Midori: A Block Cipher for Low Energy (Extended Version)

In the past few years, lightweight cryptography has become a popular research discipline with a number of ciphers and hash functions proposed. The designers\u27 focus has been predominantly to minimize the hardware area, while other goals such as low latency have been addressed rather recently only. However, the optimization goal of low energy for block cipher design has not been explicitly addressed so far. At the same time, it is a crucial measure of goodness for an algorithm. Indeed, a cipher optimized with respect to energy has wide applications, especially in constrained environments running on a tight power/energy budget such as medical implants. This paper presents the block cipher Midori that is optimized with respect to the energy consumed by the circuit per bit in encryption or decryption operation. We deliberate on the design choices that lead to low energy consumption in an electrical circuit, and try to optimize each component of the circuit as well as its entire architecture for energy. An added motivation is to make both encryption and decryption functionalities available by small tweak in the circuit that would not incur significant area or energy overheads. We propose two energy-efficient block ciphers Midori128 and Midori64 with block sizes equal to 128 and 64 bits respectively. These ciphers have the added property that a circuit that provides both the functionalities of encryption and decryption can be designed with very little overhead in terms of area and energy. We compare our results with other ciphers with similar characteristics: it was found that the energy consumptions of Midori64 and Midori128 are by far better when compared ciphers like PRINCE and NOEKEON

One‐dimensional patterning of cells in silicone wells via compression‐induced fracture

We have adapted our existing compression‐induced fracture technology to cell culture studies by generating linear patterns on a complex cell culture well structure rather than on simple solid constructs. We present a simple method to create one‐dimensional (1D), submicron, and linear patterns of extracellular matrix on a multilayer silicone material. We identified critical design parameters necessary to optimize compression‐induced fracture patterning on the wells, and applied stresses using compression Hoffman clamps. Finite‐element analyses show that the incorporation of the well improves stress homogeneity (stress variation = 25%), and, thus, crack uniformity over the patterned region. Notably, a shallow well with a thick base (vs. deeper wells with thinner bases) reduces out‐of‐plane deflections by greater than a sixth in the cell culture region, improving clarity for optical imaging. The comparison of cellular and nuclear shape indices of a neuroblast line cultured on patterned 1D lines and unpatterned 2D surfaces reveals significant differences in cellular morphology, which could impact many cellular functions. Because 1D cell cultures recapitulate many important phenotypical traits of 3D cell cultures, our culture system offers a simple means to further study the relationship between 1D and 3D cell culture environments, without demanding expensive engineering techniques and expertise. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 1361–1369, 2014.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106690/1/jbma34814.pd

EphB regulates L1 phosphorylation during retinocollicular mapping

Interaction of the cell adhesion molecule L1 with the cytoskeletal adaptor ankyrin is essential for topographic mapping of retinal ganglion cell (RGC) axons to synaptic targets in the superior colliculus (SC). Mice mutated in the L1 ankyrin-binding motif (FIGQY1229H) display abnormal mapping of RGC axons along the mediolateral axis of the SC, resembling mouse mutant phenotypes in EphB receptor tyrosine kinases. To investigate whether L1 functionally interacts with EphBs, we investigated the role of EphB kinases in phosphorylating L1 using a phospho-specific antibody to the tyrosine phosphorylated FIGQY1229 motif. EphB2, but not an EphB2 kinase dead mutant, induced tyrosine phosphorylation of L1 at FIGQY1229 and perturbed ankyrin recruitment to the membrane in L1-transfected HEK293 cells. Src family kinases mediated L1 phosphorylation at FIGQY1229 by EphB2. Other EphB receptors that regulate medial-lateral retinocollicular mapping, EphB1 and EphB3, also mediated phosphorylation of L1 at FIGQY1229. Tyrosine1176 in the cytoplasmic domain of L1, which regulates AP2/clathrin-mediated endocytosis and axonal trafficking, was not phosphorylated by EphB2. Accordingly mutation of Tyr1176 to Ala in L1-Y1176A knock-in mice resulted in normal retinocollicular mapping of ventral RGC axons. Immunostaining of the mouse SC during retinotopic mapping showed that L1 colocalized with phospho-FIGQY in RGC axons in retinorecipient layers. Immunoblotting of SC lysates confirmed that L1 was phosphorylated at FIGQY1229 in wild type but not L1-FIGQY1229H (L1Y1229H) mutant SC, and that L1 phosphorylation was decreased in the EphB2/B3 mutant SC. Inhibition of ankyrin binding in L1Y1229H mutant RGCs resulted in increased neurite outgrowth compared to WT RGCs in retinal explant cultures, suggesting that L1-ankyrin binding serves to constrain RGC axon growth. These findings are consistent with a model in which EphB kinases phosphorylate L1 at FIGQY1229 in retinal axons to modulate L1-ankyrin binding important for mediolateral retinocollicular topography

