1,999 research outputs found
Higher and lower supramolecular orders for the design of self-assembled heterochiral tripeptide hydrogel biomaterials
The self-assembly behaviour of the eight stereoisomers of Val\u2013Phe\u2013Phe tripeptides under physiological conditions is assessed by several spectroscopy and microscopy techniques. We report the first examples of self-organised hydrogels from tripeptides in the L\u2013D\u2013L or D\u2013L\u2013D configuration, besides the expected gels with the D\u2013L\u2013L or L\u2013D\u2013D configuration, thus widening the scope for using amino acid chirality as a tool to drive self-assembly. Importantly, the positions of D- and L-amino acids in the gelling tripeptides determine a higher or lower supramolecular order, which translates into macroscopic gels with different rheological properties and thermal behaviours. The more durable hydrogels perform well in cytotoxicity assays, and also as peptides in solution. An appropriate design of the chirality of self-assembling sequences thus allows for the fine-tuning of the properties of the gel biomaterials. In conclusion, this study adds key details of supramolecular organization that will assist in the ex novo design of assembling chiral small molecules for their use as biomaterials
Replica symmetry breaking in an adiabatic spin-glass model of adaptive evolution
We study evolutionary canalization using a spin-glass model with replica
theory, where spins and their interactions are dynamic variables whose
configurations correspond to phenotypes and genotypes, respectively. The spins
are updated under temperature T_S, and the genotypes evolve under temperature
T_J, according to the evolutionary fitness. It is found that adaptation occurs
at T_S < T_S^{RS}, and a replica symmetric phase emerges at T_S^{RSB} < T_S <
T_S^{RS}. The replica symmetric phase implies canalization, and replica
symmetry breaking at lower temperatures indicates loss of robustness.Comment: 5pages, 2 figure
Differentiation of human fetal mesenchymal stem cells into cells with an oligodendrocyte phenotype
This article is available open access through the publisher’s website at the link below. Copyright @ 2009 Landes Bioscience.The potential of mesenchymal stem cells (MSC) to differentiate into neural lineages has raised the possibility of autologous cell transplantation as a therapy for neurodegenerative diseases. We have identified a population of circulating human fetal mesenchymal stem cells (hfMSC) that are highly proliferative and can readily differentiate into mesodermal lineages such as bone, cartilage, fat and muscle. Here, we demonstrate for the first time that primary hfMSC can differentiate into cells with an oligodendrocyte phenotype both in vitro and in vivo. By exposing hfMSC to neuronal conditioned medium or by introducing the pro-oligodendrocyte gene, Olig-2, hfMSC adopted an oligodendrocyte-like morphology, expressed oligodendrocyte markers and appeared to mature appropriately in culture. Importantly we also demonstrate the differentiation of a clonal population of hfMSC into both mesodermal (bone) and ectodermal (oligodendrocyte) lineages. In the developing murine brain transplanted hfMSC integrated into the parenchyma but oligodendrocyte differentiation of these naïve hfMSC was very low. However, the proportion of cells expressing oligodendrocyte markers increased significantly (from 0.2% to 4%) by pre-exposing the cells to differentiation medium in vitro prior to transplantation. Importantly, the process of in vivo differentiation occurred without cell fusion. These findings suggest that hfMSC may provide a potential source of oligodendrocytes for study and potential therapy
Design of a hydrophobic tripeptide that self-assembles into amphiphilic superstructures forming a hydrogel biomaterial
We report the rational design of a heterochiral hydrophobic tripeptide self-assembling into amphiphilic D-superstructures that yield a self-supportive hydrogel at physiological pH. The material endures cell culture conditions and sustains fibroblast proliferation. Tripeptide superstructures are thoroughly analysed by several techniques
Protocol for Pertussis Immunisation and Food Allergy (PIFA): A case-control study of the association between pertussis vaccination in infancy and the risk of IgE-mediated food allergy among Australian children
© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. Introduction Atopic diseases, including food allergy, have become a predominant cause of chronic illness among children in developed countries. In Australia, a rise in hospitalisations among infants coded as anaphylaxis to foods coincided with the replacement of whole-cell pertussis (wP) vaccine with subunit acellular pertussis (aP) vaccine on the national immunisation schedule in the late 1990s. Atopy is characterised by a tendency to mount T helper type 2 (Th2) responses to otherwise innocuous environmental antigens. Compared with infants who receive aP as their first pertussis vaccine, those who receive wP appear less likely to mount Th2 immune responses to either vaccine or extraneous antigens. We therefore speculate that removal of wP from the vaccine schedule contributed to the observed rise in IgE-mediated food allergy among Australian infants. Methods and analysis This is a retrospective individually matched case-control study among a cohort of Australian children born from 1997 to 1999, the period of transition from wP to aP vaccines; we include in the cohort children listed on Australia's comprehensive population-based immunisation register as having received a first dose of either pertussis vaccine by 16 weeks old. 500 cohort children diagnosed as having IgE-mediated food allergy at specialist allergy clinics will be included as cases. Controls matched to each case by date and jurisdiction of birth and regional socioeconomic index will be sampled from the immunisation register. Conditional logistic regression will be used to estimate OR (±95% CI) of receipt of wP (vs aP) as the first vaccine dose among cases compared with controls. Ethics and dissemination The study is approved by all relevant human research ethics committees: Western Australia Child and Adolescent Health Services (2015052EP), Women's and Children's Hospital (HREC/15/WCHN/162), Royal Children's Hospital (35230A) and Sydney Children's Hospital Network (HREC/15/SCHN/405). Outcomes will be disseminated through publication and scientific presentation. Trial registration number NCT02490007
