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  • Ovid Technologies (Wolters Kluwer Health)  (18)
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  • 1
    Online Resource
    Online Resource
    Efforts to Improve Survival Outcomes of Out-of-Hospital Cardiac Arrest in China: BASIC-OHCA
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation: Cardiovascular Quality and Outcomes
    Details
    In: Circulation: Cardiovascular Quality and Outcomes, Ovid Technologies (Wolters Kluwer Health)
    Abstract: Establishing registries to collect demographic characteristics, processes of care, and outcomes of patients with out-of-hospital cardiac arrest (OHCA) can better understand epidemiological trends, measure care quality, and identify opportunities for improvement. This study aimed to describe the design, implementation, and scientific significance of a nationwide registry―the BASIC-OHCA (Baseline Investigation of Out-of-Hospital Cardiac Arrest)―in China. Methods: BASIC-OHCA was designed as a prospective, multicenter, observational, population-based study. The BASIC-OHCA registry was developed based on Utstein templates. BASIC-OHCA includes all OHCA patients confirmed by emergency medical services (EMS) personnel regardless of age, sex, or cause. Patients declared dead at the scene by EMS personnel for any reasons are also included. To fully characterize an OHCA event, BASIC-OHCA collects data from 3 sources—EMS, the receiving hospital, and patient follow-up—and links them to form a single record. Once data entry is completed and quality is checked, individual identifiers are stripped from the record. Results: Currently, 32 EMS agencies in 7 geographic regions contribute data to BASIC-OHCA. They are distributed in the urban and rural areas, covering ≈9% of the population of mainland China. Data collection started on August 1, 2019. By July 31, 2020, a total of 92 913 EMS-assessed OHCA patients were enrolled. Among 28969 (31.18%) EMS-treated OHCAs‚ the mean age was 65.79±17.36 years, and 68.35% were males. The majority of OHCAs (76.85%) occurred at home or residence. A shockable initial rhythm was reported in 5.43% of patients. Any return of spontaneous circulation, survival to hospital discharge, and favorable neurological outcome at hospital discharge were 5.98%, 1.15%, and 0.83%, respectively. Conclusions: BASIC-OHCA is the first nationwide registry on OHCA in China. It can be used as a public health surveillance system and as a platform to produce evidence-based practices to help identify opportunities for improvement. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03926325.
    Type of Medium: Online Resource
    ISSN: 1941-7713 , 1941-7705
    URL: Article
    DOI: 10.1161/CIRCOUTCOMES.121.008856
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2453882-6
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  • 2
    Online Resource
    Online Resource
    ALDH2 (Aldehyde Dehydrogenase 2) Protects Against Hypoxia-Induced Pulmonary Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 39, No. 11 ( 2019-11), p. 2303-2319
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 11 ( 2019-11), p. 2303-2319
    Abstract: Hypoxia-induced pulmonary hypertension (HPH) increases lipid peroxidation with generation of toxic aldehydes that are metabolized by detoxifying enzymes, including ALDH2 (aldehyde dehydrogenase 2). However, the role of lipid peroxidation and ALDH2 in HPH pathogenesis remain undefined. Approach and Results: To determine the role of lipid peroxidation and ALDH2 in HPH, C57BL/6 mice, ALDH2 transgenic mice, and ALDH2 knockout (ALDH2 −/− ) mice were exposed to chronic hypoxia, and recombinant tissue-specific ALDH2 overexpression adeno-associated viruses were introduced into pulmonary arteries via tail vein injection for ALDH2 overexpression. Human pulmonary artery smooth muscle cells were used to elucidate underlying mechanisms in vitro. Chronic hypoxia promoted lipid peroxidation due to the excessive production of reactive oxygen species and increased expression of lipoxygenases in lung tissues. 