(Table 1) Lipid content and organohalogen contaminant concentration in plasma of incubating glaucous gulls (Larus hyperboreus) from Bjørnøya, Norwegian Arctic in 2006

The factors influencing prolactin (PRL) variation in birds and in wildlife in general have rarely been investigated with respect to the physiological impacts of exposure to environmental contaminants. We investigated the associations between circulating baseline PRL levels and concentrations of eight persistent organohalogen contaminant (OHC) classes (i.e., major organochlorines and brominated flame retardants, and associated metabolic products) in blood (plasma) of free-ranging glaucous gulls (Larus hyperboreus), a top predator in the Norwegian Arctic, engaged in the process of incubation. We further examined whether plasma OHC concentrations were associated with the variation of PRL in glaucous gulls exposed to a standardized capture/restraint protocol. Plasma OHC concentrations in male glaucous gulls were 2-to 3-fold higher relative to females. Baseline PRL levels tended to be higher in females compared to males, although not significantly (p = 0.20). In both males and females, the 30-min capture/restraint protocol led on average to a 26% decrease in PRL levels, which resulted in a rate of PRL decrease of 0.76 ng/mL/min. The baseline PRL levels and the rate of decrease in PRL levels tended to vary negatively with plasma OHC concentrations in males, but not in females, although several of these associations did not adhere with the criterion of significance (alpha = 0.05). Present results suggest that in highly OHC-exposed male glaucous gulls, the control of PRL release may be affected by the direct or indirect modulating actions of OHCs and/or their metabolically derived products. We conclude that potentially OHC-mediated impact on PRL secretion in glaucous gulls (males) may be a contributing factor to the adverse effects observed on the reproductive behavior, development and population size of glaucous gulls breeding in the Norwegian Arctic.

Social stress and the reactivation of latent herpes simplex virus type 1

Psychological stress is thought to contribute to reactivation of latent herpes simplex virus (HSV). Although several animal models have been developed in an effort to reproduce different pathogenic aspects of HSV keratitis or labialis, until now, no good animal model existed in which application of a psychological laboratory stressor results in reliable reactivation of the virus. Reported herein, disruption of the social hierarchy within colonies of mice increased aggression among cohorts, activated the hypothalamic-pituitary-adrenal axis, and caused reactivation of latent HSV type 1 in greater than 40% of latently infected animals. However, activation of the hypothalamic-pituitary-adrenal axis using restraint stress did not activate the latent virus. Thus, the use of social stress in mice provides a good model in which to investigate the neuroendocrine mechanisms that underlie behaviorally mediated reactivation of latent herpesviruses.

Experimental diabetes in rats causes hippocampal dendritic and synaptic reorganization and increased glucocorticoid reactivity to stress

We report that 9 d of uncontrolled experimental diabetes induced by streptozotocin (STZ) in rats is an endogenous chronic stressor that produces retraction and simplification of apical dendrites of hippocampal CA3 pyramidal neurons, an effect also observed in nondiabetic rats after 21 d of repeated restraint stress or chronic corticosterone (Cort) treatment. Diabetes also induces morphological changes in the presynaptic mossy fiber terminals (MFT) that form excitatory synaptic contacts with the proximal CA3 apical dendrites. One effect, synaptic vesicle depletion, occurs in diabetes as well as after repeated stress and Cort treatment. However, diabetes produced other MFT structural changes that differ qualitatively and quantitatively from other treatments. Furthermore, whereas 7 d of repeated stress was insufficient to produce dendritic or synaptic remodeling in nondiabetic rats, it potentiated both dendritic atrophy and MFT synaptic vesicle depletion in STZ rats. These changes occurred in concert with adrenal hypertrophy and elevated basal Cort release as well as hypersensitivity and defective shutoff of Cort secretion after stress. Thus, as an endogenous stressor, STZ diabetes not only accelerates the effects of exogenous stress to alter hippocampal morphology; it also produces structural changes that overlap only partially with those produced by stress and Cort in the nondiabetic state.

Transcriptionally active Stat1 is required for the antiproliferative effects of both interferon alpha and interferon gamma.

