The optical properties of plant surfaces are strongly determined by the shape of epidermal cells and by the patterning of the cuticle on top of the cells. Combinations of particular cell shapes with particular nanoscale structures can generate a wide range of optical effects. Perhaps most notably, the development of ordered ridges of cuticle on top of flat petal cells can produce diffraction-grating-like structures. A diffraction grating is one of a number of mechanisms known to produce 'structural colours', which are more intense and pure than chemical colours and can appear iridescent. We explore the concept that mechanical buckling of the cuticle on the petal epidermis might explain the formation of cuticular ridges, using a theoretical model that accounts for the development of compressive stresses in the cuticle arising from competition between anisotropic expansion of epidermal cells and isotropic cuticle production. Model predictions rationalize cuticle patterns, including those with long-range order having the potential to generate iridescence, for a range of different flower species.
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http://dx.doi.org/10.1098/rsif.2012.0847 | DOI Listing |
Immune cells determine the role of the tumor microenvironment during tumor progression, either suppressing tumor formation or promoting tumorigenesis. We analyzed the profile of immune cells in the tumor microenvironment of control mouse skins and skin tumors at the single-cell level. We identified 15 CD45 immune cell clusters, which broadly represent the most functionally characterized immune cell types including macrophages, Langerhans cells (LC), conventional type 1 dendritic cells (cDC1), conventional type 2 dendritic cells (cDC2), migratory/mature dendritic cells (mDC), dendritic epidermal T cells (DETC), dermal γδ T cells (γδT), T cells, regulatory T cells (Tregs), natural killer cells (NK), type 2 innate lymphoid cells (ILC2), neutrophils (Neu), mast cells (Mast), and two proliferating populations (Prolif.
View Article and Find Full Text PDFWhile the genetic paradigm of cancer etiology has proven powerful, it remains incomplete as evidenced by the widening spectrum of non-cancer cell-autonomous "hallmarks" of cancer. Studies have demonstrated the commonplace presence of high oncogenic mutational burdens in homeostatically-stable epithelia. Hence, the presence of driver mutations alone does not result in cancer.
View Article and Find Full Text PDFRSC Adv
January 2025
Department of Chemistry, College of Science, King Saud University P. O. Box 2455 Riyadh 11451 Saudi Arabia
The search for effective anti-cancer therapies has led to the exploration of dual inhibition strategies targeting multiple key molecular pathways. In this study, we aimed to design a novel candidate capable of dual inhibition targeting both EGFR (Epidermal Growth Factor Receptor) and PARP-1 (poly(ADP-ribose)polymerase-1), two crucial proteins implicated in cancer progression and resistance mechanisms. Through molecular hybridization and structure-based drug design approaches, we synthesized a series of compounds based on spirooxindole with triazole scaffolds with the potential for dual EGFR and PARP-1 inhibition.
View Article and Find Full Text PDFInflamm Res
January 2025
Departments of Oral Medicine, Stomatological Hospital, School of Stomatology, Southern Medical University, Guangzhou, Guangdong Province, China.
Mucosal-associated invariant T (MAIT) cells, a type of T lymphocytes with innate-like characteristics, are crucial in bridging innate and adaptive immunity. When activated, MAIT cells release various inflammatory molecules and swiftly respond to antigens. Notably, numerous studies highlight the significant impact of MAIT cells on tumors and various immune disorders by influencing the immune microenvironment.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Genetics, Yale School of Medicine, New Haven, CT, USA.
Skin epithelial stem cells correct aberrancies induced by oncogenic mutations. Oncogenes invoke different strategies of epithelial tolerance; while wild-type cells outcompete β-catenin-gain-of-function (βcatGOF) cells, Hras cells outcompete wild-type cells. Here we ask how metabolic states change as wild-type stem cells interface with mutant cells and drive different cell-competition outcomes.
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