The Finite Element Sea Ice-Ocean Model (FESOM) v.1.4: formulation of an ocean general circulation model

The Finite Element Sea Ice-Ocean Model (FESOM) is the first global ocean general circulation model based on unstructured-mesh methods that has been developed for the purpose of climate research. The advantage of unstructured-mesh models is their flexible multi-resolution modelling functionality. In this study, an overview of the main features of FESOM will be given; based on sensitivity experiments a number of specific parameter choices will be explained; and directions of future developments will be outlined. It is argued that FESOM is sufficiently mature to explore the benefits of multi-resolution climate modelling and that its applications will provide information useful for the advancement of climate modelling on unstructured meshes

Hungry for change: the Sydney Food Fairness Alliance

The Sydney Food Fairness Alliance is one of a growing number of nascent food movements in Australia to have emerged out of concern for the country’s food future, as well as the deleterious effect the present food system is having on its citizens’ health and the continent’s fragile environment. The Alliance’s structure and activities clearly position it as a new social movement (NSM) engaged in collective action on a specific issue, in this instance, food security/justice, and operating outside the political sphere while aiming to influence and affect societal change. Food security as a human right lies at the heart of the Alliance’s philosophy, and equitable, sustainable food policies for New South Wales are a core focus of its advocacy work. The authors argue that the Alliance is a distinctive food movement in that it positions itself as an \u27umbrella\u27 organization representing a wide range of stakeholders in the food system. This chapter reflects on the values, achievements, issues of concern, strengths and weaknesses, and future of the Sydney Food Fairness Alliance. This resource is Chapter 8 in \u27Food Security in Australia: Challenges and Prospects for the Future\u27 published by Springer in 2013

Altered serological and cellular reactivity to H-2 antigens after target cell infection with vaccinia virus

MICE generate cytotoxic T lymphocytes (CTL) which are able to lyse virus infected target cells in vitro after infection with lymphocytic choriomeningitis virus (LCMV) and pox-viruses1−3. CTL kill syngeneic and semiallogenic infected cells but not allogenic infected targets. Target cell lysis in these systems seems to be restricted by H-2 antigens, especially by the K or D end of the major histocompatibility complex (MHC). In experiments where virus specific sensitised lymphocytes kill virus infected allogenic target cells4 the effector lymphocytes have not been characterised exactly. Recent investigations suggest that the active cell in this assay, at least in the measles infection, is a non-thymus derived cell (H. Kreth, personal communication). An H-2 restriction of cell mediated cytolysis (CMC) to trinitrophenol (TNP)-modified lymphocytes has also been described5. Zinkernagel and Doherty6 postulated that the CTL is directed against syngeneic H-2 antigens and viral antigens and they suggested an alteration of H-2 induced by the LCMV infection. Earlier7 we found a close topological relationship between H-2 antigens and the target antigen(s) responsible for CMC in the vaccinia system. Here we report experiments which were carried out to prove alteration of H-2 after infection of L-929 fibroblasts with vaccinia virus

Allograft and patient survival after sequential HSCT and kidney transplantation from the same donorA multicenter analysis

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Visualizing the activation of encephalitogenic T cells in the ileal lamina propria by in vivo two- photon imaging

Autoreactive encephalitogenic T cells exist in the healthy immune repertoire but need a trigger to induce CNS inflammation. The underlying mechanisms remain elusive, whereby microbiota were shown to be involved in the manifestation of CNS autoim-munity. Here, we used intravital imaging to explore how microbiota affect the T cells as trigger of CNS inflammation. Encephalitogenic CD4(+) T cells transduced with the calcium-sensing protein Twitch -2B showed calcium signaling with higher frequency than polyclonal T cells in the small intestinal lamina propria (LP) but not in Peyer's patches. Interestingly, nonencephalitogenic T cells specific for OVA and LCMV also showed calcium signaling in the LP, indicating a general stimulating effect of microbiota. The observed calcium signaling was microbiota and MHC class II dependent as it was significantly reduced in germfree animals and after administration of anti- MHC class II antibody, respectively. As a consequence of T cell stimulation in the small intestine, the encephalitogenic T cells start expressing Th17- axis genes. Finally, we show the migration of CD4(+) T cells from the small intestine into the CNS. In summary, our direct in vivo visualization revealed that microbiota induced T cell activation in the LP, which directed T cells to adopt a Th17- like phenotype as a trigger of CNS inflammation

Does the East Greenland Current exist in the northern Fram Strait?

Warm Atlantic Water (AW) flows around the Nordic Seas in a cyclonic boundary current loop. Some AW enters the Arctic Ocean where it is transformed to Arctic Atlantic Water (AAW) before exiting through the Fram Strait. There the AAW is joined by recirculating AW. Here we present the first summer synoptic study targeted at resolving this confluence in the Fram Strait which forms the East Greenland Current (EGC). Absolute geostrophic velocities and hydrography from observations in 2016, including four sections crossing the east Greenland shelf break, are compared to output from an eddy-resolving configuration of the sea ice–ocean model FESOM. Far offshore (120&thinsp;km at 80.8°&thinsp;N) AW warmer than 2&thinsp;°C is found in the northern Fram Strait. The Arctic Ocean outflow there is broad and barotropic, but gets narrower and more baroclinic toward the south as recirculating AW increases the cross-shelf-break density gradient. This barotropic to baroclinic transition appears to form the well-known EGC boundary current flowing along the shelf break farther south where it has been previously described. In this realization, between 80.2 and 76.5°&thinsp;N, the southward transport along the east Greenland shelf break increases from roughly 1&thinsp;Sv to about 4&thinsp;Sv and the proportion of AW to AAW also increases fourfold from 19±8&thinsp;% to 80±3&thinsp;%. Consequently, in the southern Fram Strait, AW can propagate into the Norske Trough on the east Greenland shelf and reach the large marine-terminating glaciers there. High instantaneous variability observed in both the synoptic data and the model output is attributed to eddies, the representation of which is crucial as they mediate the westward transport of AW in the recirculation and thus structure the confluence forming the EGC.</p

