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1 repressor of selenoprotein synthesis during selenium deficiency.
2 sts that patients with cirrhosis do not have selenium deficiency.
3 use of compensation for a chemically induced selenium deficiency.
4 o severe neurodegeneration and death in mild selenium deficiency.
5 hepatocyte selenium to peripheral tissues in selenium deficiency.
6 worsening clinical manifestations of dietary selenium deficiency.
7 in, zinc, vitamin A, kwashiorkor, biotin and selenium deficiencies, along with the clinical entities
10 bowel disease (IBD) demonstrate nutritional selenium deficiencies and are at greater risk of develop
13 wn-regulated by MsrB1 small interfering RNA, selenium deficiency, and selenocysteine tRNA mutations;
14 This effect was not explained by uniform selenium deficiency because methionine sulfoxide reducta
15 oped severe neurodegeneration caused by mild selenium deficiency, brain selenium was approximately 35
21 In studies of coxsackievirus infection and selenium deficiency in mice, we found that mice fed a se
22 that severe cirrhosis causes mild functional selenium deficiency in some patients that is associated
23 trate that deletion of Sepp1, and presumably selenium deficiency in the brain, produce both neuronal
24 cquired immunodeficiency syndrome (AIDS) and selenium deficiency, indicating a protective role for th
31 al dysfunction and death under conditions of selenium deficiency, suggesting an interaction of apoER2
32 ther cirrhosis is associated with functional selenium deficiency (the lack of selenium for the proces
34 luding liver can be substantially reduced by selenium deficiency without any apparent change in pheno