Lineage-Specific Transcriptional Profiles of Symbiodinium spp. Unaltered by Heat Stress in a Coral Host

Dinoflagellates of the genus Symbiodinium form an endosymbiosis with reef building corals, in which photosynthetically derived nutrients comprise the majority of the coral energy budget. An extraordinary amount of functional and genetic diversity is contained within the coral-associated Symbiodinium, with some phylotypes (i.e., genotypic groupings), conferring enhanced stress tolerance to host corals. Recent advances in DNA sequencing technologies have enabled transcriptome-wide profiling of the stress response of the cnidarian coral host; however, a comprehensive understanding of the molecular response to stress of coral-associated Symbiodinium, as well as differences among physiologically susceptible and tolerant types, remains largely unexplored. Here, we examine the transcriptome-wide response to heat stress via RNA-Seq of two types of Symbiodinium, the putatively thermotolerant type D2 and the more susceptible type C3K, resident within the same coral host species, Acropora hyacinthus. Contrary to previous findings with coral hosts, we find no detectable change in gene expression across the dinoflagellate transcriptome after 3 days of elevated thermal exposure, despite physical evidence of symbiosis breakdown. However, hundreds of genes identified as orthologs between the C and D types exhibited significant expression differences within treatments (i.e., attributable solely to type, not heat exposure). These include many genes related to known thermotolerance mechanisms including heat shock proteins and chloroplast membrane components. Additionally, both the between-treatment similarities and between-type differences remained pervasive after 12-18 months of common garden acclimation and in mixed Symbiodinium assemblages within the same coral host colony

Gene therapy for articular cartilage repair

Articular cartilage serves as the gliding surface of joints. It is susceptible to damage from trauma and from degenerative diseases. Restoration of damaged articular cartilage may be achievable through the use of cell-regulatory molecules that augment the reparative activities of the cells, inhibit the cells\u27; degradative activities, or both. A variety of such molecules have been identified. These include insulin-like growth factor I, fibroblast growth factor 2, bone morphogenetic proteins 2, 4, and 7, and interleukin-1 receptor antagonist. It is now possible to transfer the genes encoding such molecules into articular cartilage and synovial lining cells. Although preliminary, data from in-vitro and in-vivo studies suggest that gene therapy can deliver such potentially therapeutic agents to protect existing cartilage and to build new cartilage. Keywords: gene therapy, vectors, articular cartilage, arthritis, animal model

Sociology and postcolonialism: another 'missing' revolution?

Sociology is usually represented as having emerged alongside European modernity. The latter is frequently understood as sociology's special object with sociology itself a distinctively modern form of explanation. The period of sociology's disciplinary formation was also the heyday of European colonialism, yet the colonial relationship did not figure in the development of sociological understandings. While the recent emergence of postcolonialism appears to have initiated a reconsideration of understandings of modernity, with the development of theories of multiple modernities, I suggest that this engagement is more an attempt at recuperating the transformative aspect of postcolonialism than engaging with its critiques. In setting out the challenge of postcolonialism to dominant sociological accounts, I also address `missing feminist/queer revolutions', suggesting that by engaging with postcolonialism there is the potential to transform sociological understandings by opening up a dialogue beyond the simple pluralism of identity claims

Turbulent superfluid profiles in a counterflow channel

We have developed a two-dimensional model of quantised vortices in helium II moving under the influence of applied normal fluid and superfluid in a counterflow channel. We predict superfluid and vortex-line density profiles which could be experimentally tested using recently developed visualization techniques.Comment: 3 double figures, 9 page

The Computational Complexity of Generating Random Fractals

In this paper we examine a number of models that generate random fractals. The models are studied using the tools of computational complexity theory from the perspective of parallel computation. Diffusion limited aggregation and several widely used algorithms for equilibrating the Ising model are shown to be highly sequential; it is unlikely they can be simulated efficiently in parallel. This is in contrast to Mandelbrot percolation that can be simulated in constant parallel time. Our research helps shed light on the intrinsic complexity of these models relative to each other and to different growth processes that have been recently studied using complexity theory. In addition, the results may serve as a guide to simulation physics.Comment: 28 pages, LATEX, 8 Postscript figures available from [email protected]

