Sport Analytics: Using Open Source Logistic Regression Software to Classify Upcoming Play Type in the NFL

The purpose of this study was to utilize data analytics as means to classify National Football League offensive play types. The open source software R was employed to create a logistic regression based on data for the Cleveland Browns and Pittsburgh Steelers from 13 recent seasons. The regression is based on all first, second, and third downs within regulation play, totaling 26,310 data points. The initial algorithms classify rush or pass for each offense. Revealed through differing coefficients of the independent variables, each team shows a slightly different approach to play selections in response to in-game situations. Identifying the driving factors to play selection is possible by isolating each attribute within the regression. Further examination could yield improved precision to control for changes in head coach, offensive coordinators, player personnel and other factors such as weather because these may influence play type. Logistic regression shows promise as an in-game aid to determining opponent behavior. Specifically, Cleveland\u27s offensive play selection algorithm was correct for 66.4% of plays versus 66.9% for Pittsburgh. Use of open source software and logistic regression of NFL play selection could be beneficial in aiding future game decisions. Further research is recommended to explore possible improvement of the algorithm accuracy

Molecular Mechanisms of Vascular Disease in Patients with Rare Variants in MYH11

Thoracic aortic aneurysms and dissections (TAAD) are the primary disease affecting the thoracic ascending aorta, with an incidence rate of 10.4/100,000. Although about 20% of patients carry a mutation in a single gene that causes their disease, the remaining 80% of patients may also have genetic factors that increase their risk for developing TAAD. Many of the genes that predispose to TAAD encode proteins involved in smooth muscle cell (SMC) contraction and the disease-causing mutations are predicted to disrupt contractile function. SMCs are the predominant cell type in the ascending aortic wall. Mutations in MYH11, encoding the smooth muscle specific myosin heavy chain, are a rare cause of inherited TAAD. However, rare but recurrent non-synonymous variants in MYH11 are present in the general population but do not cause inherited TAAD. The goal of this study was to assess the potential role of these rare variants in vascular diseases. Two distinct variants were selected: the most commonly seen rare variant, MYH11 R247C, and a duplication of the chromosomal region spanning the MYH11 locus at 16p13.1. Genetic analyses indicated that both of these variants were significantly enriched in patients with TAAD compared with controls. A knock-in mouse model of the Myh11 R247C rare variant was generated, and these mice survive and reproduce normally. They have no structural abnormalities of the aorta or signs of aortic disease, but do have decreased aortic contractility. Myh11R247C/R247C mice also have increased proliferative response to vascular injury in vivo and increased proliferation of SMCs in vitro. Myh11R247C/R247C SMCs have decreased contractile gene and protein expression and are dedifferentiated. In fibroblasts, myosin force generation is required for maturation of focal adhesions, and enhancers of RhoA activity replace enhancers of Rac1 activity as maturation occurs. Consistent with these previous findings, focal adhesions are smaller in Myh11R247C/R247C SMCs, and there is decreased RhoA activation. A RhoA activator (CN03) rescues the dedifferentiated phenotype of Myh11R247C/R247C SMCs. Myh11R247C/R247C mice were bred with an existing murine model of aneurysm formation, the Acta2-/- mouse. Over time, mice carrying the R247C allele in conjunction with heterozygous or homozygous loss of Acta2 had significantly increased aortic diameter, and a more rapid accumulation of pathologic markers. These results suggest that the Myh11 R247C rare variant acts as a modifier gene increasing the risk for and severity of TAAD in mice. In patients with 16p13.1 duplications, aortic MYH11 expression is increased, but there is no corresponding increase in smooth muscle myosin heavy chain protein. Using SMCs that overexpress Myh11, we identified alterations in SMC phenotype leading to excessive protein turnover. All contractile proteins, not just myosin, are affected, and the proteins are turned over by autophagic degradation. Surprisingly, these cells are also more contractile compared with wild-type SMCs. The results described in this dissertation firmly establish that rare variants in MYH11 significantly affect the phenotype of SMCs. Further, the data suggests that these rare variants do increase the risk of TAAD via pathways involving altered SMC phenotype and contraction. Therefore, this study validates that these rare genetic variants alter vascular SMCs and provides model systems to explore the contribution of rare variants to disease

The ‘Nordstrom Tower’: a landmark daylight injury study

This paper describes a landmark daylight injury study whereby measures predicted using climate-based daylight modelling formed part of the legal agreement for the development of a skyscraper building in New York. Now known as the Nordstrom Tower, when completed in 2018 it will become the world’s tallest residential building. The evaluation was carried out in two stages: original design proposal in 2005, and the final design in 2013. The background/context for the study, and the daylight injury evaluations carried out at both stages are described. The potential implications of this unique study for planning guidelines are discussed

