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Theodore C. White

Researcher at University of Missouri–Kansas City

Publications -  98
Citations -  12535

Theodore C. White is an academic researcher from University of Missouri–Kansas City. The author has contributed to research in topics: Candida albicans & Corpus albicans. The author has an hindex of 48, co-authored 95 publications receiving 11171 citations. Previous affiliations of Theodore C. White include Netherlands Cancer Institute & Fred Hutchinson Cancer Research Center.

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Hidden Killers: Human Fungal Infections

TL;DR: The importance of fungi as human pathogens is highlighted and the challenges the authors face in combating the devastating invasive infections caused by these microorganisms are discussed, in particular in immunocompromised individuals.
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Clinical, cellular, and molecular factors that contribute to antifungal drug resistance.

TL;DR: This review summarizes the factors that contribute to antifungal drug resistance on three levels: clinical factors that result in the inability to successfully treat refractory disease; cellular factors associated with a resistant fungal strain; and molecular factors that are ultimately responsible for the resistance phenotype in the cell.
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Increased mRNA levels of ERG16, CDR, and MDR1 correlate with increases in azole resistance in Candida albicans isolates from a patient infected with human immunodeficiency virus.

TL;DR: A compilation of the genetic alterations identified in this series suggests that resistance develops gradually and is the sum of several different changes, all of which contribute to the final resistant phenotype.
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Candidemia in Allogeneic Blood and Marrow Transplant Recipients: Evolution of Risk Factors after the Adoption of Prophylactic Fluconazole

TL;DR: The use of prophylactic fluconazole is associated with a low incidence of candidemia and attributable mortality, despite colonization with azole-resistant Candida species in BMT recipients.
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Resistance Mechanisms in Clinical Isolates of Candida albicans

TL;DR: The analyses suggest that the resistance mechanisms identified in matched sets of susceptible and resistant isolates are not sufficient to explain resistance in a collection of unmatched clinical isolates and that additional mechanisms have yet to be discovered.