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- Haagsma, JA, et al.
(författare)
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Burden of injury along the development spectrum: associations between the Socio-demographic Index and disability-adjusted life year estimates from the Global Burden of Disease Study 2017
- 2020
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Ingår i: Injury prevention : journal of the International Society for Child and Adolescent Injury Prevention. - : BMJ. - 1475-5785 .- 1353-8047. ; 26:SUPP_1Supp 1, s. 12-26
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Tidskriftsartikel (refereegranskat)abstract
- The epidemiological transition of non-communicable diseases replacing infectious diseases as the main contributors to disease burden has been well documented in global health literature. Less focus, however, has been given to the relationship between sociodemographic changes and injury. The aim of this study was to examine the association between disability-adjusted life years (DALYs) from injury for 195 countries and territories at different levels along the development spectrum between 1990 and 2017 based on the Global Burden of Disease (GBD) 2017 estimates.MethodsInjury mortality was estimated using the GBD mortality database, corrections for garbage coding and CODEm—the cause of death ensemble modelling tool. Morbidity estimation was based on surveys and inpatient and outpatient data sets for 30 cause-of-injury with 47 nature-of-injury categories each. The Socio-demographic Index (SDI) is a composite indicator that includes lagged income per capita, average educational attainment over age 15 years and total fertility rate.ResultsFor many causes of injury, age-standardised DALY rates declined with increasing SDI, although road injury, interpersonal violence and self-harm did not follow this pattern. Particularly for self-harm opposing patterns were observed in regions with similar SDI levels. For road injuries, this effect was less pronounced.ConclusionsThe overall global pattern is that of declining injury burden with increasing SDI. However, not all injuries follow this pattern, which suggests multiple underlying mechanisms influencing injury DALYs. There is a need for a detailed understanding of these patterns to help to inform national and global efforts to address injury-related health outcomes across the development spectrum.
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- Crous, P. W., et al.
(författare)
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Fungal Planet description sheets: 1478-1549
- 2023
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Ingår i: Persoonia. - 0031-5850. ; 50, s. 158-310
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Tidskriftsartikel (refereegranskat)abstract
- Novel species of fungi described in this study include those from various countries as follows: Australia, Aschersonia mackerrasiae on whitefly, Cladosporium corticola on bark of Melaleuca quinquenervia, Penicillium nudgee from soil under Melaleuca quinquenervia, Pseudocercospora blackwoodiae on leaf spot of Persoonia fal- cata, and Pseudocercospora dalyelliae on leaf spot of Senna alata. Bolivia, Aspicilia lutzoniana on fully submersed siliceous schist in high-mountain streams, and Niesslia parviseta on the lower part and apothecial discs of Erioderma barbellatum on a twig. Brazil, Cyathus bonsai on decaying wood, Geastrum albofibrosum from moist soil with leaf litter, Laetiporus pratigiensis on a trunk of a living unknown hardwood tree species, and Scytalidium synnematicum on dead twigs of unidentified plant. Bulgaria, Amanita abscondita on sandy soil in a plantation of Quercus suber. Canada, Penicillium acericola on dead bark of Acer saccharum, and Penicillium corticola on dead bark of Acer saccharum. China, Colletotrichum qingyuanense on fruit lesion of Capsicum annuum. Denmark, Helminthosphaeria leptospora on corticioid Neohypochnicium cremicolor. Ecuador (Galapagos), Phaeosphaeria scalesiae on Scalesia sp. Finland, Inocybe jacobssonii on calcareous soils in dry forests and park habitats. France, Cortinarius rufomyr- rheus on sandy soil under Pinus pinaster, and Periconia neominutissima on leaves of Poaceae. India, Coprinopsis fragilis on decaying bark of logs, Filoboletus keralensis on unidentified woody substrate, Penicillium sankaranii from soil, Physisporinus tamilnaduensis on the trunk of Azadirachta indica, and Poronia nagaraholensis on elephant dung. Iran, Neosetophoma fici on infected leaves of Ficus elastica. Israel, Cnidariophoma eilatica (incl. Cnidario- phoma gen. nov.) from Stylophora pistillata. Italy, Lyophyllum obscurum on acidic soil. Namibia, Aureobasidium faidherbiae on dead leaf of Faidherbia albida, and Aureobasidium welwitschiae on dead leaves of Welwitschia mirabilis. Netherlands, Gaeumannomycella caricigena on dead culms of Carex elongata, Houtenomyces caricicola (incl. Houtenomyces gen. nov.) on culms of Carex disticha, Neodacampia ulmea (incl. Neodacampia gen. nov.) on branch of Ulmus laevis, Niesslia phragmiticola on dead standing culms of Phragmites australis, Pseudopyricularia caricicola on culms of Carex disticha, and