32 research outputs found
Experiences in deploying metadata analysis tools for institutional repositories
Current institutional repository software provides few tools to help metadata librarians understand and analyze their collections. In this article, we compare and contrast metadata analysis tools that were developed simultaneously, but independently, at two New Zealand institutions during a period of national investment in research repositories: the Metadata Analysis Tool (MAT) at The University of Waikato, and the Kiwi Research Information Service (KRIS) at the National Library of New Zealand.
The tools have many similarities: they are convenient, online, on-demand services that harvest metadata using OAI-PMH; they were developed in response to feedback from repository administrators; and they both help pinpoint specific metadata errors as well as generating summary statistics. They also have significant differences: one is a dedicated tool wheres the other is part of a wider access tool; one gives a holistic view of the metadata whereas the other looks for specific problems; one seeks patterns in the data values whereas the other checks that those values conform to metadata standards. Both tools work in a complementary manner to existing Web-based administration tools. We have observed that discovery and correction of metadata errors can be quickly achieved by switching Web browser views from the analysis tool to the repository interface, and back. We summarize the findings from both tools' deployment into a checklist of requirements for metadata analysis tools
Role of atrial tissue remodeling on rotor dynamics an in vitro study
The objective of this article is to present an in vitro model of atrial cardiac tissue that could serve to study the mechanisms of remodeling related to atrial fibrillation (AF). We analyze the modification on gene expression and modifications on rotor dynamics following tissue remodeling. Atrial murine cells (HL-1 myocytes) were maintained in culture after the spontaneous initiation of AF and analyzed at two time points: 3.1 +/- 1.3 and 9.7 +/- 0.5 days after AF initiation. The degree of electrophysiological remodeling (i.e., relative gene expression of key ion channels) and structural inhomogeneity was compared between early and late cell culture times both in nonfibrillating and fibrillating cell cultures. In addition, the electrophysiological characteristics of in vitro fibrillation [e.g., density of phase singularities (PS/cm2), dominant frequency, and rotor meandering] analyzed by means of optical mapping were compared with the degree of electrophysiological remodeling. Fibrillating cell cultures showed a differential ion channel gene expression associated with atrial tissue remodeling (i.e., decreased SCN5A, CACN1C, KCND3, and GJA1 and increased KCNJ2) not present in nonfibrillating cell cultures. Also, fibrillatory complexity was increased in late- vs. early stage cultures (1.12 +/- 0.14 vs. 0.43 +/- 0.19 PS/cm(2), P < 0.01), which was associated with changes in the electrical reentrant patterns (i.e., decrease in rotor tip meandering and increase in wavefront curvature). HL-1 cells can reproduce AF features such as electrophysiological remodeling and an increased complexity of the electrophysiological behavior associated with the fibrillation time that resembles those occurring in patients with chronic AF.This work was supported in part by grants from the Spanish Ministry of Science and Innovation (PLE2009-0152), the Instituto de Salud Carlos III (Ministry of Economy and Competitiveness, Spain: PI13-01882, PI13-00903, and TEC2013-50391-EXP), and the Red de Investigacion Cardiovacular (RIC) from Instituto de Salud Carlos III (Ministry of Economy and Competitiveness, Spain).Climent, A.; Guillem Sánchez, MS.; Fuentes, L.; Lee, P.; Bollensdorff, C.; Fernandez-Santos, M.; Suarez-Sancho, S.... (2015). Role of atrial tissue remodeling on rotor dynamics an in vitro study. AJP - Heart and Circulatory Physiology. 