National early warning scores in care homes: do policy imperatives reflect a genuine need?

Background the National Early Warning Score (NEWS) is a tool based on vital signs that aims to standardise detection of, and response to, clinical deterioration in adults. NEWS has been adopted in hospitals but not adapted for other settings. This study aimed to explore the feasibility of measuring the NEWS in care homes and describe the distribution of NEWS readings amongst care home residents. Methods descriptive analysis of all NEWS readings recorded in a 30-month period (2016–19) across 46 care homes in one Clinical Commissioning Group in England. Comparisons were made between measurements taken as a routine reading and those prompted by concern about acute illness. Results a total of 19,604 NEWS were recorded from 2,424 older adults (≥65 years; mean age 85). Median NEWS was 2. Two thirds (66%) of residents had a low NEWS (≤2), and 28% had a score of 0. Of the total NEWS readings, 6,277 (32%) were known to be routine readings and 2,256 (12%) were measured because of staff concerns. Median NEWS was 1 for routine and 2 for concern recordings. Overall, only 12% of NEWS were high (≥5), but a higher proportion were elevated when there were concerns about acute illness (18%), compared with routine recordings (7%). Conclusions use of NEWS in care homes appears to be feasible. The majority of NEWS were not elevated, and the distribution of scores is consistent with other out-of-hospital settings. Further work is required to know if NEWS is triggering the most appropriate response and improving care home resident outcomes. Keywords care homes, track and trigger systems, National Early Warning Score, older people Topic internship and residencyprecipitating factorsvital signselderlymedical residenciesnational early warning score (news

Report: The 62nd Annual Caddo Conference and 27th Annual East Texas Archeological Conference, Tyler, Texas, February 28 and 29, 2020

The 62nd Caddo Conference and 27th East Texas Archeological Conference was held at the University Center on the campus of the University of Texas at Tyler on February 28 and 29, 2020. The conference was dedicated to the rebuilding of public facilities at Caddo Mounds State Historic Site. These facilities had been destroyed by a tornado in 2019. The conference organizers were Thomas Guderjan, Colleen Hanratty, Cory Sills, Christy Simmons (University of Texas at Tyler), Keith Eppich (Tyler Junior College), Anthony Souther (Caddo Mounds State Historic Site), Amanda Regnier (Oklahoma Archeological Survey), Mark Walters (Texas Historical Commission Steward). Sponsors included The Center for Social Science Research and Department of Social Sciences, University of Texas at Tyler, Humanities Texas, Kevin Stingley, Arkansas Archeological Survey, Beta Analytic, Inc., Friends of Northeast Texas Archeology, East Texas Archeological Society, Maya Research Program, Tejas Archeology, Tyler Junior College, Gregg County Historical Museum, the American Indian Heritage Day of Texas organization, and the Caddo Nation. Before the formal program began, a preconference gathering was held at ETX Brewing Company at 221 S Broadway Avenue in Tyler on Thursday evening, February 27th. Approximately 250 people participated in the joint conferences

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Acceptance and Commitment Therapy plus usual care for improving quality of life in people with motor neuron disease (COMMEND) : a multicentre, parallel, randomised controlled trial in the UK

Background Motor neuron disease is a progressive, fatal neurodegenerative disease for which there is no cure. Acceptance and Commitment Therapy (ACT) is a psychological therapy incorporating acceptance, mindfulness, and behaviour change techniques. We aimed to evaluate the effectiveness of ACT plus usual care, compared with usual care alone, for improving quality of life in people with motor neuron disease. Methods We conducted a parallel, multicentre, two-arm randomised controlled trial in 16 UK motor neuron disease care centres or clinics. Eligible participants were aged 18 years or older with a diagnosis of definite or laboratory-supported probable, clinically probable, or possible familial or sporadic amyotrophic lateral sclerosis; progressive muscular atrophy; or primary lateral sclerosis; which met the World Federation of Neurology's El Escorial diagnostic criteria. Participants were randomly assigned (1:1) to receive up to eight sessions of ACT adapted for people with motor neuron disease plus usual care or usual care alone by a web-based system, stratified by site. Participants were followed up at 6 months and 9 months post-randomisation. Outcome assessors and trial statisticians were masked to treatment allocation. The primary outcome was quality of life using the McGill Quality of Life Questionnaire-Revised (MQOL-R) at 6 months post-randomisation. Primary analyses were multi-level modelling and modified intention to treat among participants with available data. This trial was pre-registered with the ISRCTN Registry (ISRCTN12655391). Findings Between Sept 18, 2019, and Aug 31, 2022, 435 people with motor neuron disease were approached for the study, of whom 206 (47%) were assessed for eligibility, and 191 were recruited. 97 (51%) participants were randomly assigned to ACT plus usual care and 94 (49%) were assigned to usual care alone. 80 (42%) of 191 participants were female and 111 (58%) were male, and the mean age was 63·1 years (SD 11·0). 155 (81%) participants had primary outcome data at 6 months post-randomisation. After controlling for baseline scores, age, sex, and therapist clustering, ACT plus usual care was superior to usual care alone for quality of life at 6 months (adjusted mean difference on the MQOL-R of 0·66 [95% CI 0·22–1·10]; d=0·46 [0·16–0·77]; p=0·0031). Moderate effect sizes were clinically meaningful. 75 adverse events were reported, 38 of which were serious, but no adverse events were deemed to be associated with the intervention. Interpretation ACT plus usual care is clinically effective for maintaining or improving quality of life in people with motor neuron disease. As further evidence emerges confirming these findings, health-care providers should consider how access to ACT, adapted for the specific needs of people with motor neuron disease, could be provided within motor neuron disease clinical services

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

FEDSM2003-45657 RELATION OF POLYMER DRAG REDUCTION TO STRUCTURE AND MOLECULAR WEIGHT

ABSTRACT The influence of molecular weight distribution on polymer drag reduction was studied for solutions of partially hydrolyzed polyacrylamide by analyzing the solution over a period of time during which the polymer was degrading. No relation was observed between the effectiveness of this polymer solution and molecular weight

Meta-analysis of randomised controlled trials with N-acetylcysteine in the treatment of schizophrenia

Objective: There is accumulating evidence that adjunctive treatment with N-acetylcysteine may be effective for schizophrenia. This study aimed to conduct a comprehensive meta-analysis examining the efficacy of randomised control trials investigating N-acetylcysteine as an adjunct treatment for schizophrenia and the first to investigate cognition as an outcome. Methods: We systematically reviewed Medline, EmCare, PsycINFO, Embase, CINAHL Complete, China Knowledge Resource Integrated Database and the Cochrane Clinical Trials online registry for randomised control trials of N-acetylcysteine for schizophrenia. We undertook pairwise meta-analyses of N-acetylcysteine vs placebo for psychosis symptoms and cognition. Results: Seven studies, including n = 220 receiving N-acetylcysteine and n = 220 receiving placebo, met inclusion criteria for the pairwise meta-analyses. Positive and Negative Syndrome Scale negative and total scores were significantly improved in the N-acetylcysteine group after 24 weeks of treatment. The cognitive domain of working memory improved with N-acetylcysteine supplementation. Conclusion: Evidence supports the notion that N-acetylcysteine may be a useful adjunct to standard treatment for the improvement of schizophrenia symptoms, as well as the cognitive domain of working memory. Treatment effects were observed at the later time point (> 24 weeks), suggesting that longer interventions are required for the success of N-acetylcysteine treatment