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Pathogenesis of Fungal Keratitis
Published in Mahendra Rai, Marcelo Luís Occhiutto, Mycotic Keratitis, 2019
Phenotypic switching or morphogenesis is a process of adaptation used by some microorganisms to survive in unfavorable micro-environments (San-Blas et al. 2000), such as inside the infected hosts, especially under antimicrobial therapy. The presence of intrahyphal hyphae was unequivocally observed in culture from a case of human mycotic keratitis caused by Lasiodiplodia theobromae (Thomas et al. 1991). Kiryu and co-workers induced Fusarium solani keratitis of rabbits to study the mode of fungal invasion into the corneal stroma, the interactions between F. solani and inflammatory cells under the influence of topical dexamethasone treatment, and the survival mechanism of the fungi in the dexamethasone-treated cornea. In the dexamethasone-treated corneal lesions, a significant increase in both size and number of fungal peroxisomes was noted. Moreover, the hyphae surrounded by neutrophils, showed double or triple cell wall formation or occasionally a hypha-in-hypha structure was observed (Kyriu et al. 1991).
Atherosclerosis and Mechanical Forces
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
Experimental data regarding the impact of stretch on SMC phenotype are contradicting, depending on the model used. In vitro studies on cultured cells have demonstrated that in response to cyclic stretch, vascular SMCs undergo phenotypic switching from contractile to synthetic phenotype (Hu 2014; Rodríguez 2015). By contrast, in ex vivo model, where the stretch was applied to a segment of portal vein, SMCs adopted a contractile pattern (Turczynska 2012). The discrepancy between both models may be explained by the fact that, in the wall of a real vessel, an interaction occurs between SMCs and ECs (Mantella 2015). Vascular SMCs cocultured with ECs display different gene expressions as compared with monocultured SMCs (Heydarkhan-Hagvall 2003).
Amphotericin B Lipid Complex (ABLC)
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
AmB possesses a broad spectrum of antifungal activity that includes the endemic dimorphic fungi and most of the opportunistic yeast and molds observed in humans (for an overview table of MIC values, please see Chapter 141, Table 141.1). Resistance to AmB has been associated with quantitative or qualitative alterations in the sterol composition of the fungal cell membrane, but may also be related to phenotypic switching such as increased catalase activity with decreased susceptibility to oxidative damage (Chamilos et al., 2005; Groll et al., 2003; Hamilton-Miller, 1972; Kelly et al., 1994; Pierce et al., 1978; Subden et al., 1977; Woods, 1971).
Size-optimized simvastatin-loaded TPGS modified lipid nanocapsules for targeting epithelial-to-mesenchymal transition in hepatocellular carcinoma: Role of PTEN/AKT signaling
Published in Expert Opinion on Drug Delivery, 2023
Khaled Mahmoud, Mahmoud Teaima, Yasmeen Attia, Mohamed El-Nabarawi, Shady Swidan
During cancer progression, the acquisition of the mesenchymal phenotype along with the loss of the epithelial phenotype are considered hallmarks of the EMT program to reinforce the chemoresistance and stemness of cancer cells. To this end, the expression of N- and E-cadherins, the mesenchymal and epithelial markers, respectively, are commonly used to dictate the EMT status in cancer cells. In the present study, the levels of N-cadherin were 27.58% lower in the SIM-LNC50-treated cells, as compared to SIM-treated cells (Figure 2A). Both treatments demonstrated lower N-cadherin levels compared to control untreated cells. Consistent with these findings, E-cadherin levels were found to be higher in SIM-LNC50-treated cells by 1.4 folds compared to free SIM (Figure 2B). These results might imply the phenotypic switching from the mesenchymal to the epithelial form in HCC cells following treatment with SIM-loaded LNC.
MicroRNA-144 silencing attenuates intimal hyperplasia by directly targeting PTEN
Published in Clinical and Experimental Hypertension, 2022
Vascular smooth muscle cells (VSMCs) within the middle layer of the vessel wall are not terminally differentiated that can alter their phenotype in response to changing local environmental cues, which the cellular transition is well recognized as phenotypic switching of VSMC (1). Specifically, the mature VSMCs show contractile or differentiated character with extremely low rates of proliferation and migration. Upon the various cellular stimuli, the differentiated VSMCs transform into a synthetic phenotype, characterized as increased rates of proliferation, migration, and synthesis of extracellular matrix components, as well as reduced expression of differentiation markers, including smooth muscle α-actin, smooth muscle 22α, and smooth muscle myosin heavy chain (2). Importantly, intimal hyperplasia contributed by VSMC phenotypic switching is the major cause of failure in atherosclerosis-related coronary heart diseases, followed by vascular revascularization therapy, including angioplasty, vascular stenting (3). However, the potential target and molecular mechanisms underlying VSMC phenotypic switching and intimal hyperplasia still need to be widely investigated. .
Agent-based model of diffusion of N-acyl homoserine lactones in a multicellular environment of Pseudomonas aeruginosa and Candida albicans
Published in Biofouling, 2018
Gael Pérez-Rodríguez, Sónia Dias, Martín Pérez-Pérez, Florentino Fdez-Riverola, Nuno F. Azevedo, Anália Lourenço
Agent-based simulations studied the impact of spatial location over cell phenotypic switching. Simulations included multiple scenarios of cell distribution and each simulation was replicated six times. For simplicity, the simulation environment was dimensioned to fit the population of cells studied in each group of simulations (ie cell volume times the number of cells) and a minimal volume of extracellular space (ie a realistic spacing between the cells).