The post-stroke young adult brain has limited capacity to re-express the gene expression patterns seen during early postnatal brain development.

The developmental origins of the brain's response to injury can play an important role in recovery after a brain lesion. In this study, we investigated whether the ischemic young adult brain can re-express brain plasticity genes that were active during early postnatal development. Differentially expressed genes in the cortex of juvenile post-natal day 3 and the peri-infarcted cortical areas of young, 3-month-old post-stroke rats were identified using fixed-effects modeling within an empirical Bayes framework through condition-specific comparison. To further analyze potential biological processes, upregulated and downregulated genes were assessed for enrichment using GSEA software. The genes showing the highest expression changes were subsequently verified through RT-PCR. Our findings indicate that the adult brain partially recapitulates the gene expression profile observed in the juvenile brain but fails to upregulate many genes and pathways necessary for brain plasticity. Of the upregulated genes in post-stroke brains, specific roles have not been assigned to Apobec1, Cenpf, Ect2, Folr2, Glipr1, Myo1f, and Pttg1. New genes that failed to upregulate in the adult post-stroke brain include Bex4, Cd24, Klhl1/Mrp2, Trim67, and St8sia2. Among the upregulated pathways, the largest change was observed in the KEGG pathway "One carbon pool of folate," which is necessary for cellular proliferation, followed by the KEGG pathway "Antifolate resistance," whose genes mainly encode the family of ABC transporters responsible for the efflux of drugs that have entered the brain. We also noted three less-described downregulated KEGG pathways in experimental models: glycolipid biosynthesis, oxytocin, and cortisol pathways, which could be relevant as therapeutic targets. The limited brain plasticity of the adult brain is illustrated through molecular and histological analysis of the axonal growth factor, KIF4. Collectively, these results strongly suggest that further research is needed to decipher the complex genetic mechanisms that prevent the re-expression of brain plasticity-associated genes in the adult brain.

Perception of biological motion in visual agnosia.

Over the past 25 years, visual processing has been discussed in the context of the dual stream hypothesis consisting of a ventral ("what") and a dorsal ("where") visual information processing pathway. Patients with brain damage of the ventral pathway typically present with signs of visual agnosia, the inability to identify and discriminate objects by visual exploration, but show normal perception of motion perception. A dissociation between the perception of biological motion and non-biological motion has been suggested: perception of biological motion might be impaired when "non-biological" motion perception is intact and vice versa. The impact of object recognition on the perception of biological motion remains unclear. We thus investigated this question in a patient with severe visual agnosia, who showed normal perception of non-biological motion. The data suggested that the patient's perception of biological motion remained largely intact. However, when tested with objects constructed of coherently moving dots ("Shape-from-Motion"), recognition was severely impaired. The results are discussed in the context of possible mechanisms of biological motion perception.

Functional analysis of metagenomes and metatranscriptomes using SEED and KEGG.

BACKGROUND: Metagenomics is the study of microbial organisms using sequencing applied directly to environmental samples. Technological advances in next-generation sequencing methods are fueling a rapid increase in the number and scope of metagenome projects. While metagenomics provides information on the gene content, metatranscriptomics aims at understanding gene expression patterns in microbial communities. The initial computational analysis of a metagenome or metatranscriptome addresses three questions: (1) Who is out there? (2) What are they doing? and (3) How do different datasets compare? There is a need for new computational tools to answer these questions. In 2007, the program MEGAN (MEtaGenome ANalyzer) was released, as a standalone interactive tool for analyzing the taxonomic content of a single metagenome dataset. The program has subsequently been extended to support comparative analyses of multiple datasets. RESULTS: The focus of this paper is to report on new features of MEGAN that allow the functional analysis of multiple metagenomes (and metatranscriptomes) based on the SEED hierarchy and KEGG pathways. We have compared our results with the MG-RAST service for different datasets. CONCLUSIONS: The MEGAN program now allows the interactive analysis and comparison of the taxonomical and functional content of multiple datasets. As a stand-alone tool, MEGAN provides an alternative to web portals for scientists that have concerns about uploading their unpublished data to a website.

Perception of global gestalt by temporal integration in simultanagnosia.

Patients with bilateral parieto-occipital brain damage may show intact processing of individual objects, while their perception of multiple objects is disturbed at the same time. The deficit is termed 'simultanagnosia' and has been discussed in the context of restricted visual working memory and impaired visuo-spatial attention. Recent observations indicated that the recognition of global shapes can be modulated by the spatial distance between individual objects in patients with simultanagnosia and thus is not an all-or-nothing phenomenon depending on spatial continuity. However, grouping mechanisms not only require the spatial integration of visual information, but also involve integration processes over time. The present study investigated motion-defined integration mechanisms in two patients with simultanagnosia. We applied hierarchical organized stimuli of global objects that consisted of coherently moving dots ('shape-from-motion'). In addition, we tested the patients' ability to recognize biological motion by presenting characteristic human movements ('point-light-walker'). The data revealed largely preserved perception of biological motion, while the perception of motion-defined shapes was impaired. Our findings suggest separate mechanisms underlying the recognition of biological motion and shapes defined by coherently moving dots. They thus argue against a restriction in the overall capacity of visual working memory over time as a general explanation for the impaired global shape recognition in patients with simultanagnosia.