ARCHANGEL: Tamper-proofing Video Archives using Temporal Content Hashes on the Blockchain

We present ARCHANGEL; a novel distributed ledger based system for assuring the long-term integrity of digital video archives. First, we describe a novel deep network architecture for computing compact temporal content hashes (TCHs) from audio-visual streams with durations of minutes or hours. Our TCHs are sensitive to accidental or malicious content modification (tampering) but invariant to the codec used to encode the video. This is necessary due to the curatorial requirement for archives to format shift video over time to ensure future accessibility. Second, we describe how the TCHs (and the models used to derive them) are secured via a proof-of-authority blockchain distributed across multiple independent archives. We report on the efficacy of ARCHANGEL within the context of a trial deployment in which the national government archives of the United Kingdom, Estonia and Norway participated.Comment: Accepted to CVPR Blockchain Workshop 201

Statistical significance and sports medicine trials

Objectives: Lowering the threshold for statistical significance in medical research from a P value of .05 to .005 was recently proposed to reduce misinterpretation of study results. What effect this proposal would have on orthopaedic sports medicine literature is currently unclear.Research Question/Hypothesis: We seek to determine how the newly proposed threshold could affect the interpretation of previously published sports medicine RCTs.Methods: We searched PubMed from January 01, 2016 to December 31, 2017 for RCTs published in the American Journal of Sports Medicine, Arthroscopy, and Knee Surgery, Sports Traumatology, Arthroscopy. We extracted P value data for primary endpoints, since RCTs are most often powered for these endpoints. We used Google Forms for data extraction and STATA 13.1 for the data analysis.Results: Of the 159 studies, only 13 (8%) of the studies have endpoints in which all P values are below the new threshold of .005. 40 (25%) of the studies have endpoints in which some would meet the new P value threshold of .005, and some would not meet this new threshold. 106 (67%) of the studies have no endpoints in which the P value(s) was less than .005. Overall, 38% (59/157) of the previously statistically significant primary endpoints were less than .005, while 62% (98/157) would be reclassified as suggestive.Conclusions: Of statistically significant endpoints in our sample, only 17% (59/350) would maintain their statistical significance with a P value threshold of less than .005, and only 8% of studies would maintain their overall significance with all P values falling below the new threshold

Gender gap in surgery: Can integrated surgical programs increase the number of women in surgery?

Objective: To determine if the creation of integrated surgical programs has increased the recruitment of women into surgical residencies.Summary Background Data: Historically, there have been disproportionately lower numbers of women entering surgical residency programs compared to the percentage of women physicians. Per the ACGME, in 2017, women comprised 45.8% of all residents in training but just 29.9% of surgical residents. We sought to determine if certain factors, specifically integrated surgical programs, have made an impact on the number of women in surgical specialties.Methods: Data regarding surgical residents and physicians was extracted from the Accreditation Council of Graduate Medical Education (ACGME) Data Resource Books and ACGME Association of American Medical Colleges (AAMC) Physician Specialty Data Reports from 2007-2018.Results: Overall, integrated surgical programs consistently report increased percentages of women compared to non- integrated surgical programs.Conclusions: The creation of integrated surgical programs has increased and will likely continue to increase the proportion of women in surgical residencies

Mortality and pulmonary complications in patients undergoing surgery with perioperative SARS-CoV-2 infection: an international cohort study

Background: The impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on postoperative recovery needs to be understood to inform clinical decision making during and after the COVID-19 pandemic. This study reports 30-day mortality and pulmonary complication rates in patients with perioperative SARS-CoV-2 infection. Methods: This international, multicentre, cohort study at 235 hospitals in 24 countries included all patients undergoing surgery who had SARS-CoV-2 infection confirmed within 7 days before or 30 days after surgery. The primary outcome measure was 30-day postoperative mortality and was assessed in all enrolled patients. The main secondary outcome measure was pulmonary complications, defined as pneumonia, acute respiratory distress syndrome, or unexpected postoperative ventilation. Findings: This analysis includes 1128 patients who had surgery between Jan 1 and March 31, 2020, of whom 835 (74·0%) had emergency surgery and 280 (24·8%) had elective surgery. SARS-CoV-2 infection was confirmed preoperatively in 294 (26·1%) patients. 30-day mortality was 23·8% (268 of 1128). Pulmonary complications occurred in 577 (51·2%) of 1128 patients; 30-day mortality in these patients was 38·0% (219 of 577), accounting for 81·7% (219 of 268) of all deaths. In adjusted analyses, 30-day mortality was associated with male sex (odds ratio 1·75 [95% CI 1·28–2·40], p\textless0·0001), age 70 years or older versus younger than 70 years (2·30 [1·65–3·22], p\textless0·0001), American Society of Anesthesiologists grades 3–5 versus grades 1–2 (2·35 [1·57–3·53], p\textless0·0001), malignant versus benign or obstetric diagnosis (1·55 [1·01–2·39], p=0·046), emergency versus elective surgery (1·67 [1·06–2·63], p=0·026), and major versus minor surgery (1·52 [1·01–2·31], p=0·047). Interpretation: Postoperative pulmonary complications occur in half of patients with perioperative SARS-CoV-2 infection and are associated with high mortality. Thresholds for surgery during the COVID-19 pandemic should be higher than during normal practice, particularly in men aged 70 years and older. Consideration should be given for postponing non-urgent procedures and promoting non-operative treatment to delay or avoid the need for surgery. Funding: National Institute for Health Research (NIHR), Association of Coloproctology of Great Britain and Ireland, Bowel and Cancer Research, Bowel Disease Research Foundation, Association of Upper Gastrointestinal Surgeons, British Association of Surgical Oncology, British Gynaecological Cancer Society, European Society of Coloproctology, NIHR Academy, Sarcoma UK, Vascular Society for Great Britain and Ireland, and Yorkshire Cancer Research