309(11):H1964-H1973. doi:10.1152/ajpheart.00055.2015SH1964H197330911Allessie, M. (2002). Electrical, contractile and structural remodeling during atrial fibrillation. Cardiovascular Research, 54(2), 230-246. doi:10.1016/s0008-6363(02)00258-4Allessie, M. A., de Groot, N. M. S., Houben, R. P. M., Schotten, U., Boersma, E., Smeets, J. L., & Crijns, H. J. (2010). Electropathological Substrate of Long-Standing Persistent Atrial Fibrillation in Patients With Structural Heart Disease. Circulation: Arrhythmia and Electrophysiology, 3(6), 606-615. doi:10.1161/circep.109.910125Atienza, F., Almendral, J., Jalife, J., Zlochiver, S., Ploutz-Snyder, R., Torrecilla, E. G., … Berenfeld, O. (2009). Real-time dominant frequency mapping and ablation of dominant frequency sites in atrial fibrillation with left-to-right frequency gradients predicts long-term maintenance of sinus rhythm. Heart Rhythm, 6(1), 33-40. doi:10.1016/j.hrthm.2008.10.024Atienza, F., Almendral, J., Ormaetxe, J. M., Moya, Á., Martínez-Alday, J. D., Hernández-Madrid, A., … Jalife, J. (2014). Comparison of Radiofrequency Catheter Ablation of Drivers and Circumferential Pulmonary Vein Isolation in Atrial Fibrillation. Journal of the American College of Cardiology, 64(23), 2455-2467. doi:10.1016/j.jacc.2014.09.053Bikou, O., Thomas, D., Trappe, K., Lugenbiel, P., Kelemen, K., Koch, M., … Bauer, A. (2011). Connexin 43 gene therapy prevents persistent atrial fibrillation in a porcine model. Cardiovascular Research, 92(2), 218-225. doi:10.1093/cvr/cvr209Bollmann, A., Sonne, K., Esperer, H.-D., Toepffer, I., & Klein, H. U. (2002). Patients with Persistent Atrial Fibrillation Taking Oral Verapamil Exhibit a Lower Atrial Frequency on the ECG. Annals of Noninvasive Electrocardiology, 7(2), 92-97. doi:10.1111/j.1542-474x.2002.tb00148.xBRUNDEL, B. (2004). Calpain inhibition prevents pacing-induced cellular remodeling in a HL-1 myocyte model for atrial fibrillation. Cardiovascular Research, 62(3), 521-528. doi:10.1016/j.cardiores.2004.02.007Calkins, H., Kuck, K. H., Cappato, R., Brugada, J., Camm, A. J., Chen, S.-A., … Wilber, D. (2012). 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design. Heart Rhythm, 9(4), 632-696.e21. doi:10.1016/j.hrthm.2011.12.016Claycomb, W. C., Lanson, N. A., Stallworth, B. S., Egeland, D. B., Delcarpio, J. B., Bahinski, A., & Izzo, N. J. (1998). HL-1 cells: A cardiac muscle cell line that contracts and retains phenotypic characteristics of the adult cardiomyocyte. Proceedings of the National Academy of Sciences, 95(6), 2979-2984. doi:10.1073/pnas.95.6.2979Filgueiras-Rama, D., Price, N. F., Martins, R. P., Yamazaki, M., Avula, U. M. R., Kaur, K., … Berenfeld, O. (2012). Long-Term Frequency Gradients During Persistent Atrial Fibrillation in Sheep Are Associated With Stable Sources in the Left Atrium. Circulation: Arrhythmia and Electrophysiology, 5(6), 1160-1167. doi:10.1161/circep.111.969519Haïssaguerre, M., Jaïs, P., Shah, D. C., Takahashi, A., Hocini, M., Quiniou, G., … Clémenty, J. (1998). Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins. New England Journal of Medicine, 339(10), 659-666. doi:10.1056/nejm199809033391003Haralick, R. M., Shanmugam, K., & Dinstein, I. (1973). Textural Features for Image Classification. IEEE Transactions on Systems, Man, and Cybernetics, SMC-3(6), 610-621. doi:10.1109/tsmc.1973.4309314Jalife, J. (2010). Deja vu in the theories of atrial fibrillation dynamics. Cardiovascular Research, 89(4), 766-775. doi:10.1093/cvr/cvq364Koivumäki, J. T., Seemann, G., Maleckar, M. M., & Tavi, P. (2014). In Silico Screening of the Key Cellular Remodeling Targets in Chronic Atrial Fibrillation. PLoS Computational Biology, 10(5), e1003620. doi:10.1371/journal.pcbi.1003620Lee, P., Klos, M., Bollensdorff, C., Hou, L., Ewart, P., Kamp, T. J., … Herron, T. J. (2012). Simultaneous Voltage and Calcium Mapping of Genetically Purified Human Induced Pluripotent Stem Cell–Derived Cardiac Myocyte Monolayers. Circulation Research, 110(12), 1556-1563. doi:10.1161/circresaha.111.262535Lieu, D. K., Fu, J.-D., Chiamvimonvat, N., Tung, K. C., McNerney, G. P., Huser, T., … Li, R. A. (2013). Mechanism-Based Facilitated Maturation of Human Pluripotent Stem Cell–Derived Cardiomyocytes. Circulation: Arrhythmia and Electrophysiology, 6(1), 191-201. doi:10.1161/circep.111.973420Liu, X., Shi, H., Tan, H., Wang, X., Zhou, L., & Gu, J. (2009). Decreased Connexin 43 and Increased Fibrosis in Atrial Regions Susceptible to Complex Fractionated Atrial Electrograms. Cardiology, 114(1), 22-29. doi:10.1159/000210398Mansour, M., Mandapati, R., Berenfeld, O., Chen, J., Samie, F. H., & Jalife, J. (2001). Left-to-Right Gradient of Atrial Frequencies During Acute Atrial Fibrillation in the Isolated Sheep Heart. Circulation, 103(21), 2631-2636. doi:10.1161/01.cir.103.21.2631Martins, R. P., Kaur, K., Hwang, E., Ramirez, R. J., Willis, B. C., Filgueiras-Rama, D., … Jalife, J. (2014). Dominant Frequency Increase Rate Predicts Transition from Paroxysmal to Long-Term Persistent Atrial Fibrillation. Circulation, 129(14), 1472-1482. doi:10.1161/circulationaha.113.004742McDowell, K. S., Vadakkumpadan, F., Blake, R., Blauer, J., Plank, G., MacLeod, R. S., & Trayanova, N. A. (2013). Mechanistic Inquiry into the Role of Tissue Remodeling in Fibrotic Lesions in Human Atrial Fibrillation. Biophysical Journal, 104(12), 2764-2773. doi:10.1016/j.bpj.2013.05.025Narayan, S. M., Krummen, D. E., Shivkumar, K., Clopton, P., Rappel, W.