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Background Previous articles have assessed the evidence-base for the treatment of burns, but the latest was published in 2010, examining data up to and inclusive of 2008. The aim of this article is to examine the trend in the number of high-evidence publications over the subsequent 11-year period and quality-assess RCTs within this timeframe. Materials and Methods All articles published in Burns and Journal of Burn Care and Research (JBCR) were identified using PubMed Search Tools and its Single Citation Matcher function. These journals were manually screened from 01/01/2009 to 01/06/2020 inclusive. Additionally, a PubMed search was conducted searching for RCTs and meta-analyses in English with the MESH term burns to identify meta-analyses and RCTs in all other journals. The reporting of RCTs was assessed using a modified CONsolidated Standards of Reporting Trials (CONSORT) checklist. Results A total of 5,145 articles were evaluated from Burns and JBCR, with 3,230 (62.78%) from Burns and 1,915 (37.22%) from JBCR. 0.012% were meta-analyses of RCTs, 0.30% were other meta-analyses, and 2.52% were initially identified as RCTs. Whilst a significant increase in the number of high-evidence publications is observed, these represent 2.83% (n=237) of the total. An additional 95 RCTs were identified in other journals, 58 being included in quality-analysis. A total 128 RCTs were thus eligible for quality-assessment, the most popular individual topic being wound healing (n=28; 21.88%). The most highly reported criterion was listed inclusion and exclusion criteria (n=111; 86.72%) and the least reported criterion was allocation concealment (n=22; 13.92%). Conclusions This study observes a positive trend in high-evidence publications. The reporting of several CONSORT criteria in RCTs remains poor. Observation to standard reporting guidelines is advocated to improve the quality of reporting.

International audience; BACKGROUND & AIMS: NADPH oxidase 1 (NOX1) has emerged as a prime regulator of intestinal mucosa immunity and homeostasis. Dysregulation of NOX1 may cause inflammatory bowel disease (IBD). It is not clear how NOX1 is regulated in vivo under inflammatory conditions. We studied the role of CK2 in this process.METHODS: The NOX1 organizer subunit, NADPH oxidase organizer 1 (NOXO1), was immunoprecipitated from cytokine-treated colon epithelial cells, and bound proteins were identified by mass spectrometry analysis. Sites on NOXO1 phosphorylated by CK2 were identified by nanoscale liquid chromatography coupled to tandem mass spectrometry. NOX1 activity was determined in colon epithelial cells and colonoids in the presence or absence of CX-4945, a CK2 specific inhibitor. Acute colitis was induced by administration of trinitrobenzenesulfonic acid in mice treated or not with CX-4945. Colon tissues were analyzed by histologic examination, quantitative polymerase chain reaction, and Western blots. CK2 activity, markers of inflammation, and oxidative stress were assessed.RESULTS: We identified CK2 as a major partner of NOXO1 in colon epithelial cells under inflammatory conditions. CK2 directly binds NOXO1 at the C-terminus containing the Phox homology domain and phosphorylates NOXO1 on several sites. CX-4945 increased ROS generation by NOX1 in human colon epithelial cells and organoids. Strikingly, CK2 activity was reduced in trinitrobenzenesulfonic acid-induced acute colitis, and CX-4945 exacerbated colitis inflammation as shown by increased levels of CXCL1, ROS generation, lipid peroxidation, and colon damage.CONCLUSIONS: The ubiquitous protein kinase CK2 limits NOX1 activity via NOXO1 binding and phosphorylation in colonic epithelial cells and lessens experimental colitis. Loss of CK2 activity during acute colitis results in excessive ROS production, contributing to the pathogenesis. Strategies to activate CK2 could be an effective novel therapeutic approach in IBD.

There is an old saying that if you think you have discovered something new then it is because you don't read the German literature and there is some truth in this. When Plastic Surgery is mentioned the usual reply is "Ah, Gillies" as though he was the fons et origo of Plastic and Reconstructive surgery. The fact is that there were many more pioneering plastic surgeons outside the British Empire, whose work preceded and even surpassed Gilles. In 1818, Karl Ferdinand von Graefe published "Rhinoplastik" and coined the term plastic surgery (Plastische Chirurgie). Eduard Zeis, in 1838 published the textbook "Handbuch der plastischen Chirurgie" and established its meaning based on hundreds of references. Undoubtably, the first decades of the 20th century, especially the war between 1914 and 1918, were the genesis of most modern developments in plastic surgery and there were many more pioneering plastic surgeons outside the British Empire, whose work preceded, equalled and even surpassed Gillies, despite his admirable achievements.

The incidence of oropharyngeal cancer induced by human papillomavirus (HPV) infection is steadily increasing in developed countries. These tumors are more chemoradiosensitive and have a better prognosis than HPV-negative one. In addition, they occur in younger and better-off patients with longer life expectancy. Current radiotherapy and chemotherapy protocols are currently being questioned as they may expose HPV-positive patients to excessive treatment and unnecessary toxic effects. Less intensive treatment regimens could possibly achieve similar efficacy with lower toxicity and improved quality of life. The aim of this work was to summarize the knowledge on these tumors and their implications for radiation oncologists. In this update, we will discuss ongoing de-escalation trials and highlight the issues raised by these studies. We will also comment on the results of recently published de-intensification studies. Three main strategies are analyzed in the present article: the de-escalation of the drug associated with radiotherapy, the de-escalation of the radiotherapy dose (in concomitant chemoradiotherapy, after induction chemotherapy, in a postoperative setting) and de-escalation of radiation target volumes. Our findings ultimately indicate that clinicians should not change the management of oropharyngeal cancer patients outside of clinical trials.

Proteinase 3 (PR3) is the main target antigen of antineutrophil cytoplasmic antibodies (ANCAs) in PR3-ANCA–associated vasculitis. A small fraction of PR3 is constitutively exposed on the surface of quiescent blood neutrophils in a proteolytically inactive form. When activated, neutrophils expose an induced form of membrane-bound PR3 (PR3(mb)) on their surface as well, which is enzymatically less active than unbound PR3 in solution due to its altered conformation. In this work, our objective was to understand the respective role of constitutive and induced PR3(mb) in the immune activation of neutrophils triggered by murine anti-PR3 mAbs and human PR3-ANCA. We quantified immune activation of neutrophils by the measurement of the production of superoxide anions and secreted protease activity in the cell supernatant before and after treatment of the cells by alpha-1 protease inhibitor that clears induced PR3(mb) from the cell surface. Incubation of TNFα-primed neutrophils with anti-PR3 antibodies resulted in a significant increase in superoxide anion production, membrane activation marker exposition, and secreted protease activity. When primed neutrophils were first treated with alpha-1 protease inhibitor, we observed a partial reduction in antibody-induced neutrophil activation, suggesting that constitutive PR3(mb) is sufficient to activate neutrophils. The pretreatment of primed neutrophils with purified antigen-binding fragments used as competitor significantly reduced cell activation by whole antibodies. This led us to the conclusion that PR3(mb) promoted immune activation of neutrophils. We propose that blocking and/or elimination of PR3(mb) offers a new therapeutic strategy to attenuate neutrophil activation in patients with PR3-ANCA–associated vasculitis.