Lost Ground: Neoliberalism, Charter Schools, and the End of Desegregation in St. Louis, Missouri

During the final decades of the twentieth century, U.S. urban education policy experienced a sea change in its orientation toward equity. Mid-century social liberalism and its programs for expanding access to public education resources through desegregation and more equitable funding gave way to neoliberal reforms focused on improving outcomes through deregulation, accountability regimes, and market discipline. Charter schools are the vanguard of neoliberal education reform. While much of the research on charters aims at either substantiating or critiquing their success claims relative to traditional public schools, in this dissertation, I examine the role of charter schools within the larger processes of urbanization. Specifically, I focus on St. Louis, Missouri, where, in 1998, a single piece of education reform legislation (Senate Bill 781) legalized charter schools and set an end for the largest and longest-running school desegregation program in U.S. history. Rather than legalize charters statewide, SB 781 restricted them to St. Louis and Kansas City, Missouri’s only two metropolitan areas to have operated court-enforced desegregation programs. Combining critical policy analysis and economic geography, I link both desegregation and charter schools to urban neoliberalization, arguing that racialized processes of accumulation structured (and continue to structure) uneven development in such a way to make educational equity-based reforms necessary and their failures inevitable. Here too, St. Louis has an important story to tell. With deindustrialization and suburbanization resulting in a 63 percent decline in population in just over 60 years, St. Louis, like many other Rust Belt cities, has wholly embraced neoliberalism’s entrepreneurial ethos. Through public-private partnerships and a portfolio of tax incentives, St. Louis has sacrificed public education in its efforts to attract capital back to the city. Rather than mitigating these issues, the neoliberal restructuring of public education in St. Louis has embraced the same market logics that contributed to educational divestment and school segregation. I argue for a more expansive approach to critical policy analysis in education, one that addresses the limitations of reform within the existing political economy and relocates educational issues and their solutions within a larger struggle for racial and economic justice

In Defense of Academic Free dom and Faculty Governance: John Dewey, the 100th Anniversary of the AAU P, and the Threat of Corporatization

This essay situates John Dewey in the context of the founding of the American Association of University Professors (AAUP) in 1915. We argue that the 1915 Declaration of Principles, together with World War I, provides contemporary academics important historical justification for rethinking academic freedom and faculty governance in light of neoliberalism and what we argue is an increased corporatization of higher education in the United States. By revisiting the founding of the AAUP and John Dewey’s role in the various debates surrounding the establishment of the organization—including his broader role as a public intellectual confronted by war, questions of duty and freedom, and the shifting boundaries of the professoriate—we argue that professors today should demonstrate academic freedom and reclaim faculty governance for the public good over private interests

Secondhand Smoke Exposure and Preclinical Markers of Cardiovascular Risk in Toddlers

Objective: Links between secondhand smoke (SHS) exposure and cardiovascular disease in adults are well established but seldom reported during childhood. Although rates of smoking have decreased, young children from low-income backgrounds remain likely to be exposed to SHS. The purpose of this study was to investigate relationships between SHS exposure in young children and several preclinical markers of cardiovascular risk that have been established as relevant to adult populations. Methods: 139 children, 2–5 years of age, were enrolled in a cross-sectional study. SHS exposure was objectively determined by hair nicotine level; a comprehensive panel of clinical markers (AM blood pressure, fasting glucose & insulin, lipid profiles, inflammation) and research markers (markers of oxidation, endothelial stress, and endothelial repair) of cardiovascular risk status were assessed. Univariate and multivariate linear regression were used to evaluate relationships between SHS exposure and cardiovascular risk markers. Results: Hair nicotine levels were directly correlated with blood pressure and serum CRP, and inversely correlated with serum HDL and endothelial cell progenitor cell prevalence. In multivariate analyses, these relationships remained when controlled for age, sex, BMI z-score, maternal education, and method of payment. Additionally, in multivariate analyses, hair nicotine level was significantly negatively correlated with total anti-oxidant capacity. Conclusions: These results support the view that SHS exposure in the very young has a detectable relationship with several markers of cardiovascular risk, long before the emergence of clinical disease. Further studies to define mechanisms and strategies to prevent and mitigate these risks early in life are warranted

Molecular characterization of a marine turtle tumor epizootic, profiling external, internal and postsurgical regrowth tumors

