bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of H3N8 influenza A virus with multiple mammalian-adaptive mutations in a rescued Grey seal (Halichoerus grypus) pup
Authors: Venkatesh Divya , Bianco Carlo , Núñez Alejandro , Collins Rachael , Thorpe Darryl , Reid Scott M , Brookes Sharon M , Essen Steve , McGinn Natalie , Seekings James , Cooper Jayne , Brown Ian H , Lewis Nicola S 
Published: February 2020

Abstract
Avian influenza A viruses (IAVs) in different species of seals display a spectrum of pathogenicity, from sub-clinical infection to mass mortality events. Here we present an investigation of avian IAV infection in a 3- to 4-month-old Grey seal (Halichoerus grypus) pup, rescued from St Michael’s Mount, Cornwall in 2017. The pup underwent medical treatment but died after two weeks; post-mortem examination and histology indicated sepsis as the cause of death. IAV NP antigen was detected by immunohistochemistry in the nasal mucosa, and sensitive real-time reverse transcription polymerase chain reaction assays detected trace amounts of viral RNA within the lower respiratory tract, suggesting that the infection may have been cleared naturally. IAV prevalence among Grey seals may therefore be underestimated. Moreover, contact with humans during the rescue raised concerns about potential zoonotic risk. Nucleotide sequencing revealed the virus to be of subtype H3N8. Combining a GISAID database BLAST search and time-scaled phylogenetic analyses, we inferred that the seal virus originated from an unsampled, locally circulating (in Northern Europe) viruses, likely from wild Anseriformes. From examining the protein alignments, we found several residue changes in the seal virus that did not occur in the bird viruses, including D701N in the PB2 segment, a rare mutation, and a hallmark of mammalian adaptation of bird viruses. IAVs of H3N8 subtype have been noted for their particular ability to cross the species barrier and cause productive infections, including historical records suggesting that they may have caused the 1889 pandemic. Therefore, infections such as the one we report here may be of interest to pandemic surveillance and risk and help us better understand the determinants and drivers of mammalian adaptation in influenza.
Terminal Ulcers, SCALE, Skin Failure, and Unavoidable Pressure Injuries: Results of the 2019 Terminology Survey
Authors: Sibbald R. Gary , Ayello Elizabeth A. 
Published: February 2020

ABSTRACT
This article reports the results of a global wound care community survey on Kennedy terminal ulcers, Skin Changes At Life’s End, Trombley-Brennan terminal tissue injuries, skin failure, and unavoidable pressure injury terminology. The survey consisted of 10 respondent-ranked statements to determine their level of agreement. There were 505 respondents documented. Each statement required 80% of respondents to agree (either “strongly agree” or “somewhat agree”) for the statement to reach consensus. Nine of the 10 statements reached consensus. Comments from two additional open-ended questions were grouped by theme. Conclusions and suggested recommendations for next steps are discussed. This summary is designed to improve clinical care and foster research into current criteria for unavoidable skin changes at the end of life.

GENERAL PURPOSE
To present the results of the 2019 study of healthcare professionals’ consensus and opinions regarding terminology for terminal ulcers, Skin Changes At Life’s End, skin failure, and unavoidable pressure injuries to improve clinical care and to foster research into current criteria for unavoidable skin changes at the end of life.

TARGET AUDIENCE
This continuing education activity is intended for physicians, physician assistants, NPs, and nurses with an interest in skin and wound care.

LEARNING OBJECTIVES/OUTCOMES
After completing this continuing education activity, the participant should be better able to:
1. Explain the survey methodology and identify the consensus statements.
2. Synthesize the open-ended questions and respondent comments and their implications for clinical care and research.
Pressure Ulcer Risk Factors in Persons with Mobility-Related Disabilities
Authors: Sprigle Stephen , McNair Douglas , Sonenblum Sharon 
Published: February 2020

ABSTRACT

OBJECTIVE
To assess pressure ulcer (PU) risk in persons with mobility impairments using a large data set to identify demographic, laboratory, hemodynamic, and pharmacologic risk factors.

METHODS
The cohort of interest was persons with disabilities who have mobility impairments and are diagnostically at risk of PUs. To define this cohort, diagnoses that qualify patients for skin protection wheelchair cushions were used. Data were obtained from the Cerner Health Facts data warehouse. Two cohorts were defined: persons with and without a history of PUs. Analysis included descriptive statistics and multivariate logistic regression modeling. Variables retained in the model were identified using LASSO, gradient boosting, and Bayesian model averaging.

