Predispositions and the Political Behavior of American Economic Elites: Evidence from Technology Entrepreneurs

Economic elites regularly seek to exert political influence. But what policies do they support? Many accounts implicitly assume economic elites are homogeneous and that increases in their political power will increase inequality. We shed new light on heterogeneity in economic elites' political preferences, arguing that economic elites from an industry can share distinctive preferences due in part to sharing distinctive predispositions. Consequently, how increases in economic elites' influence affect inequality depends on which industry's elites are gaining influence and which policy issues are at stake. We demonstrate our argument with four original surveys, including the two largest political surveys of American economic elites to date: one of technology entrepreneurs—whose influence is burgeoning—and another of campaign donors. We show that technology entrepreneurs support liberal redistributive, social, and globalistic policies but conservative regulatory policies—a bundle of preferences rare among other economic elites. These differences appear to arise partly from their distinctive predispositions

A Uniform Analysis of the Ly-alpha Forest at z=0 - 5: V. The extragalactic ionizing background at low redshift

In Paper III of our series "A Uniform Analysis of the Ly-alpha forest at z=0 - 5", we presented a set of 270 quasar spectra from the archives of the Faint Object Spectrograph on the Hubble Space Telescope. A total of 151 of these spectra, yielding 906 lines, are suitable for using the proximity effect signature to measure J(\nu_0), the mean intensity of the hydrogen-ionizing background radiation field, at low redshift. Using a maximum likelihood technique and the best estimates possible for each QSO's Lyman limit flux and systemic redshift, we find J(\nu_0)= 7.6^+9.4_-3.0 x 10^-23 ergs s^-1 cm^-2 Hz^-1 sr^-1 at at 0.03 < z < 1.67. This is in good agreement with the mean intensity expected from models of the background which incorporate only the known quasar population. When the sample is divided into two subsamples, consisting of lines with z 1, the values of J(\nu_0) found are 6.5^+38._-1.6 x 10^-23 ergs s^-1 cm^-2 Hz^-1 sr^-1, and 1.0^+3.8_-0.2 x 10^-22 ergs s^-1 cm^-2 Hz^-1 sr^-1, respectively, indicating that the mean intensity of the background is evolving over the redshift range of this data set. Relaxing the assumption that the spectral shapes of the sample spectra and the background are identical, the best fit HI photoionization rates are found to be 6.7 x 10^-13 s^-1 for all redshifts, and 1.9 x 10^-13 s^-1 and 1.3 x 10^-12 s^-1 for z 1, respectively. This work confirms that the evolution of the number density of Ly-alpha lines is driven by a decrease in the ionizing background from z ~ 2 to z ~ 0 as well as by the formation of structure in the intergalactic medium. (Abridged)Comment: 71 LaTeX pages, 20 encapsulated Postscript figures, Accepted for publication in ApJ, Figure 4 available at http://lithops.as.arizona.edu/~jill/QuasarSpectra/ or http://hea-www.harvard.edu/QEDT/QuasarSpectra

A Mouse Model of Zika Virus Pathogenesis

SummaryThe ongoing Zika virus (ZIKV) epidemic and unexpected clinical outcomes, including Guillain-Barré syndrome and birth defects, has brought an urgent need for animal models. We evaluated infection and pathogenesis with contemporary and historical ZIKV strains in immunocompetent mice and mice lacking components of the antiviral response. Four- to six-week-old Irf3−/− Irf5−/− Irf7−/− triple knockout mice, which produce little interferon α/β, and mice lacking the interferon receptor (Ifnar1−/−) developed neurological disease and succumbed to ZIKV infection, whereas single Irf3−/−, Irf5−/−, and Mavs−/− knockout mice exhibited no overt illness. Ifnar1−/− mice sustained high viral loads in the brain and spinal cord, consistent with evidence that ZIKV causes neurodevelopmental defects in human fetuses. The testes of Ifnar1−/− mice had the highest viral loads, which is relevant to sexual transmission of ZIKV. This model of ZIKV pathogenesis will be valuable for evaluating vaccines and therapeutics as well as understanding disease pathogenesis

