The state of the science of nurse work environments in the United States: A systematic review

A healthy nurse work environment is a workplace that is safe, empowering, and satisfying. Many research studies were conducted on nurse work environments in the last decade; however, it lacks an overview of these research studies. The purpose of this review is to identify, evaluate, and summarize the major foci of studies about nurse work environments in the United States published between January 2005 and December 2017 and provide strategies to improve nurse work environments. Databases searched included MEDLINE via PubMed, CINAHL, PsycINFO, Nursing and Allied Health, and the Cochrane Library. The literature search followed the PRISMA guideline. Fifty-four articles were reviewed. Five major themes emerged: 1) Impacts of healthy work environments on nurses' outcomes such as psy- chological health, emotional strains, job satisfaction, and retention; 2) Associations between healthy work environments and nurse interpersonal relationships at workplaces, job performance, and pro- ductivity; 3) Effects of healthy work environments on patient care quality; 4) Influences of healthy work environments on hospital accidental safety; and 5) Relationships between nurse leadership and healthy work environments. This review shows that nurses, as frontline patient care providers, are the foun- dation for patient safety and care quality. Promoting nurse empowerment, engagement, and interper- sonal relationships at work is rudimental to achieve a healthy work environment and quality patient care. Healthier work environments lead to more satisfied nurses who will result in better job perfor- mance and higher quality of patient care, which will subsequently improve healthcare organizations' financial viability. Fostering a healthy work environment is a continuous effort

Psychiatric framing affects positive but not negative schizotypy scores in psychology and medical students

When testing risk for psychosis, we regularly rely on self-report questionnaires. Yet, the more that people know about this condition, the more they might respond defensively, in particular with regard to the more salient positive symptom dimension. In two studies, we investigated whether framing provided by questionnaire instructions might modulate responses on self-reported positive and negative schizotypy. The O-LIFE (UK study) or SPQ (New Zealand study) questionnaire was framed in either a “psychiatric” “creativity” or “personality” (NZ only) context. We tested psychology students (without taught knowledge about psychosis) and medical students (with taught knowledge about psychosis; UK only). We observed framing effects in psychology students in both studies: positive schizotypy scores were lower after the psychiatric compared to the creativity instruction. However, schizotypy scores did not differ between the creativity and personality framing conditions, suggesting that the low scores with psychiatric framing reflect defensive responding. The same framing effect was also observed in medical students, despite their lower positive schizotypy scores overall. Negative schizotypy scores were not affected by framing in either study. These results highlight the need to reduce response biases when studying schizotypy, because these might blur schizotypy-behaviour relationships.</p

A systematic review of supportive interventions to promote women's comfort and well-being during induction of labour

© 2020 John Wiley & Sons Ltd Aims: To evaluate the effectiveness of non-pharmacological non-invasive supportive interventions for impacts on women's comfort and well-being during induction of labour. Design: A quantitative systematic review without meta-analysis. Data Sources: Databases were searched for primary research published in English between 2000–2019: AMED, CINAHL, Medline, Maternity and Infant Care database, PsycINFO, and ProQuest. The quality of studies was evaluated using JBI levels of evidence and established critical appraisal tools. Studies describing measures of comfort, coping, and well-being for women during induction of labour were included. Results: Two articles met the criteria for inclusion. There is limited evidence to suggest that women having outpatient cervical priming were more satisfied with their experience than women having inpatient cervical priming and that outpatient cervical priming did not increase women's anxiety. A specifically designed information brochure explaining the induction process improved women's knowledge and understanding. Review Methods: The quantitative systematic review followed the Centre for Reviews and Dissemination guidelines and Cochrane Effective Practice and Organisation of Care guidance. Quality appraisal was conducted using JBI levels of evidence, Cochrane Risk of Bias, and other established tools. A narrative description of the quantitative data was undertaken. There was insufficient evidence to perform a narrative synthesis or meta-analysis due to the nature of the study designs and insufficient outcome data. Conclusions: Globally, the number of women having an induction of labour is increasing and there is a lack of evidence on the effectiveness of supportive interventions. Components of supportive care for women having induction of labour require urgent evaluation. Measurement tools which capture the complexity of supportive care for women having induction of labour need to be developed and validated. Impact: This is the first review to evaluate non-pharmacological, non-invasive supportive interventions for women having induction of labour. The findings of this review identify the urgent need to develop an evidence base for effective supportive

Risk Factors Associated With Infection in Open Fractures of the Upper and Lower Extremities

