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.

Social capital and social quilts : network patterns of favor exchange

Abstract: We examine the informal exchange of favors in societies such that any two individuals interact too infrequently to sustain exchange, but such that the social pressure of the possible loss of multiple relationships can sustain exchange. Patterns of exchange that are locally enforceable and renegotiation-proof necessitate that all links are “supported”: any two individuals exchanging favors have a common friend. In symmetric settings, such robust networks are “social quilts”: tree-like unions of completely connected subnetworks. Examining favor exchange networks in 75 villages in rural India, we find high levels of support and identify characteristics that correlate with support.

Dimensionality of consumer search space drives trophic interaction strengths

Abstract: Interactions between the feeding habits of different organisms in a food chain or web trophic interactions can take place in two or three dimensions, and many communities show a mix of the two. By relating search rate and consumption rate to body mass, the authors show that the relationship between trophic-interaction strength and body size scales sublinearly in two-dimensional interactions but superlinearly in three-dimensional ones. They develop a model to show how this explains differences between, for example, aquatic and terrestrial ecosystems because the extra dimension provides an additional niche or opportunity in which to find resources. As an example, the model predicts that a foraging Galpagos sea lion could enjoy a consumption rate up to 30 times higher in a pelagic zone near the surface of the ocean (in three dimensions) than deep-down in a benthic zone (in two dimensions).

Scaling of number, size, and metabolic rate of cells with body size in mammals

Abstract: The size and metabolic rate of cells affect processes from the molecular to the organismal level. We present a quantitative, theoretical framework for studying relationships among cell volume, cellular metabolic rate, body size, and whole-organism metabolic rate that helps reveal the feedback between these levels of organization. We use this framework to show that average cell volume and average cellular metabolic rate cannot both remain constant with changes in body size because of the well known body-size dependence of whole-organism metabolic rate. Based on empirical data compiled for 18 cell types in mammals, we find that many cell types, including erythrocytes, hepatocytes, fibroblasts, and epithelial cells, follow a strategy in which cellular metabolic rate is body size dependent and cell volume is body size invariant. We suggest that this scaling holds for all quickly dividing cells, and conversely, that slowly dividing cells are expected to follow a strategy in which cell volume is body size dependent and cellular metabolic rate is roughly invariant with body size. Data for slowly dividing neurons and adipocytes show that cell volume does indeed scale with body size. From these results, we argue that the particular strategy followed depends on the structural and functional properties of the cell type. We also discuss consequences of these two strategies for cell number and capillary densities. Our results and conceptual framework emphasize fundamental constraints that link the structure and function of cells to that of whole organisms.

Covariation of mutations in the V3 loop of human immunodeficiency virus type 1 envelope protein: an information theoretic analysis.

Abstract: The V3 loop of the human immunodeficiency virus type 1 (HIV-1) envelope protein is a highly variable region that is both functionally and immunologically important. Using available amino acid sequences from the V3 region, we have used an information theoretic quantity called mutual information, a measure of covariation, to quantify dependence between mutations in the loop. Certain pairs of sites, including non-contiguous sites along the sequence, do not have independent mutations but display considerable, statistically significant, covarying mutations as measured by mutual information. For the pairs of sites with the highest mutual information, specific amino acids were identified that were highly predictive of amino acids in the linked site. The observed interdependence between variable sites may have implications for structural or functional relationships; separate experimental evidence indicates functional linkage between some of the pairs of sites with high mutual information. Further specific mutational studies of the V3 loop's role in determining viral phenotype are suggested by our analyses. Also, the implications of our results may be important to consider for V3 peptide vaccine design. The methods used here are generally applicable to the study of variable proteins.

Clustering Patterns of Cytotoxic T-Lymphocyte Epitopes in Human Immunodeficiency Virus Type 1 (HIV-1) Proteins Reveal Imprints of Immune Evasion on HIV-1 Global Variation

Abstract: The human cytotoxic T-lymphocyte (CTL) response to human immunodeficiency virus type 1 (HIV-1) has been intensely studied, and hundreds of CTL epitopes have been experimentally defined, published, and compiled in the HIV Molecular Immunology Database. Maps of CTL epitopes on HIV-1 protein sequences reveal that defined epitopes tend to cluster. Here we integrate the global sequence and immunology databases to systematically explore the relationship between HIV-1 amino acid sequences and CTL epitope distributions. CTL responses to five HIV-1 proteins, Gag p17, Gag p24, reverse transcriptase (RT), Env, and Nef, have been particularly well characterized in the literature to date. Through comparing CTL epitope distributions in these five proteins to global protein sequence alignments, we identified distinct characteristics of HIV amino acid sequences that correlate with CTL epitope localization. First, experimentally defined HIV CTL epitopes are concentrated in relatively conserved regions. Second, the highly variable regions that lack epitopes bear cumulative evidence of past immune escape that may make them relatively refractive to CTLs: a paucity of predicted proteasome processing sites and an enrichment for amino acids that do not serve as C-terminal anchor residues. Finally, CTL epitopes are more highly concentrated in alpha-helical regions of proteins. Based on amino acid sequence characteristics, in a blinded fashion, we predicted regions in HIV regulatory and accessory proteins that would be likely to contain CTL epitopes; these predictions were then validated by comparison to new sets of experimentally defined epitopes in HIV-1 Rev, Tat, Vif, and Vpr.