Effects of Farnesol on Drug-Resistant and Non-Resistant Candida albicans: Implications for Cosmetic and Pharmaceutical Applications
Creator:
Larsen, Bryan, Wittman, Emma OMS-2, Yar, Neela, de Seta, Francesco, and Schaut, Dominic
Description:
Background: Farnesol is added to numerous consumer products that intentionally, or inadvertently come in contact with tissues that may harbor the opportunistic yeast, Candida albicans. Objective: This study explores biological consequences of the exposure of Candida albicans from community infections or from a panel of antifungal drug resistant organisms on growth and survival of these organisms when exposed to farnesol. Methods: ATCC supplied Candida albicans from the MP8 drug resistance panel and an additional 12 strains of community-acquired Candida albicans were cultured in the presence of farnesol. With standard micobiologic techniques and flow cytometry evaluation, a series of experiments considered growth, morphology, viability and entrance into the quiescent persister phenotype of Candida with emphasis on differences between drug resistant and community organisms. Results: Differences growth yield, relative cell size and heat susceptibility distinguished the community organisms from the drug-resistant organisms. Using a subset of these organisms, exposure to farnesol resulted in diminished growth, inhibited hyphal growth, diminished cell membrane integrity and increased heat stress susceptibility. Data provided suggest that exposure to farnesol pushes cultures of Candida albicans toward the quiescent persister phenotype. Conclusion: Exposure of drug resistant and community strains of Candida albicans are modestly affected by farnesol in ways that may lessen their pathogenic potential. In contrast, the tendency of farnesol to engender greater numbers of quiescent organisms could support persistence of Candida.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
Language:
English
Identifier:
10.4236/aim.2020.108028
Type:
Article
Keyword:
Antifungal Resistance, Farnesol, Quorum Sensing, Candida albicans, and Persister Phenotype
Exploring Phenotypic and Neurocognitive Profiles in BCL11B Gene Mutations: A Case Study of a Family with Three Siblings
Creator:
Medernach, Kevin, Chapman, L., Thibodaux, L., and Curtin, Michelle
Contributor:
Wake Forest University School of Medicine
Description:
BCL11B is a transcription factor gene that encodes a zinc finger domain, which is thought to play an important role in DNA binding, that is critical to the development of the nervous and immune system. Mutations in this gene are rare in the general population but associated with a range of neurodevelopmental abnormalities, intellectual disability, craniofacial dysmorphology, movement disorders, atopic disorders, and immune deficiencies. Most mutations in BCL11B arise de novo, with missense mutations often leading to the most severe neurodevelopmental defects. The findings of this poster aim to summarize current literature and to expand understanding regarding the phenotypic and neurodevelopmental abnormalities associated with mutations in the BCL11B gene.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
Language:
English
Type:
Poster
Keyword:
BCL11B , transcription factor gene, DNA binding, gene mutations, neurodevelopmental defects, and phenotypic defects
Extracranial hypoglossal neurofibroma with a variant ansa cervicalis: a case report
Creator:
Dykstra, Chandler, Dwenger, Emma, Parent, Elizabeth, and Sakthi-Velavan, Sumathilatha
Related Url Tesim:
PubMed: https://pubmed.ncbi.nlm.nih.gov/36723635/, Available from publisher: https://link.springer.com/article/10.1007/s00276-023-03085-z, and Available from the library catalog: https://marianunivindianapolis.on.worldcat.org/oclc/9754729532
Description:
Purpose: This case report aims to explore a rare combination of findings in a cadaver donor: variant ansa cervicalis, vagus (CN X) and hypoglossal (CN XII) nerve fusion, and extracranial hypoglossal neurofibroma.
Background: The type of ansa cervicalis variation presented in this report has been documented in less than 1% of described cases. The CN X-CN XII fusion has been reported in one prior study. Additionally, hypoglossal neurofibromas are benign neoplasms of the peripheral nerve sheath. There are only two known cases of extracranial hypoglossal neurofibroma described in the literature.