Sea turtle populations are under threat from an epizootic tumor disease (animal epidemic) known as fibropapillomatosis. Fibropapillomatosis continues to spread geographically, with prevalence of the disease also growing at many longer-affected sites globally. However, we do not yet understand the precise environmental, mutational and viral events driving fibropapillomatosis tumor formation and progression. Here we perform transcriptomic and immunohistochemical profiling of five fibropapillomatosis tumor types: external new, established and postsurgical regrowth tumors, and internal lung and kidney tumors. We reveal that internal tumors are molecularly distinct from the more common external tumors. However, they have a small number of conserved potentially therapeutically targetable molecular vulnerabilities in common, such as the MAPK, Wnt, TGFβ and TNF oncogenic signaling pathways. These conserved oncogenic drivers recapitulate remarkably well the core pan-cancer drivers responsible for human cancers. Fibropapillomatosis has been considered benign, but metastatic-related transcriptional signatures are strongly activated in kidney and established external tumors. Tumors in turtles with poor outcomes (died/euthanized) have genes associated with apoptosis and immune function suppressed, with these genes providing putative predictive biomarkers. Together, these results offer an improved understanding of fibropapillomatosis tumorigenesis and provide insights into the origins, inter-tumor relationships, and therapeutic treatment for this wildlife epizootic

KELT-8b: A highly inflated transiting hot Jupiter and a new technique for extracting high-precision radial velocities from noisy spectra

We announce the discovery of a highly inflated transiting hot Jupiter discovered by the KELT-North survey. A global analysis including constraints from isochrones indicates that the V = 10.8 host star (HD 343246) is a mildly evolved, G dwarf with $T_{\rm eff} = 5754_{-55}^{+54}$ K, $\log{g} = 4.078_{-0.054}^{+0.049}$, $[Fe/H] = 0.272\pm0.038$, an inferred mass $M_{*}=1.211_{-0.066}^{+0.078}$ M$_{\odot}$, and radius $R_{*}=1.67_{-0.12}^{+0.14}$ R$_{\odot}$. The planetary companion has mass $M_P = 0.867_{-0.061}^{+0.065}$ $M_{J}$, radius $R_P = 1.86_{-0.16}^{+0.18}$ $R_{J}$, surface gravity $\log{g_{P}} = 2.793_{-0.075}^{+0.072}$, and density $\rho_P = 0.167_{-0.038}^{+0.047}$ g cm$^{-3}$. The planet is on a roughly circular orbit with semimajor axis $a = 0.04571_{-0.00084}^{+0.00096}$ AU and eccentricity $e = 0.035_{-0.025}^{+0.050}$. The best-fit linear ephemeris is $T_0 = 2456883.4803 \pm 0.0007$ BJD$_{\rm TDB}$ and $P = 3.24406 \pm 0.00016$ days. This planet is one of the most inflated of all known transiting exoplanets, making it one of the few members of a class of extremely low density, highly-irradiated gas giants. The low stellar $\log{g}$ and large implied radius are supported by stellar density constraints from follow-up light curves, plus an evolutionary and space motion analysis. We also develop a new technique to extract high precision radial velocities from noisy spectra that reduces the observing time needed to confirm transiting planet candidates. This planet boasts deep transits of a bright star, a large inferred atmospheric scale height, and a high equilibrium temperature of $T_{eq}=1675^{+61}_{-55}$ K, assuming zero albedo and perfect heat redistribution, making it one of the best targets for future atmospheric characterization studies.Comment: Submitted to ApJ, feedback is welcom

The Distance of Five Type II Supernovae Using the Expanding Photosphere Method and the Value of H 0

We have used observations gathered at CTIO to measure distances by the expanding photosphere method (EPM) to five Type II supernovae. These supernovae lie at redshifts from cz = 1100 km s^-1^ to cz = 5500 km s^- 1^, and increase to 18 the number of distances measured Using EPM. We compare distances derived to 11 Type II supernovae with distances to their host galaxies measured Using the Tully-Fisher method. We find that the Tully-Fisher distances average 11% +/- 17% smaller. The comparison shows no significant evidence of any large distance-dependent bias in the Tully-Fisher distances. We employ the sample of EPM distances from 4.5 Mpc to 180 Mpc to derive a value for the Hubble constant. We find H_0_ = 73 +/- 6(statistical) +/-7(systematic)km s^-1^ Mpc^-1^

The Peculiar SN 2005hk: Do Some Type Ia Supernovae Explode as Deflagrations?

