Attracting and Retaining Teachers in High-Need Schools: Do Financial Incentives Make Financial Sense?

This study synthesizes what we know and do not know about policies to attract and retain teachers in high-need schools and assesses the relative cost-effectiveness of two types of policies. Research consistently shows that teacher quality is likely to be lower in schools with higher proportions of students from disadvantaged backgrounds. This pattern is likely a result of several factors but the most well-documented is teachers’ mobility choices within and across districts. Although there are numerous programs across the country intended to attract and retain highly-skilled teachers in high-need schools, there is very little assessment of their effectiveness. Given the lack of evidence on specific interventions, I use the results from existing studies of teacher mobility and attrition to compare the effect of salary incentives and induction or mentoring programs. Although financial incentives are arguably the most straightforward policies for states and districts to adopt, high-need schools may be better served if policymakers and researchers devoted more attention to more cost-effective alternatives.

Private Contributions and Public School Resources

In the wake of school finance reforms that limit local tax revenue and, more recently, state budget cuts that have threatened K-12 education spending, an increasing number of schools and school districts have appealed to parents and communities for voluntary contributions to augment school resources. Of course, not all schools benefit equally from these contributions leading to a common concern that voluntary contributions create inequities in school funding across communities. In this paper we examine the size and distribution of voluntary contributions to California’s K-12 public schools in 2001. In addition, we examine how contributions have affected the distribution of resources across schools. Our results indicate that while some schools have been quite successful in raising voluntary contributions, overall, contributions have not led to large inequities in the distribution of resources among high- and low-income schools. Specifically, schools raising particularly high levels of contributions, over $500 per pupil, do tend to have more resources, but these schools are rare and very small. Over ninety-nine percent of California elementary students attend schools where contributions have almost no effect on inputs.Voluntary Contributions, Public School Finance, School Resources

Demonstration of intrahepatic accumulated microbubble on ultrasound represents the grade of hepatic fibrosis

OBJECTIVES: To examine the feasibility of perflubutane-based ultrasound for grading hepatic fibrosis. METHODS: This prospective study included 202 subjects; main study (controls:33, F0–1:35, F2:26, F3:23, cirrhosis:29) and subsequent study (controls:16, F0–1:7, F2:20, F3:7, cirrhosis:6). Diagnostic abilities for assessing fibrosis grade were compared between contrast findings and FIB4 (age × AST/[platelet count × ALT(0.5)]). RESULTS: High-power emission produced an intrahepatic band-like structure, and the three-layer appearance was less frequent and monolayer appearance was more frequent in cirrhosis than controls/chronic hepatitis (P < 0.0001). Intensity difference at 15-min phase showed most significant correlation with fibrosis grade (ρ = 0.79, P < 0.0001), and the best areas under the receiver operating characteristic curves are 0.88 for marked fibrosis, 0.95 for advanced fibrosis and 0.97 for cirrhosis, which were significantly higher than those of FIB4, 0.85 for marked fibrosis, 0.89 for advanced fibrosis and 0.90 for cirrhosis. Sensitivity, specificity and efficiency of the intensity difference were 88%, 72% and 81% for marked fibrosis, 85%, 91% and 89% for advanced fibrosis and 97%, 90% and 91% for cirrhosis, respectively. The subsequent study validated the main study results; significant correlation between the intensity difference and the fibrosis grade (ρ = 0.73–0.77, P < 0.0001). CONCLUSIONS: Perflubutane-based ultrasound accurately predicts the grade of hepatic fibrosis. KEY POINTS: • The behaviour of intrahepatic microbubbles depends on the severity of hepatic fibrosis. • Layer enhancement pattern simply represents the degree of chronic liver disease. • Parenchymal intensity change due to high-power emission predicts the hepatic fibrosis grade

Hepatitis B Virus e Antigen Physically Associates With Receptor-Interacting Serine/Threonine Protein Kinase 2 and Regulates IL-6 Gene Expression

