Constructive Noncooperation: Living in Truth

Mohandas Gandhi often indicated that nonviolence was “a science,” and he appears to have meant this literally. Consistent with this vision, in this paper, we outline and apply principles of behavioral systems science, an emerging data-based approach to understanding the dynamics of complex cultural systems, to the practice of constructive noncooperation (Gandhi’s “constructive programme”). Although Gandhi emphasized that constructive action was the most important and potent of nonviolent strategic options, constructive alternatives have been the least developed in the literature of nonviolent struggle. The reconceptualization of constructive noncooperation in behavioral systems terms offered here suggests that rigorous analysis of Havel’s “living in truth” and Gandhi’s “truth force” may be both possible and practically useful in challenging oppression and supporting human rights

Human teaching and cumulative cultural evolution

This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme under grant agreement No. 648841 RATCHETCOG ERC-2014-CoG.Although evidence of teaching behaviour has been identified in some nonhuman species, human teaching appears to be unique in terms of both the breadth of contexts within which it is observed, and in its responsiveness to needs of the learner. Similarly, cultural evolution is observable in other species, but human cultural evolution appears strikingly distinct. This has led to speculation that the evolutionary origins of these capacities may be causally linked. Here we provide an overview of contrasting perspectives on the relationship between teaching and cultural evolution in humans, and briefly review previous research which suggests that cumulative culture (here meaning cultural evolution featuring a trend towards improving functionality) can occur without teaching. We then report the results of a novel experimental study in which we investigated how the benefits of teaching may depend on the complexity of the skill to be acquired. Participants were asked to tie knots of varying complexity. In our Teaching condition, opportunities to interact with an experienced partner aided transmission of the most complex knots, but not simpler equivalents, relative to exposure to completed products alone (End State Only condition), and also relative to information about the process of completion (Intermediate States condition). We conclude by considering the plausibility of various accounts of the evolutionary relationship between teaching and cultural evolution in humans.Publisher PDFPeer reviewe

Stem Cells to Insulin Secreting Cells: Two Steps Forward and Now a Time to Pause?

Two groups recently reported the in vitro differentiation of human embryonic stem cells into insulin-secreting cells, achieving an elusive goal for regenerative medicine. Herein we provide a perspective regarding these developments, compare phenotypes of the insulin-containing cells to human β cells, and discuss implications for type 1 diabetes research and clinical care

Increased risk for T cell autoreactivity to ß-cell antigens in the mice expressing the Avy obesity-associated gene.

There has been considerable debate as to whether obesity can act as an accelerator of type 1 diabetes (T1D). We assessed this possibility using transgenic mice (MIP-TF mice) whose ß-cells express enhanced green fluorescent protein (EGFP). Infecting these mice with EGFP-expressing murine herpes virus-68 (MHV68-EGFP) caused occasional transient elevation in their blood glucose, peri-insulitis, and Th1 responses to EGFP which did not spread to other ß-cell antigens. We hypothesized that obesity-related systemic inflammation and ß-cell stress could exacerbate the MHV68-EGFP-induced ß-cell autoreactivity. We crossed MIP-TF mice with Avy mice which develop obesity and provide models of metabolic disease alongside early stage T2D. Unlike their MIP-TF littermates, MHV68-EGFP-infected Avy/MIP-TF mice developed moderate intra-insulitis and transient hyperglycemia. MHV68-EGFP infection induced a more pronounced intra-insulitis in older, more obese, Avy/MIP-TF mice. Moreover, in MHV68-EGFP-infected Avy/MIP-TF mice, Th1 reactivity spread from EGFP to other ß-cell antigens. Thus, the spreading of autoreactivity among ß-cell antigens corresponded with the transition from peri-insulitis to intra-insulitis and occurred in obese Avy/MIP-TF mice but not lean MIP-TF mice. These observations are consistent with the notion that obesity-associated systemic inflammation and ß-cell stress lowers the threshold necessary for T cell autoreactivity to spread from EGFP to other ß-cell autoantigens

A Humanistic Approach to Understanding Child Consumer Socialization in US Homes

We present findings from a qualitative, multisite, multi-method, longitudinal study of parents and their preschool-aged children that explores the intersections of marketing influences in the home and in the larger outside world of children. Findings indicate that preschoolers represent complicated and nuanced “consumers in training” beyond predictions based on their “perceptual stage of development.” Specifically, our data revealed interesting ways in which marketing and consumer culture can foster a number of pro-social consumer outcomes (e.g., charity, gift-giving, financial literacy). We also noted an emerging understanding by preschoolers of the social meanings of goods for identity construction and product evaluation. Finally, through a presentation of an idiographic case, we show how consumer socialization cannot be attributed to one factor such as media but is based on multiple and concurrent factors—parents, siblings, peers, and home environment—that act to moderate, mediate, and provide meaning for marketing messages