MAIN RESULTS
The resulting cohorts included more than 87,000 persons with a history of PUs and more than 1.1 million persons who did not have a PU. The data revealed seven disability groups with the greatest prevalence of PUs: those with Alzheimer disease, cerebral palsy, hemiplegia, multiple sclerosis, paraplegia/quadriplegia, Parkinson disease, and spina bifida. Ulcers in the pelvic region accounted for 82% of PUs. Persons with disabilities who were male or black had a greater prevalence of PUs. Physiologic risk factors included the presence of kidney or renal disease, decreased serum albumin, and increased serum C-reactive protein.

CONCLUSIONS
The results indicate that, although persons with disabilities can exhibit a wide functional range, they remain at risk of PUs and should be evaluated for proper preventive measures, including support surfaces and wheelchair cushions.
Critical Illness Factors Associated With Long-Term Mortality and Health-Related Quality of Life Morbidity Following Community-Acquired Pediatric Septic Shock*
Authors: Zimmerman Jerry J. , Banks Russell , Berg Robert A. , Zuppa Athena , Newth Christopher J. , Wessel David , Pollack Murray M. , Meert Kathleen L. , Hall Mark W. , Quasney Michael , Sapru Anil , Carcillo Joseph A. , McQuillen Patrick S. , Mourani Peter M. , Wong Hector , Chima Ranjit S. , Holubkov Richard , Coleman Whitney , Sorenson Samuel , Varni James W. , McGalliard Julie , Haaland Wren , Whitlock Kathryn , Dean J. Michael , Reeder Ron W. 
Published: February 2020

Objectives:
A companion article reports the trajectory of long-term mortality and significant health-related quality of life disability among children encountering septic shock. In this article, the investigators examine critical illness factors associated with these adverse outcomes.

Design:
Prospective, cohort-outcome study, conducted 2013–2017.

Setting:
Twelve United States academic PICUs.

Patients:
Critically ill children, 1 month to 18 years, with community-acquired septic shock requiring vasoactive-inotropic support.

Interventions:
Illness severity, organ dysfunction, and resource utilization data were collected during PICU admission. Change from baseline health-related quality of life at the month 3 follow-up was assessed by parent proxy-report employing the Pediatric Quality of Life Inventory or the Stein-Jessop Functional Status Scale.

Measurements and Main Results:
In univariable modeling, critical illness variables associated with death and/or persistent, serious health-related quality of life deterioration were candidates for multivariable modeling using Bayesian information criterion. The most clinically relevant multivariable models were selected among models with near-optimal statistical fit. Three months following septic shock, 346 of 389 subjects (88.9%) were alive and 43 of 389 had died (11.1%); 203 of 389 (52.2%) had completed paired health-related quality of life surveys. Pediatric Risk of Mortality, cumulative Pediatric Logistic Organ Dysfunction scores, PICU and hospital durations of stay, maximum and cumulative vasoactive-inotropic scores, duration of mechanical ventilation, need for renal replacement therapy, extracorporeal life support or cardiopulmonary resuscitation, and appearance of pathologic neurologic signs were associated with adverse outcomes in univariable models. In multivariable regression analysis (odds ratio [95% CI]), summation of daily Pediatric Logistic Organ Dysfunction scores, 1.01/per point (1.01–1.02), p < 0.001; highest vasoactive-inotropic score, 1.02/per point (1.00–1.04), p = 0.003; and any acute pathologic neurologic sign/event, 5.04 (2.15–12.01), p < 0.001 were independently associated with death or persistent, serious deterioration of health-related quality of life at month 3.

Conclusions and Relevance:
Biologically plausible factors related to sepsis-associated critical illness organ dysfunction and its treatment were associated with poor outcomes at month 3 follow-up among children encountering septic shock.
Trajectory of Mortality and Health-Related Quality of Life Morbidity Following Community-Acquired Pediatric Septic Shock*
Authors: Zimmerman Jerry J. , Banks Russell , Berg Robert A. , Zuppa Athena , Newth Christopher J. , Wessel David , Pollack Murray M. , Meert Kathleen L. , Hall Mark W. , Quasney Michael , Sapru Anil , Carcillo Joseph A. , McQuillen Patrick S. , Mourani Peter M. , Wong Hector , Chima Ranjit S. , Holubkov Richard , Coleman Whitney , Sorenson Samuel , Varni James W. , McGalliard Julie , Haaland Wren , Whitlock Kathryn , Dean J. Michael , Reeder Ron W. 
Published: February 2020

Objectives:
In-hospital pediatric sepsis mortality has decreased substantially, but long-term mortality and morbidity among children initially surviving sepsis, is unknown. Accordingly, the Life After Pediatric Sepsis Evaluation investigation was conducted to describe the trajectory of mortality and health-related quality of life morbidity for children encountering community-acquired septic shock.

