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  • 1
    Online Resource
    Online Resource
    Angiographic Complete versus Clinical Selective Incomplete Percutaneous Revascularization in Heart Failure Patients with Multivessel Coronary Disease
    Hindawi Limited ; 2020
    In:  Journal of Interventional Cardiology Vol. 2020 ( 2020-07-27), p. 1-8
    Details
    In: Journal of Interventional Cardiology, Hindawi Limited, Vol. 2020 ( 2020-07-27), p. 1-8
    Abstract: Background . Patients with multivessel disease (MVD) often pursue complete revascularization (CR) during percutaneous coronary intervention (PCI) to improve prognosis. However, angiographic CR is not always feasible and is associated with some procedure-related complications in heart failure (HF) patients with MVD. Clinical selective incomplete revascularization (IR) may be reasonable for these high-risk patients, but its role in long-term outcomes remains uncertain. Methods . Six hundred patients with HF and MVD submitted to PCI were enrolled. Major adverse cardiac events (MACEs) were defined as a composite of recurrent myocardial infarction, any revascularization, and all-cause mortality at 5 years. Results . During a mean follow-up period of 3.7 ± 1.9 years, there was no significant difference in 5-year MACEs between selective IR and successful angiographic CR in HF patients with MVD. However, patients who failed CR had a significantly greater incidence of 5-year MACEs than those in the other two groups (failed CR: 46.4% vs. selective IR: 27.7% vs. successful CR: 27.8%, p 〈 0.001 ). Conclusions . Long-term outcomes of selective IR were comparable with those of successful angiographic CR in HF patients with MVD. However, patients that failed CR showed 2.53-fold increased risk of MACEs compared to patients undergoing either selective IR or successful angiographic CR. A more comprehensive planning strategy should be devised before PCI in HF patients with MVD.
    Type of Medium: Online Resource
    ISSN: 0896-4327 , 1540-8183
    URL: Article
    DOI: 10.1155/2020/9506124
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2103585-4
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  • 2
    Online Resource
    Online Resource
    Table_1.DOCX
    Frontiers Media SA ; 2022
    In:  Frontiers in Cardiovascular Medicine Vol. 9 ( 2022-4-14)
    Details
    In: Frontiers in Cardiovascular Medicine, Frontiers Media SA, Vol. 9 ( 2022-4-14)
    Abstract: Coronary perfusion pressure (CPP) and coronary artery stenosis are responsible for myocardial perfusion. However, how CPP-related survival outcome affects revascularization is unclear. Objective The aim of this study is to investigate the prognostic role of CPP in patients with left ventricular systolic dysfunction (LVSD) undergoing percutaneous coronary intervention (PCI) with complete revascularization (CR) or reasonable incomplete revascularization (RIR). Methods We retrospectively screened 6,076 consecutive patients in a registry. The residual synergy between percutaneous coronary intervention with Taxus and cardiac surgery (SYNTAX) score (rSS) was used to define CR (rSS = 0) and RIR (0 & lt;rSS≤8). Propensity score matching was performed to reduce bias between RIR and CR. The primary endpoint was all-cause mortality. Results In total, 816 patients with LVSD who underwent CR or RIR were enrolled. After a mean follow-up of 4.6 years, 134 patients died. Both CPP and RIR independently predicted mortality in the total population. After 1:1 matching, 175 pairs of RIR and CR were found in patients with CPP & gt; 42 mmHg. Moreover, 101 pairs of RIR and CR were present in patients with CPP ≤ 42 mmHg. In patients with CPP & gt; 42 mmHg, RIR was not significantly different from CR in long-term mortality [hazard ratio (HR) 1.20; 95% confidence interval (CI):0.70–2.07; p = 0.513]; However, in patients with CPP≤42 mmHg, RIR had a significantly higher mortality risk than CR (HR 2.39; 95% CI: 1.27–4.50; p = 0.007). Conclusions The CPP had a risk stratification role in selecting different revascularization strategies in patients with LVSD. When patients with LVSD had CPP & gt; 42 mmHg, RIR was equivalent to CR in survival. However, when patients with LVSD had CPP ≤ 42 mmHg, RIR had a significantly higher mortality risk than CR.
