Cheuk-Kwan Sun

E-Da Hospital, Kao-hsiung-shih, Kaohsiung, Taiwan

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Publications (145)414.32 Total impact

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    ABSTRACT: We hypothesized that lung cancer patient's circulating microparticles (Lc-MPs) could promote angiogenesis, blood flow in ischemic zone and ischemic recovery in rat critical limb ischemia (CLI). To investigate the impact of MP therapy on reversing the setting of CLI, adult-male Sprague-Dawley rats (n=50) equally randomized into sham control (SC) (group 1), SC-Lc-MPs (1.0 x 10(7) particles) (group 2), CLI (group 3), CLI-Hs-MPs (MPs from healthy-subject) (group 4), and CLI-Lc-MPs (group 5) were sacrificed by post-CLI day-14. In vitro study showed that Lc-MPs enhanced VEGFR2 expression, angiogenesis, nitric-oxide production, and endothelial cell proliferation (all p<0.005). By days 7 and 14, Laser Doppler showed significantly higher ischemic/normal blood-flow ratio in groups 1 and 2 compared with group 3, and was significantly higher in group 4 and further elevated in group 5 (p<0.0001). Numbers of small vessels and endothelial markers (CD31(+) and vWF(+) cells) and protein expressions (eNOS, CD31) exhibited a pattern identical to Lasre Doppler among the five groups (all p<0.001). Pro-angiogenic factors (VEGF, CXCR4, SDF-1α, HGF) at cellular and protein levels showed a significant step-wise increase from groups 1 and 2 to groups 3, 4, and 5 (all p<0.001). Protein expressions of fibrotic (Smad3, TGF-β) and apoptotic (mitochondrial Bax, cleaved caspase 3, and PARP) biomarkers displayed an opposite pattern compared to that of Laser Doppler, whereas the protein expressions of anti-fibrotic (Smad1/5, BMP-2) and anti-apoptotic (Bcl-2) biomarkers showed an identical pattern compared with that of Laser Doppler among groups 1 to 3, and 5 (all p<0.001). Administration of Lc-MPs augmented angiogenesis and restored blood flow in a rat of CLI.
    Journal of Translational Medicine 12/2015; 13(1). DOI:10.1186/s12967-015-0381-8 · 3.99 Impact Factor
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    ABSTRACT: Skull and intracranial metastases from hepatocellular carcinoma (HCC) have seldom been reported. A skull metastasis of HCC with a tumor bleeding resulting in spontaneous subdural hematoma (SDH) is extremely unusual. We report the first case of acute spontaneous SDH in a 69-year-old woman who presented with acute onset of headache, because of tumor bleeding caused by skull metastasis of HCC. A 69-year-old woman was referred to our hospital because of progressive headache, nausea, and vomiting for 3 days. Brain computed tomography (CT) performed in the emergency department (ED) revealed a left temporal SDH with a slight mass effect and a small left temporal bone erosion. Tri-phasic abdominal CT demonstrated a large right lobe liver tumor compatible with HCC. She experienced progressive deterioration of consciousness in the intensive care unit. Follow-up CT showed an enlargement of the SDH. An emergency craniotomy for hematoma evacuation and removal of skull tumor was performed. She regained consciousness and had no neurological deficits during the postoperative course. Pathological examination of the skull specimen indicated metastasis of a HCC. Patients with acute SDH without a history of head injury are rarely encountered in the ED. Metastatic carcinoma with bleeding should be included as a differential diagnosis for acute spontaneous SDH. Before an operation for SDH, the possibility of metastatic lesion of the skull should be considered in the surgical planning and the origin of malignancy should be sought.
    BMC Surgery 05/2015; 15(1):60. DOI:10.1186/s12893-015-0045-x · 1.24 Impact Factor
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    ABSTRACT: We hypothesized that combined therapy with shock wave (SW) and autologous bone marrow-derived mesenchymal stem cells (BMDMSCs) is superior to either alone for alleviating left ventricular (LV) dysfunction.
