ASU Scholarship Showcase

We recommend using backward design to develop course-based undergraduate research experiences (CUREs). The defining hallmark of CUREs is that students in a formal lab course explore research questions with unknown answers that are broadly relevant outside the course. Because CUREs lead to novel research findings, they represent a unique course design challenge, as the dual nature of these courses requires course designers to consider two distinct, but complementary, sets of goals for the CURE: 1) scientific discovery milestones (i.e., research goals) and 2) student learning in cognitive, psychomotor, and affective domains (i.e., pedagogical goals). As more undergraduate laboratory courses are re-imagined as CUREs, how do we thoughtfully design these courses to effectively meet both sets of goals? In this Perspectives article, we explore this question and outline recommendations for using backward design in CURE development.

Although insulin resistance in skeletal muscle is well-characterized, the role of circulating whole blood in the metabolic syndrome phenotype is not well understood. We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered in expression in the whole blood of individuals with metabolic syndrome. We further wanted to examine whether similar relationships that we have found previously in skeletal muscle exist in peripheral whole blood cells. All subjects (n=184) were Latino descent from the Arizona Insulin Resistance registry. Subjects were classified based on the metabolic syndrome phenotype according to the National Cholesterol Education Program’s Adult Treatment Panel III. Of the 184 Latino subjects in the study, 74 were classified with the metabolic syndrome and 110 were without. Whole blood gene expression profiling was performed using the Agilent 4x44K Whole Human Genome Microarray. Whole blood microarray analysis identified 1,432 probes that were altered in expression ≥1.2 fold and P<0.05 after Benjamini-Hochberg in the metabolic syndrome subjects. KEGG pathway analysis revealed significant enrichment for pathways including ribosome, oxidative phosphorylation and MAPK signaling (all Benjamini-Hochberg P<0.05). Whole blood mRNA expression changes observed in the microarray data were confirmed by quantitative RT-PCR. Transcription factor binding motif enrichment analysis revealed E2F1, ELK1, NF-kappaB, STAT1 and STAT3 significantly enriched after Bonferroni correction (all P<0.05). The results of the present study demonstrate that whole blood is a useful tissue for studying the metabolic syndrome and its underlying insulin resistance although the relationship between blood and skeletal muscle differs.

Women who start college in one of the natural or physical sciences leave in greater proportions than their male peers. The reasons for this difference are complex, and one possible contributing factor is the social environment women experience in the classroom. Using social network analysis, we explore how gender influences the confidence that college-level biology students have in each other’s mastery of biology. Results reveal that males are more likely than females to be named by peers as being knowledgeable about the course content. This effect increases as the term progresses, and persists even after controlling for class performance and outspokenness. The bias in nominations is specifically due to males over-nominating their male peers relative to their performance. The over-nomination of male peers is commensurate with an overestimation of male grades by 0.57 points on a 4 point grade scale, indicating a strong male bias among males when assessing their classmates. Females, in contrast, nominated equitably based on student performance rather than gender, suggesting they lacked gender biases in filling out these surveys. These trends persist across eleven surveys taken in three different iterations of the same Biology course. In every class, the most renowned students are always male. This favoring of males by peers could influence student self-confidence, and thus persistence in this STEM discipline.

Our previous studies show reduced abundance of the β-subunit of mitochondrial H+-ATP synthase (β-F1-ATPase) in skeletal muscle of obese individuals. The β-F1-ATPase forms the catalytic core of the ATP synthase, and it is critical for ATP production in muscle. The mechanism(s) impairing β-F1-ATPase metabolism in obesity, however, are not completely understood. First, we studied total muscle protein synthesis and the translation efficiency of β-F1-ATPase in obese (BMI, 36±1 kg/m²) and lean (BMI, 22±1 kg/m²) subjects. Both total protein synthesis (0.044±0.006 vs 0.066±0.006%·h^-1) and translation efficiency of β-F1-ATPase (0.0031±0.0007 vs 0.0073±0.0004) were lower in muscle from the obese subjects when compared to the lean controls (P<0.05). We then evaluated these same responses in a primary cell culture model, and tested the specific hypothesis that circulating non-esterified fatty acids (NEFA) in obesity play a role in the responses observed in humans. The findings on total protein synthesis and translation efficiency of β-F1-ATPase in primary myotubes cultured from a lean subject, and after exposure to NEFA extracted from serum of an obese subject, were similar to those obtained in humans. Among candidate microRNAs (i.e., non-coding RNAs regulating gene expression), we identified miR-127-5p in preventing the production of β-F1-ATPase. Muscle expression of miR-127-5p negatively correlated with β-F1-ATPase protein translation efficiency in humans (r = – 0.6744; P<0.01), and could be modeled in vitro by prolonged exposure of primary myotubes derived from the lean subject to NEFA extracted from the obese subject. On the other hand, locked nucleic acid inhibitor synthesized to target miR-127-5p significantly increased β-F1-ATPase translation efficiency in myotubes (0.6±0.1 vs 1.3±0.3, in control vs exposure to 50 nM inhibitor; P<0.05). Our experiments implicate circulating NEFA in obesity in suppressing muscle protein metabolism, and establish impaired β-F1-ATPase translation as an important consequence of obesity.

