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ObjectiveTo develop sex-specific and age-specific normative values for the nine Eurofit tests in European children and adolescents aged 9–17 years.MethodsA systematic review was undertaken to identify papers that explicitly reported descriptive results for at least one of nine Eurofit tests (measuring balance, muscular strength, muscular endurance, muscular power, flexibility, speed, speed-agility and cardiorespiratory fitness (CRF)) on children and adolescents. Data were included on apparently healthy (free from known disease/injury) children and adolescents aged 9–17 years. Following harmonisation for methodological variation where appropriate, pseudodata were generated using Monte Carlo simulation, with population-weighted sex-specific and age-specific normative centiles generated using the Lambda Mu Sigma (LMS) method. Sex-specific and age-specific differences were expressed as standardised differences in means, with the percentage of children and adolescents with healthy CRF estimated at the sex-age level.ResultsNorms were displayed as tabulated centiles and as smoothed centile curves for the nine Eurofit tests. The final dataset included 2 779 165 results on children and adolescents from 30 European countries, extracted from 98 studies. On average, 78% of boys (95% CI 72% to 85%) and 83% of girls (95% CI 71% to 96%) met the standards for healthy CRF, with the percentage meeting the standards decreasing with age. Boys performed substantially (standardised differences >0.2) better than girls on muscular strength, muscular power, muscular endurance, speed-agility and CRF tests, but worse on the flexibility test. Physical fitness generally improved at a faster rate in boys than in girls, especially during the teenage years.ConclusionThis study provides the largest and most geographically representative sex-specific and age-specific European normative values for children and adolescents, which have utility for health and fitness screening, profiling, monitoring and surveillance.

Cellular senescence is a plausible mediator of inflammation-related tissue dysfunction. In the aged brain, senescent cell identities and the mechanisms by which they exert adverse influence are unclear. Here we used high-dimensional molecular profiling, coupled with mechanistic experiments, to study the properties of senescent cells in the aged mouse brain. We show that senescence and inflammatory expression profiles increase with age and are brain region- and sex-specific. p16 -positive myeloid cells exhibiting senescent and disease-associated activation signatures, including upregulation of chemoattractant factors, accumulate in the aged mouse brain. Senescent brain myeloid cells promote peripheral immune cell chemotaxis in vitro. Activated resident and infiltrating immune cells increase in the aged brain and are partially restored to youthful levels through p16-positive senescent cell clearance in female p16-InkAttac mice, which is associated with preservation of cognitive function. Our study reveals dynamic remodeling of the brain immune cell landscape in aging and suggests senescent cell targeting as a strategy to counter inflammatory changes and cognitive decline. The authors discovered that proinflammatory senescent myeloid cells may recruit peripheral immune cells in the aged mouse brain. Their findings implicate senescent cell clearance as a strategy to counter aged brain inflammation and cognitive decline.

Neutrinos interact only very weakly with matter, but giant detectors have succeeded in detecting small numbers of astrophysical neutrinos. Aside from a diffuse background, only two individual sources have been identified: the Sun and a nearby supernova in 1987. A multiteam collaboration detected a high-energy neutrino event whose arrival direction was consistent with a known blazar—a type of quasar with a relativistic jet oriented directly along our line of sight. The blazar, TXS 0506+056, was found to be undergoing a gamma-ray flare, prompting an extensive multiwavelength campaign. Motivated by this discovery, the IceCube collaboration examined lower-energy neutrinos detected over the previous several years, finding an excess emission at the location of the blazar. Thus, blazars are a source of astrophysical neutrinos. Science , this issue p. 147 , p. eaat1378 A high-energy neutrino was emitted by a blazar during a flare, prompting observations across the electromagnetic spectrum. Previous detections of individual astrophysical sources of neutrinos are limited to the Sun and the supernova 1987A, whereas the origins of the diffuse flux of high-energy cosmic neutrinos remain unidentified. On 22 September 2017, we detected a high-energy neutrino, IceCube-170922A, with an energy of ~290 tera–electron volts. Its arrival direction was consistent with the location of a known γ-ray blazar, TXS 0506+056, observed to be in a flaring state. An extensive multiwavelength campaign followed, ranging from radio frequencies to γ-rays. These observations characterize the variability and energetics of the blazar and include the detection of TXS 0506+056 in very-high-energy γ-rays. This observation of a neutrino in spatial coincidence with a γ-ray–emitting blazar during an active phase suggests that blazars may be a source of high-energy neutrinos.

