GLORIA — GEOMAR Library Ocean Research Information Access

1

Unknown

Angle-resolved Photoemission Spectroscopy Study on the Surface States of the Correlated Topological Insulator YbB6 (2014)

M. Xia; J. Jiang; Z. R. Ye; Y. H. Wang; Y. Zhang; S. D. Chen; X. H. Niu; D. F. Xu; F. Chen; X. H. Chen; B. P. Xie; T. Zhang; D. L. Feng

Nature Publishing Group (NPG)

In: Scientific Reports

add to mindlist on the mindlist

Details

Publication Date: 2014-08-09

Description: YbB6 is recently predicted to be a moderately correlated topological insulator, which provides a playground to explore the interplay between correlation and topological properties. With angle-resolved photoemission spectroscopy, we directly observed almost linearly dispersive bands around the time-reversal invariant momenta and with negligible kz dependence, consistent with odd number of surface states crossing the Fermi level in a Z2 topological insulator. Circular dichroism photoemission spectra suggest that these in-gap states possess chirality of orbital angular momentum, which is related to the chiral spin texture, further indicative of their topological nature. The observed insulating gap of YbB6 is about 100 meV, larger than that found by theoretical calculations. Our results present strong evidence that YbB6 is a correlated topological insulator and provide a foundation for further studies of this promising material. Scientific Reports 4 doi: 10.1038/srep05999

Electronic ISSN: 2045-2322

Topics: Natural Sciences in General

Published by Nature Publishing Group (NPG)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

2

Unknown

GADD45B mediates podocyte injury in zebrafish by activating the ROS-GADD45B-p38 pathway (2016)

Z Chen; X Wan; Q Hou; S Shi; L Wang; P Chen; X Zhu; C Zeng; W Qin; W Zhou; Z Liu

Nature Publishing Group (NPG)

In: Cell Death & Disease

add to mindlist on the mindlist

Details

Publication Date: 2016-01-22

Description: GADD45B mediates podocyte injury in zebrafish by activating the ROS-GADD45B-p38 pathway Cell Death and Disease 7, e2068 (January 2016). doi:10.1038/cddis.2015.300 Authors: Z Chen, X Wan, Q Hou, S Shi, L Wang, P Chen, X Zhu, C Zeng, W Qin, W Zhou & Z Liu

Electronic ISSN: 2041-4889

Topics: Biology , Medicine

Published by Nature Publishing Group (NPG)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

3

Unknown

Hepatocyte growth factor-modified mesenchymal stem cells improve ischemia/reperfusion-induced acute lung injury in rats (2017)

S Chen; X Chen; X Wu; S Wei; W Han; J Lin; M Kang; L Chen

Nature Publishing Group (NPG)

In: Gene Therapy

add to mindlist on the mindlist

Details

Publication Date: 2017-01-27

Description: Hepatocyte growth factor-modified mesenchymal stem cells improve ischemia/reperfusion-induced acute lung injury in rats Gene Therapy 24, 3 (January 2017). doi:10.1038/gt.2016.64 Authors: S Chen, X Chen, X Wu, S Wei, W Han, J Lin, M Kang & L Chen

Print ISSN: 0969-7128

Electronic ISSN: 1476-5462

Topics: Biology , Medicine

Published by Nature Publishing Group (NPG)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

4

Unknown

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)

Wang, Y., Chen, J., Zhang, Y., Yu, W., Zhang, C., Gong, L., Shao, L., Lu, J., Gao, Y., Chen, X., Chen, X., Hui, R.

American Heart Association (AHA)

In: Circulation: Cardiovascular Genetics

add to mindlist on the mindlist

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)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

5

Unknown

Deletion of Interleukin-6 Attenuates Pressure Overload-Induced Left Ventricular Hypertrophy and Dysfunction [Integrative Physiology] (2016)

Zhao, L., Cheng, G., Jin, R., Afzal, M. R., Samanta, A., Xuan, Y.-T., Girgis, M., Elias, H. K., Zhu, Y., Davani, A., Yang, Y., Chen, X., Ye, S., Wang, O.-L., Chen, L., Hauptman, J., Vincent, R. J., Dawn, B.

American Heart Association (AHA)