    Type of Medium: Online Resource
    ISSN: 2297-055X
    URL: Article
    URL: Article
    DOI: 10.3389/fcvm.2022.860346
    DOI: 10.3389/fcvm.2022.860346.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2781496-8
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  • 3
    Online Resource
    Online Resource
    Comparison of long-term outcomes of complete vs. incomplete revascularization in elderly patients (≥75 years) with acute coronary syndrome and multi-vessel disease undergoing percutaneous coronary intervention
    Frontiers Media SA ; 2023
    In:  Frontiers in Cardiovascular Medicine Vol. 10 ( 2023-7-25)
    Details
    In: Frontiers in Cardiovascular Medicine, Frontiers Media SA, Vol. 10 ( 2023-7-25)
    Abstract: The optimal revascularization strategy for elderly patients with acute coronary syndrome (ACS) remains uncertain. We evaluated the impact of complete revascularization (CR) vs. incomplete revascularization (IR) in elderly ACS patients with multivessel disease (MVD) undergoing percutaneous coronary intervention (PCI). Methods Using registry data from 2011 to 2019, we conducted a propensity-score matched cohort study. Elderly patients (≥75 years) with ACS and MVD who underwent PCI were divided into CR and IR groups based on angiography during index hospitalization. Major adverse cardiovascular events (MACEs), including all-cause mortality, recurrent non-fatal myocardial infarction, and any revascularization, were assessed at 3-year follow-up. Results Among 1,018 enrolled patients, 496 (48.7%) underwent CR and 522 (51.3%) received IR. After 1:1 propensity-score matching, we analyzed 395 pairs. At 3-year follow-up, CR was significantly associated with lower MACE risk compared to IR (16.7% vs. 25.6%, HR = 0.65, 95% CI: 0.47–0.88, p  = 0.006), driven by reduced all-cause mortality. This benefit was consistent across all pre-specified subgroups, particularly in ST segment elevation (STE)-ACS patients. In non-STE (NSTE)-ACS subgroup analysis, CR was also associated with a lower risk of cardiac mortality compared to IR (HR = 0.30, 95% CI: 0.12–0.75, p  = 0.01). Conclusion In elderly ACS patients with MVD undergoing PCI, CR demonstrates superior long-term outcomes compared to IR, irrespective of STE- or NSTE-ACS presentation.
    Type of Medium: Online Resource
    ISSN: 2297-055X
    URL: Article
    DOI: 10.3389/fcvm.2023.1037392
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2781496-8
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  • 4
    Online Resource
    Online Resource
    Hepatitis B virus pre‐ S 2 mutant large surface protein inhibits DNA double‐strand break repair and leads to genome instability in hepatocarcinogenesis
    Wiley ; 2015
    In:  The Journal of Pathology Vol. 236, No. 3 ( 2015-07), p. 337-347
    Details
    In: The Journal of Pathology, Wiley, Vol. 236, No. 3 ( 2015-07), p. 337-347
    Abstract: Although hepatitis B virus ( HBV ) has been established to cause hepatocellular carcinoma ( HCC ), the exact mechanism remains to be clarified. Type II ground glass hepatocytes ( GGHs ) harbouring the HBV pre‐ S 2 mutant large surface protein ( LHBS ) have been recognized as a morphologically distinct hallmark of HCC in the advanced stages of chronic HBV infection. Considering its preneoplastic nature, we hypothesized that type II GGH may exhibit high genomic instability, which is important for the carcinogenic process in chronic HBV carriers. In this study we found that pre‐ S 2 mutant LHBS directly interacted with importin α1, the key factor that recognizes cargos undergoing nuclear transportation mediated by the importin α/β‐associated nuclear pore complex ( NPC ). By interacting with importin α1, which inhibits its function as an NPC factor, pre‐ S 2 mutant LHBS blocked nuclear transport of an essential DNA repair and recombination factor, Nijmegen breakage syndrome 1 ( NBS1 ), upon DNA damage, thereby delaying the formation of nuclear foci at the sites of DNA double‐strand breaks ( DSBs ). Pre‐ S 2 mutant LHBS was also found to block NBS1 ‐mediated homologous recombination repair and induce multi‐nucleation of cells. In addition, pre‐ S 2 mutant LHBS transgenic mice showed genomic instability, indicated by increased global gene copy number variations ( CNVs ), which were significantly higher than those in hepatitis B virus X mice, indicating that pre‐ S 2 mutant LHBS is the major viral oncoprotein inducing genomic instability in HBV ‐infected hepatocytes. Consistently, the human type II GGHs in HCC patients exhibited increased DNA DSBs representing significant genomic instability. In conclusion, type II GGHs harbouring HBV pre‐ S 2 mutant oncoprotein represent a high‐risk marker for the loss of genome integrity in chronic HBV carriers and explain the complex chromosome changes in HCCs . Mouse array CGH raw data: GEO Accession No. GSE61378 ( http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc= GSE61378 ) Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0022-3417 , 1096-9896