Type I (alpha, beta) and type II (gamma) interferons (IFNs) can restrict the growth of many cell types. INF-stimulated gene transcription, a key early event in IFN response, acts through the Janus kinase-signal transducers and activators of transcription pathway, in which both IFN-alpha and IFN-gamma activate the transcription factor Stat1. A cell line lacking Stat1 (U3A) was not growth-arrested by IFN-alpha or IFN-gamma, and experiments were carried out with U3A cells permanently expressing normal or various mutant forms of Stat1 protein. Only cells in which complete Stat1 activity was available (Stat1alpha) were growth-inhibited by IFN-gamma. A mutant that supports 20-30% normal transcription did not cause growth restraint. In contrast, IFN-alpha growth restraint was imposed by cells producing Stat1beta, which lacks transcriptional activation potential. This parallels earlier results showing the truncated Stat1 can function in IFN-alpha gene activation. In addition to experiments on long-term cultured cells, we also found that wild-type primary mouse embryonic fibroblasts were inhibited by IFNs, but fibroblasts from Stat1-deficient mouse embryos were not inhibited by IFNs.

The Drivers of Current Account Surplus in Germany and the Politics of Rebalancing in the Eurozone. EU Centre, Singapore Working Paper No. 24, April 2015

Current account deficits have caught the public’s attention as they have contributed to the European debt crisis. However, surpluses also constitute an issue as a deficit in any country must be financed through a surplus in another country. In 2013, Germany, now the world’s largest surplus economy, registered a record high US$273 billion surplus. This paper looks at what accounts for Germany’s surplus, revealing that the major driving factors include strong global demand for quality German exports, domestic wage restraint, an undervalued single currency, high domestic savings rate and interest rate convergence in the euro area. This paper echoes the US Treasury’s view that a persistent German surplus makes it harder for the eurozone as a whole and the southern peripheral economies in particular to recover from the current financial crisis by imposing a Europe-wide “deflationary bias” through pushing up the exchange rate of the euro, exporting feeble German inflation and projecting its ultra-tight macroeconomic policies onto crisis economies. This paper contends that Germany’s trade surplus is likely to endure as Germany and other eurozone countries uphold diverging views on the nature of the surplus engage in a blame-game amidst a sluggish rebalancing process. Prizing the surplus as a reflection of hard work and economic competitiveness, German authorities urge their southern eurozone colleagues to undertake bold structural reforms to correct the imbalance, while the hand-tied governments in crisis-stricken economies call on Germany to do its “homework” by boosting German demands for European goods and services.

Evaluation of New York State's Mandatory Occupant Restraint Law. Volume II - attitudinal surveys of licensed drivers in New York state. Final report.

National Highway Traffic Safety Administration, Washington, D.C.

Upgrade Volvo production restraint systems. Final report.

National Highway Traffic Safety Administration, Washington, D.C.

Augmentation of research and analysis capabilities for timely support of automotive fuel economy activities. Final report.

National Highway Traffic Safety Administration, Washington, D.C.

Cases on restraint of trade.

Mode of access: Internet.

Performance testing of an improved driver restraint system for subcompact cars. Volume II - final report.

National Highway Traffic Safety Administration, Washington, D.C.

Development of a test methodology for evaluating crash compatibility and aggressiveness. Test report 1: 1975 Honda Civic CVCC-to-NHTSA test device.

National Highway Traffic Safety Administration, Washington, D.C.

Development of a test methodology for evaluating crash compatibility and aggressiveness. Test report 2: 1975 Ford Torino-to-NHTSA test device.

National Highway Traffic Safety Administration, Washington, D.C.

Safety systems optimization model (SSOM). Final report. Volume 1 - introduction and executive summary.

National Highway Traffic Safety Administration, Washington, D.C.

Identification of approaches for the control of health, environmental, and safety hazards associated with air bag use and disposal. Final report.

National Highway Traffic Safety Administration, Washington, D.C.

Child restraint systems testing. Appendix. Final report.

Mode of access: Internet.