27 research outputs found
Two-particle correlations in azimuthal angle and pseudorapidity in inelastic p + p interactions at the CERN Super Proton Synchrotron
Results on two-particle ΔηΔϕ correlations in inelastic p + p interactions at 20, 31, 40, 80, and 158 GeV/c are presented. The measurements were performed using the large acceptance NA61/SHINE hadron spectrometer at the CERN Super Proton Synchrotron. The data show structures which can be attributed mainly to effects of resonance decays, momentum conservation, and quantum statistics. The results are compared with the Epos and UrQMD models.ISSN:1434-6044ISSN:1434-605
The regional species richness and genetic diversity of Arctic vegetation reflect both past glaciations and current climate
AIM : The Arctic has experienced marked climatic differences between glacial and interglacial periods and is now subject to a rapidly warming climate. Knowledge of the effects of historical processes on current patterns of diversity may aid predictions
of the responses of vegetation to future climate change. We aim to test whether plant species and genetic diversity patterns are correlated with time since deglaciation at regional and local scales. We also investigate whether species richness is correlated with genetic diversity in vascular plants. LOCATION : Circumarctic.
METHODS : We investigated species richness of the vascular plant flora of 21 floristic provinces and examined local species richness in 6215 vegetation plots distributed across the Arctic. We assessed levels of genetic diversity inferred from amplified fragment length polymorphism variation across populations of 23 common Arctic
species. Correlations between diversity measures and landscape age (time since deglaciation) as well as variables characterizing current climate were analysed using spatially explicit simultaneous autoregressive models. RESULTS : lts Regional species richness of vascular plants and genetic diversity were correlated with each other, and both showed a positive relationship with landscape
age. Plot species richness showed differing responses for vascular plants, bryophytes and lichens. At this finer scale, the richness of vascular plants was not significantly related to landscape age, which had a small effect size compared to the models of bryophyte and lichen richness. MAIN CONCLUSION : Our study suggests that imprints of past glaciations in Arctic vegetation diversity patterns at the regional scale are still detectable today. Since Arctic vegetation is still limited by post-glacial migration lag, it will most probably
also exhibit lags in response to current and future climate change. Our results also suggest that local species richness at the plot scale is more determined by local habitat factors.Compilation of the species richness data was made possible through the TFI Networks grant to CD,
“Effect Studies and Adaptation to Climate Change,” under the Norforsk initiative (2011 – 2014) which supported two CBIONET-AVA workshops held in Denmark during 2013. The genetic studies were funded by the Research Council of Norway (grant nos. 150322/720 and 170952/V40 to CB).http://http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1466-82382017-04-30hb2016Plant Production and Soil Scienc
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Global burden of 288 causes of death and life expectancy decomposition in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021
BACKGROUND Regular, detailed reporting on population health by underlying cause of death is fundamental for public health decision making. Cause-specific estimates of mortality and the subsequent effects on life expectancy worldwide are valuable metrics to gauge progress in reducing mortality rates. These estimates are particularly important following large-scale mortality spikes, such as the COVID-19 pandemic. When systematically analysed, mortality rates and life expectancy allow comparisons of the consequences of causes of death globally and over time, providing a nuanced understanding of the effect of these causes on global populations. METHODS The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 cause-of-death analysis estimated mortality and years of life lost (YLLs) from 288 causes of death by age-sex-location-year in 204 countries and territories and 811 subnational locations for each year from 1990 until 2021. The analysis used 56 604 data sources, including data from vital registration and verbal autopsy as well as surveys, censuses, surveillance systems, and cancer registries, among others. As with previous GBD rounds, cause-specific death rates for most causes were estimated using the Cause of Death Ensemble model-a modelling tool developed for GBD to assess the out-of-sample predictive validity of different statistical models and covariate permutations and combine those results to produce cause-specific mortality estimates-with alternative strategies adapted to model causes with insufficient data, substantial changes in reporting over the study period, or unusual epidemiology. YLLs were computed as the product of the number of deaths for each cause-age-sex-location-year and the