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  • American Heart Association (AHA)  (46)
  • American Association for the Advancement of Science (AAAS)  (35)
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  • 1
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    Common Genetic Variants of MGP Are Associated With Calcification on the Arterial Wall but Not With Calcification Present in the Atherosclerotic Plaques [Original Articles] (2013)
    American Heart Association (AHA)
    Details
    Publication Date: 2013-06-19
    Description: Background— Two endophenotypes of arterial calcification, calcification on arterial wall and calcification in atherosclerotic plaques, are associated with different types of cardiovascular events. Mgp -deficient mice showed matrix Gla protein (MGP) is strongly associated with calcification on arterial wall without atherosclerotic plaques, and MGP variants were not significantly associated with myocardial infarction. MGP may play different roles in the 2 endophenotypes. Methods and Results— We analyzed the associations of MGP variants rs4236, rs1800801, and rs1800802 with the 2 endophenotypes determined by multidetector computed tomography angiography. A total of 585 with calcification on coronary artery wall, 675 with calcification in coronary atherosclerotic plaques, 454 with calcification on aortic wall, and 725 controls were enrolled. After Bonferroni correction, rs4236 and rs1800801 were still associated with calcification on arterial wall, the odds ratios were 0.708 (95% confidence interval, 0.540–0.928) for rs4236 and 0.652 (95% confidence interval, 0.479–0.888) for rs1800801 in coronary artery wall calcification, and 0.699 (95% confidence interval, 0.525–0.931) for rs4236 and 0.650 (95% confidence interval, 0.467–0.905) for rs1800801 in aortic wall calcification, respectively. The variants were correlated with calcification severity by ln(CAC Agatston score+1) in coronary artery wall calcification but not in atherosclerotic plaque calcification. In accordance with their associations with calcification on arterial wall, rs4236C and rs1800801A were associated with higher MGP plasma levels, whereas rs1800802C was associated with lower MGP levels in normal controls. Because of the role of calcification in plaque vulnerability, their associations with acute myocardial infarction were also determined in 771 controls and 752 patients, no association was found. Conclusions— MGP genetic variants showed association with calcification on arterial wall but not with calcification in atherosclerotic plaques.
    Keywords: Clinical genetics, Risk Factors, Acute myocardial infarction, Other Vascular biology
    Print ISSN: 1942-325X
    Electronic ISSN: 1942-3268
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 2
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    Anderson localization of electrons in single crystals: LixFe7Se8 (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-02-21
    Description: Anderson (disorder-induced) localization, proposed more than half a century ago, has inspired numerous efforts to explore the absence of wave diffusions in disordered media. However, the proposed disorder-induced metal-insulator transition (MIT), associated with the nonpropagative electron waves, has hardly been observed in three-dimensional (3D) crystalline materials, let alone single crystals. We report the observation of an MIT in centimeter-size single crystals of Li x Fe 7 Se 8 induced by lattice disorder. Both specific heat and infrared reflectance measurements reveal the presence of considerable electronic states in the vicinity of the Fermi level when the MIT occurs, suggesting that the transition is not due to Coulomb repulsion mechanism. The 3D variable range hopping regime evidenced by electrical transport measurements at low temperatures indicates the localized nature of the electronic states on the Fermi level. Quantitative analyses of carrier concentration, carrier mobility, and simulated density of states (DOS) fully support that Li x Fe 7 Se 8 is an Anderson insulator. On the basis of these results, we provide a unified DOS picture to explain all the experimental results, and a schematic diagram for finding other potential Anderson insulators. This material will thus serve as a rich playground for both theoretical and experimental investigations on MITs and disorder-induced phenomena.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    A single transcription factor promotes both yield and immunity in rice (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-07
    Description: Plant immunity often penalizes growth and yield. The transcription factor Ideal Plant Architecture 1 (IPA1) reduces unproductive tillers and increases grains per panicle, which results in improved rice yield. Here we report that higher IPA1 levels enhance immunity. Mechanistically, phosphorylation of IPA1 at amino acid Ser 163 within its DNA binding domain occurs in response to infection by the fungus Magnaporthe oryzae and alters the DNA binding specificity of IPA1. Phosphorylated IPA1 binds to the promoter of the pathogen defense gene WRKY45 and activates its expression, leading to enhanced disease resistance. IPA1 returns to a nonphosphorylated state within 48 hours after infection, resuming support of the growth needed for high yield. Thus, IPA1 promotes both yield and disease resistance by sustaining a balance between growth and immunity.