Introduction: Open fractures are associated with a high risk of infection. The prevention of infection is the single most important goal, influencing perioperative care of patients with open fractures. Using data from 2,500 participants with open fracture wounds enrolled in the Fluid Lavage of Open Wounds trial, we conducted a multivariable analysis to determine the factors that are associated with infections 12 months postfracture. Methods: Eighteen predictor variables were identified for infection a priori from baseline data, fracture characteristics, and surgical data from the Fluid Lavage of Open Wounds trial. Twelve predictor variables were identified for deep infection, which included both surgically and nonoperatively managed infections.We used multivariable Cox proportional hazards regression analyses to identify the factors associated with infection. Irrigation solution and pressure were included as variables in the analysis. The results were reported as adjusted hazard ratios (HRs), 95% confidence intervals (CIs), and associated P values. All tests were two tailed with alpha = 0.05. Results: Factors associated with any infection were fracture location (tibia: HR 5.13 versus upper extremity, 95% CI 3.28 to 8.02; other lower extremity: HR 3.63 versus upper extremity, 95% CI 2.38 to 5.55; overall P\u3c 0.001), low energy injury (HR 1.64, 95% CI 1.08 to 2.46; P = 0.019), degree of wound contamination (severe: HR 2.12 versus mild, 95% CI 1.35 to 3.32; moderate: HR 1.08 versus mild, 95% CI 0.78 to 1.49; overall P = 0.004), and need for flap coverage (HR 1.82, 95% CI 1.11 to 2.99; P = 0.017). Discussion: The results of this study provide a better understanding of which factors are associated with a greater risk of infection in open fractures. In addition, it can allow for surgeons to better counsel patients regarding prognosis, helping patients to understand their individual risk of infection

Risk Factors Associated With Infection in Open Fractures of the Upper and Lower Extremities

Introduction: Open fractures are associated with a high risk of infection. The prevention of infection is the single most important goal, influencing perioperative care of patients with open fractures. Using data from 2,500 participants with open fracture wounds enrolled in the Fluid Lavage of Open Wounds trial, we conducted a multivariable analysis to determine the factors that are associated with infections 12 months postfracture. Methods: Eighteen predictor variables were identified for infection a priori from baseline data, fracture characteristics, and surgical data from the Fluid Lavage of Open Wounds trial. Twelve predictor variables were identified for deep infection, which included both surgically and nonoperatively managed infections.We used multivariable Cox proportional hazards regression analyses to identify the factors associated with infection. Irrigation solution and pressure were included as variables in the analysis. The results were reported as adjusted hazard ratios (HRs), 95% confidence intervals (CIs), and associated P values. All tests were two tailed with alpha = 0.05. Results: Factors associated with any infection were fracture location (tibia: HR 5.13 versus upper extremity, 95% CI 3.28 to 8.02; other lower extremity: HR 3.63 versus upper extremity, 95% CI 2.38 to 5.55; overall P\u3c 0.001), low energy injury (HR 1.64, 95% CI 1.08 to 2.46; P = 0.019), degree of wound contamination (severe: HR 2.12 versus mild, 95% CI 1.35 to 3.32; moderate: HR 1.08 versus mild, 95% CI 0.78 to 1.49; overall P = 0.004), and need for flap coverage (HR 1.82, 95% CI 1.11 to 2.99; P = 0.017). Discussion: The results of this study provide a better understanding of which factors are associated with a greater risk of infection in open fractures. In addition, it can allow for surgeons to better counsel patients regarding prognosis, helping patients to understand their individual risk of infection

Mitochondrial ROS regulate thermogenic energy expenditure and sulfenylation of UCP1

Brown adipose tissue (BAT) can dissipate chemical energy as heat through thermogenic respiration, which requires uncoupling protein 1 (UCP1)1,2. Thermogenesis from BAT and beige adipose can combat obesity and diabetes3, encouraging investigation of factors that control UCP1-dependent respiration in vivo. Herein we show that acutely activated BAT thermogenesis is defined by a substantial increase in mitochondrial reactive oxygen species (ROS) levels. Remarkably, this process supports in vivo BAT thermogenesis, as pharmacological depletion of mitochondrial ROS results in hypothermia upon cold exposure, and inhibits UCP1-dependent increases in whole body energy expenditure. We further establish that thermogenic ROS alter BAT cysteine thiol redox status to drive increased respiration, and Cys253 of UCP1 is a key target. UCP1 Cys253 is sulfenylated during thermogenesis, while mutation of this site desensitizes the purine nucleotide inhibited state of the carrier to adrenergic activation and uncoupling. These studies identify BAT mitochondrial ROS induction as a mechanism that drives UCP1-dependent thermogenesis and whole body energy expenditure, which opens the way to develop improved therapeutic strategies for combating metabolic disorders

Assessment of brain age in posttraumatic stress disorder: Findings from the ENIGMA PTSD and brain age working groups