    International Journal of Cardiology 03/2015; DOI:10.1016/j.ijcard.2015.03.044 · 6.18 Impact Factor
  • International Journal of Cardiology 03/2015; DOI:10.1016/j.ijcard.2015.03.137 · 6.18 Impact Factor
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    ABSTRACT: Sitagliptin, a new antidiabetic drug that inhibits dipeptidyl peptidase (DPP)-4 enzyme activity, has been reported to possess neuroprotective property. We tested the protective effects of sitagliptin against chronic cerebral hypoperfusion (CHP) in mice after bilateral carotid artery stenosis (BCAS). Thirty C57BL/6 mice were divided into three groups: sham control (n = 10), CHP (n = 10) and CHP-sitagliptin (orally 600 mg/kg/day) (n = 10). Working memory was assessed with novel-object recognition test. MRI was performed at day 0 and day 90 after BCAS procedure prior to sacrifice. Immunohistochemical (IHC) staining showed significantly enhanced white matter lesions, microglia activation and astrocytosis of white matter in CHP group than in sham control, but the changes were significantly suppressed after sitagliptin treatment (all P < 0.01). The mRNA expressions of inflammatory [tumour necrosis factor-alpha (TNF-α), monocyte chemoattractant protein (MCP-1) and matrix metalloproteinase (MMP)-2] and apoptotic (Bax) biomarkers showed an identical pattern, whereas the anti-inflammatory (interleukin, IL-10) and antiapoptotic (Bcl-2) biomarkers showed an opposite pattern compared with that of IHC among all groups (all P < 0.01). The protein expressions of oxidative stress (NOX-I, NOX-II, nitrotyrosin, oxidized protein), inflammatory [nuclear factor-kappa B (NF-κB), TNF-α and MMP-2], apoptotic [mitochondrial Bax, cleaved poly(ADP-ribose) polymerase (PARP)] and DNA-damage (γ-H2AX) markers showed an identical pattern, while expression pattern of antiapoptotic marker (Bcl-2) was opposite to that of IHC (all P < 0.01). Glycogen-like peptide-1 receptor protein expression progressively increased from sham control to CHP-sitagliptin (P < 0.01). The short-term working-memory loss and MRI/diffusion tensor imaging (DTI) showed a pattern identical to that of IHC in all groups (all P < 0.01). Sitagliptin protected against cognitive impairment and brain damage in a murine CHP model.
    Journal of Hypertension 02/2015; DOI:10.1097/HJH.0000000000000529 · 4.22 Impact Factor
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    ABSTRACT: This study hypothesized that combined serum-deprived (Sd) and healthy (He) adipose-derived mesenchymal stem cell (ADMSC) therapy is superior to either alone in reducing acute lung ischemia-reperfusion injury (ALIRI). Adult male Sprague-Dawley (SD) rats (n = 30) were equally randomized into group 1 (sham control), group 2 (ALIRI + culture medium), group 3 (ALIRI + intravenous autologous 1.2 × 10(6) He-ADMSCs at 30 minute, 6 h, and 24 h following lung ischemia/reperfusion for 45 minutes/72 hours, respectively), group 4 (ALIRI + 1.2 × 10(6) Sd-ADMSCs at identical time points after ischemia/reperfusion), and group 5 (ALIRI + 1.2 × 10(6) combined Sd-ADMSC/He-ADMSC 1:1). Blood oxygen saturation (%) was lowest in group 2, lower in groups 3 to 5 than in group 1, and lower in group 5 than in group 1, whereas right ventricular systolic pressure (RVSP) showed a reverse pattern among the five groups (all p < 0.001). Additionally, changes in histological scoring of lung parenchymal damage, inflammatory and apoptotic biomarkers showed identical pattern compared to that of RVSP in all groups (all p < 0.001). Protein expressions of VCAM-1, ICAM-1, oxidative stress, TNF-α, nuclear factor-κB, and number of CD68 + cells were highest in group 2, higher in groups 3 to 5 than in group 1, and higher in groups 3 and 4 than in group 5, whereas NQO-1 and HO-1 activities and number of CD31 + and vWF + cells showed opposite changes compared with those of inflammatory biomarkers (all p < 0.001). Combined Sd-ADMSC/He-ADMSC therapy offered superior benefit to either option alone in minimizing rodent ALIRI through suppressing oxidative stress and inflammatory reaction.