    Keywords: Botany
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Hematoma Volume Measurement in Gradient Echo MRI Using Quantitative Susceptibility Mapping [Brief Reports] (2013)
    American Heart Association (AHA)
    In: Stroke
    Details
    Publication Date: 2013-07-23
    Description: Background and Purpose— A novel quantitative susceptibility mapping (QSM) processing technology has been developed to map tissue susceptibility property without blooming artifacts. We hypothesize that hematoma volume measurement on QSM is independent of imaging parameters, eliminating its echo time dependence on gradient echo MRI. Methods— Gradient echo MRI of 16 patients with intracerebral hemorrhage was processed with susceptibility-weighted imaging, R 2 * (=1/T2*) mapping, and QSM at various echo times. Hematoma volumes were measured from these images. Results— Linear regression of hematoma volume versus echo time showed substantial slopes for gradient echo magnitude (0.45±0.31 L/s), susceptibility-weighted imaging (0.52±0.46), and R 2 * (0.39±0.30) but nearly zero slope for QSM (0.01±0.05). At echo time=20 ms, hematoma volume on QSM was 0.80 x that on gradient echo magnitude image ( R 2 =0.99). Conclusions— QSM can provide reliable measurement of hematoma volume, which can be performed rapidly and accurately using a semiautomated segmentation tool.
    Keywords: CT and MRI, Intracerebral Hemorrhage, Aneurysm, AVM, hematoma
    Print ISSN: 0039-2499
    Electronic ISSN: 1524-4628
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 5
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    Nebivolol Induces Distinct Changes in Profibrosis MicroRNA Expression Compared With Atenolol, in Salt-Sensitive Hypertensive Rats [Heart] (2013)
    American Heart Association (AHA)
    Details
    Publication Date: 2013-04-18
    Description: Nebivolol is a selective β1-blocker with nitric oxide–enhancing effects. MicroRNAs are small noncoding RNA molecules that downregulate gene expression. We compared the effects of nebivolol and atenolol, a first generation β1-selective blocker, on left ventricular hypertrophy, fibrosis, and function and microRNA expression in a rodent model of hypertension. Dahl salt-sensitive rats received either low-salt chow (control) or AIN-76A high-salt (8% NaCl) diet and randomized to vehicle (high-salt), nebivolol (20 mg/kg per day), or atenolol (50 mg/kg per day) for 8 weeks. High-salt induced left ventricular hypertrophy and fibrosis and decreased the expression of miR-27a, -29a, and -133a. Nebovolol attenuated deterioration of left ventricular systolic function, remodeling, and fibrosis more than atenolol, despite similar effects on heart rate and blood pressure. Nebivolol, but not atenolol, prevented the decrease in miR-27a and -29a induced by high-salt. Nebivolol and atenolol equally attenuated the decrease in miR-133a. In vitro overexpression of miR-27a,-29a, and -133a inhibited cardiomyocyte hypertrophy and reduced collagen expression. Both miR-27a and -29a target Sp1, and miR-133a targets Cdc42. Pharmacological inhibition of Sp1 and Cdc42 decreased myocardial fibrosis and hypertrophy. Our data support a differential microRNAs expression profile in salt-induced hypertension. Nebivolol substantially attenuated cardiac remodeling, hypertrophy, and fibrosis more than atenolol. These effects are related to attenuation of the hypertension-induced decrease in miR-27a and -29a (with a subsequent decrease in Sp1 expression) and miR-133a (with a subsequent decrease in Cdc42).
