Technology in Higher Education Mathematics: a Mixed Methods Study

The integration of technology has become a high priority at various levels of education, including higher education. This study focused on discovering and describing the technology being used in higher education mathematics content courses by faculty members at colleges and universities. The research questions focused on what technology was being used by higher education mathematics faculty, how it was being used, what factors would encourage the incorporation of technology, the description of an adopter of technology, who is most likely to use technology to engage students in learning, and challenges that must be overcome to implement technology. The study uses an explanatory sequential mixed methods design which allowed for gathering qualitative data through semi-structured interviews and a vignette to support the quantitative data, which was gathered from a general technology survey administered electronically. The participants included 68 faculty members from research universities, regional public and private universities, and community colleges in a Midwestern state. Results from the study found that technology used by faculty included computers, projector systems, calculators, word processing software, learning management systems, e-mail communication, and the Internet. Technology was found to be predominately used for classroom instruction as a visual aid to present multiple forms of mathematical representations. Factors that could influence the integration of technology into mathematics content courses include the need for a technology resource bank that has appropriate and high-quality tasks that correspond to content and the need for additional time to investigate and implement new technologies. The description of an adopter of technology that evolved during the study was not adequate, but the analysis did show that the attitudes and beliefs of faculty toward technology influenced technology-use preferences. Future research is needed to identify a complete description of an adopter of technology. The study also reinforced the idea that technology-rich classrooms offer an avenue to engage students in learning mathematics. Lastly, the study highlighted challenges that faculty encounter when integrating technology including demands from administration, time for exploration, the need for additional training opportunities, and the lack of technical support.Education (all programs

Public Health Liberation – An Emerging Transdiscipline to Elucidate and Transform the Public Health Economy

Public Health Liberation (PHL) is an innovative general theory of public health aimed at accelerating health equity. This paper provides a rich synthesis of philosophical traditions, novel theories, and approaches to establish the basis for a new public health transdiscipline. The authors argue that the public health economy as a single analytic lens elucidates the contradictions and tensions that reproduce vast health inequity. Authored by a majority of Black women, community experiences and perspectives are a major strength of this paper because they draw upon leadership experiences with contemporary issues. The authors begin by describing their background in public health advocacy and by demonstrating the need for PHL using lead-contaminated water crises from Flint, Michigan and Washington, DC. They discuss the benefits of horizontal and vertical integration that broaden public health discourse to include affected populations and that seek opportunities throughout the public health economy. Their philosophical and theoretical reasoning reinterprets and adopts disciplinary concepts in political theory, sociology, women\u27s studies, African American emancipatory writing, anti-racism, and community psychology to form a culturally relevant worldview and cogent thesis. Several new constructs emerge that do not appear elsewhere in the literature - Gaze of the Enslaved, Morality Principle, liberation, illiberation, liberation safe spaces, public health realism, and hegemony. The authors use their ethical and theoretical assumptions to guide practice and community self-help. Public Health Liberation presents a major challenge to assumptions about public health effectiveness in addressing vast health inequity

In it together! Cultivating space for intergenerational dialogue, empathy and hope in a climate of uncertainty

The urgent and interlocking social, economic and ecological crises faced by societies around the world require dialogue, empathy and above all, hope that transcends social divides. At a time of uncertainty and crisis, many societies are divided, with distrust and divides exacerbated by media representations pitting different groups against one another. Acknowledging intersectional interrelationships, this collaborative paper considers one type of social distinction – generation – and focuses on how trust can be rebuilt across generations. To do this, we collate key insights from eight projects that shared space within a conference session foregrounding creative, intergenerational responses to the climate and related crises. Prompted by a set of reflective questions, presenters commented on the methodological resources that were co-developed in intergenerational research and action spaces. Most of the work outlined was carried out in the UK, situated in challenges that are at once particular to local contexts, and systematic of a wider malaise that requires intergenerational collaboration. Reflecting across the projects, we suggest fostering ongoing, empathetic dialogues across generations is key to addressing these challenges of the future, securing communities that are grounded as collaborative and culturally responsive, and resilient societies able to adapt to and mitigate the impacts of change

