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m.OBJECTIVE Digital subtraction imaging (DSI) decreases the risk of intravascular injection during cervical transforaminal epidural steroid injection (CTFESI); however, sequence acquisition and interpretation are operator-dependent skills. This study tests the reliability of a grading system to determine adequate DSI during CTFESI. SETTING Academic tertiary medical center. METHODS A grading scheme for adequate DSI quality during CTFESI was created by the study authors based on patient positioning, mask image, and volume of contrast injected. The inter-rater and intrarater reliability values of this grading scheme were tested using 50 DSI images evaluated by three raters during two distinct sessions separated by four weeks. Based on a power analysis, a sample of 50 scans was sufficient to detect significant correlations. Inter-rater reliability was determined by percent agreement between graders for dichotomized categories of "quality of DSI is adequate for safe C-TFESI" vs "quality of DSI is inadequate for saferved. For permissions, please e-mail journals.permissions@oup.com.Xyloglucan is a major hemicellulose in plant cell walls and exists in two distinct types, XXXG and XXGG. While the XXXG-type xyloglucan from dicot species only contains O-acetyl groups on side-chain galactose (Gal) residues, the XXGG-type xyloglucan from Poaceae (grasses) and Solanaceae bear O-acetyl groups on backbone glucosyl (Glc) residues. Although O-acetyltransferases responsible for xyloglucan Gal acetylation have been characterized, the biochemical mechanism underlying xyloglucan backbone acetylation remains to be elucidated. In this study, we showed that recombinant proteins of a group of DUF231 members from rice and tomato were capable of transferring acetyl groups onto O-6 of Glc residues in cello-oligomer acceptors, indicating that they are xyloglucan backbone 6-O-acetyltransferases (XyBATs). We further demonstrated that XyBAT-acetylated cellohexaose oligomers could be readily xylosylated by AtXXT1 (Arabidopsis xyloglucan xylosyltransferase1) to generate acetylated, xylosylated cello-oligomers, whecom.Peripheral neuropathy is a common disorder with many possible etiologies including metabolic diseases, inflammatory conditions, infections, malignancy, inherited diseases, drugs, and toxins. In most instances, diagnosis and treatment plan can be established based on clinical presentation, family history, laboratory results, genetic testing, and electrophysiological studies. But in some situations, a peripheral nerve biopsy remains a valuable tool. This is especially true in patients with rapidly progressive disease, with atypical presentation or for whom other approaches fail to yield a definitive diagnosis. The pathologic examination starts with basic decisions about specimen triage. A few basic questions help to provide an initial framework for the assessment of a nerve biopsy-is the specimen adequate; are there inflammatory changes; are there vascular changes; is there amyloid; are there changes to axonal density and the Schwann cell-myelin-axon unit. In the appropriate context and with such an approach peripheral nerve biopsies can still represent a clinically helpful test. © 2020 American Association of Neuropathologists, Inc. All rights reserved.The dN/dS ratio provides evidence of adaptation or functional constraint in protein-coding genes by quantifying the relative excess or deficit of amino acid-replacing versus silent nucleotide variation. Inexpensive sequencing promises a better understanding of parameters such as dN/dS, but analysing very large datasets poses a major statistical challenge. Here I introduce genomegaMap for estimating within-species genome-wide variation in dN/dS, and I apply it to 3,979 genes across 10,209 tuberculosis genomes to characterize the selection pressures shaping this global pathogen. GenomegaMap is a phylogeny-free method that addresses two major problems with existing approaches (i) it is fast no matter how large the sample size and (ii) it is robust to recombination, which causes phylogenetic methods to report artefactual signals of adaptation. GenomegaMap uses population genetics theory to approximate the distribution of allele frequencies under general, parent-dependent mutation models. Coalescent simulations show that substitution parameters are well-estimated even when genomegaMap's simplifying assumption of independence among sites is violated. I demonstrate the ability of genomegaMap to detect genuine signatures of selection at antimicrobial resistance-conferring substitutions in M. tuberculosis and describe a novel signature of selection in the cold-shock DEAD-box protein A gene deaD/csdA. The genomegaMap approach helps accelerate the exploitation of big data for gaining new insights into evolution within species. © The Author(s) 2020. selleck compound Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.Gerstmann-Sträussler-Scheinker (GSS) disease with P102L mutation and familial Creutzfeldt-Jakob disease (CJD) with V180I mutation are 2 major hereditary prion diseases in Japan. GSS and some familial CJD [V180I] exhibit characteristic prion protein (PrP) plaques. Overexpression of the astrocytic water channel proteins aquaporin (AQP) 1 and AQP4 was recently reported in sporadic CJD. To clarify the pathological characteristics of AQP1 and AQP4 in prion disease patient brains with plaque-type deposition, we investigated 5 patients with GSS, 2 patients with CJD [V180I], and 2 age-matched control cases without neurological diseases using immunohistochemistry and double immunofluorescence methods. We demonstrated that there is the intense expression of AQP1 and AQP4 around prion plaques, especially in distal astrocytic processes deep inside these plaques. Similar results have been reported in the senile plaques and ghost tangles of Alzheimer disease brains and a protective role of AQP4 in which AQP4 is redistributed toward the plaques and works as a barrier against the deleterious effects of these plaques has been suggested. Our results, which show a similar clustering of AQPs around PrP plaques, therefore support the possibility that AQPs also have a protective role in plaque formation in prion diseases. © 2020 American Association of Neuropathologists, Inc. 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