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1.
J. Am. Coll. Cardiol ; J. Am. Coll. Cardiol;74(13 supl): 176-176, Oct., 2019.
Article in English | Sec. Est. Saúde SP, SESSP-IDPCPROD, Sec. Est. Saúde SP | ID: biblio-1024953

ABSTRACT

BACKGROUND: The Fantom sirolimus-eluting bioresorbable coronary scaffold (BRS) (REVA Medical, San Diego, California) was previously studied with angiographic late lumen loss at 6, 9, and 24 months with clinical events being followed through 36 months. However, a functional evaluation has not previously been performed. The aim of this study was to assess serial functional changes after percutaneous coronary intervention (PCI) with the Fantom BRS implantation. METHODS: The FANTOM II trial was a prospective, multicenter, single-arm study that enrolled 240 patients with stable coronary artery disease or unstable angina and single de novo native coronary lesions, of which 235 patients received the Fantom BRS and are included in the present analysis. Serial quantitative flow ratio (QFR) analysis was performed in an independent core laboratory at baseline, after PCI, and at 6- or 9-month and 24-month follow-up. RESULTS: QFR was analyzable in 178 patients at baseline, 185 post-PCI, 178 at 6- or 9-month follow-up, and 31 at 24-month follow-up. At baseline, 59 patients (33.1%) had QFR >0.80, whereas 12 (6.5%) at post-PCI, 13 (7.3%) at 6- or 9-month followup, and 3 (9.7%) at 24-month follow-up had QFR _0.80. In the paired analyses, QFR was significantly increased from baseline to post-PCI (0.73 _ 0.12 vs. 0.94 _ 0.07; p < 0.001), while it decreased from post-PCI to 6- or 9-month follow-up (0.94 _ 0.07 vs. 0.92 _ 0.08; p < 0.001) and from 6- or 9-month to 24-month follow-up (0.93 _ 0.07 vs. 0.91 _ 0.09; p » 0.03). CONCLUSION: Serial angiographic analysis showed significant increase in QFR values between baseline and post-PCI. A slight decrease was observed in QFR values with the Fantom BRS over 24 months. (AU)


Subject(s)
Angiography/methods , Drug-Eluting Stents , Percutaneous Coronary Intervention
2.
BMC Complement Altern Med ; 15(1): 421, 2015 Nov 26.
Article in English | MEDLINE | ID: mdl-26611539

ABSTRACT

BACKGROUND: Exposure to ultraviolet A (UVA) irradiation is the major cause of human skin aging. Suppression of UVA irradiation-induced skin fibroblast cell damage protects the skin against aging. An oxidative stress response transcription factor nuclear factor-(erythroid-derived 2)-related factor 2 (Nrf2) has an important role as a cytoprotective system against oxidative stress in the human skin and other organs. Propolis has been commonly used as a traditional medicine since ancient times. The water extract of propolis (WEP) mainly contains caffeoylquinic acids. In our previous study, we reported that WEP and its major constituents protected immortalized human skin fibroblast cells (NB1-RGB) against UVA irradiation-induced cell death. In this study, we examined the mechanism of WEP-mediated skin protection and the possible involvement of Nrf2/antioxidant response element (ARE) pathways. METHODS: Brazilian green propolis was used in the present study (Minas Gerais State, Brazil), Baccharis dracunculifolia is its main source. The Baccharis propolis was extracted with water at 50 °C to yield water extract. The NB1-RGB cell cultures were incubated for 23 h. After replenishing the medium, WEP or its constituents were added to the cell cultures. After 1 h, the cells were exposed to 10 J/cm(2) of UVA light (365 nm UVA light source, CL-1000 L UV Closslinkers, Ultraviolet Products Ltd., Cambridge, UK). Heme oxygenase-1 (HO-1) expression levels in NB1-RGB cells were evaluated using western blotting. Nrf2 nuclear translocation changes in NB1-RGB cells were indicated using immunostaining. RESULTS: We demonstrated that WEP pretreatment up-regulated HO-1 expression level after UVA irradiation at earlier time points than vehicle pretreatment did, and three main constituents of WEP showed similar effects. Furthermore, WEP pretreatment also accelerated Nrf2 nuclear translocation after UVA irradiation. CONCLUSIONS: Our findings indicated that WEP acts as an early inducer of HO-1 and rapid activator of Nrf2 to protect against UVA-induced oxidative stress.


Subject(s)
Antioxidants/pharmacology , Heme Oxygenase-1/biosynthesis , NF-E2-Related Factor 2/biosynthesis , Propolis , Antioxidant Response Elements/drug effects , Apoptosis/drug effects , Apoptosis/radiation effects , Cells, Cultured , Fibroblasts/drug effects , Fibroblasts/metabolism , Fibroblasts/radiation effects , Humans , Oxidative Stress/radiation effects , Plant Extracts/pharmacology , Quinic Acid/analogs & derivatives , Quinic Acid/pharmacology , Skin/drug effects , Skin/metabolism , Ultraviolet Rays/adverse effects , Up-Regulation/drug effects
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