Rhodoveronaea nieuwwulvenica on dead bamboo sticks. Norway, Arrhenia similis half-buried and moss-covered pieces of rotting wood in grass-grown path. Pakistan, Mallocybe ahmadii on soil. Poland, Beskidomyces laricis (incl. Beskidomyces gen. nov.) from resin of Larix decidua ssp. polonica, Lapi- domyces epipinicola from sooty mould community on Pinus nigra, and Leptographium granulatum from a gallery of Dendroctonus micans on Picea abies. Portugal, Geoglossum azoricum on mossy areas of laurel forest areas planted with Cryptomeria japonica, and Lunasporangiospora lusitanica from a biofilm covering a biodeteriorated limestone wall. Qatar, Alternaria halotolerans from hypersaline sea water, and Alternaria qatarensis from water sample collected from hypersaline lagoon. South Africa, Alfaria thamnochorti on culm of Thamnochortus fraternus, Knufia aloeicola on Aloe gariepensis, Muriseptatomyces restionacearum (incl. Muriseptatomyces gen. nov. ) on culms of Restionaceae, Neocladosporium arctotis on nest of cases of bag worm moths (Lepidoptera, Psychidae) on Arctotis auriculata, Neodevriesia scadoxi on leaves of Scadoxus puniceus, Paraloratospora schoenoplecti on stems of Schoenoplectus lacustris, Tulasnella epidendrea from the roots of Epidendrum x obrienianum, and Xenoidriella cinnamomi (incl. Xenoidriella gen. nov.) on leaf of Cinnamomum camphora. South Korea, Lemonniera fraxinea on decaying leaves of Fraxinus sp. from pond. Spain, Atheniella lauri on the bark of fallen trees of Laurus nobilis, Halocryptovalsa endophytica from surface-sterilised, asymptomatic roots of Salicornia patula, Inocybe amygda- liolens on soil in mixed forest, Inocybe pityusarum on calcareous soil in mixed forest, Inocybe roseobulbipes on acidic soils, Neonectria borealis from roots of Vitis berlandieri x Vitis rupestris, Sympoventuria eucalyptorum on leaves of Eucalyptus sp., and Tuber conchae from soil. Sweden, Inocybe bidumensis on calcareous soil. Thailand, Cordyceps sandindaengensis on Lepidoptera pupa, buried in soil, Ophiocordyceps kuchinaraiensis on Coleoptera larva, buried in soil, and Samsoniella winandae on Lepidoptera pupa, buried in soil. Taiwan region (China), Neo- phaeosphaeria livistonae on dead leaf of Livistona rotundifolia. Turkiye, Melanogaster anatolicus on clay loamy soils. UK, Basingstokeomyces allii (incl. Basingstokeomyces gen. nov.) on leaves of Allium schoenoprasum. Ukraine, Xenosphaeropsis corni on recently dead stem of Cornus alba. USA, Nothotrichosporon aquaticum (incl. Nothotrichosporon gen. nov.) from water, and Periconia philadelphiana from swab of coil surface. Morphological and culture characteristics for these new taxa are supported by DNA barcodes.
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- Charalampous, P., et al.
(författare)
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Methodological considerations in injury burden of disease studies across Europe: a systematic literature review
- 2022
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Ingår i: Bmc Public Health. - : Springer Science and Business Media LLC. - 1471-2458. ; 22:1
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Forskningsöversikt (refereegranskat)abstract
- Background Calculating the disease burden due to injury is complex, as it requires many methodological choices. Until now, an overview of the methodological design choices that have been made in burden of disease (BoD) studies in injury populations is not available. The aim of this systematic literature review was to identify existing injury BoD studies undertaken across Europe and to comprehensively review the methodological design choices and assumption parameters that have been made to calculate years of life lost (YLL) and years lived with disability (YLD) in these studies. Methods We searched EMBASE, MEDLINE, Cochrane Central, Google Scholar, and Web of Science, and the grey literature supplemented by handsearching, for BoD studies. We included injury BoD studies that quantified the BoD expressed in YLL, YLD, and disability-adjusted life years (DALY) in countries within the European Region between early-1990 and mid-2021. Results We retrieved 2,914 results of which 48 performed an injury-specific BoD assessment. Single-country independent and Global Burden of Disease (GBD)-linked injury BoD studies were performed in 11 European countries. Approximately 79% of injury BoD studies reported the BoD by external cause-of-injury. Most independent studies used the incidence-based approach to calculate YLDs. About half of the injury disease burden studies applied disability weights (DWs) developed by the GBD study. Almost all independent injury studies have determined YLL using national life tables. Conclusions Considerable methodological variation across independent injury BoD assessments was observed; differences were mainly apparent in the design choices and assumption parameters towards injury YLD calculations, implementation of DWs, and the choice of life table for YLL calculations. Development and use of guidelines for performing and reporting of injury BoD studies is crucial to enhance transparency and comparability of injury BoD estimates across Europe and beyond.
