This suggests that individual studies may be prone to Type II errors, but also that our results represent the most robustly replicated group differences. Finally, our metaanalysis provides an estimate of how consistently clusters of differential activation occur in particular brain regions when comparing groups of individuals, and not the mean activation difference in these regions. Therefore traditional measures of heterogeneity and publication bias that are based on the effect size of group differences are not applicable. Borrelia burgdorferi is the causative agent of Lyme disease, the most prevalent vector-borne disease in the United States and Europe. In Sorafenib nature, B. burgdorferi cycles between rodent reservoirs and Ixodes scapularis ticks. This complex enzootic life cycle requires successful colonization and coordinated transmission between strikingly different host and vector environments. It is thought that differential gene expression plays an important role in allowing the spirochete to navigate the transitions between hosts and in establishing persistent infection. Due to the availability of excellent murine models of Lyme disease, B. burgdorferi gene expression through the tick-rodent transmission cycle can be examined in the laboratory. These efforts may provide important clues for understanding functions of microbial gene products that support B. burgdorferi persistence in nature. The genes encoding the Complement Regulator-Acquiring Surface Proteins of B. burgdorferi are differentially expressed in the pathogen life cycle. As many as five BbCRASPs were identified that bind host proteins of the factor H family, and possibly contribute to the spirochete defense against host complement-mediating killing. BbCRASP-1 and BbCRASP-2, located on linear plasmids lp54 and lp28-3 respectively, share little sequence homology with other BbCRASP sequences. In contrast, BbCRASP-3, -4 and -5 are sequentially similar and belong to the erp paralog GDC-0941 family and are known as erpP, erpC and erpA, respectively. Collectively these erp genes are also known as ospE, and are encoded on multiple cp32 plasmids. The gene erpC and one of the three erpA genes currently lack TIGR database annotations, as the sequenced B31 M1 isolate lost these plasmids. Of all the BbCRASP genes, BbCRASP-2 is the only gene without paralogous family members, and is therefore unique in B. burgdorferi. Evasion of host complement is especially important for B. burgdorferi, as it establishes an extracellular and disseminated infection in many tissue environments where the complement system is readily available through host vasculature or body fluids. The complement system includes soluble membrane binding proteins which, upon contact with foreign cells, become activated, and are then capable of direct chemical lysis via membrane disruption. Specific regulatory proteins, such as FH family proteins, protect the host from self-inflicted damage by preventing unwarranted complement activation.