Nell I. Mock
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Also affiliated: University of Iowa (1988–1998); Arkansas Children's Hospital (1995–2003); University of California, San Francisco (1983); University of Arkansas Medical Center (2003); University of Iowa Hospitals and Clinics (2003); University of Texas Health Science Center at Dallas (1982); Maine Medical Center (1998); Clinical Research Management (2005)
Formerly Arkansas Affiliated with UAMS through 2008.
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Biography and Research Information
OverviewAI-generated summary
Nell I. Mock's research has focused on the role of biotin in human and animal health, with particular attention to its status during pregnancy and its indicators. Her work has investigated marginal biotin deficiency in both humans and animal models, including ICR mice, examining its teratogenic effects and identifying sensitive early indicators of decreased biotin status. These indicators include increased urinary excretion of 3-hydroxyisovaleric acid and decreased urinary excretion of biotin. Mock has also explored methods for assessing biotin status, such as using biotinylated red blood cells to measure circulating red blood cell volume in neonates and comparing it to hematocrit. Her publications also touch upon the composition of circulating substances, noting that biotin accounts for only half of the total avidin-binding substances in human serum. Mock's research has been recognized with a designation as a highly cited researcher, with an h-index of 21 and over 1,149 citations across 31 publications.
Metrics
- h-index: 21
- Publications: 31
- Citations: 1,149
Selected Publications
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Red Cell Volume Can Be Accurately Determined in Sheep Using a Nonradioactive Biotin Label (2008)
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Lymphocyte propionyl-CoA carboxylase and its activation by biotin are sensitive indicators of marginal biotin deficiency in humans (2006)
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Lymphocyte propionyl-CoA carboxylase and its activation by biotin are sensitive indicators of marginal biotin deficiency in humans 1–3 (2006)
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Instability of the biotin–protein bond in human plasma (2004)
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Release of biotin from biotinylated proteins occurs enzymatically and nonenzymatically in human plasma (2004)
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A biotin–protein bond with stability in plasma (2004)
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Marginal Biotin Deficiency Is Teratogenic in ICR Mice (2003)
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Lymphocyte Propionyl-CoA Carboxylase Is an Early and Sensitive Indicator of Biotin Deficiency in Rats, but Urinary Excretion of 3-Hydroxypropionic Acid Is Not (2002)
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Marginal biotin deficiency during normal pregnancy (2002)
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Lymphocyte propionyl-CoA carboxylase and accumulation of odd-chain fatty acid in plasma and erythrocytes are useful indicators of marginal biotin deficiency☆ (2002)
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Indicators of marginal biotin deficiency and repletion in humans: validation of 3-hydroxyisovaleric acid excretion and a leucine challenge,, (2002)
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Certain Immune Markers Are Not Good Indicators of Mild to Moderate Biotin Deficiency in Rats (2001)
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MATERNAL BIOTIN DEFICIENCY CAUSES FETAL MALFORMATIONS BY INDUCING FETAL BIOTIN DEFICIENCY (1999)
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Disturbances in Biotin Metabolism in Children Undergoing Long‐Term Anticonvulsant Therapy (1998)
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Disturbances in Biotin Metabolism in Children Undergoing Long-Term Anticonvulsant Therapy (1998)
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