676 research outputs found

    Genome-wide signatures of convergent evolution in echolocating mammals

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    Evolution is typically thought to proceed through divergence of genes, proteins, and ultimately phenotypes(1-3). However, similar traits might also evolve convergently in unrelated taxa due to similar selection pressures(4,5). Adaptive phenotypic convergence is widespread in nature, and recent results from a handful of genes have suggested that this phenomenon is powerful enough to also drive recurrent evolution at the sequence level(6-9). Where homoplasious substitutions do occur these have long been considered the result of neutral processes. However, recent studies have demonstrated that adaptive convergent sequence evolution can be detected in vertebrates using statistical methods that model parallel evolution(9,10) although the extent to which sequence convergence between genera occurs across genomes is unknown. Here we analyse genomic sequence data in mammals that have independently evolved echolocation and show for the first time that convergence is not a rare process restricted to a handful of loci but is instead widespread, continuously distributed and commonly driven by natural selection acting on a small number of sites per locus. Systematic analyses of convergent sequence evolution in 805,053 amino acids within 2,326 orthologous coding gene sequences compared across 22 mammals (including four new bat genomes) revealed signatures consistent with convergence in nearly 200 loci. Strong and significant support for convergence among bats and the dolphin was seen in numerous genes linked to hearing or deafness, consistent with an involvement in echolocation. Surprisingly we also found convergence in many genes linked to vision: the convergent signal of many sensory genes was robustly correlated with the strength of natural selection. This first attempt to detect genome-wide convergent sequence evolution across divergent taxa reveals the phenomenon to be much more pervasive than previously recognised

    Maladaptive spinal plasticity opposes spinal learning and recovery in spinal cord injury

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    Synaptic plasticity within the spinal cord has great potential to facilitate recovery of function after spinal cord injury (SCI). Spinal plasticity can be induced in an activity-dependent manner even without input from the brain after complete SCI. A mechanistic basis for these effects is provided by research demonstrating that spinal synapses have many of the same plasticity mechanisms that are known to underlie learning and memory in the brain. In addition, the lumbar spinal cord can sustain several forms of learning and memory, including limb-position training. However, not all spinal plasticity promotes recovery of function. Central sensitization of nociceptive (pain) pathways in the spinal cord may emerge in response to various noxious inputs, demonstrating that plasticity within the spinal cord may contribute to maladaptive pain states. In this review we discuss interactions between adaptive and maladaptive forms of activity-dependent plasticity in the spinal cord below the level of SCI. The literature demonstrates that activity-dependent plasticity within the spinal cord must be carefully tuned to promote adaptive spinal training. Prior work from our group has shown that stimulation that is delivered in a limb position-dependent manner or on a fixed interval can induce adaptive plasticity that promotes future spinal cord learning and reduces nociceptive hyper-reactivity. On the other hand, stimulation that is delivered in an unsynchronized fashion, such as randomized electrical stimulation or peripheral skin injuries, can generate maladaptive spinal plasticity that undermines future spinal cord learning, reduces recovery of locomotor function, and promotes nociceptive hyper-reactivity after SCI. We review these basic phenomena, how these findings relate to the broader spinal plasticity literature, discuss the cellular and molecular mechanisms, and finally discuss implications of these and other findings for improved rehabilitative therapies after SCI

    Metaplasticity and behavior: how training and inflammation affect plastic potential within the spinal cord and recovery after injury

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    Research has shown that spinal circuits have the capacity to adapt in response to training, nociceptive stimulation and peripheral inflammation. These changes in neural function are mediated by physiological and neurochemical systems analogous to those that support plasticity within the hippocampus (e.g., long-term potentiation and the NMDA receptor). As observed in the hippocampus, engaging spinal circuits can have a lasting impact on plastic potential, enabling or inhibiting the capacity to learn. These effects are related to the concept of metaplasticity. Behavioral paradigms are described that induce metaplastic effects within the spinal cord. Uncontrollable/unpredictable stimulation, and peripheral inflammation, induce a form of maladaptive plasticity that inhibits spinal learning. Conversely, exposure to controllable or predictable stimulation engages a form of adaptive plasticity that counters these maladaptive effects and enables learning. Adaptive plasticity is tied to an up-regulation of brain derived neurotrophic factor (BDNF). Maladaptive plasticity is linked to processes that involve kappa opioids, the metabotropic glutamate (mGlu) receptor, glia, and the cytokine tumor necrosis factor (TNF). Uncontrollable nociceptive stimulation also impairs recovery after a spinal contusion injury and fosters the development of pain (allodynia). These adverse effects are related to an up-regulation of TNF and a down-regulation of BDNF and its receptor (TrkB). In the absence of injury, brain systems quell the sensitization of spinal circuits through descending serotonergic fibers and the serotonin 1A (5HT 1A) receptor. This protective effect is blocked by surgical anesthesia. Disconnected from the brain, intracellular Cl- concentrations increase (due to a down-regulation of the cotransporter KCC2), which causes GABA to have an excitatory effect. It is suggested that BDNF has a restorative effect because it up-regulates KCC2 and re-establishes GABA-mediated inhibition

