Numerical simulation of a flat back airfoil for wind turbine applications.

Wind energy provides an attractive power source as an alternative to fossil fuels because it is abundant, clean, and produces no harmful emissions. To extract more energy from the wind we need to increase the wind turbine size. However, the increase in size has begun to reach a limit in terms of material composition and structural stability. To quell the trend of increasing size in wind power systems alternative wind turbine blade designs are investigated and evaluated to increase power production and efficiency of present size machines. Flat back airfoils have been proposed for the inboard region of large wind turbine blades because they provide structural and aerodynamic advantages. In this work we will investigate the aerodynamic performance of flat back airfoils with computational fluid dynamics techniques. To reduce the drag and noise inherent from the blunt trailing edge, a splitter plate with varying lengths is added to the trailing edge of the airfoils. Comparisons are made with experimental data. Excellent agreement is achieved with the measurements. Our numerical simulations show that the flat back airfoil can increase lift production as much as 20%. The splitter can effectively reduce drag by as much as 20% and tonal noise by as much as 20 dB

A History of Financial Aid to Students

The history of financial aid in higher education covers a board range of philanthropic-, scholarship-, and loan-based approaches. This article comprehensively covers the history of American financial aid to students from influences of European medieval institutions to contemporary aid systems. A broad history of financial aid is covered, revealing an evolution from a system primarily based upon local philanthropic efforts, to a more formal system of scholarships and grants, to, finally, a complex federal system of loans. As the history of financial aid is chronologically covered, attention is paid to describing how financial aid policies and practices were a response to societal and political contexts of their times and how need- and merit-based philosophies have given way to political agenda-based philosophies of aid

Tap the Screen: Technology Integration in Our Students’ Lives

The focus of this study is to document and describe the integration of technology in the everyday lives of students in Grades 3–8 attending a high-performing public school district in an affluent Chicago suburb. The following research questions guide this study: How do students in Grades 3–8 integrate technology into their lives? What are the implications of students’ technology integration for teaching and learning? How can teachers capitalize upon students’ technology integration in ways that inform instructional practice? A review of the literature presents related information in areas that explore the increasingly digital world of our students; curriculum, instruction, and research; innovation, creativity, and learning environments; student social and cognitive development; and student technology use. In this ethnographic study, qualitative research methods are used to interview 55 students in 17 focus groups. An analysis of focus group data is presented in the following categories: technology device access and use; gaming; electronic book readers; television and online video; imposed limits on technology; communicating using technology; and technology in the school environment. Student technology use information is presented in the student voice and is then discussed in the context of improving teaching and learning. This study recommends that both parents and teachers should intentionally seek to understand the technology-enabled pursuits of children to better understand the “whole child.” Further, teachers and other school leaders are encouraged to welcome student-owned technology in school and encourage project-based learning opportunities

Slide to Unlock: Creating a Technology-Integrated Environment for Our Students

The focus of this study is to explore how to support teachers in capitalizing on students’ technology skills, experiences, and preferences to offer enhanced teaching and learning experiences in school. Using a framework developed by Wagner et al. (2006), technology integration is systemically examined in terms of “4 Cs:” context, culture, conditions, and competencies to construct an “As-Is” picture of a school district based upon current realities. Next, a series of changes are proposed and the 4 Cs are used to describe the “To-Be” picture of the organization at the end of the proposed change journey. The three teachers who participated in this study used a protocol developed by the researcher with over 150 students that allowed the teachers to learn about their students’ technology skills, experiences, and preferences both in and outside of school. Information from the survey data was used by the researcher and participating teachers to co-plan technology-integrated projects that matched the students’ technology skills, experiences, and preferences. An analysis of the student projects and teacher interview data resulted in a set of eight strategies for educators, Creating a Technology-Integrated Environment for Our Students, presented in two themes. Theme one offers, Provide Technology-Integrated Student Learning Opportunities: (1) engage students by allowing choices; (2) share learning experiences (student-to-student; student-to-teacher); (3) create with digital tools, learn outside of school, and simplify learning experiences; and (4) practice student-centered assessment. Theme two offers, Provide a Technology- Integrated Environment: (5) seek student opinions and match tools with student interests; (6) build capacity in the classroom; (7) provide models for all teachers; and (8) allow students to take the lead

