Santa Fe Institute

About: Santa Fe Institute is a nonprofit organization based out in Santa Fe, New Mexico, United States. It is known for research contribution in the topics: Population & Context (language use). The organization has 558 authors who have published 4558 publications receiving 396015 citations. The organization is also known as: SFI.

Heat freezes niche evolution

Abstract: Climate change is altering phenology and distributions of many species and further changes are projected. Can species physiologically adapt to climate warming? We analyse thermal tolerances of a large number of terrestrial ectotherm (n = 697), endotherm (n = 227) and plant (n = 1816) species worldwide, and show that tolerance to heat is largely conserved across lineages, while tolerance to cold varies between and within species. This pattern, previously documented for ectotherms, is apparent for this group and for endotherms and plants, challenging the longstanding view that physiological tolerances of species change continuously across climatic gradients. An alternative view is proposed in which the thermal component of climatic niches would overlap across species more than expected. We argue that hard physiological boundaries exist that constrain evolution of tolerances of terrestrial organisms to high temperatures. In contrast, evolution of tolerances to cold should be more frequent. One consequence of conservatism of upper thermal tolerances is that estimated niches for cold-adapted species will tend to underestimate their upper thermal limits, thereby potentially inflating assessments of risk from climate change. In contrast, species whose climatic preferences are close to their upper thermal limits will unlikely evolve physiological tolerances to increased heat, thereby being predictably more affected by warming.

The first T cell response to transmitted/founder virus contributes to the control of acute viremia in HIV-1 infection

Abstract: Identification of the transmitted/founder virus makes possible, for the first time, a genome-wide analysis of host immune responses against the infecting HIV-1 proteome. A complete dissection was made of the primary HIV-1–specific T cell response induced in three acutely infected patients. Cellular assays, together with new algorithms which identify sites of positive selection in the virus genome, showed that primary HIV-1–specific T cells rapidly select escape mutations concurrent with falling virus load in acute infection. Kinetic analysis and mathematical modeling of virus immune escape showed that the contribution of CD8 T cell–mediated killing of productively infected cells was earlier and much greater than previously recognized and that it contributed to the initial decline of plasma virus in acute infection. After virus escape, these first T cell responses often rapidly waned, leaving or being succeeded by T cell responses to epitopes which escaped more slowly or were invariant. These latter responses are likely to be important in maintaining the already established virus set point. In addition to mutations selected by T cells, there were other selected regions that accrued mutations more gradually but were not associated with a T cell response. These included clusters of mutations in envelope that were targeted by NAbs, a few isolated sites that reverted to the consensus sequence, and bystander mutations in linkage with T cell–driven escape.

The predominance of quarter-power scaling in biology

Abstract: Summary 1. Recent studies have resurrected the debate over the value for the allometric scaling exponent that relates whole-organism metabolic rate to body size. Is it 3 / 4 or 2 / 3 ? This question has been raised before and resolved in favour of 3 / 4 . Like previous ones, recent claims for a value of 2 / 3 are based almost entirely on basal metabolic rate (BMR) in mammals. 2. Here we compile and analyse a new, larger data set for mammalian BMR. We show that interspecific variation in BMR, as well as field metabolic rates of mammals, and basal or standard metabolic rates for many other organisms, including vertebrates, invertebrates, protists and plants, all scale with exponents whose confidence intervals include 3 / 4 and exclude 2 / 3 . Our analysis of maximal metabolic rate gives a slope that is greater than and confidence intervals that exclude both 3 / 4 and 2 / 3 . 3. Additionally, numerous other physiological rates that are closely tied to metabolism in a wide variety of organisms, including heart and respiratory rates in mammals, scale as M − 1/4 . 4. The fact that quarter-power allometric scaling is so pervasive in biology suggests that different allometric relations have a common, mechanistic origin and provides an empirical basis for theoretical models that derive these scaling exponents.

Financial Networks and Contagion

Abstract: *We study cascades of failures in a network of interdependent financial organizations: how discontinuous changes in asset values (e.g., defaults and shutdowns) trigger further failures, and how this depends on network structure. Integration (greater dependence on counterparties) and diversification (more counterparties per organization) have different, nonmonotonic effects on the extent of cascades. Diversification connects the network initially, permitting cascades to travel; but as it increases further, organizations are better insured against one another’s failures. Integration also faces trade-offs: increased dependence on other organizations versus less sensitivity to own investments. Finally, we illustrate the model with data on European debt cross-holdings. (JEL D85, F15, F34, F36, F65, G15, G32, G33, G38) Globalization brings with it increased financial interdependencies among many kinds of organizations—governments, central banks, investment banks, firms, etc.— that hold each other’s shares, debts, and other obligations. Such interdependencies can lead to cascading defaults and failures, which are often avoided through massive bailouts of institutions deemed “too big to fail.” Recent examples include the US government’s interventions in AIG, Fannie Mae, Freddie Mac, and General Motors; and the European Commission’s interventions in Greece and Spain. Although such bailouts circumvent the widespread failures that were more prevalent in the nineteenth and early twentieth centuries, they emphasize the need to study the risks created by a network of interdependencies. Understanding these risks is crucial to designing incentives and regulatory responses which defuse cascades before they are imminent. In this paper we develop a general model that produces new insights regarding financial contagions and cascades of failures among organizations linked through a network of financial interdependencies. Organizations’ values depend on each other—e.g., through cross-holdings of shares, debt, or other liabilities. If an