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Paul L. Fidel

Researcher at LSU Health Sciences Center New Orleans

Publications -  77
Citations -  8154

Paul L. Fidel is an academic researcher from LSU Health Sciences Center New Orleans. The author has contributed to research in topics: Candida albicans & Corpus albicans. The author has an hindex of 46, co-authored 70 publications receiving 7769 citations. Previous affiliations of Paul L. Fidel include Wayne State University & University Medical Center New Orleans.

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Candida glabrata: review of epidemiology, pathogenesis, and clinical disease with comparison to C. albicans

TL;DR: This review summarizes all known clinical and experimental information about C. glabrata infections with comparisons to C. albicans as a means of contrasting the two species commonly observed and emphasizing the many recognized differences.
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Requirement of Interleukin-17A for Systemic Anti-Candida albicans Host Defense in Mice

TL;DR: The data suggest that the mIL- 17A/mIL-17AR system is required for normal fungal host defense in vivo, and IL-17A could have potential as a therapeutic cytokine for systemic C. albicans infections in immunocompromised patients with cancer or advanced acquired immunodeficiency syndrome.
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Adhesive and Mammalian Transglutaminase Substrate Properties of Candida albicans Hwp1

TL;DR: A hypha-specific surface protein, Hwp1, with similarities to mammalian small proline-rich proteins was shown to serve as a substrate for mammalian transglutaminases, representing a paradigm for microbial adhesion that implicates essential host enzymes.
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The diagnostic and prognostic value of amniotic fluid white blood cell count, glucose, interleukin-6, and Gram stain in patients with preterm labor and intact membranes

TL;DR: Interleukin-6 concentrations in amniotic fluid are better indicators of microbial invasion of the amniotics cavity, amniocentesis-to-delivery interval, and neonatal complications than the ammiotic fluid Gram stain, glucose concentration, or white blood cell count.
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Immunopathogenesis of recurrent vulvovaginal candidiasis.

TL;DR: The results of both clinical studies and studies in an animal model of experimental vaginitis suggest that systemic CMI may not be the predominant host defense mechanism against C. albicans vaginal infections, and locally acquired mucosal immunity is under consideration as an important host defense at the vaginal mucosa.