The critical question for Cognitive Scientists is what does Cognitive Science do, if anything, for people? Cognitive Science is primarily concerned with human cognition but has fallen short in continuously and critically assessing the who in human cognition. This complacency in a world where white supremacist and patriarchal structures leave Cognitive Science in the unfortunate position of potentially supporting those structures. We take it that many Cognitive Scientists operate on the assumption that the study of human cognition is both interesting and important. We want to invoke that importance to note that Cognitive Scientists must continue to work to show how the field is useful to all of humanity and reflects a humanity that is not white by default. We wonder how much the field has done, and can do, to show that it is useful not only in the sense that we might make connections with researchers in other fields, win grants and write papers, even of the highest quality, but useful in some material way to the billions of non-Cognitive Scientists across the globe.

This article describes two studies testing the efficacy of a commercial one-on-one cognitive training program (LearningRx) and its computer-based version (Brainskills) in laboratory and school settings. Study 1 tested Brainskills in a laboratory setting with 322 middle school students. Paired t-tests revealed significant gains on all cognitive measures and math performance after 3 weeks of training. Study 2, a randomized control study, included 225 high school students randomly assigned to one of three conditions: LearningRx, Brainskills, or study hall (control) in a school setting for a 15-week training period. Univariate ANCOVAs revealed significantly higher scores for the treatment groups compared with controls on working memory, logic and reasoning, and three of four math attitude measures but not for math performance. Implications for school-based interventions are discussed.

The unfolded protein endoplasmic reticulum stress response has emerged as a cellular physiological target to invoke tumor cell killing due to its homeostatic and cytoprotective functions. In this study, thapsigargin and tunicamycin, two endoplasmic reticulum stress inducers, were investigated for their efficacy on glioblastomas. We demonstrate that clinically relevant concentrations of thapsigargin and tunicamycin eliminate the glioblastoma cell reproductive capacity as a consequence of cell death. The mode of glioblastoma-induced cell death was determined to be via apoptosis as supported by increased C/EBP homologous protein (CHOP) levels and caspase 3 activity, two proteins with established roles in endoplasmic reticulum stress-induced cell death. In conclusion, this study provides evidence that glioblastomas are responsive to endoplasmic reticulum stress induction as a cellular program to eradicate this tumor via programmed cell death.

In neurons, the interaction of laminin with its receptor, beta 1 integrin, is accompanied by an increase in cytosolic Ca2+. Neuronal behavior is influenced by CaMK-II, the type II Ca2+/calmodulin-dependent protein kinase, which is enriched in axons of mouse embryonic neurons. In this study, we sought to determine whether CaMK-II is activated by laminin, and if so, how CaMK-II influences axonal growth and stability. Axons grew up to 200 mu m within 1 day of plating P19 embryoid bodies on laminin-1 (EHS laminin). Activated CaMK-II was found enriched along the axon and in the growth cone as detected using a phospho-Thr(287) specific CaMK-II antibody. beta 1 integrin was found in a similar pattern along the axon and in the growth cone. Direct inhibition of CaMK-II in 1-day-old neurons immediately froze growth cone dynamics, disorganized F-actin and ultimately led to axon retraction. Collapsed axonal remnants exhibited diminished phospho-CaMK-II levels. Treatment of 1-day neurons with a beta 1 integrin-blocking antibody (CD29) also reduced axon length and phospho-CaMK-II levels and, like CaMK-II inhibitors, decreased CaMK-II activation. Among several CaMK-II variants detected in these cultures, the S2-kDa delta variant preferentially associated with actin and beta(3) tubulin as determined by reciprocal immunoprecipitation. our findings indicate that persistent activation of delta CaMK-II by laminin stabilizes nascent embryonic axons through its influence on the actin cytoskeleton. (c) 2006 Elsevier B.V. All rights reserved.