Inferring behavior from partial social information plays little or no role in the cultural transmission of adaptive traits

This project has received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program under grant agreement No. 648841 RATCHETCOG ERC‐2014‐CoG.Many human cultural traits become increasingly beneficial as they are repeatedly transmitted, thanks to an accumulation of modifications made by successive generations. But how do later generations typically avoid modifications which revert traits to less beneficial forms already sampled and rejected by earlier generations? And how can later generations do so without direct exposure to their predecessors' behavior? One possibility is that learners are sensitive to cues of non‐random production in others' behavior, and that particular variants (e.g., those containing structural regularities unlikely to occur spontaneously) have been produced deliberately and with some effort. If this non‐random behavior is attributed to an informed strategy, then the learner may infer that apparent avoidance of certain possibilities indicates that these have already been sampled and rejected. This could potentially prevent performance plateaus resulting from learners modifying inherited behaviors randomly. We test this hypothesis in four experiments in which participants, either individually or in interacting dyads, attempt to locate rewards in a search grid, guided by partial information about another individual's experience of the task. We find that in some contexts, valid inferences about another's behavior can be made from partial information, and these inferences can be used in a way which facilitates trait adaptation. However, the benefit of these inferences appears to be limited, and in many contexts—including some which have the potential to make inferring the experience of another individual easier—there appears to be no benefit at all. We suggest that inferring previous behavior from partial social information plays a minimal role in the adaptation of cultural traits.Publisher PDFPeer reviewe

Interleukin‐12p70-dependent interferon‐γ production is crucial for resistance in African trypanosomiasis

African trypanosomiasis encompasses diseases caused by pathogenic trypanosomes, infecting both humans and animals. In the present article, we dissected the possible role of members of the interleukin ( IL)-12 family during infection with Trypanosoma brucei brucei and Trypanosoma evansi in mice. IL-12p35(-/-) , IL-12p40(-/-) , and IL-12p35(-/-)/p40(-/-) mice were susceptible to both pathogens, as was demonstrated by the increased mortality among these mice, compared with wild-type C57BL/6 mice. The different IL-12p70(-/-) mouse strains showed similar mortality kinetics, suggesting that IL-12p70 - but not the IL-12p80 homodimer or IL-23 plays a crucial role in survival. Although there were similar plasma levels of immunoglobulin (Ig) M and IgG2a in IL-12-deficient mice and wild-type mice, interferon (IFN) - g production, especially during early infection, was severely impaired in all IL-12p70(-/-) mouse strains, demonstrating an IL-12p70 - dependent mechanism for IFN-gamma production. Because IFN-gamma receptor-deficient mice (IFN-gamma R-/(-)) were also highly susceptible to both Trypanosoma species, IL-12p70 - dependent IFN-gamma production seems to be the important mechanism involved in resistance against both pathogens

Rho GTPases show differential sensitivity to nucleotide triphosphate depletion in a model of ischemic cell injury

Rho GTPases are critical for actin cytoskeletal regulation, and alterations in their activity may contribute to altered cytoskeletal organization that characterizes many pathological conditions, including ischemia. G protein activity is a function of the ratio of GTP-bound (active) to GDP-bound (inactive) protein, but the effect of altered energy metabolism on Rho protein activity has not been determined. We used antimycin A and substrate depletion to induce depletion of intracellular ATP and GTP in the kidney proximal tubule cell line LLC-PK10 and measured the activity of RhoA, Rac1, and Cdc42 with GTPase effector binding domains fused to glutathione S-transferase. RhoA activity decreased in parallel with the concentration of ATP and GTP during depletion, so that by 60 min there was no detectable RhoA-GTP, and recovered rapidly when cells were returned to normal culture conditions. Dissociation of the membrane-actin linker ezrin, a target of RhoA signaling, from the cytoskeletal fraction paralleled the decrease in RhoA activity and was augmented by treatment with the Rho kinase inhibitor Y27632. The activity of Cdc42 did not decrease significantly during depletion or recovery. Rac1 activity decreased moderately to a minimum at 30 min of depletion but then increased from 30 to 90 min of depletion, even as ATP and GTP levels continued to fall. Our data are consistent with a principal role for RhoA in cytoskeletal reorganization during ischemia and demonstrate that the activity of Rho GTPases can be maintained even at low GTP concentrations