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Abstract This “work in progress” paper describes a multiyear project to study the development of engineering identity in a chemical and biological engineering program at Montana State University. The project focuses on how engineering identity may be impacted by a series of interventions utilizing subject material in a senior-level capstone design course and has the senior capstone design students serve as peer-mentors to first- and second-year students. A more rapid development of an engineering identity by first- and second-year students is suspected to increase retention and persistence in this engineering program. Through a series of timed interventions scheduled to take place in the first and second year, which includes cohorts that will serve as negative controls (no intervention), we hope to ascertain the following: (1) the extent to which, relative to a control group, exposure to a peer mentor increases a students’ engineering identity development over time compared to those who do not receive peer mentoring and (2) if the quantity and/or timing of the peer interactions impact engineering identity development. While the project includes interventions for both first- and second-year students, this work in progress paper focuses on the experiences of first year freshman as a result of the interventions and their development of an engineering identity over the course of the semester. Early in the fall semester, freshman chemical engineering students enrolled in an introductory chemical engineering course and senior students in a capstone design course were administered a survey which contained a validated instrument to assess engineering identity. The first-year course has 107 students and the senior-level course has 92 students and approximately 50% of the students in both cohorts completed the survey. Mid-semester, after the first-year students were introduced to the concepts of process flow diagrams and material balances in their course, senior design student teams gave presentations about their capstone design projects in the introductory course. The presentations focused on the project goals, design process and highlighted the process flow diagrams. After the presentations, freshman and senior students attended small group dinners as part of a homework assignment wherein the senior students were directed to communicate information about their design projects as well as share their experiences in the chemical engineering program. Dinners occurred overall several days, with up to ten freshman and five seniors attending each event. Freshman students were encouraged to use this time to discover more about the major, inquire about future course work, and learn about ways to enrich their educational experience through extracurricular and co-curricular activities. Several weeks after the dinner experience, senior students returned to give additional presentations to the freshman students to focus on the environmental and societal impacts of their design projects. We report baseline engineering identity in this paper. 

Glioblastoma ranks among the most lethal of primary brain malignancies, with glioblastoma stem cells (GSCs) at the apex of tumor cellular hierarchies. Here, to discover novel therapeutic GSC targets, we interrogated gene expression profiles from GSCs, differentiated glioblastoma cells (DGCs), and neural stem cells (NSCs), revealing EYA2 as preferentially expressed by GSCs. Targeting EYA2 impaired GSC maintenance and induced cell cycle arrest, apoptosis, and loss of self-renewal. EYA2 displayed novel localization to centrosomes in GSCs, and EYA2 tyrosine (Tyr) phosphatase activity was essential for proper mitotic spindle assembly and survival of GSCs. Inhibition of the EYA2 Tyr phosphatase activity, via genetic or pharmacological means, mimicked EYA2 loss in GSCs in vitro and extended the survival of tumor-bearing mice. Supporting the clinical relevance of these findings, EYA2 portends poor patient prognosis in glioblastoma. Collectively, our data indicate that EYA2 phosphatase function plays selective critical roles in the growth and survival of GSCs, potentially offering a high therapeutic index for EYA2 inhibitors. 

Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors activate cell death and confer disease resistance by unknown mechanisms. We demonstrate that plant Toll/interleukin-1 receptor (TIR) domains of NLRs are enzymes capable of degrading nicotinamide adenine dinucleotide in its oxidized form (NAD + ). Both cell death induction and NAD + cleavage activity of plant TIR domains require known self-association interfaces and a putative catalytic glutamic acid that is conserved in both bacterial TIR NAD + -cleaving enzymes (NADases) and the mammalian SARM1 (sterile alpha and TIR motif containing 1) NADase. We identify a variant of cyclic adenosine diphosphate ribose as a biomarker of TIR enzymatic activity. TIR enzymatic activity is induced by pathogen recognition and functions upstream of the genes enhanced disease susceptibility 1 ( EDS1 ) and N requirement gene 1 ( NRG1 ), which encode regulators required for TIR immune function. Thus, plant TIR-NLR receptors require NADase function to transduce recognition of pathogens into a cell death response.