An analysis of average annual pay and cost-of-living in U.S. metropolitan regions: Working paper series--02-28

One of the key factors in the decision to relocate or migrate from one location to another involves whether or not the migrant's economic status is enhanced by the move. The potential for improved economic status plays a significant role in the migration decision. Therefore, it is important to know whether relocation to a new area improves the economic welfare of the migrant. One means to determine the answer is to compare annual pay in each region with the relative cost-of-living there. This paper examines the relationship between "average annual pay" in 2000 for cities in 219 metropolitan areas and the cost of living in these same locations. A regression analysis was performed for cities in the 219 Metropolitan Statistical Areas. Additional regressions were performed after grouping these cities within the four U.S. Census Regions. The results allow us to determine the strength of the relationship between annual pay and cost-of-living variables in these locations, and also if different patterns emerge among the four census regions of the economy. Additional variables were included to determine if city size, climate, or education impact the relationship

Logical extremes, beta, and the power of the test: Working paper series--02-03

There is a potential misuse of the power function under the logical extreme when the null hypothesis is true. The power function is defined to measure the probability of rejecting the null given any value of the parameter being tested. It can be used to obtain the power and the ? values only under the alternative hypothesis. When the null is true, the power function can be used to obtain the size of the test. The power and the probability of committing a type II error are, however, undefined and, hence, the power function should not be used to obtain these values

Economic or amenity driven migration? A cluster-based analysis of county migration in the American southwest: Working paper series--08-01

This paper initially analyzes the determinants of net domestic migration which occurred from 1995 to 2000 at the county level in the 4-Corners Region of the U.S. (Arizona, Colorado, New Mexico and Utah.) Regression techniques were used to explain approximately 70 percent of the variation in net migration rates within the region for counties whose populations exceeded 10,000 persons at the beginning of the period. The results of the study suggest net migration flows in the region are a dual function of both economic and non-economic characteristics existing within each county. The analysis is extended through the use of additional multivariate techniques in order to group the counties into clusters that reflect natural groupings based on a similar profile of variables used in the analysis. Migration activity differed statistically from cluster to cluster based upon variations in the predictor variables used in the analysis. Further research is suggested in order to extend these results to the broader economy

Assessing domestic migration at the county level in the 4-corners region: Working paper series--07-06

This paper analyzes net domestic migration which occurred between 1995 and 2000 at the county level for the 4-Corners Region (Arizona, Colorado, New Mexico, and Utah.) Regression techniques were used to explain approximately 70 percent of the variation in net migration rates within the region for all counties whose populations exceeded 10,000 persons at the beginning of the period. The results of the study suggest net migration rates in the region are a function of both economic and non-economic characteristics existing within each county. Initially, a number of amenity-related, recreation and socio-demographic variables were considered along with traditional economic indicators; however, only a few of the traditional variables were correlated with migration activity to and from this region. Further research is needed in order to explain the differences in migration rates for these locations compared with results discovered in other regions

Group finding in the stellar halo using M-giants in 2MASS: An extended view of the Pisces Overdensity?

A density based hierarchical group-finding algorithm is used to identify stellar halo structures in a catalog of M-giants from the Two Micron All Sky Survey (2MASS). The intrinsic brightness of M-giant stars means that this catalog probes deep into the halo where substructures are expected to be abundant and easy to detect. Our analysis reveals 16 structures at high Galactic latitude (greater than 15 degree), of which 10 have been previously identified. Among the six new structures two could plausibly be due to masks applied to the data, one is associated with a strong extinction region and one is probably a part of the Monoceros ring. Another one originates at low latitudes, suggesting some contamination from disk stars, but also shows protrusions extending to high latitudes, implying that it could be a real feature in the stellar halo. The last remaining structure is free from the defects discussed above and hence is very likely a satellite remnant. Although the extinction in the direction of the structure is very low, the structure does match a low temperature feature in the dust maps. While this casts some doubt on its origin, the low temperature feature could plausibly be due to real dust in the structure itself. The angular position and distance of this structure encompass the Pisces overdensity traced by RR Lyraes in Stripe 82 of the Sloan Digital Sky Survey (SDSS). However, the 2MASS M-giants indicate that the structure is much more extended than what is visible with the SDSS, with the point of peak density lying just outside Stripe 82. The morphology of the structure is more like a cloud than a stream and reminiscent of that seen in simulations of satellites disrupting along highly eccentric orbits.Comment: Accepted for publication in Ap

Extracellular Vesicles from Infected Cells Are Released Prior to Virion Release

Here, we have attempted to address the timing of EV and virion release from virally infected cells. Uninfected (CEM), HIV-1-infected (J1.1), and human T cell leukemia virus-1 (HTLV-1)-infected (HUT102) cells were synchronized in G0. Viral latency was reversed by increasing gene expression with the addition of serum-rich media and inducers. Supernatants and cell pellets were collected post-induction at different timepoints and assayed for extracellular vesicle (EV) and autophagy markers; and for viral proteins and RNAs. Tetraspanins and autophagy-related proteins were found to be differentially secreted in HIV-1- and HTLV-1-infected cells when compared with uninfected controls. HIV-1 proteins were present at 6 h and their production increased up to 24 h. HTLV-1 proteins peaked at 6 h and plateaued. HIV-1 and HTLV-1 RNA production correlated with viral protein expression. Nanoparticle tracking analysis (NTA) showed increase of EV concentration over time in both uninfected and infected samples. Finally, the HIV-1 supernatant from the 6-h samples was found not to be infectious; however, the virus from the 24-h samples was successfully rescued and infectious. Overall, our data indicate that EV release may occur prior to viral release from infected cells, thereby implicating a potentially significant effect of EVs on uninfected recipient cells prior to subsequent viral infection and spread

