Microphytobenthos of Arctic Kongsfjorden (Svalbard, Norway): biomass and potential primary production along the shore line

During summer 2007, Arctic microphytobenthic potential primary production was measured at several stations around the coastline of Kongsfjorden (Svalbard, Norway) at ?5 m water depth and at two stations at five different water depths (5, 10, 15, 20, 30 m). Oxygen planar optode sensor spots were used ex situ to determine oxygen exchange in the overlying water of intact sediment cores under controlled light (ca. 100 ?mol photons m?2 s?1) and temperature (2–4°C) conditions. Patches of microalgae (mainly diatoms) covering sandy sediments at water depths down to 30 m showed high biomass of up to 317 mg chl a m?2. In spite of increasing water depth, no significant trend in “photoautotrophic active biomass” (chl a, ratio living/dead cells, cell sizes) and, thus, in primary production was measured at both stations. All sites from ?5 to 30 m water depth exhibited variable rates of net production from ?19 to +40 mg O2 m?2 h?1 (?168 to +360 mg C m?2 day?1) and gross production of about 2–62 mg O2 m?2 h?1 (17–554 mg C m?2 day?1), which is comparable to other polar as well as temperate regions. No relation between photoautotrophic biomass and gross/net production values was found. Microphytobenthos demonstrated significant rates of primary production that is comparable to pelagic production of Kongsfjorden and, hence, emphasised the importance as C source for the zoobenthos

Different osteosyntheses for Colles' fracture: A mechanical study in 42 cadaver bones

Background and purpose In recent years several different plate designs for internal fixation of fractures of the distal radius have been developed. However, few biomechanical studies have been performed to compare these new implants. The purpose of this study was to compare the mechanical properties of 5 different commercially available plates (3 volar and 2 dorsal) with standard K-wire fixation using a distal radial cadaver model

Replicating viral vector platform exploits alarmin signals for potent CD8⁺ T cell-mediated tumour immunotherapy.

Viral infections lead to alarmin release and elicit potent cytotoxic effector T lymphocyte (CTL <sup>eff</sup> ) responses. Conversely, the induction of protective tumour-specific CTL <sup>eff</sup> and their recruitment into the tumour remain challenging tasks. Here we show that lymphocytic choriomeningitis virus (LCMV) can be engineered to serve as a replication competent, stably-attenuated immunotherapy vector (artLCMV). artLCMV delivers tumour-associated antigens to dendritic cells for efficient CTL priming. Unlike replication-deficient vectors, artLCMV targets also lymphoid tissue stroma cells expressing the alarmin interleukin-33. By triggering interleukin-33 signals, artLCMV elicits CTL <sup>eff</sup> responses of higher magnitude and functionality than those induced by replication-deficient vectors. Superior anti-tumour efficacy of artLCMV immunotherapy depends on interleukin-33 signalling, and a massive CTL <sup>eff</sup> influx triggers an inflammatory conversion of the tumour microenvironment. Our observations suggest that replicating viral delivery systems can release alarmins for improved anti-tumour efficacy. These mechanistic insights may outweigh safety concerns around replicating viral vectors in cancer immunotherapy

IFNγ and IL-12 restrict Th2 responses during Helminth/Plasmodium co-infection and promote IFNγ from Th2 cells

Parasitic helminths establish chronic infections in mammalian hosts. Helminth/Plasmodium co-infections occur frequently in endemic areas. However, it is unclear whether Plasmodium infections compromise anti-helminth immunity, contributing to the chronicity of infection. Immunity to Plasmodium or helminths requires divergent CD4+ T cell-driven responses, dominated by IFNγ or IL-4, respectively. Recent literature has indicated that Th cells, including Th2 cells, have phenotypic plasticity with the ability to produce non-lineage associated cytokines. Whether such plasticity occurs during co-infection is unclear. In this study, we observed reduced anti-helminth Th2 cell responses and compromised anti-helminth immunity during Heligmosomoides polygyrus and Plasmodium chabaudi co-infection. Using newly established triple cytokine reporter mice (Il4gfpIfngyfpIl17aFP635), we demonstrated that Il4gfp+ Th2 cells purified from in vitro cultures or isolated ex vivo from helminth-infected mice up-regulated IFNγ following adoptive transfer into Rag1-/- mice infected with P. chabaudi. Functionally, Th2 cells that up-regulated IFNγ were transcriptionally re-wired and protected recipient mice from high parasitemia. Mechanistically, TCR stimulation and responsiveness to IL-12 and IFNγ, but not type I IFN, was required for optimal IFNγ production by Th2 cells. Finally, blockade of IL-12 and IFNγ during co-infection partially preserved anti-helminth Th2 responses. In summary, this study demonstrates that Th2 cells retain substantial plasticity with the ability to produce IFNγ during Plasmodium infection. Consequently, co-infection with Plasmodium spp. may contribute to the chronicity of helminth infection by reducing anti-helminth Th2 cells and converting them into IFNγ-secreting cells