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| 11. |
- Feigin, Valery L., et al.
(författare)
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Global, regional, and national burden of neurological disorders, 1990–2016 : a systematic analysis for the Global Burden of Disease Study 2016
- 2019
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Ingår i: Lancet Neurology. - : Elsevier. - 1474-4422 .- 1474-4465. ; 18:5, s. 459-480
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Tidskriftsartikel (refereegranskat)abstract
- Background: Neurological disorders are increasingly recognised as major causes of death and disability worldwide. The aim of this analysis from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 is to provide the most comprehensive and up-to-date estimates of the global, regional, and national burden from neurological disorders.Methods: We estimated prevalence, incidence, deaths, and disability-adjusted life-years (DALYs; the sum of years of life lost [YLLs] and years lived with disability [YLDs]) by age and sex for 15 neurological disorder categories (tetanus, meningitis, encephalitis, stroke, brain and other CNS cancers, traumatic brain injury, spinal cord injury, Alzheimer's disease and other dementias, Parkinson's disease, multiple sclerosis, motor neuron diseases, idiopathic epilepsy, migraine, tension-type headache, and a residual category for other less common neurological disorders) in 195 countries from 1990 to 2016. DisMod-MR 2.1, a Bayesian meta-regression tool, was the main method of estimation of prevalence and incidence, and the Cause of Death Ensemble model (CODEm) was used for mortality estimation. We quantified the contribution of 84 risks and combinations of risk to the disease estimates for the 15 neurological disorder categories using the GBD comparative risk assessment approach.Findings: Globally, in 2016, neurological disorders were the leading cause of DALYs (276 million [95% UI 247–308]) and second leading cause of deaths (9·0 million [8·8–9·4]). The absolute number of deaths and DALYs from all neurological disorders combined increased (deaths by 39% [34–44] and DALYs by 15% [9–21]) whereas their age-standardised rates decreased (deaths by 28% [26–30] and DALYs by 27% [24–31]) between 1990 and 2016. The only neurological disorders that had a decrease in rates and absolute numbers of deaths and DALYs were tetanus, meningitis, and encephalitis. The four largest contributors of neurological DALYs were stroke (42·2% [38·6–46·1]), migraine (16·3% [11·7–20·8]), Alzheimer's and other dementias (10·4% [9·0–12·1]), and meningitis (7·9% [6·6–10·4]). For the combined neurological disorders, age-standardised DALY rates were significantly higher in males than in females (male-to-female ratio 1·12 [1·05–1·20]), but migraine, multiple sclerosis, and tension-type headache were more common and caused more burden in females, with male-to-female ratios of less than 0·7. The 84 risks quantified in GBD explain less than 10% of neurological disorder DALY burdens, except stroke, for which 88·8% (86·5–90·9) of DALYs are attributable to risk factors, and to a lesser extent Alzheimer's disease and other dementias (22·3% [11·8–35·1] of DALYs are risk attributable) and idiopathic epilepsy (14·1% [10·8–17·5] of DALYs are risk attributable).Interpretation: Globally, the burden of neurological disorders, as measured by the absolute number of DALYs, continues to increase. As populations are growing and ageing, and the prevalence of major disabling neurological disorders steeply increases with age, governments will face increasing demand for treatment, rehabilitation, and support services for neurological disorders. The scarcity of established modifiable risks for most of the neurological burden demonstrates that new knowledge is required to develop effective prevention and treatment strategies.Funding: Bill & Melinda Gates Foundation.
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| 13. |
- DeWitt, Douglas S., et al.
