Leadership through Collaborative Strategic Planning: One School’s Journey

Educational administrators, school board members, and policy makers have been mandated to account for the learning and performance of the highly diverse students that comprise today’s classrooms. The No Child Left Behind Act (NCLB) of 2002 and the Individuals with Disabilities Education Improvement Act (IDEIA 2004) have presented a set of challenges for educating all children using data-driven decisions in a standards-based curriculum with culturally responsive practices. These mandates from federal and state legislation demand a change in administrative culture. These challenges require school personnel to develop plans to adjust their practices to meet the academic and behavioral needs of all students. Additionally, federal and state laws require local educational agencies (LEAs) to meet rigorous standards and provide evidence of progress through academic yearly progress (AYP) reports

Reduction of \u3ci\u3eStabilin-2\u3c/i\u3e Contributes to a Protection Against Atherosclerosis

We have previously identified a novel atherosclerosis quantitative trait locus (QTL), Arch atherosclerosis 5 (Aath5), on mouse chromosome 10 by three-way QTL analyses between Apoe−/− mice on a DBA/2J, 129S6 and C57BL/6J background. The DBA/2J haplotype at the Aath5 locus was associated with smaller plaque size. One of the candidate genes underlying Aath5 was Stabilin-2 (Stab2), which encodes a clearance receptor for hyaluronan (HA) predominantly expressed in liver sinusoidal endothelial cells (LSECs). However, the role of Stab2 in atherosclerosis is unknown. A congenic line of Apoe−/− mice carrying Aath5 covering the Stab2DBA allele on a background of 129S6 confirmed the small reductions of atherosclerotic plaque development. To further determine whether Stab2 is an underlying gene for Aath5, we generated Stab2−/−Apoe−/− mice on a C57BL/6J background. When fed with a Western diet for 8 weeks, Stab2−/−Apoe−/− males developed approximately 30% smaller plaques than Stab2+/+Apoe−/− mice. HA was accumulated in circulation but not in major organs in the Stab2 deficient mice. STAB2-binding molecules that are involved in atherosclerosis, including acLDL, apoptotic cells, heparin and vWF were not likely the direct cause of the protection in the Stab2−/−Apoe−/− males. These data indicate that reduction of Stab2 is protective against atherosclerotic plaque development, and that Stab2 is a contributing gene underlying Aath5, although its effect is small. To test whether non-synonymous amino acid changes unique to DBA/2J affect the function of STAB2 protein, we made HEK293 cell lines expressing STAB2129 or STAB2DBA proteins, as well as STAB2129 proteins carrying each of five DBA-unique replacements that have been predicted to be deleterious. These mutant cells were capable of internalizing 125I -HA and DiI-acLDL similarly to the control cells. These results indicate that the amino acid changes unique to DBA/2J are not affecting the function of STAB2 protein, and support our previous observation that the reduced transcription of Stab2 in the liver sinusoid as a consequence of the insertion of a viral-derived sequence, intracisternal A particle, is the primary contributor to the athero-protection conferred by the DBA/2J allele

Reduction of Stabilin-2 Contributes to a Protection Against AtherosclerosisStabilin

We have previously identified a novel atherosclerosis quantitative trait locus (QTL), Arch atherosclerosis 5 (Aath5), on mouse chromosome 10 by three-way QTL analyses between Apoe−/− mice on a DBA/2J, 129S6 and C57BL/6J background. The DBA/2J haplotype at the Aath5 locus was associated with smaller plaque size. One of the candidate genes underlying Aath5 was Stabilin-2 (Stab2), which encodes a clearance receptor for hyaluronan (HA) predominantly expressed in liver sinusoidal endothelial cells (LSECs). However, the role of Stab2 in atherosclerosis is unknown. A congenic line of Apoe−/− mice carrying Aath5 covering the Stab2DBA allele on a background of 129S6 confirmed the small reductions of atherosclerotic plaque development. To further determine whether Stab2 is an underlying gene for Aath5, we generated Stab2−/−Apoe−/− mice on a C57BL/6J background. When fed with a Western diet for 8 weeks, Stab2−/−Apoe−/− males developed approximately 30% smaller plaques than Stab2+/+Apoe−/− mice. HA was accumulated in circulation but not in major organs in the Stab2 deficient mice. STAB2-binding molecules that are involved in atherosclerosis, including acLDL, apoptotic cells, heparin and vWF were not likely the direct cause of the protection in the Stab2−/−Apoe−/− males. These data indicate that reduction of Stab2 is protective against atherosclerotic plaque development, and that Stab2 is a contributing gene underlying Aath5, although its effect is small. To test whether non-synonymous amino acid changes unique to DBA/2J affect the function of STAB2 protein, we made HEK293 cell lines expressing STAB2129 or STAB2DBA proteins, as well as STAB2129 proteins carrying each of five DBA-unique replacements that have been predicted to be deleterious. These mutant cells were capable of internalizing 125I -HA and DiI-acLDL similarly to the control cells. These results indicate that the amino acid changes unique to DBA/2J are not affecting the function of STAB2 protein, and support our previous observation that the reduced transcription of Stab2 in the liver sinusoid as a consequence of the insertion of a viral-derived sequence, intracisternal A particle, is the primary contributor to the athero-protection conferred by the DBA/2J allele