We previously reported that hepatitis B virus (HBV) e antigen (HBeAg) inhibits production of interleukin 6 by suppressing NF-κB activation. NF-κB is known to be activated through receptor-interacting serine/threonine protein kinase 2 (RIPK2), and we examined the mechanisms of interleukin 6 regulation by HBeAg. HBeAg inhibits RIPK2 expression and interacts with RIPK2, which may represent 2 mechanisms through which HBeAg blocks nucleotide-binding oligomerization domain-containing protein 1 ligand-induced NF-κB activation in HepG2 cells. Our findings identified novel molecular mechanisms whereby HBeAg modulates intracellular signaling pathways by targeting RIPK2, supporting the concept that HBeAg could impair both innate and adaptive immune responses to promote chronic HBV infectio

Idiosyncratic Risk and Expected Returns in REITs

The Modern Portfolio Theory (MPT) argues that all unsystematic risk can be diversified away thus there should be no relationship between idiosyncratic risk and return. Ooi, Wang and Webb (2009) employ the Fama-French (1993) three-factor model (FF3) to estimate the level of nonsystematic return volatility in REITs as a proxy for idiosyncratic risk. They find a significant positive relationship between expected returns and conditionally estimated idiosyncratic risk contrary to the MPT. In this research, I examine other potential sources of systematic risk in REITs which may explain the seeming violation of the MPT found by Ooi et al (2009). I re-examine the proportion of idiosyncratic risk in REITs with Carhart’s (1997) momentum factor, which is largely applied on the FF3 to control for the persistency of stock returns as supplemental risk in the finance literature. Next, I conduct cross-sectional regression and test the significance of the relationship between idiosyncratic risk and expected returns. I further analyze the role of property sector on idiosyncratic risk as well as on its relationship with expected returns. I argue three conclusions. First, momentum has a relatively minor effect on the idiosyncratic risk consistent with the financial literature. Second, the effect of momentum is not strong enough to cause a significant change in the relationship between idiosyncratic risk and expected returns. Third, a REIT portfolio diversified across property sectors neutralizes the relationship between idiosyncratic risk and expected returns, though the contribution of each property sector is not statistically significant

The Daily Tulean Dispatch, October 5, 1942

https://scholarlycommons.pacific.edu/tulean/1068/thumbnail.jp

The Daily Tulean Dispatch, October 22, 1942

https://scholarlycommons.pacific.edu/tulean/1075/thumbnail.jp

The Daily Tulean Dispatch, November 2, 1942

https://scholarlycommons.pacific.edu/tulean/1078/thumbnail.jp

The Daily Tulean Dispatch, December 15, 1942

https://scholarlycommons.pacific.edu/tulean/1106/thumbnail.jp

Hepatitis C Virus Nonstructural 5A Protein Inhibits Lipopolysaccharide-Mediated Apoptosis of Hepatocytes by Decreasing Expression of Toll-Like Receptor 4

Background. Hepatitis C virus (HCV) nonstructural protein 5A (NS5A) has been shown to modulate multiple cellular processes, including apoptosis. The aim of this study was to assess the effects of HCV NS5A on apoptosis induced by Toll-like receptor (TLR) 4 ligand, lipopolysaccharide (LPS). Methods. Apoptotic responses to TLR4 ligands and the expression of molecules involved in TLR signaling pathways in human hepatocytes were examined with or without expression of HCV NS5A. Results. HCV NS5A protected HepG2 hepatocytes against LPS-induced apoptosis, an effect linked to reduced TLR4 expression. A similar downregulation of TLR4 expression was observed in Huh-7-expressing genotype 1b and 2a. In agreement with these findings, NS5A inhibited the expression of numerous genes encoding for molecules involved in TLR4 signaling, such as CD14, MD-2, myeloid differentiation primary response gene 88, interferon regulatory factor 3, and nuclear factor-κB2. Consistent with a conferred prosurvival advantage, NS5A diminished the poly(adenosine diphosphate-ribose) polymerase cleavage and the activation of caspases 3, 7, 8, and 9 and increased the expression of anti-apoptotic molecules Bcl-2 and c-FLIP. Conclusions. HCV NS5A downregulates TLR4 signaling and LPS-induced apoptotic pathways in human hepatocytes, suggesting that disruption of TLR4-mediated apoptosis may play a role in the pathogenesis of HCV infectio