Suspense is an affective state that contributes to our enjoy-ment of experiences such as movies and sports. Ely, Frankel,and Kamenica (2015) proposed a formal definition of suspensewhich depends on the variance of subjective future beliefsabout an outcome of interest (e.g., winning a game). In orderto evaluate this theory, we designed a task based on the cardgame Blackjack where a variety of suspense dynamics can beexperimentally induced. By presenting participants with iden-tical sequences of information (i.e., card draws), but manip-ulating contextual knowledge (i.e., their understanding of therules of the game) we were able to show that self-reported sus-pense follows the predictions of the model. Follow-up modelcomparison further showed an advantage for the “suspense asvariance of future beliefs” account over a number of alterna-tive definitions of suspense, including some that depend onlyon current uncertainty (not the future). This paper is an initialattempt to link aspects of formal models of information anduncertainty with affective cognitive states.

What are the major topics of the Cognitive Science Societyconference? How have they changed over the years? To an-swer these questions, we applied an unsupervised learning al-gorithm known as dynamic topic modeling (Blei & Lafferty,2006) to the 2000–2017 Proceedings of the Cognitive Sci-ence Society. Unlike traditional topic models, a dynamic topicmodel is sensitive to the temporal context of documents andcan characterize the evolution of each topic across years. Us-ing this model, we identify historical trends in the popularity oftopics over time, and shifts in word use within topics indicativeof changing focuses within the field. We also measure the cor-relation across topics, and use the model to highlight the topicstructure of particular papers and labs. We believe dynamictopic models present an important tool towards understandingCognitive Science as it continues to grow and evolve over time

TRK fusions are rare but targetable mutations which occur across a wide variety of cancer types. We report the prevalence of approximately 0.7% for NTRK-positive colorectal cancer (CRC) by genetically profiling 2519 colonic and rectal tumors. The aberrations of APC and TP53 frequently co-occurred with NTRK gene fusions, whereas RAS/BRAF oncogenic alterations and NTRK fusions were almost always mutually exclusive. NTRK-driven colorectal cancer patients demonstrated increased TMB (median = 53 mut/MB, 95% CI: 36.8-68.0 mut/MB), high microsatellite instability, and an enrichment for POLE/POLD1 mutations when compared to molecularly unstratified colorectal cancer population. These data shed light on possible future approach of multimodality treatment regimen including TRK-targeted therapy and immune checkpoint inhibitor therapy in NTRK-positive CRCs.

The IkappaB kinase (IKK) complex is composed of three subunits, IKKalpha, IKKbeta, and IKKgamma (NEMO). While IKKalpha and IKKbeta are highly similar catalytic subunits, both capable of IkappaB phosphorylation in vitro, IKKgamma is a regulatory subunit. Previous biochemical and genetic analyses have indicated that despite their similar structures and in vitro kinase activities, IKKalpha and IKKbeta have distinct functions. Surprisingly, disruption of the Ikkalpha locus did not abolish activation of IKK by proinflammatory stimuli and resulted in only a small decrease in nuclear factor (NF)-kappaB activation. Now we describe the pathophysiological consequence of disruption of the Ikkbeta locus. IKKbeta-deficient mice die at mid-gestation from uncontrolled liver apoptosis, a phenotype that is remarkably similar to that of mice deficient in both the RelA (p65) and NF-kappaB1 (p50/p105) subunits of NF-kappaB. Accordingly, IKKbeta-deficient cells are defective in activation of IKK and NF-kappaB in response to either tumor necrosis factor alpha or interleukin 1. Thus IKKbeta, but not IKKalpha, plays the major role in IKK activation and induction of NF-kappaB activity. In the absence of IKKbeta, IKKalpha is unresponsive to IKK activators.