(författare)
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Pre-clinical testing of therapies for traumatic brain injury
- 2018
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Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 35:23, s. 2737-2754
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Tidskriftsartikel (refereegranskat)abstract
- Despite the large number of promising neuroprotective agents identified in experimental traumatic brain injury (TBI) studies, none has yet shown meaningful improvements in long-term outcome in clinical trials. To develop recommendations and guidelines for pre-clinical testing of pharmacological or biological therapies for TBI, the Moody Project for Translational Traumatic Brain Injury Research hosted a symposium attended by investigators with extensive experience in pre-clinical TBI testing. The symposium participants discussed issues related to pre-clinical TBI testing including experimental models, therapy and outcome selection, study design, data analysis, and dissemination. Consensus recommendations included the creation of a manual of standard operating procedures with sufficiently detailed descriptions of modeling and outcome measurement procedures to permit replication. The importance of the selection of clinically relevant outcome variables, especially related to behavior testing, was noted. Considering the heterogeneous nature of human TBI, evidence of therapeutic efficacy in multiple, diverse (e.g., diffuse vs. focused) rodent models and a species with a gyrencephalic brain prior to clinical testing was encouraged. Basing drug doses, times, and routes of administration on pharmacokinetic and pharmacodynamic data in the test species was recommended. Symposium participants agreed that the publication of negative results would reduce costly and unnecessary duplication of unsuccessful experiments. Although some of the recommendations are more relevant to multi-center, multi-investigator collaborations, most are applicable to pre-clinical therapy testing in general. The goal of these consensus guidelines is to increase the likelihood that therapies that improve outcomes in pre-clinical studies will also improve outcomes in TBI patients.
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- Zhang, Zhiqun, et al.
(författare)
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Human traumatic brain injury induces autoantibody response against glial fibrillary acidic protein and its breakdown products
- 2014
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Ingår i: PLOS ONE. - San Francisco, USA : Public Library of Science (PLoS). - 1932-6203. ; 9:3
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Tidskriftsartikel (refereegranskat)abstract
- The role of systemic autoimmunity in human traumatic brain injury (TBI) and other forms of brain injuries is recognized but not well understood. In this study, a systematic investigation was performed to identify serum autoantibody responses to brain-specific proteins after TBI in humans. TBI autoantibodies showed predominant immunoreactivity against a cluster of bands from 38-50 kDa on human brain immunoblots, which were identified as GFAP and GFAP breakdown products. GFAP autoantibody levels increased by 7 days after injury, and were of the IgG subtype predominantly. Results from in vitro tests and rat TBI experiments also indicated that calpain was responsible for removing the amino and carboxyl termini of GFAP to yield a 38 kDa fragment. Additionally, TBI autoantibody staining co-localized with GFAP in injured rat brain and in primary rat astrocytes. These results suggest that GFAP breakdown products persist within degenerating astrocytes in the brain. Anti-GFAP autoantibody also can enter living astroglia cells in culture and its presence appears to compromise glial cell health. TBI patients showed an average 3.77 fold increase in anti-GFAP autoantibody levels from early (0-1 days) to late (7-10 days) times post injury. Changes in autoantibody levels were negatively correlated with outcome as measured by GOS-E score at 6 months, suggesting that TBI patients with greater anti-GFAP immune-responses had worse outcomes. Due to the long lasting nature of IgG, a test to detect anti-GFAP autoantibodies is likely to prolong the temporal window for assessment of brain damage in human patients.
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| 20. |
- Büki, Andras, 1966-, et al.
(författare)
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BIOMARKERS OF TRAUMATIC BRAIN- AND SPINAL CORD INJURY
- 2022
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Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert. - 0897-7151 .- 1557-9042. ; 39:15-16, s. A7-A7
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Biomarkers of traumatic brain injury have long been investigated, yet their application in real life clinical practice is less than widespread.Research efforts under the umbrella of InTBIR and specifically CENTER TBI provided novel results based on a bulk of data collected.The symposium aims to provide an update on contemporary knowledge on purported clinical application of core biomarkers while also sharing novel data on emerging markers and novel technologies and approaches that may further improve our diagnostic and prognostic capabilities in the treatment of traumatic brain injury.The session will provide a critical review and update on biomarkers of spinal cord injury.
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| 21. |
- Constantinescu, Radu, 1966, et al.