4-hydroxynonenal but not malondialdehyde level was increased in hypoxic lung tissues which might reflect differences in detoxifying enzymes. ALDH2 overexpression attenuated the development of HPH, whereas ALDH2 knockout aggravated it. Specific overexpression of ALDH2 using AAV1 (adeno-associated virus)-ICAM (intercellular adhesion molecule) 2p-ALDH2 and AAV2-SM22αp (smooth muscle 22 alpha)-ALDH2 viral vectors in pulmonary artery smooth muscle cells, but not endothelial cells, prevented the development of HPH. Hypoxia or 4-hydroxynonenal increased stabilization of HIF (hypoxia-inducible factor)-1α, phosphorylation of Drp1 (dynamin-related protein 1) at serine 616, mitochondrial fission, and pulmonary artery smooth muscle cells proliferation, whereas ALDH2 activation suppressed the latter 3. Conclusions: Increased 4-hydroxynonenal level plays a critical role in the development of HPH. ALDH2 attenuates the development of HPH by regulating mitochondrial fission and smooth muscle cell proliferation suggesting ALDH2 as a potential new therapeutic target for pulmonary hypertension.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.119.312946
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1494427-3
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  • 3
    Online Resource
    Online Resource
    Two-dimensional strain technique to detect the function of coronary collateral circulation
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Coronary Artery Disease Vol. 23, No. 3 ( 2012-05), p. 188-194
    Details
    In: Coronary Artery Disease, Ovid Technologies (Wolters Kluwer Health), Vol. 23, No. 3 ( 2012-05), p. 188-194
    Type of Medium: Online Resource
    ISSN: 0954-6928
    URL: Article
    DOI: 10.1097/MCA.0b013e32834f1b56
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2042449-8
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  • 4
    Online Resource
    Online Resource
    Therapies for diabetic gastroparesis : A protocol for a systematic review and network meta-analysis
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Medicine Vol. 99, No. 21 ( 2020-05-22), p. e20461-
    Details
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 99, No. 21 ( 2020-05-22), p. e20461-
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    URL: Article
    DOI: 10.1097/MD.0000000000020461
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2049818-4
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  • 5
    Online Resource
    Online Resource
    Trends in percutaneous coronary intervention in China: analysis of China PCI Registry Data from 2010 to 2018
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Cardiology Plus Vol. 7, No. 3 ( 2022-07), p. 118-124
    Details
    In: Cardiology Plus, Ovid Technologies (Wolters Kluwer Health), Vol. 7, No. 3 ( 2022-07), p. 118-124
    Abstract: In the past 30 to 40 years, percutaneous coronary intervention (PCI) in China has greatly improved. The State Ministry of Health established a quality control (QC) system in 2009, and all medical centers were required to report their PCI cases. We analyzed the data from the QC system to describe the current status and development of PCI in China. Methods: PCI case data during a period from 2010 to 2018 were extracted from the online QC system. Data quality was audited by QC centers at the provincial level. Statistical analysis was mainly descriptive. Trend analysis was conducted by recoding the year as a continuous variable in linear regression or logistic regression. Results: The number of medical centers reporting PCI cases was 941 in 2010, and increased to 1,788 in 2018. Total number of PCI cases reported online to the QC system was 236,717 in 2010, and increased to 705,970 in 2018. Estimate of the actual case number that included those reported offline only (based on offline audit by provincial QC centers) was 284,936 in 2010, and increased to 915,256 in 2018. The most common indication for PCI was unstable angina (52.9%–59.1%), followed by ST elevation myocardial infarction (STEMI; 25.0%–27.4%). Majority of the PCI procedures were performed via the radial artery (65.4% in 2010 and 90.7% in 2018). Angiography detected a left main lesion in 5%, single-vessel disease in 38.7% to 44.4%, two-vessel disease in 22.3% to 27.5%, and three-vessel disease in 27.0% to 28.7% of the patients. The rate of primary PCI for STEMI in all STEMI cases was 28.0% in 2010, and increased to 45.9% in 2018. The average number of stents implanted per case was 1.63 in 2010, and decreased to 1.46 in 2018. There was a trend for decreasing mortality (0.31% in 2010; 0.26% in 2018). Conclusions: The number of PCI cases in China increased steadily during a period from 2010 to 2018, with stable mortality rate. Transradial access is the dominant PCI route. The rate of primary PCI for STEMI increased substantially, but remained relatively low.
