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Of those, 378 (10.3%) were oral and maxillofacial injuries. Most of the oral and maxillofacial injuries were attributed to powered bikes (321 out of 378; 84.92%) and the rest to powered scooters. There was a constant increase in general as well as the oral and maxillofacial injuries during the study years. Almost 20% of the cases involved injuries to the teeth. Overall, 291 pedestrians were reported to be injured due to electric-powered bikes and scooters; 29 (9.97%) of them, suffered from oral and maxillofacial injuries. Most of those were children aged 0-15 years (41.38%) and elders older than 60 years (37.39%). CONCLUSIONS Trauma related to electric-powered bikes and scooters is an increasing concern. Dental professionals should be actively involved in educational and legislative efforts focusing on the prevention of e-bike and scooter related injuries, in general, and specifically maxillofacial injuries. This article is protected by copyright. All rights reserved.OBJECTIVE To foster trial-readiness of COQ8A-ataxia, we map the clinico-genetic, molecular and neuroimaging spectrum of COQ8A-ataxia in a large worldwide cohort, and provide first progression data, including treatment response to coenzyme Q10 (CoQ10). METHODS Cross-modal analysis of a multicenter cohort of 59 COQ8A patients, including genotype-phenotype correlations, 3D-protein modelling, in vitro mutation analyses, MRI markers, disease progression and CoQ10 response data. RESULTS 59 patients (39 novel) with 44 pathogenic COQ8A variants (18 novel) were identified. Missense variants demonstrated a pleiotropic range of detrimental effects upon protein modelling and in vitro analysis of purified variants. COQ8A-ataxia presented as variable multisystemic, early-onset cerebellar ataxia, with complicating features ranging from epilepsy (32%) and cognitive impairment (49%) to exercise intolerance (25%) and hyperkinetic movement disorders (41%), including dystonia and myoclonus as presenting symptoms. Multisystemic involvement was more prevalent in missense than biallelic loss-of-function variants (82-93% vs. 53%, p&nbsp;=&nbsp;0.029). Cerebellar atrophy was universal on MRI (100%), with cerebral atrophy or dentate and pontine T2 hyperintensities observed in 28%. Cross-sectional (n&nbsp;=&nbsp;34) and longitudinal (n&nbsp;=&nbsp;7) assessments consistently indicated mild-to-moderate progression of ataxia (SARA 0.45/year). CoQ10 treatment led to improvement by clinical report in 14/30 patients, and by quantitative longitudinal assessments in 8/11 patients (SARA -0.81/year). Explorative sample size calculations indicate that ≥48 patients per arm may suffice to demonstrate efficacy for interventions that reduce progression by 50%. INTERPRETATION This study provides a deeper understanding of the disease, and paves the way towards large-scale natural history studies and treatment trials in COQ8A-ataxia. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.Successful treatment of viral infections has proven to be huge challenge for modern medicine with the most effective approach being prior vaccination. The problem with vaccination is the time it takes to develop an effective vaccine, validate its safety and manufacture it in large quantities. Facing Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), we simply do not have the time to develop the vaccine before thousands of people die. Therefore, any treatment which can decrease the severe symptoms due to lung damage may help attenuate mortality rates. Inactivation of ACE2 during virus fusion into the host cell may be one of the underlying reasons for intense immunological reaction seen in the lung tissue. This overreaction is probably mediated through the bradykinin receptor activation. Noscapine, a medication used for the treatment of cough, has been shown to inhibit bradykinin enhanced cough response in man. As it is already marketed in a number of countries as a cough medicine, even for children, a suitable formulation with all the required licenses is available that can be rapidly utilized in preliminary trials. © 2020 Wiley Periodicals, Inc.Atherosclerosis (AS) is the principal cause of heart attack, sudden cardiac death, stroke, and necrosis of the extremities, in which significant changes in gene expression associated with inflammation are found. However, the molecular mechanisms of AS are not clearly elucidated. In this study, ApoE-/- mice were fed with a high fat diet for 12&nbsp;weeks to induce atherosclerosis and half of the mice were treated with tanshinone IIA (TAN). Then sequencing analysis was performed to investigate the expression patterns of ncRNAs in AS plaques obtained from mice treated with TAN and AS Model mice. A total of 22 long noncoding RNAs (lncRNAs), 74 microRNAs (miRNAs), 13 circular RNAs (circRNAs), and 1359 mRNAs in AS plaque were more significantly regulated from TAN mice, compared with model mice. Bioinformatics tools and databases were employed to investigate the potential ncRNA functions and their interaction. [https://www.selleckchem.com/products/pkm2-inhibitor-compound-3k.html see more] Our data showed that the most significantly pathways regulated by TAN were associated with inflammation, and involved in the signaling pathways of Ras, Rap1, MAPK, cAMP, T cell receptor, and so on. In addition, the competitive endogenous RNA (ceRNA) network had been constructed and the core nodes included circ-Tns3/let-7d-5p/Ctsl, circ-Wdr91/miR-378a-5p/Msr1, and circ-Cd84/ miR-30c/ Tlr2. The DERNAs were validated by quantitative RT-PCR and dual luminescence reporter assay in RAW264.7 cells in vitro. This study identified ceRNAs network regulated by TAN and elucidated the ncRNAs profile and signal pathways to attenuate AS comprehensively. This research would contribute to further research on the pathogenesis of AS, and facilitate the development of novel therapeutics targeting ncRNAs. © 2020 The Authors. Journal of Leukocyte Biology published by Wiley Periodicals, Inc. on behalf of Society for Leukocyte Biology.Cyanophages, widespread in aquatic systems, are a class of viruses that specifically infect cyanobacteria. Though they play important roles in modulating the homeostasis of cyanobacterial populations, little is known about the freshwater cyanophages, especially those hypothetical proteins of unknown function. Mic1 is a freshwater siphocyanophage isolated from the Lake Chaohu. It encodes three hypothetical proteins Gp65, Gp66 and Gp72, which share an identity of 61.6% ~ 83%. However, we find these three homologous proteins differ from each other in oligomeric state. Moreover, we solve the crystal structure of Gp72 at 2.3&nbsp;å, which represents a novel fold in the α + β class. Structural analyses combined with redox assays enable us to propose a model of disulfide bond mediated oligomerization for Gp72. Altogether, these findings provide structural and biochemical basis for further investigations on the freshwater cyanophage Mic1. This article is protected by copyright. All rights reserved. © 2020 Wiley Periodicals, Inc.