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The handbook of linguistics
\"The Handbook of Linguistics is a general introductory volume designed to address this gap in knowledge about language\"-- Provided by publisher.
Book
How can we make plants grow faster? A source–sink perspective on growth rate
Growth is a major component of fitness in all organisms, an important mediator of competitive interactions in plant communities, and a central determinant of yield in crops. Understanding what limits plant growth is therefore of fundamental importance to plant evolution, ecology, and crop science, but each discipline views the process from a different perspective. This review highlights the importance of source–sink interactions as determinants of growth. The evidence for source- and sink-limitation of growth, and the ways in which regulatory molecular feedback systems act to maintain an appropriate source:sink balance, are first discussed. Evidence clearly shows that future increases in crop productivity depend crucially on a quantitative understanding of the extent to which sources or sinks limit growth, and how this changes during development. To identify bottlenecks limiting growth and yield, a holistic view of growth is required at the whole-plant scale, incorporating mechanistic interactions between physiology, resource allocation, and plant development. Such a holistic perspective on source–sink interactions will allow the development of a more integrated, whole-system level understanding of growth, with benefits across multiple disciplines.
Journal Article
Sex-specific disease modifiers in juvenile myoclonic epilepsy
Juvenile myoclonic epilepsy (JME) is a common idiopathic generalised epilepsy with variable seizure prognosis and sex differences in disease presentation. Here, we investigate the combined epidemiology of sex, seizure types and precipitants, and their influence on prognosis in JME, through cross-sectional data collected by The Biology of Juvenile Myoclonic Epilepsy (BIOJUME) consortium. 765 individuals met strict inclusion criteria for JME (female:male, 1.8:1). 59% of females and 50% of males reported triggered seizures, and in females only, this was associated with experiencing absence seizures (OR = 2.0,
p
< 0.001). Absence seizures significantly predicted drug resistance in both males (OR = 3.0,
p
= 0.001) and females (OR = 3.0,
p
< 0.001) in univariate analysis. In multivariable analysis in females, catamenial seizures (OR = 14.7,
p
= 0.001), absence seizures (OR = 6.0,
p
< 0.001) and stress-precipitated seizures (OR = 5.3,
p
= 0.02) were associated with drug resistance, while a photoparoxysmal response predicted seizure freedom (OR = 0.47,
p
= 0.03). Females with both absence seizures and stress-related precipitants constitute the prognostic subgroup in JME with the highest prevalence of drug resistance (49%) compared to females with neither (15%) and males (29%), highlighting the unmet need for effective, targeted interventions for this subgroup. We propose a new prognostic stratification for JME and suggest a role for circuit-based risk of seizure control as an avenue for further investigation.
Journal Article
Integral projection models for populations in temporally varying environments
Most plant and animal populations have substantial interannual variability in survival, growth rate, and fecundity. They also exhibit substantial variability among individuals in traits such as size, age, condition, and disease status that have large impacts on individual fates and consequently on the future of the population. We present here methods for constructing and analyzing a stochastic integral projection model (IPM) incorporating both of these forms of variability, illustrated through a case study of the monocarpic thistle Carlina vulgaris. We show how model construction can exploit the close correspondence between stochastic IPMs and statistical analysis of trait-fate relationships in a \"mixed\" or \"hierarchical\" models framework. This correspondence means that IPMs can be parameterized straightforwardly from data using established statistical techniques and software (vs. the largely ad hoc methods for stochastic matrix models), properly accounting for sampling error and between-year sample size variation and with vastly fewer parameters than a conventional stochastic matrix model. We show that the many tools available for analyzing stochastic matrix models (such as stochastic growth rate, $\\lambda _s$, small variance approximations, elasticity/sensitivity analysis, and life table response experiment [LTRE] analysis) can be used for IPMs, and we give computational formulas for elasticity/sensitivity analyses. We develop evolutionary analyses based on the connection between growth rate sensitivity and selection gradients and present a new method using techniques from functional data analysis to study the evolution of function-valued traits such as size-dependent flowering probability. For Carlina we found consistent selection against variability in both state-specific transition rates and the fitted functions describing state dependence in demographic rates. For most of the regression parameters defining the IPM there was also selection against temporal variance; however, in some cases the effects of nonlinear averaging were big enough to favor increased temporal variation. The LTRE analysis identified year-to-year variation in survival as the dominant factor in population growth variability. Evolutionary analysis of flowering strategy showed that the entire functional relationship between plant size and flowering probability is at or near an evolutionarily stable strategy (ESS) shaped by the size-specific trade-off between the benefit (fecundity) and cost (mortality) of flowering in a temporally varying environment.
Journal Article
Complement activation and increased anaphylatoxin receptor expression are associated with cortical grey matter lesions and the compartmentalised inflammatory response of multiple sclerosis
The extent of cortical pathology is an important determinant of multiple sclerosis (MS) severity. Cortical demyelination and neurodegeneration are related to inflammation of the overlying leptomeninges, a more inflammatory CSF milieu and with parenchymal microglia and astroglia activation. These are all components of the compartmentalised inflammatory response. Compartmentalised inflammation is a feature of progressive MS, which is not targeted by disease modifying therapies. Complement is differentially expressed in the MS CSF and complement, and complement receptors, are associated with demyelination and neurodegeneration.