Background: Posttraumatic stress disorder (PTSD) is associated with markers of accelerated aging. Estimates of brain age, compared to chronological age, may clarify the effects of PTSD on the brain and may inform treatment approaches targeting the neurobiology of aging in the context of PTSD. Method: Adult subjects (N = 2229; 56.2% male) aged 18–69 years (mean = 35.6, SD = 11.0) from 21 ENIGMA-PGC PTSD sites underwent T1-weighted brain structural magnetic resonance imaging, and PTSD assessment (PTSD+, n = 884). Previously trained voxel-wise (brainageR) and region-of-interest (BARACUS and PHOTON) machine learning pipelines were compared in a subset of control subjects (n = 386). Linear mixed effects models were conducted in the full sample (those with and without PTSD) to examine the effect of PTSD on brain predicted age difference (brain PAD; brain age − chronological age) controlling for chronological age, sex, and scan site. Results: BrainageR most accurately predicted brain age in a subset (n = 386) of controls (brainageR: ICC = 0.71, R = 0.72, MAE = 5.68; PHOTON: ICC = 0.61, R = 0.62, MAE = 6.37; BARACUS: ICC = 0.47, R = 0.64, MAE = 8.80). Using brainageR, a three-way interaction revealed that young males with PTSD exhibited higher brain PAD relative to male controls in young and old age groups; old males with PTSD exhibited lower brain PAD compared to male controls of all ages. Discussion: Differential impact of PTSD on brain PAD in younger versus older males may indicate a critical window when PTSD impacts brain aging, followed by age-related brain changes that are consonant with individuals without PTSD. Future longitudinal research is warranted to understand how PTSD impacts brain aging across the lifespan

Autoantibodies Against Proteins Previously Associated With Autoimmunity in Adult and Pediatric Patients With COVID-19 and Children With MIS-C

The antibody profile against autoantigens previously associated with autoimmune diseases and other human proteins in patients with COVID-19 or multisystem inflammatory syndrome in children (MIS-C) remains poorly defined. Here we show that 30% of adults with COVID-19 had autoantibodies against the lung antigen KCNRG, and 34% had antibodies to the SLE-associated Smith-D3 protein. Children with COVID-19 rarely had autoantibodies; one of 59 children had GAD65 autoantibodies associated with acute onset of insulin-dependent diabetes. While autoantibodies associated with SLE/Sjögren’s syndrome (Ro52, Ro60, and La) and/or autoimmune gastritis (gastric ATPase) were detected in 74% (40/54) of MIS-C patients, further analysis of these patients and of children with Kawasaki disease (KD), showed that the administration of intravenous immunoglobulin (IVIG) was largely responsible for detection of these autoantibodies in both groups of patients. Monitoring in vivo decay of the autoantibodies in MIS-C children showed that the IVIG-derived Ro52, Ro60, and La autoantibodies declined to undetectable levels by 45-60 days, but gastric ATPase autoantibodies declined more slowly requiring >100 days until undetectable. Further testing of IgG and/or IgA antibodies against a subset of potential targets identified by published autoantigen array studies of MIS-C failed to detect autoantibodies against most (16/18) of these proteins in patients with MIS-C who had not received IVIG. However, Troponin C2 and KLHL12 autoantibodies were detected in 2 of 20 and 1 of 20 patients with MIS-C, respectively. Overall, these results suggest that IVIG therapy may be a confounding factor in autoantibody measurements in MIS-C and that antibodies against antigens associated with autoimmune diseases or other human proteins are uncommon in MIS-C

Immunopathological signatures in multisystem inflammatory syndrome in children and pediatric COVID-19

: Pediatric Coronavirus Disease 2019 (pCOVID-19) is rarely severe; however, a minority of children infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) might develop multisystem inflammatory syndrome in children (MIS-C), with substantial morbidity. In this longitudinal multi-institutional study, we applied multi-omics (analysis of soluble biomarkers, proteomics, single-cell gene expression and immune repertoire analysis) to profile children with COVID-19 (n = 110) and MIS-C (n = 76), along with pediatric healthy controls (pHCs; n = 76). pCOVID-19 was characterized by robust type I interferon (IFN) responses, whereas prominent type II IFN-dependent and NF-κB-dependent signatures, matrisome activation and increased levels of circulating spike protein were detected in MIS-C, with no correlation with SARS-CoV-2 PCR status around the time of admission. Transient expansion of TRBV11-2 T cell clonotypes in MIS-C was associated with signatures of inflammation and T cell activation. The association of MIS-C with the combination of HLA A*02, B*35 and C*04 alleles suggests genetic susceptibility. MIS-C B cells showed higher mutation load than pCOVID-19 and pHC. These results identify distinct immunopathological signatures in pCOVID-19 and MIS-C that might help better define the pathophysiology of these disorders and guide therapy