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This semester-long research project examined the use of social studies trade books to thematically teach about six individuals who served as change agents in the United States during the late 19th century and early 20th century. Three of the individuals were African American men, Robert Smalls, Frederick Douglass, and John Roy Lynch, who took civic action to address racial discrimination faced by the Black community in the half century following the U.S. Civil War. The other three indivduals were women women, Ida B. Wells, Clara Lemlich, and Jane Addams, who challenged social inequities and injustices within their communities. Over the course of the semester-long research project, sixth-grade U.S. history students read selected trade books, examined primary sources, completed graphic organizers, and crafted writing assessments about each of the six individuals. Students demonstrated complex historical thinking, integrated economic and civic thinking, and communicated thematic ideas of systemic oppression of minorities, women, and the poor. They struggled to make connections between examples of historic oppression and contemporary examples of societal oppression. [ABSTRACT FROM AUTHOR]

Full‐scale sampling at 16 facilities illustrated that NDMA precursor concentrations, measured by adding chloramine under Uniform Formation Conditions (NDMAUFC), increased across biofiltration at 7 of 16 facilities (by 3–48 ng/L or 12%–296%) but stayed the same or decreased (by up to 5 ng/L or 24%) at the other nine facilities. Increases in NDMAUFC concentrations were attributed to both particulate and soluble precursors. Only two facilities had an increase in NDMAUFC greater than 10 ng/L. However, NDMAUFC concentrations in the biofilter effluent from five facilities exceeded 10 ng/L during one or more sampling events. For these facilities, testing at multiple scales showed that mitigation steps could include pretreatment with ozone (which resulted in overall lower NDMAUFC), increased free chlorine contact time prior to ammonia addition, and/or optimized biofilter design and operation. [ABSTRACT FROM AUTHOR]

Calculates initial state selected reaction probabilities, reaction cross sections and rate constants for the chemical reaction N[sup +]+H[sub 2] on the potential energy surface of Wilhelmson, Siegbahn and Schinke using the time-dependent wave packet method. Reactive scattering calculations; Implementation for J=0; Implementation for J>0.

The peroxisome proliferator-activated receptors (PPARs) are dietary lipid sensors that regulate fatty acid and carbohydrate metabolism. The hypolipidemic effects of the fibrate drugs and the antidiabetic effects of the glitazone drugs in humans are due to activation of the [Alpha] (NR1C1) and [Gamma] (NR1C3) subtypes, respectively. By contrast, the therapeutic potential of the [Delta] (NR1C2) subtype is unknown, due in part to the lack of selective ligands. We have used combinatorial chemistry and structure-based drug design to develop a potent and subtype-selective PPAR[Delta] agonist, GW501516. In macrophages, fibroblasts, and intestinal cells, GW501516 increases expression of the reverse cholesterol transporter ATP-binding cassette A1 and induces apolipoprotein A1-specific cholesterol efflux. When dosed to insulin-resistant middle-aged obese rhesus monkeys, GW501516 causes a dramatic dose-dependent rise in serum high density lipoprotein cholesterol while lowering the levels of small-dense low density lipoprotein, fasting triglycerides, and fasting insulin. Our results suggest that PPAR[Delta] agonists may be effective drugs to increase reverse cholesterol transport and decrease cardiovascular disease associated with the metabolic syndrome X.

The PRP17/CDC40 gene of Saccharomyces cerevisiae functions in two different cellular processes: pre-mRNA splicing and cell cycle progression. The Prp17/Cdc40 protein participates in the second step of the splicing reaction and, in addition, prp17/cdc40 mutant cells held at the restrictive temperature arrest in the G2 phase of the cell cycle. Here we describe the identification of nine genes that, when mutated, show synthetic lethality with the prp17/cdc40[Delta] allele. Six of these encode known splicing factors: Prp8p, Slu7p, Prp16p, Prp22p, Slt11p, and U2 snRNA. The other three, SYF1, SYF2, and SYF3, represent genes also involved in cell cycle progression and in pre-mRNA splicing. Syf1p and Syf3p are highly conserved proteins containing several copies of a repeated motif, which we term RTPR. This newly defined motif is shared by proteins involved in RNA processing and represents a subfamily of the known TPR (tetratricopeptide repeat) motif. Using two-hybrid interaction screens and biochemical analysis, we show that the SYF gene products interact with each other and with four other proteins: Isy1p, Cef1p, Prp22p, and Ntc20p. We discuss the role played by these proteins in splicing and cell cycle progression.

Biochemical and genetic experiments have shown that the PRP17 gene of the yeast Saccharomyces cerevisiae encodes a protein that plays a role during the second catalytic step of the splicing reaction. It was found recently that PRP17 is identical to the cell division cycle CDC40 gene.cdc40 mutants arrest at the restrictive temperature after the completion of DNA replication. Although the PRP17/CDC40 gene product is essential only at elevated temperatures, splicing intermediates accumulate in prp17 mutants even at the permissive temperature. In this report we describe extensive genetic interactions between PRP17/CDC40 and the PRP8 gene. PRP8 encodes a highly conserved U5 snRNP protein required for spliceosome assembly and for both catalytic steps of the splicing reaction. We show that mutations in the PRP8 gene are able to suppress the temperature-sensitive growth phenotype and the splicing defect conferred by the absence of the Prp17 protein. In addition, these mutations are capable of suppressing certain alterations in the conserved PyAG trinucleotide at the 3' splice junction, as detected by an ACT1-CUP1 splicing reporter system. Moreover, other PRP8 alleles exhibit synthetic lethality with the absence of Prp17p and show a reduced ability to splice an intron bearing an altered 3' splice junction. On the basis of these findings, we propose a model for the mode of interaction between the Prp8 and Prp17 proteins during the second catalytic step of the splicing reaction.