Early Numerical Competencies and Students with Mathematics Difficulty

Children start elementary school with variable mathematics ski11s. Some childrenunderstand the fundamentals of numbers and mathematics, while others struggle with basic counting, number recognition, understanding of symbols, quantity discrimination, and concepts of addition and subtraction. Often, this set of early numerical competencies is referred to as number sense or early numeracy competencies. Students need to establish and understand these competencies before moving on to more complex mathematical tasks. This article describes important early num erical competencies and provides a description of how these competencies can be taught to students who struggle with mathematics

Do word problem features differentially affect problem difficulty as a function of students’ mathematics difficulty with and without reading difficulty

This study examined whether and, if so, how word-problem features differentially affect problem difficulty as a function of mathematics difficulty (MD) status: no MD (n = 109), MD only (n = 109), or MD in combination with reading difficulties (MDRD; n = 109). The problem features were problem type (total, difference, or change) and position of missing information in the number sentence representing the word problem (first, second, or third position). Students were assessed on 14 word problems near the beginning of third grade. Consistent with the hypothesis that mathematical cognition differs as a function of MD subtype, problem type affected problem difficulty differentially for MDRD versus MD-only students; however, the position of missing information in word problems did not. Implications for MD subtyping and for instruction are discussed

Accelerating mathematics word problem-solving performance and efficacy with think-aloud strategies

Background: The previous body of research literature has reported several separate cognitive processes relevant in solving mathematics wps. Therefore, it is of the essence to seek for effective intervention and instruction for students in need for support in learning.Aim: This article reports the outcome of an intervention targeted at mathematics word problem (wp) skills.Setting: This study included three data collection points: (1) Premeasurements, (2) post-measurements and (3) follow-up measurements. Pre-measurements were performed in August, post-measurements immediately after the intervention period in October and follow-up measurements in December.Methods: A programme, which included face-to-face support in mathematics wp strategies with the think-aloud protocol, was applied. The participants were 28 Finnish third-graders (14 training group students and 14 control students). Their mathematics wp skills were tested three times (pre-, post- and follow-up assessments). The groups were matched by gender, family type and the mathematics wp pre-measurement score level. The groups differed neither by literacy skills (i.e. technical reading, reading comprehension) nor by task orientation at baseline.Results: Some acceleration of mathematics wp skills among the training group students was found but the growth dramatically declined as soon as the face-to-face support stopped. The results further showed improvement in the efficacy of correct answers or attempted mathematics wp items among training group students.Conclusion: The results suggested that training consisting of face-to-face support is crucial for accelerating mathematics wp strategies among students struggling with mathematics. Repeated, cyclic periods of support are suggested for sustained effect.</p

Influences of Neural Pathway Integrity on Children's Response to Reading Instruction

As the education field moves toward using responsiveness to intervention to identify students with disabilities, an important question is the degree to which this classification can be connected to a student's neurobiological characteristics. A few functional neuroimaging studies have reported a relationship between activation and response to instruction; however, whether a similar correlation exists with white matter (WM) is not clear. To investigate this issue, we acquired high angular resolution diffusion images from a group of first grade children who differed in their levels of responsiveness to a year-long reading intervention. Using probabilistic tractography, we calculated the strength of WM connections among nine cortical regions of interest and correlated these estimates with participants’ scores on four standardized reading measures. We found eight significant correlations, four of which were connections between the insular cortex and angular gyrus. In each of the correlations, a relationship with children's response to intervention was evident

Targeting NETs using dual-active DNase1 variants

Background: Neutrophil Extracellular Traps (NETs) are key mediators of immunothrombotic mechanisms and defective clearance of NETs from the circulation underlies an array of thrombotic, inflammatory, infectious, and autoimmune diseases. Efficient NET degradation depends on the combined activity of two distinct DNases, DNase1 and DNase1-like 3 (DNase1L3) that preferentially digest double-stranded DNA (dsDNA) and chromatin, respectively. Methods: Here, we engineered a dual-active DNase with combined DNase1 and DNase1L3 activities and characterized the enzyme for its NET degrading potential in vitro. Furthermore, we produced a mouse model with transgenic expression of the dual-active DNase and analyzed body fluids of these animals for DNase1 and DNase 1L3 activities. We systematically substituted 20 amino acid stretches in DNase1 that were not conserved among DNase1 and DNase1L3 with homologous DNase1L3 sequences. Results: We found that the ability of DNase1L3 to degrade chromatin is embedded into three discrete areas of the enzyme's core body, not the C-terminal domain as suggested by the state-of-the-art. Further, combined transfer of the aforementioned areas of DNase1L3 to DNase1 generated a dual-active DNase1 enzyme with additional chromatin degrading activity. The dual-active DNase1 mutant was superior to native DNase1 and DNase1L3 in degrading dsDNA and chromatin, respectively. Transgenic expression of the dual-active DNase1 mutant in hepatocytes of mice lacking endogenous DNases revealed that the engineered enzyme was stable in the circulation, released into serum and filtered to the bile but not into the urine. Conclusion: Therefore, the dual-active DNase1 mutant is a promising tool for neutralization of DNA and NETs with potential therapeutic applications for interference with thromboinflammatory disease states

Contributions Made by CDC25 Phosphatases to Proliferation of Intestinal Epithelial Stem and Progenitor Cells

The CDC25 protein phosphatases drive cell cycle advancement by activating cyclin-dependent protein kinases (CDKs). Humans and mice encode three family members denoted CDC25A, -B and -C and genes encoding these family members can be disrupted individually with minimal phenotypic consequences in adult mice. However, adult mice globally deleted for all three phosphatases die within one week after Cdc25 disruption. A severe loss of absorptive villi due to a failure of crypt epithelial cells to proliferate was observed in the small intestines of these mice. Because the Cdc25s were globally deleted, the small intestinal phenotype and loss of animal viability could not be solely attributed to an intrinsic defect in the inability of small intestinal stem and progenitor cells to divide. Here, we report the consequences of deleting different combinations of Cdc25s specifically in intestinal epithelial cells. The phenotypes arising in these mice were then compared with those arising in mice globally deleted for the Cdc25s and in mice treated with irinotecan, a chemotherapeutic agent commonly used to treat colorectal cancer. We report that the phenotypes arising in mice globally deleted for the Cdc25s are due to the failure of small intestinal stem and progenitor cells to proliferate and that blocking cell division by inhibiting the cell cycle engine (through Cdc25 loss) versus by inducing DNA damage (via irinotecan) provokes a markedly different response of small intestinal epithelial cells. Finally, we demonstrate that CDC25A and CDC25B but not CDC25C compensate for each other to maintain the proliferative capacity of intestinal epithelial stem and progenitor cells