Background: A limitation of traditional outcome studies from behavioral interventions is the lack of attention given to evaluating the influence of moderating variables. This study examined possible moderation effect of baseline activity levels on physical activity change as a result of the Ready for Recess intervention.

Methods: Ready for Recess (August 2009-September 2010) was a controlled trial with twelve schools randomly assigned to one of four conditions: control group, staff supervision, equipment availability, and the combination of staff supervision and equipment availability. A total of 393 children (181 boys and 212 girls) from grades 3 through 6 (8–11 years old) were asked to wear an Actigraph monitor during school time on 4–5 days of the week. Assessments were conducted at baseline (before intervention) and post intervention (after intervention).

Results: Initial MVPA moderated the effect of Staff supervision (β = −0.47%; p < .05), but not Equipment alone and Staff + Equipment (p > .05). Participants in the Staff condition that were 1 standard deviation (SD) below the mean for baseline MVPA (classified as “low active”) had lower MVPA levels at post-intervention when compared with their low active peers in the control condition (Mean_diff = −10.8 ± 2.9%; p = .005). High active individuals (+1SD above the mean) in the Equipment treatment also had lower MVPA values at post-intervention when compared with their highly active peers in the control group (Mean_diff = −9.5 ± 2.9%; p = .009).

Conclusions: These results indicate that changes in MVPA levels at post-intervention were reduced in highly active participants when recess staff supervision was provided. In this study, initial MVPA moderated the effect of Staff supervision on children’s MVPA after 6 months of intervention. Staff training should include how to work with inactive youth but also how to assure that active children remain active.

Background: Obesity is a metabolic disease caused by environmental and genetic factors. However, the epigenetic mechanisms of obesity are incompletely understood. The aim of our study was to investigate the role of skeletal muscle DNA methylation in combination with transcriptomic changes in obesity.

Results: Muscle biopsies were obtained basally from lean (n = 12; BMI = 23.4 ± 0.7 kg/m[superscript 2]) and obese (n = 10; BMI = 32.9 ± 0.7 kg/m[superscript 2]) participants in combination with euglycemic-hyperinsulinemic clamps to assess insulin sensitivity. We performed reduced representation bisulfite sequencing (RRBS) next-generation methylation and microarray analyses on DNA and RNA isolated from vastus lateralis muscle biopsies. There were 13,130 differentially methylated cytosines (DMC; uncorrected P < 0.05) that were altered in the promoter and untranslated (5' and 3'UTR) regions in the obese versus lean analysis. Microarray analysis revealed 99 probes that were significantly (corrected P < 0.05) altered. Of these, 12 genes (encompassing 22 methylation sites) demonstrated a negative relationship between gene expression and DNA methylation. Specifically, sorbin and SH3 domain containing 3 (SORBS3) which codes for the adapter protein vinexin was significantly decreased in gene expression (fold change −1.9) and had nine DMCs that were significantly increased in methylation in obesity (methylation differences ranged from 5.0 to 24.4 %). Moreover, differentially methylated region (DMR) analysis identified a region in the 5'UTR (Chr.8:22,423,530–22,423,569) of SORBS3 that was increased in methylation by 11.2 % in the obese group. The negative relationship observed between DNA methylation and gene expression for SORBS3 was validated by a site-specific sequencing approach, pyrosequencing, and qRT-PCR. Additionally, we performed transcription factor binding analysis and identified a number of transcription factors whose binding to the differentially methylated sites or region may contribute to obesity.

Conclusions: These results demonstrate that obesity alters the epigenome through DNA methylation and highlights novel transcriptomic changes in SORBS3 in skeletal muscle.

Background: In the United States, approximately one in 110 pregnancies end in stillbirth affecting more than 26,000 women annually. Women experiencing stillbirth have a threefold greater risk of developing depressive symptoms compared to women experiencing live birth. Depression contributes negatively to health outcomes for both mothers and babies subsequent to stillbirth. Physical activity may improve depression in these women, however, little is known about acceptable physical activity interventions for women after stillbirth. This is the purpose of this descriptive exploratory study.