Increased apoptosis of immunoreactive host cells and augmented donor leukocyte chimerism, not sustained inhibition of B7 molecule expression are associated with prolonged cardiac allograft survival in mice preconditioned with immature donor dendritic cells plus anti-CD40L mAb

Background. We previously reported the association among donor leukocyte chimerism, apoptosis of presumedly IL-2-deficient graft-infiltrating host cells, and the spontaneous donor-specific tolerance induced by liver but not heart allografts in mice. Survival of the rejection-prone heart allografts in the same strain combination is modestly prolonged by the pretransplant infusion of immature, costimulatory molecule-(CM) deficient donor dendritic cells (DC), an effect that is markedly potentiated by concomitant CM blockade with anti-CD40L (CD154) monoclonal antibody (mAb). We investigated whether the long survival of the heart allografts in the pretreated mice was associated with donor leukocyte chimerism and apoptosis of graft-infiltrating cells, if these end points were similar to those in the spontaneously tolerant liver transplant model, and whether the pretreatment effect was dependent on sustained inhibition of CM expression of the infused immature donor DC. In addition, apoptosis was assessed in the host spleen and lymph nodes, a critical determination not reported in previous studies of either spontaneous or 'treatment-aided' organ tolerance models. Methods. Seven days before transplantation of hearts from B10 (H-2b) donors, 2 x 106 donor- derived immature DC were infused i.v. into C3H (H-2(k)) recipient mice with or without a concomitant i.p. injection of anti-CD40L mAb. Donor cells were detected posttransplantation by immunohistochemical staining for major histocompatibility complex class II (I-Ab) in the cells of recipient lymphoid tissue. CM expression was determined by two-color labeling. Host responses to donor alloantigen were quantified by mixed leukocyte reaction, and cytotoxic T lymphocyte (CTL) assays. Apoptotic death in graft- infiltrating cells and in areas of T-dependent lymphoid tissue was visualized by terminal deoxynucleotidyltransferase-catalyzed dUTP-digoxigenin nick-end labeling and quantitative spectrofluorometry. Interleukin-2 production and localization were estimated by immunohistochemistry. Results. Compared with control heart transplantation or heart transplantation after only DC administration, concomitant pretreatment with immature donor DC and anti- CD40L mAb caused sustained elevation of donor (I-Ab+) cells (microchimerism) in the spleen including T cell areas. More than 80% of the I-Ab+ cells in combined treatment animals also were CD86+, reflecting failure of the mAb to inhibit CD40/CD80/CD86 up-regulation on immature DC in vitro after their interaction with host T cells. Donor-specific CTL activity in graft-infiltrating cells and spleen cell populations of these animals was present on day 8, but decreased strikingly to normal control levels by day 14. The decrease was associated with enhanced apoptosis of graft-infiltrating cells and of cells in the spleen where interleukin-2 production was inhibited. The highest levels of splenic microchimerism were found in mice with long surviving grafts (> 100 days). In contrast, CTL activity was persistently elevated in control heart graft recipients with comparatively low levels of apoptotic activity and high levels of interleukin-2. Conclusion. The donor-specific acceptance of rejection-prone heart allografts by recipients pretreated with immature donor DC and anti-CD40L mAb is not dependent on sustained inhibition of donor DC CM (CD86) expression. Instead, the pretreatment facilitates a tolerogenic cascade similar to that in spontaneously tolerant liver recipients that involves: (1) chimerism-driven immune activation, succeeded by deletion of host immune responder cells by apoptosis in the spleen and allograft that is linked to interleukin-2 deficiency in both locations and (2) persistence of comparatively large numbers of donor-derived leukocytes. These tolerogenic mechanisms are thought to be generic, explaining the tolerance induced by allografts spontaneously, or with the aid of various kinds of immunosuppression

Reliability of self-report of health in juvenile offenders

The aim of the present study was to investigate the accuracy of self-reports of juvenile offenders on physical factors (e.g., sleep difficulties, weight related behaviors and weight perceptions), health risk behaviors (e.g., alcohol use), trauma history (e.g., physical and sexual abuse) and psychological factors (e.g., anxiety, suicidal and self-harm behaviors). Self-reports obtained via a Health Questionnaire from 242 incarcerated juvenile offenders were compared with standardized measures (Body Mass Index, Adolescent Psychopathology Scale and Child Trauma Questionnaire) to investigate the reliability (via construct validity) and veracity of their self-report. Using kappa estimates and receiver operating characteristic curves, results generally showed high agreement across measures, suggesting that self-report questions from the health survey could all be used reliably. The degree of accuracy indicated that young offenders are as reliable as clinical and community samples of adolescents in their self-report. These findings have implications for routine assessments and practice evaluations that rely on self-report as the method of data collection and as the basis for clinical formulation and treatment planning