Examining the dissociative basis for body image disturbances

Although dissociative symptoms have been linked with both food- and appearance-related aspects of eating disorders, the psychological mechanisms underlying these relationships remain unclear. The present study evaluated the hypothesis that the disturbances of self-identity attributed to dissociation can manifest as disturbances of body image and, in turn, undermine body-specific self-evaluations relevant to disordered eating (i.e., body comparison, body dissatisfaction, and internalization of the thin ideal). Ninety-three female university students completed self-report measures of dissociation and body-related aspects of disordered eating. In addition, the method of constant stimuli was used to experimentally derive three measures of body image disturbance: (1) accuracy of body size estimations (body image distortion), (2) ability to discriminate between different body sizes (body image sensitivity), and (3) consistency in one&rsquo;s body size estimations (body image variability). The findings show that dissociation is related to symptoms of disordered eating, and that these relationships may be mediated by body image instability. Collectively, these findings support the notion that the body image attitudes and behaviours that characterize eating disorders may derive from proprioceptive deficits due to dissociation.<br /

Isometric tuples are hyperreflexive

An $n$-tuple of operators $(V_1,...,V_n)$ acting on a Hilbert space $H$ is said to be isometric if the row operator $(V_1,...,V_n) : H^n \to H$ is an isometry. We prove that every isometric $n$-tuple is hyperreflexive, in the sense of Arveson. For $n = 1$, the hyperreflexivity constant is at most 95. For $n \geq 2$, the hyperreflexivity constant is at most 6.Comment: 11 page

The Parvovirus Minute Virus of Mice modulates the DNA damage response to facilitate viral replication and a pre-mitotic cell cycle block /

