ASU Scholarship Showcase

The estimation of energy demand (by power plants) has traditionally relied on historical energy use data for the region(s) that a plant produces for. Regression analysis, artificial neural network and Bayesian theory are the most common approaches for analysing these data. Such data and techniques do not generate reliable results. Consequently, excess energy has to be generated to prevent blackout; causes for energy surge are not easily determined; and potential energy use reduction from energy efficiency solutions is usually not translated into actual energy use reduction. The paper highlights the weaknesses of traditional techniques, and lays out a framework to improve the prediction of energy demand by combining energy use models of equipment, physical systems and buildings, with the proposed data mining algorithms for reverse engineering. The research team first analyses data samples from large complex energy data, and then, presents a set of computationally efficient data mining algorithms for reverse engineering. In order to develop a structural system model for reverse engineering, two focus groups are developed that has direct relation with cause and effect variables. The research findings of this paper includes testing out different sets of reverse engineering algorithms, understand their output patterns and modify algorithms to elevate accuracy of the outputs.

Small and medium office buildings consume a significant parcel of the U.S. building stock energy consumption. Still, owners lack resources and experience to conduct detailed energy audits and retrofit analysis. We present an eight-steps framework for an energy retrofit assessment in small and medium office buildings. Through a bottom-up approach and a web-based retrofit toolkit tested on a case study in Arizona, this methodology was able to save about 50% of the total energy consumed by the case study building, depending on the adopted measures and invested capital. While the case study presented is a deep energy retrofit, the proposed framework is effective in guiding the decision-making process that precedes any energy retrofit, deep or light.

Commercial buildings’ consumption is driven by multiple factors that include occupancy, system and equipment efficiency, thermal heat transfer, equipment plug loads, maintenance and operational procedures, and outdoor and indoor temperatures. A modern building energy system can be viewed as a complex dynamical system that is interconnected and influenced by external and internal factors. Modern large scale sensor measures some physical signals to monitor real-time system behaviors. Such data has the potentials to detect anomalies, identify consumption patterns, and analyze peak loads. The paper proposes a novel method to detect hidden anomalies in commercial building energy consumption system. The framework is based on Hilbert-Huang transform and instantaneous frequency analysis. The objectives are to develop an automated data pre-processing system that can detect anomalies and provide solutions with real-time consumption database using Ensemble Empirical Mode Decomposition (EEMD) method. The finding of this paper will also include the comparisons of Empirical mode decomposition and Ensemble empirical mode decomposition of three important type of institutional buildings.

There are many data mining and machine learning techniques to manage large sets of complex energy supply and demand data for building, organization and city. As the amount of data continues to grow, new data analysis methods are needed to address the increasing complexity. Using data from the energy loss between the supply (energy production sources) and demand (buildings and cities consumption), this paper proposes a Semi-Supervised Energy Model (SSEM) to analyse different loss factors for a building cluster. This is done by deep machine learning by training machines to semi-supervise the learning, understanding and manage the process of energy losses. Semi-Supervised Energy Model (SSEM) aims at understanding the demand-supply characteristics of a building cluster and utilizes the confident unlabelled data (loss factors) using deep machine learning techniques. The research findings involves sample data from one of the university campuses and presents the output, which provides an estimate of losses that can be reduced. The paper also provides a list of loss factors that contributes to the total losses and suggests a threshold value for each loss factor, which is determined through real time experiments. The conclusion of this paper provides a proposed energy model that can provide accurate numbers on energy demand, which in turn helps the suppliers to adopt such a model to optimize their supply strategies.

Background: The discovery of genetic associations is an important factor in the understanding of human illness to derive disease pathways. Identifying multiple interacting genetic mutations associated with disease remains challenging in studying the etiology of complex diseases. And although recently new single nucleotide polymorphisms (SNPs) at genes implicated in immune response, cholesterol/lipid metabolism, and cell membrane processes have been confirmed by genome-wide association studies (GWAS) to be associated with late-onset Alzheimer's disease (LOAD), a percentage of AD heritability continues to be unexplained. We try to find other genetic variants that may influence LOAD risk utilizing data mining methods.

Methods: Two different approaches were devised to select SNPs associated with LOAD in a publicly available GWAS data set consisting of three cohorts. In both approaches, single-locus analysis (logistic regression) was conducted to filter the data with a less conservative p-value than the Bonferroni threshold; this resulted in a subset of SNPs used next in multi-locus analysis (random forest (RF)). In the second approach, we took into account prior biological knowledge, and performed sample stratification and linkage disequilibrium (LD) in addition to logistic regression analysis to preselect loci to input into the RF classifier construction step.

Results: The first approach gave 199 SNPs mostly associated with genes in calcium signaling, cell adhesion, endocytosis, immune response, and synaptic function. These SNPs together with APOE and GAB2 SNPs formed a predictive subset for LOAD status with an average error of 9.8% using 10-fold cross validation (CV) in RF modeling. Nineteen variants in LD with ST5, TRPC1, ATG10, ANO3, NDUFA12, and NISCH respectively, genes linked directly or indirectly with neurobiology, were identified with the second approach. These variants were part of a model that included APOE and GAB2 SNPs to predict LOAD risk which produced a 10-fold CV average error of 17.5% in the classification modeling.

Conclusions: With the two proposed approaches, we identified a large subset of SNPs in genes mostly clustered around specific pathways/functions and a smaller set of SNPs, within or in proximity to five genes not previously reported, that may be relevant for the prediction/understanding of AD.