Preventing Cholesterol-Induced Perk (Protein Kinase RNA-Like Endoplasmic Reticulum Kinase) Signaling in Smooth Muscle Cells Blocks Atherosclerotic Plaque Formation

BACKGROUND: Vascular smooth muscle cells (SMCs) undergo complex phenotypic modulation with atherosclerotic plaque formation in hyperlipidemic mice, which is characterized by de-differentiation and heterogeneous increases in the expression of macrophage, fibroblast, osteogenic, and stem cell markers. An increase of cellular cholesterol in SMCs triggers similar phenotypic changes in vitro with exposure to free cholesterol due to cholesterol entering the endoplasmic reticulum, triggering endoplasmic reticulum stress and activating Perk (protein kinase RNA-like endoplasmic reticulum kinase) signaling. METHODS: We generated an SMC-specific RESULTS: SMC-specific deletion of Perk reduces atherosclerotic plaque formation in male hyperlipidemic mice by 80%. Single-cell transcriptomic data identify 2 clusters of modulated SMCs in hyperlipidemic mice, one of which is absent when CONCLUSIONS: Our results indicate that hypercholesterolemia drives both Perk-dependent and Perk-independent SMC modulation and that deficiency of Perk significantly blocks atherosclerotic plaque formation

Smooth muscle hyperplasia due to loss of smooth muscle α-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-β

Mutations in ACTA2, encoding the smooth muscle cell (SMC)-specific isoform of α-actin (α-SMA), cause thoracic aortic aneurysms and dissections and occlusive vascular diseases, including early onset coronary artery disease and stroke. We have shown that occlusive arterial lesions in patients with heterozygous ACTA2 missense mutations show increased numbers of medial or neointimal SMCs. The contribution of SMC hyperplasia to these vascular diseases and the pathways responsible for linking disruption of α-SMA filaments to hyperplasia are unknown. Here, we show that the loss of Acta2 in mice recapitulates the SMC hyperplasia observed in ACTA2 mutant SMCs and determine the cellular pathways responsible for SMC hyperplasia. Acta2−/− mice showed increased neointimal formation following vascular injury in vivo, and SMCs explanted from these mice demonstrated increased proliferation and migration. Loss of α-SMA induced hyperplasia through focal adhesion (FA) rearrangement, FA kinase activation, re-localization of p53 from the nucleus to the cytoplasm and increased expression and ligand-independent activation of platelet-derived growth factor receptor beta (Pdgfr-β). Disruption of α-SMA in wild-type SMCs also induced similar cellular changes. Imatinib mesylate inhibited Pdgfr-β activation and Acta2−/− SMC proliferation in vitro and neointimal formation with vascular injury in vivo. Loss of α-SMA leads to SMC hyperplasia in vivo and in vitro through a mechanism involving FAK, p53 and Pdgfr-β, supporting the hypothesis that SMC hyperplasia contributes to occlusive lesions in patients with ACTA2 missense mutation

From 3D landscape visualization to environmental simulation: The contribution of sound to the perception of virtual environments

This research investigated the perceptual interaction of combining sound with 3D landscape visualizations. Images sourced from Google Earth at St. James’s Park, London, UK, showing terrain only,terrain with built form or terrain with primarily vegetation were paired with four sound conditions using recordings from the park (i.e. ‘no sound’, anthropogenic, mechanical and natural). Perceived realism and preference were evaluated using a survey delivered via the Internet and in a controlled laboratory environment (N = 199 total). Analysis using repeated measures ANOVA indicated the interaction of sound and 3D visualizations significantly alters environmental perception both positively and negatively. Sounds and visuals that are congruent receive higher realism and preference ratings while the more incongruent the combination is, the lower the corresponding ratings. The lowest realism and preference ratings are given to visualizations showing terrain only combined with speech. The highest realism ratings overall correspond to visualization with built form combined with speech, and visualizations showing primarily vegetation paired with a birdcall. The absolute highest realism rating was for the visualization with primarily vegetation and some built form paired with speech, while the highest preference ratings correspond to visualizations showing vegetation paired with birdcall or no sound. Aural-visual data collected via the web-based survey was comparable to data collected in the laboratory and overall realism ratings for the Google Earth visualizations were low (e.g. below 3 on a 1–5 likert type scale). The results suggest there is an opportunity to increase experiential authenticity of 3D landscape visualizations with sound