Design:
Prospective, cohort-outcome study, conducted 2013–2017.

Setting:
Twelve academic PICUs in the United States.

Patients:
Critically ill children, 1 month to 18 years, with community-acquired septic shock requiring vasoactive-inotropic support.

Interventions:
Demographic, infection, illness severity, organ dysfunction, and resource utilization data were collected daily during PICU admission. Serial parent proxy-report health-related quality of life assessments were obtained at baseline, 7 days, and 1, 3, 6, and 12 months following PICU admission utilizing the Pediatric Quality of Life Inventory or Stein-Jessop Functional Status Scale.

Measurements and Main Results:
Among 389 children enrolled, mean age was 7.4 ± 5.8 years; 46% were female; 18% were immunocompromised; and 51% demonstrated chronic comorbidities. Baseline Pediatric Overall Performance Category was normal in 38%. Median (Q1–Q3) Pediatric Risk of Mortality and Pediatric Logistic Organ Dysfunction scores at PICU admission were 11.0 (6.0–17.0) and 9.0 (6.0–11.0); durations of vasoactive-inotropic and mechanical ventilation support were 3.0 days (2.0–6.0 d) and 8.0 days (5.0–14.0 d); and durations of PICU and hospital stay were 9.4 days (5.6–15.4 d) and 15.7 days (9.2–26.0 d). At 1, 3, 6, and 12 months following PICU admission for the septic shock event, 8%, 11%, 12%, and 13% of patients had died, while 50%, 37%, 30%, and 35% of surviving patients had not regained their baseline health-related quality of life.

Conclusions:
This investigation provides the first longitudinal description of long-term mortality and clinically relevant, health-related quality of life morbidity among children encountering community-acquired septic shock. Although in-hospital mortality was 9%, 35% of survivors demonstrated significant, health-related quality of life deterioration from baseline that persisted at least 1 year following hospitalization for septic shock.
The contribution of residential greenness to mortality among men with prostate cancer: a registry-based cohort study of Black and White men
Authors: Iyer Hari S. , Valeri Linda , James Peter , Chen Jarvis T. , Hart Jaime E. , Laden Francine , Holmes Michelle D. , Rebbeck Timothy R. 
Published: February 2020

Background:
Black men with prostate cancer (CaP) experience excess mortality compared with White men. Residential greenness, a health promoting contextual factor, could explain racial disparities in mortality among men with CaP.

Methods:
We identified Pennsylvania Cancer Registry cases diagnosed between January 2000 and December 2015. Totally, 128,568 participants were followed until death or 1 January 2018, whichever occurred first. Residential exposure at diagnosis was characterized using the Normalized Difference Vegetation Index (NDVI) with 250 m resolution. We estimated hazard ratios (HRs) using Cox models, adjusting for area-level socioeconomic status, geographic healthcare access, and segregation. To determine whether increasing residential greenness could reduce racial disparities, we compared standardized 10-year mortality Black-White risk differences under a hypothetical intervention fixing NDVI to the 75th percentile of NDVI experienced by White men.

Results:
We observed 29,978 deaths over 916,590 person-years. Comparing men in the highest to lowest NDVI quintile, all-cause (adjusted HR [aHR]: 0.88, 95% confidence interval [CI]: 0.84, 0.92, P
trend < 0.0001), prostate-specific (aHR: 0.88, 95% CI: 0.80, 0.99, P
trend= 0.0021), and cardiovascular-specific (aHR: 0.82, 95% CI: 0.74, 0.90, P
trend < 0.0001) mortality were lower. Inverse associations between an interquartile range increase in NDVI and cardiovascular-specific mortality were observed in White (aHR: 0.90, 95% CI: 0.86, 0.93) but not Black men (aHR: 0.97, 95% CI: 0.89, 1.06; P
het = 0.067). Hypothetical interventions to increase NDVI led to nonsignificant reductions in all-cause (−5.3%) and prostate-specific (−23.2%), but not cardiovascular-specific mortality disparities (+50.5%).