The DNA damage response (DDR) is a critical cellular network that affords cells the ability to repair DNA damage they have incurred from endogenous and exogenous sources. Recently, it has become appreciated that viruses, both DNA and RNA, can induce the DDR and have evolved the ability to interact with this ancient antiviral mechanism. Viruses can choose to inactivate or utilize this host response, which typically requires specific modulation for either case. Importantly, it has been shown that MVM utilizes this response to facilitate its replication in an ATM-dependent manner. MVM induces a DDR-dependent pre-mitotic, G2/M cell cycle block via activation of the checkpoint kinase, Chk2, and depletion of the RNA and protein of the key mitotic cyclin, cyclin B1. Unexpectedly, this cell cycle block was shown to be p21- and Chk1-independent. MVM infection results in the recruitment and activation of numerous DDR proteins including Chk2, RPA32 and p53. Upon activation, via phosphorylation, p53, a critical tumor suppressor, is known to transactivate several hundred genes including the well-characterized CDK inhibitor, p21. However, previous work demonstrated a sustained, proteasome-dependent loss of p21 during infection, which was required for efficient replication. This depletion of p21 during infection was unexpected, given the activation of p53 during infection, and because p21 is a known, potent cell cycle inhibitor. We investigated the loss of p21 during infection and found that siRNA knockdown of specific components of the CRL4Cdt2 E3 ubiquitin ligaseCul4A, DDB1 and Cdt2stabilized p21 during MVM infection. Importantly, siRNA knockdown of specific components of CRL4Cdt2 reduced viral replication. DDB1 and Cdt2, the adapter protein and substrate recognition factor of the CRL4Cdt2, respectively, were recruited to viral replication factories, termed autonomous parvovirus-associated replication (APAR) bodies, suggesting that MVM may be hijacking this important E3 ubiquitin ligase. The recruitment and utilization of this ligase is likely specific, as the APC/CCDC20 E3 ubiquitin ligase, which also targets p21 for proteasome-dependent degradation, was not recruited to APAR bodies nor did siRNA knockdown of specific components of this ligase stabilize p21 during infection. Taken together, these results suggest that MVM specifically utilizes the CRL4Cdt2 E3 ubiquitin ligase to target p21 for degradation and that the activity of this E3 ubiquitin ligase is required for efficient MVM replication. The requirements for the activity of CRL4Cdt2 gave us a hint as to why MVM would target p21 for degradation. It has been shown that CRL4Cdt2 activity requires interaction with PCNA, a DNA polymerase d cofactor, and chromatin. Importantly, p21 is an inhibitor of PCNA activity. As PCNA and DNA polymerase d are known to be required for parvoviral rolling hairpin replication, we hypothesized that MVM must target p21 for depletion to allow for PCNA activity, which is required for viral replication. p21 mutants that were unable to interact with either CRL4Cdt2 or PCNA were stable during MVM infection, suggesting that p21 needed to interact with both the E3 ubiquitin ligase and PCNA for degradation during MVM infection. We next constructed p21 mutants that were resistant to ubiquitination, by mutating the seven lysine residues in p21 to arginine, and maintained or lost their ability to interact with PCNA. Importantly, a stable p21 mutant that interacted with PCNA resulted in the significant depletion of MVM replication whereas a stable p21 mutant that no longer interacted with PCNA had no effect on replication. Taken together, this data suggests that MVM co-opts a cellular E3 ubiquitin ligase to target the CDK inhibitor p21 for degradation, which is required to allow the PCNA activity that MVM needs for efficient replication. To induce a pre-mitotic G2/M cell cycle block, MVM depletes the key mitotic cyclin, cyclin B1, which is preceded by the loss of its encoding RNA. We next sought to determine how MVM programs the depletion of cyclin B1 RNA. Initial studies indicated a loss of cyclin B1 RNA between 18 and 24 hours post-infection in a NS2-independent manner. This loss of RNA and protein was seen in both human and murine cells lines, suggesting that programming the depletion of cyclin B1 is a critical hallmark of MVM infection. Interestingly, the viral mechanism which targets cyclin B1 could overcome the effects of an exogenous DNA damaging agent known to induce cyclin B1 levels. The stability of cyclin B1 RNA during MVM infection is comparable to doxorubicin-treated cells, while the production of nascent cyclin B1 RNA is substantially depleted. Importantly, the chromatin landscape of the cyclin B1 promoter during MVM infection was consistent with an open conformation, yet significantly lower levels of RNA polymerase II (RNA pol II) were found to occupy the cyclin B1 gene. The NF-Y transcription factor and B-myb, a component of MuvB-B-Myb (MMB) complex, were both found to bind the cyclin B1 promoter during infection. However, the key G2/M transcription factor, FoxM1, was found to occupy the cyclin B1 promoter at significantly lower levels in MVM infected cells compared to mock- or doxorubicin-treated cells. FoxM1, which requires hyperphosphorylation to activate its transcriptional activity, was found to have lower levels of phosphorylation during MVM infection, compared to mock- or doxorubicin-treated cells. Reconstitution of FoxM1 to the cyclin B1 promoter, via catalytically inactive Cas9 fused to the FoxM1 transactivation domain, upregulated cyclin B1 RNA and protein during MVM infection. Taken together, these results suggest that MVM prevents the activation and binding of the critical transcription factor FoxM1 to the cyclin B1 promoter, thereby reducing RNA pol II transcriptional activity and the production of nascent cyclin B1 RNA and its encoded protein, ultimately facilitating establishment of a pre-mitotic G2/M block. An important RNA-binding protein, HuR, known to regulate two cyclins important for MVM infection, cyclin A and cyclin B1, was also investigated. We observed the predominantly nuclear HuR was heavily relocalized to the cytoplasm during MVM infection. Ectopic expression of NS1, but not NS2, resulted in the cytoplasmic relocalization of HuR in a Crm1-independent manner. Importantly, siRNA knockdown of HuR during MVM infection resulted in a further reduction of cyclin B1 protein, but not cyclin B1 RNA. This data suggested that HuR may promote the translation of specific RNAs during MVM infection. HuR was also shown to bind MVM RNA. While more work needs to be undertaken to fully understand the ramifications of this interaction, HuR is likely to be an important regulator of MVM RNA stability or translation. Taken together, these observations suggest that MVM expertly modulates the DDR and other components of the cellular machinery to ensure an environment conducive to facilitation of viral replication. To establish this environment, MVM targets several core cellular mechanisms including proteasome-mediated protein degradation, RNA transcription, RNA translation and subcellular localization of cellular proteins.David J. Pintel, Dissertation Supervisor.|Includes vita.Includes bibliographical references (pages 178-209)