To better understand if complement activation in the leptomeninges is associated with underlying cortical demyelination, inflammation, and microglial activation, we performed a neuropathological study of progressive MS (
= 22, 14 females), neuroinflammatory (
= 8), and non-neurological disease controls (
= 10). We then quantified the relative extent of demyelination, connective tissue inflammation, complement, and complement receptor positive microglia/macrophages.
Complement was elevated at the leptomeninges, subpial, and within and around vessels of the cortical grey matter. The extent of complement C1q immunoreactivity correlated with connective tissue infiltrates, whilst activation products C4d, Bb, and C3b associated with grey matter demyelination, and C3a receptor 1+ and C5a receptor 1+ microglia/macrophages closely apposed C3b labelled cells. The density of C3a receptor 1+ and C5a receptor 1+ cells was increased at the expanding edge of subpial and leukocortical lesions. C5a receptor 1+ cells expressed TNFα, iNOS and contained puncta immunoreactive for proteolipid protein, neurofilament and synaptophysin, suggesting their involvement in grey matter lesion expansion.
The presence of products of complement activation at the brain surfaces, their association with the extent of underlying pathology and increased complement anaphylatoxin receptor positive microglia/macrophages at expanding cortical grey matter lesions, could represent a target to modify compartmentalised inflammation and cortical demyelination.
Journal Article
Building integral projection models: a user's guide
In order to understand how changes in individual performance (growth, survival or reproduction) influence population dynamics and evolution, ecologists are increasingly using parameterized mathematical models. For continuously structured populations, where some continuous measure of individual state influences growth, survival or reproduction, integral projection models (IPMs) are commonly used. We provide a detailed description of the steps involved in constructing an IPM, explaining how to: (i) translate your study system into an IPM; (ii) implement your IPM; and (iii) diagnose potential problems with your IPM. We emphasize how the study organism's life cycle, and the timing of censuses, together determine the structure of the IPM kernel and important aspects of the statistical analysis used to parameterize an IPM using data on marked individuals. An IPM based on population studies of Soay sheep is used to illustrate the complete process of constructing, implementing and evaluating an IPM fitted to sample data. We then look at very general approaches to parameterizing an IPM, using a wide range of statistical techniques (e.g. maximum likelihood methods, generalized additive models, nonparametric kernel density estimators). Methods for selecting models for parameterizing IPMs are briefly discussed. We conclude with key recommendations and a brief overview of applications that extend the basic model. The online Supporting Information provides commented R code for all our analyses.
Journal Article
Evolutionary bet-hedging in the real world: empirical evidence and challenges revealed by plants
Understanding the adaptations that allow species to live in temporally variable environments is essential for predicting how they may respond to future environmental change. Variation at the intergenerational scale can allow the evolution of bet-hedging strategies: a novel genotype may be favoured over an alternative with higher arithmetic mean fitness if the new genotype experiences a sufficiently large reduction in temporal fitness variation; the successful genotype is said to have traded off its mean and variance in fitness in order to ‘hedge its evolutionary bets’. We review the evidence for bet-hedging in a range of simple plant systems that have proved particularly tractable for studying bet-hedging under natural conditions. We begin by outlining the essential theory, reiterating the important distinction between conservative and diversified bet-hedging strategies. We then examine the theory and empirical evidence for the canonical example of bet-hedging: diversification via dormant seeds in annual plants. We discuss the complications that arise when moving beyond this simple case to consider more complex life-history traits, such as flowering size in semelparous perennial plants. Finally, we outline a framework for accommodating these complications, emphasizing the central role that model-based approaches can play.
Journal Article
Complement is activated in progressive multiple sclerosis cortical grey matter lesions
Background
The symptoms of multiple sclerosis (MS) are caused by damage to myelin and nerve cells in the brain and spinal cord. Inflammation is tightly linked with neurodegeneration, and it is the accumulation of neurodegeneration that underlies increasing neurological disability in progressive MS. Determining pathological mechanisms at play in MS grey matter is therefore a key to our understanding of disease progression.
Methods
We analysed complement expression and activation by immunocytochemistry and in situ hybridisation in frozen or formalin-fixed paraffin-embedded post-mortem tissue blocks from 22 progressive MS cases and made comparisons to inflammatory central nervous system disease and non-neurological disease controls.
Results
Expression of the transcript for
C1qA
was noted in neurons and the activation fragment and opsonin C3b-labelled neurons and glia in the MS cortical and deep grey matter. The density of immunostained cells positive for the classical complement pathway protein C1q and the alternative complement pathway activation fragment Bb was significantly increased in cortical grey matter lesions in comparison to control grey matter. The number of cells immunostained for the membrane attack complex was elevated in cortical lesions, indicating complement activation to completion. The numbers of classical (C1-inhibitor) and alternative (factor H) pathway regulator-positive cells were unchanged between MS and controls, whilst complement anaphylatoxin receptor-bearing microglia in the MS cortex were found closely apposed to cortical neurons. Complement immunopositive neurons displayed an altered nuclear morphology, indicative of cell stress/damage, supporting our finding of significant neurodegeneration in cortical grey matter lesions.
Conclusions
Complement is activated in the MS cortical grey matter lesions in areas of elevated numbers of complement receptor-positive microglia and suggests that complement over-activation may contribute to the worsening pathology that underlies the irreversible progression of MS.
Journal Article