In: Circulation Research

add to mindlist on the mindlist

Details

Publication Date: 2016-06-10

Description: Rationale: The role of interleukin (IL)-6 in the pathogenesis of cardiac myocyte hypertrophy remains controversial. Objective: To conclusively determine whether IL-6 signaling is essential for the development of pressure overload–induced left ventricular (LV) hypertrophy and to elucidate the underlying molecular pathways. Methods and Results: Wild-type and IL-6 knockout ( IL-6 –/– ) mice underwent sham surgery or transverse aortic constriction (TAC) to induce pressure overload. Serial echocardiograms and terminal hemodynamic studies revealed attenuated LV hypertrophy and superior preservation of LV function in IL-6 –/– mice after TAC. The extents of LV remodeling, fibrosis, and apoptosis were reduced in IL-6 –/– hearts after TAC. Transcriptional and protein assays of myocardial tissue identified Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) and signal transducer and activator of transcription 3 (STAT3) activation as important underlying mechanisms during cardiac hypertrophy induced by TAC. The involvement of these pathways in myocyte hypertrophy was verified in isolated cardiac myocytes from wild-type and IL-6 –/– mice exposed to prohypertrophy agents. Furthermore, overexpression of CaMKII in H9c2 cells increased STAT3 phosphorylation, and exposure of H9c2 cells to IL-6 resulted in STAT3 activation that was attenuated by CaMKII inhibition. Together, these results identify the importance of CaMKII-dependent activation of STAT3 during cardiac myocyte hypertrophy via IL-6 signaling. Conclusions: Genetic deletion of IL-6 attenuates TAC-induced LV hypertrophy and dysfunction, indicating a critical role played by IL-6 in the pathogenesis of LV hypertrophy in response to pressure overload. CaMKII plays an important role in IL-6–induced STAT3 activation and consequent cardiac myocyte hypertrophy. These findings may have significant therapeutic implications for LV hypertrophy and failure in patients with hypertension.

Keywords: Growth Factors/Cytokines, Cardiomyopathy, Hypertrophy

Print ISSN: 0009-7330

Electronic ISSN: 1524-4571

Topics: Medicine

Published by American Heart Association (AHA)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

6

Unknown

Angiotensin-Converting Enzyme in Smooth Muscle Cells Promotes Atherosclerosis--Brief Report [Basic Sciences] (2016)

Chen, X., Howatt, D. A., Balakrishnan, A., Moorleghen, J. J., Wu, C., Cassis, L. A., Daugherty, A., Lu, H.

American Heart Association (AHA)

In: Arteriosclerosis, Thrombosis, and Vascular Biology

add to mindlist on the mindlist

Details

Publication Date: 2016-05-26

Description: Objective— Angiotensin-converting enzyme (ACE) is present in many cell types of atherosclerotic lesions. This study determined whether ACE activity in endothelial and smooth muscle cells (SMCs), 2 major resident cell types of the aorta, contributes to hypercholesterolemia-induced atherosclerosis. Approach and Results— All study mice were in low-density lipoprotein receptor –/– background. To determine the contribution of ACE on endothelial cells to atherosclerosis, female ACE floxed mice were bred to male Tie2-Cre transgenic mice. Endothelial cell–specific deletion of ACE significantly decreased serum ACE activity, but had no effect on systolic blood pressure and atherosclerosis. Because ACE protein is present on SMCs, the most abundant cell type of the aorta, we then determined whether ACE on SMCs contributes to atherosclerosis. ACE was depleted from SMCs by breeding female ACE floxed mice with male SM22-Cre transgenic mice. SMC-specific deficiency of ACE did not affect ACE activity in serum, but ablated its presence and activity in the aortic media. Although SMC-specific deficiency of ACE had no effect on systolic blood pressure, it significantly attenuated hypercholesterolemia-induced atherosclerosis in both male and female mice. Conclusions— These studies provide direct evidence that ACE derived from endothelial cells does not play a critical role in atherosclerosis. Rather, SMC-derived ACE contributes to atherosclerosis, independent of circulating ACE activity and blood pressure.

Keywords: Atherosclerosis

Print ISSN: 1079-5642

Electronic ISSN: 1524-4636

Topics: Medicine

Published by American Heart Association (AHA)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

7

Unknown

CD123 targeting oncolytic adenoviruses suppress acute myeloid leukemia cell proliferation in vitro and in vivo (2014)

G Li; X Li; H Wu; X Yang; Y Zhang; L Chen; X Wu; L Cui; L Wu; J Luo; X Y Liu

Nature Publishing Group (NPG)

In: Blood Cancer Journal

add to mindlist on the mindlist

Details

Publication Date: 2014-03-22

Description: CD123 targeting oncolytic adenoviruses suppress acute myeloid leukemia cell proliferation in vitro and in vivo Blood Cancer Journal 4, e194 (March 2014). doi:10.1038/bcj.2014.15 Authors: G Li, X Li, H Wu, X Yang, Y Zhang, L Chen, X Wu, L Cui, L Wu, J Luo & X Y Liu

Electronic ISSN: 2044-5385

Topics: Medicine

Published by Nature Publishing Group (NPG)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

8

Unknown

Interferon Regulatory Factor 1 Is Required for Cardiac Remodeling in Response to Pressure Overload [Heart] (2014)

Jiang, D.-S., Li, L., Huang, L., Gong, J., Xia, H., Liu, X., Wan, N., Wei, X., Zhu, X., Chen, Y., Chen, X., Zhang, X.-D., Li, H.