Case report: The study investigated a swelling of the right CN XII in a 90-year-old female cadaver donor. Detailed dissection, examination of the region, and histopathological analysis of the mass followed. The entire course of CN XII and other cranial nerves were examined to exclude concurrent pathology. A fusiform enlargement of the right CN XII was observed in the submandibular region, measuring ~ 1.27 × 1.27 cm. The superior portion of the right CN XII was fused to the right CN X, exiting the jugular foramen. The superior root of ansa cervicalis, normally a branch of CN XII, was found to arise from CN X on the right side. The left CN XII and CN X were unremarkable. Histopathological examination revealed benign neurofibroma.
Conclusion: The anatomical variation and rare location of the tumor necessitate further investigation to better understand pathogenesis, clinical correlation, and surgical implications. This study furthers knowledge of this condition and contributes to the currently limited body of research.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
License Tesim:
https://creativecommons.org/licenses/by/4.0/
Language:
English
Publisher:
Springer
Identifier:
DOI: 10.1007/s00276-023-03085-z and PMID: 36723635
Type:
Article
Keyword:
Anatomical variation, Ansa cervicalis, Extracranial neurofibroma, and Neurofibroma
HCAHPS scores as a surrogate for quality does not correlate with TQIP quality measures at a level 1 trauma center
Creator:
Thoma-Perry, Carley OMS-4, Jacobsen, L., Blocher-Smith, Ethan C. OMS-4, and Saxe, J.
Related Url Tesim:
Article available at the following link: https://pubmed.ncbi.nlm.nih.gov/30149936/
Description:
BACKGROUND: The Trauma Quality Improvement Program was designed by the American College of Surgeons to measure quality benchmarks across American College of Surgeons-certified trauma centers. The Hospital Consumer Assessment of Healthcare Providers and Systems survey was developed to report patient satisfaction with inpatient care and has been used as a surrogate for quality of care by the Affordable Care Act. The purpose of this study was to determine the correlation of hospitals' Hospital Consumer Assessment of Healthcare Providers and Systems data to the Trauma Quality Improvement Program quality analysis. METHODS: A retrospective review of available Trauma Quality Improvement Program and Hospital Consumer Assessment of Healthcare Providers and Systems results from an American College of Surgeons level 1 trauma center 2016-2017 was performed. Trauma Quality Improvement Program and Hospital Consumer Assessment of Healthcare Providers and Systems data were represented as either above, at, or below the mean of national data and were analyzed using the Fisher exact test. RESULTS: Hospital Consumer Assessment of Healthcare Providers and Systems scores from wards participating in care of trauma patients were summarized by perceived level of quality. Trauma Quality Improvement Program data for risk-adjusted mortality were included in analysis for all trauma admissions. The Fisher exact test was used to analyze contingency tables of data and was found to support the null hypothesis (P?=?.1109). CONCLUSION: Overall Hospital Consumer Assessment of Healthcare Providers and Systems rating is most significant for hospitals because it is a global view of patient satisfaction and is used to determine a portion of hospital reimbursement. It is believed that higher patient satisfaction is correlated with lower readmission rates and improved outcomes, thus resulting in cost savings for hospitals. However, it appears that overall Hospital Consumer Assessment of Healthcare Providers and Systems rating does not correlate with measured outcomes in terms of risk-adjusted mortality for trauma admissions. It is suggested from these data that trauma patients be considered independently from other hospitalizations and that Hospital Consumer Assessment of Healthcare Providers and Systems may not be an appropriate tool to determine reimbursement for trauma admission.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
Language:
English
Identifier:
10.1016/j.surg.2018.07.032
Type:
Article
Keyword:
HCAHPS, level 1 trauma center, quality benchmarks, American College of Surgeons, and TQIP
How Medical Students' Perceptions of Online Learning Change After Matriculation
Creator:
Zaheer, Meesam, Schmiedeknecht, Madeline, Svendsen, John, Asper, Joseph, Mihalic, Taylor, Montgomery, Zachary, Reed, Wyatt, Hudson, Asia, and Hum, Julia
Description:
The COVID-19 pandemic has accelerated the adoption of online learning across various academic disciplines, including medical education. This study aims to investigate how medical students' perceptions of online learning change before and after matriculation. A comparative thematic analysis was conducted at an osteopathic medical school in Indianapolis, IN, to explore the factors influencing these perceptions and the potential impact on students' educational experiences. The findings highlight the effects that one semester of medical school can have on changing the opinions of students regarding online learning.
