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Correction to: Environ. Eng. Sci. 2017;34(1):51-61. DOI: 10.1089/ees.2016.0223.

ABSTRACT: [This corrects the article DOI: 10.1089/ees.2016.0223.].

SUBMITTER:

PROVIDER: S-EPMC5564049 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Correction: Two distinct ontogenies confer heterogeneity to mouse brain microglia (doi: 10.1242/dev.152306).

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Project description:Duchenne muscular dystrophy (DMD) is caused by genetic mutations that result in the absence of dystrophin protein expression. Oligonucleotide-induced exon skipping can restore the dystrophin reading frame and protein production. However, this requires continuous drug administration and may not generate complete skipping of the targeted exon. In this study, we apply genome editing with zinc finger nucleases (ZFNs) to permanently remove essential splicing sequences in exon 51 of the dystrophin gene and thereby exclude exon 51 from the resulting dystrophin transcript. This approach can restore the dystrophin reading frame in ~13% of DMD patient mutations. Transfection of two ZFNs targeted to sites flanking the exon 51 splice acceptor into DMD patient myoblasts led to deletion of this genomic sequence. A clonal population was isolated with this deletion and following differentiation we confirmed loss of exon 51 from the dystrophin mRNA transcript and restoration of dystrophin protein expression. Furthermore, transplantation of corrected cells into immunodeficient mice resulted in human dystrophin expression localized to the sarcolemmal membrane. Finally, we quantified ZFN toxicity in human cells and mutagenesis at predicted off-target sites. This study demonstrates a powerful method to restore the dystrophin reading frame and protein expression by permanently deleting exons.

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Correction: Chow, J.W. and Stokic, D.S. Longitudinal Changes in Temporospatial Gait Characteristics during the First Year Post-Stroke. Brain Sci. 2021, 11, 1648

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Project description:Spinal cord injury (SCI) is characterized by secondary degeneration, which leads to tissue loss at the epicenter and subsequent functional deficits. This review provides insight into the pathophysiology of microvascular dysfunction and endothelial cell loss, which are among the earliest responses during the first postinjury day. The enigmatic role of the angiogenic response in the penumbra around the lost tissue, which occurs during the first 2 weeks, is also discussed. The importance of stabilizing and rescuing the injured vasculature is now well-recognized, and several pharmacological and genetic treatments have emerged in the past few years. We conclude with suggestions for future experimental research, including development of vascular-selective treatments and exploitation of genetic models. In summary, vascular dysfunction following SCI is an important contributor to neurological deficits, as proposed long ago. However, there now appears to be new and potentially powerful opportunities for treating acute SCI by targeting the vascular responses.

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Correction: Xingchen Zhou, et al. Whole Exome Sequencing in Psoriasis Patients Contributes to Studies of Acitretin Treatment Difference. Int. J. Mol. Sci. 2017, 18, 295.

Project description:We would like to submit the following correction to the published paper [1], the reason for this action is that the data in Table 3 were reanalyzed by one more accurate statistic method: On page 12, the sentence of paragraph three "OR and 95% CI were calculated by limited backward-LR (likelihood ratio) logistic regression analysis with adjustment by clinical variables" should be corrected into "OR and 95% CI were calculated by limited enter logistic regression analysis with adjustment by clinical variables".[...].

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Correction To: TSAVOURELOU, A., STYLIANIDES, N., PAPADOPOULOS, A., DIKAIAKOS, M. D., NANAS, S., KYPRIANOU, T., TOKMAKIDIS, S. P. (2016). TELEREHABILITATION SOLUTION CONCEPTUAL PAPER FOR COMMUNITY-BASED EXERCISE REHABILITATION OF PATIENTS DISCHARGED AFTER CRITICAL ILLNESS. INTERNATIONAL JOURNAL OF TELEREHABILITATION, 8(2), 61-70. DOI: 10.5195/IJT.2016.6205.

Project description:[This corrects the article on p. 61 in vol. 8, PMID: 28775802.].

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