Tambora and the Mackerel Year: Phenology and Fisheries During an Extreme Climate Event

Global warming has increased the frequency of extreme climate events, yet responses of biological and human communities are poorly understood, particularly for aquatic ecosystems and fisheries. Retrospective analysis of known outcomes may provide insights into the nature of adaptations and trajectory of subsequent conditions. We consider the 1815 eruption of the Indonesian volcano Tambora and its impact on Gulf of Maine (GoM) coastal and riparian fisheries in 1816. Applying complex adaptive systems theory with historical methods, we analyzed fish export data and contemporary climate records to disclose human and piscine responses to Tambora’s extreme weather at different spatial and temporal scales while also considering sociopolitical influences. Results identified a tipping point in GoM fisheries induced by concatenating social and biological responses to extreme weather. Abnormal daily temperatures selectively affected targeted fish species—alewives, shad, herring, and mackerel—according to their migration and spawning phenologies and temperature tolerances. First to arrive, alewives suffered the worst. Crop failure and incipient famine intensified fishing pressure, especially in heavily settled regions where dams already compromised watersheds. Insufficient alewife runs led fishers to target mackerel, the next species appearing in abundance along the coast; thus, 1816 became the “mackerel year.” Critically, the shift from riparian to marine fisheries persisted and expanded after temperatures moderated and alewives recovered. We conclude that contingent human adaptations to extraordinary weather permanently altered this complex system. Understanding how adaptive responses to extreme events can trigger unintended consequences may advance long-term planning for resilience in an uncertain future

Non-compact Lattice QED with Two Charges: Phase Diagram and Renormalization Group Flow

The phase diagram of non-compact lattice QED in four dimensions with staggered fermions of charges 1 and $-1/2$ is investigated. The renormalized charges are determined and found to be in agreement with perturbation theory. This is an indication that there is no continuum limit with non-vanishing renormalized gauge coupling, and that the theory has a validity bound for every finite value of the renormalized coupling. The renormalization group flow of the charges is investigated and an estimate for the validity bound as a function of the cut-off is obtained. Generalizing this estimate to all fermions in the Standard Model,it is found that a cut-off at the Planck scale implies that $\alpha_R$ has to be less than $1/80$. Due to spontaneous chiral symmetry breaking, strongly bound fermion-antifermion composite states are generated. Their spectrum is discussed.Comment: 35 pages, LATEX, 26 PostScript figures (uuencoded

Cytotoxicity of CD56bright NK Cells towards Autologous Activated CD4+ T Cells Is Mediated through NKG2D, LFA-1 and TRAIL and Dampened via CD94/NKG2A

In mouse models of chronic inflammatory diseases, Natural Killer (NK) cells can play an immunoregulatory role by eliminating chronically activated leukocytes. Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distinguished as CD16+CD56dim and CD16dim/−CD56bright. An expansion in the CD56bright NK cell subset has been associated with clinical responses to therapy in various autoimmune diseases, suggesting an immunoregulatory role for this subset in vivo. Here we compared the regulation of activated human CD4+ T cells by CD56dim and CD56bright autologous NK cells in vitro. Both subsets efficiently killed activated, but not resting, CD4+ T cells. The activating receptor NKG2D, as well as the integrin LFA-1 and the TRAIL pathway, played important roles in this process. Degranulation by NK cells towards activated CD4+ T cells was enhanced by IL-2, IL-15, IL-12+IL-18 and IFN-α. Interestingly, IL-7 and IL-21 stimulated degranulation by CD56bright NK cells but not by CD56dim NK cells. NK cell killing of activated CD4+ T cells was suppressed by HLA-E on CD4+ T cells, as blocking the interaction between HLA-E and the inhibitory CD94/NKG2A NK cell receptor enhanced NK cell degranulation. This study provides new insight into CD56dim and CD56bright NK cell-mediated elimination of activated autologous CD4+ T cells, which potentially may provide an opportunity for therapeutic treatment of chronic inflammation

Type I Interferons Induce T Regulatory 1 Responses and Restrict Humoral Immunity during Experimental Malaria

We thank Christopher Hunter and Bob Axtell for critical feedback, and the Flow Cytometry Laboratory at OUHSC for technical assistance.Author Summary Humoral immunity is essential for host resistance to pathogens that trigger highly inflammatory immune responses, including Plasmodium parasites, the causative agents of malaria. Long-lived, secreted antibody responses depend on a specialized subset of CD4 T cells called T follicular helper (Tfh) cells. However, anti-Plasmodium humoral immunity is often short-lived, non-sterilizing, and immunity rapidly wanes, leaving individuals susceptible to repeated bouts of malaria. Here we explored the relationship between inflammatory type I interferons, the regulation of pathogen-specific CD4 T cell responses, and humoral immunity using models of experimental malaria and systemic virus infection. We identified that type I interferons promote the formation and accumulation of pathogen-specific CD4 T regulatory 1 cells that co-express interferon-gamma and interleukin-10. Moreover, we show that the combined activity of interferon-gamma and interleukin-10 limits the magnitude of infection-induced Tfh responses, the secretion of parasite-specific secreted antibody, and parasite control. Our study provides new insight into the regulation of T regulatory 1 responses and humoral immunity during inflammatory immune reactions against systemic infections.Yeshttp://www.plospathogens.org/static/editorial#pee

Suffering for our sakes: the soteriological thought process of Ignatius of Antioch

This thesis provides a comprehensive account of the understanding of salvation in the letters of Ignatius of Antioch. Ignatius' surviving writings date from the first quarter of the second century and are some of the few surviving writings from that period. They are indispensable for tracing developments in Christian thought and the evolution of theological ideas between the writings of the New Testament and the much better documented times of the third and fourth centuries. Since Ignatian soteriology has rarely been the focus of scholarly investigation, the present thesis examines the soteriological language employed by Ignatius of Antioch with the goal of weaving the dominant threads into a comprehensive and clear presentation of Ignatian soteriology. The argument of the thesis is therefore developed in three main sections with each arranged thematically to address a basic soteriological question. Part I opens by explaining why Ignatius believed humanity required salvation. Humanity’s threefold predicament with sin (Chapter 2), with the forces of evil (Chapter 3), and with death and the wrath of God (Chapter 4) all necessitated deliverance. Chapter 5 concludes by examining the way Ignatius segmented humanity based on one’s response to the incarnational gospel narrative that, if ignored, could result in misinterpreting many of the warning passages in the letters. Next, Part II addresses the question of what salvation entailed for Ignatius. After exploring Jesus Christ as the central savior figure in Chapter 6, Chapter 7 presents Ignatius’ varying descriptions of salvation. Chapter 8 then explores Ignatius’ primary conception of salvation as the reception of life. Part III concludes by examining how salvation was obtained. After exploring Ignatius’ description of faith as the means of salvation, the section concludes by evaluating several theories regarding additional avenues of salvation