(författare)
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Cerebrospinal fluid biomarker candidates for Parkinsonian disorders
- 2013
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Ingår i: Frontiers in Neurology. - : Frontiers Media SA. - 1664-2295. ; 3 JAN
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Tidskriftsartikel (refereegranskat)abstract
- The Parkinsonian disorders are a large group of neurodegenerative diseases including idiopathic Parkinson's disease (PD) and atypical Parkinsonian disorders (APD), such as multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, and dementia with Lewy bodies. The etiology of these disorders is not known although it is considered to be a combination of genetic and environmental factors. One of the greatest obstacles for developing efficacious disease-modifying treatment strategies is the lack of biomarkers. Reliable biomarkers are needed for early and accurate diagnosis, to measure disease progression, and response to therapy. In this review several of the most promising cerebrospinal biomarker candidates are discussed. Alpha-synuclein seems to be intimately involved in the pathogenesis of synucleinopathies and its levels can be measured in the cerebrospinal fluid and in plasma. In a similar way, tau protein accumulation seems to be involved in the pathogenesis of tauopathies. Urate, a potent antioxidant, seems to be associated to the risk of developing PD and with its progression. Neurofilament light chain levels are increased in APD compared with PD and healthy controls. The new "omics" techniques are potent tools offering new insights in the patho-etiology of these disorders. Some of the difficulties encountered in developing biomarkers are discussed together with future perspectives. © 2013 Constantinescu and Mondello.
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| 22. |
- Nichols, Emma, et al.
(författare)
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Global, regional, and national burden of Alzheimer's disease and other dementias, 1990-2016 : a systematic analysis for the Global Burden of Disease Study 2016
- 2019
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Ingår i: Lancet Neurology. - : Elsevier. - 1474-4422 .- 1474-4465. ; 18:1, s. 88-106
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Tidskriftsartikel (refereegranskat)abstract
- Background: The number of individuals living with dementia is increasing, negatively affecting families, communities, and health-care systems around the world. A successful response to these challenges requires an accurate understanding of the dementia disease burden. We aimed to present the first detailed analysis of the global prevalence, mortality, and overall burden of dementia as captured by the Global Burden of Diseases, Injuries, and Risk Factors (GBD) Study 2016, and highlight the most important messages for clinicians and neurologists.Methods: GBD 2016 obtained data on dementia from vital registration systems, published scientific literature and surveys, and data from health-service encounters on deaths, excess mortality, prevalence, and incidence from 195 countries and territories from 1990 to 2016, through systematic review and additional data-seeking efforts. To correct for differences in cause of death coding across time and locations, we modelled mortality due to dementia using prevalence data and estimates of excess mortality derived from countries that were most likely to code deaths to dementia relative to prevalence. Data were analysed by standardised methods to estimate deaths, prevalence, years of life lost (YLLs), years of life lived with disability (YLDs), and disability-adjusted life-years (DALYs; computed as the sum of YLLs and YLDs), and the fractions of these metrics that were attributable to four risk factors that met GBD criteria for assessment (high body-mass index [BMI], high fasting plasma glucose, smoking, and a diet high in sugarsweetened beverages).Findings: In 2016, the global number of individuals who lived with dementia was 43.8 million (95% uncertainty interval [UI] 3 7. 8-51.0), increased from 20.2 million (17. 4-23 5) in 1990. This increase of 117% (95% UI 114-121) contrasted with a minor increase in age-standardised prevalence of 1.7% (1.0-2.4), from 701 cases (95% UI 602-815) per 100 000 population in 1990 to 712 cases (614-828) per 100 000 population in 2016. More women than men had dementia in 2016 (27.0 million, 95% UI 23 .3-31. 4, vs 16.8 million, 14.4-19.6), and dementia was the fifth leading cause of death globally, accounting for 2.4 million (95% UI 2.1-2.8) deaths. Overall, 28.8 million (95% UI 24. 5-34. 0) DALYs were attributed to dementia; 6.4 million (95% UI 3 .4-10. 5) of these could be attributed to the modifiable GBD risk factors of high BMI, high fasting plasma glucose, smoking, and a high intake of sugar-sweetened beverages.Interpretation: The global number of people living with dementia more than doubled from 1990 to 2016, mainly due to increases in population ageing and growth. Although differences in coding for causes of death and the heterogeneity in case-ascertainment methods constitute major challenges to the estimation of the burden of dementia, future analyses should improve on the methods for the correction of these biases. Until breakthroughs are made in prevention or curative treatment, dementia will constitute an increasing challenge to health-care systems worldwide.
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