A Simple Artificial Life Model Explains Irrational Behavior in Human Decision-Making

Although praised for their rationality, humans often make poor decisions, even in simple situations. In the repeated binary choice experiment, an individual has to choose repeatedly between the same two alternatives, where a reward is assigned to one of them with fixed probability. The optimal strategy is to perseverate with choosing the alternative with the best expected return. Whereas many species perseverate, humans tend to match the frequencies of their choices to the frequencies of the alternatives, a sub-optimal strategy known as probability matching. Our goal was to find the primary cognitive constraints under which a set of simple evolutionary rules can lead to such contrasting behaviors. We simulated the evolution of artificial populations, wherein the fitness of each animat (artificial animal) depended on its ability to predict the next element of a sequence made up of a repeating binary string of varying size. When the string was short relative to the animats’ neural capacity, they could learn it and correctly predict the next element of the sequence. When it was long, they could not learn it, turning to the next best option: to perseverate. Animats from the last generation then performed the task of predicting the next element of a non-periodical binary sequence. We found that, whereas animats with smaller neural capacity kept perseverating with the best alternative as before, animats with larger neural capacity, which had previously been able to learn the pattern of repeating strings, adopted probability matching, being outperformed by the perseverating animats. Our results demonstrate how the ability to make predictions in an environment endowed with regular patterns may lead to probability matching under less structured conditions. They point to probability matching as a likely by-product of adaptive cognitive strategies that were crucial in human evolution, but may lead to sub-optimal performances in other environments

Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML

Occurrence of the BCR-ABL[superscript T315I] gatekeeper mutation is among the most pressing challenges in the therapy of chronic myeloid leukemia (CML). Several BCR-ABL inhibitors have multiple targets and pleiotropic effects that could be exploited for their synergistic potential. Testing combinations of such kinase inhibitors identified a strong synergy between danusertib and bosutinib that exclusively affected CML cells harboring BCR-ABL[superscript T315I]. To elucidate the underlying mechanisms, we applied a systems-level approach comprising phosphoproteomics, transcriptomics and chemical proteomics. Data integration revealed that both compounds targeted Mapk pathways downstream of BCR-ABL, resulting in impaired activity of c-Myc. Using pharmacological validation, we assessed that the relative contributions of danusertib and bosutinib could be mimicked individually by Mapk inhibitors and collectively by downregulation of c-Myc through Brd4 inhibition. Thus, integration of genome- and proteome-wide technologies enabled the elucidation of the mechanism by which a new drug synergy targets the dependency of BCR-ABL[superscript T315I] CML cells on c-Myc through nonobvious off targets

Search for Neutrinoless tau Decays Involving the K_S^0 Meson

We have searched for lepton flavor violating decays of the tau lepton with one or two KS0 mesons in the final state. The data used in the search were collected with the CLEO II and II.V detectors at the Cornell Electron Storage Ring (CESR) and correspond to an integrated luminosity of 13.9 fb^-1 at the Upsilon(4S) resonance. No evidence for signals were found, therefore we have set 90% confidence level (C.L.) upper limits on the branching fractions B(tau -> e KS0) mu KS0) e 2KS0) < 2.2e-6, and B(tau -> mu 2KS0) < 3.4e-6. These represent significantly improved upper limits on the two-body decays and first upper limits on the three-body decays.Comment: 9 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, submitted to PRD Rapid Communication

Record book of business statistics. A background of facts from earlier years for comparision with data published monthly in the Survey of current business. Textiles Section.

Mode of access: Internet.conv cj

The amygdala and the experience of affect

The current study examined the hypothesis that amygdala activation serves as a neural precondition for negative affective experience. Participants’ affective experience was measured by asking them to report on their momentary experiences several times a day over the course of a month using an electronic experience-sampling procedure. One year later, participants viewed backwardly masked depictions of fear while functional magnetic resonance imaging was used to measure their amygdala and fusiform gyrus activation. Negative affect, as measured during the experience-sampling procedure 1-year prior, was positively correlated with amygdala activation in response to these brief presentations of fear depictions. Furthermore, descriptive analyses indicated that fusiform gyrus activation and negative affective experience in the scanner were associated for participants reporting increased nervousness during the imaging procedure. The results are consistent with the interpretation that the amygdala contributes to negative affective experience by increasing perceptual sensitivity for negative stimuli

Undifferentiated recurrent fevers in pediatrics are clinically distinct from PFAPA syndrome but retain an IL-1 signature

Autoinflammatory disorders of the innate immune system present with recurrent episodes of inflammation often beginning in early childhood. While there are now more than 30 genetically-defined hereditary fever disorders, many patients lack a clear diagnosis. Many pediatric patients are often grouped with patients with periodic fever, aphthous stomatitis, pharyngitis, and adenitis (PFAPA) syndrome despite failing to meet diagnostic criteria. Here, we categorize these patients as syndrome of undifferentiated recurrent fever (SURF), and identify the unique features which distinguish them from the PFAPA syndrome. SURF patients were more likely to report gastrointestinal symptoms of nausea, vomiting and abdominal pain, and experienced inconsistent responses to on-demand steroid therapy compared to PFAPA patients. For this previously undefined cohort, an optimal course of therapy remains uncertain, with medical and surgical therapies largely driven by parental preference. A subset of patients with SURF underwent tonsillectomy with complete resolution. Flow cytometric evaluation demonstrates leukocytic populations distinct from PFAPA patients, with reduced CD3+ T cell numbers. SURF patient tonsils were predominantly characterized by an IL-1 signature compared to PFAPA, even during the afebrile period. Peripheral blood signatures were similar between groups suggesting that PFAPA and SURF patient tonsils have localized, persistent inflammation, without clinical symptoms. These data suggest that SURF is a heterogenous syndrome on the autoinflammatory disease spectrum