AGL StimSelect: Software for automated selection of stimuli for artificial grammar learning

Artificial Grammar Learning (AGL) is an experimental paradigm that has been used extensively in cognitive research for many years to study implicit learning, associative learning, and generalization based either on similarity or rules. Without computer assistance it is virtually impossible to generate appropriate grammatical training stimuli along with grammatical or non-grammatical test stimuli that control relevant psychological variables. We present the first flexible, fully automated software for selecting AGL stimuli. The software allows users to specify a grammar of interest, and to manipulate characteristics of training and test sequences, and their relationship to each other. The user thus has direct control over stimulus features that may influence learning and generalization in AGL tasks. The software enables researchers to develop AGL designs that would not be feasible without automatic stimulus selection. It is implemented in Matlab

A Large Gene Network in Immature Erythroid Cells Is Controlled by the Myeloid and B Cell Transcriptional Regulator PU.1

PU.1 is a hematopoietic transcription factor that is required for the development of myeloid and B cells. PU.1 is also expressed in erythroid progenitors, where it blocks erythroid differentiation by binding to and inhibiting the main erythroid promoting factor, GATA-1. However, other mechanisms by which PU.1 affects the fate of erythroid progenitors have not been thoroughly explored. Here, we used ChIP-Seq analysis for PU.1 and gene expression profiling in erythroid cells to show that PU.1 regulates an extensive network of genes that constitute major pathways for controlling growth and survival of immature erythroid cells. By analyzing fetal liver erythroid progenitors from mice with low PU.1 expression, we also show that the earliest erythroid committed cells are dramatically reduced in vivo. Furthermore, we find that PU.1 also regulates many of the same genes and pathways in other blood cells, leading us to propose that PU.1 is a multifaceted factor with overlapping, as well as distinct, functions in several hematopoietic lineages

Directing the Deposition of Ferromagnetic Cobalt onto Pt-tipped CdSe@CdS Nanorods: Synthetic and Mechanistic Insights

A methodology providing access to dumbbell-tipped, metal-semiconductor and metal oxide-semiconductor heterostructured nanorods has been developed. The synthesis and characterization of CdSe@CdS nanorods incorporating ferromagnetic cobalt domains at both nanorod termini (dumbbell morphology) are presented. Cobalt nanoparticle tips are then selectively oxidized to afford CdSe@CdS nanorods with cobalt oxide domains at both termini. In the case of longer nanorods, self assembly of dipolar cobalt domains prior to oxidation resulted in the colloidal polymerization of the ferromagnetic cobalt domains to afford cobalt oxide domains which were fused due to the nanoscale Kirkendall effect. Intact wurtzite CdS nanorod domains were confirmed via XRD and HRTEM power spectrum analysis. Four lengths of CdSe@CdS nanorods with comparable diameters (6-7 nm) and lengths ranging from 40-174 nm were modified in this fashion. The total synthesis required five steps from commercially available reagents. Key synthetic considerations are discussed, with particular emphasis on isolation of intermediates, yields, and increasing scale of intermediate reactions. We show that installing platinum at CdSe@CdS nanorod termini effectively activates these nanorods towards facile cobalt deposition using our polymeric ligand methodology. Exposing unmodified CdSe@CdS nanorods to identical cobalt deposition conditions resulted only in the formation of free cobalt nanoparticles (CoNPs) and unmodified nanorods. We find that the enabling platinum-tipping step provides a mixture of matchstick and dumbbell PtNP-tipped nanorods. Kinetic investigations and control experiments reveal that other reagents in this key step (besides platinum) can activate CdSe@CdS nanorods towards Co deposition to a lesser extent. A mechanism involving both Pt-assisted Co deposition, and nanorod activation by chemical etching/ligand exchange is proposed

Additivity in the Analysis and Design of HIV Protease Inhibitors

We explore the applicability of an additive treatment of substituent effects to the analysis and design of HIV protease inhibitors. Affinity data for a set of inhibitors with a common chemical framework were analyzed to provide estimates of the free energy contribution of each chemical substituent. These estimates were then used to design new inhibitors whose high affinities were confirmed by synthesis and experimental testing. Derivations of additive models by least-squares and ridge-regression methods were found to yield statistically similar results. The additivity approach was also compared with standard molecular descriptor-based QSAR; the latter was not found to provide superior predictions. Crystallographic studies of HIV protease−inhibitor complexes help explain the perhaps surprisingly high degree of substituent additivity in this system, and allow some of the additivity coefficients to be rationalized on a structural basis