Publications (277)840.93 Total impact
- [Show abstract] [Hide abstract] ABSTRACT: Significance: Autologous adipose-derived mesenchymal stem cell-assisted ciprofloxacin therapy offered an additional benefit by reducing acute urogenital organ damage in rats.
- [Show abstract] [Hide abstract] ABSTRACT: Aim: Antioxidant peptide SS-31 is a class of cell-permeable small peptides, which selectively resides on the inner mito¬chondrial membrane and possesses intrinsic mitochondrial protective capacities. In this study we inves¬tigated the therapeutic effects of antioxidant peptide SS-31 on transverse aortic constriction (TAC)-induced pulmonary arterial hypertension (PAH) in a murine model. Methods: Adult male mice were divided into 3 groups: sham-operated mice, TAC mice, and TAC+SS-31 mice that underwent TAC surgery and received SS-31 (2 mg/d, ip) for 60 d. The right ventricular systolic blood pressure (RVSBP) was measured on d 60 prior to sacrificing the mice; then their right heart and lung tissues were collected for histological and biochemical examinations. Lung injury scores were defined by the increased crowded area and decreased number of alveolar sacs. Results: TAC mice showed significantly higher RVSBP compared with sham-operated mice, the elevation was substantially suppressed in TAC+SS-31 mice. The same pattern of changes was found in pulmonary levels of oxidative stress proteins (NOX-1/NOX-2/oxidized proteins), cytosolic cytochrome c, biomarkers related to inflammation (MMP-9/TNF-α/iNOS), calcium overload index (TRPC1, 2, 4, 6), apoptosis (mitochondrial BAX, cleaved caspase 3/PARP), fibrosis (Smad3/TGF-β), hypoxic (HIF-1α), DNA damage (γ-H2AX) and endothelial function (eNOS/ET-1R), as well as in lung injury score, number of muscularized vessels in lungs, number of TRPC1(+) and HIF-1α(+) cells in pulmonary artery, and number of γ-H2AX(+) and Ki-67(+) cells in lung parenchyma. An opposite pattern of changes was observed in pulmonary anti-fibrotic markers (Smad1/5, BMP-2), number of small vessels, and number of alveolar sacs. In contrast, the levels of antioxidant proteins (HO-1/NQO-1/GR/GPx) in lung parenchyma were progressively and significantly increased from sham-operated mice, TAC mice to TAC+SS-31 mice. Conclusion: Antioxidant peptide SS-31 administration effectively attenuates TAC-induced PAH in mice.
- [Show abstract] [Hide abstract] ABSTRACT: Microparticles (MPs) are substantially increased in patients with operable stage non-small cell lung cancer (NSCLC) prior to lung resection surgery. This study tested the hypothesis that there is a decrease in MPs after surgical intervention. Between March 2012 and January 2015, 33 patients who had operable stage NSCLC were consecutively and prospectively enrolled into the study. Additionally, 31 healthy subjects who were consecutively enrolled in the study period served as age- and gender-matched controls. Circulating MPs (EDAc-MPs, EDAp-MPs, PDAc-MPs, PDAp-MPs) were measured by flow cytometry once in control subjects and twice (i.e., prior to and three months later after surgical intervention) in NSCLC patients. Compared with control subjects, these four types of circulating MPs were significantly higher in NSCLC patients prior to operation (all P < 0.005), but did not differ among the controls and NSCLC patients at 3 months after surgery (all P > 0.2). Additionally, a receiver operating characteristic curve (ROC) showed that these four types of MPs were significantly valuable predictors for detecting early stage NSCLC (all P < 0.004). Circulating MPs which were remarkably increased in the operable stage of NSCLC prior to surgery were substantially decreased 3 months later after surgery. These findings show that circulating MPs might be an accessory biomarker for monitoring those of NSCLC after receiving lung resection surgery.