-J., & Miller, J. M. (2012). Treatment of Atrial Fibrillation by the Ablation of Localized Sources. Journal of the American College of Cardiology, 60(7), 628-636. doi:10.1016/j.jacc.2012.05.022Noguchi, K., Masumiya, H., Takahashi, K., Kaneko, K., Higuchi, S., Tanaka, H., & Shigenobu, K. (1997). Comparative effects of gallopamil and verapamil on the mechanical and electrophysiological parameters of isolated guinea-pig myocardium. Canadian Journal of Physiology and Pharmacology, 75(12), 1316-1321. doi:10.1139/y97-161Pandit, S. V., Berenfeld, O., Anumonwo, J. M. B., Zaritski, R. M., Kneller, J., Nattel, S., & Jalife, J. (2005). Ionic Determinants of Functional Reentry in a 2-D Model of Human Atrial Cells During Simulated Chronic Atrial Fibrillation. Biophysical Journal, 88(6), 3806-3821. doi:10.1529/biophysj.105.060459Pandit, S. V., & Jalife, J. (2013). Rotors and the Dynamics of Cardiac Fibrillation. Circulation Research, 112(5), 849-862. doi:10.1161/circresaha.111.300158Riccio, M. L., Koller, M. L., & Gilmour, R. F. (1999). Electrical Restitution and Spatiotemporal Organization During Ventricular Fibrillation. Circulation Research, 84(8), 955-963. doi:10.1161/01.res.84.8.955Samie, F. H., Mandapati, R., Gray, R. A., Watanabe, Y., Zuur, C., Beaumont, J., & Jalife, J. (2000). A Mechanism of Transition From Ventricular Fibrillation to Tachycardia. Circulation Research, 86(6), 684-691. doi:10.1161/01.res.86.6.684Samie, F. H., Berenfeld, O., Anumonwo, J., Mironov, S. F., Udassi, S., Beaumont, J., … Jalife, J. (2001). Rectification of the Background Potassium Current. Circulation Research, 89(12), 1216-1223. doi:10.1161/hh2401.100818Smith, A. W., Segar, C. E., Nguyen, P. K., MacEwan, M. R., Efimov, I. R., & Elbert, D. L. (2012). Long-term culture of HL-1 cardiomyocytes in modular poly(ethylene glycol) microsphere-based scaffolds crosslinked in the phase-separated state. Acta Biomaterialia, 8(1), 31-40. doi:10.1016/j.actbio.2011.08.021Tsai, C.-T., Chiang, F.-T., Chen, W.-P., Hwang, J.-J., Tseng, C.-D., Wu, C.-K., … Lin, J.-L. (2011). Angiotensin II induces complex fractionated electrogram in a cultured atrial myocyte monolayer mediated by calcium and sodium-calcium exchanger. Cell Calcium, 49(1), 1-11. doi:10.1016/j.ceca.2010.10.005Tsai, C.-T., Chiang, F.-T., Tseng, C.-D., Yu, C.-C., Wang, Y.-C., Lai, L.-P., … Lin, J.-L. (2011). Mechanical Stretch of Atrial Myocyte Monolayer Decreases Sarcoplasmic Reticulum Calcium Adenosine Triphosphatase Expression and Increases Susceptibility to Repolarization Alternans. Journal of the American College of Cardiology, 58(20), 2106-2115. doi:10.1016/j.jacc.2011.07.039Tuomi, J. M., Tyml, K., & Jones, D. L. (2011). Atrial tachycardia/fibrillation in the connexin 43 G60S mutant (Oculodentodigital dysplasia) mouse. American Journal of Physiology-Heart and Circulatory Physiology, 300(4), H1402-H1411. doi:10.1152/ajpheart.01094.2010White, S. M., Constantin, P. E., & Claycomb, W. C. (2004). Cardiac physiology at the cellular level: use of cultured HL-1 cardiomyocytes for studies of cardiac muscle cell structure and function. American Journal of Physiology-Heart and Circulatory Physiology, 286(3), H823-H829. doi:10.1152/ajpheart.00986.2003Wijffels, M. C. E. F., Kirchhof, C. J. H. J., Dorland, R., & Allessie, M. A. (1995). Atrial Fibrillation Begets Atrial Fibrillation. Circulation, 92(7), 1954-1968. doi:10.1161/01.cir.92.7.1954Zlochiver, S., Muñoz, V., Vikstrom, K. L., Taffet, S. M., Berenfeld, O., & Jalife, J. (2008). Electrotonic Myofibroblast-to-Myocyte Coupling Increases Propensity to Reentrant Arrhythmias in Two-Dimensional Cardiac Monolayers. Biophysical Journal, 95(9), 4469-4480. doi:10.1529/biophysj.108.13647
Assessment of contractility in intact ventricular cardiomyocytes using the dimensionless ‘Frank–Starling Gain’ index