Defining new therapeutics using a more immunocompetent mouse model of antibody-enhanced dengue virus infection

With over 3.5 billion people at risk and approximately 390 million human infections per year, dengue virus (DENV) disease strains health care resources worldwide. Previously, we and others established models for DENV pathogenesis in mice that completely lack subunits of the receptors (Ifnar and Ifngr) for type I and type II interferon (IFN) signaling; however, the utility of these models is limited by the pleotropic effect of these cytokines on innate and adaptive immune system development and function. Here, we demonstrate that the specific deletion of Ifnar expression on subsets of murine myeloid cells (LysM Cre(+) Ifnar(flox/flox) [denoted as Ifnar(f/f) herein]) resulted in enhanced DENV replication in vivo. The administration of subneutralizing amounts of cross-reactive anti-DENV monoclonal antibodies to LysM Cre(+) Ifnar(f/f) mice prior to infection with DENV serotype 2 or 3 resulted in antibody-dependent enhancement (ADE) of infection with many of the characteristics associated with severe DENV disease in humans, including plasma leakage, hypercytokinemia, liver injury, hemoconcentration, and thrombocytopenia. Notably, the pathogenesis of severe DENV-2 or DENV-3 infection in LysM Cre(+) Ifnar(f/f) mice was blocked by pre- or postexposure administration of a bispecific dual-affinity retargeting molecule (DART) or an optimized RIG-I receptor agonist that stimulates innate immune responses. Our findings establish a more immunocompetent animal model of ADE of infection with multiple DENV serotypes in which disease is inhibited by treatment with broad-spectrum antibody derivatives or innate immune stimulatory agents

Phase III Randomized Trial of Chemotherapy With or Without Bevacizumab in Patients With Recurrent or Metastatic Head and Neck Cancer.

PURPOSE: We evaluated the addition of bevacizumab, a humanized monoclonal antibody that targets vascular endothelial growth factor, to platinum-based chemotherapy in recurrent or metastatic squamous cell carcinoma of the head and neck (SCCHN). PATIENTS AND METHODS: Patients with chemotherapy-naïve (or with prior platinum as part of multimodal therapy completed ≥ 4 months earlier) recurrent or metastatic SCCHN were randomly assigned to receive a platinum-based chemotherapy doublet with or without bevacizumab 15 mg/kg given intravenously every 3 weeks until disease progression. Chemotherapy could be discontinued after six cycles if a maximum response was achieved. RESULTS: The study randomly assigned 403 patients. Median overall survival (OS) was 12.6 months with bevacizumab plus chemotherapy (BC) and 11.0 months with chemotherapy alone (hazard ratio, 0.87; 95% CI, 0.70 to 1.09; P = .22). At 2, 3, and 4 years, the OS rates were 25.2% v 18.1%, 16.4% v 10.0%, and 11.8% v 6.4% for BC versus chemotherapy, respectively. In an analysis of 365 eligible patients who started treatment, the hazard ratio was 0.82 (95% CI, 0.65 to 1.04; P = .10), with a median OS of 14.2 months on BC v 11.1 months on chemotherapy. Median progression-free survival with BC was 6.0 months v 4.3 months with chemotherapy (P = .0014). Overall response rates were 35.5% with BC and 24.5% with chemotherapy (P = .016). There was increased toxicity, including a higher rate of treatment-related grade 3 to 5 bleeding events (6.7% v 0.5%; P \u3c .001) and treatment-related deaths (9.3% v 3.5%; P = .022) with BC versus chemotherapy. CONCLUSION: The addition of bevacizumab to chemotherapy did not improve OS but improved the response rate and progression-free survival with increased toxicities. These results encourage biomarker-driven studies of angiogenesis inhibitors with better toxicity profiles in select patients with SCCHN

Zika virus pathogenesis in rhesus macaques is unaffected by pre-existing immunity to dengue virus

Zika virus (ZIKV) is a re-emerging virus that has recently spread into dengue virus (DENV) endemic regions and cross-reactive antibodies (Abs) could potentially affect ZIKV pathogenesis. Using DENV-immune serum, it has been shown in vitro that antibody-dependent enhancement (ADE) of ZIKV infection can occur. Here we study the effects of pre-existing DENV immunity on ZIKV infection in vivo. We infect two cohorts of rhesus macaques with ZIKV; one cohort has been exposed to DENV 2.8 years earlier and a second control cohort is naïve to flaviviral infection. Our results, while confirming ADE in vitro, suggest that pre-existing DENV immunity does not result in more severe ZIKV disease. Rather our results show a reduction in the number of days of ZIKV viremia compared to naïve macaques and that the previous exposure to DENV may result in modulation of the immune response without resulting in enhancement of ZIKV pathogenesis