The Interdependence of School Outcomes and School and Neighborhood Crime

In this paper, we estimate the effects of neighborhood crime and in-school crime on educational outcomes for elementary and secondary schools in the city of Atlanta over the period 1999 to 2002. We specify a model that accounts for the joint determination of both types of crime along with school outcomes. Despite the large empirical literature on both education production functions and crime incidence, there has been little empirical work on crime's effect on school outcomes. One exception is Grogger (1997) who used individual data from the High School and Beyond study to estimate the effect of school violence on measures of individual student performance. After controlling for individual and school characteristics, he found that moderate and severe levels of school violence had substantial negative consequences for school outcomes. Our study both updates and expands on his work, using current data and better measures of neighborhood violence. Working Paper 07-1

Sample Selection in Models of Academic Performance

This article shows how admission and enrollment processes affect the interpretation of simple validation studies of academic performance. In a competitive market for students, optimal behavior of admissions committees and applicants drives the simple correlation between test scores and performance toward zero, regardless of the relationship in the population of prospective students. Data from our university’s MBA program support the prediction that applicants exhibit a higher correlation between test scores and undergraduate GPAs than do current students. This suggests that standard validation studies will understate the importance of GMAT scores in predicting performance of potential MBA students

Identification by Disaggregation

Standard economic theory predicts that the actions of individual participants in competitive markets have negligible effects on market-determined aggregates. Applied researchers, and even some econometric textbooks, incorrectly infer from this that market prices can be modeled as econometrically exogenous with respect to the quantity demanded of an individual consumer. This faulty inference has even led some researchers (for example, Robert Engle, 1978; Nicholas Kiefer, 1984; Roger Waud, 1974) to employ an estimation strategy we call identification by disaggregation (IBD). This procedure attempts to circumvent the simultaneity problem in a macro regression by disaggregating the dependent variable and estimating the relationship for individual agents or sectors. This note provides a simple proof that estimates using disaggregated dependent variables suffer, on average, from the same degree of simultaneity bias as the estimates using aggregate data

The Effect of a Smoke-Free Ordinance on Eating and Drinking Places in Lincoln, Nebraska

The Lincoln Smoking Regulation Act which prohibited smoking in most public places and places of employment in Lincoln, Nebraska including restaurants and bars was implemented in January 2005. This report examines the impact of the ordinance on the following measures of business activity in Lincoln: • Sales revenue of eating and drinking places • Employment of eating and drinking places • Gross revenues from keno. We examine the impact of the ordinance during the year 2005, the first year that the ordinance was in effect. While restaurant and bar activity in Lincoln rose during 2005 by some measures, we focus on performance relative to Omaha in order to isolate the impact of Lincoln’s ordinance. The estimated first-year impacts of the ordinance were as follows

Photophysical and Electrochemical Properties of meso-Substituted Thien-2-yl Zn(II) Porphyrins

The influence of the thiophene ring on the ground and excited state properties of the porphyrin ring is investigated, when substituted at the meso-position. A series of mono-, di-, tri-, and tetra-meso-thien-2-yl porphyrins are studied and discussed with respect to the reference compounds zinc(II)-5,10,15,20-tetra(thien-2′-yl)porphyrin (1a) and zinc(II)-5,10,15,20-tetraphenylporphyrin (ZnTPP). The extended conjugated system zinc(II)-5-(5′-(5′′-ethynyl-2′′-thiophenecarboxaldehyde)thien-2′-yl)-10,15,20-triphenylporphyrin (4d) is also studied and shows enhanced charge transfer character due to the presence of the terminal aldehyde accepting group. A detailed analysis of ground and excited state UV−vis absorption, steady-state and time-resolved fluorescence, laser flash photolysis, and electrochemical data all point toward substantial electronic communication between the central Zn(II) porphyrin ring and the meso-thien-2-yl substituents, which is evident from excited state charge transfer character

Transcriptional Repressive H3K9 and H3K27 Methylations Contribute to DNMT1-Mediated DNA Methylation Recovery

DNA methylation and histone modifications are two major epigenetic events regulating gene expression and chromatin structure, and their alterations are linked to human carcinogenesis. DNA methylation plays an important role in tumor suppressor gene inactivation, and can be revised by DNA methylation inhibitors. The reversible nature of DNA methylation forms the basis of epigenetic cancer therapy. However, it has been reported that DNA re-methylation and gene re-silencing could occur after removal of demethylation treatment and this may significantly hamper the therapeutic value of DNA methylation inhibitors. In this study we have provided detailed evidence demonstrating that mammalian cells possess a bona fide DNA methylation recovery system. We have also shown that DNA methylation recovery was mediated by the major human DNA methyltransferase, DNMT1. In addition, we found that H3K9-tri-methylation and H3K27-tri-methylation were closely associated with this DNA methylation recovery. These persistent transcriptional repressive histone modifications may have a crucial role in regulating DNMT1-mediated DNA methylation recovery. Our findings may have important implications towards a better understanding of epigenetic regulation and future development of epigenetic therapeutic intervention

Treatable childhood neuronopathy caused by mutations in riboflavin transporter RFVT2.

Childhood onset motor neuron diseases or neuronopathies are a clinically heterogeneous group of disorders. A particularly severe subgroup first described in 1894, and subsequently called Brown-Vialetto-Van Laere syndrome, is characterized by progressive pontobulbar palsy, sensorineural hearing loss and respiratory insufficiency. There has been no treatment for this progressive neurodegenerative disorder, which leads to respiratory failure and usually death during childhood. We recently reported the identification of SLC52A2, encoding riboflavin transporter RFVT2, as a new causative gene for Brown-Vialetto-Van Laere syndrome. We used both exome and Sanger sequencing to identify SLC52A2 mutations in patients presenting with cranial neuropathies and sensorimotor neuropathy with or without respiratory insufficiency. We undertook clinical, neurophysiological and biochemical characterization of patients with mutations in SLC52A2, functionally analysed the most prevalent mutations and initiated a regimen of high-dose oral riboflavin. We identified 18 patients from 13 families with compound heterozygous or homozygous mutations in SLC52A2. Affected individuals share a core phenotype of rapidly progressive axonal sensorimotor neuropathy (manifesting with sensory ataxia, severe weakness of the upper limbs and axial muscles with distinctly preserved strength of the lower limbs), hearing loss, optic atrophy and respiratory insufficiency. We demonstrate that SLC52A2 mutations cause reduced riboflavin uptake and reduced riboflavin transporter protein expression, and we report the response to high-dose oral riboflavin therapy in patients with SLC52A2 mutations, including significant and sustained clinical and biochemical improvements in two patients and preliminary clinical response data in 13 patients with associated biochemical improvements in 10 patients. The clinical and biochemical responses of this SLC52A2-specific cohort suggest that riboflavin supplementation can ameliorate the progression of this neurodegenerative condition, particularly when initiated soon after the onset of symptoms