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Determining multi-functional bioactive peptide features making use of multi-label heavy mastering.
Of 923 consecutive patients who tested COVID-19 positive, 592 (64%) flagged at risk for thromboembolism, 241/923 (26%) for cytokine storm and 361/923 (39%) for ARDS. Thromboembolism and cytokine storm flags were met in the ED for 342 (37.1%) patients. Of the 318 (34.5%) patients receiving thromboembolism flags, 49 (5.3% of all patients) were for suspected thromboembolism, 103 (11.1%) were high-risk and 166 (18.0%) were medium-risk. Of the 89 (9.6%) who received a cytokine storm flag from the ED, 18 (2.0% of all patients) were for suspected cytokine storm, 13 (1.4%) were high-risk and 58 (6.3%) were medium-risk. Males were more likely to receive a specific traffic light flag. In conclusion, ED predictors were used to identify high proportions of COVID-19 admissions at risk of clinical deterioration due to severity of disease, enabling accelerated care targeted to those more likely to benefit. Larger prospective studies are encouraged.On 12 March 2020 the UK entered the 'delay phase' of the COVID-19 pandemic response. The Public Health England Emergency Department Syndromic Surveillance System (EDSSS) carries out daily (near real-time) public health surveillance of emergency department (ED) attendances across England. This retrospective observational analysis of EDSSS data aimed to describe changes in ED attendances during March-April 2020, and identify the attendance types with the largest impact. Type 1 ED attendances were selected from 109 EDs that reported data to EDSSS for the period 1 January 2019 to 26 April 2020. The daily numbers of attendances were plotted by age group and acuity of presentation. The 2020 'COVID-19' period (12 March 2020 to 26 April 2020) attendances were compared with the equivalent 2019 'pre-COVID-19' period (14 March 2019 to 28 April 2019) in total; by hour and day of the week; age group( less then 1, 1-4, 15-14, 15-44, 45-64 and 65+ years); gender; acuity; and for selected syndromic indicators(acute respiratoity of EDSSS allowed rapid development of new indicators (including COVID-19-like) and reporting methods.
For the prehospital diagnosis of raised intracranial pressure (ICP), clinicians are reliant on clinical signs such as the Glasgow Coma Score (GCS), pupillary response and/or Cushing's triad (hypertension, bradycardia and an irregular breathing pattern). #link# This study aimed to explore the diagnostic accuracy of these signs as indicators of a raised ICP.

We performed a retrospective cohort study of adult patients attended by a Helicopter Emergency Medical Service (Air Ambulance Kent, Surrey Sussex), who had sustained a traumatic brain injury (TBI), requiring prehospital anaesthesia between 1 January 2016 and 1 January 2018. We established optimal cut-off values for clinical signs to identify patients with a raised ICP and investigated diagnostic accuracy for combinations of these values.

Outcome data for 249 patients with TBI were available, of which 87 (35%) had a raised ICP. Optimal cut-off points for systolic blood pressure (SBP), heart rate (HR) and pupil diameter to discriminate patients with a raised Iould identify more accurate clinical signs or alternative non-invasive diagnostic aids in the prehospital environment.
Since its emergence in late December 2019, COVID-19 has rapidly developed into a pandemic in mid of March with many countries suffering heavy human loss and declaring emergency conditions to contain its spread. The impact of the disease, while it has been relatively low in the sub-Saharan Africa (SSA) as of May 2020, is feared to be potentially devastating given the less developed and fragmented healthcare system in the continent. In addition, most emergency measures practised may not be effective due to their limited affordability as well as the communal way people in SSA live in relative isolation in clusters of large as well as smaller population centres.

To address the acute need for estimates of the potential impacts of the disease once it sweeps through the African region, we developed a process-based model with key parameters obtained from recent studies, taking local context into consideration. We further used the model to estimate the number of infections within a year of sustained local transmisprevent several millions of infections and thousands of deaths across the continent.It is widely recognized that noncoding genetic variants play important roles in many human diseases, but there are multiple challenges that hinder the identification of functional disease-associated noncoding variants. TAE684 order of noncoding variants can be many times that of coding variants; many of them are not functional but in linkage disequilibrium with the functional ones; different variants can have epistatic effects; different variants can affect the same genes or pathways in different individuals; and some variants are related to each other not by affecting the same gene but by affecting the binding of the same upstream regulator. To overcome these difficulties, we propose a novel analysis framework that considers convergent impacts of different genetic variants on protein binding, which provides multiscale information about disease-associated perturbations of regulatory elements, genes, and pathways. Applying it to our whole-genome sequencing data of 918 short-segment Hirschsprung disease patients and matched controls, we identify various novel genes not detected by standard single-variant and region-based tests, functionally centering on neural crest migration and development. Our framework also identifies upstream regulators whose binding is influenced by the noncoding variants. Using human neural crest cells, we confirm cell stage-specific regulatory roles of three top novel regulatory elements on our list, respectively in the RET, RASGEF1A, and PIK3C2B loci. In the PIK3C2B regulatory element, we further show that a noncoding variant found only in the patients affects the binding of the gliogenesis regulator NFIA, with a corresponding up-regulation of multiple genes in the same topologically associating domain.The V(DD)J recombination is currently viewed as an aberrant and inconsequential variant of the canonical V(D)J recombination. Moreover, since the classical 12/23 rule for the V(D)J recombination fails to explain the V(DD)J recombination, the molecular mechanism of tandem D-D fusions has remained unknown since they were discovered three decades ago. Revealing this mechanism is a biomedically important goal since tandem fusions contribute to broadly neutralizing antibodies with ultralong CDR3s. We reveal previously overlooked cryptic nonamers in the recombination signal sequences of human IGHD genes and demonstrate that these nonamers explain the vast majority of tandem fusions in human repertoires. We further reveal large clonal lineages formed by tandem fusions in antigen-stimulated immunosequencing data sets, suggesting that such data sets contain many more tandem fusions than previously thought and that about a quarter of large clonal lineages with unusually long CDR3s are generated through tandem fusions. Finally, we developed the SEARCH-D algorithm for identifying D genes in mammalian genomes and applied it to the recently completed Vertebrate Genomes Project assemblies, nearly doubling the number of mammalian species with known D genes.
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