    American Journal of Translational Research 01/2015; 7(2):209-31. · 3.23 Impact Factor
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    ABSTRACT: Obstructive sleep apnea (OSA) is an independent cardiovascular risk factor to which autonomic nervous dysfunction has been reported to be an important contributor. Ninety subjects recruited from the sleep center of a single medical center were divided into four groups: normal snoring subjects without OSA (apnea hypopnea index, AHI < 5, n = 11), mild OSA (5 <= AHI < 15, n = 10), moderate OSA (15 <= AHI < 30, n = 24), and severe OSA (AHI >= 30, n = 45). Demographic (i.e., age, gender), anthropometric (i.e., body mass index, neck circumference), and polysomnographic (PSG) data were recorded and compared among the different groups. For each subject, R-R intervals (RRI) from 10 segments of 10-minute electrocardiogram recordings during non-rapid eye movement sleep at stage N2 were acquired and analyzed for heart rate variability (HRV) and sample entropy using multiscale entropy index (MEI) that was divided into small scale (MEISS, scale 1-5) and large scale (MEILS, scale 6-10). Our results not only demonstrated that MEISS could successfully distinguish normal snoring subjects and those with mild OSA from those with moderate and severe disease, but also revealed good correlation between MEISS and AHI with Spearman correlation analysis (r = -0.684, p < 0.001). Therefore, using the two parameters of EEG and ECG, MEISS may serve as a simple preliminary screening tool for assessing the severity of OSA before proceeding to PSG analysis.
    Entropy 01/2015; 17(1):231-243. DOI:10.3390/e17010231 · 1.56 Impact Factor
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    ABSTRACT: Background We investigated whether attenuating dipeptidyl peptidase-IV (DPP4) enzyme activity protected rat heart from ischemia-reperfusion (IR) injury (40-min left anterior descending coronary artery ligation followed by 72 h reperfusion).Methods and resultsAdult male Fischer 344 rats (n¿=¿24) were equally divided into sham-control (WT-SC), WT-IR, and WT-IR-Sita (oral sitagliptin 400 mg/kg/day for 3 days) groups, whereas adult male DPP4-deficiency (DPP4D) rats (n¿=¿16) were equally divided into DPP4D-SC and DPP4D-IR groups. Animals were sacrificed at 72 h after reperfusion with collection of heart specimens. Infarct area (H&E), collagen deposition (Sirius-red stain), fibrotic area (Masson's trichrome), and fluorescent-ROS intensity (H2DCFDA-labeling myocardium) of left ventricle were significantly higher in WT-IR than those in other groups, significantly higher in WT-IR-Sita and DPP4D-IR groups than in WT-SC and DPP4D-SC groups (all p¿<¿0.001), but there was no difference between the latter two groups. Protein expressions of oxidative stress (oxidized protein), reactive oxygen species (NOX-1, NOX-2), inflammation (TNF-¿, NF-¿B, MMP-9, VCAM-1), apoptosis (mitochondrial Bax, cleaved caspase-3 and PARP), myocardial damage markers (cytosolic cytochrome-C, ¿-H2AX), and number of inflammatory cells (CD14+, CD68+, CD40+ cells) showed a pattern identical to that of histological changes among all groups (all p¿<¿0.005), whereas markers of anti-apoptosis (Bcl-2) and mitochondrial integrity (mitochondrial cytochrome-C) as well as left ventricular ejection fraction showed an opposite pattern (all p¿<¿0.001). Protein expressions of anti-oxidants (HO-1, NQO-1), angiogenesis factors (SDF-1¿, CXCR4), and glycogen-like-peptide-1-receptor were significantly higher inWT-IR-Sita and DPP4D-IR than those in other groups (all p¿<¿0.001).Conclusion Abrogation of DPP4 activity protects against myocardial IR injury and preserved heart function.
    Journal of Translational Medicine 12/2014; 12(1):357. DOI:10.1186/s12967-014-0357-0 · 3.99 Impact Factor
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    ABSTRACT: We applied multiscale entropy (MSE) to assess variation in crest time (CT), a parameter in arterial waveform analysis, in diagnosing patients with diabetes. Data on digital volume pulse were obtained from 93 individuals in three groups [Healthy young (Group 1, 20< age ≤40, n = 30), healthy upper-middle-aged (Group 2, age >40, n = 30), and diabetic (Group 3, n = 33) subjects]. Crest time, normalized crest time, crest time ratio (CTR), small- and large-scale MSE on CT [MSESS(CT) and MSELS(CT), respectively] were computed and correlated with anthropometric (i.e., body weight/height, waist circumference), hemodynamic (i.e., blood pressure), and biochemical parameters (i.e., serum triglyceride, high-density lipoprotein, fasting blood sugar, and glycosylated hemoglobin). The results demonstrated higher variability in CT in healthy subjects (Groups 1 and 2) compared with that in diabetic patients (Group 3) as reflected in significantly elevated MSESS(CT) and MSELS(CT) in the former (p < 0.003 and p < 0.001, respectively). MSELS(CT) also showed significant association with waist circumference and fasting blood sugar (i.e., two diagnostic criteria of metabolic syndrome) as well as glycosylated hemoglobin concentration. In conclusion, using MSE analysis for assessing CT variation successfully distinguished diabetic patients from healthy subjects. MSESS(CT) and MSELS(CT) therefore may serve as noninvasive tools for identifying subjects with diabetes and those at risk.