Turbulence characteristics across a range of idealized urban canopy geometries

Good representation of turbulence in urban canopy models is necessary for accurate prediction of momentum and scalar distribution in and above urban canopies. To develop and improve turbulence closure schemes for one-dimensional multi-layer urban canopy models, turbulence characteristics are investigated here by analyzing existing large-eddy simulation and direct numerical simulation data. A range of geometries and flow regimes are analyzed that span packing densities of 0.0625 to 0.44, different building array configurations (cubes and cuboids, aligned and staggered arrays, and variable building height), and different incident wind directions (0 degrees and 45 degrees with regards to the building face). Momentum mixing-length profiles share similar characteristics across the range of geometries, making a first-order momentum mixing-length turbulence closure a promising approach. In vegetation canopies turbulence is dominated by mixing-layer eddies of a scale determined by the canopy top shear length scale. No relationship was found between the depth-averaged momentum mixing length within the canopy and the canopy top shear length scale in the present study. By careful specification of the intrinsic averaging operator in the canopy, an often-overlooked term that accounts for changes in plan area density with height, is included in a first-order momentum mixing-length turbulence closure model. For an array of variable-height buildings, its omission leads to velocity overestimation of up to 17%. Additionally, we observe that the von Karman coefficient varies between 0.20 and 0.51 across simulations, which is the first time such a range of values has been documented. When driving flow is oblique to the building faces, the ratio of dispersive to turbulent momentum flux is larger than unity in the lower half of the canopy, and wake production becomes significant compared to shear production of turbulent momentum flux. It is probable that dispersive momentum fluxes are more significant than previously thought in real urban settings, where the wind direction is almost always oblique

The Lantern Vol. 1, No. 1, May 1933

• Remember: Translation of Rappelle-toi by Alfred de Musset • Lighting the Lantern • Footfalls • To a Lovely Lady • The Sons of Martha • Strategy • Lumine Lunae • Poetry in Retrospect • Nirvana • A Domestic Episode • At Night • Haman and Hitler • This is What He Said • Bookocracy • Four Loves • Cities and Personalitieshttps://digitalcommons.ursinus.edu/lantern/1000/thumbnail.jp

A Quasi-Experimental Evaluation of Tuition Reimbursement in Municipal Government

An evaluation of the tuition reimbursement program for a mid-sized mid-Atlantic city was undertaken using both surveys and quasi-experimental techniques. Contrary to recent criticisms of tuition reimbursement programs, the survey findings indicate generally perceived benefits of the program among participants, supervisors and non-participant co-workers. The quasi-experi mental phase of the research determined a 56% higher promotion rate among participants than among non-participants; moreover, program participants were much more likely to remain in city employment than were non-participants.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Reduction of Stabilin-2 Contributes to a Protection Against Atherosclerosis

We have previously identified a novel atherosclerosis quantitative trait locus (QTL), Arch atherosclerosis 5 (Aath5), on mouse chromosome 10 by three-way QTL analyses between Apoe−/− mice on a DBA/2J, 129S6 and C57BL/6J background. The DBA/2J haplotype at the Aath5 locus was associated with smaller plaque size. One of the candidate genes underlying Aath5 was Stabilin-2 (Stab2), which encodes a clearance receptor for hyaluronan (HA) predominantly expressed in liver sinusoidal endothelial cells (LSECs). However, the role of Stab2 in atherosclerosis is unknown. A congenic line of Apoe−/− mice carrying Aath5 covering the Stab2DBA allele on a background of 129S6 confirmed the small reductions of atherosclerotic plaque development. To further determine whether Stab2 is an underlying gene for Aath5, we generated Stab2−/−Apoe−/− mice on a C57BL/6J background. When fed with a Western diet for 8 weeks, Stab2−/−Apoe−/− males developed approximately 30% smaller plaques than Stab2+/+Apoe−/− mice. HA was accumulated in circulation but not in major organs in the Stab2 deficient mice. STAB2-binding molecules that are involved in atherosclerosis, including acLDL, apoptotic cells, heparin and vWF were not likely the direct cause of the protection in the Stab2−/−Apoe−/− males. These data indicate that reduction of Stab2 is protective against atherosclerotic plaque development, and that Stab2 is a contributing gene underlying Aath5, although its effect is small. To test whether non-synonymous amino acid changes unique to DBA/2J affect the function of STAB2 protein, we made HEK293 cell lines expressing STAB2129 or STAB2DBA proteins, as well as STAB2129 proteins carrying each of five DBA-unique replacements that have been predicted to be deleterious. These mutant cells were capable of internalizing 125I -HA and DiI-acLDL similarly to the control cells. These results indicate that the amino acid changes unique to DBA/2J are not affecting the function of STAB2 protein, and support our previous observation that the reduced transcription of Stab2 in the liver sinusoid as a consequence of the insertion of a viral-derived sequence, intracisternal A particle, is the primary contributor to the athero-protection conferred by the DBA/2J allele