Human fluids alter DNA-acquisition in Acinetobacter baumannii

Transformation is one of the mechanisms of acquisition of foreign genetic material leading to the emergence of multidrug resistant (MDR) bacteria. Recently, human serum albumin (HSA) was shown to specifically increase transformation frequency in the nosocomial pathogen Acinetobacter baumannii. To further assess the relevance of HSA as a possible modulator of A. baumannii transformation in host-pathogen interactions, in this work we examined the effect of different human fluids. We observed a significant increase in transformation frequencies in the presence of pleural fluid, whole blood cells and liquid ascites, and to a lesser extent with urine. The observed effects correlate with both HSA and bacterial content found in the assayed patient fluids. Taken together, these results are in agreement with our previous findings that highlight HSA as a possible host signal with the ability to trigger natural transformation in A. baumannii.Fil: Martinez, Jasmine. California State University; Estados UnidosFil: Liu, Christine. California State University; Estados UnidosFil: Rodman, Nyah. California State University; Estados UnidosFil: Fernandez, Jennifer S.. California State University; Estados UnidosFil: Barberis, Claudia. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; ArgentinaFil: Sieira, Rodrigo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Perez, Federico. Louis Stokes Cleveland Department of Veterans Affairs Medical Center; Estados UnidosFil: Bonomo, Robert A.. Louis Stokes Cleveland Department of Veterans Affairs Medical Center; Estados Unidos. Case Western Reserve University; Estados UnidosFil: Ramirez, Maria Soledad. California State University; Estados Unido

Cervical cancer control for Hispanic women in Texas: Strategies from research and practice

Hispanic women in Texas have among the highest rates of cervical cancer incidence and mortality in the country. Increasing regular Papanicolaou test screening and HPV vaccination are crucial to reduce the burden of cervical cancer among Hispanics. This paper presents lessons learned from community-based cervical cancer control programs in Texas and highlights effective intervention programs, methods and strategies

A Uniform Analysis of the Ly-alpha forest at z = 0 - 5: II. Measuring the mean intensity of the extragalactic ionizing background using the proximity effect

A homogeneous sample of 99 moderate resolution QSO spectra at z > 1.7 were presented in Paper I, including 39 previously unpublished spectra from the Multiple Mirror Telescope. The statistics of the Lyman alpha forest were discussed. In this analysis, we demonstrate that a proximity effect is present in the data, ie. there exists a significant (5.5$\sigma$) deficit of lines at $z_{abs} \approx z_{em}$. Within 1.5 $h^{-1}$ Mpc of the QSO emission redshift, the significance does depend on QSO luminosity, in accordance with the theory that this effect is caused by enhanced ionization of hydrogen in the vicinity of the QSO from UV photons from the QSO itself. The photoionization model of Bajtlik, Duncan, and Ostriker (1988) permits an estimate of the mean intensity of the extragalactic background radiation at the Lyman limit. We compare the results of this standard analysis with those obtained using a maximum likelihood technique. The best fit value for $J(\nu_{0})$ is 7.0$^{+3.4}_{-4.4}$ x 10$^{-22}$ ergs/s/cm$^{2}$/Hz/sr, over the redshift range 1.7 < z < 3.8, using QSO redshifts based on narrow emission lines. The best fit value for the HI ionization rate is 1.9$^{+1.2}_{-1.0}$ x 10$^{-12}$ s$^{-1}$, in good agreement with models of the background which incorporate QSOs only. This large absorption line sample and these techniques for measuring the background and understanding the systematics involved allow us to place what we believe are are the firmest limits on the background at these redshifts.Comment: revised figures 13 and 14, and other minor corrections, 42 Latex pages, 23 encapsulated Postscript figures, uses emulateapj.sty, To appear in the Sept. 2000 ApJ

A Mediterranean Low-Glycemic-Load Diet alone or in Combination with a Medical Food Improves Insulin Sensitivity and Reduces Inflammation in Women with Metabolic Syndrome

Aim: To determine the effects of a Mediterranean-style low-glycemic load diet alone or in combination with a medical food (MF) on insulin resistance and inflammation in women with metabolic syndrome (MetS). Study design: Two groups, Parallel study with control. Place and Duration of Study: Department of Nutritional Sciences, University of Connecticut, Storrs, CT; Department of Emergency Medicine, University of Florida, Jacksonville, FL; Department of Medicine, University of California, Irvine, CA. The study was carried out from September of 2009 to May 2010. Methodology: Eighty three women (20-75 y) with MetS. Participants were randomly allocated to consume diet alone (control group) or the diet plus the MF (MF group) for 12 wk. Body composition was measured at baseline, week 8 and week 12 by use of bioelectrical impedance in all participants while Dual-emission X-ray absorptiometry was used for 37 of the subjects. Insulin resistance, plasma insulin, leptin, adiponectin and the inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin-6 (IL-6), adhesion molecules, sICAM-1 and sVCAM-1, were measured at the same time points. Results: Independent of group allocation, women had decreases in body mass index (p \u3c 0.0001) and body and trunk fat (p \u3c 0.0001). Plasma insulin, insulin resistance, and leptin were also significantly decreased over time (p \u3c 0.0001), while plasma adiponectin levels did not change. Regarding inflammatory markers, significant reductions were found in TNF-α (p \u3c 0.0001) and sICAM-1 levels (p \u3c 0.001), but not in IL-6 or sVCAM-1. At 12 wk, sICAM was reduced only in the MF group (

