Number Talks for Multilingual Learners

Educators know that profound learning occurs when students are able to make meaningful connections and engage in academic discourse with their teachers and peers (Kazemi & Hintz, 2014; Moschkovich, 1999; Zwiers, 2008). We know that success in mathematics depends upon a strong foundation of number sense (Boaler, 2015). An interest in synthesising the most promising practices for language acquisition and the most promising practices for mathematics instruction led to the research question: How can Number Talks affect academic achievement and language development of fourth grade multilingual learners? The purpose of this project was to incorporate Number Talks into the fourth grade math curriculum in order to develop number sense and promote student interaction and engagement in the language of mathematics. More specifically, the objective was to teach the language of mathematics and provide students with a daily routine and structure to produce and interact in this mathematical register. As a teacher of English Learners (ELs), the routine of Number Talks proved to be a promising instructional strategy that could be implemented in support of ELs, as well as their native English speaking peers in the mainstream classroom. Research resulted in the instructional materials needed for teaching the first 21 days of the Number Talks routine, in the format of Google slides

Short-term operating plan for farms and ranches

"Timely decision making is essential for farm and ranch businesses. Decisions are a part of daily operations and vary greatly from prioritizing tasks to choosing inputs and deciding how much product to sell at a certain price. Most operations have primary decision makers who routinely make these decisions. It is important however, that others know how to proceed if the key decision maker(s) is/are unable to make decisions. This plan was developed to help farm and ranch families continue operating their businesses with minimal interruptions should the primary decision maker(s) be unable to make short-term decisions. The plan could be helpful in an unexpected situation such as hospitalization or military deployment. For this plan, the short term is generally considered two weeks to six months. The purpose is to have organized information for family members to use to continue operating the farm or ranch business. Locating key information is stressful and time consuming, and this plan will help to reduce stress and save time."--First page.The following authors contributed to this plan: Mary Sobba (Field Specialist, Agricultural Business and Policy, MU Extension), Joni Harper (Community Engagement Specialist, Agriculture and Environment, MU Extension), Catherine Neuner (Community Engagement Specialist, Agriculture and Environment, MU Extension), Kyle Whittaker (Community Engagement Specialist, Agriculture and Environment, MU Extension)New 07/202

Short-term operating plan for farms and ranches

stats082022upload"Timely decision making is essential for farm and ranch businesses. Decisions are a part of daily operations and vary greatly from prioritizing tasks to choosing inputs and deciding how much product to sell at a certain price. Most operations have primary decision makers who routinely make these decisions. It is important however, that others know how to proceed if the key decision maker(s) is/are unable to make decisions. This plan was developed to help farm and ranch families continue operating their businesses with minimal interruptions should the primary decision maker(s) be unable to make short-term decisions. The plan could be helpful in an unexpected situation such as hospitalization or military deployment."--Page 1.Mary Sobba (Field Specialist, Agricultural Business and Policy), Joni Harper (Community Engagement Specialist, Agriculture and Environment), Catherine Neuner (Community Engagement Specialist, Agriculture and Environment), Kyle Whittaker (Community Engagement Specialist, Agriculture and Environment

Knockdown of heterochromatin protein 1 binding protein 3 recapitulates phenotypic, cellular, and molecular features of aging.

Identifying genetic factors that modify an individual\u27s susceptibility to cognitive decline in aging is critical to understanding biological processes involved and mitigating risk associated with a number of age-related disorders. Recently, heterochromatin protein 1 binding protein 3 (Hp1bp3) was identified as a mediator of cognitive aging. Here, we provide a mechanistic explanation for these findings and show that targeted knockdown of Hp1bp3 in the hippocampus by 50%-75% is sufficient to induce cognitive deficits and transcriptional changes reminiscent of those observed in aging and Alzheimer\u27s disease brains. Specifically, neuroinflammatory-related pathways become activated following Hp1bp3 knockdown in combination with a robust decrease in genes involved in synaptic activity and neuronal function. To test the hypothesis that Hp1bp3 mediates susceptibility to cognitive deficits via a role in neuronal excitability, we performed slice electrophysiology demonstrate transcriptional changes after Hp1bp3 knockdown manifest functionally as a reduction in hippocampal neuronal intrinsic excitability and synaptic plasticity. In addition, as Hp1bp3 is a known mediator of miRNA biogenesis, here we profile the miRNA transcriptome and identify mir-223 as a putative regulator of a portion of observed mRNA changes, particularly those that are inflammatory-related. In summary, work here identifies Hp1bp3 as a critical mediator of aging-related changes at the phenotypic, cellular, and molecular level and will help inform the development of therapeutics designed to target either Hp1bp3 or its downstream effectors in order to promote cognitive longevity

Genetic background modifies CNS-mediated sensorimotor decline in the AD-BXD mouse model of genetic diversity in Alzheimer\u27s disease.

