A study of the types of structural and grammatical errors appearing in the writing of 170 freshmen and 170 juniors and seniors at the University of Kansas and of 114 boys of superior mental ability at St. Louis Country Day School

Thesis (M.A.Ed.)--University of Kansas, Education, 1928

Prone-only SPECT myocardial perfusion imaging: An alternative standard in clinical practice?

N

The Wife of the Alcoholic; Sexist Stereotypes in the Alcoholism Literature

Current alcoholism literature, alcoholism education, and alcoholism treatment suggests that the wife of the alcoholic is every bit as sick (physically, mentally, and spiritually) as her practicing alcoholic husband. How did we come to this view of the wife of the alcoholic? This paper will review 1) how the wife of the alcoholic has been regarded over the years; 2) how these portraits of the wife of the alcoholic that appeared in the scholarly literature have influenced current thinking and treatment, and 3) how this body of literature and the popular concepts of the wife of the alcoholic that evolved from it, carry sexual biases and stereotyping that can potentially interfere with optimum treatment, full recovery, and effective marital and family functioning

Caspase-mediated loss of mitochondrial function and generation of reactive oxygen species during apoptosis

During apoptosis, the permeabilization of the mitochondrial outer membrane allows the release of cytochrome c, which induces caspase activation to orchestrate the death of the cell. Mitochondria rapidly lose their transmembrane potential (ΔΨm) and generate reactive oxygen species (ROS), both of which are likely to contribute to the dismantling of the cell. Here we show that both the rapid loss of ΔΨm and the generation of ROS are due to the effects of activated caspases on mitochondrial electron transport complexes I and II. Caspase-3 disrupts oxygen consumption induced by complex I and II substrates but not that induced by electron transfer to complex IV. Similarly, ΔΨm generated in the presence of complex I or II substrates is disrupted by caspase-3, and ROS are produced. Complex III activity measured by cytochrome c reduction remains intact after caspase-3 treatment. In apoptotic cells, electron transport and oxygen consumption that depends on complex I or II was disrupted in a caspase-dependent manner. Our results indicate that after cytochrome c release the activation of caspases feeds back on the permeabilized mitochondria to damage mitochondrial function (loss of ΔΨm) and generate ROS through effects of caspases on complex I and II in the electron transport chain

Quality Rating Improvement System (QRIS)

With funding from the Race-to-the-Top grant, we are working with Oregon State University researchers to conduct a validation study to support the state’s Quality Rating Improvement System (QRIS). The QRIS provides technical assistance to child care facilities to improve quality, as well as ratings for child care facilities to help parents in decision-making. Center staff are collecting standardized observational measures of child care quality statewide to assess the extent to which QRIS ratings correspond to observed quality

2001-2002 Birthday Celebration Concert - Wolfgang Amadeus Mozart

https://spiral.lynn.edu/conservatory_otherseasonalconcerts/1093/thumbnail.jp

2003-2004 Beethoven\u27s Birthday Concert

https://spiral.lynn.edu/conservatory_otherseasonalconcerts/1058/thumbnail.jp

Endothelial heme oxygenase-1 induction by hypoxia. Modulation by inducible nitric-oxide synthase and S-nitrosothiols.

The stress protein heme oxygenase-1 (HO-1) is induced in endothelial cells exposed to nitric oxide (NO)-releasing agents, and this process is finely modulated by thiols (Foresti, R., Clark, J. E., Green, C. J., and Motterlini R. (1997) J. Biol. Chem. 272, 18411–18417). Here, we report that up-regulation of HO-1 in aortic endothelial cells by severe hypoxic conditions (pO2 ≤ 2 mm Hg) is preceded by increased inducible NO synthase and NO synthase activity. This effect is accompanied by oxidation of intracellular glutathione and formation of S-nitrosothiols. Incubation of cells with a selective inhibitor of inducible NO synthase (S-(2-aminoethyl)-isothiourea) or a NO scavenger ([2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide]) significantly attenuated the increase in heme oxygenase activity caused by reduced oxygen availability. A series of antioxidant agents did not prevent the elevation in heme oxygenase activity by hypoxia; however, the precursor of glutathione synthesis and thiol donor,N-acetylcysteine, completely abolished HO-1 induction. We also found that the hypoxia-mediated increase in endothelial heme oxygenase activity was potentiated by the presence ofS-nitrosoglutathione. These results indicate that intracellular interaction of thiols with NO is an important determinant in the mechanism leading to HO-1 induction by reduced oxygen levels. We suggest that in addition to oxidative stress, HO-1 gene expression can be regulated by redox reactions involving NO andS-nitrosothiols (nitrosative stress), emphasizing a versatile role for the heme oxygenase pathway in the cellular adaptation to a variety of stressful conditions

2002-2003 Chamber Music Concert

https://spiral.lynn.edu/conservatory_otherseasonalconcerts/1072/thumbnail.jp