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Argus--a new database system for Web-based analysis of multiple microarray data sets.

Genome research

Comander J, Weber GM, Gimbrone MA, García-Cardeña G.
PMID: 11544205
Genome Res. 2001 Sep;11(9):1603-10. doi: 10.1101/gr.186601.

The ongoing revolution in microarray technology allows biologists studying gene expression to routinely collect >10(5) data points in a given experiment. Widely accessible and versatile database software is required to process this large amount of raw data into a...

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Comander J, Weber GM, Gimbrone MA, et al. Argus--a new database system for Web-based analysis of multiple microarray data sets. Genome Res. 2001;11(9):1603-10doi: 10.1101/gr.186601.
Comander, J., Weber, G. M., Gimbrone, M. A., & García-Cardeña, G. (2001). Argus--a new database system for Web-based analysis of multiple microarray data sets. Genome research, 11(9), 1603-10. https://doi.org/10.1101/gr.186601
Comander, J, et al. "Argus--a new database system for Web-based analysis of multiple microarray data sets." Genome research vol. 11,9 (2001): 1603-10. doi: https://doi.org/10.1101/gr.186601
Comander J, Weber GM, Gimbrone MA, García-Cardeña G. Argus--a new database system for Web-based analysis of multiple microarray data sets. Genome Res. 2001 Sep;11(9):1603-10. doi: 10.1101/gr.186601. PMID: 11544205; PMCID: PMC311087.
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Heparan Sulfate Regrowth Profiles Under Laminar Shear Flow Following Enzymatic Degradation.

Cellular and molecular bioengineering

Giantsos-Adams KM, Koo AJ, Song S, Sakai J, Sankaran J, Shin JH, Garcia-Cardena G, Dewey CF.
PMID: 23805169
Cell Mol Bioeng. 2013 Jun;6(2):160-174. doi: 10.1007/s12195-013-0273-z. Epub 2013 Feb 20.

The local hemodynamic shear stress waveforms present in an artery dictate the endothelial cell phenotype. The observed decrease of the apical glycocalyx layer on the endothelium in atheroprone regions of the circulation suggests that the glycocalyx may have a...

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Giantsos-Adams KM, Koo AJ, Song S, et al. Heparan Sulfate Regrowth Profiles Under Laminar Shear Flow Following Enzymatic Degradation. Cell Mol Bioeng. 2013;6(2):160-174doi: 10.1007/s12195-013-0273-z.
Giantsos-Adams, K. M., Koo, A. J., Song, S., Sakai, J., Sankaran, J., Shin, J. H., Garcia-Cardena, G., & Dewey, C. F. (2013). Heparan Sulfate Regrowth Profiles Under Laminar Shear Flow Following Enzymatic Degradation. Cellular and molecular bioengineering, 6(2), 160-174. https://doi.org/10.1007/s12195-013-0273-z
Giantsos-Adams, Kristina M, et al. "Heparan Sulfate Regrowth Profiles Under Laminar Shear Flow Following Enzymatic Degradation." Cellular and molecular bioengineering vol. 6,2 (2013): 160-174. doi: https://doi.org/10.1007/s12195-013-0273-z
Giantsos-Adams KM, Koo AJ, Song S, Sakai J, Sankaran J, Shin JH, Garcia-Cardena G, Dewey CF. Heparan Sulfate Regrowth Profiles Under Laminar Shear Flow Following Enzymatic Degradation. Cell Mol Bioeng. 2013 Jun;6(2):160-174. doi: 10.1007/s12195-013-0273-z. Epub 2013 Feb 20. PMID: 23805169; PMCID: PMC3689914.
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Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment.

JACC. Basic to translational science

Oh NA, Hong X, Doulamis IP, Meibalan E, Peiseler T, Melero-Martin J, García-Cardeña G, Del Nido PJ, Friehs I.
PMID: 35024504
JACC Basic Transl Sci. 2021 Dec 27;6(12):984-999. doi: 10.1016/j.jacbts.2021.10.002. eCollection 2021 Dec.

Endocardial fibroelastosis (EFE) is defined by fibrotic tissue on the endocardium and forms partly through aberrant endothelial-to-mesenchymal transition. However, the pathologic triggers are still unknown. In this study, we showed that abnormal flow induces EFE partly through endothelial-to-mesenchymal transition...

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Oh NA, Hong X, Doulamis IP, et al. Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC Basic Transl Sci. 2021;6(12):984-999doi: 10.1016/j.jacbts.2021.10.002.
Oh, N. A., Hong, X., Doulamis, I. P., Meibalan, E., Peiseler, T., Melero-Martin, J., García-Cardeña, G., Del Nido, P. J., & Friehs, I. (2021). Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC. Basic to translational science, 6(12), 984-999. https://doi.org/10.1016/j.jacbts.2021.10.002
Oh, Nicholas A, et al. "Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment." JACC. Basic to translational science vol. 6,12 (2021): 984-999. doi: https://doi.org/10.1016/j.jacbts.2021.10.002
Oh NA, Hong X, Doulamis IP, Meibalan E, Peiseler T, Melero-Martin J, García-Cardeña G, Del Nido PJ, Friehs I. Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC Basic Transl Sci. 2021 Dec 27;6(12):984-999. doi: 10.1016/j.jacbts.2021.10.002. eCollection 2021 Dec. PMID: 35024504; PMCID: PMC8733675.
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Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment.

