g., smoking with changes to brain volume) may be unidirectional, bidirectional, or mediated by other shared factors. In addition, there currently exists a paucity of research assessing a particular pathway in concert with smoking and anxiety. Few prospective data are available assessing the impact of changes to specific systems on anxiety symptoms in response to cigarette smoking. In addition, aside from Inhibitors,research,lifescience,medical the inherent difficulties

in translating animal model data to humans, many of the above associations displayed variability in results depending upon study variables, including animal model used or experimental design. In addition, much of the literature has focused solely on the role of nicotine and not the other known toxic ingredients of cigarette smoke including free radicals Inhibitors,research,lifescience,medical and metals. There was also significant variability in expression and function of these systems between different groups (e.g., men vs. women) and individuals within these groups, and hence

much further work is required to ascertain how these influences draw together. Understanding reasons underpinning differential expression between groups may help clarify further key elements to anxiety development. Women, for example, are known to exhibit higher rates of anxiety disorders, which likely relates to a combination of biological (e.g., different hormonal compositions) and Inhibitors,research,lifescience,medical psychological factors, and hence further analysis of these effects on the described pathways may prove enlightening. Inhibitors,research,lifescience,medical The acute and long-term effects of any agent that causes a robust homeostatic adaptation are often quite different; this needs to be taken into account in interpretation of acute data, and in extrapolating to management strategies. Future research efforts in this area should attempt to address some of these Paclitaxel challenges. First, it would be useful to ascertain the effects of nicotine versus other cigarette constituents to the above pathways in humans.

The use of Inhibitors,research,lifescience,medical populations with high consumption of Snus, such as Norway, presents as opportunity for such analyses to be conducted prospectively, and combined with follow-up behavioral assessments, serum analysis of relevant markers (e.g., inflammatory or O&NS), assessment of genetic function, and functional and structural imaging. Such studies could be extended over time to investigate specific changes between different anxiety disorders (e.g., Drug_discovery PD, GAD, PTSD), different subsets of the promotion info population (e.g., cultural or gender groups), and in individuals with other risk elements known to influence these similar pathways (e.g., history of childhood trauma, comorbid medical illness). It is likely that interindividual differences in genetics and epigenetic alterations will also complicate these effects, and as such further exploration of this evolving area will be of foremost importance.