- [Show abstract] [Hide abstract] ABSTRACT: Angina pectoris is a treatable symptom that is associated with mortality and decreased quality of life. Angina eradication is a primary care goal of care after an acute myocardial infarction (AMI). Our aim was to evaluate factors influencing angina pectoris 1 year after an AMI.From January 2005 to December 2013, 1547 patient received primary percutaneous intervention in our hospital for an acute ST-segment elevation myocardial infarction (MI). Of these patients, 1336 patients did not experience post-MI angina during a 1-year follow-up, and 211 patients did. Univariate and multivariate logistic regression analyses were performed to identify the factors influencing angina pectoris 1 year after an AMI. Propensity score matched analyses were performed for subgroups analyses.The average age of the patients was 61.08 ± 12.77 years, with a range of 25 to 97 years, and 82.9% of the patients were male. During 1-year follow-up, 13.6% of the patients experienced post-MI angina. There was a longer chest pain-to-reperfusion time in the post-MI angina group (P = 0.01), as well as a higher fasting sugar level, glycohemoglobin (HbA1C), serum creatinine, troponin-I and creatine kinase MB (CK-MB). The post-MI angina group also had a higher prevalence of multiple-vessel disease. Manual thrombectomy, and distal protective device and intracoronary glycoprotein IIb/IIIa inhibitor injection were used frequently in the no post-MI angina group. Antiplatelet agents and post-MI medication usage were similar between the 2 groups. Multivariate logistic regression analyses demonstrated that prior MI was a positive independent predictor of occurrence of post-MI angina. Manual thrombectomy use and drug-eluting stent implantation were negative independent predictors of post-MI angina. Higher troponin-I and longer chest pain-to-reperfusion time exhibited a trend toward predicting post-MI angina.Prior MIs were strong, independent predictors of post-MI angina. Manual thrombectomy and drug-eluting stent implantation could decrease the occurrence of angina pectoris 1 year after an AMI, decrease long-term healthy costs, and increase post-MI quality of life.
- [Show abstract] [Hide abstract] ABSTRACT: Background: This study tested the hypothesis that preactivated and disaggregated shape-changed platelet (PreD-SCP) therapy attenuates lung injury from acute respiratory distress syndrome (ARDS) induced by 100% oxygen inhalation and complicated by sepsis through peritoneal administration of 1.5 mg/kg lipopolysaccharide (LPS). Methods: Adult male Sprague-Dawley rats, weighing 325-350 g, were randomized into group 1 [normal controls (NC)], group 2 [NC + PreD-SCP (3.0 x 10, intravenous administration)], group 3 (ARDS-LPS), and group 4 (ARDS-LPS + PreD-SCP) and sacrificed by 72 h after ARDS induction. Results: The lung injury score was significantly higher in group 3 than that in other groups, and significantly higher in group 4 than that in groups 1 and 2, whereas the numbers of alveolar sacs and oxygen saturation (%) showed a reversed pattern compared to that of lung injury score among the four groups (all p < 0.0001) without significant difference between groups 1 and 2. The expressions of pro-inflammatory cells [CD11+, CD14+, CD68+] and proteins (TNF-α, NF-κB, IL-1β, MMP-9, iNOS, ICAM-1) exhibited a pattern identical to the lung injury score. Circulating levels of WBC, IL-6, TNF-α, MPO and CCL5, and pulmonary protein expressions of oxidative stress (NOX-1/NOX-2, oxidized protein), apoptotic (Bax, cleaved caspase 3/PARP), fibrotic (Smad3, TGF-β), and DNA damage (γ-H2AX) biomarkers showed an identical pattern, whereas protein expressions of anti-fibrotic (Smad1/5, BMP-2) and anti-inflammatory (Bcl-2) biomarkers demonstrated an opposite pattern compared to the pro-inflammatory indices among the four groups (all p < 0.001). Conclusions: PreD-SCP therapy effectively improved lung injury in ARDS complicated by sepsis.
