Social Promotion of High School Students

With new standards and increasing pressure on educators from state and national governments, it is essential that schools are able to keep up with the increasing demands placed upon them. However, increasing standards has led to an increase in the number of students that fail to meet grade level requirements. In the attempt to help more students to meet standards, the issue of social promotion, or the policy of allowing a student who did not meet requirements to continue on to the next grade, has come under fire. In this thesis, the objective was to analyze the effectiveness of the policy of social promotion. To do this, a simple survey was given to students to assess attitudes towards school in general, homework, respect for authority, and parental involvement. To gain additional data, several students volunteered access to their permanent records for analysis of their major exams and grade level scores. The scores were averaged, and based upon the results students were assigned to one of three groups: Control, At Risk, or Socially Promoted. The groups were then reassessed after the final exam in June 2006 to see if their original grouping was a good indicator of their final grade. In addition, the socially promoted group was analyzed to see how many students were able to pass after being allowed to continue on after previous failure. The major contribution of this study was to add new research on the topic of social promotion. It was found throughout the course of this study that students who were socially promoted from one grade to another continued to do poorly in school. It was also observed that students who were deemed to be at risk continued to pass by the slightest of margins

Symmetry and Duplication

The symmetry and duplication in bee hives and ant colonies will be compared to tiling the plane in TI-84

A multispecies tree ring reconstruction of Potomac River streamflow (950-2001)

Millennial length reconstruction of Potomac River StreamflowInstrumental record does represent the past milleniumImprovement upon the previous reconstructio

Vegetation Production Responses to October Grazing in the Nebraska Sandhills

Understanding the long-term effect of summer grazing date and fall stocking rate on herbage production is critical to extending the grazing season in the Nebraska Sandhills. A study was conducted from 1997 to 2002 at the Gudmundsen Sandhills Laboratory located near Whitman, Nebraska, to determine the herbage production response to summer grazing date and October stocking rate on two different sites. Site 1 was dominated by warm-season grasses and site 2 was dominated by cool- season graminoids. At each site, three 0.37-ha pastures were constructed in each of four blocks before application of summer grazing treatments. Pastures in each block were grazed at 0.5 animal-unit months (AUM) ha-1 in June or July, or were deferred from summer grazing. Following summer grazing treatments, October stocking rate treatments (no grazing or 1.0, 2.0, or 3.0 AUM ha-1) were applied to subunits of each summer grazing date pasture during mid-October. Vegetation was sampled in each pasture in mid-June and mid-August and sorted by functional group to determine the effect of 5 yr of grazing treatments on herbage production and residual herbage. Herbage production was not affected by summer or October grazing treatments on the warm-season grass-dominated site. Increasing October stocking rate, however, reduced cool-season graminoid production and subsequent herbage production 25% by year 5 of the study. Residual herbage at both sites at the end of the October grazing periods explained as much as 16% to 34% of subsequent year’s herbage production. Grazing managers in the Nebraska Sandhills can extend the grazing season by lightly stocking pastures in the summer to facilitate additional fall grazing. Heavy stocking in October over several years on cool-season-, but not warm-season-, dominated sites will reduce production of cool- season graminoids on these sites.The Rangeland Ecology & Management archives are made available by the Society for Range Management and the University of Arizona Libraries. Contact [email protected] for further information.Migrated from OJS platform August 202

NUP98 and RAE1 sustain progenitor function through HDAC-dependent chromatin targeting to escape from nucleolar localization

Abstract Self-renewing somatic tissues rely on progenitors to support the continuous tissue regeneration. The gene regulatory network maintaining progenitor function remains incompletely understood. Here we show that NUP98 and RAE1 are highly expressed in epidermal progenitors, forming a separate complex in the nucleoplasm. Reduction of NUP98 or RAE1 abolishes progenitors’ regenerative capacity, inhibiting proliferation and inducing premature terminal differentiation. Mechanistically, NUP98 binds on chromatin near the transcription start sites of key epigenetic regulators (such as DNMT1, UHRF1 and EZH2) and sustains their expression in progenitors. NUP98’s chromatin binding sites are co-occupied by HDAC1. HDAC inhibition diminishes NUP98’s chromatin binding and dysregulates NUP98 and RAE1’s target gene expression. Interestingly, HDAC inhibition further induces NUP98 and RAE1 to localize interdependently to the nucleolus. These findings identified a pathway in progenitor maintenance, where HDAC activity directs the high levels of NUP98 and RAE1 to directly control key epigenetic regulators, escaping from nucleolar aggregation

Use of whole exome sequencing for the identification of Ito-based arrhythmia mechanism and therapy

Identified genetic variants are insufficient to explain all cases of inherited arrhythmia. We tested whether the integration of whole exome sequencing with well-established clinical, translational, and basic science platforms could provide rapid and novel insight into human arrhythmia pathophysiology and disease treatment

Impact of schizophrenia GWAS loci converge onto distinct pathways in cortical interneurons vs glutamatergic neurons during development

Remarkable advances have been made in schizophrenia (SCZ) GWAS, but gleaning biological insight from these loci is challenging. Genetic influences on gene expression (e.g., eQTLs) are cell type-specific, but most studies that attempt to clarify GWAS loci\u27s influence on gene expression have employed tissues with mixed cell compositions that can obscure cell-specific effects. Furthermore, enriched SCZ heritability in the fetal brain underscores the need to study the impact of SCZ risk loci in specific developing neurons. MGE-derived cortical interneurons (cINs) are consistently affected in SCZ brains and show enriched SCZ heritability in human fetal brains. We identified SCZ GWAS risk genes that are dysregulated in iPSC-derived homogeneous populations of developing SCZ cINs. These SCZ GWAS loci differential expression (DE) genes converge on the PKC pathway. Their disruption results in PKC hyperactivity in developing cINs, leading to arborization deficits. We show that the fine-mapped GWAS locus in the ATP2A2 gene of the PKC pathway harbors enhancer marks by ATACseq and ChIPseq, and regulates ATP2A2 expression. We also generated developing glutamatergic neurons (GNs), another population with enriched SCZ heritability, and confirmed their functionality after transplantation into the mouse brain. Then, we identified SCZ GWAS risk genes that are dysregulated in developing SCZ GNs. GN-specific SCZ GWAS loci DE genes converge on the ion transporter pathway, distinct from those for cINs. Disruption of the pathway gene CACNA1D resulted in deficits of Ca2+ currents in developing GNs, suggesting compromised neuronal function by GWAS loci pathway deficits during development. This study allows us to identify cell type-specific and developmental stage-specific mechanisms of SCZ risk gene function, and may aid in identifying mechanism-based novel therapeutic targets