Many patients with Alzheimer\u27s dementia (AD) also exhibit noncognitive symptoms such as sensorimotor deficits, which can precede the hallmark cognitive deficits and significantly impact daily activities and an individual\u27s ability to live independently. However, the mechanisms underlying sensorimotor dysfunction in AD and their relationship with cognitive decline remains poorly understood, due in part to a lack of translationally relevant animal models. To address this, we recently developed a novel model of genetic diversity in Alzheimer\u27s disease, the AD-BXD genetic reference panel. In this study, we investigated sensorimotor deficits in the AD-BXDs and the relationship to cognitive decline in these mice. We found that age- and AD-related declines in coordination, balance and vestibular function vary significantly across the panel, indicating genetic background strongly influences the expressivity of the familial AD mutations used in the AD-BXD panel and their impact on motor function. Although young males and females perform comparably regardless of genotype on narrow beam and inclined screen tasks, there were significant sex differences in aging- and AD-related decline, with females exhibiting worse decline than males of the same age and transgene status. Finally, we found that AD motor decline is not correlated with cognitive decline, suggesting that sensorimotor deficits in AD may occur through distinct mechanisms. Overall, our results suggest that AD-related sensorimotor decline is strongly dependent on background genetics and is independent of dementia and cognitive deficits, suggesting that effective therapeutics for the entire spectrum of AD symptoms will likely require interventions targeting each distinct domain involved in the disease

Translational approaches to understanding resilience to Alzheimer\u27s disease.

Individuals who maintain cognitive function despite high levels of Alzheimer\u27s disease (AD)-associated pathology are said to be \u27resilient\u27 to AD. Identifying mechanisms underlying resilience represents an exciting therapeutic opportunity. Human studies have identified a number of molecular and genetic factors associated with resilience, but the complexity of these cohorts prohibits a complete understanding of which factors are causal or simply correlated with resilience. Genetically and phenotypically diverse mouse models of AD provide new and translationally relevant opportunities to identify and prioritize new resilience mechanisms for further cross-species investigation. This review will discuss insights into resilience gained from both human and animal studies and highlight future approaches that may help translate these insights into therapeutics designed to prevent or delay AD-related dementia

Identification of Pre-symptomatic Gene Signatures That Predict Resilience to Cognitive Decline in the Genetically Diverse AD-BXD Model

Across the population, individuals exhibit a wide variation of susceptibility or resilience to developing Alzheimer’s disease (AD). Identifying specific factors that promote resilience would provide insight into disease mechanisms and nominate potential targets for therapeutic intervention. Here, we use transcriptome profiling to identify gene networks present in the pre-symptomatic AD mouse brain relating to neuroinflammation, brain vasculature, extracellular matrix organization, and synaptic signaling that predict cognitive performance at an advanced age. We highlight putative drivers of these observed relationships, including Itgb2, Fcgr2b, Slc6a14, and Gper1, which represent prime targets through which to promote resilience prior to overt symptom onset. In addition, we identify a genomic region on chromosome 2 containing variants that directly modulate resilience network expression. Overall, work here highlights new potential drivers of resilience to AD and contributes significantly to our understanding of early, potentially causal, disease mechanisms

Identifying the molecular systems that influence cognitive resilience to Alzheimer\u27s disease in genetically diverse mice.

Individual differences in cognitive decline during normal aging and Alzheimer\u27s disease (AD) are common, but the molecular mechanisms underlying these distinct outcomes are not fully understood. We utilized a combination of genetic, molecular, and behavioral data from a mouse population designed to model human variation in cognitive outcomes to search for the molecular mechanisms behind this population-wide variation. Specifically, we used a systems genetics approach to relate gene expression to cognitive outcomes during AD and normal aging. Statistical causal-inference Bayesian modeling was used to model systematic genetic perturbations matched with cognitive data that identified astrocyte and microglia molecular networks as drivers of cognitive resilience to AD. Using genetic mapping, we identifie

Identifying Mechanisms of Normal Cognitive Aging Using a Novel Mouse Genetic Reference Panel.

Developing strategies to maintain cognitive health is critical to quality of life during aging. The basis of healthy cognitive aging is poorly understood; thus, it is difficult to predict who will have normal cognition later in life. Individuals may have higher baseline functioning (cognitive reserve) and others may maintain or even improve with age (cognitive resilience). Understanding the mechanisms underlying cognitive reserve and resilience may hold the key to new therapeutic strategies for maintaining cognitive health. However, reserve and resilience have been inconsistently defined in human studies. Additionally, our understanding of the molecular and cellular bases of these phenomena is poor, compounded by a lack of longitudinal molecular and cognitive data that fully capture the dynamic trajectories of cognitive aging. Here, we used a genetically diverse mouse population (B6-BXDs) to characterize individual differences in cognitive abilities in adulthood and investigate evidence of cognitive reserve and/or resilience in middle-aged mice. We tested cognitive function at two ages (6 months and 14 months) using y-maze and contextual fear conditioning. We observed heritable variation in performance on these traits