Engineering biomolecular microenvironments for cell instructive biomaterials

Engineered cell instructive microenvironments with the ability to stimulate specific cellular responses is a topic of high interest in the fabrication and development of biomaterials for application in tissue engineering. Cells are inherently sensitive to the in vivo microenvironment that is often designed as the cell “niche”. The cell “niche” comprising the extracellular matrix and adjacent cells, influences not only cell architecture and mechanics, but also cell polarity and function. Extensive research has been performed to establish new tools to fabricate biomimetic advanced materials for tissue engineering that incorporate structural, mechanical and biochemical signals that interact with cells in a controlled manner and to recapitulate the in vivo dynamic microenvironment. Bioactive tunable microenvironments using micro and nanofabrication have been successfully developed and proven to be extremely powerful to control intracellular signaling and cell function. This review is focused in the assortment of biochemical signals that have been explored to fabricate bioactive cell microenvironments and the main technologies and chemical strategies to encode them in engineered biomaterials with biological information.The authors thank Fundacao para a Ciencia e Tecnologia for C.A.C.'s PhD grant (SFRH/BD/61390/2009). This work was carried out under the scope of the European Union's Seventh Framework Programme (FP7/2007-2013) under grant agreement no REGPOT-CT2012-316331-POLARIS

Cell and Matrix Interactions during Branching Morphogenesis

During embryonic development when tissues are particularly plastic, cells within a tissue can often interact with their surrounding extracellular matrix in a reciprocal manner: the cells remodel the matrix, but the matrix can induce signaling and changes in cell behavior, which in turn can affect matrix remodeling to sculpt tissue architecture. A specialized type of extracellular matrix is the basement membrane, which underlies or encapsulates epithelial tissues. We have used the embryonic mouse salivary gland as a model to study cell-basement membrane interactions during branching morphogenesis. We first focused on whether the cells in contact with the basement membrane (termed outer bud cells) behave differently from cells that remain in contact only with other epithelial cells (inner bud cells). Using a transgenic mouse expressing a photoconvertible fluorescent probe to optically highlight small populations of cells within developing salivary glands, we tracked their migration. The outer cells migrated much more rapidly than the inner cells and each cell population required different proteins for their migration. Therefore, there are two distinct populations of epithelial cells that utilize two different modes of migration in the salivary gland. We also found that the basement membrane was remarkably dynamic, being remodeled on a local and global scale. There are hundreds of tiny perforations in the basement membrane surrounding the tips of rapidly expanding end buds in embryonic lung, kidney, and salivary gland. The entire basement membrane also translocates rearward and accumulates to stabilize the duct. Both the micro-perforations and translocation are dependent on myosin II and protease activity. We speculate that the micro-perforations locally increase the distensibility of the basement membrane, allowing directed expansion of the epithelium and basement membrane translocation. Interestingly, the perforations could also allow increased epithelial cell exposure to the mesenchyme, which could stimulate the motility of the outer cells. In summary, we have described a dynamic, bidirectional system in which the cells modify the basement membrane, which in turn affects cell behavior and matrix remodeling to sculpt tissue architecture during branching of the embryonic mouse salivary gland.Doctor of Philosoph