The Long-Run Impacts of Same-Race Teachers

Black primary-school students matched to a same-race teacher perform better on standardized tests and face more favorable teacher perceptions, yet little is known about the long-run, sustained impacts of student-teacher demographic match. We show that assigning a black male to a black teacher in the third, fourth, or fifth grades significantly reduces the probability that he drops out of high school, particularly among the most economically disadvantaged black males. Exposure to at least one black teacher in grades 3-5 also increases the likelihood that persistently low-income students of both sexes aspire to attend a four-year college. These findings are robust across administrative data from two states and multiple identification strategies, including an instrumental variables strategy that exploits within-school, intertemporal variation in the proportion of black teachers, family fixed-effects models that compare siblings who attended the same school, and the random assignment of students and teachers to classrooms created by the Project STAR class-size reduction experiment

Demonstration of Universal Parametric Entangling Gates on a Multi-Qubit Lattice

We show that parametric coupling techniques can be used to generate selective entangling interactions for multi-qubit processors. By inducing coherent population exchange between adjacent qubits under frequency modulation, we implement a universal gateset for a linear array of four superconducting qubits. An average process fidelity of $\mathcal{F}=93\%$ is estimated for three two-qubit gates via quantum process tomography. We establish the suitability of these techniques for computation by preparing a four-qubit maximally entangled state and comparing the estimated state fidelity against the expected performance of the individual entangling gates. In addition, we prepare an eight-qubit register in all possible bitstring permutations and monitor the fidelity of a two-qubit gate across one pair of these qubits. Across all such permutations, an average fidelity of $\mathcal{F}=91.6\pm2.6\%$ is observed. These results thus offer a path to a scalable architecture with high selectivity and low crosstalk

Rrp1b, a New Candidate Susceptibility Gene for Breast Cancer Progression and Metastasis

A novel candidate metastasis modifier, ribosomal RNA processing 1 homolog B (Rrp1b), was identified through two independent approaches. First, yeast two-hybrid, immunoprecipitation, and functional assays demonstrated a physical and functional interaction between Rrp1b and the previous identified metastasis modifier Sipa1. In parallel, using mouse and human metastasis gene expression data it was observed that extracellular matrix (ECM) genes are common components of metastasis predictive signatures, suggesting that ECM genes are either important markers or causal factors in metastasis. To investigate the relationship between ECM genes and poor prognosis in breast cancer, expression quantitative trait locus analysis of polyoma middle-T transgene-induced mammary tumor was performed. ECM gene expression was found to be consistently associated with Rrp1b expression. In vitro expression of Rrp1b significantly altered ECM gene expression, tumor growth, and dissemination in metastasis assays. Furthermore, a gene signature induced by ectopic expression of Rrp1b in tumor cells predicted survival in a human breast cancer gene expression dataset. Finally, constitutional polymorphism within RRP1B was found to be significantly associated with tumor progression in two independent breast cancer cohorts. These data suggest that RRP1B may be a novel susceptibility gene for breast cancer progression and metastasis

Venous thromboembolism after inpatient surgery in administrative data vs NSQIP: a multi-institutional study

Previous studies have documented significant differences between administrative data and registry data in the determination of postoperative venous thromboembolism (VTE). The goal of this study was to characterize the discordance between administrative and registry data in the determination of postoperative VTE.This study was performed using data from the American College of Surgeons NSQIP merged with administrative data from 8 different hospitals (5 different medical centers) between 2013 and 2015. Occurrences of postoperative vein thrombosis (VT) and pulmonary embolism (PE) as ascertained by administrative data and NSQIP data were compared. In each situation where the 2 sources disagreed (discordance), a 2-clinician chart review was performed to characterize the reasons for discordance.The cohort used for analysis included 43,336 patients, of which 53.3% were female and the mean age was 59.5 years. Concordance between administrative and NSQIP data was worse for VT (κ 0.57; 95% CI 0.51 to 0.62) than for PE (κ 0.83; 95% CI 0.78 to 0.89). A total of 136 cases of discordance were noted in the assessment of VT; of these, 50 (37%) were explained by differences in the criteria used by administrative vs NSQIP systems. In the assessment of postoperative PE, administrative data had a higher accuracy than NSQIP data (odds ratio for accuracy 2.86; 95% CI 1.11 to 7.14) when compared with the 2-clinician chart review.This study identifies significant problems in ability of both NSQIP and administrative data to assess postoperative VT/PE. Administrative data functioned more accurately than NSQIP data in the identification of postoperative PE. The mechanisms used to translate VTE measurement into quality improvement should be standardized and improved

Genes, Education, and Labor Market Outcomes: Evidence from the Health and Retirement Study

Recent advances have led to the discovery of specific genetic variants that predict educational attainment. We study how these variants, summarized as a genetic score variable, are associated with human capital accumulation and labor market outcomes in the Health and Retirement Study (HRS). We demonstrate that the same genetic score that predicts education is also associated with higher wages, but only among individuals with a college education. Moreover, the genetic gradient in wages has grown in more recent birth cohorts, consistent with interactions between technological change and labor market ability. We also show that individuals who grew up in economically disadvantaged households are less likely to go to college when compared to individuals with the same genetic score, but from higher socioeconomic status households. Our findings provide support for the idea that childhood socioeconomic status is an important moderator of the economic returns to genetic endowments. Moreover, the finding that childhood poverty limits the educational attainment of high-ability individuals suggests the existence of unrealized human potential

Gain-of-function RHOA mutations promote focal adhesion kinase activation and dependency in diffuse gastric cancer

Diffuse gastric cancer (DGC) is a lethal malignancy lacking effective systemic therapy. Among the most provocative recent results in DGC has been that of highly recurrent missense mutations in the GTPase RHOA. The function of these mutations has remained unresolved. We demonstrate that RHOAY42C, the most common RHOA mutation in DGC, is a gain-of-function oncogenic mutant, and that expression of RHOAY42C with inactivation of the canonical tumor suppressor Cdh1 induces metastatic DGC in a mouse model. Biochemically, RHOAY42C exhibits impaired Y42C GTP hydrolysis and enhances interaction with its effector ROCK. RHOA mutation and Cdh1 loss induce actin/cytoskeletal rearrangements and activity of focal adhesion kinase (FAK), which activates YAP–TAZ, PI3K–AKT, and β-catenin. RHOAY42C murine models were sensitive to FAK inhibition and to combined YAP and PI3K pathway blockade. These results, coupled with sensitivity to FAK inhibition in patient-derived DGC cell lines, nominate FAK as a novel target for these cancers. SIGNIFICANCE: The functional significance of recurrent RHOA mutations in DGC has remained unresolved. Through biochemical studies and mouse modeling of the hotspot RHOAY42C mutation, we establish that these mutations are activating, detail their effects upon cell signaling, and define how RHOA-mediated FAK activation imparts sensitivity to pharmacologic FAK inhibitors