We present extensive u'g'r'i'BVRIYJHKs photometry and optical spectroscopy of SN 2005hk. These data reveal that SN 2005hk was nearly identical in its observed properties to SN 2002cx, which has been called ``the most peculiar known type Ia supernova.'' Both supernovae exhibited high ionization SN 1991T-like pre-maximum spectra, yet low peak luminosities like SN 1991bg. The spectra reveal that SN 2005hk, like SN 2002cx, exhibited expansion velocities that were roughly half those of typical type Ia supernovae. The R and I light curves of both supernovae were also peculiar in not displaying the secondary maximum observed for normal type Ia supernovae. Our YJH photometry of SN 2005hk reveals the same peculiarity in the near-infrared. By combining our optical and near-infrared photometry of SN 2005hk with published ultraviolet light curves obtained with the Swift satellite, we are able to construct a bolometric light curve from ~10 days before to ~60 days after B maximum. The shape and unusually low peak luminosity of this light curve, plus the low expansion velocities and absence of a secondary maximum at red and near-infrared wavelengths, are all in reasonable agreement with model calculations of a 3D deflagration which produces ~0.25 M_sun of 56Ni.Comment: Accepted by PASP, to appear in April 2007 issue, 63 pages, 16 figures, 11 table

The Expanding Photosphere Method Applied to SN 1992 AM At cz=14 600km/s

We present photometry and spectroscopy of SN 1992am for five months following its discovery by the Calan/CTIO SN search. These data show SN 1992am to be type II-P, displaying hydrogen in its spectrum and the typical shoulder in its light curve. The photometric data and the distance from our own analysis are used to construct the supernova's bolometric light curve. Using the bolometric light curve, we estimate SN 1992am ejected approximately 0.30 M_sun_ of ^56^Ni, an amount four times larger than that of other well studied SNe II. SN 1992am's; host galaxy lies at a redshift of cz = 14600 km s ~, making it one of the most distant SNe II discovered, and an important application of the Expanding Photosphere Method. Since z = 0.05 is large enough for redshift-dependent effects to matter, we develop the technique to derive luminosity distances with the Expanding Photosphere Method at any redshift, and apply this method to SN 1992am, The derived distance, D = 180_-25_^+30^ Mpc, is independent of all other rungs in the extragalactic distance ladder. The redshift of SN 1992am's host galaxy is sufficiently large that uncertainties due to perturbations in the smooth Hubble flow should be smaller than 10%. The Hubble ratio derived from the distance and redshift of this single object is H_0_ = 81_-15_^+17^ km s^-1^ Mpc^-1^. In the future with more of these distant objects, we hope to establish an independent and statistically robust estimate of H_0_ based solely on type II supernovae.Supernova research at Harvard University is supported by NSF Grant No. AST 92-18475, and NASA Grants Nos. NAG 5-841 and NGT-51002. M.H. and J.M. gratefully acknowledge financial support from Grant No. 92/0312 from Fondo Nacional de Ciencias y Tecnologia (Fondecyt-Chile). The Berkeley group was financially supported by NSF Grants Nos. AST-8957063 and AST-9115174 to A. V. F, by an NSF Graduate Fellowship to T.M., and by the NSF Cooperative Agreement No. AST-8809616. N.D.T. acknowledges support from NSF Grant No. AST-931469

Genetic Mapping and Exome Sequencing Identify Variants Associated with Five Novel Diseases

The Clinic for Special Children (CSC) has integrated biochemical and molecular methods into a rural pediatric practice serving Old Order Amish and Mennonite (Plain) children. Among the Plain people, we have used single nucleotide polymorphism (SNP) microarrays to genetically map recessive disorders to large autozygous haplotype blocks (mean = 4.4 Mb) that contain many genes (mean = 79). For some, uninformative mapping or large gene lists preclude disease-gene identification by Sanger sequencing. Seven such conditions were selected for exome sequencing at the Broad Institute; all had been previously mapped at the CSC using low density SNP microarrays coupled with autozygosity and linkage analyses. Using between 1 and 5 patient samples per disorder, we identified sequence variants in the known disease-causing genes SLC6A3 and FLVCR1, and present evidence to strongly support the pathogenicity of variants identified in TUBGCP6, BRAT1, SNIP1, CRADD, and HARS. Our results reveal the power of coupling new genotyping technologies to population-specific genetic knowledge and robust clinical data