Impact of a Self-Determination Intervention on the Reading Fluency of Struggling Elementary Students

Struggling readers are likely to face life-long challenges in achieving success in school and life as a result of their struggles with reading (Armbruster et al., 2001; Arnold, 2010; Hernandez, 2011). Third-grade students with reading disabilities are an exceptionally critical group who may experience enhanced risk during the year that the focus of schooling switches from learning to read to reading to learn (Lesnick et al., 2010). Students with learning disabilities need a robust rate of improvement to close the gap with their peers and access grade-level content. Oral reading fluency (ORF), assessed using reading-curriculum-based measures (R-CBM), provides a standardized measure of a student's overall progress in reading, including the rate of improvement (Roehrig et al., 2008). By the end of first grade, poor readers will likely experience significant and declining levels of motivation and engagement (Armbruster et al., 2001; Didion, 2019; Stanovich, 1986; Toste et al., 2020). Confidence in reading, or a student's view of themselves as readers, is integral to reading achievement and thus has been added as a vital component of the Nation's Report Card on the National Assessment of Educational Progress (NAEP) reading assessment (NAEP, 2019). Together, these research findings and public policy changes provide evidence that reading skills and self-determination skills such as motivation, engagement, and confidence are intertwined and affect one another. Thus, struggling students may need interventions addressing reading and self-determination skill sets to facilitate achievement (Wehmeyer et al., 2017). This single case experimental design study provided a self-determination intervention to three third-grade students with learning disabilities who were already receiving a research-based reading intervention. Intervention procedures were based on the Self-Determined Learning Model of Instruction (SDLMI) with the training component from Data Mountain. Both programs SUMMARY (Continued) are research-based and teach students to become self-regulated learners through a continual process of goal setting, action planning, progress monitoring, and reflection (Didion, 2019; Shogren et al., 2017). The central research question of this study was whether elementary students with reading disabilities would demonstrate increased oral reading fluency performance (level and trend) when participating in a self-determination intervention. Specifically, the study tested the effects of using the SDLMI and Data Mountain procedures on the ORF growth of third-grade students already receiving an evidence-based reading intervention. Visual inspection and the effect size metric found mixed results on the effectiveness of the intervention. Implications for practice and future research are discussed

The dense core transmembrane vesicle protein IA-2 is a regulator of vesicle number and insulin secretion

IA-2 is an enzymatically inactive member of the transmembrane protein tyrosine phosphate family located in dense core secretory vesicles and a major autoantigen in type 1 diabetes. Recent studies showed that targeted disruption of the IA-2 gene in mice resulted in impairment of insulin secretion and glucose intolerance. Insulin homeostasis, however, is a complex process involving a cascade of regulatory factors, and IA-2 is widely expressed in neuroendocrine cells throughout the body. Consequently, it is uncertain whether the impairment of insulin secretion in IA-2 knockout mice is a direct result of the knockout of IA-2 in beta cells or to counter regulatory alterations resulting from IA-2 knockout in other neuroendocrine cells. To define the function of IA-2, we studied the secretion of insulin in a single cell type, MIN-6, by overexpressing and knocking down IA-2. Our experiments showed that overexpression of IA-2 resulted in a 6-fold increase in glucose- or K+-induced insulin secretion and a ?3-fold increase in the number of secretory vesicles and the insulin content of cells. In contrast, knockdown of endogenous IA-2 by short interfering RNA resulted in nearly a complete loss of glucose-induced insulin secretion and a 50% decrease in basal insulin release. The half-life of insulin in cells overexpressing IA-2 was nearly twice as great as that in mock-transfected cells, suggesting that IA-2 was stabilizing the insulin-containing vesicles. From these results we conclude that in beta cells, IA-2 is an important regulator of dense core vesicle number and glucose-induced and basal insulin secretion. © 2005 by the National Academy of Sciences of the USA.</p

Expression of the protein tyrosine phosphatase-like protein IA-2 during pancreatic islet development

A tyrosine phosphatase-like protein, IA-2, is a major autoantigen in Type 1 diabetes but its role in islet function is unclear. Tyrosine phosphorylation mediates regulation of cellular processes such as exocytosis, cell growth, and cell differentiation. To investigate the potential involvement of IA-2 in islet differentiation and insulin secretion, we analyzed by immunohistochemistry expression of IA-2 during islet development in fetal rats and during the maturation of insulin secretory responses after birth. In the fetus, IA-2 immunoreactivity was detected in primitive islets positive for insulin and glucagon at 12 days' gestation. Subsequently, IA-2 was only weakly detectable in the fetal pancreas. In neonatal rat, a progressive increase in IA-2 immunoreactivity was observed in islets from very low levels at 1 day of age to moderate labeling at 10 days. In the adult, relatively high levels of IA-2 were detected in islets, with heterogeneous expression in individual cells within each islet. IA-2 marks a population of endocrine cells that transiently appear early in pancreatic ontogeny. Islet IA-2 expression reappears after birth concomitant with the development of mature insulin secretory responses, consistent with a role for this protein in regulated hormone secretion.</p