Teachers observed 51 university-level science, technology, engineering, and mathematics (STEM) courses and collected information on the active-engagement nature of instruction. These results give a comprehensive view of the diversity of STEM instruction and student in-class behavior at a campus-wide level. The authors discuss how these results could be used to design targeted professional development.

The P1 plasmid addiction operon is a compact genetic structure consisting of promoter, operator, antitoxin gene (phd), and toxin gene (doc). The 73-amino-acid antitoxin protein, Phd, has two distinct functions: it represses transcription (by binding to its operator) and it prevents host death (by binding and neutralizing the toxin). Here, we show that the N terminus of Phd is required for repressor but not antitoxin activity. Conversely, the C terminus is required for antitoxin but not repressor activity. Only a quarter of the protein, the resolution limit of this analysis, was required for both activities. We suggest that the plasmid addiction operon is a composite of two evolutionarily separable modules, an operator-repressor module and an antitoxintoxin module. Consideration of similar antitoxin proteins and their surroundings indicates that modular exchange may contribute to antitoxin and operon diversity.Protein-ligand interactions. The economy and structure of the cell is dependent upon the specificity of myriad proteinligand interactions. The antitoxin proteins of toxin-antitoxin or plasmid addiction modules are a diverse group of small proteins, typically 72 to 104 amino acid residues in length, with multiple macromolecular ligands. Thus, they are a potentially rich source of novel protein-ligand motifs whose characterization may contribute to our understanding of protein-ligand interactions.P1 plasmid addiction operon. Phd is a bifunctional repressor/antitoxin protein encoded by the plasmid addiction operon of the P1 plasmid (which is the plasmid prophage of bacteriophage P1). Escherichia coli grows well without the P1 plasmid. Upon acquiring the P1 plasmid it continues to grow well, but upon losing the plasmid the cells become sick and cease growth. Thus, the cells have acquired a physiological addiction to the plasmid. This effect is mediated by the P1 plasmid addiction operon. This operon encodes a toxin, Doc, which causes death on curing, and an antitoxin, Phd, which prevents host death (33). While the plasmid is retained, the antitoxin is present in sufficient quantity to neutralize the toxin. However, the antitoxin is unstable, due to the action of the host-encoded ClpXP protease (34). When the plasmid is lost, the continuing proteolysis of the antitoxin, unreplenished by new synthesis, unveils the toxin and arrests the cell. By poisoning plasmid-free segregants, the module increases the apparent stability of the plasmid and eliminates competition from plasmid-free sister cells.Autoregulation of the P1 plasmid addiction operon. The P1 addiction operon is negatively autoregulated (37). The antitoxin binds as a dimer (18) to two palindromic sequences in the promoter region of the P1 addiction operon and thus inhibits transcription (37). The antitoxin interacts with toxin both in solution and in the repressive complex (17,38). In the repressive complex, the toxin mediates cooperative interactions between the two palindromic sites and thereby enhances repression (38).

This report provides a brief overview of aspects of training nonhuman primates who have been, and continue to be, used in this laboratory. The research context involves applied behavioral studies in which animals are trained to perform complex operant behavioral sequences, often in their homecage environment. In such studies, animals have freedom to choose whether to engage in appetitively reinforced behavioral tests that employ neither food deprivation nor fluid management. This background of operant conditioning has provided an insight to, and a context for, animal training both as an adjunct to general laboratory management and as a way to expedite scientific procedures. Thus, training has potential implications for both well-being and scientific quality, although it must be considered an adjunct to the provision of socialization with conspecifics in high quality diverse housing systems and not as an alternative to such provision. The importance of discussion and consideration of alternative procedures cannot be overemphasized.

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Bryostatin 1 transiently inhibits Na-K-Cl cotransport and Cl secretion, possibly through a PKC isoform also targeted by phorbol esters. Unlike phorbol esters, bryostatin 1 does not impair barrier function. The data imply that bryostatin 1 and phorbol esters differentially affect a PKC isoform involved in junctional regulation, and that epithelial transport and barrier function may be regulated by distinct PKC isoforms.