standard life expectancy at each age. As part of the modelling process, uncertainty intervals (UIs) were generated using the 2·5th and 97·5th percentiles from a 1000-draw distribution for each metric. We decomposed life expectancy by cause of death, location, and year to show cause-specific effects on life expectancy from 1990 to 2021. We also used the coefficient of variation and the fraction of population affected by 90% of deaths to highlight concentrations of mortality. Findings are reported in counts and age-standardised rates. Methodological improvements for cause-of-death estimates in GBD 2021 include the expansion of under-5-years age group to include four new age groups, enhanced methods to account for stochastic variation of sparse data, and the inclusion of COVID-19 and other pandemic-related mortality-which includes excess mortality associated with the pandemic, excluding COVID-19, lower respiratory infections, measles, malaria, and pertussis. For this analysis, 199 new country-years of vital registration cause-of-death data, 5 country-years of surveillance data, 21 country-years of verbal autopsy data, and 94 country-years of other data types were added to those used in previous GBD rounds. FINDINGS The leading causes of age-standardised deaths globally were the same in 2019 as they were in 1990; in descending order, these were, ischaemic heart disease, stroke, chronic obstructive pulmonary disease, and lower respiratory infections. In 2021, however, COVID-19 replaced stroke as the second-leading age-standardised cause of death, with 94·0 deaths (95% UI 89·2-100·0) per 100 000 population. The COVID-19 pandemic shifted the rankings of the leading five causes, lowering stroke to the third-leading and chronic obstructive pulmonary disease to the fourth-leading position. In 2021, the highest age-standardised death rates from COVID-19 occurred in sub-Saharan Africa (271·0 deaths [250·1-290·7] per 100 000 population) and Latin America and the Caribbean (195·4 deaths [182·1-211·4] per 100 000 population). The lowest age-standardised death rates from COVID-19 were in the high-income super-region (48·1 deaths [47·4-48·8] per 100 000 population) and southeast Asia, east Asia, and Oceania (23·2 deaths [16·3-37·2] per 100 000 population). Globally, life expectancy steadily improved between 1990 and 2019 for 18 of the 22 investigated causes. Decomposition of global and regional life expectancy showed the positive effect that reductions in deaths from enteric infections, lower respiratory infections, stroke, and neonatal deaths, among others have contributed to improved survival over the study period. However, a net reduction of 1·6 years occurred in global life expectancy between 2019 and 2021, primarily due to increased death rates from COVID-19 and other pandemic-related mortality. Life expectancy was highly variable between super-regions over the study period, with southeast Asia, east Asia, and Oceania gaining 8·3 years (6·7-9·9) overall, while having the smallest reduction in life expectancy due to COVID-19 (0·4 years). The largest reduction in life expectancy due to COVID-19 occurred in Latin America and the Caribbean (3·6 years). Additionally, 53 of the 288 causes of death were highly concentrated in locations with less than 50% of the global population as of 2021, and these causes of death became progressively more concentrated since 1990, when only 44 causes showed this pattern. The concentration phenomenon is discussed heuristically with respect to enteric and lower respiratory infections, malaria, HIV/AIDS, neonatal disorders, tuberculosis, and measles. INTERPRETATION Long-standing gains in life expectancy and reductions in many of the leading causes of death have been disrupted by the COVID-19 pandemic, the adverse effects of which were spread unevenly among populations. Despite the pandemic, there has been continued progress in combatting several notable causes of death, leading to improved global life expectancy over the study period. Each of the seven GBD super-regions showed an overall improvement from 1990 and 2021, obscuring the negative effect in the years of the pandemic. Additionally, our findings regarding regional variation in causes of death driving increases in life expectancy hold clear policy utility. Analyses of shifting mortality trends reveal that several causes, once widespread globally, are now increasingly concentrated geographically. These changes in mortality concentration, alongside further investigation of changing risks, interventions, and relevant policy, present an important opportunity to deepen our understanding of mortality-reduction strategies. Examining patterns in mortality concentration might reveal areas where successful public health interventions have been implemented. Translating these successes to locations where certain causes of death remain entrenched can inform policies that work to improve life expectancy for people everywhere. FUNDING Bill & Melinda Gates Foundation
Chronic stress, cortisol regulation, interpersonal relatedness, cognitive burden, and depressive symptoms among community -dwelling survivors of brain injury.