    Type of Medium: Online Resource
    ISSN: 2470-7511
    URL: Article
    DOI: 10.1097/CP9.0000000000000021
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2987027-6
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  • 6
    Online Resource
    Online Resource
    Pentoxifylline Ameliorates Cardiac Fibrosis, Pathological Hypertrophy, and Cardiac Dysfunction in Angiotensin II-induced Hypertensive Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of Cardiovascular Pharmacology Vol. 67, No. 1 ( 2016-01), p. 76-85
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 67, No. 1 ( 2016-01), p. 76-85
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000316
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    Platelet IκB Kinase-β Deficiency Increases Mouse Arterial Neointima Formation via Delayed Glycoprotein Ibα Shedding
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 33, No. 2 ( 2013-02), p. 241-248
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 2 ( 2013-02), p. 241-248
    Abstract: On the luminal surface of injured arteries, platelet activation and leukocyte–platelet interactions are critical for the initiation and progression of arterial restenosis. The transcription factor nuclear factor-κB is a critical molecule in platelet activation. Here, we investigated the role of the platelet nuclear factor-κB pathway in forming arterial neointima after arterial injury. Methods and Results— We performed carotid artery wire injuries in low-density lipoprotein receptor-deficient (LDLR –/– ) mice with a platelet-specific deletion of IκB kinase-β (IKKβ) (IKKβ fl/fl /PF4 cre /LDLR –/– ) and in control mice (IKKβ fl/fl /LDLR –/– ). The size of the arterial neointima was 61% larger in the IKKβ fl/fl /PF4 cre /LDLR –/– mice compared with the littermate control IKKβ fl/fl /LDLR –/– mice. Compared with the control mice, the IKKβ fl/fl /PF4 cre /LDLR –/– mice exhibited more leukocyte adhesion at the injured area. The extent of glycoprotein Ibα shedding after platelet activation was compromised in the IKKβ-deficient platelets. This effect was associated with a low level of the active form of A Disintegrin And Metalloproteinase 17, the key enzyme involved in mediating glycoprotein Ibα shedding in activated IKKβ-deficient platelets. Conclusion— Platelet IKKβ deficiency increases the formation of injury-induced arterial neointima formation. Thus, nuclear factor-κB–related inhibitors should be carefully evaluated for use in patients after an arterial intervention.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.112.300781
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1494427-3
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  • 8
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    Abstract 699: Mitochondrial Aldehyde Dehydrogenase (aldh-2) Protects Against Lipopolysaccharide-induced Myocardial Contractile Dysfunction by Suppression of ER Stress via Regulation of Autophagy
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 35, No. suppl_1 ( 2015-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. suppl_1 ( 2015-05)
    Abstract: Lipopolysaccharide (LPS), a constituent of the outer membrane of Gram-negative bacteria, is the principal culprit factor responsible for the development of multi-organ failure including septic heart failure - a major contributor to increased mortality in patients with sepsis. However, there is still no efficacious treatment for septic cardiomyophathy. ALDH2 is well-known for its distinct beneficial role in cardiac pathologies including heart failure, ischemia and reperfusion injury. Little is known with regards to its effect on septic cardiomyopathy and the underlying mechanism. This study was designed to examine whether ALDH2 affects LPS-induced myocardial dysfunction and the underlying mechanism involved with a focus on ER stress and autophagy. WT and ALDH2 transgenic mice were subjected to LPS (4 mg/kg, 4 h). Myocardial mechanical and intracellular Ca2+ properties were examined in FVB wild-type and ALDH2 transgenic mice using echocardiography and IonOptix SoftEdge techniques. Protein markers for ER stress, autophagy and related signaling molecules were evaluated. LPS compromised cardiac contractile function shown as reduced fractional shortening, peak shortening, maximal velocity of shortening/relengthening, prolonged relengthening duration and impaired intracellular Ca2+ homeostasis, associated with overt ER stress, upregulated autophagy, suppressed phosphorylation of Akt and its downstream signal molecule mTOR, the effects of which were attenuated by ALDH2. In vitro study revealed that the ER stress inducer tunicamycin exacerbated LPS-induced myocardial dysfunction, which was abrogated by the ALDH2 activator Alda-1 and the autophagy inhibitor 3-MA. Interestingly, the beneficial effect of Alda-1 was obliterated by the autophagy inducer rapamycin, Akt inhibitor AktI and mTOR inhibitor RAD001. We conclude that ALDH2 protects against LPS-induced myocardial dysfunction possibly through suppression of ER stress and inhibition of autophagy.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.35.suppl_1.699
