The Cell and Tissue Imaging Core A is comprised of a centralized, cutting-edge microscopy facility, absolutely essential to the research goals of the 4 Projects in this PO1 application entitled """"""""New therapies for liver fibrosis and hyperproliferation in alpha1-AT deficiency (ATD)"""""""". The facility is housed within the Center for Biologic Imaging (CBI) (www.cbi.pitt.edu) at the main campus of the University of Pittsburgh Medical Center. All Project Pis have made, and continue to make, heavy and diverse use of the CBI for facility-specific imaging methodologies. Evidence of the longevity of this use is seen in co-authored publications between the PI of Core A (Stolz), and/or other faculty and staff members at the Center for Biologic Imaging and Pi's ofthe individual projects. The imaging specialties afforded by CBI include all ultrastructural electron microscopy (transmission electron microscopy, scanning electron microscopy, immuno-electron SEM and TEM, negative staining), light and fluorescence microscopy (macro, dissecting, light and fluorescence, epi-fluorescence, confocal scanning and multi-photon imaging), live cell microscopy (transmitted light and fluorescence) and advanced fluorescence specialties like FRET;FRAP spectral analysis and ratiometric imaging. Also critical to data processing, a wide range of image analysis, quantitative evaluation software and technical assistance is available to program investigators and their laboratory staff. Since the expertise and equipment is located in one centralized facility, seamless integration among imaging modalities can be realized. Furthermore, instrumentation is accessible via programmable key card and is available 24/7 by trained users. Trained users can sign up for time through our on-line scheduling website which also serves as an internet-based data sharing venue among Pis.
The Cell and Tissue) Imaging Core A is highly relevant to all the projects within this Program Project application. Each of the 4 projects requires a variety of imaging technologies to achieve the goals outlined in the specific aims. Pis of this program receive considerable access to expertise on design of imaging experiments, preparation of samples, and analysis of imaging data. Consequently, the CBI can serve as a clearinghouse of information and reagents that results in efficient sharing of data and resources among Pis.
|Yokota, Shinichiro; Ono, Yoshihiro; Nakao, Toshimasa et al. (2018) Partial Bile Duct Ligation in the Mouse: A Controlled Model of Localized Obstructive Cholestasis. J Vis Exp :|
|Khan, Zahida; Orr, Anne; Michalopoulos, George K et al. (2017) Immunohistochemical Analysis of the Stem Cell Marker LGR5 in Pediatric Liver Disease. Pediatr Dev Pathol 20:16-27|
|Liu, Bing; Oltvai, Zoltán N; Bay?r, Hülya et al. (2017) Quantitative assessment of cell fate decision between autophagy and apoptosis. Sci Rep 7:17605|
|Khan, Zahida; Yokota, Shinichiro; Ono, Yoshihiro et al. (2017) Bile Duct Ligation Induces ATZ Globule Clearance in a Mouse Model of ?-1 Antitrypsin Deficiency. Gene Expr 17:115-127|
|Li, Hongchun; Chang, Yuan-Yu; Lee, Ji Young et al. (2017) DynOmics: dynamics of structural proteome and beyond. Nucleic Acids Res 45:W374-W380|
|Khan, Zahida; Venkat, Veena L; Soltys, Kyle A et al. (2017) A Challenging Case of Severe Infantile Cholestasis in Alpha-1 Antitrypsin Deficiency. Pediatr Dev Pathol 20:176-181|
|Polgar, Zsuzsanna; Li, Yanfeng; Li Wang, Xia et al. (2017) Gunn Rats as a Surrogate Model for Evaluation of Hepatocyte Transplantation-Based Therapies of Crigler-Najjar Syndrome Type 1. Methods Mol Biol 1506:131-147|
|Roy-Chowdhury, Jayanta; Schilsky, Michael L (2016) Gene therapy of Wilson disease: A ""golden"" opportunity using rAAV on the 50th anniversary of the discovery of the virus. J Hepatol 64:265-267|
|Khan, Zahida; Venkat, Veena L; Soltys, Kyle A et al. (2016) A CHALLENGING CASE OF SEVERE INFANTILE CHOLESTASIS IN ALPHA-1 ANTITRYPSIN DEFICIENCY. Pediatr Dev Pathol :|
|Paranjpe, Shirish; Bowen, William C; Mars, Wendy M et al. (2016) Combined systemic elimination of MET and epidermal growth factor receptor signaling completely abolishes liver regeneration and leads to liver decompensation. Hepatology 64:1711-1724|
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