Using Root Cause Analysis for the Reduction of Fall Accidents

Chang Ya-Hui,Chang Huei-Lan 한국간호과학회 2015 한국간호과학회 학술대회 Vol.2015 No.10

Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis

Hsieh, Wei-Chung,Hsu, Pei-Chen,Liao, Ya-Fan,Young, Shu-Ting,Wang, Zeng-Wei,Lin, Chih-Li,Tsay, Gregory J.,Lee, Huei,Hung, Hui-Chih,Liu, Guang-Yaw Korean Society for Molecular and Cellular Biology 2010 Molecules and cells Vol.30 No.4

Ornithine decarboxylase (ODC), the key enzyme of polyamine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC prevents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/endoplasmic reticulum (ER) $Ca^{2+}$ ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpression of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspse-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homologous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC preserved the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and downstream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-mediated apoptotic pathway, induced by TG. Finally, overexpression of ODC maintains the protein and mRNA expression of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.

Astaxanthine Secured Apoptotic Death of PC12 Cells Induced by β-Amyloid Peptide 25–35: Its Molecular Action Targets

Chi-Huang Chang,Chung-Yin Chen,Jueen-Ya Chiou,Robert Y. Peng,Chiung-Huei Peng 한국식품영양과학회 2010 Journal of medicinal food Vol.13 No.3

Astaxanthine (ASTx) is a novel carotenoid nutraceutical occurring in many crustaceans and red yeasts. It has potent antioxidant, photoprotective, hepatodetoxicant, and anti-inflammatory activities. Documented effect of ASTx on treatment of neurodegenerative disease is still lacking. We used the β-amyloid peptide (Aβ) 25–35-treated PC12 model to investigate the neuron-protective effect of ASTx. The parameters examined included cell viability, caspase activation, and various apoptotic biomarkers that play their critical roles in the transduction pathways independently or synergistically. Results indicated that Aβ25–35 at 30μM suppressed cell viability by 55%, whereas ASTx was totally nontoxic below a dose of 5.00μM. ASTx at 0.1μM protected PC12 cells from damaging effects of Aβ25–35 in several ways: (1) by securing the cell viability; (2) by partially down-regulating the activation of caspase 3; (3) by inhibiting the expression of Bax; (4) by completely eliminating the elevation of interleukin-1β and tumor necrosis factor-α; (5) by inhibiting the nuclear translocation of nuclear factor κB; (6) by completely suppressing the phosphorylation of p38 mitogen-activated protein kinase; (7) by completely abolishing the calcium ion influx to effectively maintain calcium homeostasis; and (8) by suppressing the majority (about 75%) of reactive oxygen species production. Conclusively, ASTx may have merit to be used as a very potential neuron protectant and an anti–early-stage Alzheimer's disease adjuvant therapy.

Controlled Release of Clenbuterol from a Hydroxyapatite Carrier for the Treatment of Alzheimer’s Disease

Yi-Wen Lin,Chih-Hsiang Fang,Ya-Jyun Liang,Ching-Yun Yang,Wei-Ting Kuo,Feng-Huei Lin 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00

Background Alzheimer’s disease is a neurodegenerative disorder, and Aβ aggregation is considered to be the central process implicated in its pathogenesis. Current treatments are faced by challenges such as serious side effects and reduced drug bioavailability. In this study, we developed a drug delivery system for intramuscular injection that uses cellular activity to achieve constant and long-term drug release. Methods Synthesized mesoporous hydroxyapatite (SHAP) was prepared via co-precipitation, and hydrophobic surface modification using stearic acid was then used to load clenbuterol by physical absorption, thus creating the drug delivery system. Clenbuterol release was achieved through cellular activity, with macrophage uptake triggering lysosome/endosome disruption, cytoplasmic release, extracellular exocytosis, and subsequent systemic circulation. Results We found that clenbuterol-loaded SHAP enabled sustained release for more than 2 weeks and effectively modulated inflammation, reduced Aβ oligomer-induced toxicity, and prevented Aβ aggregation. Conclusions Our findings suggest that treatment with clenbuterol loaded in this SHAP delivery system could be a promising strategy for treating Alzheimer’s disease.

Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis

Wei-Chung Hsieh,Pei-Chen Hsu,Ya-Fan Liao,Shu-Ting Young,Zeng-Wei Wang,Chih-Li Lin,Gregory J. Tsay,Huei Lee,Hui-Chih Hung,Guang-Yaw Liu 한국분자세포생물학회 2010 Molecules and cells Vol.30 No.4

Ornithine decarboxylase (ODC), the key enzyme of poly-amine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC pre-vents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/en-doplasmic reticulum (ER) Ca2+ ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpres-sion of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspse-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homolo-gous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC pre-served the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and downstream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-medi-ated apoptotic pathway, induced by TG. Finally, overex-pression of ODC maintains the protein and mRNA expres-sion of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.

Cilostazol ameliorates diabetic nephropathy by inhibiting highglucose-induced apoptosis

Chien-Wen Chian,Yung-Shu Lee,Yi-Ju Lee,Ya-Hui Chen,Chi-Ping Wang,Wen-Chin Lee,Huei-Jane Lee 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.5

Diabetic nephropathy (DN) is a hyperglycemia-induced progressive development of renal insufficiency. Excessive glucose can increase mitochondrial reactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction. Our previous study indicated that cilostazol (CTZ) can reduce ROS levels and decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes. This study investigated the potential mechanisms of CTZ in rats with DN and in high glucose-treated mesangial cells. Male Sprague-Dawley rats were fed 5 mg/kg/day of CTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealed that CTZ reduced the thickness of the glomerular basement membrane and improved mitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatment reduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemia and interacted with the intrinsic pathway for regulating cell apoptosis as an antiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROS production, altered the apoptotic status, and down-regulated transforming growth factor beta (TGF-β) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB). Base on the results of our previous and current studies, CTZ deceleration of hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenance of the mitochondrial function and reduction in TGF-β and NF-κB levels.

The simple and easy way to manufacture counter electrode for dye-sensitized solar cells

Jo-Lin Lan,Yung-Yun Wang,Chi-Chao Wan,Tzu-Chien Wei,Hsien-Ping Feng,Chao Peng,Hai-Peng Cheng,Ya-Huei Chang,Wen-Chi Hsu 한국물리학회 2010 Current Applied Physics Vol.10 No.2

We previously developed poly-N-vinyl-2-pyrrolidone (PVP)-capped Pt nanoclusters on ITO glass via a simple ‘‘2-step dip coating process” as counter electrode for DSSC. This new counter electrode was examined by transmission electron microscopy (TEM), inductively coupled plasma-atomic emission spectroscopy (ICP-AES), electrochemical impedance spectroscopy (EIS), cyclic voltammetry (CV), and current–voltage curve (I–V curve). The TEM results revealed that PVP-capped Pt nanoclusters’ size is about 3 nm, and the amount of Pt deposited on ITO glass is about 5 ㎍/㎠. Comparing with sputtered Pt and Solaronix thermal cluster Pt-catalyst T/SP, the PVP-capped Pt counter electrode has lower amount of Pt deposited on TCO glass,more positive potential of tri-iodide reduction, and better performance for the charge-transfer resistance (RCT) and the cell efficiency (g).