ASU Scholarship Showcase

This study dealt with emotional responses elicited by certain products, which helped to understand the attributes of the product leading to emotional responses. Emotional Design is a way of design that is using emotions generated by people as reference and measurement. Making good use of emotional design could let the user discover resonance in the interaction between user and product, which could help the product to be more attractive to users. This research proposes to apply qualitative research method to uncover the secrets of emotional bonds between users and products This study also offered an useful tool to examine the strength and weakness of a certain product from perspective of emotion, and the insights could help designers to refine the product to become emotional attractive, thus create better user experience and bigger opportunity for the product on the market in the future.

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.

An urban forest assessment is essential for developing a baseline from which to measure changes and trends. The most precise way to assess urban forests is to measure and record every tree on a site, but although this may work well for relatively small populations (e.g., street trees, small parks), it is prohibitively expensive for large tree populations. Thus, random sampling offers a cost-effective way to assess urban forest structure and the associated ecosystem services for large-scale assessments. The methodology applied to assess ecosystem services in this study can also be used to assess the ecosystem services provided by vacant land in other urban contexts and improve urban forest policies, planning, and the management of vacant land. The study’s findings support the inclusion of trees on vacant land and contribute to a new vision of vacant land as a valuable ecological resource by demonstrating how green infrastructure can be used to enhance ecosystem health and promote a better quality of life for city residents.

Communicating climate risks is crucial when engaging the public to support climate action planning and addressing climate justice. How does evidence-based communication influence local residents’ risk perception and potential behavior change in support of climate planning? Built upon our previous study of Climate Justice maps illustrating high scores of both social and ecological vulnerability in Michigan’s Huron River watershed, USA, a quasi-experiment was conducted to examine the effects of Climate Justice mapping intervention on residents’ perceptions and preparedness for climate change associated hazards in Michigan. Two groups were compared: residents in Climate Justice areas with high social and ecological vulnerability scores in the watershed (n=76) and residents in comparison areas in Michigan (n=69). Measurements for risk perception include perceived exposure, sensitivity, and adaptability to hazards. Results indicate that risk information has a significant effect on perceived sensitivity and level of preparedness for future climate extremes among participants living in Climate Justice areas. Findings highlight the value of integrating scientific risk assessment information in risk communication to align calculated and perceived risks. This study suggests effective risk communication can influence local support of climate action plans and implementation of strategies that address climate justice and achieve social sustainability in local communities.

Background: Although principles based in motor learning, rehabilitation, and human-computer interfaces can guide the design of effective interactive systems for rehabilitation, a unified approach that connects these key principles into an integrated design, and can form a methodology that can be generalized to interactive stroke rehabilitation, is presently unavailable.

Results: This paper integrates phenomenological approaches to interaction and embodied knowledge with rehabilitation practices and theories to achieve the basis for a methodology that can support effective adaptive, interactive rehabilitation. Our resulting methodology provides guidelines for the development of an action representation, quantification of action, and the design of interactive feedback. As Part I of a two-part series, this paper presents key principles of the unified approach. Part II then describes the application of this approach within the implementation of the Adaptive Mixed Reality Rehabilitation (AMRR) system for stroke rehabilitation.

Conclusions: The accompanying principles for composing novel mixed reality environments for stroke rehabilitation can advance the design and implementation of effective mixed reality systems for the clinical setting, and ultimately be adapted for home-based application. They furthermore can be applied to other rehabilitation needs beyond stroke.

Background: Few existing interactive rehabilitation systems can effectively communicate multiple aspects of movement performance simultaneously, in a manner that appropriately adapts across various training scenarios. In order to address the need for such systems within stroke rehabilitation training, a unified approach for designing interactive systems for upper limb rehabilitation of stroke survivors has been developed and applied for the implementation of an Adaptive Mixed Reality Rehabilitation (AMRR) System.

Results: The AMRR system provides computational evaluation and multimedia feedback for the upper limb rehabilitation of stroke survivors. A participant's movements are tracked by motion capture technology and evaluated by computational means. The resulting data are used to generate interactive media-based feedback that communicates to the participant detailed, intuitive evaluations of his performance. This article describes how the AMRR system's interactive feedback is designed to address specific movement challenges faced by stroke survivors. Multimedia examples are provided to illustrate each feedback component. Supportive data are provided for three participants of varying impairment levels to demonstrate the system's ability to train both targeted and integrated aspects of movement.

Conclusions: The AMRR system supports training of multiple movement aspects together or in isolation, within adaptable sequences, through cohesive feedback that is based on formalized compositional design principles. From preliminary analysis of the data, we infer that the system's ability to train multiple foci together or in isolation in adaptable sequences, utilizing appropriately designed feedback, can lead to functional improvement. The evaluation and feedback frameworks established within the AMRR system will be applied to the development of a novel home-based system to provide an engaging yet low-cost extension of training for longer periods of time.

Type 2 diabetes (T2D) is a complex metabolic disease that is more prevalent in ethnic groups such as Mexican Americans, and is strongly associated with the risk factors obesity and insulin resistance. The goal of this study was to perform whole genome gene expression profiling in adipose tissue to detect common patterns of gene regulation associated with obesity and insulin resistance. We used phenotypic and genotypic data from 308 Mexican American participants from the Veterans Administration Genetic Epidemiology Study (VAGES). Basal fasting RNA was extracted from adipose tissue biopsies from a subset of 75 unrelated individuals, and gene expression data generated on the Illumina BeadArray platform. The number of gene probes with significant expression above baseline was approximately 31,000. We performed multiple regression analysis of all probes with 15 metabolic traits. Adipose tissue had 3,012 genes significantly associated with the traits of interest (false discovery rate, FDR ≤ 0.05). The significance of gene expression changes was used to select 52 genes with significant (FDR ≤ 10^-4) gene expression changes across multiple traits. Gene sets/Pathways analysis identified one gene, alcohol dehydrogenase 1B (ADH1B) that was significantly enriched (P < 10^-60) as a prime candidate for involvement in multiple relevant metabolic pathways. Illumina BeadChip derived ADH1B expression data was consistent with quantitative real time PCR data. We observed significant inverse correlations with waist circumference (2.8 x 10[superscript -9]), BMI (5.4 x 10^-6), and fasting plasma insulin (P < 0.001). These findings are consistent with a central role for ADH1B in obesity and insulin resistance and provide evidence for a novel genetic regulatory mechanism for human metabolic diseases related to these traits.

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: 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: 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.