness to TNF-α-treated endothelial cells: evidence for an anti-inflammatory cascade mediated by the miR-221/222/AMPK/p38/NF-κB pathway
Resveratrol, an edible polyphenolic phytoalexin, improves endothelial dysfunction and attenuates inflammation. However, the mechanisms have not been thoroughly elucidated. Therefore, we investigated the molecular basis of the effects of resveratrol on TNF-α-induced ICAM-1 expression in HUVECs. The resveratrol treatment significantly attenuated the TNF-α-induced ICAM-1 expression. The inhibition of p38 phosphorylation mediated the reduction in ICAM-1 expression caused by resveratrol. Resveratrol also decreased TNF-α-induced IκB phosphorylation and the phosphorylation, acetylation, and translocation of NF-κB p65. Moreover, resveratrol induced the AMPK phosphorylation and the SIRT1 expression in TNF-α-treated HUVECs. Furthermore, TNF-α significantly suppressed miR-221/-222 expression, which was reversed by resveratrol. miR-221/-222 overexpression decreased p38/NF-κB and ICAM-1 expression, which resulted in reduced monocyte adhesion to TNF-α-treated ECs. In a mouse model of acute TNF-α-induced inflammation, resveratrol effectively attenuated ICAM-1 expression in the aortic ECs of TNF-α-treated wild-type mice. These beneficial effects of resveratrol were lost in miR-221/222 knockout mice. Our data showed that resveratrol counteracted the TNF-α-mediated reduction in miR-221/222 expression and decreased the TNF-α-induced activation of p38 MAPK and NF-κB, thereby suppressing ICAM-1 expression and monocyte adhesion. Collectively, our results show that resveratrol attenuates endothelial inflammation by reducing ICAM-1 expression and that the protective effect was mediated partly through the miR-221/222/AMPK/p38/NF-κB pathway.
- Open Access
- 3 July 2015
- Published by Springer Nature in Discover Nano
- Vol. 10 (1) , 1-7
Assaying Carcinoembryonic Antigens by Normalized Saturation Magnetization
Biofunctionalized magnetic nanoparticles (BMNs) that provide unique advantages have been extensively used to develop immunoassay methods. However, these developed magnetic methods have been used only for specific immunoassays and not in studies of magnetic characteristics of materials. In this study, a common vibration sample magnetometer (VSM) was used for the measurement of the hysteresis loop for different carcinoembryonic antigens (CEA) concentrations (Φ CEA) based on the synthesized BMNs with anti-CEA coating. Additionally, magnetic parameters such as magnetization (M), remanent magnetization (M R), saturation magnetization (M S), and normalized parameters (ΔM R/M R and ΔM S/M S) were studied. Here, ΔM R and ΔM s were defined as the difference between any ΦCEA and zero Φ CEA. The parameters M, ΔM R, and ΔM S increased with Φ CEA, and ΔM S showed the largest increase. Magnetic clusters produced by the conjugation of the BMNs to CEAs showed a ΔM S greater than that of BMNs. Furthermore, the relationship between ΔM S/M S and Φ CEA could be described by a characteristic logistic function, which was appropriate for assaying the amount of CEAs. This analytic ΔM S/M S and the BMNs used in general magnetic immunoassays can be used for upgrading the functions of the VSM and for studying the magnetic characteristics of materials.
- 3 July 2015
- Published by Springer Nature in Discover Nano
- Vol. 10 (1) , 1-7
Open AccessAssaying Carcinoembryonic Antigens by Normalized Saturation Magnetization
Biofunctionalized magnetic nanoparticles (BMNs) that provide unique advantages have been extensively used to develop immunoassay methods. However, these developed magnetic methods have been used only for specific immunoassays and not in studies of magnetic characteristics of materials. In this study, a common vibration sample magnetometer (VSM) was used for the measurement of the hysteresis loop for different carcinoembryonic antigens (CEA) concentrations (Φ CEA) based on the synthesized BMNs with anti-CEA coating. Additionally, magnetic parameters such as magnetization (M), remanent magnetization (M R), saturation magnetization (M S), and normalized parameters (ΔM R/M R and ΔM S/M S) were studied. Here, ΔM R and ΔM s were defined as the difference between any ΦCEA and zero Φ CEA. The parameters M, ΔM R, and ΔM S increased with Φ CEA, and ΔM S showed the largest increase. Magnetic clusters produced by the conjugation of the BMNs to CEAs showed a ΔM S greater than that of BMNs. Furthermore, the relationship between ΔM S/M S and Φ CEA could be described by a characteristic logistic function, which was appropriate for assaying the amount of CEAs. This analytic ΔM S/M S and the BMNs used in general magnetic immunoassays can be used for upgrading the functions of the VSM and for studying the magnetic characteristics of materials.