We present a method that uses microcontact printing of alkanethiols on gold to generate patterned substrates presenting "islands" of extracellular matrix (ECM) surrounded by nonadhesive regions such that single cells attach and spread only on the adhesive regions. We have used this micropatterning technology to demonstrate that mammalian cells can be switched between growth and apoptosis programs in the presence of saturating concentrations of growth factors by either promoting or preventing cell spreading (1). From the perspective of fundamental cell biology, these results suggested that the local differentials in growth and viability that are critical for the formation of complex tissue patterns may be generated by local changes in cell-ECM interactions. In the context of cell culture technologies, such as bioreactors and cellular engineering applications, the regulation of cell function by cell shape indicates that the adhesive microenvironment around cells can be carefully optimized by patterning a substrate in addition to using soluble factors (2). Micropatterning technology will play a central role both in our understanding how ECM and cell shape regulate cell physiology and in facilitating the development of cellular biosensor and tissue engineering applications (3-5).
No abstract is provided for this article.
No abstract is provided for this article.
Save every clone! In phage display, clones displaying ligands that hinder growth of phage are lost in amplification. Competition of slowly (S) and rapidly (R) growing phage is mitigated in monodisperse emulsions generated by a simple microfluidic device. Separating R and S in ca. 107 droplets maintains R/S ratio throughout amplification. Competition-free amplification of phage preserves ligands that are usually lost in phage display screen. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Type 2 diabetes (T2D) is thought to arise from the complex interplay of both genetic and environmental factors. Since the advent of genome-wide association studies (GWAS), we have seen considerable progress in our understanding of the role that genetics and gene-environment interactions play in the development of T2D. Recent work suggests that the adverse effect of several T2D loci may be abolished or at least attenuated by higher physical activity levels or healthy lifestyle, whereas low physical activity and dietary factors characterizing a Western dietary pattern may augment it. However, there still remain inconsistencies warranting further investigation. Lack of statistical power and measurement errors for the environmental factors continue to challenge our efforts for characterizing interactions. Although our recent focus on established T2D loci is reasonable, we may be overlooking many other potential loci not captured by recent T2D GWAS. Agnostic approaches to the discovery of gene and environment interactions may address this possibility, but their application to the field is currently limited and still faces conceptual challenges. Nonetheless, continued investment in gene-environment interaction studies through large collaborative efforts holds promise in furthering our understanding of the interplay between genetic and environmental factors.
A series of model experiments have been conducted to compare observations on buckling-driven delamination of thin films under plane-strain compression with an existing analysis. The results are consistent within the range considered by the theory, which applies when the delamination crack is open to the tip. However, the observations indicate that delamination can occur beyond this range, when the crack tip is closed and undergoing mode-II advance. The theory was extended to incorporate the effect of a contact region in which frictional effects shields the crack tip. A comparison of the analysis with the data indicates that the frictional stress required to explain the apparent toughness observed in this regime is larger than the shear yield strength of the interface. It is inferred that large-scale plasticity may have a significant effect on the results, but this effect has not been included in the analysis.