Clustering of galaxies at 3.6 microns in the Spitzer Wide-area Infrared Extragalactic legacy survey
We investigate the clustering of galaxies selected in the 3.6 micron band of
the Spitzer Wide-area Infrared Extragalactic (SWIRE) legacy survey. The angular
two-point correlation function is calculated for eleven samples with flux
limits of S_3.6 > 4-400 mujy, over an 8 square degree field. The angular
clustering strength is measured at >5-sigma significance at all flux limits,
with amplitudes of A=(0.49-29)\times10^{-3} at one degree, for a power-law
model, A\theta^{-0.8}. We estimate the redshift distributions of the samples
using phenomological models, simulations and photometric redshifts, and so
derive the spatial correlation lengths. We compare our results with the GalICS
(Galaxies In Cosmological Simulations) models of galaxy evolution and with
parameterized models of clustering evolution. The GalICS simulations are
consistent with our angular correlation functions, but fail to match the
spatial clustering inferred from the phenomological models or the photometric
redshifts. We find that the uncertainties in the redshift distributions of our
samples dominate the statistical errors in our estimates of the spatial
clustering. At low redshifts (median z<0.5) the comoving correlation length is
approximately constant, r_0=6.1\pm0.5h^{-1} Mpc, and then decreases with
increasing redshift to a value of 2.9\pm0.3h^{-1} Mpc for the faintest sample,
for which the median redshift is z=1. We suggest that this trend can be
attributed to a decrease in the average galaxy and halo mass in the fainter
flux-limited samples, corresponding to changes in the relative numbers of
early- and late-type galaxies. However, we cannot rule out strong evolution of
the correlation length over 0.5<z<1.Comment: 14 pages, 9 (colour) figures. Published in MNRA
Systems developmental biology: the use of ontologies in annotating models and in identifying gene function within and across species
Systems developmental biology is an approach to the study of embryogenesis that attempts to analyze complex developmental processes through integrating the roles of their molecular, cellular, and tissue participants within a computational framework. This article discusses ways of annotating these participants using standard terms and IDs now available in public ontologies (these are areas of hierarchical knowledge formalized to be computationally accessible) for tissues, cells, and processes. Such annotations bring two types of benefit. The first comes from using standard terms: This allows linkage to other resources that use them (e.g., GXD, the gene-expression [G-E] database for mouse development). The second comes from the annotation procedure itself: This can lead to the identification of common processes that are used in very different and apparently unrelated events, even in other organisms. One implication of this is the potential for identifying the genes underpinning common developmental processes in different tissues through Boolean analysis of their G-E profiles. While it is easiest to do this for single organisms, the approach is extendable to analyzing similar processes in different organisms. Although the full computational infrastructure for such an analysis has yet to be put in place, two examples are briefly considered as illustration. First, the early development of the mouse urogenital system shows how a line of development can be graphically formalized using ontologies. Second, Boolean analysis of the G-E profiles of the mesenchyme-to-epithelium transitions that take place during mouse development suggest Lhx1, Foxc1, and Meox1 as candidate transcription factors for mediating this process
Mapping between dissipative and Hamiltonian systems
Theoretical studies of nonequilibrium systems are complicated by the lack of
a general framework. In this work we first show that a transformation
introduced by Ao recently (J. Phys. A {\bf 37}, L25 (2004)) is related to
previous works of Graham (Z. Physik B {\bf 26}, 397 (1977)) and Eyink {\it et
al.} (J. Stat. Phys. {\bf 83}, 385 (1996)), which can also be viewed as the
generalized application of the Helmholtz theorem in vector calculus. We then
show that systems described by ordinary stochastic differential equations with
white noise can be mapped to thermostated Hamiltonian systems. A steady-state
of a dissipative system corresponds to the equilibrium state of the
corresponding Hamiltonian system. These results provides a solid theoretical
ground for corresponding studies on nonequilibrium dynamics, especially on
nonequilibrium steady state. The mapping permits the application of established
techniques and results for Hamiltonian systems to dissipative non-Hamiltonian
systems, those for thermodynamic equilibrium states to nonequilibrium steady
states. We discuss several implications of the present work.Comment: 18 pages, no figure. final version for publication on J. Phys. A:
Math & Theo
Shaping Robust System through Evolution
Biological functions are generated as a result of developmental dynamics that
form phenotypes governed by genotypes. The dynamical system for development is
shaped through genetic evolution following natural selection based on the
fitness of the phenotype. Here we study how this dynamical system is robust to
noise during development and to genetic change by mutation. We adopt a
simplified transcription regulation network model to govern gene expression,
which gives a fitness function. Through simulations of the network that
undergoes mutation and selection, we show that a certain level of noise in gene
expression is required for the network to acquire both types of robustness. The
results reveal how the noise that cells encounter during development shapes any
network's robustness, not only to noise but also to mutations. We also
establish a relationship between developmental and mutational robustness
through phenotypic variances caused by genetic variation and epigenetic noise.
A universal relationship between the two variances is derived, akin to the
fluctuation-dissipation relationship known in physics
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