    Medical & Biological Engineering & Computing 10/2014; DOI:10.1007/s11517-014-1220-4 · 1.50 Impact Factor
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    ABSTRACT: The role of nerve growth factor (NGF) in liver injury induced by bile duct ligation (BDL) remains elusive. This study aimed to investigate the relationship between inflammation and hepatic NGF expression, to explore the possible upstream molecules up-regulating NGF, and to determine whether NGF could protect hepatocytes from oxidative liver injury. Biochemical and molecular detection showed that NGF was up-regulated in cholestatic livers and plasma, and well correlated with systemic and hepatic inflammation. Conversely, systemic immunosuppression reduced serum NGF levels and resulted in higher mortality in BDL-treated mice. Immunohistochemistry showed that the up-regulated NGF was mainly localized in parenchymal hepatocytes. In vitro mechanistic study further demonstrated that TGF-β1 up-regulated NGF expression in clone-9 and primary rat hepatocytes. Exogenous NGF supplementation and endogenous NGF overexpression effectively protected hepatocytes against TGF-β1- and oxidative stress-induced cell death in vitro, along with reduced formation of oxidative adducted proteins modified by 4-HNE and 8-OHdG. TUNEL staining confirmed the involvement of anti-apoptosis in the NGF-exhibited hepatoprotection. Moreover, NGF potently induced Akt phosphorylation and increased Bcl-2 to Bax ratios, whereas these molecular alterations by NGF were only seen in the H2O2-, but not TGF-β1-treated hepatocytes. In conclusion, NGF exhibits anti-oxidative and hepatoprotective effects and is suggested to be therapeutically applicable in treating cholestatic liver diseases.
    PLoS ONE 10/2014; DOI:10.1371/journal.pone.0112113 · 3.53 Impact Factor
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    ABSTRACT: This study investigated the pro-fibrogenic role of high mobility group box 1 (HMGB1) peptides in liver fibrogenesis. An animal model of carbon tetrachloride (CCl4)-induced liver fibrosis was used to examine the serum HMGB1 levels and its intrahepatic distribution. The increased serum HMGB1 levels were positively correlated with elevation of transforming growth factor-β1 (TGF-β1) and collagen deposition during fibrogenesis. The cytoplasmic distribution of HMGB1 was noted in the parenchymal hepatocytes of fibrotic livers. In vitro studies confirmed that exposure to hydrogen peroxide and CCl4 induced an intracellular mobilization and extracellular release of nuclear HMGB1 peptides in clone-9 and primary hepatocytes, respectively. An uptake of exogenous HMGB1 by hepatic stellate cells (HSCs) T6 cells indicated a possible paracrine action of hepatocytes on HSCs. Moreover, HMGB1 dose-dependently stimulated HSC proliferation, up-regulated de novo synthesis of collagen type I and α-smooth muscle actin (α-SMA), and triggered Smad2 phosphorylation and its nuclear translocation through a TGF-β1-independent mechanism. Blockade with neutralizing antibodies and gene silencing demonstrated the involvement of the receptor for advanced glycation end-products (RAGE), but not toll-like receptor 4, in cellular uptake of HMGB1 and the HMGB1-mediated Smad2 and ERK1/2 phosphorylation as well as α-SMA up-regulation in HSC-T6 cells. Furthermore, anti-RAGE treatment significantly ameliorated CCl4-induced liver fibrosis. In conclusion, the nuclear HMGB1 peptides released from parenchymal hepatocytes during liver injuries may directly activate HSCs through stimulating HSC proliferation and transformation, eventually leading to the fibrotic changes of livers. Blockade of HMGB1/RAGE signaling cascade may constitute a therapeutic strategy for treatment of liver fibrosis.