Depression after traumatic brain injury is one of the most common and problematic mood disorders, affecting more than a third of those in the recovery process. Efforts to empirically examine this topic have failed to elucidate theoretical explanations and mechanisms. As part of the theory building process this study, using regression analysis, provided a cross-sectional examination of how major concepts, chronic stress, cortisol regulation, interpersonal relatedness and cognitive burden, which were derived from nursing and other disciplines could be related to post-brain injury depression. These concepts were empirically rooted in studies of depression. Thus, hypotheses were stated which posited explanatory relationships between depressive symptoms and these concepts. Seventy-five participants and their significant others were recruited from outpatient rehabilitation clinics. All had sustained a mild-to-moderate brain injury and were within two years of the trauma. Participants with TBI were asked to complete a computerized battery of cognitive tests on short-term memory and directed attention, provide a 12-hour profile of salivary cortisol and complete self-report questionnaires. Relative versions of the depression instruments were also completed. Overall, it was determined that when time-since-injury was included in regression models, pre- and post-injury stress explained a significant amount of the variability in depressive symptoms. Furthermore, a lowered sense-of-belonging, not social support, was a strong correlate of depressive symptoms. As in other studies, cognitive test results failed to provide clarity about the relationship between depressed mood and cognition. Post-injury stress and belonging account for nearly 75% of the variability of depressive symptoms. Cortisol regulation, determined by a 12-hour salivary cortisol profile of 50 of these participants, displayed circadian rhythm variation but demonstrated a lack of association with measures of cognition, head injury indices, depressive symptoms and post-injury stress. This study provides a foundation for further study of TBI and depression. Longitudinal studies, including pre-injury variables such as childhood adversities and the frequency of major stressful life events require further examination to develop knowledge regarding TBI and eventual nursing interventions.Ph.D.Health and Environmental SciencesNursingPhysical therapyPsychobiologyPsychologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/127111/2/3029291.pd
De stad als klaslokaal en onderzoekslab: Ervaringen en dilemma's
Hoger-onderwijsinstellingen zien ‘de stad’ steeds meer als een interessante leer- en onderzoeksomgeving, vol met boeiende vragen en uitdagingen. Tegelijkertijd zijn stedelijke beleidsmakers en andere urban stakeholders op zoek naar manieren om studenten en onderzoekers te betrekken bij hun strategieën, beleid en praktijk. Hoe komen de stad, onderwijs en onderzoek samen? Er gebeurt al van alles, maar hoe werkt deze samenwerking eigenlijk, en hoe kan het beter
Roadmap for action on Risk Assessment of Combined Exposure to Multiple Chemicals (RACEMiC)
EFSA's aim by 2030, is that the Agency and its partners will be equipped for the routine implementation of human health risk assessment to multiple chemicals, across EFSA's domains of activity. To facilitate this effort, a roadmap for action has been developed by mapping the methods, data and tools that are currently available for mixture risk assessment and identifying current scientific gaps including challenges and blockers. The results shows that extensive methods, data and tools are available for dietary mixture risk assessment for pesticides, but that several scientific gaps still exist for the non-dietary mixture exposure to pesticides. For food additives and for certain contaminants, the regulatory readiness for mixture risk assessment was also found to be fairly high compared to food contact materials and cross-silo mixture risk assessment. The scientific gaps identified were prioritised according to their impact on the implementation of mixture risk assessment and, as a result, ten multi-annual project proposals were defined to address these scientific gaps on the short-term, mid-term and long-term. The roadmap also proposes and prioritises a number of working areas in the regulatory domains of pesticides, food contact materials, contaminants, food additives, as well as in the overarching domain of chemicals. Besides the scientific proposals, recommendations to improve stakeholder engagement and communication on mixture risk assessment was investigated. These included, among others, creating an online catalogue of tools, methods and data for mixture risk assessment, as well as the organisation of regular webinars/workshop to promote exchange of information between stakeholders and making more efficient use of national communication hubs for food safety in communicating with the general public