Integration of GWAS SNPs and tissue specific expression profiling reveal discrete eQTLs for human traits in blood and brain

Our knowledge of the transcriptome has become much more complex since the days of the central dogma of molecular biology. We now know that splicing takes place to create potentially thousands of isoforms from a single gene, and we know that RNA does not always faithfully recapitulate DNA if RNA editing occurs. Collectively, these observations show that the transcriptome is amazingly rich with intricate regulatory mechanisms for overall gene expression, splicing, and RNA editing. Genetic variability can play a role in controlling gene expression, which can be identified by examining expression quantitative trait loci (eQTLs). eQTLs are genomic regions where genetic variants, including single nucleotide polymorphisms (SNPs) show a statistical association with expression of mRNA transcripts. In humans, many SNPs are also associated with disease, and have been identified using genome wide association studies (GWAS) but the biological effects of those SNPs are usually not known. If SNPs found in GWAS are also found in eQTLs, then one could hypothesize that expression levels may contribute to disease risk. Performing eQTL analysis with GWAS SNPs in both blood and brain, specifically the frontal cortex and the cerebellum, we found both shared and tissue unique eQTLS. The identification of tissue-unique eQTLs supports the argument that choice of tissue type is important in eQTL studies (Paper I). Aging is a complex process with the mechanisms underlying aging still being poorly defined. There is evidence that the transcriptome changes with age, and hence we used the brain dataset from our first paper as a discovery set, with an additional replication dataset, to investigate any aging-gene expression associations. We found evidence that many genes were associated with aging. We further found that there were more statically significant expression changes in the frontal cortex versus the cerebellum, indicating that brain regions may age at different rates. As the brain is a heterogeneous tissue including both neurons and non-neuronal cells, we used LCM to capture Purkinje cells as a representative neuronal type and repeated the age analysis. Looking at the discovery, replication and Purkinje cell datasets we found five genes with strong, replicated evidence of age-expression associations (Paper II). Being able to capture and quantify the depth of the transcriptome has been a lengthy process starting with methods that could only measure a single gene to genome-wide techniques such as microarray. A recently developed technology, RNA-Seq, shows promise in its ability to capture expression, splicing, and editing and with its broad dynamic range quantification is accurate and reliable. RNA-Seq is, however, data intensive and a great deal of computational expertise is required to fully utilize the strengths of this method. We aimed to create a small, well-controlled, experiment in order to test the performance of this relatively new technology in the brain. We chose embryonic versus adult cerebral cortex, as mice are genetically homogenous and there are many known differences in gene expression related to brain development that we could use as benchmarks for analysis testing. We found a large number of differences in total gene expression between embryonic and adult brain. Rigorous technical and biological validation illustrated the accuracy and dynamic range of RNA-Seq. We were also able to interrogate differences in exon usage in the same dataset. Finally we were able to identify and quantify both well-known and novel A-to-I edit sites. Overall this project helped us develop the tools needed to build usable pipelines for RNA-Seq data processing (Paper III). Our studies in the developing brain (Paper III) illustrated that RNA-Seq was a useful unbiased method for investigating RNA editing. To extend this further, we utilized a genetically modified mouse model to study the transcriptomic role of the RNA editing enzyme ADAR2. We found that ADAR2 was important for editing of the coding region of mRNA as a large proportion of RNA editing sites in coding regions had a statistically significant decrease in editing percentages in Adar2 -/-Gria2 R/R mice versus controls. However, despite indications in the literature that ADAR2 may also be involved in splicing and expression regulatory machinery we found no changes in gene expression or exon utilization in Adar2 -/-Gria2 R/R mice as compared to their littermate controls (Paper IV). In our final study, based on the methods developed in Papers III and IV, we revisited the idea of age related gene expression associations from Paper II. We used a subset of human frontal cortices for RNA sequencing. Interestingly we found more gene expression changes with aging compared to the previous data using microarrays in Paper II. When the significant gene lists were analysed for gene ontology enrichment, we found that there was a large number of downregulated genes involved in synaptic function while those that were upregulated had enrichment in immune function. This dataset illustrates that the aging brain may be predisposed to the processes found in neurodegenerative diseases (Paper V)

