Objective: The aim of this study was to evaluate whether fluconazole (FLZ) could affect the bioactivity and cellular structure of Candida albicans or Candida glabrata biofilms grown in the presence of FLZ.
Materials And Methods: Tokens were fabricated using poly(methylmethacrylate) resin (PMMA) in a hot water bath. Salivary pellicles were formed on the PMMA surface, and biofilms of a reference strain and two clinical isolates of C. albicans (ATCC 90028, P01 and P34) and C. glabrata (ATCC 2001, P11 and P31) were developed for a period of 48 h. Control and experimental groups were formed. FLZ at the bioavailable concentration in saliva (2.56 μg/mL) was added to the medium of the experimental group. The culture mediums of the control and experimental groups were changed after 24h. The bioactivities of the biofilms were evaluated using an XTT reduction colorimetric assay. The cellular structure was analysed by confocal scanning laser microscopy and by transmission electron microscopy. The data were analysed by the independent sample Student's t-test, with the significance level set at 5%.
Results: The presence of FLZ decreased the bioactivity of all C. albicans biofilms (p<0.001), however, it did not change the cellular structure of C. albicans P34. Regarding the C. glabrata biofilm bioactivity and structure, no statistically significant differences were found between the control and experimental groups.
Conclusion: FLZ, at the bioavailable concentration present in saliva, interferes with the development of C. albicans biofilms, but does not interfere with the development of C. glabrata biofilms.
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http://dx.doi.org/10.1016/j.archoralbio.2011.04.006 | DOI Listing |
Sci Rep
December 2024
Department of Psychiatry and Behavioral Sciences and Weill Center for Neurosciences, University of California, San Francisco, CA, 94107, USA.
Telomere attrition is a hallmark of biological aging, contributing to cellular replicative senescence. However, few studies have examined the determinants of telomere attrition in vivo in humans. Mitochondrial Health Index (MHI), a composite marker integrating mitochondrial energy-transformation capacity and content, may be one important mediator of telomere attrition, as it could impact telomerase activity, a direct regulator of telomere maintenance.
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December 2024
Department of Biological Sciences and Biotechnology, College of Life Sciences and Nanotechnology, Hannam University, Daejeon, Korea.
The NS1 binding protein, known for interacting with the influenza A virus protein, is involved in RNA processing, cancer, and nerve cell growth regulation. However, its role in stress response independent of viral infections remains unclear. This study investigates NS1 binding protein's function in regulating stress granules during oxidative stress through interactions with GABARAP subfamily proteins.
View Article and Find Full Text PDFThe proximity ligation-based Hi-C and derivative methods are the mainstream tools to study genome-wide chromatin interactions. These methods often fragment the genome using enzymes functionally irrelevant to the interactions per se, restraining the efficiency in identifying structural features and the underlying regulatory elements. Here we present Footprint-C, which yields high-resolution chromatin contact maps built upon intact and genuine footprints protected by transcription factor (TF) binding.
View Article and Find Full Text PDFNat Commun
December 2024
IRCCS Azienda Ospedaliero-Universitaria di Bologna, Istituto di Ematologia "Seràgnoli", Bologna, Italy.
Acute myeloid leukemia (AML) is an aggressive disease with a high relapse rate. In this study, we map the metabolic profile of CD34(CD38) AML cells and the extracellular vesicle signatures in circulation from AML patients at diagnosis. CD34 AML cells display high antioxidant glutathione levels and enhanced mitochondrial functionality, both associated with poor clinical outcomes.
View Article and Find Full Text PDFNat Commun
December 2024
Department of Neuroscience, Baylor College of Medicine, Houston, TX, 77030, USA.
The bipolar disorder (BD) risk gene ANK3 encodes the scaffolding protein AnkyrinG (AnkG). In neurons, AnkG regulates polarity and ion channel clustering at axon initial segments and nodes of Ranvier. Disruption of neuronal AnkG causes BD-like phenotypes in mice.
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