Irregular Migration, Trafficking and Smuggling of Human Beings: Policy Dilemmas in the EU. CEPS Paperback, 22 February 2016

The expert contributors to this edited volume, representing a multidisciplinary selection of academics, examine the treatment of irregular migration, human trafficking and smuggling in EU law and policy. The various chapters explore the policy dilemmas encountered in efforts to criminalise irregular migration and humanitarian assistance to irregular immigrants. The book aims to provide academic input to informed policy-making in the next phase of the European Agenda on Migration. In his Foreword, Matthias Ruete, Director General of DG Home Affairs of the European Commission, writes: “This initiative aims to stimulate evidence-based policy-making and to bring fresh thinking to develop more effective policies. The European Commission welcomes the valuable contribution of this initiative to help close the wide gap in our knowledge about the smuggling of migrants, and especially the functioning of smuggling networks.”

Characteristics of nonpoint source urban runoff and its effects on stream ecosystems /

Mode of access: Internet.

Surfactant effects on pesticide photochemistry in water and soil /

Grant no. R-802959.

Sulfuric acid rain effects on crop yield and foliar injury /

Mode of access: Internet.

Photochemical oxidant air pollution effects on a mixed conifer forest ecosystem : final report /

Mode of access: Internet.

Age effects on symbol sign recognition. Final report.

Federal Highway Administration, Washington, D.C.

Effect of chlorination on human enteric viruses in partially treated water from the Potomac River estuary : study report /

At head of cover title: Northeastern United States Water Supply Study.

Trends in wastepaper exports and their effects on domestic markets /

Mode of access: Internet.

Environmental carcinogens and human cancer : estimation of exposure to carcinogens in the ambient air /

Sponsored by Health Effects Research Laboratory, Research Triangle Park, N.C.

Assessing effects on water quality by boating activity. --

Mode of access: Internet.

Pollution effects on adult steelhead migration in the Snake River,

Prepared for Office of Research and Development, U.S. Environmental Protection Agency under project 18050DMB, program element 1B1021.

Relative effects on stream biota of chlorine and ammonia occurring in secondary sewage /

"Project no. 20./32."

Soil, Clay, and caustic soda effects on solubility, sorption, and mobility of hexachlorocyclopentadiene /

Bibliography: p. 51-54.

High glucose-mediated effects on endothelial cell proliferation occur via p38 MAP kinase

The mitogen-activated protein ( MAP) kinases contribute to altered cell growth and function in a variety of disease states. However, their role in the endothelial complications of diabetes mellitus remains unclear. Human endothelial cells were exposed for 72 h to 5 mM ( control) or 25 mM ( high) glucose or 5 mM glucose plus 20 mM mannitol ( osmotic control). The roles of p38 and p42/44 MAP kinases in the high glucose-induced growth effects were determined by assessment of phosphorylated MAP kinases and their downstream activators by Western blot and by pharmacological inhibition of these MAP kinases. Results were expressed as a percentage ( means +/- SE) of control. High glucose increased the activity of total and phosphorylated p38 MAP kinase ( P < 0.001) and p42/44 MAP kinase ( P < 0.001). Coexposure of p38 MAP kinase blocker with high glucose reversed the antiproliferative but not the hypertrophic effects associated with high-glucose conditions. Transforming growth factor (TGF)-beta1 increased the levels of phosphorylated p38 MAP kinase, and p38 MAP kinase blockade reversed the antiproliferative effects of this cytokine. The high glucose-induced increase in phosphorylated p38 MAP kinase was reversed in the presence of TGF-beta1 neutralizing antibody. Although hyperosmolarity also induced antiproliferation (P < 0.0001) and cell hypertrophy (P < 0.05), there was no change in p38 activity, and therefore inhibition of p38 MAP kinase had no influence on these growth responses. Blockade of p42/44 MAP kinase had no effect on the changes in endothelial cell growth induced by either high glucose or hyperosmolarity. High glucose increased p42/44 and p38 MAP kinase activity in human endothelial cells, but only p38 MAP kinase mediated the antiproliferative growth response through the effects of autocrine TGF-beta1. High glucose-induced endothelial cell hypertrophy was independent of activation of the MAP kinases studied. In addition, these effects were independent of any increase in osmolarity associated with high-glucose exposure.

Genetic effects on alcohol dependence risk: re-evaluating the importance of psychiatric and other heritable risk factors

Background. Genetic influences have been shown to play a major role in determining the risk of alcohol dependence (AD) in both women and men; however, little attention has been directed to identifying the major sources of genetic variation in AD risk. Method. Diagnostic telephone interview data from young adult Australian twin pairs born between 1964 and 1971 were analyzed. Cox regression models were fitted to interview data from a total of 2708 complete twin pairs (690 MZ female, 485 MZ male, 500 DZ female, 384 DZ male, and 649 DZ female/male pairs). Structural equation models were fitted to determine the extent of residual genetic and environmental influences on AD risk while controlling for effects of sociodemographic and psychiatric predictors on risk. Results. Risk of AD was increased in males, in Roman Catholics, in those reporting a history of major depression, social anxiety problems, and conduct disorder, or (in females only) a history of suicide attempt and childhood sexual abuse; but was decreased in those reporting Baptist, Methodist, or Orthodox religion, in those who reported weekly church attendance, and in university-educated males. After allowing for the effects of sociodemographic and psychiatric predictors, 47 % (95 % CI 28-55) of the residual variance in alcoholism risk was attributable to additive genetic effects, 0 % (95 % CI 0-14) to shared environmental factors, and 53 % (95 % CI 45-63) to non-shared environmental influences. Conclusions. Controlling for other risk factors, substantial residual heritability of AD was observed, suggesting that psychiatric and other risk factors play a minor role in the inheritance of AD.