Ocean acidification (OA) may alter the behaviour of sediment-bound metals, modifying their bioavailability and thus toxicity. We provide the first experimental test of this hypothesis with the amphipod Corophium volutator. Amphipods were exposed to two test sediments, one with relatively high metals concentrations (Σmetals 239 mg kg(-1) ) and a reference sediment with lower contamination (Σmetals 82 mg kg(-1) ) under conditions that mimic current and projected conditions of OA (390-1140 μatm pCO2 ). Survival and DNA damage was measured in the amphipods, whereas the flux of labile metals was measured in the sediment and water column (WC) using Diffusive Gradients in Thin-films. The contaminated sediments became more acutely toxic to C. volutator under elevated pCO2 (1140 μatm). There was also a 2.7-fold increase in DNA damage in amphipods exposed to the contaminated sediment at 750 μatm pCO2 , as well as increased DNA damage in organisms exposed to the reference sediment, but only at 1140 μatm pCO2 . The projected pCO2 concentrations increased the flux of nickel and zinc to labile states in the WC and pore water. However, the increase in metal flux at elevated pCO2 was equal between the reference and contaminated sediments or, occasionally, greater from reference sediments. Hence, the toxicological interaction between OA and contaminants could not be explained by e ffects of pH on metal speciation. We propose that the additive physiological effects of OA and contaminants will be more important than changes in metal speciation in determining the responses of benthos to contaminated sediments under OA. Our data demonstrate clear potential for near-future OA to increase the susceptibility of benthic ecosystems to contaminants. Environmental policy should consider contaminants within the context of changing environmental conditions. Specifically, sediment metals guidelines may need to be reevaluated to afford appropriate environmental protection under future conditions of OA.
Recognition of lipopolysaccharide (LPS) by Toll-like receptor (TLR)4 initiates an intracellular signaling pathway leading to the activation of nuclear factor-B (NF-B). Although LPS-induced activation of NF-B isThe innate immune response to microbial pathogens begins when pathogen-associated molecular patterns meet their cognate Toll-like receptors (TLRs) 8 on effector cells of the immune system, such as monocytes and macrophages (1). Lipopolysaccharide (LPS), an integral cell wall component of Gram-negative bacteria and one of the most potent stimulators in innate immunity, is recognized by the TLR4-MD2 receptor complex (2). In the past years, much progress has been made in understanding the intracellular signaling cascades that are initiated when LPS stimulates TLR4 (reviewed in Refs. 3 and 4). Ligation of the TLR4-MD2 complex by LPS initially results in the recruitment of myeloid differentiation factor (MyD)88 and MyD88-adaptor like (Mal), also called TIRAP, to the receptor cytoplasmic domain. MyD88 then facilitates recruitment of the serine/threonine kinases IL-1R-associated kinase (IRAK)-1 and -4, thus enabling IRAK4 to phosphorylate IRAK1. The latter subsequently dissociates from the receptor complex and associates with tumor necrosis factor (TNF) receptor-associated factor (TRAF)6, constituting a cytoplasmic signaling complex. Upon ubiquitination, TRAF6 activates transforming growth factor--activated kinase 1, which in turn activates the inhibitor of B kinase (IKK) complex that consists of the regulatory subunit IKK␥ (also known as NEMO) and the kinases IKK␣ and IKK. The latter eventually phosphorylates the inhibitory IB proteins, resulting in their ubiquitination and degradation. This allows the transcription factor NF-B to translocate to the nucleus and initiate transcription of inflammatory cytokines, such as TNF, which contribute to mounting an inflammatory response. Apart from this MyD88-dependent signaling pathway, TLR4 also initiates a MyD88-independent signaling pathway that is mediated by the adaptor proteins Toll/IL-1 receptor domain domain-containing adaptor-inducing interferon- (TRIF; also known as TICAM-1) and TRIFrelated adaptor molecule (also known as TICAM-2). Although
42Ostreid herpesvirus (OsHV) can cause mass mortality events in Pacific oyster indicating a significant but low heritability for the binary trait of survival and also for 60 viral load measures (h2 0.12 -0.25). A genome-wide association study highlighted a 61 region of linkage group 6 containing a significant QTL affecting host resistance. 62These results are an important step towards identification of genes underlying 63 resistance to OsHV in oyster, and a step towards applying genomic data to enhance 64 selective breeding for disease resistance in oyster aquaculture.
Affinity chromatography is among the most powerful separation techniques, achieving the finest separation with high yields even in the most challenging feed streams. Incorporating affinity chromatography in vaccine purification has long been attempted by researchers to improve unit yield and purity with the secondary goal of reducing the number of downstream process operations. Despite the success in laboratory-scale proof of concept, implementation of this technique in pilot or cGMP manufacturing has rarely been realised due to technical and economic challenges in design and manufacturing of ideal ligands as well as availability of high-productivity chromatography media. This paper reviews evolving technologies in engineered ligands and chromatography media that are encouraging companies to re-visit the possible use of affinity chromatography in larger scale vaccine purification. It is postulated that commercial-scale implementation of high throughput single-use affinity chromatography can significantly simplify process architecture, improve productivity and flexibility, and reduce cost of goods.
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