- [Show abstract] [Hide abstract] ABSTRACT: We tested the hypothesis that melatonin (Mel) enhances exogenous mitochondria (Mito) treatment against rodent hepatic ischemia-reperfusion (IR) injury. In vitro study utilized three groups of hepatocytes (i.e., non-treatment, menadione, and menadione-melatonin treatment, 4.0 x 10(5) each), while in vivo study involved adult male Sprague-Dawley rats (n=40) equally divided into sham-control (SC), IR (60-min left lobe ischemia + 72-hr reperfusion), IR-Mel (melatonin at 30 min/6h/8h after reperfusion), IR-Mito (mitochondria 15000 μg/rat 30 min after reperfusion), and IR-Mel-Mito. Following menadione treatment in vitro, oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptotic (cleaved caspase-3/PARP), DNA-damage (γ-H2AX/CD90/XRCC1), mitochondria-damage (cytosolic cytochrome-C) biomarkers and mitochondrial permeability transition were lower, whereas mitochondrial cytochrome-C were higher in hepatocytes with melatonin treatment compared to those without (all p<0.001). In vivo study demonstrated highest liver injury score and serum AST in IR group but lowest in SC group, higher in IR-Mito group than that in groups IR-Mel and IR-Mel-Mito, and higher in IR-Mel group than that in IR-Mel-Mito group after 72-hour reperfusion (all p<0.003). Protein expressions of inflammatory (TNF-α/NF-κB/IL-1β/MMP-9), oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptotic (caspase-3/PARP/Bax), mitochondria-damage (cytosolic cytochrome-C) biomarkers displayed an identical pattern, whereas mitochondria integrity marker (mitochondrial cytochrome-C) showed an opposite pattern compared to that of liver injury score (all p<0.001) among five groups. Microscopically, expressions of apoptotic nuclei, inflammatory (MPO(+) /CD68(+) /CD14(+) cells) and DNA-damage (γ-H2AX(+) cells) biomarkers exhibited an identical pattern compared to that of liver injury score (all p<0.001) among five groups. Melatonin-supported mitochondria treatment offered additional benefit of alleviating hepatic IR injury. This article is protected by copyright. All rights reserved.
Article: Carotid stenting and endarterectomy[Show abstract] [Hide abstract] ABSTRACT: Stroke, either ischemic or hemorrhagic, remains the second commonest cause of death worldwide in the last decade. Etiologies for ischemic stroke (IS) vary widely. Atherothrombotic occlusion is an essential cause to which carotid artery stenosis (CAS) is a major contributor. Administration of anti-platelet agent to patients with CAS has been shown to reduce incidence of long-term IS. In additional, in patients with symptomatic CAS, clinical trials have demonstrated that carotid endarterectomy (CEA) is superior to medical therapy for prevention of future CAS-related IS. However, CEA is not suitable for CAS post-radiotherapy or those located at higher level of the internal carotid artery; and major complications of this procedure including cranial nerve injuries have stimulated the interest of using percutaneous transfemoral carotid stenting as an alternative approach. Although transfemoral arterial approach of carotid stenting is not inferior to CEA in improving clinical outcomes, it has been reported to be associated with vascular complication and has its limitations in patients with athero-occlusive disease of abdominal aorta or bilateral iliac arteries, level II or III aortic arch, or bovine type carotid arterial anatomy. Therefore, transradial/transbrachial arterial approach has emerged as a novel method for carotid stenting. This article provides a critical review on interventional approaches for the treatment of CAS.