    Keywords: Remodeling, Animal models of human disease, Hypertrophy
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 6
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    Prolyl Hydroxylase Domain Protein 2 Silencing Enhances the Survival and Paracrine Function of Transplanted Adipose-Derived Stem Cells in Infarcted Myocardium [Integrative Physiology] (2013)
    American Heart Association (AHA)
    Details
    Publication Date: 2013-07-19
    Description: Rationale: Transplantation of stem cells into damaged hearts has had modest success as a treatment for ischemic heart disease. One of the limitations is the poor stem cell survival in the diseased microenvironment. Prolyl hydroxylase domain protein 2 (PHD2) is a cellular oxygen sensor that regulates 2 key transcription factors involved in cell survival and inflammation: hypoxia-inducible factor and nuclear factor-B. Objective: We studied whether and how PHD2 silencing in human adipose-derived stem cells (ADSCs) enhances their cardioprotective effects after transplantation into infarcted hearts. Methods and Results: ADSCs were transduced with lentiviral short hairpin RNA against prolyl hydroxylase domain protein 2 (shPHD2) to silence PHD2. ADSCs, with or without shPHD2, were transplanted after myocardial infarction in mice. ADSCs reduced cardiomyocyte apoptosis, fibrosis, and infarct size and improved cardiac function. shPHD2-ADSCs exerted significantly more protection. PHD2 silencing induced greater ADSC survival, which was abolished by short hairpin RNA against hypoxia-inducible factor-1α. Conditioned medium from shPHD2-ADSCs decreased cardiomyocyte apoptosis. Insulin-like growth factor-1 (IGF-1) levels were significantly higher in the conditioned medium of shPHD2-ADSCs versus ADSCs, and depletion of IGF-1 attenuated the cardioprotective effects of shPHD2-ADSC–conditioned medium. Nuclear factor-B activation was induced by shPHD2 to induce IGF-1 secretion via binding to IGF-1 gene promoter. Conclusions: PHD2 silencing promotes ADSCs survival in infarcted hearts and enhances their paracrine function to protect cardiomyocytes. The prosurvival effect of shPHD2 on ADSCs is hypoxia-inducible factor-1α dependent, and the enhanced paracrine function of shPHD2-ADSCs is associated with nuclear factor-B–mediated IGF-1 upregulation. PHD2 silencing in stem cells may be a novel strategy for enhancing the effectiveness of stem cell therapy after myocardial infarction.
    Keywords: Animal models of human disease, Apoptosis, Heart failure - basic studies, Acute myocardial infarction
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 7
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    Genetic and Functional Evidence Supports LPAR1 as a Susceptibility Gene for Hypertension [Genetics] (2015)
    American Heart Association (AHA)
    Details
    Publication Date: 2015-08-13
    Description: Essential hypertension is a complex disease affected by genetic and environmental factors and serves as a major risk factor for cardiovascular diseases. Serum lysophosphatidic acid correlates with an elevated blood pressure in rats, and lysophosphatidic acid interacts with 6 subtypes of receptors. In this study, we assessed the genetic association of lysophosphatidic acid receptors with essential hypertension by genotyping 28 single-nucleotide polymorphisms from genes encoding for lysophosphatidic acid receptors, LPAR1 , LPAR2 , LPAR3 , LPAR4 , LPAR5 , and LPAR6 and their flanking sequences, in 3 Han Chinese cohorts consisting of 2630 patients and 3171 controls in total. We identified a single-nucleotide polymorphism, rs531003 in the 3'-flanking genomic region of LPAR1 , associated with hypertension (the Bonferroni corrected P =1.09 x 10 –5 , odds ratio [95% confidence interval]=1.23 [1.13–1.33]). The risk allele C of rs531003 is associated with the increased expression of LPAR1 and the susceptibility of hypertension, particularly in those with a shortage of sleep ( P =4.73 x 10 –5 , odds ratio [95% confidence interval]=1.75 [1.34–2.28]). We further demonstrated that blood pressure elevation caused by sleep deprivation and phenylephrine-induced vasoconstriction was both diminished in LPAR1 -deficient mice. Together, we show that LPAR1 is a novel susceptibility gene for human essential hypertension and that stress, such as shortage of sleep, increases the susceptibility of patients with risk allele to essential hypertension.