Background: Glioblastoma is the most aggressive primary central nervous tumor and carries a very poor prognosis. Invasion precludes effective treatment and virtually assures tumor recurrence. In the current study, we applied analytical and bioinformatics approaches to identify a set of microRNAs (miRs) from several different human glioblastoma cell lines that exhibit significant differential expression between migratory (edge) and migration-restricted (core) cell populations. The hypothesis of the study is that differential expression of miRs provides an epigenetic mechanism to drive cell migration and invasion.

Results: Our research data comprise gene expression values for a set of 805 human miRs collected from matched pairs of migratory and migration-restricted cell populations from seven different glioblastoma cell lines. We identified 62 down-regulated and 2 up-regulated miRs that exhibit significant differential expression in the migratory (edge) cell population compared to matched migration-restricted (core) cells. We then conducted target prediction and pathway enrichment analysis with these miRs to investigate potential associated gene and pathway targets. Several miRs in the list appear to directly target apoptosis related genes. The analysis identifies a set of genes that are predicted by 3 different algorithms, further emphasizing the potential validity of these miRs to promote glioblastoma.

Conclusions: The results of this study identify a set of miRs with potential for decreased expression in invasive glioblastoma cells. The verification of these miRs and their associated targeted proteins provides new insights for further investigation into therapeutic interventions. The methodological approaches employed here could be applied to the study of other diseases to provide biomedical researchers and clinicians with increased opportunities for therapeutic interventions.

Introduction: Abundance of immune cells has been shown to have prognostic and predictive significance in many tumor types. Beyond abundance, the spatial organization of immune cells in relation to cancer cells may also have significant functional and clinical implications. However there is a lack of systematic methods to quantify spatial associations between immune and cancer cells.

Methods: We applied ecological measures of species interactions to digital pathology images for investigating the spatial associations of immune and cancer cells in breast cancer. We used the Morisita-Horn similarity index, an ecological measure of community structure and predator–prey interactions, to quantify the extent to which cancer cells and immune cells colocalize in whole-tumor histology sections. We related this index to disease-specific survival of 486 women with breast cancer and validated our findings in a set of 516 patients from different hospitals.

Results: Colocalization of immune cells with cancer cells was significantly associated with a disease-specific survival benefit for all breast cancers combined. In HER2-positive subtypes, the prognostic value of immune-cancer cell colocalization was highly significant and exceeded those of known clinical variables. Furthermore, colocalization was a significant predictive factor for long-term outcome following chemotherapy and radiotherapy in HER2 and Luminal A subtypes, independent of and stronger than all known clinical variables.

Conclusions: Our study demonstrates how ecological methods applied to the tumor microenvironment using routine histology can provide reproducible, quantitative biomarkers for identifying high-risk breast cancer patients. We found that the clinical value of immune-cancer interaction patterns is highly subtype-specific but substantial and independent to known clinicopathologic variables that mostly focused on cancer itself. Our approach can be developed into computer-assisted prediction based on histology samples that are already routinely collected.

In a meta-analysis published by myself and co-authors, we report differences in the life history risk factors for estrogen receptor negative (ER−) and estrogen receptor positive (ER+) breast cancers. Our meta-analysis did not find the association of ER− breast cancer risk with fast life history characteristics that Hidaka and Boddy suggest in their response to our article. There are a number of possible explanations for the differences between their conclusions and the conclusions we drew from our meta-analysis, including limitations of our meta-analysis and methodological challenges in measuring and categorizing estrogen receptor status. These challenges, along with the association of ER+ breast cancer with slow life history characteristics, may make it challenging to find a clear signal of ER− breast cancer with fast life history characteristics, even if that relationship does exist. The contradictory results regarding breast cancer risk and life history characteristics illustrate a more general challenge in evolutionary medicine: often different sub-theories in evolutionary biology make contradictory predictions about disease risk. In this case, life history models predict that breast cancer risk should increase with faster life history characteristics, while the evolutionary mismatch hypothesis predicts that breast cancer risk should increase with delayed reproduction. Whether life history tradeoffs contribute to ER− breast cancer is still an open question, but current models and several lines of evidence suggest that it is a possibility.

It has long been accepted that modern reproductive patterns are likely contributors to breast cancer susceptibility because of their influence on hormones such as estrogen and the importance of these hormones in breast cancer. We conducted a meta-analysis to assess whether this ‘evolutionary mismatch hypothesis’ can explain susceptibility to both estrogen receptor positive (ER-positive) and estrogen receptor negative (ER-negative) cancer. Our meta-analysis includes a total of 33 studies and examines parity, age of first birth and age of menarche broken down by estrogen receptor status. We found that modern reproductive patterns are more closely linked to ER-positive than ER-negative breast cancer. Thus, the evolutionary mismatch hypothesis for breast cancer can account for ER-positive breast cancer susceptibility but not ER-negative breast cancer.

Cancer therapy selects for cancer cells resistant to treatment, a process that is fundamentally evolutionary. To what extent, however, is the evolutionary perspective employed in research on therapeutic resistance and relapse? We analyzed 6,228 papers on therapeutic resistance and/or relapse in cancers and found that the use of evolution terms in abstracts has remained at about 1% since the 1980s. However, detailed coding of 22 recent papers revealed a higher proportion of papers using evolutionary methods or evolutionary theory, although this number is still less than 10%. Despite the fact that relapse and therapeutic resistance is essentially an evolutionary process, it appears that this framework has not permeated research. This represents an unrealized opportunity for advances in research on therapeutic resistance.