- [Show abstract] [Hide abstract] ABSTRACT: Background: We tested the hypothesis that extracorporeal shock wave (ECSW) therapy can effectively protect sciatic nerve (SN) from diabetes mellitus (DM)-induced neuropathy in leptin-deficient (ob/ob) mice. Methods and results: Eighteen-week C57BL/6 mice (n=8) served as age-matched controls (group 1) and ob/ob mice (n=16) were categorized into DM (group 2) and DM + ECSW (0.12 mJ/mm(2) for 4 times of 200 impulses at 3-week intervals) (group 3). The animals were sacrificed two weeks post-ECSW. In vitro results showed that the protein expressions of oxidative stress (NOX-1, NOX-2, oxidized protein), inflammation (MMP-9, TNF-α, iNOS), apoptosis (Bax, cleaved caspase-3, & PARP), and DNA-damage marker (γ-H2AX) were significantly higher in RT4-D6P2T (schwannoma cell line) treated by menadione (25 µM) compared with control group and were significantly reversed after ECSW (0.12 mJ/mm(2), 200 impulses) (all p<0.001). mRNA expressions of inflammation (MMP-9, TNF-α, iNOS), oxidative stress (NOX-1, NOX-2) and apoptosis (Bax, caspase-3) in SN were significantly higher in group 2 than in group 1 and were significantly reversed in group 3, whereas the mRNA expressions of anti-oxidants (HO-1, NQO1) progressively increased from group 1 to group 3 (all p<0.001). Cellular expressions of F4/80+, CD14+, γ-H2AX+ cells, and number of vacuolar formation in SN showed a pattern identical to that of inflammation markers among all groups (all p<0.001). Microscopic findings of Schwann cells and myelin-sheath scores, and number of eNOS+ cells in SN showed a reversed pattern compared to that of inflammation among all groups (all p<0.001). Conclusions: ECSW therapy protected SN against DM-induced neuropathy.
- [Show abstract] [Hide abstract] ABSTRACT: Despite advancements in pharmacological therapy and refinement of the tools and technique of primary percutaneous coronary intervention (PCI) and coronary artery bypass surgery, patients with acute myocardial infarction (AMI) complicated by profound cardiogenic shock (CS) still have unacceptably high in-hospital mortality and unfavorable long-term outcome. Thus, there is an imminent need of a new and safe treatment modality in the management of AMI complicated by profound CS. Growing evidence suggests that extracorporeal membrane oxygenator (ECMO)-supported primary PCI is an effective therapeutic option for saving lives under such conditions. In this review, we describe and interpret the potential role of circulatory mechanical support by ECMO in the setting of AMI complicated by profound CS for improving clinical outcomes.
- [Show abstract] [Hide abstract] ABSTRACT: Purpose: This study aimed to test the hypothesis that lung cancer patient-derived circulating microparticles (LCC-MPs) enhance metastatic lung tumors in a rat model. Procedures: The controls (n = 6) and LCC-MP-treated rats (n = 6) with N1S1-induced pulmonary metastatic hepatocellular carcinoma (HCC) underwent dual-source CT (DSCT) on days 10, 15, and 20. Cellular and molecular studies were performed subsequently. Results: DSCT revealed slow progression of metastatic lung tumors in the controls. Compared with the controls, the LCC-MP-treated rats exhibited significantly more and larger metastatic tumors on days 15 and 20 on DSCT, enhanced angiogenesis with higher microvessel count (CD34+), more CXCR4+ and VEGF+ cells in immunohistofluorescence studies, and higher protein expression levels of eNOS, angiopoietin, vascular endothelial growth factor, and CD31 on western blotting (Mann-Whitney test, all P < 0.05). Conclusions: LCC-MPs can elicit oncogenic stimulation and accelerate metastatic HCC growth in rat lung as demonstrated on DSCT and enhanced tumoral angiogenesis as confirmed in cellular and molecular studies.
- [Show abstract] [Hide abstract] 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.
- [Show abstract] [Hide abstract] ABSTRACT: Mortality and disability following ischemic stroke (IS) remains unacceptably high with respect to the conventional therapies. This study tested the effect of erythropoietin (EPO) on long-term neurological outcome in patients after acute IS. This study aimed to evaluate the safety and efficacy of two consecutive doses of EPO (5,000 IU/dose, subcutaneously administered at 48 hours and 72 hours after acute IS) on improving the 90-day combined endpoint of recurrent stroke or death that has been previously reported. A secondary objective was to evaluate the long-term (that is, five years) outcome of patients who received EPO. This was a prospective, randomized, placebo-controlled trial that was conducted between October 2008 and March 2010 in a tertiary referral center. IS stroke patients who were eligible for EPO therapy were enrolled into the study. The results showed that long-term recurrent stroke and mortality did not differ between group 1 (placebo-control; n = 71) and group 2 (EPO-treated; n = 71). Long-term Barthel index of <35 (defining a severe neurological deficit) was lower in group 2 than group 1 (P = 0.007). Multiple-stepwise logistic-regression analysis showed that EPO therapy was significantly and independently predictive of freedom from a Barthel index of <35 (P = 0.029). Long-term major adverse neurological event (MANE; defined as: death, recurrent stroke, or long-term Barthel index < 35) was lower in group 2 than group 1 (P = 0.04). Log-Rank test showed that MANE-free rate was higher in group 2 than group 1 (P = 0.031). Multiple-stepwise Cox-regression analysis showed that EPO therapy and higher Barthel Index at day 90 were independently predictive of freedom from long-term MANE (all P <0.04). EPO therapy significantly improved long-term neurological outcomes in patients after IS. ISRCTN71371114 . Registered 10 October 2008.