    Keywords: Other hypertension, Endothelium/vascular type/nitric oxide
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 8
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    Chronic Kidney Disease in Patients With Lacunar Stroke: Association With Enlarged Perivascular Spaces and Total Magnetic Resonance Imaging Burden of Cerebral Small Vessel Disease [Clinical Sciences] (2015)
    American Heart Association (AHA)
    In: Stroke
    Details
    Publication Date: 2015-07-28
    Description: Background and Purpose— The relationship between chronic kidney disease and cerebral small vessel disease (cSVD), especially enlarged perivascular spaces (EPVS), has not been fully understood. This study aimed to investigate the association of chronic kidney disease and EPVS, as well as the total burden of cSVD on magnetic resonance imaging, expressed by the simultaneous presence of multiple markers of cSVD, among patients with first-ever lacunar stroke. Methods— Four hundred and thirteen consecutive patients were prospectively enrolled. Centrum semiovale and basal ganglia EPVS on T2-weighted magnetic resonance imaging, as well as other imaging markers of cSVD, including lacune, white matter lesions, and cerebral microbleeds, were rated using validated scales. Chronic kidney disease was defined as either reduced estimated glomerular filtration rate or the presence of proteinuria. Results— After adjustments for potential confounders by logistic regression, proteinuria and impaired estimated glomerular filtration rate were correlated with the severity of EPVS in both centrum semiovale (odds ratio [OR] 2.59; 95% confidence interval [CI] 1.19–5.64 and OR 2.37; 95% CI 1.19–4.73) and basal ganglia (OR 5.12; 95% CI 2.70–12.10 and OR 4.17; 95% CI 2.08–8.37). A similar association was also found between proteinuria and low estimated glomerular filtration rate levels and the comprehensive cSVD burden (OR 2.13; 95% CI 1.10–4.14 and OR 5.59; 95% CI 2.58–12.08). Conclusions— Proteinuria and impaired estimated glomerular filtration rate are associated with increasing EPVS severity and, furthermore, accumulated magnetic resonance imaging burden of cSVD in patients with first-ever acute lacunar stroke.
    Keywords: Acute Cerebral Infarction, Computerized tomography and Magnetic Resonance Imaging
    Print ISSN: 0039-2499
    Electronic ISSN: 1524-4628
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 9
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    Unraveling the storage mechanism in organic carbonyl electrodes for sodium-ion batteries (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-09-20
    Description: Organic carbonyl compounds represent a promising class of electrode materials for secondary batteries; however, the storage mechanism still remains unclear. We take Na 2 C 6 H 2 O 4 as an example to unravel the mechanism. It consists of alternating Na-O octahedral inorganic layer and -stacked benzene organic layer in spatial separation, delivering a high reversible capacity and first coulombic efficiency. The experiment and calculation results reveal that the Na-O inorganic layer provides both Na + ion transport pathway and storage site, whereas the benzene organic layer provides electron transport pathway and redox center. Our contribution provides a brand-new insight in understanding the storage mechanism in inorganic-organic layered host and opens up a new exciting direction for designing new materials for secondary batteries.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    Direct Interaction of Kindlin-3 With Integrin {alpha}IIb{beta}3 in Platelets Is Required for Supporting Arterial Thrombosis in Mice [Basic Sciences] (2014)
    American Heart Association (AHA)
    Details
    Publication Date: 2014-08-21
    Description: Objective— Kindlin-3 is a critical supporter of integrin function in platelets. Lack of expression of kindlin-3 protein in patients impairs integrin αIIbβ3–mediated platelet aggregation. Although kindlin-3 has been categorized as an integrin-binding partner, the functional significance of the direct interaction of kindlin-3 with integrin αIIbβ3 in platelets has not been established. Here, we evaluated the significance of the binding of kindlin-3 to integrin αIIbβ3 in platelets in supporting integrin αIIbβ3–mediated platelet functions. Approach and Results— We generated a strain of kindlin-3 knockin (K3KI) mice that express a kindlin-3 mutant that carries an integrin-interaction defective substitution. K3KI mice could survive normally and express integrin αIIbβ3 on platelets similar to their wild-type counterparts. Functional analysis revealed that K3KI mice exhibited defective platelet function, including impaired integrin αIIbβ3 activation, suppressed platelet spreading and platelet aggregation, prolonged tail bleeding time, and absence of platelet-mediated clot retraction. In addition, whole blood drawn from K3KI mice showed resistance to in vitro thrombus formation and, as a consequence, K3KI mice were protected from in vivo arterial thrombosis. Conclusions— These observations demonstrate that the direct binding of kindlin-3 to integrin αIIbβ3 is involved in supporting integrin αIIbβ3 activation and integrin αIIbβ3-dependent responses of platelets and consequently contributes significantly to arterial thrombus formation.
    Keywords: Aggregation, Platelets
    Print ISSN: 1079-5642
    Electronic ISSN: 1524-4636
    Topics: Medicine
    Published by American Heart Association (AHA)
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