Impact of Local Curvature and Structural Defects on Graphene–C₆₀ Fullerene Fusion Reaction Barriers

Self-consistent charge density functional tight-binding and density functional theory calculations have been employed to study the energetics of the graphene–C₆₀ fullerene fusion. We show that there is an optimal value of the bond-puckering angle of single-layer graphene-like systems, which facilitates fusion with other low-dimension carbon systems. Specifically, chemical attachment of a C₆₀ fullerene to a single-layer graphene sheet is not feasible from the energetic point of view due to lack of puckering of the pristine graphene surface, but may occur for systems with some surface curvature. The presence of various defects in the graphene surface, including formation of four- and five-membered rings, Stone–Wales defects, or single and double vacancies may create some surface strain leading to formation of reactive sites in graphene, which are susceptive to binding with a fullerene. As an example, we show that a single vacancy in the graphene surface can lead to formation of a stable chemical bond with a fullerene

Calcium signaling regulates histamine-mediated contraction in capillary-like networks.

<p>(A-C) Shrinkage of capillary-like networks after treatment with (A) histamine, (B) histamine and BAPTA, and (C) histamine with 18β-GA. Left and middle columns indicate bright-field images of the networks before and after treatment. Right column shows overlays of cell structure profiles before (red) and after (black) histamine treatment. Scale bar, 100 μm. (D) Quantification of the relative shrinkage area. Data are representative from seven independent experiments (Bonferroni's multiple comparison test; ***, P<0.001).</p

Collective calcium signaling depends on the number of coupled cells in linear networks.

<p>(A–C) Histamine-induced calcium oscillations in linear cell networks with the width of (A) 20 μm, (B) 40 μm and (C) 100 μm. Scale bar, 100 μm. Red circles indicate the oscillating cells. The calcium response curves were shifted vertically for clarity. (D-E) Quantification of the mean decay rate and calcium oscillation occurrence rate in linear cell networks with different widths (n = 8; 233 cells for 20 μm; 432 cells for 40 μm; 806 cells for 100 μm; Bonferroni's multiple comparison test; ns, not significant; *, P<0.05; ***, P<0.001).</p

Calcium signaling in HUVEC depends on the cellular architecture.

<p>(A–D) Histamine-induced calcium dynamics in (A) individual cells (100 cells/mm²), (B) cells in monolayers (800 cells/mm²), (C) capillary-like networks (CLN), and (D) microengineered hexagonal cell networks (hexagon). The numbers at the upper left corners indicate the time in seconds after histamine treatment. White arrows indicate cells exhibiting calcium oscillations. (E–H) Calcium dynamics in 12 selected cells in different configurations. Red arrows indicate the time of histamine addition. The calcium response curves were shifted vertically for clarity. Images are representative from three to eight independent experiments (n = 6 for individual cells; n = 6 for monolayer; n = 3 for CLN; n = 8 for hexagon). Scale bar, 200 μm. Random regions of interest at 405 μm×405 μm were chosen to ensure enough cells for representing the calcium signaling in various cell architectures. For individual cells, cells were numbered randomly. For monolayers and cell networks, cells were numbered to illustrate the spatial locations.</p

Cellular Architecture Regulates Collective Calcium Signaling and Cell Contractility

<div><p>A key feature of multicellular systems is the ability of cells to function collectively in response to external stimuli. However, the mechanisms of intercellular cell signaling and their functional implications in diverse vascular structures are poorly understood. Using a combination of computational modeling and plasma lithography micropatterning, we investigate the roles of structural arrangement of endothelial cells in collective calcium signaling and cell contractility. Under histamine stimulation, endothelial cells in self-assembled and microengineered networks, but not individual cells and monolayers, exhibit calcium oscillations. Micropatterning, pharmacological inhibition, and computational modeling reveal that the calcium oscillation depends on the number of neighboring cells coupled via gap junctional intercellular communication, providing a mechanistic basis of the architecture-dependent calcium signaling. Furthermore, the calcium oscillation attenuates the histamine-induced cytoskeletal reorganization and cell contraction, resulting in differential cell responses in an architecture-dependent manner. Taken together, our results suggest that endothelial cells can sense and respond to chemical stimuli according to the vascular architecture via collective calcium signaling.</p></div

Architecture-dependent calcium signaling is mediated through gap junctions.

<p>(A-B) Quantification of the mean decay rate of the initial calcium spike and calcium oscillation occurrence rate in various configurations in the presence or absence of 18β-GA, a gap junction blocker. Data represent mean ± s.e.m. (Bonferroni's multiple comparison test; ns, not significant; *, P<0.05; **, P<0.01; ***, P<0.001; n = 6 for individual cells; n = 3 for CLN; n = 3 for CLN with 18β-GA; n = 8 for hexagon; n = 3 for hexagon with 18β-GA). (C) Histograms of the half decay times of the initial calcium spikes. Total cells analyzed were 256, 2776, 466, 377, 884, and 324 for individual cells, monolayer, CLN, CLN with 18β-GA, hexagon, and hexagon with 18β-GA respectively.</p