American Heart Association (AHA)

In: Hypertension

add to mindlist on the mindlist

Details

Publication Date: 2014-06-12

Description: Interferon regulatory factor 1 (IRF1), a critical member of the IRF family, was previously shown to be associated with the immune system and to be involved in apoptosis and tumor suppression. However, the role of IRF1 in pressure overload–induced cardiac remodeling has remained unclear. Using genetic approaches, we established a central role for the IRF1 transcription factor in the regulation of cardiac remodeling both in vivo and in vitro, and we determined the mechanism underlying this process. The expression level of IRF1 was remarkably altered in both failing human hearts and hypertrophic murine hearts. Transgenic mice with cardiac-specific IRF1 overexpression exacerbated aortic banding–induced cardiac hypertrophy, ventricular dilation, fibrosis, and dysfunction, whereas IRF1-deficient (knockout) mice exhibited a significant reduction in the hypertrophic response. Similar results were observed in a global IRF1-knockout rat model. Mechanistically, the prohypertrophic effects elicited by IRF1 in response to pathological stimuli were associated with the direct activation of inducible nitric oxide synthase (iNOS). Furthermore, we identified 1 IRF1-binding site in the promoter region of the iNOS gene, which was essential for its transcription. To examine the IRF1-iNOS axis in vivo, we generated IRF1-transgenic/iNOS-knockout mice. IRF1 exerted profoundly detrimental effects in these mice; however, these effects were nullified by iNOS ablation. These data suggest the IRF1–iNOS axis as a crucial regulator of cardiac remodeling and that IRF1 could be a potent therapeutic target for cardiac remodeling.

Keywords: Remodeling, Animal models of human disease, Hypertrophy

Print ISSN: 0194-911X

Topics: Medicine

Published by American Heart Association (AHA)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

9

Unknown

Caspase Recruitment Domain 6 Protects Against Cardiac Hypertrophy in Response to Pressure Overload [Heart] (2014)

Li, L., Chen, W., Zhu, Y., Wang, X., Jiang, D.-S., Huang, F., Wang, L., Xiang, F., Qin, W., Wang, Q., Zhang, R., Zhu, X., Li, H., Chen, X.

American Heart Association (AHA)

In: Hypertension

add to mindlist on the mindlist

Details

Publication Date: 2014-06-12

Description: Caspase recruitment domain 6 (CARD6), a crucial member of the CARD family, was initially shown to be involved in the immune system and oncogenesis. However, the role of CARD6 in chronic pressure overload–induced cardiac hypertrophy remains unexplored. To evaluate the impact of CARD6 on pathological cardiac hypertrophy, cardiac-specific CARD6 knockout mice and transgenic mice with cardiac-specific CARD6 overexpression were generated and subjected to aortic banding for 4 weeks. Our results demonstrated that CARD6-deficient mice aggravated aortic banding–triggered cardiac hypertrophy, ventricular dilation, fibrosis, and dysfunction, as measured by echocardiography, immunostaining, and molecular/biochemical analyses. Conversely, CARD6-overexpressing mice exhibited an attenuated hypertrophic response to chronic pressure overload. Similarly, using cultured neonatal rat cardiomyocytes, we found that adenovirus vector–driven overexpression of CARD6 dramatically limited angiotensin II–induced myocyte hypertrophy, whereas knockdown of CARD6 by AdshCARD6 (adenoviral short hairpin CARD6) exhibited the opposite phenotypes. Furthermore, analysis of the signaling events in vitro and in vivo revealed that CARD6-mediated protection against cardiac hypertrophy was attributed to the interruption of mitogen-activated protein kinase kinase (MEK) kinase-1–dependent MEK-extracellular signal-regulated protein kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase 1/2 (JNK1/2) activation. Altogether, these data indicated that CARD6 serves as a novel cardioprotective factor via negative regulation of MEK kinase-1–dependent MEK-ERK1/2 and JNK1/2 signaling. Thus, our study suggests that CARD6 may be a novel target for the treatment of pathological cardiac hypertrophy and failure.

Keywords: Congestive, Remodeling, Animal models of human disease, Hypertrophy, Myocardial cardiomyopathy disease

Print ISSN: 0194-911X

Topics: Medicine

Published by American Heart Association (AHA)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext

10

Unknown

RIP1 maintains DNA integrity and cell proliferation by regulating PGC-1α-mediated mitochondrial oxidative phosphorylation and glycolysis (2014)

W Chen; Q Wang; L Bai; W Chen; X Wang; C S Tellez; S Leng; M T Padilla; T Nyunoya; S A Belinsky; Y Lin

Nature Publishing Group (NPG)

In: Cell Death and Differentiation

add to mindlist on the mindlist

Details

Publication Date: 2014-06-10

Description: RIP1 maintains DNA integrity and cell proliferation by regulating PGC-1α-mediated mitochondrial oxidative phosphorylation and glycolysis Cell Death and Differentiation 21, 1061 (July 2014). doi:10.1038/cdd.2014.25 Authors: W Chen, Q Wang, L Bai, W Chen, X Wang, C S Tellez, S Leng, M T Padilla, T Nyunoya, S A Belinsky & Y Lin

Keywords: receptor-interacting protein 1metabolismPGC-1αglycolysisoxidative phosphorylationDNA damage

Print ISSN: 1350-9047

Electronic ISSN: 1476-5403

Topics: Biology , Medicine

Published by Nature Publishing Group (NPG)

Permalink

	Location	Call Number	Limitation	Availability

Others were also interested in ...

PAPER CURRENT

Fulltext