Presented at the American Medical Muslim Student Association Conference. A work pertaining to the OMS-3 Class of 2025.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
Language:
English
Type:
Poster
Keyword:
COVID-19, online learning adoption, medical education, and medical students' perceptions
Identification of a bone morphogenetic protein type 2 receptor neutralizing antibody
Creator:
Hum, Julia M. , Totten, Madeline, Gorrell, Ruthann, Schoerning, Laura, Newby, Jordan B., Lowery, Jonathan W., Geyman, Logan J., and Lawless, Warren
Related Url Tesim:
http://creativecommons.org/licenses/by/4.0/
Description:
Originally appearing in BMC Research Notes as an open access article under the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/)., The bone morphogenetic protein (BMP) signaling pathway comprises the largest subdivision of the transforming growth factor (TGFβ) superfamily. BMP signaling plays essential roles in both embryonic development and postnatal tissue homeostasis. Dysregulated BMP signaling underlies human pathologies ranging from pulmonary arterial hypertension to heterotopic ossification. Thus, understanding the basic mechanisms and regulation of BMP signaling may yield translational opportunities. Unfortunately, limited tools are available to evaluate this pathway, and genetic approaches are frequently confounded by developmental requirements or ability of pathway components to compensate for one another. Specific inhibitors for type 2 receptors are poorly represented. Thus, we sought to identify and validate an antibody that neutralizes the ligand-binding function of BMP receptor type 2 (BMPR2) extracellular domain (ECD)., and Ruthann E. Gorrell, Madeline H. Totten share equal contribution to this work.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
Identifier:
10.1186/s13104-019-4367-0
Type:
Article
Keyword:
Bone Morphogenetic Protein and Osteopathic Medicine
Identification of a bone morphogenetic protein type 2 receptor neutralizing antibody
Creator:
Newby, Jordan B., Hum, Julia M., Gorrell, Ruthann, Schoerning, Laura, Lowery, Jonathan W., Lawless, Warren, Totten, Madeline, and Geyman, Logan J.
Description:
The bone morphogenetic protein (BMP) signaling pathway comprises the largest subdivision of the transforming growth factor (TGF?) superfamily. BMP signaling plays essential roles in both embryonic development and postnatal tissue homeostasis. Dysregulated BMP signaling underlies human pathologies ranging from pulmonary arterial hypertension to heterotopic ossification. Thus, understanding the basic mechanisms and regulation of BMP signaling may yield translational opportunities. Unfortunately, limited tools are available to evaluate this pathway, and genetic approaches are frequently confounded by developmental requirements or ability of pathway components to compensate for one another. Specific inhibitors for type 2 receptors are poorly represented. Thus, we sought to identify and validate an antibody that neutralizes the ligand-binding function of BMP receptor type 2 (BMPR2) extracellular domain (ECD).
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
Language:
English
Identifier:
10.1186/s13104-019-4367-0
Type:
Article
Keyword:
Bone morphogenetic protein, Bone morphogenetic protein receptor type 2, BMP, BMPR2, Neutralizing antibody, and SMAD
Identification of p38 MAPK as a novel therapeutic target for Friedreich's ataxia.
