Exploring the Latino Paradox: How Economic and Citizenship Status Impact Health

We examined the contributions of economic status (ES) and citizenship status to health differences between European Americans, Latino Americans, and non-citizen Latinos. The investigation was framed using social identity and comparison theories. Southern California residents (N = 2164) were randomly selected to complete a telephone interview. Increases in ES predicted health improvements for European Americans across ES levels. For Latino citizens and non-citizens, ES improvements had no effect on objective health. For subjective health, the Latino paradox existed at the lowest ES level for Latino Americans, and did not exist for non-citizens. For objective health, the paradox existed in both Latino groups at low ES, and additionally for Latino Americans at mid ES. Our findings suggest that compared to Latinos, improvements in ES have a stronger positive impact on the health of European Americans, which is likely due to the social comparisons being made by each cultural group

Ethnic and Immigration Status Differences on Child Indicators of Health for European Americans and Latinos

This study examined the effects of ethnicity and immigration status on subjective and objective health (Body Mass Index; BMI) for Latino and European American children. Social identity and comparison theories were used to frame the investigation. Southern California parents were randomly selected to complete a telephone interview about their children’s health yielding a sample of 165 European American and 152 Latino participants. Compared to European Americans, Latinos evidenced poorer subjective and objective health. Latino children who had a caregiver who was a citizen had better subjective health than Latino children whose caregiver was not a citizen. BMI was correlated with subjective health for European American children but not for Latinos. Our findings add to the literature on the Latino Paradox and the healthy immigrant effect, specifically as it relates to children

Post-processing V&V level II ASC milestone (2360) results.

The 9/30/2007 ASC Level 2 Post-Processing V&V Milestone (Milestone 2360) contains functionality required by the user community for certain verification and validation tasks. These capabilities include loading of edge and face data on an Exodus mesh, run-time computation of an exact solution to a verification problem, delivery of results data from the server to the client, computation of an integral-based error metric, simultaneous loading of simulation and test data, and comparison of that data using visual and quantitative methods. The capabilities were tested extensively by performing a typical ALEGRA HEDP verification task. In addition, a number of stretch criteria were met including completion of a verification task on a 13 million element mesh

Enhanced insulin sensitivity associated with provision of mono and polyunsaturated fatty acids in skeletal muscle cells involves counter modulation of PP2A

International audienceAims/Hypothesis: Reduced skeletal muscle insulin sensitivity is a feature associated with sustained exposure to excess saturated fatty acids (SFA), whereas mono and polyunsaturated fatty acids (MUFA and PUFA) not only improve insulin sensitivity but blunt SFA-induced insulin resistance. The mechanisms by which MUFAs and PUFAs institute these favourable changes remain unclear, but may involve stimulating insulin signalling by counter-modulation/repression of protein phosphatase 2A (PP2A). This study investigated the effects of oleic acid (OA; a MUFA), linoleic acid (LOA; a PUFA) and palmitate (PA; a SFA) in cultured myotubes and determined whether changes in insulin signalling can be attributed to PP2A regulation. Principal Findings: We treated cultured skeletal myotubes with unsaturated and saturated fatty acids and evaluated insulin signalling, phosphorylation and methylation status of the catalytic subunit of PP2A. Unlike PA, sustained incubation of rat or human myotubes with OA or LOA significantly enhanced Akt-and ERK1/2-directed insulin signalling. This was not due to heightened upstream IRS1 or PI3K signalling nor to changes in expression of proteins involved in proximal insulin signalling, but was associated with reduced dephosphorylation/inactivation of Akt and ERK1/2. Consistent with this, PA reduced PP2Ac demethylation and tyrosine 307 phosphorylation-events associated with PP2A activation. In contrast, OA and LOA strongly opposed these PA-induced changes in PP2Ac thus exerting a repressive effect on PP2A.Conclusions/Interpretation: Beneficial gains in insulin sensitivity and the ability of unsaturated fatty acids to oppose palmitate-induced insulin resistance in muscle cells may partly be accounted for by counter-modulation of PP2A

Endogenous cholinergic inputs and local circuit mechanisms govern the phasic mesolimbic dopamine response to nicotine

Nicotine exerts its reinforcing action by stimulating nicotinic acetylcholine receptors (nAChRs) and boosting dopamine (DA) output from the ventral tegmental area (VTA). Recent data have led to a debate about the principal pathway of nicotine action: direct stimulation of the DAergic cells through nAChR activation, or disinhibition mediated through desensitization of nAChRs on GABAergic interneurons. We use a computational model of the VTA circuitry and nAChR function to shed light on this issue. Our model illustrates that the α4β2-containing nAChRs either on DA or GABA cells can mediate the acute effects of nicotine. We account for in vitro as well as in vivo data, and predict the conditions necessary for either direct stimulation or disinhibition to be at the origin of DA activity increases. We propose key experiments to disentangle the contribution of both mechanisms. We show that the rate of endogenous acetylcholine input crucially determines the evoked DA response for both mechanisms. Together our results delineate the mechanisms by which the VTA mediates the acute rewarding properties of nicotine and suggest an acetylcholine dependence hypothesis for nicotine reinforcement.Peer reviewe

Event-by-event fluctuations in Mean pTp_T and Mean eTe_T in sqrt(s_NN) = 130 GeV Au+Au Collisions

