Using infrared-visible sum-frequency generation we have obtained the OH stretch vibrational spectra of water at the vapor/water interface. From the spectra, we deduce that more than 20% of the surface water molecules have one free OH projecting into the vapor. The spectrum is weakly temperature dependent from 10 to 80 C. A monolayer of fatty alcohol on water surface terminates the free OH groups and induces an icelike structure in the spectrum.
The curling of a graphitic sheet to form carbon nanotubes produces a class of materials that seem to have extraordinary electrical and mechanical properties. In particular, the high elastic modulus of the graphite sheets means that the nanotubes might be stiffer and stronger than any other known material, with beneficial consequences for their application in composite bulk materials and as individual elements of nanometre-scale devices and sensors. The mechanical properties are predicted to be sensitive to details of their structure and to the presence of defects, which means that measurements on individual nanotubes are essential to establish these properties. Here we show that multiwalled carbon nanotubes can be bent repeatedly through large angles using the tip of an atomic force microscope, without undergoing catastrophic failure. We observe a range of responses to this high-strain deformation, which together suggest that nanotubes are remarkably flexible and resilient.
Mechanical forces influence many aspects of cell behavior. Forces are detected and transduced into biochemical signals by force bearing molecular elements located at the cell surface, in adhesion complexes or in cytoskeletal structures1. The nucleus is physically connected to the cell surface through the cytoskeleton and the linker of nucleoskeleton and cytoskeleton (LINC) complex, allowing rapid mechanical stress transmission from adhesions to the nucleus2. Whereas it has been demonstrated that nuclei experience force3, the direct effect of force on the nucleus is not known. Here we show that isolated nuclei are able to respond to force by adjusting their stiffness to resist the applied tension. Using magnetic tweezers, we found that applying force on nesprin-1 triggers nuclear stiffening that does not involve chromatin or nuclear actin, but requires an intact nuclear lamina and emerin, a protein of the inner nuclear membrane. Emerin becomes tyrosine phosphorylated in response to force and mediates the nuclear mechanical response to tension. Our results demonstrate that mechanotransduction is not restricted to cell surface receptors and adhesions but can occur within the nucleus.
Cancer cells are defined by their ability to invade through the basement membrane, a critical step during metastasis. While increased secretion of proteases, which facilitates degradation of the basement membrane, and alterations in the cytoskeletal architecture of cancer cells have been previously studied, the contribution of the mechanical properties of cells in invasion is unclear. Here we apply a magnetic tweezer system to establish that stiffness of patient tumor cells and cancer cell lines inversely correlates with migration and invasion through three-dimensional basement membranes, a correlation known as a power law. We found that cancer cells with the highest migratory and invasive potential are five times less stiff than cells with the lowest migration and invasion potential. Moreover, decreasing cell stiffness by pharmacological inhibition of myosin II increases invasiveness, while increasing cell stiffness by restoring expression of the metastasis suppressor TβRIII/betaglycan decreases invasiveness. These findings are the first demonstration of the power law relation between the stiffness and the invasiveness of cancer cells and show that mechanical phenotypes can be used to grade the metastatic potential of cell populations with the potential for single cell grading. The measurement of a mechanical phenotype, taking minutes rather than hours needed for invasion assays, is promising as a quantitative diagnostic method and as a discovery tool for therapeutics. By demonstrating that altering stiffness predictably alters invasiveness, our results indicate that pathways regulating these mechanical phenotypes are novel targets for molecular therapy of cancer.
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