    Population structure of the predatory mite Neoseiulus womersleyi in a tea field based on an analysis of microsatellite DNA markers

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    The predatory mite Neoseiulus womersleyi (Schicha) (Acari: Phytoseiidae) is an important natural enemy of the Kanzawa spider mite, Tetranychus kanzawaki Kishida (Acari: Tetranychidae), in tea fields. Attraction and preservation of natural enemies by habitat management to reduce the need for acaricide sprays is thought to enhance the activity of N. womersleyi. To better conserve N. womersleyi in the field, however, it is essential to elucidate the population genetic structure of this species. To this end, we developed ten microsatellite DNA markers for N. womersleyi. We then evaluated population structure of N. womersleyi collected from a tea field, where Mexican sunflower, Tithonia rotundifolia (Mill.), was planted to preserve N. womersleyi. Seventy-seven adult females were collected from four sites within 200 m. The fixation indexes FST among subpopulations were not significantly different. The kinship coefficients between individuals did not differ significantly within a site as a function of the sampling dates, but the coefficients gradually decreased with increasing distance. Bayesian clustering analysis revealed that the population consisted of three genetic clusters, and that subpopulations within 100 m, including those collected on T. rotundifolia, were genetically similar to each other. Given the previously observed population dynamics of N. womersleyi, it appears that the area inhabited by a given cluster of the mite did not exceed 100 m. The estimation of population structure using microsatellite markers will provide valuable information in conservation biological control

    Physical activity and nutrition behaviour outcomes of a cluster-randomized controlled trial for adults with metabolic syndrome in Vietnam

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    Background: Metabolic syndrome is prevalent among Vietnamese adults, especially those aged 50-65 years. This study evaluated the effectiveness of a 6 month community-based lifestyle intervention to increase physical activity levels and improve dietary behaviours for adults with metabolic syndrome in Vietnam. Methods: Ten communes, involving participants aged 50-65 years with metabolic syndrome, were recruited from Hanam province in northern Vietnam. The communes were randomly allocated to either the intervention (five communes, n = 214) or the control group (five communes, n = 203). Intervention group participants received a health promotion package, consisting of an information booklet, education sessions, a walking group, and a resistance band. Control group participants received one session of standard advice during the 6 month period. Data were collected at baseline and after the intervention to evaluate programme effectiveness. The International Physical Activity Questionnaire - Short Form and a modified STEPS questionnaire were used to assess physical activity and dietary behaviours, respectively, in both groups. Pedometers were worn by the intervention participants only for 7 consecutive days at baseline and post-intervention testing. To accommodate the repeated measures and the clustering of individuals within communes, multilevel mixed regression models with random effects were fitted to determine the impacts of intervention on changes in outcome variables over time and between groups. Results: With a retention rate of 80.8%, the final sample comprised 175 intervention and 162 control participants. After controlling for demographic and other confounding factors, the intervention participants showed significant increases in moderate intensity activity (P = 0.018), walking (P < 0.001) and total physical activity (P = 0.001), as well as a decrease in mean sitting time (P < 0.001), relative to their control counterparts. Significant improvements in dietary behaviours were also observed, particularly reductions in intake of animal internal organs (P = 0.001) and in using cooking oil for daily meal preparation (P = 0.001). Conclusions: The prescribed community-based physical activity and nutrition intervention programme successfully improved physical activity and dietary behaviours for adults with metabolic syndrome in Vietnam. Trial registration: Australian New Zealand Clinical Trials Registry, ACTRN12614000811606. Registered on 31 July 201

    NO Dioxygenase Activity in Hemoglobins Is Ubiquitous In Vitro, but Limited by Reduction In Vivo

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    Genomics has produced hundreds of new hemoglobin sequences with examples in nearly every living organism. Structural and biochemical characterizations of many recombinant proteins reveal reactions, like oxygen binding and NO dioxygenation, that appear general to the hemoglobin superfamily regardless of whether they are related to physiological function. Despite considerable attention to “hexacoordinate” hemoglobins, which are found in nearly every plant and animal, no clear physiological role(s) has been assigned to them in any species. One popular and relevant hypothesis for their function is protection against NO. Here we have tested a comprehensive representation of hexacoordinate hemoglobins from plants (rice hemoglobin), animals (neuroglobin and cytoglobin), and bacteria (Synechocystis hemoglobin) for their abilities to scavenge NO compared to myoglobin. Our experiments include in vitro comparisons of NO dioxygenation, ferric NO binding, NO-induced reduction, NO scavenging with an artificial reduction system, and the ability to substitute for a known NO scavenger (flavohemoglobin) in E. coli. We conclude that none of these tests reveal any distinguishing predisposition toward a role in NO scavenging for the hxHbs, but that any hemoglobin could likely serve this role in the presence of a mechanism for heme iron re-reduction. Hence, future research to test the role of Hbs in NO scavenging would benefit more from the identification of cognate reductases than from in vitro analysis of NO and O2 binding