Flow Phase Diagram for the Helium Superfluids

The flow phase diagram for He II and $^3$He-B is established and discussed based on available experimental data and the theory of Volovik [JETP Letters {\bf{78}} (2003) 553]. The effective temperature - dependent but scale - independent Reynolds number $Re_{eff}=1/q=(1+\alpha')/\alpha$, where $\alpha$ and $\alpha'$ are the mutual friction parameters and the superfluid Reynolds number characterizing the circulation of the superfluid component in units of the circulation quantum are used as the dynamic parameters. In particular, the flow diagram allows identification of experimentally observed turbulent states I and II in counterflowing He II with the turbulent regimes suggested by Volovik.Comment: 2 figure

The Complexity of Computing Minimal Unidirectional Covering Sets

Given a binary dominance relation on a set of alternatives, a common thread in the social sciences is to identify subsets of alternatives that satisfy certain notions of stability. Examples can be found in areas as diverse as voting theory, game theory, and argumentation theory. Brandt and Fischer [BF08] proved that it is NP-hard to decide whether an alternative is contained in some inclusion-minimal upward or downward covering set. For both problems, we raise this lower bound to the Theta_{2}^{p} level of the polynomial hierarchy and provide a Sigma_{2}^{p} upper bound. Relatedly, we show that a variety of other natural problems regarding minimal or minimum-size covering sets are hard or complete for either of NP, coNP, and Theta_{2}^{p}. An important consequence of our results is that neither minimal upward nor minimal downward covering sets (even when guaranteed to exist) can be computed in polynomial time unless P=NP. This sharply contrasts with Brandt and Fischer's result that minimal bidirectional covering sets (i.e., sets that are both minimal upward and minimal downward covering sets) are polynomial-time computable.Comment: 27 pages, 7 figure

The inhibitor of differentiation-2 promotes synovial fibroblast-dependent osteoclastogenesis in rheumatoid arthritis

Objectives: Despite indirect evidence suggesting that low oxygen levels might occur in the rheumatoid arthritis (RA) synovium, direct proof of the presence of hypoxia in the arthritic synovium as well as the relevance of low oxygen levels for joint destruction is lacking. The aim of this study was to analyse the distribution of hypoxia in arthritic joints and to evaluate the molecular effects of the hypoxic environment on the phenotype of RA synovial fibroblasts (SF).<p></p> Methods: The hypoxia marker EF-5 was applied in mice with the collagen-induced arthritis (CIA). Expression profile analysis with hypoxic and normoxic SF was performed using subtractive hybridization and microarray. The expression of the inhibitor of differentiation-2 (Id-2), CD68 (macrophage marker) and prolyl hydroxylase (fibroblast marker) was evaluated by immunohistochemistry on synovial tissues from RA, osteoarthritis patients and CIA mice. To evaluate the function of Id-2 in SF, cells were transfected with the pcDNA3.1 containing cDNA for Id-2 or Id-2-specific siRNA or mock controls. The expression of Id-2 and genes regulated by Id-2 in transfected SF was evaluated by SYBR Green real-time PCR and western blot. SF stably transfected with Id-2 were cocultured with bone marrow cells in a transwell system. The expression of the receptor activator of NF-κB ligand (RANKL) and osteoprotegerin were measured by real-time PCR. The development of osteoclasts was evaluated by visualization of the activity of tartrate-resistant acid phosphatase.<p></p> Results: Using the hypoxia marker EF-5 we found that in mice with CIA, synovial cells invading bone and cartilage are exposed to reduced oxygen levels. Expression profile studies identified Id-2 as being upregulated under low oxygen conditions. In addition, IL-1beta stimulation increased the expression of Id-2 in these cells. Histological studies of RA synovium and CIA synovium showed strong expression of Id-2 in SF at sites of synovial invasion into bone. Overproduction of Id-2 in SF by stable transfection triggered the expression of several genes promoting osteoclastogenesis, including BMP-2, PTHrP, Wnt5a and vascular endothelial growth factor. Conversely, the suppression of endogenous Id-2 led to the downregulation of the expression of these molecules. Consistent with these findings coculture of Id-2 transfected SF with bone marrow cells increased the expression of the osteoclast differentiation factor RANKL, and decreased the expression of the osteoclast inhibitory factor osteoprotegerin in bone marrow stromal cells, which was followed by an increase in the number of osteoclasts.<p></p> Conclusion: Taken together, our data provide evidence that hypoxia is present at sites of synovial invasion in RA and that Id-2 induced by hypoxia contributes at these sites to joint destruction by promoting SF-dependent osteoclastogenesis