The Histopathology Core of the NEI is devoted to supporting the patient care, vision research, and mission of the NEI and other collaborative institutes at the NIH. This consists of processing human tissues (mainly ocular tissues) removed in surgeries and collected at autopsies. The Core grosses the tissues, sections and stains slides for light and/or transmission electron microscopy. The Histopathology Core serves the Clinical Branch and all NEI laboratories under the NEI Intramural Research Program, as well as other NIH institutes, which perform research involving ocular and related tissues. In addition, the Core receives clinical and experimental specimens submitted by clinicians and investigators outside NIH (USA and abroad) for consultation or collaboration. During FY13, the Histopathology Core received and processed approximately 5076 specimens and yielded over 6153 slides stained. Additionally, the laboratory processed case materials sent for ultrastructure, which produced 4208 electron microscopic images. This fiscal year, 91 clinical cases were also received and processed. The patient specimens produced 2113 histological slides and 173 electronic microscopic images. There are over 20 publications that include work performed by the Core. Although about 95% of our effort is devoted to NEI duties, the Histopathology Core also performs services for research projects inside and outside the NIH. The core follows the guidelines for the conduct of research in the intramural research program at the NIH and other standards set by the NIH.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Scientific Cores Intramural Research (ZIC)
Project #
1ZICEY000461-06
Application #
8737697
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
6
Fiscal Year
2013
Total Cost
$525,163
Indirect Cost
Name
U.S. National Eye Institute
Department
Type
DUNS #
City
State
Country
Zip Code
Sun, Xun; Park, James H; Gumerson, Jessica et al. (2016) Loss of RPGR glutamylation underlies the pathogenic mechanism of retinal dystrophy caused by TTLL5 mutations. Proc Natl Acad Sci U S A 113:E2925-34
Ma, Wenxin; Wong, Wai T (2016) Aging Changes in Retinal Microglia and their Relevance to Age-related Retinal Disease. Adv Exp Med Biol 854:73-8
Wang, Xu; Zhao, Lian; Zhang, Jun et al. (2016) Requirement for Microglia for the Maintenance of Synaptic Function and Integrity in the Mature Retina. J Neurosci 36:2827-42
Hinshaw, Samuel J H; Ogbeifun, Osato; Wandu, Wambui S et al. (2016) Digoxin Inhibits Induction of Experimental Autoimmune Uveitis in Mice, but Causes Severe Retinal Degeneration. Invest Ophthalmol Vis Sci 57:1441-7
Wang, Yujuan; Hanus, Jakub W; Abu-Asab, Mones S et al. (2016) NLRP3 Upregulation in Retinal Pigment Epithelium in Age-Related Macular Degeneration. Int J Mol Sci 17:
Silver, Phyllis B; Horai, Reiko; Chen, Jun et al. (2015) Correction: Retina-Specific T Regulatory Cells Bring About Resolution and Maintain Remission of Autoimmune Uveitis. J Immunol 195:393
Mattapallil, Mary J; Silver, Phyllis B; Cortes, Lizette M et al. (2015) Characterization of a New Epitope of IRBP That Induces Moderate to Severe Uveoretinitis in Mice With H-2b Haplotype. Invest Ophthalmol Vis Sci 56:5439-49
Indaram, Maanasa; Ma, Wenxin; Zhao, Lian et al. (2015) 7-Ketocholesterol increases retinal microglial migration, activation, and angiogenicity: a potential pathogenic mechanism underlying age-related macular degeneration. Sci Rep 5:9144
Dalal, Monica; Casady, Megan; Moriarty, Emily et al. (2014) Diagnostic procedures in vitreoretinal lymphoma. Ocul Immunol Inflamm 22:270-6
Schaal, Shlomit; Kagan, Aleksandr; Wang, Yujuan et al. (2014) Acute retinal necrosis associated with Epstein-Barr virus: immunohistopathologic confirmation. JAMA Ophthalmol 132:881-2

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