- [Show abstract] [Hide abstract] ABSTRACT: The management of ostial lesions is one of the challenges of percutaneous coronary intervention (PCI) in recent medicine. Although stent implantation has increased the accuracy of the results and improved long-term outcomes, in-stent restenosis (ISR) occurs more frequency following the treatment of ostial lesions than the treatment of non-ostial lesions. When additional stenting is not desirable, PCI with drug-eluting balloons (DEBs) has emerged as an adjunctive strategy. However, little data regarding the effects of DEBs in ostial ISR lesions are available. Our study aimed to assess the efficacy of the use of DEBs in coronary ostial instent restenotic lesions.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: The aim of this study was to evaluate the clinical effects of different strategies for preventing coronary microvascular obstruction in ST elevation myocardial infarction (STEMI) patients with a high thrombus-burden plaque. Methods: Between January, 2007 and December, 2012, 354 patients suffering from STEMI with high thrombus-burden were enrolled and divided into three groups as the first group received a GP IIb/IIIa inhibitor, and the second group received a distal protective device, and the third group was treated with primary PCI alone. Results: A high percentage of patients in the GP IIb/IIIa inhibitor (96.8% and 90.5%), distal protective device (99.3% and 87.6%) had better thirty-day and one-year symptom-free outcomes when compared with PCI only group (91.6% and 65.6%) (P = 0.008 and P < 0.001; respectively). Conclusions: Treatment with intracoronary GP IIb/IIIa inhibitor injection or distal protection device to prevent coronary microvascular obstruction was demonstrated to increase the occurrences of thirty-day and one-year symptom-free outcomes; thus, these treatments can help decrease post-MI medical care costs.
- [Show abstract] [Hide abstract] ABSTRACT: Background: We tested the hypothesis that tissue plasminogen activator (tPA) deficiency protected against acute ischemic stroke (AIS)-induced brain injury. Methods and results: Wild-type mice (n=54) were categorized into group 1 (sham control, n=18) and group 3 [AIS by permanent ligation of left common carotid artery (CCA) and cramping right CCA for 1h and then reperfusion followed by hypoxia (11% of oxygen supply for 2h), n=36]. Similarly, tPA knockout (tPA(-/-)) mice (n=54) were randomized into group 2 (sham control, n=18) and group 4 (AIS, n=36). By day 28 after AIS procedure, mortality rate was higher in group 3 (77.8%) than in group 4 (38.9%) and lowest in groups 1 (0%) and 2 (0%) (p<0.001). By days 3 and 28, MRI demonstrated a pattern of changes in brain-infarct volume identical to that of mortality among four groups (p<0.001). By day 28, protein expressions of inflammatory (MMP-9, TNF-α, NF-κB, iNOS, PAI-1, RANTES), oxidative (NOX-1, NOX-2, oxidized protein), apoptotic (cleaved caspase-3 & PARP, Bax), and fibrotic (Smad3, TGF-β) biomarkers and cellular expressions of inflammation (CD11, F4/80, GFAP), DNA-damage (γ-H2AX) and brain-edema (AQP4) markers exhibited an identical pattern compared to that of mortality (all p<0.001), whereas protein expressions of endothelial (eNOS, CD31), anti-fibrotic (Smad1/5, BMP-2) biomarkers, and number of small vessels displayed an opposite pattern (all p<0.001) among four groups. Expressions of protein and cellular angiogenesis markers (VEGF, SDF-1α, CXCR4) were progressively increased from groups 1 and 2 to group 4 (all p<0.0001). Conclusion: tPA deficiency protected the brain from AIS injury.