Search for gravitational-lensing signatures in the full third observing run of the LIGO-Virgo network

Gravitational lensing by massive objects along the line of sight to the source causes distortions of gravitational wave-signals; such distortions may reveal information about fundamental physics, cosmology and astrophysics. In this work, we have extended the search for lensing signatures to all binary black hole events from the third observing run of the LIGO--Virgo network. We search for repeated signals from strong lensing by 1) performing targeted searches for subthreshold signals, 2) calculating the degree of overlap amongst the intrinsic parameters and sky location of pairs of signals, 3) comparing the similarities of the spectrograms amongst pairs of signals, and 4) performing dual-signal Bayesian analysis that takes into account selection effects and astrophysical knowledge. We also search for distortions to the gravitational waveform caused by 1) frequency-independent phase shifts in strongly lensed images, and 2) frequency-dependent modulation of the amplitude and phase due to point masses. None of these searches yields significant evidence for lensing. Finally, we use the non-detection of gravitational-wave lensing to constrain the lensing rate based on the latest merger-rate estimates and the fraction of dark matter composed of compact objects

Partnership between the aryl hydrocarbon receptor (AHR) and RELB regulates cigarette smoke-induced cyclooxygenase-2 (COX-2) expression

Chronic obstructive pulmonary disease (COPD) is an inflammatory disease of the lungs caused by cigarette smoke exposure; COPD is also now the third leading cause of death worldwide. Controlling lung inflammation is a priority in COPD patients, but currently-available medications offer little relief. Thus, new therapeutic targets represent a major unmet need. Previously, the aryl hydrocarbon receptor (AHR) has been shown to suppress cigarette smoke-induced inflammation. The AHR is a ligand-activated transcription factor, and well-established for its response to xenobiotic ligands. AHR-mediated suppression of smoke-induced inflammation requires the NF-κβ family member RELB. To date, nothing is known about the expression of AHR or RELB in subjects with COPD. Therefore, we investigated the expression of the AHR and RELB in human lung fibroblasts derived from Control (Non-smoker), Smoker and COPD subjects, as well as the mechanism through which they repress the production of the inflammatory protein cycloxygenase-2 (COX-2) in response to cigarette smoke extract (CSE). There was reduced AHR expression in COPD subjects, which was associated with increased expression of COX-2 protein (but not mRNA) in quiescent COPD fibroblasts. Inhibition of AHR activity in lung fibroblasts by the pharmacological AHR antagonist CH-223191 increased COX-2 protein induction by CSE. Mechanistically, this increase in COX-2 protein corresponded with increased cytoplasmic shuttling of the RNA binding protein HUR which is known to prolong the half-life of RNA transcripts - including COX-2. HUR was observed to be cytoplasmically-localized in lung tissue from COPD subjects, but not Control, suggesting altered regulation of HUR in COPD subjects. Another protein associated with the suppressive function of the AHR- RElB, was reduced in both Smoker and COPD lung fibroblasts, suggesting cigarette smoke may contribute to the reduced expression. siRNA-knockdown of RELB increased the production of Cox-2 mRNA in response to CSE or IL-1β, supporting that RELB contributes to the suppression of Cox-2. We hypothesized this may be due to miR-146a, an anti-inflammatory microRNA (miRNA) which targets Cox-2 mRNA for degradation. miR-146a basal expression was not significantly different between the subject groups. However, only Control fibroblasts increased miR-146a expression in response to CSE. siRNA knockdown of RELB abrogated the expression of miR-146a in response to IL-1β, but not CSE, suggesting RELB repression of Cox-2 mRNA does not involve miR-146a, but that RELB may regulate miR-146a under certain stimuli. Collectively, these data support the regulatory role of AHR and RELB in cigarette smoke-induced inflammation, and thus represent promising new cellular targets with the potential for controlling