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Volumn 220, Issue 7, 2003, Pages 499-502

Ocular manifestation in LCAT deficiency - A clinicopathological correlation;Okuläre manifestation bei LCAT-Mangel - Eine klinisch-histopathologische korrelation

Author keywords

Arteriosclerosis; Bilateral; Corneal opacification; Genotype; HDL deficiency; Histology; LCAT deficiency; Lipoid arc; Penetrating keratoplasty; Secondary amyloidosis

Indexed keywords

HIGH DENSITY LIPOPROTEIN; PHOSPHATIDYLCHOLINE STEROL ACYLTRANSFERASE;

EID: 0041325085     PISSN: 00232165     EISSN: None     Source Type: Journal    
DOI: 10.1055/s-2003-40943     Document Type: Article
Times cited : (7)

References (17)
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  • 5
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    • A molecular defect causing fish eye disease: An amino acid exchange in lecithin-cholesterol acyltransferase (LCAT) leads to the selective loss of α-LCAT activity
    • Funke H, Eckardstein A von, Pritchard PH, Albers JJ, Kastelein JJ, Droste C, Assmann G. A molecular defect causing fish eye disease: An amino acid exchange in lecithin-cholesterol acyltransferase (LCAT) leads to the selective loss of α-LCAT activity. Proc Natl Acad Sci 1991; 88: 4855-4859
    • (1991) Proc Natl Acad Sci , vol.88 , pp. 4855-4859
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    • Corneal opacity in familial cholesterol ester deficiency
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    • Corneal and fundus changes in familial LCAT-deficiency
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* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.