52 research outputs found
Superlubricity - a new perspective on an established paradigm
Superlubricity is a frictionless tribological state sometimes occurring in
nanoscale material junctions. It is often associated with incommensurate
surface lattice structures appearing at the interface. Here, by using the
recently introduced registry index concept which quantifies the registry
mismatch in layered materials, we prove the existence of a direct relation
between interlayer commensurability and wearless friction in layered materials.
We show that our simple and intuitive model is able to capture, down to fine
details, the experimentally measured frictional behavior of a hexagonal
graphene flake sliding on-top of the surface of graphite. We further predict
that superlubricity is expected to occur in hexagonal boron nitride as well
with tribological characteristics very similar to those observed for the
graphitic system. The success of our method in predicting experimental results
along with its exceptional computational efficiency opens the way for modeling
large-scale material interfaces way beyond the reach of standard simulation
techniques.Comment: 18 pages, 7 figure
Transforming a Pair of Orthogonal tRNA-aminoacyl-tRNA Synthetase from Archaea to Function in Mammalian Cells
A previously engineered Methanocaldococcus jannaschii –tyrosyl-tRNA synthetase pair orthogonal to Escherichia coli was modified to become orthogonal in mammalian cells. The resulting -tyrosyl-tRNA synthetase pair was able to suppress an amber codon in the green fluorescent protein, GFP, and in a foldon protein in mammalian cells. The methodology reported here will allow rapid transformation of the much larger collection of existing tyrosyl-tRNA synthetases that were already evolved for the incorporation of an array of over 50 unnatural amino acids into proteins in Escherichia coli into proteins in mammalian cells. Thus we will be able to introduce a large array of possibilities for protein modifications in mammalian cells
Income redistribution going awry: The reversal power of the concern for relative deprivation
p53 Silencing by Lentiviral Vector Mediated RNA Interference in Murine Hematopoietic Cells and the Development of a Myelogenous Proliferative Disease.
Human-Induced Neurons from Presenilin 1 Mutant Patients Model Aspects of Alzheimer’s Disease Pathology
Traditional approaches to studying Alzheimer’s disease (AD) using mouse models and cell lines have advanced our understanding of AD pathogenesis. However, with the growing divide between model systems and clinical therapeutic outcomes, the limitations of these approaches are increasingly apparent. Thus, to generate more clinically relevant systems that capture pathological cascades within human neurons, we generated human-induced neurons (HiNs) from AD and non-AD individuals to model cell autonomous disease properties. We selected an AD patient population expressing mutations in presenilin 1 (mPS1), which is linked to increased amyloid production, tau pathology, and calcium signaling abnormalities, among other features. While these AD components are detailed in model systems, they have yet to be collectively identified in human neurons. Thus, we conducted molecular, immune-based, electrophysiological, and calcium imaging studies to establish patterns of cellular pathology in this patient population. We found that mPS1 HiNs generate increased Aβ42 and hyperphosphorylated tau species relative to non-AD controls, and exaggerated ER calcium responses that are normalized with ryanodine receptor (RyR) negative allosteric modulators. The inflammasome product, interleukin-18 (IL-18), also increased PS1 expression. This work highlights the potential for HiNs to model AD pathology and validates their role in defining cellular pathogenesis and their utility for therapeutic screening
The orthogonality of the <i>M. jannaschii</i> TyrRS- pair was verified on western blots probed with anti-V5 antibodies.
<p>Expression of full-length foldon was monitored when various tRNAs were introduced into the HEK 293T cells. Note that the tRNA mutants used in these experiments were slightly different from those depicted in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0011263#pone-0011263-g001" target="_blank">figure 1</a>.</p
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