Translating Strong Mobility into Weak Mobility

Mobile agents are software objects that can be transmitted over the net together with data and code, or can autonomously migrate to a remote computer and execute automatically on arrival. However many frameworks and languages for mobile agents only provide weak mobility: agents do not resume their execution from the instruction following the migration action, instead they are always restarted from a given point. In this paper we present a purely syntactic translation process for transforming programs that use strong mobility into programs that rely only on weak mobility, while preserving the original semantics.This transformation applies to programs written in a procedural language and can be adapted to other languages, like Java, that provide means to send data and code, but not the execution state.It has actually been exploited for implementing our language for mobile agents X-Klaim, that has linguistic constructs for strong mobility

Attachment and mentalization as predictors of outcome in family therapy for adolescent anorexia nervosa

Particulate matter in aquatic systems is an important vehicle for the transport of particulate organic carbon (POC). Its accurate measurement is of central importance for the understanding of marine carbon cycling. Previous work has shown that GF/F-filter-based bottle-sample-derived concentration estimates of POC are generally close to or higher than large-volume in-situ-pump-derived values (and in some rare cases in subzero waters are up to two orders of magnitude higher). To further investigate this phenomenon, water samples from the surface and mid-water Northeast Atlantic and the Baltic Sea were analyzed. Our data support a bias of POC concentration estimates caused by adsorption of nitrogen-rich dissolved organic material onto GF/F filters. For surface-ocean samples the mass per unit area of exposed filter and composition of adsorbed material depended on the filtered volume. Amounts of adsorbed OC were enhanced in the surface ocean (typically 0.5 ?mol cm? 2 of exposed filter) as compared to the deep ocean (typically 0.2 ?mol cm? 2 of exposed filter). These dependencies should be taken into account for future POC methodologies. Bottle/pump differences of samples that were not corrected for adsorption were higher in the deep ocean than in the surface ocean. This discrepancy increased in summer. It is shown that POC concentration estimates that were not corrected for adsorption depend not only on the filtered volume, true POC concentration and mass of adsorbed OC, but also on the filter area. However, in all cases we studied, correction for adsorption was important, but not sufficient, to explain bottle/pump differences. Artificial formation of filterable particles and/or processes leading to filterable material being lost from and/or missed by sample-processing procedures must be considered. It can be deduced that the maximum amounts of POC and particulate organic nitrogen (PON) that can be artificially formed per liter of filtered ocean water are 3–4 ?M OC (5–10% of dissolved OC) and 0.2–0.5 ?M ON (2–10% of dissolved ON), respectively. The relative sensitivities of bottle and pump procedures, and of surface- and deep-ocean material, to artificial particle formation and the missing/losing of material are evaluated. As present procedures do not exist to correct for all possible biasing effects due to artificial particle formation and/or miss/loss of filterable material, uncertainties of filtration-based estimates of POC concentrations need further testing. The challenge now is to further constrain the magnitude of the biasing effects that add to the adsorption effect to reduce the uncertainties of estimates of POC concentrations, inventories and fluxes in the ocean

Chemical Genetics Reveals Negative Regulation of Abscisic Acid Signaling by a Plant Immune Response Pathway

SummaryCoordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptation and survival. Initial abiotic stress can interfere with disease-resistance signaling [1–6]. Conversely, initial plant immune signaling may interrupt subsequent abscisic acid (ABA) signal transduction [7, 8]. However, the processes involved in this crosstalk between these signaling networks have not been determined. By screening a 9600-compound chemical library, we identified a small molecule [5-(3,4-dichlorophenyl)furan-2-yl]-piperidine-1-ylmethanethione (DFPM) that rapidly downregulates ABA-dependent gene expression and also inhibits ABA-induced stomatal closure. Transcriptome analyses show that DFPM also stimulates expression of plant defense-related genes. Major early regulators of pathogen-resistance responses, including EDS1, PAD4, RAR1, and SGT1b, are required for DFPM—and notably also for Pseudomonas—interference with ABA signal transduction, whereas salicylic acid, EDS16, and NPR1 are not necessary. Although DFPM does not interfere with early ABA perception by PYR/RCAR receptors or ABA activation of SnRK2 kinases, it disrupts cytosolic Ca2+ signaling and downstream anion channel activation in a PAD4-dependent manner. Our findings provide evidence that activation of EDS1/PAD4-dependent plant immune responses rapidly disrupts ABA signal transduction and that this occurs at the level of Ca2+ signaling, illuminating how the initial biotic stress pathway interferes with ABA signaling