    URL: Issue
    URL: Article
    DOI: 10.1002/path.2015.236.issue-3
    DOI: 10.1002/path.4531
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 1475280-3
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  • 5
    Online Resource
    Online Resource
    Video_1.MP4
    Frontiers Media SA ; 2022
    In:  Frontiers in Neuroscience Vol. 16 ( 2022-11-16)
    Details
    In: Frontiers in Neuroscience, Frontiers Media SA, Vol. 16 ( 2022-11-16)
    Abstract: The dynamic vascular responses during cortical spreading depolarization (CSD) are causally related to pathophysiological consequences in numerous neurovascular conditions, including ischemia, traumatic brain injury, cerebral hemorrhage, and migraine. Monitoring of the hemodynamic responses of cerebral penetrating vessels during CSD is motivated to understand the mechanism of CSD and related neurological disorders. Six SD rats were used, and craniotomy surgery was performed before imaging. CSDs were induced by topical KCl application. Ultrasound dynamic ultrafast Doppler was used to access hemodynamic changes, including cerebral blood volume (CBV) and flow velocity during CSD, and further analyzed those in a single penetrating arteriole or venule. The CSD-induced hemodynamic changes with typical duration and propagation speed were detected by ultrafast Doppler in the cerebral cortex ipsilateral to the induction site. The hemodynamics typically showed triphasic changes, including initial hypoperfusion and prominent hyperperfusion peak, followed by a long-period depression in CBV. Moreover, different hemodynamics between individual penetrating arterioles and venules were proposed by quantification of CBV and flow velocity. The negative correlation between the basal CBV and CSD-induced change was also reported in penetrating vessels. These results indicate specific vascular dynamics of cerebral penetrating vessels and possibly different contributions of penetrating arterioles and venules to the CSD-related pathological vascular consequences. We proposed using ultrasound dynamic ultrafast Doppler imaging to investigate CSD-induced cerebral vascular responses. With this imaging platform, it has the potential to monitor the hemodynamics of cortical penetrating vessels during brain injuries to understand the mechanism of CSD in advance.
    Type of Medium: Online Resource
    ISSN: 1662-453X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fnins.2022.1015843
    DOI: 10.3389/fnins.2022.1015843.s001
    DOI: 10.3389/fnins.2022.1015843.s002
    DOI: 10.3389/fnins.2022.1015843.s003
    DOI: 10.3389/fnins.2022.1015843.s004
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2411902-7
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  • 6
    Online Resource
    Online Resource
    Large False Lumen Prevailed After Coronary Dissection and Intramural Haematoma Fenestration With Cutting Balloon
    Elsevier BV ; 2022
    In:  Heart, Lung and Circulation Vol. 31, No. 5 ( 2022-05), p. e82-e83
    Details
    In: Heart, Lung and Circulation, Elsevier BV, Vol. 31, No. 5 ( 2022-05), p. e82-e83
    Type of Medium: Online Resource
    ISSN: 1443-9506
    URL: Article
    DOI: 10.1016/j.hlc.2021.12.009
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 2026333-8
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  • 7
    Online Resource
    Online Resource
    Pholiota nameko Polysaccharides Protect against Ultraviolet A-Induced Photoaging by Regulating Matrix Metalloproteinases in Human Dermal Fibroblasts
    MDPI AG ; 2022
    In:  Antioxidants Vol. 11, No. 4 ( 2022-04-08), p. 739-
    Details
    In: Antioxidants, MDPI AG, Vol. 11, No. 4 ( 2022-04-08), p. 739-
    Abstract: Ultraviolet-A (UVA) exposure is a major cause of skin aging and can induce oxidative damage and accelerate skin wrinkling. Many natural polysaccharides exhibit a UV protective effect. In research on Pholiota nameko polysaccharides (PNPs), a natural macromolecular polysaccharide (4.4–333.487 kDa), studies have shown that PNPs can significantly decrease elastase activity to protect against UVA-induced aging in Hs68 human dermal fibroblasts. Cellular experiments in the present study indicated that PNPs can protect against UVA-induced oxidative damage in Hs68 cells by inhibiting the production of reactive oxygen species. Furthermore, PNPs significantly attenuated UVA-induced cell aging by decreasing the protein expression of matrix metalloproteinase 1, 3, and 9. Pretreatment of Hs68 cells with PNP-40, PNP-60, and PNP-80 before UVA irradiation increased protein expression of tissue inhibitor metalloproteinase 1 by 41%, 42%, and 56% relative to untreated cells. In conclusion, this study demonstrates that PNPs are a natural resource with potentially beneficial effects in protecting against UVA-induced skin aging.