JACC. Basic to translational science

Oh NA, Hong X, Doulamis IP, Meibalan E, Peiseler T, Melero-Martin J, García-Cardeña G, Del Nido PJ, Friehs I.
PMID: 35024504
JACC Basic Transl Sci. 2021 Dec 27;6(12):984-999. doi: 10.1016/j.jacbts.2021.10.002. eCollection 2021 Dec.

Endocardial fibroelastosis (EFE) is defined by fibrotic tissue on the endocardium and forms partly through aberrant endothelial-to-mesenchymal transition. However, the pathologic triggers are still unknown. In this study, we showed that abnormal flow induces EFE partly through endothelial-to-mesenchymal transition...

Cite
Oh NA, Hong X, Doulamis IP, et al. Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC Basic Transl Sci. 2021;6(12):984-999doi: 10.1016/j.jacbts.2021.10.002.
Oh, N. A., Hong, X., Doulamis, I. P., Meibalan, E., Peiseler, T., Melero-Martin, J., García-Cardeña, G., Del Nido, P. J., & Friehs, I. (2021). Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC. Basic to translational science, 6(12), 984-999. https://doi.org/10.1016/j.jacbts.2021.10.002
Oh, Nicholas A, et al. "Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment." JACC. Basic to translational science vol. 6,12 (2021): 984-999. doi: https://doi.org/10.1016/j.jacbts.2021.10.002
Oh NA, Hong X, Doulamis IP, Meibalan E, Peiseler T, Melero-Martin J, García-Cardeña G, Del Nido PJ, Friehs I. Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC Basic Transl Sci. 2021 Dec 27;6(12):984-999. doi: 10.1016/j.jacbts.2021.10.002. eCollection 2021 Dec. PMID: 35024504; PMCID: PMC8733675.
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Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment.

JACC. Basic to translational science

Oh NA, Hong X, Doulamis IP, Meibalan E, Peiseler T, Melero-Martin J, García-Cardeña G, Del Nido PJ, Friehs I.
PMID: 35024504
JACC Basic Transl Sci. 2021 Dec 27;6(12):984-999. doi: 10.1016/j.jacbts.2021.10.002. eCollection 2021 Dec.

Endocardial fibroelastosis (EFE) is defined by fibrotic tissue on the endocardium and forms partly through aberrant endothelial-to-mesenchymal transition. However, the pathologic triggers are still unknown. In this study, we showed that abnormal flow induces EFE partly through endothelial-to-mesenchymal transition...

Cite
Oh NA, Hong X, Doulamis IP, et al. Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC Basic Transl Sci. 2021;6(12):984-999doi: 10.1016/j.jacbts.2021.10.002.
Oh, N. A., Hong, X., Doulamis, I. P., Meibalan, E., Peiseler, T., Melero-Martin, J., García-Cardeña, G., Del Nido, P. J., & Friehs, I. (2021). Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC. Basic to translational science, 6(12), 984-999. https://doi.org/10.1016/j.jacbts.2021.10.002
Oh, Nicholas A, et al. "Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment." JACC. Basic to translational science vol. 6,12 (2021): 984-999. doi: https://doi.org/10.1016/j.jacbts.2021.10.002
Oh NA, Hong X, Doulamis IP, Meibalan E, Peiseler T, Melero-Martin J, García-Cardeña G, Del Nido PJ, Friehs I. Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment. JACC Basic Transl Sci. 2021 Dec 27;6(12):984-999. doi: 10.1016/j.jacbts.2021.10.002. eCollection 2021 Dec. PMID: 35024504; PMCID: PMC8733675.
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Current in vitro models of leukocyte migration : methods and interpretation.

Methods in molecular medicine

Allport JR, García-Cardeña G, Lim YC, Luscinskas FW.
PMID: 21336913
Methods Mol Med. 2001;56:357-65. doi: 10.1385/1-59259-151-5:357.

A large component of airway inflammatory disease is the recruitment of activated leukocytes (primarily eosinophils and T lymphocytes) from the lung vasculature into the bronchial walls resulting in lung edema. Ultimately, many of the infiltrating leukocytes progress across the...

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Allport JR, García-Cardeña G, Lim YC, et al. Current in vitro models of leukocyte migration : methods and interpretation. Methods Mol Med. 2001;56:357-65doi: 10.1385/1-59259-151-5:357.
Allport, J. R., García-Cardeña, G., Lim, Y. C., & Luscinskas, F. W. (2001). Current in vitro models of leukocyte migration : methods and interpretation. Methods in molecular medicine, 56357-65. https://doi.org/10.1385/1-59259-151-5:357
Allport, J R, et al. "Current in vitro models of leukocyte migration : methods and interpretation." Methods in molecular medicine vol. 56 (2001): 357-65. doi: https://doi.org/10.1385/1-59259-151-5:357
Allport JR, García-Cardeña G, Lim YC, Luscinskas FW. Current in vitro models of leukocyte migration : methods and interpretation. Methods Mol Med. 2001;56:357-65. doi: 10.1385/1-59259-151-5:357. PMID: 21336913.
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Showing 1 to 6 of 6 entries