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 09/2014; 1842(9):1720-32. DOI:10.1016/j.bbadis.2014.06.017. · 5.09 Impact Factor
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    ABSTRACT: This study investigates the therapeutic potential of intracoronary tacrolimus against acute myocardial infarction (AMI) in minipigs with serial cardiac magnetic resonance (CMR) and changes at histological and protein levels. Twelve minipigs subjected to permanent left anterior descending artery ligation were randomized as tac-treated group (n = 6, with intracoronary tacrolimus treatment) and controls (n = 6). CMR with cine and late gadolinium enhancement (LGE) studies were performed on postoperative days 2, 5, and 21. There were no significant differences in left ventricular function (LVF), contractility, and LGE between the two groups on day 2. On day 5, the tac-treated group showed a significantly higher ejection fraction, smaller infarct, and lower day-5/day-2 infarct ratio than controls. On day 21, the controls demonstrated further deterioration of LVF and infarct. Contrastingly, the tac-treated animals demonstrated preservation of LVF, contractility, significantly smaller infarct, and lower day-21/day-2 infarct ratios compared with those on day 5 and controls. The in vivo CMR results were correlated with in vitro findings on histology, immunostaining, and Western blotting which revealed significantly less fibrosis, higher vascularities, less CD68+ and CD40+ inflammatory cells, lower expressions of inflammatory (MMP-9, NF-κB, and TNF-α), and apoptotic (Bax, Caspase-3, c-PARP) biomarkers, respectively, in tac-treated AMI minipigs than controls.
    BioMed Research International 07/2014; 2014:524078. DOI:10.1155/2014/524078 · 2.71 Impact Factor
  • Entropy 07/2014; 16(7):4032-4043. DOI:10.3390/e16074032 · 1.56 Impact Factor
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    ABSTRACT: Impact of early bone marrow-derived mesenchymal stem cell (BMDMSC) implantation on left ventricular (LV) function after AMI was studied.Twelve mini-pigs were equally divided into placebo (AMI through left coronary artery ligation) and cell-treated groups [BMDMSCs (3.0 × 10(7)) implanted into infarct area (IA)] with myocardium harvested by post-AMI day 90. Six healthy animals served as controls.On post-AMI day 90, magnetic resonance imaging showed a lower LV ejection fraction but higher LV dimensions in the placebo group (P < 0.003) that also had increased IAs but reduced wall thickness (P < 0.005). Pro-apoptotic gene expressions (Bax, caspase-3) and apoptotic nucleus number in IAs and peri-IAs were highest in the placebo group (P < 0.001). Inflammatory biomarker expressions (MMP-9, oxidized protein, CD40+ cells) were highest, whereas those of angiogenesis (VEGF, CD31+ cells, SDF-1α, CXCR4) and myocardium-preservation (connexin43, troponin-I, cytochrome-C) were lowest in the placebo group (P < 0.01).BMDMSC implantation preserved LV function and alleviated remodeling at post-AMI day 90.
    International Heart Journal 06/2014; DOI:10.1536/ihj.14-007 · 1.13 Impact Factor
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    ABSTRACT: This study investigated the pro-fibrogenic role of high mobility group box 1 (HMGB1) peptides in liver fibrogenesis. An animal model of carbon tetrachloride (CCl4)-induced liver fibrosis was used to examine the serum HMGB1 levels and its intrahepatic distribution. The increased serum HMGB1 levels were positively correlated with elevation of transforming growth factor-β1 (TGF-β1) and collagen deposition during fibrogenesis. The cytoplasmic distribution of HMGB1 was noted in the parenchymal hepatocytes of fibrotic livers. In vitro studies confirmed that exposure to hydrogen peroxide and CCl4 induced an intracellular mobilization and extracellular release of nuclear HMGB1 peptides in clone-9 and primary hepatocytes, respectively. An uptake of exogenous HMGB1 by hepatic stellate cells (HSCs) T6 cells indicated a possible paracrine action of hepatocytes on HSCs. Moreover, HMGB1 dose-dependently stimulated HSC proliferation, up-regulated de novo synthesis of collagen type I and α-smooth muscle actin (α-SMA), and triggered Smad2 phosphorylation and its nuclear translocation through a TGF-β1-independent mechanism. Blockade with neutralizing antibodies and gene silencing demonstrated the involvement of the receptor for advanced glycation end-products (RAGE), but not toll-like receptor 4, in cellular uptake of HMGB1 and the HMGB1-mediated Smad2 and ERK1/2 phosphorylation as well as α-SMA up-regulation in HSC-T6 cells. Furthermore, anti-RAGE treatment significantly ameliorated CCl4-induced liver fibrosis. In conclusion, the nuclear HMGB1 peptides released from parenchymal hepatocytes during liver injuries may directly activate HSCs through stimulating HSC proliferation and transformation, eventually leading to the fibrotic changes of livers. Blockade of HMGB1/RAGE signaling cascade may constitute a therapeutic strategy for treatment of liver fibrosis.