Ex vivo loading of trussed implants for spine fusion induces heterogeneous strains consistent with homeostatic bone mechanobiology
A truss structure was recently introduced as an interbody fusion cage. As a truss system, some of the connected elements may be in a state of compression and others in tension. This study aimed to quantify both the mean and variance of strut strains in such an implant when loaded in a simulated fusion condition with vertebral body or contoured plastic loading platens ex vivo. Cages were each instrumented with 78 fiducial spheres, loaded between platens (vertebral body or contoured plastic), imaged using high resolution micro-CT, and analyzed for deformation and strain of each of the 221 struts. With repeated loading of a cage by vertebral platens, the distribution (variance, indicated by SD) of strut strains widened from 50 N control (4 ± 114 με, mean ± SD) to 1000 N (−23 ± 273 με) and 2000 N (−48 ± 414 με), and between 1000 N and 2000 N. With similar loading of multiple cages, the strain distribution at 2000 N (23 ± 389 με) increased from 50 N control. With repeated loading by contoured plastic platens, induced strains at 2000 N had a distribution similar to that induced by vertebral platens (84 ± 426 με). In all studies, cages exhibited increases in strut strain amplitude when loaded from 50 N to 1000 N or 2000 N. Correspondingly, at 2000 N, 59–64% of struts exhibited strain amplitudes consistent with mechanobiologically-regulated bone homeostasis. At 2000 N, vertically-oriented struts exhibited deformation of −2.87 ± 2.04 μm and strain of −199 ± 133 με, indicating overall cage compression. Thus, using an ex vivo 3-D experimental biomechanical analysis method, a truss implant can have strains induced by physiological loading that are heterogeneous and of amplitudes consistent with mechanobiological bone homeostasis
The Role of Antibiotic Prophylaxis in Prevention of Wound Infection After Lichtenstein Open Mesh Repair of Primary Inguinal Hernia: A Multicenter Double-Blind Randomized Controlled Trial
OBJECTIVE: To determine whether the use of prophylactic antibiotics is effective in the prevention of postoperative wound infection after Lichtenstein open mesh inguinal hernia repair. SUMMARY BACKGROUND DATA: A recent Cochrane meta-analysis (2003) concluded that “antibiotic prophylaxis for elective inguinal hernia repair cannot be firmly recommended or discarded.” METHODS: Patients with a primary inguinal hernia scheduled for Lichtenstein repair were randomized to a preoperative single dose of 1.5 g intravenous cephalosporin or a placebo. Patients with recurrent hernias, immunosuppressive diseases, or allergies for the given antibiotic were excluded. Infection was defined using the Centers for Disease Control and Prevention criteria. RESULTS: We included 1040 patients in the study between November 1998 and May 2003. According to the intention-to-treat principle, 1008 patients were analyzed. There were 8 infections (1.6%) in the antibiotic prophylaxis group and 9 (1.8%) in the placebo group (P = 0.82). There was 1 deep infection in the antibiotic prophylaxis group and 2 in the placebo group (P = 0.57). Statistical analysis showed an absolute risk reduction of 0.19% (95% confidence interval, −1.78%–1.40%) and a number needed to treat of 520 for the total number of infections. For deep infection, the absolute risk reduction is 0.20% (95% confidence interval, −0.87%–0.48%) with a number needed to treat of 508. CONCLUSIONS: A low percentage (1.7%) of wound infection after Lichtenstein open mesh inguinal (primary) hernia repair was found, and there was no difference between the antibiotic prophylaxis or placebo group. The results show that, in Lichtenstein inguinal primary hernia repair, antibiotic prophylaxis is not indicated in low-risk patients