This paper briefly recapitulates the Frank–Starling law of the heart, reviews approaches to establishing diastolic and systolic force–length behaviour in intact isolated cardiomyocytes, and introduces a dimensionless index called ‘Frank–Starling Gain’, calculated as the ratio of slopes of end-systolic and end-diastolic force–length relations. The benefits and limitations of this index are illustrated on the example of regional differences in Guinea pig intact ventricular cardiomyocyte mechanics. Potential applicability of the Frank–Starling Gain for the comparison of cell contractility changes upon stretch will be discussed in the context of intra- and inter-individual variability of cardiomyocyte properties
Surface Modification of Polytetrafluoroethylene and Polycaprolactone Promoting Cell-Selective Adhesion and Growth of Valvular Interstitial Cells
Tissue engineering concepts, which are concerned with the attachment and growth of specific cell types, frequently employ immobilized ligands that interact preferentially with cell types of interest. Creating multicellular grafts such as heart valves calls for scaffolds with spatial control over the different cells involved. Cardiac heart valves are mainly constituted out of two cell types, endothelial cells and valvular interstitial cells. To have control over where which cell type can be attracted would enable targeted cell settlement and growth contributing to the first step of an engineered construct. For endothelial cells, constituting the outer lining of the valve tissue, several specific peptide ligands have been described. Valvular interstitial cells, representing the bulk of the leaflet, have not been investigated in this regard. Two receptors, the integrin α9β1 and CD44, are known to be highly expressed on valvular interstitial cells. Here, we demonstrate that by covalently grafting the corresponding peptide and polysaccharide ligand onto an erodible, polycaprolactone (PCL), and a non-degradable, polytetrafluoroethylene (PTFE), polymer, surfaces were generated that strongly support valvular interstitial cell colonization with minimal endothelial cell and reduced platelet adhesion. The technology for covalent binding of corresponding ligands is a key element towards tissue engineered cardiac valves for in vitro applications, but also towards future in vivo application, especially in combination with degradable scaffold material
Surface Modification of Polydimethylsiloxane via Combined Aminolysis and Alcoholysis Generating Cell Adhesive and Antifouling Properties
Abstract Polydimethylsiloxane (PDMS) is an elastomeric polymer frequently used as implant material, for flexible tubing and in microfluidic devices. The pronounced hydrophobic surface of this unique material impedes many applications where a good wetting behavior is required. Consequentially, various ways of surface modifications have been used to introduce new properties. Plasma treatment is the most popular technique in this respect, but is not generally applicable, especially if hardly accessible surfaces are to be modified. A novel wet‐chemistry‐based modification scheme yielding an amino‐functionalized PDMS surface using a combined alcoholysis/aminolysis reaction is presented. Biological applications are exemplified by the conjugation of the RGD peptide, or polyethylene glycol (PEG) and heparin, yielding surfaces with cell‐adhesive or nonthrombogenic properties, respectively. The effect of subsequent conjugation with an adhesive peptide is tested in cell culture. Additionally, two antifouling surfaces generated by coupling heparin and polyethylene glycol respectively are shown to improve the materials resistance to platelet adhesion drastically while simultaneously preventing hydrophobic recovery of the PDMS surface. The findings provide a versatile means of surface functionalization of PDMS substrates and is suitable for many biomedical applications
The covalently immobilized antimicrobial peptide LL37 acts as a VEGF mimic and stimulates endothelial cell proliferation
The chemical coupling of growth factors to solid substrates are discussed as an alternative to delivery systems. Utilizing entire proteins for this application is hampered by safety and stability considerations. Instead, growth factor mimicking peptides are of great interest for biomedical applications, such as tissue engineering, due to their purity and stability. The human cathelicidin derived antimicrobial peptide LL37, beside its microbicidal activity, was shown to stimulate endothelial cell growth when used in a soluble form. Here, in a novel approach, spacer mediated immobilization, but not direct conjugation of LL37, to a gold substrate was shown to result in a pronounced mitogenic effect on endothelial cells, comparable to that of soluble vascular endothelial growth factor