The Politics of Race and Class and the Changing Spatial Fortunes of the McCarren Pool in Brooklyn, New York, 1936-2010

This paper explores the changing spatial properties of the McCarren Pool and connects them to the politics of race and class. The pool was a large liberal government project that sought to improve the leisure time of working class Brooklynites and between 1936 and the early 1970s it was a quasi-public functional space. In the 1970s and the early 1980s, the pool became a quasi-public dysfunctional space because the city government reduced its maintenance and staffing levels. Working class whites of the area engaged into neighborhood defense in order to prevent the influx of Latinos and African Americans into parts of Williamsburg and Greenpoint and this included the environs of the McCarren Pool. The pool was shut down in 1983 because of a mechanical failure. Its restoration did not take place because residents and storekeepers near the vicinity of the pool complained that by the 1970s, it was only African Americans and Latinos who patronized the pool and that their presence in the neighborhood undermined white exclusivity. For two decades, the McCarren Pool became a multi-use alternative space frequented by homeless people, graffiti artists, heroin users, teenagers, and drug dealers. Unlike previous decades, during this period, people of various racial and ethnic backgrounds frequented the pool area in a relatively harmonious manner. In the early part of the twenty-first century, a neoliberal city administration allowed a corporation to organize music concerts in the pool premises and promised to restore the facility into an operable swimming pool. The problem with this restoration project is that the history of the pool between the early 1970s and the early 2000s is downplayed and this does not serve well former or future users of the poo

Recurrent Chromosome 16p13.1 Duplications Are a Risk Factor for Aortic Dissections

Chromosomal deletions or reciprocal duplications of the 16p13.1 region have been implicated in a variety of neuropsychiatric disorders such as autism, schizophrenia, epilepsies, and attention-deficit hyperactivity disorder (ADHD). In this study, we investigated the association of recurrent genomic copy number variants (CNVs) with thoracic aortic aneurysms and dissections (TAAD). By using SNP arrays to screen and comparative genomic hybridization microarrays to validate, we identified 16p13.1 duplications in 8 out of 765 patients of European descent with adult-onset TAAD compared with 4 of 4,569 controls matched for ethnicity (P = 5.0×10−5, OR = 12.2). The findings were replicated in an independent cohort of 467 patients of European descent with TAAD (P = 0.005, OR = 14.7). Patients with 16p13.1 duplications were more likely to harbor a second rare CNV (P = 0.012) and to present with aortic dissections (P = 0.010) than patients without duplications. Duplications of 16p13.1 were identified in 2 of 130 patients with familial TAAD, but the duplications did not segregate with TAAD in the families. MYH11, a gene known to predispose to TAAD, lies in the duplicated region of 16p13.1, and increased MYH11 expression was found in aortic tissues from TAAD patients with 16p13.1 duplications compared with control aortas. These data suggest chromosome 16p13.1 duplications confer a risk for TAAD in addition to the established risk for neuropsychiatric disorders. It also indicates that recurrent CNVs may predispose to disorders involving more than one organ system, an observation critical to the understanding of the role of recurrent CNVs in human disease and a finding that may be common to other recurrent CNVs involving multiple genes

Suzanne Duchamp Does More Intelligent Things Than Paint

Suzanne Duchamp pushed the boundaries of painting by incorporating unorthodox, machine-made materials into interconnected pictorial geometries. This doctoral thesis focuses on her distinct way of combining modern elements with traditional media, situating her within dialogues on the readymade taking place between New York, Zurich, and Paris during the 1910s and 1920s. These exchanges involved a transatlantic group of artists, including her husband Jean Crotti, her older brother Marcel Duchamp, Elsa von Freytag-Loringhoven, Francis Picabia, Man Ray, Sophie Taeuber-Arp, and Beatrice Wood. While Duchamp has been summarily treated in the literature on Dada, there has been little concentrated attention devoted to her specific involvement with this avant-garde, or to her sustained artist practice. Suzanne Duchamp’s engagement ranged from correspondences with Marcel Duchamp while he was based in New York to in-person collaborations when many of these artists returned to Paris after World War I, especially Crotti, whom she married in 1919, and Picabia. This thesis is structured around four chapters focused on objects and materials that explore painting and the readymade, language and collage, dance and diagrams, and poetry and printed journals. By studying Suzanne Duchamp’s art as a body of work in its own right and in relationship to her peers, this thesis presents a richer understanding of her individual approach and sheds greater light on ideas she shared with other artists. By turning the spotlight to Suzanne Duchamp, and to her particular place within the history of Dada, renewed consideration can be given to broader conversations on readymades, language, and the shifting status of painting which were at the heart of the movement