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 06/2014; 1842(9). DOI:10.1016/j.bbadis.2014.06.017 · 5.09 Impact Factor
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    ABSTRACT: This study tested whether adipose-derived mesenchymal stem cells (ADMSC) embedded in platelet-rich fibrin (PRF) scaffold is superior to direct ADMSC implantation in improving left ventricular (LV) performance and reducing LV remodeling in a rat acute myocardial infarction (AMI) model of left anterior descending coronary artery (LAD) ligation. Twenty-eight male adult Sprague Dawley rats equally divided into group 1 [sham control], group 2 (AMI only), group 3 (AMI+direct ADMSC implantation), and group 4 (AMI+PRF-embedded autologous ADMSC) were sacrificed on day 42 after AMI. LV systolic and diastolic dimensions and volumes, and infarct/fibrotic areas were highest in group 2, lowest in group 1 and significantly higher in group 3 than in group 4, whereas LV performance and LV fractional shortening exhibited a reversed pattern (p<0.005). Protein expressions of inflammation (oxidative stress, IL-1β, MMP-9), apoptosis (mitochondrial Bax, cleaved PARP), fibrosis (Smad3, TGF-β), and pressure-overload biomarkers (BNP, MHC-β) displayed a pattern similar to that of LV dimensions, whereas anti-inflammatory (IL-10), anti-apoptotic (Bcl-2), and anti-fibrotic (Smad1/5, BMP-2) indices showed a pattern similar to that of LV performance among the four groups (all p<0.05). Angiogenesis biomarkers at protein (CXCR4, SDF-1α, VEGF), cellular (CD31+, CXCR4+, SDF-1α+), and immunohistochemical (small vessels) levels, and cardiac stem cell markers (C-kit+, Sca-1+) in infarct myocardium were highest in group 4, lowest in group 1, and significantly higher in group 3 than in group 2 (all p<0.005). PRF-embedded ADMSC is superior to direct ADMSC implantation in preserving LV function and attenuating LV remodeling.
    International journal of cardiology 03/2014; 173(3). DOI:10.1016/j.ijcard.2014.03.015 · 6.18 Impact Factor
  • Journal of Inflammation 01/2014; 11(1):27. DOI:10.1186/s12950-014-0027-2 · 2.22 Impact Factor
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    ABSTRACT: Introduction to Computer Science (ICS), which is a compulsory theoretical course for freshmen of the electrical engineering (EE) department, lays the foundation for more advanced courses. Nevertheless, since ICS covers a wide variety of concepts that are difficult to completely comprehend, incomplete understanding and a loss of learning incentive are possible problems. The aim of implementing hands-on practice (HOP) activities was to prepare the students for the actual hardware manipulation in the field of EE and also to enhance their performance in the future advanced practice courses. Through organizing optional evening hands-on practice (HOP) activities, this study investigated whether the first-year college students who participated in HOP would exhibit a better understanding in ICS compared to those who did not. The enrollment in HOP was optional in which the performance did not affect the score in the ICS course. The results showed that HOP participants not only had significantly higher academic scores (p < 0.05), but were also less stressed toward the ICS course (p < 0.05) than the non-participants. The former also showed increased interest in accepting challenges (e.g. Two HOP participants later entered the National Microcomputer Design Competition and were awarded the third prize). In conclusion, the introduction of optional HOP for freshmen of electrical engineering not only alleviated the stress that they face in response to the ICS course, but also improved the students' academic performance and class attendance rate as well as raising their interest and boosting their confidence in further challenges in the field of electrical engineering.
