Biogeodynamics of Cretaceous marine carbonate production

We have compiled stratigraphic ranges of genera of calcareous nannofossils, calcispheres, planktonic foraminifers, larger benthic foraminifers, corals and rudists bivalves, and species of dasycladalean green algae. These taxa comprise the main planktonic and benthic carbonate producers of the Cretaceous, a period of exceptionally high sea level and palaeotemperatures that was characterized by unique assemblages of benthic carbonate producers and the significant rise in pelagic carbonate sedimentation. The autecology, physiological control on calcification, and carbonate-production potential of these groups is summarized. The observed diversity patterns are compared with proxy data of Cretaceous climate and seawater chemistry to elucidate the effect of environmental change on carbonate production and sedimentation. Two characteristic patterns are recognized. Diversity of calcareous nannofossils, calcispheres, planktonic foraminifers and corals trace the evolution of Cretaceous sea-level, while the diversity of dasycladalean algae, larger benthic foraminifers, corals and rudist bivalves show significant reductions at the level of oceanic anoxic events (OAEs). Benthic carbonate producers except for corals thus appear to have been more vulnerable to environmental change, and these general patterns appear to be unrelated to the autecology of the taxa investigated. The expansion of suitable habitats during episodes of high sea level and high temperatures appears to have been a more important control of diversity in calcareous nannofossils, planktonic foraminifers, and corals than changes in seawater chemistry. Aragonitic or aragonite-dominated benthic carbonate producers are most affected during extinction events related to OAEs, and there is a general trend of decreasing aragonite dominance throughout the Cretaceous. This is compensated by the extensive formation of calcitic hemipelagic chalk since the Cenomanian. The trend of decreasing aragonite dominance is independent of the level of biological control on calcification in the different taxa affected. The demise of aragonitic or aragonite-dominated carbonate producers at OAE1a (early Aptian) and OAE2 (Cenomanian–Turonian boundary interval) may be related to short episodes of reduced seawater carbonate-saturation caused by short-lived injections of CO2 from large igneous provinces that initiated OAEs. For OAE1a, this scenario also explains the retreat of carbonate platforms to low latitudes in the early Aptian, as sea-surface water typically has a higher carbonate saturation in warm, lower than in cooler, higher latitude waters. The gradual decrease of aragonite throughout the Cretaceous matches model simulations of seawater carbonate-saturation. An increase in the relative number of azooxanthellate coral genera following OAE1a and OAE2 suggests a disruption of photosymbiosis in the course of these global events due to high temperatures. However, the relative numbers of azooxanthellate genera continued to increase during the Late Cretaceous, when global temperatures declined. Due to the short residence time of major nutrients in seawater, these may have affected carbonate-producing ecosystems regionally. The recent patterns of benthic carbonate production being highest in oligotrophic environments cannot confidently be extrapolated to the Cretaceous. Our database records ranges of genera at the substage level. Higher-resolution stratigraphical studies of neritic carbonate sequences are required to understand what aspect of environmental change in the sequences are required to understand what aspect of environmental change in the sequence of events that unfolded in the context of OAEs caused the demise of benthic carbonate producers

Antiferromagnetism and d-wave superconductivity in cuprates: a uster DMFT study

We present a new approach to investigate the coexistence of antiferromagnetism and d-wave superconductivity in the two dimensional extended Hubbard model within a numerically exact cluster dynamical mean-field approximation. Self-consistent solutions with two non-zero order parameters exists in the wide range of doping level and temperatures. A linearized equation for energy spectrum near the Fermi level have been solved. The resulting d-wave gap has the correct magnitude and k-dependence but some distortion compare to the pure d_{x^2-y^2} superconducting order parameter due to the presence of underlying antiferromagnetic ordering.Comment: 4 pages, 3 figure

Spontaneous tumor rejection by cbl-b–deficient CD8+ T cells

The concept of tumor surveillance implies that specific and nonspecific components of the immune system eliminate tumors in the early phase of malignancy. Understanding the biochemical mechanisms of tumor immunosurveillance is of paramount significance because it might allow one to specifically modulate spontaneous antitumor activity. We report that inactivation of the E3 ligase Casitas B cell lymphoma-b (Cbl-b) confers spontaneous in vivo rejection of tumor cells that express human papilloma virus antigens. Moreover, cbl-b−/− mice develop significantly fewer ultraviolet B (UVB)–induced skin malignancies and reject UVB-induced skin tumors. CD8+ T cells were identified as key players in the spontaneous tumor rejection response. Loss of Cbl-b not only enhances antitumor reactivity of CD8+ T cells but also occurs in the absence of CD4+ T cells. Mechanistically, cbl-b−/− CD8+ T cells are resistant to T regulatory cell–mediated suppression and exhibit enhanced activation and rapid tumor infiltration. Importantly, therapeutic transfer of naive cbl-b−/− CD8+ T cells is sufficient to mediate rejection of established tumors. Even up to 1 yr after the first encounter with the tumor cells, cbl-b−/− mice carry an “anticancer memory.” These data identify Cbl-b as a key signaling molecule that controls spontaneous antitumor activity of cytotoxic T cells in different cancer models. Inhibition of Cbl-b is a novel approach to stimulate long-lasting immunity against cancer

Clinical Efficacy of Blue Light Full Body Irradiation as Treatment Option for Severe Atopic Dermatitis

BACKGROUND: Therapy of atopic dermatitis (AD) relies on immunosuppression and/or UV irradiation. Here, we assessed clinical efficacy and histopathological alterations induced by blue light-treatment of AD within an observational, non-interventional study. METHODOLOGY/PRINCIPAL FINDINGS: 36 patients with severe, chronic AD resisting long term disease control with local corticosteroids were included. Treatment consisted of one cycle of 5 consecutive blue light-irradiations (28.9 J/cm(2)). Patients were instructed to ask for treatment upon disease exacerbation despite interval therapy with topical corticosteroids. The majority of patients noted first improvements after 2-3 cycles. The EASI score was improved by 41% and 54% after 3 and 6 months, respectively (p≤0.005, and p≤0.002). Significant improvement of pruritus, sleep and life quality was noted especially after 6 months. Also, frequency and intensity of disease exacerbations and the usage of topical corticosteroids was reduced. Finally, immunohistochemistry of skin biopsies obtained at baseline and after 5 and 15 days revealed that, unlike UV light, blue light-treatment did not induce Langerhans cell or T cell depletion from skin. CONCLUSIONS/SIGNIFICANCE: Blue light-irradiation may represent a suitable treatment option for AD providing long term control of disease. Future studies with larger patient cohorts within a randomized, placebo-controlled clinical trial are required to confirm this observation

TIRAP, an Adaptor Protein for TLR2/4, Transduces a Signal from RAGE Phosphorylated upon Ligand Binding

The receptor for advanced glycation end products (RAGE) is thought to be involved in the pathogenesis of a broad range of inflammatory, degenerative and hyperproliferative diseases. It binds to diverse ligands and activates multiple intracellular signaling pathways. Despite these pivotal functions, molecular events just downstream of ligand-activated RAGE have been surprisingly unknown. Here we show that the cytoplasmic domain of RAGE is phosphorylated at Ser391 by PKCζ upon binding of ligands. TIRAP and MyD88, which are known to be adaptor proteins for Toll-like receptor-2 and -4 (TLR2/4), bound to the phosphorylated RAGE and transduced a signal to downstream molecules. Blocking of the function of TIRAP and MyD88 largely abrogated intracellular signaling from ligand-activated RAGE. Our findings indicate that functional interaction between RAGE and TLRs coordinately regulates inflammation, immune response and other cellular functions