Distributions of event-by-event fluctuations of the mean transverse momentum and mean transverse energy near mid-rapidity have been measured in Au+Au collisions at sqrt(s_NN) = 130 GeV at RHIC. By comparing the distributions to what is expected for statistically independent particle emission, the magnitude of non-statistical fluctuations in mean transverse momentum is determined to be consistent with zero. Also, no significant non-random fluctuations in mean transverse energy are observed. By constructing a fluctuation model with two event classes that preserve the mean and variance of the semi-inclusive p_T or e_T spectra, we exclude a region of fluctuations in sqrt(s_NN) = 130 GeV Au+Au collisions.Comment: 10 pages, RevTeX 3, 7 figures, 4 tables, 307 authors, submitted to Phys. Rev. C on 22 March 2002. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (will be made) publicly available at http://www.phenix.bnl.gov/phenix/WWW/run/phenix/papers.htm

Contribution of Cystine-Glutamate Antiporters to the Psychotomimetic Effects of Phencyclidine

Altered glutamate signaling contributes to a myriad of neural disorders, including schizophrenia. While synaptic levels are intensely studied, nonvesicular release mechanisms, including cystine–glutamate exchange, maintain high steady-state glutamate levels in the extrasynaptic space. The existence of extrasynaptic receptors, including metabotropic group II glutamate receptors (mGluR), pose nonvesicular release mechanisms as unrecognized targets capable of contributing to pathological glutamate signaling. We tested the hypothesis that activation of cystine–glutamate antiporters using the cysteine prodrug N-acetylcysteine would blunt psychotomimetic effects in the rodent phencyclidine (PCP) model of schizophrenia. First, we demonstrate that PCP elevates extracellular glutamate in the prefrontal cortex, an effect that is blocked by N-acetylcysteine pretreatment. To determine the relevance of the above finding, we assessed social interaction and found that N-acetylcysteine reverses social withdrawal produced by repeated PCP. In a separate paradigm, acute PCP resulted in working memory deficits assessed using a discrete trial t-maze task, and this effect was also reversed by N-acetylcysteine pretreatment. The capacity of N-acetylcysteine to restore working memory was blocked by infusion of the cystine–glutamate antiporter inhibitor (S)-4-carboxyphenylglycine into the prefrontal cortex or systemic administration of the group II mGluR antagonist LY341495 indicating that the effects of N-acetylcysteine requires cystine–glutamate exchange and group II mGluR activation. Finally, protein levels from postmortem tissue obtained from schizophrenic patients revealed significant changes in the level of xCT, the active subunit for cystine–glutamate exchange, in the dorsolateral prefrontal cortex. These data advance cystine–glutamate antiporters as novel targets capable of reversing the psychotomimetic effects of PCP

Measurement of the mid-rapidity transverse energy distribution from sNN=130\sqrt{s_{NN}}=130 GeV Au+Au collisions at RHIC

The first measurement of energy produced transverse to the beam direction at RHIC is presented. The mid-rapidity transverse energy density per participating nucleon rises steadily with the number of participants, closely paralleling the rise in charged-particle density, such that E_T / N_ch remains relatively constant as a function of centrality. The energy density calculated via Bjorken's prescription for the 2% most central Au+Au collisions at sqrt(s_NN)=130 GeV is at least epsilon_Bj = 4.6 GeV/fm^3 which is a factor of 1.6 larger than found at sqrt(s_NN)=17.2 GeV (Pb+Pb at CERN).Comment: 307 authors, 6 pages, 4 figures, 1 table, submitted to PRL 4/18/2001; revised version submitted to PRL 5/24/200

Net Charge Fluctuations in Au + Au Interactions at sqrt(s_NN) = 130 GeV

Data from Au + Au interactions at sqrt(s_NN) = 130 GeV, obtained with the PHENIX detector at RHIC, are used to investigate local net charge fluctuations among particles produced near mid-rapidity. According to recent suggestions, such fluctuations may carry information from the Quark Gluon Plasma. This analysis shows that the fluctuations are dominated by a stochastic distribution of particles, but are also sensitive to other effects, like global charge conservation and resonance decays.Comment: 6 pages, RevTeX 3, 3 figures, 307 authors, submitted to Phys. Rev. Lett. on 21 March, 2002. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (will be made) publicly available at http://www.phenix.bnl.gov/phenix/WWW/run/phenix/papers.htm

Flow Measurements via Two-particle Azimuthal Correlations in Au + Au Collisions at sqrt(s_NN) = 130 GeV

Two particle azimuthal correlation functions are presented for charged hadrons produced in Au + Au collisions at RHIC sqrt(s_NN) = 130 GeV. The measurements permit determination of elliptic flow without event-by-event estimation of the reaction plane. The extracted elliptic flow values v_2 show significant sensitivity to both the collision centrality and the transverse momenta of emitted hadrons, suggesting rapid thermalization and relatively strong velocity fields. When scaled by the eccentricity of the collision zone, epsilon, the scaled elliptic flow shows little or no dependence on centrality for charged hadrons with relatively low p_T. A breakdown of this epsilon scaling is observed for charged hadrons with p_T > 1.0 GeV/c for the most central collisions.Comment: 6 pages, RevTeX 3, 4 figures, 307 authors, submitted to Phys. Rev. Lett. on 11 April 2002. Plain text data tables for the points plotted in figures for this and previous PHENIX publications are (will be made) publicly available at http://www.phenix.bnl.gov/phenix/WWW/run/phenix/papers.htm