inflammation characteristic of COPD.La maladie pulmonaire obstructive chronique (MPOC) est une maladie inflammatoire chronique des poumons causée par l'exposition à la fumée de cigarette, maintenant au troisième rang des causes de mortalité mondiaux. Le contrôle de l'inflammation pulmonaire est hautement prioritaire pour les patients atteints de MPOC, mais les médicaments actuellement disponibles ne réduisent guère cette inflammation. Les nouvelles cibles thérapeutiques restent donc un important besoin non satisfait. La RAH est bien établi comme une réponse à des ligands xénobiotiques toxiques. La suppression par l'entremise de RAH de l'inflammation causée par la fumée de cigarette nécessite un membre de la famille NFκβ. Jusqu'à date, rien n'est connu de l'expression de RAH ou RELB parmi les patients atteints de MPOC. Par conséquent nous avons examiné ci-dessus la relation entre l'expression de RAH et RELB dans les fibroblastes de poumon humains dérivés des sujets témoins (non-fumeurs), fumeurs, et sujets atteints de MPOC, ainsi que le mécanisme par lequel ils répriment la production de la protéine inflammatoire cyclo-oxygénase 2 (COX-2) en réponse à l'extrait de la fumée de cigarette (EFC). L'expression des protéines RAH a été réduite parmi les fibroblastes des sujets atteints de MPOC, qui était aussi associée avec une expression accrue de la protéine COX-2 (mais pas ARNm) parmi les fibroblastes quiescents. L'inhibition de l'activité de RAH dans les fibroblastes pulmonaires par l'antagoniste pharmacologique CH-223191 a augmenté l'induction de COX-2 par EFC. Mécaniquement, cette augmentation de la protéine COX-2 a correspondu avec un accroissement du transport cytoplasmique de la protéine de liaison d'ARN HUR, qui est connu pour prolonger la demi-vie des transcrits d'ARN, y compris COX-2. Il a été observé que HUR est cytoplasmiquement localisé dans le tissu pulmonaire des sujets atteints de MPOC, mais non pas les témoins, suggérant une régulation altérée de HUR parmi les sujets atteints de MPOC. Une autre protéine associée avec cette fonction de suppression de la RAH=RElB a été réduite parmi les fibroblastes pulmonaires des sujets-fumeurs et sujets atteints de COP, suggérant que la fumée de cigarette puisse contribuer à cette expression réduite. pARNi (ou siRNA) anéantissement de RELB accroissait la production de COX-2 ARNm en réponse à CSE ou IL-1, appuyant l'observation que RELB contribue à la suppression de COX-2. Nous avons formulé l'hypothèse que cela pourrait être du à miR-146a, un micro-ARN (miARN) qui cible COX-2 mRNA pour dégradation. L'expression basale de miR-146a ne fut pas significativement différente parmi les divers groupes de sujets. Pourtant seulement les fibroblastes des sujets témoins ont accru l'expression de miR-146 en réponse à l'EFC. pARNi (ou siRNA) anéantissement de RELB a abrogé l'expression de miR-146 en réponse à IL-1β, mais pas l'EFC, suggérant que la répression par RELB de COX-2 ARNm n'entraîne pas miR-146a, mais que RELB pourrait réglementer miR-146a soumis à certains stimuli. Collectivement, ces données étayent le rôle régulateur de RAH et RELB dans l'inflammation induite par la fumée de cigarette, et donc représentent de nouvelles cibles cellulaires prometteuses, pleines de potentiel de contrôler l'inflammation caractéristique de MPOC

The locus of Katakana-English masked phonological priming effects

Japanese–English bilinguals completed a masked phonological priming study with Japanese Katakana primes and English targets. Event related potential (ERP) data were collected in addition to lexical decision responses. A cross-script phonological priming effect was observed in both measures, and the effect did not interact with frequency. In the ERP data, the phonological priming effect was evident before the frequency effect. These data, along with analyses of response latency distributions, provide evidence that the cross-script phonological priming effects were the consequence of the activation of sublexical phonological representations in a store shared by both Japanese and English. This activation fed back to sublexical and lexical orthographic representations, influencing lexical decision latencies. The implications for the Bilingual Interactive Activation (BIA+) model of word recognition are discussed