Neutrinos interact only very weakly with matter, but giant detectors have succeeded in detecting small numbers of astrophysical neutrinos. Aside from a diffuse background, only two individual sources have been identified: the Sun and a nearby supernova in 1987. A multiteam collaboration detected a high-energy neutrino event whose arrival direction was consistent with a known blazar—a type of quasar with a relativistic jet oriented directly along our line of sight. The blazar, TXS 0506+056, was found to be undergoing a gamma-ray flare, prompting an extensive multiwavelength campaign. Motivated by this discovery, the IceCube collaboration examined lower-energy neutrinos detected over the previous several years, finding an excess emission at the location of the blazar. Thus, blazars are a source of astrophysical neutrinos. Science , this issue p. 147 , p. eaat1378 A blazar has been found to be a point source of astrophysical neutrinos, emitted over several years. A high-energy neutrino event detected by IceCube on 22 September 2017 was coincident in direction and time with a gamma-ray flare from the blazar TXS 0506+056. Prompted by this association, we investigated 9.5 years of IceCube neutrino observations to search for excess emission at the position of the blazar. We found an excess of high-energy neutrino events, with respect to atmospheric backgrounds, at that position between September 2014 and March 2015. Allowing for time-variable flux, this constitutes 3.5σ evidence for neutrino emission from the direction of TXS 0506+056, independent of and prior to the 2017 flaring episode. This suggests that blazars are identifiable sources of the high-energy astrophysical neutrino flux.

Anthropogenic landscape change can lead to increased opportunities for pathogen transmission between domestic and non-domestic animals. Pumas, bobcats, and domestic cats are sympatric in many areas of North America and share many of the same pathogens, some of which are zoonotic. We analyzed bobcat, puma, and feral domestic cat samples collected from targeted geographic areas. We examined exposure to three pathogens that are taxonomically diverse (bacterial, protozoal, viral), that incorporate multiple transmission strategies (vector-borne, environmental exposure/ingestion, and direct contact), and that vary in species-specificity. Bartonella spp., Feline Immunodeficiency Virus (FIV), and Toxoplasma gondii IgG were detected in all three species with mean respective prevalence as follows: puma 16%, 41% and 75%; bobcat 31%, 22% and 43%; domestic cat 45%, 10% and 1%. Bartonella spp. were highly prevalent among domestic cats in Southern California compared to other cohort groups. Feline Immunodeficiency Virus exposure was primarily associated with species and age, and was not influenced by geographic location. Pumas were more likely to be infected with FIV than bobcats, with domestic cats having the lowest infection rate. Toxoplasma gondii s eroprevalence was high in both pumas and bobcats across all sites; in contrast, few domestic cats were seropositive, despite the fact that feral, free ranging domestic cats were targeted in this study. Interestingly, a directly transmitted species-specific disease (FIV) was not associated with geographic location, while exposure to indirectly transmitted diseases – vector-borne for Bartonella spp. and ingestion of oocysts via infected prey or environmental exposure for T. gondii – varied significantly by site. Pathogens transmitted by direct contact may be more dependent upon individual behaviors and intra-specific encounters. Future studies will integrate host density, as well as landscape features, to better understand the mechanisms driving disease exposure and to predict zones of cross-species pathogen transmission among wild and domestic felids.

Sarcoptic mange is a globally distributed disease caused by the burrowing mite Sarcoptes scabiei , which also causes scabies in humans. A wide and increasing number of wild mammal species are reported to be susceptible to mange; however, the impacts of the disease in wildlife populations, mechanisms involved in its eco-epidemiological dynamics, and risks to public and ecosystem health are still unclear. Major gaps exist concerning S. scabiei host specificity and the mechanisms involved in the different presentations of the disease, which change between individuals and species. Immunological responses to the mite may have a relevant role explaining these different susceptibilities, as these affect the clinical signs, and consequently, the severity of the disease. Recently, some studies have suggested sarcoptic mange as an emerging threat for wildlife, based on several outbreaks with increased severity, geographical expansions, and novel wild hosts affected. Disease ecology experts convened for the “International Meeting on Sarcoptic Mange in Wildlife” on 4–5 June 2018, hosted by the Department of Fish and Wildlife Conservation at Virginia Tech in Blacksburg, Virginia, USA. The meeting had a structure of (i) pre-workshop review; (ii) presentation and discussions; and (iii) identification of priority research questions to understand sarcoptic mange in wildlife. The workgroup concluded that research priorities should be on determining the variation in modes of transmission for S. scabiei in wildlife, factors associated with the variation of disease severity among species, and long-terms effects of the mange in wildlife populations. In this note we summarize the main discussions and research gaps identified by the experts.

Some pathogens sustain transmission in multiple different host species, but how this epidemiologically important feat is achieved remains enigmatic. Sarcoptes scabiei is among the most host generalist and successful of mammalian parasites. We synthesize pathogen and host traits that mediate sustained transmission and present cases illustrating three transmission mechanisms (direct, indirect, and combined). The pathogen traits that explain the success of S. scabiei include immune response modulation, on-host movement capacity, off-host seeking behaviors, and environmental persistence. Sociality and host density appear to be key for hosts in which direct transmission dominates, whereas in solitary hosts, the use of shared environments is important for indirect transmission. In social den-using species, combined direct and indirect transmission appears likely. Empirical research rarely considers the mechanisms enabling S. scabiei to become endemic in host species—more often focusing on outbreaks. Our review may illuminate parasites’ adaptation strategies to sustain transmission through varied mechanisms across host species.

