ment designs. The present study attempts to examine the types of stressors (life events, daily, perceived) that predict relapse and define the within-person temporal relationship between stress and symptom exacerbation. In a sample of 25 CD patients undergoing a biologic treatment, an electronic diary will be used to examine the within-person variations of symptoms and stress within a day and over 8 weeks (time from initial treatment to subsequent treatment). The hypotheses are: 1. Patients who report more stress will relapse sooner compared to those who report less stress. 2. Previous reports of stress will be associated with subsequent reports of symptom exacerbation. Thus, this study will be able to not only identify if stress and disease activity are related, but also the type of stress that most impacts the clinical course of CD. In addition, within-person analyses of the temporal relationship between stress and symptoms may aid in the development of future treatment studies.

The central objective of this proposal is to determine the regulatory mechanisms controlling the accumulation of specific proteins during mouse central nervous system development. 1) The accumulation of the tissue specific enzyme glutamic acid decarboxylase will be examined to determine if the increase in the quantity of the protein is due to a change in the rate of synthesis, the rate of degradation, or a modulation of both parameters. 2) The tissue specific S-100 protein is actually a class of related proteins; we will complete experiments to determine whether each of the mouse S-100 proteins is a direct product of mRNA translation or whether they result from an interconversion process. 3) Mouse CNS mutants showing the appearance of abnormalities at 10 to 25 days postnatally will be surveyed for quantitative and qualitative alterations in soluble proteins. The mutant spastic which does have alterations in brain amino acid pool levels will be examined in detail to determine if this is a result of a change in the activity of an enzyme.