Smoking, drinking and body weight after re-employment: does unemployment experience and compensation make a difference?

<p>Abstract</p> <p>Background</p> <p>The impact of unemployment on behaviours such as smoking, drinking and body weight has been extensively researched. However, little is known about the possible protective effects of social assistance programs on these behavioural changes. This study examines the impact of unemployment periods on smoking, drinking and body weight changes among re-employed individuals and investigates whether the receipt of unemployment benefits influences these behaviours.</p> <p>Methods</p> <p>This study used panel data provided by the Panel Study of Income Dynamics. Logistic regression models were used to analyze whether a period of unemployment in 2000 resulted in an increase in smoking and drinking or fluctuations in body weight among 2001 re-employed individuals in comparison with 1999 baseline levels. A total of 3,451 respondents who had been initially healthy and who had been continuously employed between 1998 and 1999 were included in the analysis.</p> <p>Results</p> <p>Compared to stably employed respondents, those who had experienced periods of unemployment in 2000 and did not receive unemployment benefits were more likely than continuously employed individuals to report an increase in alcohol consumption (OR 1.8, 95% CI 1.0–3.1) and a decrease in body weight (OR 1.7, 95% CI 1.1–2.8) when they were already re-employed in 2001.</p> <p>Conclusion</p> <p>Our findings suggest that the receipt of unemployment benefits confers a protective effect on health behavioural changes following periods of unemployment. These findings underscore the need to monitor the impact of unemployment assistance programs on health, particularly in light of the rapidly changing structure of employment and unemployment benefits.</p

Homeostatic regulation of the endoneurial microenvironment during development, aging and in response to trauma, disease and toxic insult

The endoneurial microenvironment, delimited by the endothelium of endoneurial vessels and a multi-layered ensheathing perineurium, is a specialized milieu intérieur within which axons, associated Schwann cells and other resident cells of peripheral nerves function. The endothelium and perineurium restricts as well as regulates exchange of material between the endoneurial microenvironment and the surrounding extracellular space and thus is more appropriately described as a blood–nerve interface (BNI) rather than a blood–nerve barrier (BNB). Input to and output from the endoneurial microenvironment occurs via blood–nerve exchange and convective endoneurial fluid flow driven by a proximo-distal hydrostatic pressure gradient. The independent regulation of the endothelial and perineurial components of the BNI during development, aging and in response to trauma is consistent with homeostatic regulation of the endoneurial microenvironment. Pathophysiological alterations of the endoneurium in experimental allergic neuritis (EAN), and diabetic and lead neuropathy are considered to be perturbations of endoneurial homeostasis. The interactions of Schwann cells, axons, macrophages, and mast cells via cell–cell and cell–matrix signaling regulate the permeability of this interface. A greater knowledge of the dynamic nature of tight junctions and the factors that induce and/or modulate these key elements of the BNI will increase our understanding of peripheral nerve disorders as well as stimulate the development of therapeutic strategies to treat these disorders