Interestingly, CD36 deficiency did not attenuate the malaria induced decrease in the reflection coefficient. Recent evidence suggests that the oncotic gradient is largely determined by the sieving properties of the glycocalyx, a complex network of surface glycopoproteins that covers the luminal surface of vascular endothelial cells and extends into the intercellular clefts. Thus, it is likely that the low salb from malaria infection indicates loss of glycocalyx integrity. This putative loss of the glycocalyx appears to be a CD36-independent event, perhaps due to the activation of an endogenous heparanase by circulating cytokines. There are additional ICG-001 iRBC-related factors that may contribute to the malaria-induced increase in fluid permeability. Macrophages have been shown to be important in phagocytizing malariainfected RBCs in the spleen and are implicated in controlling the parasite load in the lungs. It is possible that parasiteactivated macrophages or other inflammatory cells also produce ROS to cause parasite killing. In addition, Gillrie et al have shown that free merozoite proteins have an adverse effect on microvascular endothelial permeability in vitro, suggesting 
that rupturing of iRBCs in lung capillaries may play a role. Further work is required to define the relative roles of CD36 ligation, ROS and other parasite-derived factors in the adverse effects on the pulmonary endothelial barrier. The in vitro data in MLMVEC monolayers and the in vivo results in malaria-infected lungs implicate Fyn kinase as a critical downstream mediator of CD36-dependent lung endothelial dysfunction. Fyn is known to regulate endothelial barrier function and to co-localize with the cytoplasmic domain of CD36 in microvascular endothelial cells. In conclusion, this study is the first to show the critical roles that CD36 and the tyrosine kinase Fyn play as mediators of the increased pulmonary endothelial permeability found in malariainfected mice. In addition, these data suggest that CD36 is necessary for the appropriate cellular compartmentalization and activation of Fyn and that infection�Cinduced ROS may serve as an enhancing factor in the mechanism that results in pulmonary edema. Although additional experiments are necessary to fully elucidate these mechanisms, our data identify new potential targets for future treatments of malaria-induced lung injury. With a lifetime prevalence of 2�C3% and a median prevalence for the total population of also 2�C3%, obsessivecompulsive disorder is one of the most frequent adult psychiatric disorders, often showing a chronic or recurrent course. The PR-171 impact of obsessions and compulsions on a person��s quality of life is considerable. In addition to the symptoms themselves, which are subdivided into different subtypes such as washing/contamination fear, controlling/checking, symmetry/ordering, hoarding, and aggressive, sexual, or religious thoughts, a number of neuropsychological impairments have been described. Neurobiological models assume an impaired serotonin and dopamine metabolism especially in the fronto-striato-thalamic system. Within these fronto-striato-thalamic loops, different feedback mechanisms are interacting with each other. The indirect loop allows for projection inhibition from thalamic to cortical regions and thus for situational appropriate and flexible behavior. It appears that in OCD patients these inhibitions of thalamo-cortical projections originating at the striatum are shifted in favor of the direct and activating loop. In more recent models, the classic fronto-striato-thalamic system that proceeds to the dorsal striatum was supplemented by a second network, including the ventral striatum and essential structures of the limbic system. The central interfaces between these systems are the orbitofrontal cortex and the anterior cingulate cortex.