- [Show abstract] [Hide abstract] ABSTRACT: This study tested for the benefits of early administration of carvedilol as protection againstdoxorubicin-induced cardiomyopathy. Thirty male-adult B6 mice were categorized into group 1 (untreated control), group 2 [doxorubicin (15 mg/every-other-day for 2-weeks, I.P.], and group 3 [carvedilol (15 mg/kg/day, from day-7 after doxorubicin for 28 days)] and euthanized by day 35 after doxorubicin treatment. By day 35, the left-ventricular injection fraction (LEVF) was significantly lower in group 2 than in groups 1 and 3, and significantly lower in group 3 than in group 1, whereas the LV end-diastolic and LV end-systolic dimensions showed an opposite pattern to LVEF among the three groups. The protein expressions of fibrotic (Smad3, TGF-β), apoptotic (BAX, cleaved caspase 3, PARP), DNA-damage (γ-H2AX), oxidative-stress (oxidized protein), mitochondrial-damage (cytosolic cytochrome-C), heart failure (BNP), hypertrophic (β-MHC) biomarkers of LV myocardium showed an opposite pattern to LVEF among the three groups. The protein expressions of anti-fibrotic (BMP-2, Smad1/5), α-MHC, and phosphorylated-Akt showed an identical pattern to LVEF among the three groups. The microscopic findings of fibrotic and collagen-deposition areas, numbers of γ-H2AX+ and 53BP1+ cells in LV myocardium, exhibited an opposite pattern, whereas the numbers of endothelial cell (CD31+, vWF+) markers showed an identical pattern to LVEF among the three groups. Cardiac stem cell markers (C-kit+, Sca-1+ cells) were significantly progressively increased from group 1 to group 3. Additionally, The in vitro study showed carvedilol treatment significantly inhibited DOX-induced cardiomyoblast DNA (CD90/XRCC1+, CD90/53BP1+ and r-H2AX+ cells) damage. Early carvedilol therapy protected against doxorubicin-induced DNA-damage and cardiomyopathy.
- [Show abstract] [Hide abstract] ABSTRACT: Emergency department and hospital crowding have become an increasing problem. The clinical outcomes of prolonged emergency department (ED) length of stay in acute ST-segment elevation myocardial infarction (STEMI) patients after reperfusion are still unknown. Between January 2008 and December 2011, 432 consecutive patients with STEMI undergoing primary PCI were recruited. Patients were divided into two groups: the immediate admission group (length of ED stay <8 h; IA group) and the prolonged ED stay group (length of ED stay ≧8 h; PS group). The median lengths of ED stay of the patients in both groups were 29.97 h in the PS group (n = 145, 33.6 %) and 1.78 h in the IA group (n = 287, 66.4 %), respectively. The age, gender, risk factors of coronary artery disease, characteristic of coronary angiography, and TIMI risk score did not differ between the two groups. During nearly 4-year clinical follow-up, the short-term and long-term clinical outcomes were similar between the two groups. B-blocker and statins were used infrequently in the ED. In addition, patients with high TIMI risk score in the PS group had higher incidence of 1-year re-MI (6.8 vs. 1.8 %; p = 0.045). In the era of primary PCI for STEMI patients after reperfusion, prolonged ED length of stay may not influence clinical outcomes. Patients with high TIMI risk score in the PS group still had a trend toward worse clinical outcome after long ED stays.