Discussion:
Residential greenness was associated with lower mortality among men with CaP, but findings suggest that increasing residential greenness would have limited impact on racial disparities in mortality.
The Victorian Institute of Sport Assessment Scale for Patellar Tendinopathy (VISA-P): A Reliability Generalization Meta-analysis
Authors: Palazón-Bru Antonio , Tomás Rodríguez María Isabel , Mares-García Emma , Hernández-Sánchez Sergio , Carbonell-Torregrosa María Ángeles , Gil-Guillén Vicente Francisco 
Published: February 2020

Objective:
The Victorian Institute of Sport Assessment-Patella (VISA-P) is a questionnaire to assess the severity of patellar tendinopathies. Its use requires good reliability indicators: internal consistency, test-retest and parallel forms. Several studies have been published examining this question, but to date the reliability of this questionnaire (meta-analysis) has not been generalized. The aim of this study was to perform a meta-analysis to generalize the reliability of the VISA-P.

Data sources:
MEDLINE, EMBASE, and Scopus.

Study selection:
Studies included were those examining the reliability coefficients of the VISA-P: Cronbach alpha, intraclass correlation coefficient (ICC), and parallel-forms (correlation coefficients compared with other scales).

Data extraction:
All coefficients were extracted and the mean reliability was obtained using fixed- or random-effects models. Sensitivity (leave-one-out analysis) was analyzed. Quality assessment was performed using the COnsensus-based Standards for the selection of health Measurement INstruments (COSMIN) checklist.

Data Synthesis:
Of 364 scientific articles, 12 fulfilled meta-analysis criteria. The summary statistic was 0.86 [95% confidence interval (CI): 0.78-0.92] for Cronbach alpha and 0.94 (95% CI: 0.89-0.97) for the ICC. Parallel forms depended on the comparative test used, ranging from −0.83 to 0.68. The sensitivity analysis found an influential study for the parallel-forms reliability in the Blazina score. We were unable to analyze the asymmetry of funnel plots and meta-regression models because of the number of studies.

Conclusions:
The reliability of VISA-P for assessing the severity of patellar tendinopathies requires greater evaluation with more scientific evidence before it can be implemented in clinical practice.
Validation of the Chinese Version of the Somatic Symptom Disorder–B Criteria Scale for Detecting DSM-5 Somatic Symptom Disorders: A Multicenter Study
Authors: Li Tao , Wei Jing , Fritzsche Kurt , Toussaint Anne Christin , Jiang Yinan , Cao Jinya , Zhang Lan , Zhang Yaoyin , Chen Hua , Wu Heng , Ma Xiquan , Li Wentian , Ren Jie , Lu Wei , Müller Anne-Maria , Leonhart Rainer 
Published: February 2020

ABSTRACT

Objective
This study aimed to validate the Chinese version of the Somatic Symptom Disorder–B Criteria Scale (SSD-12) in an outpatient sample from Chinese general hospitals and to determine the diagnostic performance of the SSD-12 as a screening tool for somatic symptom disorder (SSD).

Methods
The Chinese version of the SSD-12 was completed by 699 outpatients from nine general hospitals during a 16-month period (2016–2018). The SSD section of the Structured Clinical Interview for DSM Disorders, Fifth Edition, Research Version, was used to determine diagnostic accuracy (criterion validity). The construct validity of the SSD-12 was evaluated by examining correlations with the Whiteley Index-7, Patient Health Questionnaire-15, Patient Health Questionnaire-9, General Anxiety Disorder-7, World Health Organization Disability Assessment Schedule, and Medical Outcome Study 12-item Short Form Health Survey (SF-12).

Results
The SSD-12 had excellent internal consistency in this sample (Cronbach α = .95). Confirmatory factor analyses replicated a three-factor structure that reflects the cognitive, affective, and behavioral aspects (Comparative Fit Index = 0.963, Tucker-Lewis Index = 0.952, root mean square error of approximation = 0.08, 90% confidence interval = 0.08–0.09), but was also consistent with a general one-factor model of the SSD-12 (Comparative Fit Index = 0.957, Tucker-Lewis Index = 0.948, root mean square error of approximation = 0.09, 90% confidence interval = 0.08–0.10). The optimal cutoff point for the Structured Clinical Interview for DSM Disorders–based diagnosis of SSD was 16 (sensitivity = 0.76, specificity = 0.80). The SSD-12 sum score was significantly associated with somatic symptom burden (Patient Health Questionnaire-15: r = 0.52, p < .001), health anxiety (Whiteley Index-7: r = 0.82, p < .001), depressive symptoms (Patient Health Questionnaire-9: r = 0.63, p < .001), general anxiety (General Anxiety Disorder-7: r = 0.64, p < .001), health-related quality of life (physical component score of SF-12: r = −0.49, p < .001; mental component score of SF-12: r = −0.61, p < .001), and health-related disabilities (World Health Organization Disability Assessment Schedule: r = 0.56, p < .001).

