Cells receive signals from the extracellular matrix through receptor-dependent interactions, but they are also influenced by the mechanical properties of the matrix. Although bulk properties of substrates have been shown to affect cell behavior, we show here that nanoscale properties of collagen fibrils also play a significant role in determining cell phenotype. Type I collagen fibrils assembled into thin films provide excellent viewing of cells interacting with individual fibrils. Cells can be observed to extensively manipulate the fibrils, and this behavior seems to result in an incompletely spread stellate morphology and a nonproliferative phenotype that is typical of these cells in collagen gels. We show here that thin films of collagen fibrils can be dehydrated, and when seeded on these dehydrated fibrils, smooth muscle cells spread and proliferate extensively. The dehydrated collagen fibrils appear to be similar to the fully hydrated collagen fibrils in topology and in presentation of beta(1) integrin ligation sites, but they are mechanically stiffer. This decrease in compliance of dehydrated fibrils is seen by a failure of cell movement of dehydrated fibrils compared to their ability to rearrange fully hydrated fibrils and from direct measurements by nanoindentation and quantitative atomic force measurements. We suggest that increase in the nanoscale rigidity of collagen fibrils can cause these cells to assume a proliferative phenotype.

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We have investigated strong optical nonlinearity of monolayer MoS2(1–x)Se2x across the exciton resonance, which is directly tunable by Se doping. The quality of monolayer alloys prepared by chemical vapor deposition is verified by atomic force microscopy, Raman spectroscopy, and photoluminescence analysis. The crystal symmetry of all of our alloys is essentially D 3h , as confirmed by polarization-dependent second-harmonic generation (SHG). The spectral structure of the exciton resonance is sampled by wavelength-dependent SHG (λ = 1000–1800 nm), where the SHG resonance red-shifts in accordance with the corresponding optical gap. Surprisingly, the effect of compositional variation turns out to be much more dramatic owing to the unexpected increase of B-exciton-induced SHG, which indeed dominates over the A-exciton resonance for x ≥ 0.3. The overall effect is therefore stronger and broader SHG resonance where the latter arises from different degrees of red-shift for the two exciton states. We report the corresponding absolute SHG dispersion of monolayer alloys, χ(2), as a function of Se doping. We believe that our finding is a critical step toward engineering highly efficient nonlinear optical van der Waals materials working in a broader performance range.

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In this study, we utilized picosecond pulses from an Nd:YAG laser to investigate the nonlinear optical characteristics of monolayer MoSe 2 . Two-step growth involving the selenization of pulsed-laser-deposited MoO 3 film was employed to yield the MoSe 2 monolayer on a SiO 2 /Si substrate. Raman scattering, photoluminescence (PL) spectroscopy, and atomic force microscopy verified the high optical quality of the monolayer. The second-order susceptibility χ (2) was calculated to be ß50 pm V −1 at the second harmonic wavelength λ SH G ß810 nm, which is near the optical gap of the monolayer. Interestingly, our wavelength-dependent second harmonic scan can identify the bound excitonic states including negatively charged excitons much more efficiently, compared with the PL method at room temperature. Additionally, the MoSe 2 monolayer exhibits a strong laser-induced damage threshold ß16 GW cm −2 under picosecond-pulse excitation . Our findings suggest that monolayer MoSe 2 can be considered as a promising candidate for high-power, thin-film-based nonlinear optical devices and applications.

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We have previously reported that green tea catechins (GTC) display a potent antithrombotic activity, which might be due to antiplatelet rather than anticoagulation effects. In the current study, we investigated the antiplatelet mechanism of GTC. We tested the effects of GTC on the aggregation of human platelets and on the binding of fluorescein isothiocyanate-conjugated fibrinogen to human platelet glycoprotein (GP) IIb/IIIa. GTC inhibited the collagen-, thrombin-, adenosine diphosphate (ADP)-, and calcium ionophore A23187-induced aggregation of washed human platelets, with 50% inhibitory concentration values of 0.64, 0.52, 0.63, and 0.45 mg/ml, respectively. GTC significantly inhibited fibrinogen binding to human platelet surface GPIIb/IIIa complex but failed to inhibit binding to purified GPIIb/IIIa complex. These results indicate that the antiplatelet activity of GTC may be due to inhibition of an intracellular pathway preceding GPIIb/IIIa complex exposure. We also investigated the effects of GTC on intracellular calcium levels, which are critical in determining the activation status of platelets and on induction of platelet aggregation by thapsigargin, which is a selective inhibitor of the Ca(2+)-ATPase pump. Pretreatment of human platelets with GTC significantly inhibited the rise in intracellular Ca(2+) concentration induced by thrombin treatment, and GTC significantly inhibited the thapsigargin-induced platelet aggregation. We also examined the effect of GTC on the second messenger, inositol 1,4,5-triphosphate (IP(3)). GTC significantly inhibited the phosphoinositide breakdown induced by thrombin. Taken together, these observations suggest that the antiplatelet activity of GTC is be mediated by inhibition of cytoplasmic calcium increase, which leads to the inhibition of fibrinogen-GPIIb/IIIa binding via the activation of Ca(2+)-ATPase and inhibition of IP(3) formation.