- [Show abstract] [Hide abstract] ABSTRACT: We sought to evaluate the effects of adipose-derived mesenchymal stem cells (ADMSCs) exosomes on hepatocellular carcinoma (HCC) in rats using apparent diffusion coefficient (ADC), natural killer T-cell (NKT-cell) responses, and histopathological features. ADMSC-derived exosomes appeared as nanoparticles (30–90 nm) on electron microscopy and were positive for CD63, tumor susceptibility gene-101, and β -catenin on western blotting. The control ( n = 8 ) and exosome-treated ( n = 8 ) rats with N1S1-induced HCC underwent baseline and posttreatment day 10 and day 20 magnetic resonance imaging and measurement of ADC. Magnetic resonance imaging showed rapidly enlarged HCCs with low ADCs in the controls. The exosome-treated rats showed partial but nonsignificant tumor reduction, and significant ADC and ADC ratio increases on day 10. On day 20, the exosome-treated rats harbored significantly smaller tumors and volume ratios, higher ADC and ADC ratios, more circulating and intratumoral NKT-cells, and low-grade HCC ( P < 0.05 for all comparisons) compared to the controls. The ADC and volume ratios exhibited significant inverse correlations ( P < 0.001 , R 2 = 0.679 ). ADMSC-derived exosomes promoted NKT-cell antitumor responses in rats, thereby facilitating HCC suppression, early ADC increase, and low-grade tumor differentiation. ADC may be an early biomarker of treatment response.
- [Show abstract] [Hide abstract] ABSTRACT: Background: Intracoronary nitroprusside and thrombus aspiration have been demonstrated to improve myocardial perfusion during percutaneous coronary interventions (PCI) for ST-segment elevation acute myocardial infarction (STEMI) However, no long-term clinical studies have been performed comparing these approaches. Methods: A single medical center retrospective study was conducted to evaluate the effects of intracoronary nitroprusside administration before slow/no-reflow phenomena versus thrombus aspiration during primary PCI. Forty-three consecutive patients with STEMI were enrolled in the intracoronary nitroprusside treatment group. One hundred twenty-four consecutive STEMI patients who received thrombus aspiration were enrolled; ninety-seven consecutive STEMI patients who did not receive either thrombus aspiration or intracoronary nitroprusside treatment were enrolled and served as control subjects. Patients with cardiogenic shock, who had received platelet glycoprotein IIb/IIIa inhibitor, or intra-aortic balloon pump insertion were excluded. Thrombolysis in Myocardial Infarction (TIMI) flow grade, corrected TIMI frame count and TIMI myocardial perfusion grade (TMPG) were assessed prior to and following PCI by two independent cardiologists blinded to the procedures. The rate of major adverse cardiac events (MACE) at 30 days, 1 year, and 3 years after study enrollment as a composite of recurrent myocardial infarction, target-vessel revascularization, and cardiac death were recorded. Results: The control group had a significantly lower pre-PCI TIMI flow (≤ 1; 49.5% vs. 69.8% vs. 77.4%; p = < 0.001) compared with the nitroprusside and thrombus aspiration groups. The thrombus aspiration group had a significantly higher pre-PCI thrombus score (> 4; 98.4% vs. 88.4% vs. 74.3%; p = < 0.001) and post-PCI TMPG (3; 39.5% vs. 16.3% vs. 20.6%; p = 0.001) compared with the nitroprusside and control groups. No significant differences were noted in the post-PCI thrombus score, 30-day, 1-year and 3-year MACE rate, and Kaplan-Meier curve among 3 groups of patients. Conclusions: Although thrombus aspiration provided improved TMPG compared with early administration of intracoronary nitroprusside and neither of both during primary PCI, it did not have a significant impact on 30-day, 1-year and 3-year MACE rate. Key words: Acute myocardial infarction; Intracoronary nitroprusside; Thrombus aspiration.
I-Shou UniversityKao-hsiung-shih, Kaohsiung, Taiwan
Chang Gung University
Hsin-chu-hsien, Taiwan, Taiwan
- Department of Internal Medicine
Mackay Memorial HospitalT’ai-pei, Taipei, Taiwan
Chang Gung Memorial Hospital
T’ai-pei, Taipei, Taiwan
- • Division of Cardiology
- • Department of Internal Medicine
National Sun Yat-sen University
Kao-hsiung-shih, Kaohsiung, Taiwan
- Department of Biological Science