Cardiac Arrhythmias after Subarachnoid Hemorrhage: Risk Factors and Impact on Outcome

Objective: Serious cardiac arrhythmias have been described in approximately 5% of patients after subarachnoid hemorrhage (SAH). The aim of this study was to identify the frequency, risk factors and clinical impact of cardiac arrhythmia after SAH. Methods: We prospectively studied 580 spontaneous SAH patients and identified risk factors and complications associated with the development of clinically significant arrhythmia. Multiple logistic regression analysis was used to calculate adjusted odds ratios for the effect of arrhythmia on hospital complications and 3-month outcome, as measured by the modified Rankin Scale, after controlling for age, neurological grade, APACHE-2 physiologic subscore, brain herniation and aneurysm size. Results: Arrhythmia occurred in 4.3% (n = 25) of patients. Atrial fibrillation and flutter were the most common arrhythmias, occurring in 76% (n = 19) of these patients. Admission predictors of cardiac arrhythmia included older age, history of arrhythmia and abnormal admission electrocardiogram (all p < 0.05). After adjusting for length of stay, hospital complications associated with arrhythmia included myocardial ischemia, hyperglycemia, and herniation (all p < 0.05). Arrhythmia was associated with an excess ICU stay of 5 days (p = 0.002). After adjusting for other predictors of outcome, arrhythmia was associated with an increased risk of death (adjusted OR 8.0, 95% confidence interval 1.9–34.0, p = 0.005), and death or severe disability (adjusted OR 6.9, 95% confidence interval 1.5–32.0, p = 0.014). Conclusions: Clinically important arrhythmias, most often atrial fibrillation or flutter, occurred in 4% of SAH patients. Arrhythmias are associated with an increased risk of cardiovascular comorbidity, prolonged hospital stay and poor outcome or death after SAH, after adjusting for other predictors of poor outcome

Toll-like receptor signaling adapter proteins govern spread of neuropathic pain and recovery following nerve injury in male mice.

BackgroundSpinal Toll-like receptors (TLRs) and signaling intermediaries have been implicated in persistent pain states. We examined the roles of two major TLR signaling pathways and selected TLRs in a mononeuropathic allodynia.MethodsL5 spinal nerve ligation (SNL) was performed in wild type (WT, C57BL/6) male and female mice and in male Tlr2-/-Tlr3-/-, Tlr4-/-, Tlr5-/-, Myd88-/-, Triflps2, Myd88/Triflps2, Tnf-/-, and Ifnar1-/- mice. We also examined L5 ligation in Tlr4-/- female mice. We examined tactile allodynia using von Frey hairs. Iba-1 (microglia) and GFAP (astrocytes) were assessed in spinal cords by immunostaining. Tactile thresholds were analyzed by 1- and 2-way ANOVA and the Bonferroni post hoc test was used.ResultsIn WT male and female mice, SNL lesions resulted in a persistent and robust ipsilateral, tactile allodynia. In males with TLR2, 3, 4, or 5 deficiencies, tactile allodynia was significantly, but incompletely, reversed (approximately 50%) as compared to WT. This effect was not seen in female Tlr4-/- mice. Increases in ipsilateral lumbar Iba-1 and GFAP were seen in mutant and WT mice. Mice deficient in MyD88, or MyD88 and TRIF, showed an approximately 50% reduction in withdrawal thresholds and reduced ipsilateral Iba-1. In contrast, TRIF and interferon receptor null mice developed a profound ipsilateral and contralateral tactile allodynia. In lumbar sections of the spinal cords, we observed a greater increase in Iba-1 immunoreactivity in the TRIF-signaling deficient mice as compared to WT, but no significant increase in GFAP. Removing MyD88 abrogated the contralateral allodynia in the TRIF signaling-deficient mice. Conversely, IFNβ, released downstream to TRIF signaling, administered intrathecally, temporarily reversed the tactile allodynia.ConclusionsThese observations suggest a critical role for the MyD88 pathway in initiating neuropathic pain, but a distinct role for the TRIF pathway and interferon in regulating neuropathic pain phenotypes in male mice