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he genus Alteromonas We provide evidence that substrate-specific bioavailability is niche specific, particularly for iron complexes, indicating that transport capacity may serve as a significant control on microbial community dynamics and the resultant cycling of organic matter. Copyright © 2020 Manck et al.Action video gaming can promote neural plasticity. Short-term monocular patching drives neural plasticity in the visual system of human adults. For instance, short-term monocular patching of 0.5 to 5 hours briefly enhances the patched eye's contribution in binocular vision (i.e., short-term ocular dominance plasticity). In this study, we investigate whether action video gaming can influence this plasticity in adults with normal vision. We measured participants' eye dominance using a binocular phase combination task before and after 2.5 hours of monocular patching. Participants were asked to play action video games (PAVG), watch action video game movies (WAVG) or play non-action video games (PNAVG) during the period of monocular patching. We found that participants' change of ocular dominance after monocular patching was not significantly different either for PAVG vs WAVG (Comparison 1) or for PAVG vs PNAVG (Comparison 2). These results suggest that action video gaming does not either boost or eliminate short-term ocular dominance plasticity, and that the neural site for this type of plasticity might be in the early visual pathway.Significance Statement Recent studies have shown that short-term (0.5 to 5 hours) monocular deprivation induces a new form of short-term ocular dominance plasticity in human adults, in which the patched eye rather than the unpatched eye gets stronger, and the effect is transient. On the other hand, there is evidence that action video gaming has potential in enhancing perceptual learning induced visual plasticity in adulthood. In this study, we found that action video gaming did not impact short-term ocular dominance plasticity in visually normal adults. Our psychophysical evidence suggests that the neural site of this plasticity should be local and early in the cortical pathway. Copyright © 2020 Chen et al.In Neuroscience, the structure of a circuit has often been used to intuit function - an inversion of Louis Kahn's famous dictum, `Form follows function' (Kristan and Katz 2006). However, different brain networks may utilize different network architectures to solve the same problem. The olfactory circuits of two insects, the Locust, Schistocerca americana, and the fruit fly, Drosophila melanogaster, serve the same function - to identify and discriminate odors. The neural circuitry that achieves this shows marked structural differences. Projection neurons (PN) in the antennal lobe (AL) innervate Kenyon cells (KC) of the mushroom body (MB). In locust, each KC receives inputs from ∼50% PNs, a scheme that maximizes the difference between inputs to any two of ∼50,000 KCs. In contrast, in drosophila, this number is only 5% and appears sub-optimal. Using a computational model of the olfactory system, we show the activity of KCs is sufficiently high-dimensional that it can separate similar odors regardless of the divetream - is nearly 50%. In contrast, this number is merely 5% in drosophila. We developed computational models of these networks to understand the relative advantages of each connectivity. Our analysis reveals that the two systems exist along a continuum of possibilities that balance two conflicting goals - separating the representations of similar odors while grouping together noisy variants of the same odor. Copyright © 2020 Rajagopalan and Assisi.OBJECTIVE Determining the genetic basis of speech disorders provides insight into the neurobiology of human communication. Despite intensive investigation over the past 2 decades, the etiology of most speech disorders in children remains unexplained. To test the hypothesis that speech disorders have a genetic etiology, we performed genetic analysis of children with severe speech disorder, specifically childhood apraxia of speech (CAS). METHODS Precise phenotyping together with research genome or exome analysis were performed on children referred with a primary diagnosis of CAS. Gene coexpression and gene set enrichment analyses were conducted on high-confidence gene candidates. RESULTS Thirty-four probands ascertained for CAS were studied. In 11/34 (32%) probands, we identified highly plausible pathogenic single nucleotide (n = 10; CDK13, EBF3, GNAO1, GNB1, DDX3X, MEIS2, POGZ, SETBP1, UPF2, ZNF142) or copy number (n = 1; 5q14.3q21.1 locus) variants in novel genes or loci for CAS. Testing of parental DNA was available for 9 probands and confirmed that the variants had arisen de novo. Eight genes encode proteins critical for regulation of gene transcription, and analyses of transcriptomic data found CAS-implicated genes were highly coexpressed in the developing human brain. CONCLUSION We identify the likely genetic etiology in 11 patients with CAS and implicate 9 genes for the first time. We find that CAS is often a sporadic monogenic disorder, and highly genetically heterogeneous. Highly penetrant variants implicate shared pathways in broad transcriptional regulation, highlighting the key role of transcriptional regulation in normal speech development. CAS is a distinctive, socially debilitating clinical disorder, and understanding its molecular basis is the first step towards identifying precision medicine approaches. find more © 2020 American Academy of Neurology.Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy described in 1916 by Guillain, Barré, and Strohl. However, many similar cases had been reported earlier under various terms, with less detail and with various explanations about its pathophysiologic origin. Based on the analysis of old articles, we propose an overview of the history of acute inflammatory polyradiculoneuropathy before the official description of GBS. © 2020 American Academy of Neurology.First reported by Guillain, Barré, and Strohl during the Great War, the concept of "Guillain-Barré syndrome" (GBS) progressively emerged as a clinical entity in its own right. Despite many debates about its clinical and pathophysiologic characteristics, GBS is now recognized as a disease throughout the world. We describe here the main steps of the rich history of GBS, from 1916 to the present. © 2020 American Academy of Neurology.