    Early chronic kidney disease: diagnosis, management and models of care

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    Chronic kidney disease (CKD) is prevalent in many countries, and the costs associated with the care of patients with end-stage renal disease (ESRD) are estimated to exceed US$1 trillion globally. The clinical and economic rationale for the design of timely and appropriate health system responses to limit the progression of CKD to ESRD is clear. Clinical care might improve if early-stage CKD with risk of progression to ESRD is differentiated from early-stage CKD that is unlikely to advance. The diagnostic tests that are currently used for CKD exhibit key limitations; therefore, additional research is required to increase awareness of the risk factors for CKD progression. Systems modelling can be used to evaluate the impact of different care models on CKD outcomes and costs. The US Indian Health Service has demonstrated that an integrated, system-wide approach can produce notable benefits on cardiovascular and renal health outcomes. Economic and clinical improvements might, therefore, be possible if CKD is reconceptualized as a part of primary care. This Review discusses which early CKD interventions are appropriate, the optimum time to provide clinical care, and the most suitable model of care to adopt

    Introduction: building the history of language learning and teaching (HoLLT)

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    The papers presented in this issue are the result of a workshop held at the University of Nottingham in December 2012 as part of an Arts and Humanities Research Council research network Towards a History of Modern Foreign Language Teaching and Learning (2012–14) intended to stimulate historical research into language teaching and learning. This, the first workshop in the programme, focused on exchanging information on the history of language learning and teaching (HoLLT) across the different language traditions, for it had become clear to us that scholars working within their own language disciplines were often relatively unaware of work outside these. We hope that this special issue — with overview articles on the history of English, French, German, and Spanish as second/foreign languages — will help overcome that lack of awareness and facilitate further research collaboration. Charting the history of language teaching and learning will, in turn, make us all better informed in facing challenges and changes to policy and practice now and in the future. It is instructive in the current climate, for example, to realize that grave doubts were held about whether second foreign languages could survive alongside French in British schools in the early twentieth century (McLelland, forthcoming), or to look back at earlier attempts to establish foreign languages in primary schools (Bayley, 1989; Burstall et al., 1974; Hoy, 1977). As we write, language learning in England is undergoing yet more radical change. Language teaching for all children from the age of seven is being made compulsory in primary schools from 2014, while at Key Stage 3 (up to age 16), where a foreign language has not been compulsory since 2002, the most recent programme of study for England has virtually abandoned the recent focus on intercultural competence and now requires learners to ‘read great literature in the original language’,1 a radical change in emphasis compared to the previous half-century, which seems to reflect a very different view of what language learning is for. We seem to be little closer in 2014 than we were at the dawn of the twentieth century to answering with any certainty the questions that lie at the very foundations of language teaching: who should learn a foreign language, why learners learn, what they need to learn, and what we want to teach them — answers that we need before we can consider how we want to teach. The research programme begun under our research network is intended to help us to take ‘the long view’ on such questions

    Pervasiveness of Parasites in Pollinators

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    Many pollinator populations are declining, with large economic and ecological implications. Parasites are known to be an important factor in the some of the population declines of honey bees and bumblebees, but little is known about the parasites afflicting most other pollinators, or the extent of interspecific transmission or vectoring of parasites. Here we carry out a preliminary screening of pollinators (honey bees, five species of bumblebee, three species of wasp, four species of hoverfly and three genera of other bees) in the UK for parasites. We used molecular methods to screen for six honey bee viruses, Ascosphaera fungi, Microsporidia, and Wolbachia intracellular bacteria. We aimed simply to detect the presence of the parasites, encompassing vectoring as well as actual infections. Many pollinators of all types were positive for Ascosphaera fungi, while Microsporidia were rarer, being most frequently found in bumblebees. We also detected that most pollinators were positive for Wolbachia, most probably indicating infection with this intracellular symbiont, and raising the possibility that it may be an important factor in influencing host sex ratios or fitness in a diversity of pollinators. Importantly, we found that about a third of bumblebees (Bombus pascuorum and Bombus terrestris) and a third of wasps (Vespula vulgaris), as well as all honey bees, were positive for deformed wing virus, but that this virus was not present in other pollinators. Deformed wing virus therefore does not appear to be a general parasite of pollinators, but does interact significantly with at least three species of bumblebee and wasp. Further work is needed to establish the identity of some of the parasites, their spatiotemporal variation, and whether they are infecting the various pollinator species or being vectored. However, these results provide a first insight into the diversity, and potential exchange, of parasites in pollinator communities
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