Conclusions
Initial assessment indicates that the Chinese version of the SSD-12 has sufficient reliability and validity to warrant further testing in both research and clinical settings.
Synergism and antagonism of two distinct, but confused, Nrf1 factors in integral regulation of the nuclear-to-mitochondrial respiratory and antioxidant transcription networks
Authors: Zhang Shuwei , Deng Yangxu , Xiang Yuancai , Hu Shaofan , Qiu Lu , Zhang Yiguo 
Published: February 2020

AbstractThere is hitherto no literature available for explaining two distinct, but confused Nrf1 transcription factors, because they shared the same abbreviations from nuclear factor erythroid 2-related factor 1 (also called Nfe2l1) and nuclear respiratory factor (originally designated α-Pal). Thus, we have here identified that Nfe2l1Nrf1and α-PalNRF1exert synergistic and antagonistic roles in integrative regulation of the nuclear-to-mitochondrial respiratory and antioxidant transcription profiles. In mouse embryonic fibroblasts (MEFs), knockout ofNfe2l1–/–leads to substantial decreases in expression levels of α-PalNRF1and Nfe2l2, together with TFAM (mitochondrial transcription factor A) and other target genes. Similar inhibitory results were determined inNfe2l2–/–MEFs, with an exception thatGSTa1andAldh1a1were distinguishably up-regulated inNfe2l1–/–MEFs. Such synergistic contributions of Nfe2l1 and Nfe2l2 to the positive regulation of α-PalNRF1and TFAM were validated inKeap1–/–MEFs. However, human α-PalNRF1expression was unaltered byhNfe2l1α–/–,hNfe2l2–/–ΔTAor evenhNfe2l1α–/–+siNrf2, albeit TFAM was activated by Nfe2l1 but inhibited by Nfe2l2; such an antagonism occured in HepG2 cells. Conversely, almost all of mouse Nfe2l1, Nfe2l2 and co-target genes were down-expressed inα-PalNRF1+/–MEFs. On the contrary, up-regulation of human Nfe2l1, Nfe2l2 and relevant reporter genes took place after silencing of α-PalNRF1, but their down-regulation occurred upon ectopic expression of α-PalNRF1. Furtherly, Pitx2 (pituitary homeobox 2) was also identified as a direct upstream regulator of Nfe2l1 and TFAM, besides α-PalNRF1. Overall, these across-talks amongst Nfe2l1, Nfe2l2 and α-PalNRF1, along with Pitx2, are integrated from the endoplasmic reticulum to the nuclear-to-mitochondrial communication for targeting TFAM, in order to finely tune the cellular respiratory and antioxidant gene transcription networks, albeit they differ between the mouse and the human.
Suppressors of YpsA-mediated cell division inhibition inBacillus subtilis
Authors: Brzozowski Robert S. , Tomlinson Brooke R. , Sacco Michael D. , Chen Judy J. , Ali Anika N. , Chen Yu , Shaw Lindsey N. , Eswara Prahathees J. 
Published: February 2020

SUMMARYAlthough many bacterial cell division factors have been uncovered over the years, evidence from recent studies points to the existence of yet to be discovered factors involved in cell division regulation. Thus, it is important to identify factors and conditions that regulate cell division to obtain a better understanding of this fundamental biological process. We recently reported that in the Gram-positive organismsBacillus subtilisandStaphylococcus aureus, increased production of YpsA resulted in cell division inhibition. In this study, we isolated spontaneous suppressor mutations to uncover critical residues of YpsA and the pathways through which YpsA may exert its function. Using this technique, we were able to isolate four unique intragenic suppressor mutations inypsA(E55D, P79L, R111P, G132E) that rendered the mutated YpsA non-toxic upon overproduction. We also isolated an extragenic suppressor mutation inyfhS, a gene that encodes a protein of unknown function. Subsequent analysis confirmed that cells lackingyfhSwere unable to undergo filamentation in response to YpsA overproduction. We also serendipitously discovered that YfhS may play a role in cell size regulation.GRAPHICAL ABSTRACTABBREVIATED SUMMARYInBacillus subtilis, we discovered that increased expression ofypsAresults in cell division inhibition and impairment of colony formation on solid medium. Colonies that do arise possess compensatory suppressor mutations. Analysis of one such suppressor mutation led us to a protein of unknown function, YfhS, which appears to play a role in regulating cell length and cell width.