An Indo-Pacifc coral spawning database

The discovery of multi-species synchronous spawning of scleractinian corals on the Great Barrier Reef in the 1980s stimulated an extraordinary effort to document spawning times in other parts of the globe. Unfortunately, most of these data remain unpublished which limits our understanding of regional and global reproductive patterns. The Coral Spawning Database (CSD) collates much of these disparate data into a single place. The CSD includes 6178 observations (3085 of which were unpublished) of the time or day of spawning for over 300 scleractinian species in 61 genera from 101 sites in the Indo-Pacific. The goal of the CSD is to provide open access to coral spawning data to accelerate our understanding of coral reproductive biology and to provide a baseline against which to evaluate any future changes in reproductive phenology

On the maximum weight minimal separator

Given an undirected and connected graph G = (V, E) and two vertices s, t ∈ V, a vertex subset S that separates s and t is called an s-t separator, and an s-t separator is called minimal if no proper subset of S separates s and t. In this paper, we consider finding a minimal s-t separator with maximum weight on a vertex-weighted graph. We first prove that this problem is NP-hard. Then, we propose an twO( tw) n-time deterministic algorithm based on tree decompositions. Moreover, we also propose an O∗ (9tw W2)-time randomized algorithm to determine whether there exists a minimal s-t separator where W is its weight and tw is the treewidth of G

The role of platelet-derived growth factor receptor in eotaxin signaling of eosinophils.

BACKGROUND: Receptor tyrosine kinases (RTKs) such as epidermal growth factor receptor (EGFR) and platelet-derived growth factor receptor (PDGFR) are capable of eliciting kinase activity after ligand binding. In several cells, RTKs are activated via the G-protein-coupled receptor independent of the ligand-RTK interaction. We have previously found that EGFR is transactivated via CC chemokine receptor 3 in bronchial epithelial cells and that this pathway is important for mitogen-activated protein (MAP) kinase activation and cytokine production. It has recently been suggested that hypereosinophilic syndrome results from the fusion tyrosine kinase FIP1L1-PDGFRA. Although it is possible that the PDGFR signal is involved in eosinophil function, the details are still unclear. METHODS: Blood eosinophils were purified using Percoll and anti-CD16 antibody-coated magnetic beads. Expression of PDGFR mRNA was examined by RT-PCR. After stimulating eosinophils with eotaxin, the phosphorylation of MAP kinases was examined by Western blotting with the antiphosphospecific MAP kinase antibody. The eotaxin-induced eosinophil chemotaxis was studied using Boyden chambers. RESULTS: Eosinophils expressed PDGFRbeta mRNA in 4 out of 8 donors, while PDGFRalpha mRNA was expressed in only 1 donor. Protein expression of PDGFR was also detectable in eosinophils from some donors. AG1295, a specific inhibitor of PDGFR, showed dose-dependent inhibition of eotaxin-induced MAP kinase phosphorylation in the eosinophils expressing PDGFRbeta mRNA. The chemotaxis of these eosinophils was significantly inhibited by AG1295 (n = 3). CONCLUSIONS: Our results suggest that PDGFR modifies the CCR3-MAP kinase signaling pathway and chemotactic response in some donors. The pharmacological targeting of PDGFR may be a new strategy to treat eosinophilic disorders

EGFR signaling upregulates expression of microsomal prostaglandin E synthase-1 in cancer cells leading to enhanced tumorigenicity

In this report we describe the contribution of prostaglandin E(2) (PGE(2)) derived from the inducible microsomal PGE-synthase type-1 (mPGES-1) to the epidermal growth factor receptor (EGFR) oncogenic drive in tumor epithelial cells and in tumor-bearing mice. EGFR stimulation upregulated expression of mPGES-1 in HT-29, A431 and A549 cancer cells. Egr-1, a transcription factor induced by EGF, mediated this response. The Egr-1 rise provoked the overexpression of mPGES-1 messenger and protein, and enhanced PGE(2) formation. These changes were suppressed either by silencing Egr-1, or by upstream blockade of EGFR or ERK1/2 signals. Further, in a clonogenic assay on tumor cells, EGF induced a florid tumorigenic phenotype, which regressed when mPGES-1 was silenced or knocked down. EGF-induced mPGES-1 overexpression in epithelial cell reduced E-cadherin expression, whereas enhancing that of vimentin, suggesting an incipient mesenchymal phenotype. Additionally, inhibiting the EGFR in mice bearing the A431 tumor, the mPGES-1 expression and the tumor growth, exhibited a parallel decline. In conclusion, these findings provide novel evidence that a tight cooperation between the EGF/EGFR and mPGES-1 leads to a significant tumorigenic gain in epithelial cells, and provide clues for controlling the vicious association

No evidence for tropicalization of coral assemblages in a subtropical climate change hot spot

Climate change is causing the distribution and abundance of many organisms to change. In particular, organisms typical of the tropics are increasing in abundance in many subtropical regions, a process known as tropicalization. Here, we examine changes in coral abundance and assemblage structure in the Solitary Islands Marine Park (SIMP), over a 23-year period between 1990 and 2013–14. Total coral cover decreased at all six islands sampled with a concomitant decline in total coral cover at the regional scale (i.e. between sampling occasions). When coral taxa were classified as either cosmopolitan or subtropical, cosmopolitan corals decreased in cover at the regional scale. In contrast, subtropical coral cover did not change at the regional scale because large increases in cover at some islands, such as North Solitary Island, were matched by decreases at other islands. Of 16 common coral taxa examined at the regional level, one declined and two increased in cover with no change in the remaining 13 taxa. In particular, there was no increase in the abundance of coral taxa typically associated with tropical reefs. Similarly, multivariate analyses of coral assemblage structure using these 16 common taxa indicated changes in two of the six island assemblages but, again, provided no evidence for tropicalization. Modelling suggested very low probabilities of larval dispersal from the southern Great Barrier Reef to the SIMP suggesting that limited connectivity with tropical coral populations is one possible cause of the lack of tropicalization in the coral assemblages. We therefore conclude that, despite significant increases in mean sea surface temperature over the last few decades, there has been no tropicalization of the coral fauna in the SIMP. Furthermore, the small proportional reduction in total coral cover, despite the occasional incidence of coral bleaching, coral disease outbreaks and a number of large storms, suggest that the reefs of the SIMP were in reasonably good health at the time of the final survey in 2014. Our results suggest that factors other than temperature, in particular, a lack of dispersal, are limiting the expansion of tropical corals along the east coast of Australia