    Computers & Education 01/2014; 70:1–8. DOI:10.1016/j.compedu.2013.08.002 · 2.63 Impact Factor
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    ABSTRACT: We tested the hypothesis that Lipofectamine siRNA delivery to deplete transient receptor potential cation channel (TRPC) 1 protein expression can suppress hypoxia-induced pulmonary arterial hypertension (PAH) in mice. Adult male C57BL/6 mice were equally divided into group 1 (normal controls), group 2 (hypoxia), and group 3 (hypoxia + siRNA TRPC1). By day 28, right ventricular systolic pressure (RVSP), number of muscularized arteries, right ventricle (RV), and lung weights were increased in group 2 than in group 1 and reduced in group 3 compared with group 2. Pulmonary crowded score showed similar pattern, whereas number of alveolar sacs exhibited an opposite pattern compared to that of RVSP in all groups. Protein expressions of TRPCs, HIF-1α, Ku-70, apoptosis, and fibrosis and pulmonary mRNA expressions of inflammatory markers were similar pattern, whereas protein expressions of antifibrosis and VEGF were opposite to the pattern of RVSP. Cellular markers of pulmonary DNA damage, repair, and smooth muscle proliferation exhibited a pattern similar to that of RVSP. The mRNA expressions of proapoptotic and hypertrophy biomarkers displayed a similar pattern, whereas sarcomere length showed an opposite pattern compared to that of RVSP in all groups. Lipofectamine siRNA delivery effectively reduced TRPC1 expression, thereby attenuating PAH-associated RV and pulmonary arteriolar remodeling.
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    ABSTRACT: We investigated whether extracorporeal shock wave (ECSW) therapy can attenuate cyclophosphamide (CYP)-induced acute interstitial cystitis (AIC) in rats. Eighteen male-adult Sprague-Dawley rats were equally divided into group 1 (sham control), group 2 (AIC induced by 150 mg/kg CYP by intra-peritoneal injection) and group 3 (AIC + ECSW 200 impulses at 0.11 mJ/mm(2) to the urinary bladder at 3 and 24 h after CYP treatment). Smooth-muscle cells co-culture with menadione (25 µM) with and without ECSW treatment was performed. Western-blot results demonstrated that ECSW significant attenuated oxidative stress and inflammatory reactions in this in-vitro studies (all p < 0.001). 24-hour urine amount and microscopic findings of red-blood-cell count (i.e., hematuria) were higher in group 2 than in groups 1 and 3, and significantly higher in group 3 than in group 1 (all p < 0.001). The urine levels of albumin and interleukin-6 showed an identical pattern of hematuria among all three groups (all p < 0.001). The cellular and mRNA expressions of macrophage migration inhibitory factor (MIF)+, CD74+, CD68+, substance p+, and Cox-2+ cells in the bladder tissue exhibited an identical pattern of hematuria among all groups (all p < 0.0001). The integrity of epithelial layer and collagen-deposition area as stained by Sirius red displayed an opposite pattern of hematuria among the three groups (p < 0.0001). The protein expression of IL-12, iNOS, TNF-α, NF-κB, MMP-9, NOX-1, NOX-2, RANTES, and Oxyblot displayed an identical pattern of hematuria among all groups (all p < 0.01). ECSW therapy markedly attenuated CYP-induced AIC through inhibitions of the inflammation and oxidative stress.
    American Journal of Translational Research 01/2014; 6(6):631-48. · 3.23 Impact Factor

Publication Stats

1k Citations
414.32 Total Impact Points

Institutions

  • 2014–2015
    • E-Da Hospital
      Kao-hsiung-shih, Kaohsiung, Taiwan
    • Chung Shan Medical University
      臺中市, Taiwan, Taiwan
  • 2011–2015
    • I-Shou University
      Kao-hsiung-shih, Kaohsiung, Taiwan
  • 2011–2012
    • National Dong Hwa University
      • Department of Electrical Engineering
      Hualian, Taiwan, Taiwan
  • 2007–2012
    • Chang Gung Memorial Hospital
      • • Department of Surgery
      • • Division of General Surgery
      • • Division of Cardiology
      T’ai-pei, Taipei, Taiwan
  • 2007–2011
    • Chang Gung University
      Hsin-chu-hsien, Taiwan, Taiwan
  • 2008
    • National Pingtung University of Science and Technology
      P’ing-tung-chieh, Taiwan, Taiwan