Urban development has major impacts on connectivity among wildlife populations and is thus likely an important factor shaping pathogen transmission in wildlife. However, most investigations of wildlife diseases in urban areas focus on prevalence and infection risk rather than potential effects of urbanization on transmission itself. Feline immunodeficiency virus (FIV) is a directly transmitted retrovirus that infects many felid species and can be used as a model for studying pathogen transmission at landscape scales. We investigated phylogenetic relationships among FIV isolates sampled from five bobcat (Lynx rufus) populations in coastal southern California that appear isolated due to major highways and dense urban development. Divergence dates among FIV phylogenetic lineages in several cases reflected historical urban growth and construction of major highways. We found strong FIV phylogeographic structure among three host populations north‐west of Los Angeles, largely coincident with host genetic structure. In contrast, relatively little FIV phylogeographic structure existed among two genetically distinct host populations south‐east of Los Angeles. Rates of FIV transfer among host populations did not vary significantly, with the lack of phylogenetic structure south‐east of Los Angeles unlikely to reflect frequent contemporary transmission among populations. Our results indicate that major barriers to host gene flow can also act as barriers to pathogen spread, suggesting potentially reduced susceptibility of fragmented populations to novel directly transmitted pathogens. Infrequent exchange of FIV among host populations suggests that populations would best be managed as distinct units in the event of a severe disease outbreak. Phylogeographic inference of pathogen transmission is useful for estimating the ability of geographic barriers to constrain disease spread and can provide insights into contemporary and historical drivers of host population connectivity.

Understanding how landscape, host, and pathogen traits contribute to disease exposure requires systematic evaluations of pathogens within and among host species and geographic regions. The relative importance of these attributes is critical for management of wildlife and mitigating domestic animal and human disease, particularly given rapid ecological changes, such as urbanization. We screened >1000 samples from sympatric populations of puma (Puma concolor), bobcat (Lynx rufus), and domestic cat (Felis catus) across urban gradients in six sites, representing three regions, in North America for exposure to a representative suite of bacterial, protozoal, and viral pathogens (Bartonella sp., Toxoplasma gondii, feline herpesvirus‐1, feline panleukopenea virus, feline calicivirus, and feline immunodeficiency virus). We evaluated prevalence within each species, and examined host trait and land cover determinants of exposure; providing an unprecedented analysis of factors relating to potential for infections in domesticated and wild felids. Prevalence differed among host species (highest for puma and lowest for domestic cat) and was greater for indirectly transmitted pathogens. Sex was inconsistently predictive of exposure to directly transmitted pathogens only, and age infrequently predictive of both direct and indirectly transmitted pathogens. Determinants of pathogen exposure were widely divergent between the wild felid species. For puma, suburban land use predicted increased exposure to Bartonella sp. in southern California, and FHV‐1 exposure increased near urban edges in Florida. This may suggest interspecific transmission with domestic cats via flea vectors (California) and direct contact (Florida) around urban boundaries. Bobcats captured near urban areas had increased exposure to T. gondii in Florida, suggesting an urban source of prey. Bobcats captured near urban areas in Colorado and Florida had higher FIV exposure, possibly suggesting increased intraspecific interactions through pile‐up of home ranges. Beyond these regional and pathogen specific relationships, proximity to the wildland–urban interface did not generally increase the probability of disease exposure in wild or domestic felids, emphasizing the importance of local ecological determinants. Indeed, pathogen exposure was often negatively associated with the wildland–urban interface for all felids. Our analyses suggest cross‐species pathogen transmission events around this interface may be infrequent, but followed by self‐sustaining propagation within the new host species.

Many pathogens infect multiple hosts, and spillover from domestic to wild species poses a significant risk of spread of diseases that threaten wildlife and humans. Documentation of cross‐species transmission, and unraveling the mechanisms that drive it, remains a challenge. Focusing on co‐occurring domestic and wild felids, we evaluate possible transmission mechanisms and evidence of spillover of “Candidatus Mycoplasma haemominutum” (CMhm), an erythrocytic bacterial parasite of cats. We examine transmission and possibility of spillover by analyzing CMhm prevalence, modeling possible transmission pathways, deducing genotypes of CMhm pathogens infecting felid hosts based on sequences of the bacterial 16S rRNA gene, and conducting phylogenetic analyses with ancestral state reconstruction to identify likely cross‐species transmission events. Model selection analyses suggest both indirect (i.e., spread via vectors) and direct (i.e., via interspecific predation) pathways may play a role in CMhm transmission. Phylogenetic analyses indicate that transmission of CMhm appears to predominate within host species, with occasional spillover, at unknown frequency, between species. These analyses are consistent with transmission by predation of smaller cats by larger species, with subsequent within‐species persistence after spillover. Our results implicate domestic cats as a source of global dispersal and spillover to wild felids via predation. We contribute to the emerging documentation of predation as a common means of pathogen spillover from domestic to wild cats, including pathogens of global conservation significance. These findings suggest risks for top predators as bioaccumulators of pathogens from subordinate species. Focusing on co‐occurring domestic and wild felids, we evaluate evidence of spillover and mechanisms of transmission for an erythrocytic bacterial parasite of cats. We undertake analyses of disease prevalence, transmission modeling, pathogen genotyping based on sequences of the bacterial 16S rRNA gene, and phylogenetic analysis with ancestral state reconstruction. Our results implicate domestic cats as a source of global dispersal and spillover of pathogens to wild felids via predation.