Methods: Eligible women were between ages 19 and 45, and experienced stillbirth within one year of the study. An online survey was used to ask questions related to 1) pregnancy and family information (i.e., time since stillbirth, weight gain during pregnancy, number of other children) 2) physical activity participation, 3) depressive symptomatology, and 4) demographics.

Results: One hundred seventy-five women participated in the study (M age = 31.26 ± 5.52). Women reported participating in regular physical activity (at least 150 minutes of moderate activity weekly) before (60%) and during (47%) their pregnancy, as well as after their stillbirth (61%). Only 37% were currently meeting physical activity recommendations. Approximately 88% reported depression (i.e., score of >10 on depression scale). When asked how women cope with depression, anxiety, or grief, 38% said physical activity. Of those that reported using physical activity to cope after stillbirth, they did so to help with depression (58%), weight loss (55%), and better overall physical health (52%). To cope with stillbirth, women used walking (67%), followed by jogging (35%), and yoga (23%). Women who participated in physical activity after stillbirth reported significantly lower depressive symptoms (M = 15.10, SD = 5.32) compared to women who did not participate in physical activity (M = 18.06, SD = 5.57; t = -3.45, p = .001).

Conclusions: Physical activity may serve as a unique opportunity to help women cope with the multiple mental sequelae after stillbirth. This study provides data to inform healthcare providers about the potential role of physical activity in bereavement and recovery for women who have experienced stillbirth. Additional research is necessary in this vulnerable population.

Background: Although the effect of the fat mass and obesity-associated (FTO) gene on adiposity is well established, there is a lack of evidence whether physical activity (PA) modifies the effect of FTO variants on obesity in Latino populations. Therefore, the purpose of this study was to examine PA influences and interactive effects between FTO variants and PA on measures of adiposity in Latinos.

Results: After controlling for age and sex, participants who did not engage in regular PA exhibited higher BMI, fat mass, HC, and WC with statistical significance (P < 0.001). Although significant associations between the three FTO genotypes and adiposity measures were found, none of the FTO genotype by PA interaction assessments revealed nominally significant associations. However, several of such interactive influences exhibited considerable trend towards association.

Conclusions: These data suggest that adiposity measures are associated with PA and FTO variants in Latinos, but the impact of their interactive influences on these obesity measures appear to be minimal. Future studies with large sample sizes may help to determine whether individuals with specific FTO variants exhibit differential responses to PA interventions.

Background: The transition to parenthood is consistently associated with declines in physical activity. In particular, working parents are at risk for inactivity, but research exploring physical activity barriers and facilitators in this population has been scarce. The purpose of this study was to qualitatively examine perceptions of physical activity among working parents.

Methods: Working mothers (n = 13) and fathers (n = 12) were recruited to participate in one of four focus group sessions and discuss physical activity barriers and facilitators. Data were analyzed using immersion/crystallization in NVivo 10.

Results: Major themes for barriers included family responsibilities, guilt, lack of support, scheduling constraints, and work. Major themes for facilitators included being active with children or during children’s activities, being a role model for children, making time/prioritizing, benefits to health and family, and having support available. Several gender differences emerged within each theme, but overall both mothers and fathers reported their priorities had shifted to focus on family after becoming parents, and those who were fitting in physical activity had developed strategies that allowed them to balance their household and occupational responsibilities.

Conclusions: The results of this study suggest working mothers and fathers report similar physical activity barriers and facilitators and would benefit from interventions that teach strategies for overcoming barriers and prioritizing physical activity amidst the demands of parenthood. Future interventions might consider targeting mothers and fathers in tandem to create an optimally supportive environment in the home.

The U.S. scientific research community does not reflect America's diversity. Hispanics, African Americans, and Native Americans made up 31% of the general population in 2010, but they represented only 18 and 7% of science, technology, engineering, and mathematics (STEM) bachelor's and doctoral degrees, respectively, and 6% of STEM faculty members (National Science Foundation [NSF], 2013). Equity in the scientific research community is important for a variety of reasons; a diverse community of researchers can minimize the negative influence of bias in scientific reasoning, because people from different backgrounds approach a problem from different perspectives and can raise awareness regarding biases (Intemann, 2009). Additionally, by failing to be attentive to equity, we may exclude some of the best and brightest scientific minds and limit the pool of possible scientists (Intemann, 2009). Given this need for equity, how can our scientific research community become more inclusive?