Creator:
to be added
Description:
Friedreich ataxia (FRDA) is an autosomal recessive neuro- and cardio-degenerative disorder caused by decreased expression of frataxin, a protein that localizes to mitochondria and is critical for iron-sulfur-cluster (ISC) assembly. There are no proven effective treatments for FRDA. We previously screened a random shRNA library and identified a synthetic shRNA (gFA11) that reverses the growth defect of FRDA cells in culture. We now report that gFA11 decreases cytokine secretion in primary FRDA fibroblasts and reverts other changes associated with cell senescence. The gene-expression profile induced by gFA11 is remarkably similar to the gene-expression profile induced by the p38 MAPK inhibitor SB203580. We found that p38 phosphorylation, indicating activation of the p38 pathway, is higher in FRDA cells than in normal control cells, and that siRNA knockdown of frataxin in normal fibroblasts also increases p38 phosphorylation. Treatment of FRDA cells with p38 inhibitors recapitulates the reversal of the slow-growth phenotype induced by clone gFA11. These data highlight the involvement of the p38 MAPK pathway in the pathogenesis of FRDA and the potential use of p38 inhibitors as a treatment for FRDA.
Identification of p38 MAPK as a Novel Therapeutic Target for Friedreich’s Ataxia
Creator:
Lin, Daniel, Tobias, John W., Cotticelli, M. Gracia, Ruff, Eric, Wang, Yongping, Xia, Shujuan, Wilson, Robert B., and Kaur, Avinash
Related Url Tesim:
Article available at the following URL: https://www.nature.com/articles/s41598-018-23168-x
Description:
Friedreich ataxia (FRDA) is an autosomal recessive neuro- and cardio-degenerative disorder caused by decreased expression of frataxin, a protein that localizes to mitochondria and is critical for iron-sulfur-cluster (ISC) assembly. There are no proven effective treatments for FRDA. We previously screened a random shRNA library and identified a synthetic shRNA (gFA11) that reverses the growth defect of FRDA cells in culture. We now report that gFA11 decreases cytokine secretion in primary FRDA fibroblasts and reverts other changes associated with cell senescence. The gene-expression profile induced by gFA11 is remarkably similar to the gene-expression profile induced by the p38 MAPK inhibitor SB203580. We found that p38 phosphorylation, indicating activation of the p38 pathway, is higher in FRDA cells than in normal control cells, and that siRNA knockdown of frataxin in normal fibroblasts also increases p38 phosphorylation. Treatment of FRDA cells with p38 inhibitors recapitulates the reversal of the slow-growth phenotype induced by clone gFA11. These data highlight the involvement of the p38 MAPK pathway in the pathogenesis of FRDA and the potential use of p38 inhibitors as a treatment for FRDA.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
Language:
English
Identifier:
https://doi.org/10.1038/s41598-018-23168-x
Type:
Article
Keyword:
Cell Biology, Neurology, Genetics, and Friedreich ataxia
The impact of C. elegans ceramide glucosyltransferase enzymes on the beneficial effects of B. subtilis lifespan
Creator:
Arvin, Chelsey L., Sibila, Zachary, Lamendella, R., Chan, Jason, and Staab, Trisha
Related Url Tesim:
National Library of Medicine: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10116348/ and Available from the library catalog: https://marianunivindianapolis.on.worldcat.org/oclc/9845890846
Description:
Ceramide glucosyltransferase (CGT) adds sugar moieties to ceramide, forming glucosylceramides that play roles in immune signaling, stress response, and host-bacterial interactions. Here, we examined whether mutations in cgt block the beneficial effects of Bacillus subtilis on C. elegans lifespan. We found that loss of cgt-1 or cgt-3 reduces lifespan compared to wildtype worms, but did not prevent the lifespan-extending phenotype of B. subtilis. However, cgt-1(ok1045) and cgt-3(tm504) did play a minor role in blocking stress resistance of 5-day old worms treated with B. subtilis. Further studying CGTs may elucidate potential roles of glucosylceramides in host-bacterial interaction.
Rights statement:
http://rightsstatements.org/vocab/InC/1.0/
License Tesim:
https://creativecommons.org/licenses/by/4.0/
Language:
English
Publisher:
California Institute of Technology
Identifier:
Doi: 10.17912/micropub.biology.000758, PMID: 37090153, and PMCID: PMC10116348
Type:
Article
Keyword:
Ceramide glucosyltransferase (CGT), glucosylceramides , Bacillus subtilis, C. elegans, host-bacterial interactions, immune signaling, and stress response