    Type of Medium: Online Resource
    ISSN: 2076-3921
    URL: Article
    DOI: 10.3390/antiox11040739
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2704216-9
    SSG: 15,3
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  • 8
    Online Resource
    Online Resource
    Effects of Au-Fe Nanocluster on Neuron Differentiation with Electric Stimulation
    Elsevier BV ; 2020
    In:  Biophysical Journal Vol. 118, No. 3 ( 2020-02), p. 455a-
    Details
    In: Biophysical Journal, Elsevier BV, Vol. 118, No. 3 ( 2020-02), p. 455a-
    Type of Medium: Online Resource
    ISSN: 0006-3495
    URL: Article
    DOI: 10.1016/j.bpj.2019.11.2537
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2020
    detail.hit.zdb_id: 1477214-0
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Andrographolide, a Novel NF- κ B Inhibitor, Induces Vascular Smooth Muscle Cell Apoptosis via a Ceramide-p47phox-ROS Signaling Cascade
    Hindawi Limited ; 2013
    In:  Evidence-Based Complementary and Alternative Medicine Vol. 2013 ( 2013), p. 1-10
    Details
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2013 ( 2013), p. 1-10
    Abstract: Atherosclerosis is linked with the development of many cardiovascular complications. Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a crucial role in the development of atherosclerosis. Accordingly, the apoptosis of VSMCs, which occurs in the progression of vascular proliferation, may provide a beneficial strategy for managing cardiovascular diseases. Andrographolide, a novel nuclear factor- κ B inhibitor, is the most active and critical constituent isolated from the leaves of Andrographis paniculata . Recent studies have indicated that andrographolide is a potential therapeutic agent for treating cancer through the induction of apoptosis. In this study, the apoptosis-inducing activity and mechanisms in andrographolide-treated rat VSMCs were characterized. Andrographolide significantly induced reactive oxygen species (ROS) formation, p53 activation, Bax, and active caspase-3 expression, and these phenomena were suppressed by pretreating the cells with N-acetyl-L-cysteine, a ROS scavenger, or diphenylene iodonium, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) inhibitor. Furthermore, p47phox, a Nox subunit protein, was phosphorylated in andrographolide-treated rat VSMCs. However, pretreatment with 3-O-methyl-sphingomyelin, a neutral sphingomyelinase inhibitor, significantly inhibited andrographolide-induced p47phox phosphorylation as well as Bax and active caspase-3 expression. Our results collectively demonstrate that andrographolide-reduced cell viability can be attributed to apoptosis in VSMCs, and this apoptosis-inducing activity was associated with the ceramide-p47phox-ROS signaling cascade.
    Type of Medium: Online Resource
    ISSN: 1741-427X , 1741-4288
    URL: Article
    DOI: 10.1155/2013/821813
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2013
    detail.hit.zdb_id: 2148302-4
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  • 10
    Online Resource
    Online Resource
    Andrographolide Inhibits Nuclear Factor- κ B Activation through JNK-Akt-p65 Signaling Cascade in Tumor Necrosis Factor- α -Stimulated Vascular Smooth Muscle Cells
    Hindawi Limited ; 2014
    In:  The Scientific World Journal Vol. 2014 ( 2014), p. 1-10
    Details
    In: The Scientific World Journal, Hindawi Limited, Vol. 2014 ( 2014), p. 1-10
    Abstract: Critical vascular inflammation leads to vascular dysfunction and cardiovascular diseases, including abdominal aortic aneurysms, hypertension, and atherosclerosis. Andrographolide is the most active and critical constituent isolated from the leaves of Andrographis paniculata , a herbal medicine widely used for treating anti-inflammation in Asia. In this study, we investigated the mechanisms of the inhibitory effects of andrographolide in vascular smooth muscle cells (VSMCs) exposed to a proinflammatory stimulus, tumor necrosis factor- α (TNF- α ). Treating TNF- α -stimulated VSMCs with andrographolide suppressed the expression of inducible nitric oxide synthase in a concentration-dependent manner. A reduction in TNF- α -induced c-Jun N-terminal kinase (JNK), Akt, and p65 phosphorylation was observed in andrographolide-treated VSMCs. However, andrographolide affected neither I κ B α degradation nor p38 mitogen-activated protein kinase or extracellular signal-regulated kinase 1/2 phosphorylation under these conditions. Both treatment with LY294002, a phosphatidylinositol 3-kinase/Akt inhibitor, and treatment with SP600125, a JNK inhibitor, markedly reversed the andrographolide-mediated inhibition of p65 phosphorylation. In addition, LY294002 and SP600125 both diminished Akt phosphorylation, whereas LY294002 had no effects on JNK phosphorylation. These results collectively suggest that therapeutic interventions using andrographolide can benefit the treatment of vascular inflammatory diseases, and andrographolide-mediated inhibition of NF- κ B activity in TNF- α -stimulated VSMCs occurs through the JNK-Akt-p65 signaling cascade, an I κ B α -independent mechanism.
    Type of Medium: Online Resource
    ISSN: 2356-6140 , 1537-744X
    URL: Article
    DOI: 10.1155/2014/130381
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2014
    detail.hit.zdb_id: 2075968-X
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