RESUMO
Acute febrile illness (AFI) is a broad clinical syndrome with a wide range of potential infectious etiologies. The lack of accessible, standardized approaches to conducting AFI etiologic investigations has contributed to significant global gaps in data on the epidemiology of AFI. Based on lessons learned from years of supporting AFI sentinel surveillance worldwide, the U.S. Centers for Disease Control and Prevention developed the toolkit for planning and implementing AFI surveillance, described here. This toolkit provides a comprehensive yet flexible framework to guide researchers, public health officials, and other implementers in developing a strategy to identify and/or monitor the potential causes of AFI. The toolkit comprises a cohesive set of planning aids and supporting materials, including an implementation framework, generic protocol, several generic forms (including screening, case report, specimen collection and testing, and informed consent and assent), and a generic data dictionary. These materials incorporate key elements intended to harmonize approaches for AFI surveillance, as well as setting-specific components and considerations for adaptation based on local surveillance objectives and limitations. Appropriate adaptation and implementation of this toolkit may generate data that expand the global AFI knowledge base, strengthen countries' surveillance and laboratory capacity, and enhance outbreak detection and response efforts.
RESUMO
Adult fish produce new cells throughout their central nervous system during the course of their lives and maintain a tremendous capacity to repair damaged neural tissue. Much of the focus on understanding brain repair and regeneration in adult fish has been directed at regions of the brainstem and forebrain; however, the mesencephalon (midbrain) and diencephalon have received little attention. We sought to examine differential gene expression in the midbrain/diencephalon in response to injury in the adult fish using RNA-seq. Using the mummichog (Fundulus heteroclitus), we administered a mechanical lesion to the midbrain/diencephalon and examined differentially expressed genes (DEGs) at an acute recovery time of 1 h post-injury. Comparisons of whole transcriptomes derived from isolated RNA of intact and injured midbrain/diencephalic tissue identified 404 DEGs with the vast majority being upregulated. Using qPCR, we validated the upregulation of DEGs pim-2-like, syndecan-4-like, and cd83. Based on genes both familiar and novel regarding the adult brain response to injury, these data provide an extensive molecular profile giving insight into a range of cellular processes involved in the injury response of a brain regenerative-capable vertebrate.