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1494427-3
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  • 9
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    Online Resource
    Postinfarction Hearts Are Protected by Premature Senescent Cardiomyocytes Via GATA4‐Dependent CCN1 Secretion
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Journal of the American Heart Association Vol. 7, No. 18 ( 2018-09-18)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 7, No. 18 ( 2018-09-18)
    Abstract: Stress‐induced cell premature senescence participates in a variety of tissue and organ remodeling by secreting such proteins as proinflammatory cytokines, chemokines, and growth factors. However, the role of cardiomyocyte senescence in heart remodeling after acute myocardial infarction has not been thoroughly elucidated to date. Therefore, we sought to clarify the impact of premature myocardial senescence on postinfarction heart function. Methods and Results Senescence markers, including p16 INK 4a , p21 CIP 1/ WAF 1 , and SA ‐β‐gal staining, were analyzed in several heart disease models by immunostaining. Both postinfarction mouse hearts and ischemic human myocardium demonstrated increased senescence markers. Additionally, senescence‐related secretory phenotype was activated after acute myocardial infarction, which upregulated senescence‐related secretory phenotype factors, including CCN family member 1 ( CCN 1), interleukin‐1α, tumor necrosis factor α, and monocyte chemoattractant protein‐1. In vivo, a tail vein injection of AAV 9‐ Gata4 ‐sh RNA significantly attenuated senescence‐related secretory phenotype secretion and aggravated postinfarction heart dysfunction. Furthermore, among activated senescence‐related secretory phenotype factors, CCN 1 administration reduced myofibroblast viability in vitro and rescued the deleterious effect of AAV 9‐ Gata4 ‐sh RNA in vivo. Conclusions Myocardial premature senescence was observed in the ischemic hearts and improved postinfarction heart function, partly through the GATA‐binding factor 4‐ CCN 1 pathway.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.118.009111
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2653953-6
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  • 10
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    Online Resource
    ALDH2 Activation Inhibited Cardiac Fibroblast-to-Myofibroblast Transformation Via the TGF-β1/Smad Signaling Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Journal of Cardiovascular Pharmacology Vol. 73, No. 4 ( 2019-04), p. 248-256
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 73, No. 4 ( 2019-04), p. 248-256
    Abstract: Pathological stimulus–triggered differentiation of cardiac fibroblasts plays a major role in the development of myocardial fibrosis. Aldehyde dehydrogenase 2 (ALDH2) was reported to exert a protective role in cardiovascular disease, and whether ALDH2 is involved in cardiac fibroblast differentiation remains unclear. In this study, we used transforming growth factor-β1 (TGF-β1) to induce the differentiation of human cardiac fibroblasts (HCFs) and adopted ALDH2 activator Alda-1 to verify the influence of ALDH2 on HCF differentiation. Results showed that ALDH2 activity was obviously impaired when treating HCFs with TGF-β1. Activation of ALDH2 with Alda-1 inhibited the transformation of HCFs into myofibroblasts, demonstrated by the decreased smooth muscle actin (α-actin) and periostin expression, reduced HCF-derived myofibroblast proliferation, collagen production, and contractility. Moreover, application of Smad2/3 inhibitor alleviated TGF-β1–induced HCF differentiation and improved ALDH2 activity, which was reversed by the application of ALDH2 inhibitor daidzin. Finally, Alda-1–induced HCF alterations alleviated neonatal rat cardiomyocyte hypertrophy, supported by the immunostaining of α-actin. To summarize, activation of ALDH2 enzymatic activity inhibited the differentiation of cardiac fibroblasts via the TGF-β1/Smad signaling pathway, which might be a promising strategy to relieve myocardial fibrosis of various causes.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000655
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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