Regulatory sites for splicing in human basal ganglia are enriched for disease-relevant information

Genome-wide association studies have generated an increasing number of common genetic variants associated with neurological and psychiatric disease risk. An improved understanding of the genetic control of gene expression in human brain is vital considering this is the likely modus operandum for many causal variants. However, human brain sampling complexities limit the explanatory power of brain-related expression quantitative trait loci (eQTL) and allele-specific expression (ASE) signals. We address this, using paired genomic and transcriptomic data from putamen and substantia nigra from 117 human brains, interrogating regulation at different RNA processing stages and uncovering novel transcripts. We identify disease-relevant regulatory loci, find that splicing eQTLs are enriched for regulatory information of neuron-specific genes, that ASEs provide cell-specific regulatory information with evidence for cellular specificity, and that incomplete annotation of the brain transcriptome limits interpretation of risk loci for neuropsychiatric disease. This resource of regulatory data is accessible through our web server, http://braineacv2.inf.um.es/

New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk

To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P<5 × 10−8), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk

Resolving the polymorphism-in-probe problem is critical for correct interpretation of expression QTL studies.

Polymorphisms in the target mRNA sequence can greatly affect the binding affinity of microarray probe sequences, leading to false-positive and false-negative expression quantitative trait locus (QTL) signals with any other polymorphisms in linkage disequilibrium. We provide the most complete solution to this problem, by using the latest genome and exome sequence reference data to identify almost all common polymorphisms (frequency >1% in Europeans) in probe sequences for two commonly used microarray panels (the gene-based Illumina Human HT12 array, which uses 50-mer probes, and exon-based Affymetrix Human Exon 1.0 ST array, which uses 25-mer probes). We demonstrate the impact of this problem using cerebellum and frontal cortex tissues from 438 neuropathologically normal individuals. We find that although only a small proportion of the probes contain polymorphisms, they account for a large proportion of apparent expression QTL signals, and therefore result in many false signals being declared as real. We find that the polymorphism-in-probe problem is insufficiently controlled by previous protocols, and illustrate this using some notable false-positive and false-negative examples in MAPT and PRICKLE1 that can be found in many eQTL databases. We recommend that both new and existing eQTL data sets should be carefully checked in order to adequately address this issue

<em>MAPT </em>expression and splicing is differentially regulated by brain region: relation to genotype and implication for tauopathies

The MAPT (microtubule-associated protein tau) locus is one of the most remarkable in neurogenetics due not only to its involvement in multiple neurodegenerative disorders, including progressive supranuclear palsy, corticobasal degeneration, Parksinson's disease and possibly Alzheimer's disease, but also due its genetic evolution and complex alternative splicing features which are, to some extent, linked and so all the more intriguing. Therefore, obtaining robust information regarding the expression, splicing and genetic regulation of this gene within the human brain is of immense importance. In this study, we used 2011 brain samples originating from 439 individuals to provide the most reliable and coherent information on the regional expression, splicing and regulation of MAPT available to date. We found significant regional variation in mRNA expression and splicing of MAPT within the human brain. Furthermore, at the gene level, the regional distribution of mRNA expression and total tau protein expression levels were largely in agreement, appearing to be highly correlated. Finally and most importantly, we show that while the reported H1/H2 association with gene level expression is likely to be due to a technical artefact, this polymorphism is associated with the expression of exon 3-containing isoforms in human brain. These findings would suggest that contrary to the prevailing view, genetic risk factors for neurodegenerative diseases at the MAPT locus are likely to operate by changing mRNA splicing in different brain regions, as opposed to the overall expression of the MAPT gene

Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP

Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention