Acquired traumatic central nervous system (CNS) injuries, including traumatic brain injury (TBI) and spinal cord injury (SCI), are devastating conditions with limited treatment options. Neuroinflammation plays a pivotal role in secondary damage, making it a prime target for therapeutic intervention. Emerging therapeutic strategies are designed to modulate the inflammatory response, ultimately promoting neuroprotection and neuroregeneration. The use of anti-inflammatory agents has yielded limited support in improving outcomes in patients, creating a critical need to re-envision novel approaches to both quell deleterious inflammatory processes and upend the progressive cycle of neurotoxic inflammation. This demands a comprehensive exploration of individual, age, and sex differences, including the use of advanced imaging techniques, multi-omic profiling, and the expansion of translational studies from rodents to humans. Moreover, a holistic approach that combines pharmacological intervention with multidisciplinary neurorehabilitation is crucial and must include both acute and long-term care for the physical, cognitive, and emotional aspects of recovery. Ongoing research into neuroinflammatory biomarkers could revolutionize our ability to predict, diagnose, and monitor the inflammatory response in real time, allowing for timely adjustments in treatment regimens and facilitating a more precise evaluation of therapeutic efficacy. The management of neuroinflammation in acquired traumatic CNS injuries necessitates a paradigm shift in our approach that includes combining multiple therapeutic modalities and fostering a more comprehensive understanding of the intricate neuroinflammatory processes at play.

A formidable challenge for global change biologists is to predict how natural populations will respond to the emergence of conditions not observed at present, termed novel climates. Popular approaches to predict population vulnerability are based on the expected degree of novelty relative to the amplitude of historical climate fluctuations experienced by a population. Here, we argue that predictions focused on amplitude may be inaccurate because they ignore the predictability of environmental fluctuations in driving patterns of evolution and responses to climate change. To address this disconnect, we review major findings of evolutionary theory demonstrating the conditions under which phenotypic plasticity is likely to evolve in natural populations, and how plasticity decreases population vulnerability to novel environments. We outline key criteria that experimental studies should aim for to effectively test theoretical predictions, while controlling for the degree of climate novelty. We show that such targeted tests of evolutionary theory are rare, with marine systems being overall underrepresented in this venture despite exhibiting unique opportunities to test theory. We conclude that with more robust experimental designs that manipulate both the amplitude and predictability of fluctuations, while controlling for the degree of novelty, we may better predict population vulnerability to climate change.

Latex occurs in 10% of plant families, has evolved independently many times, and is the most effective defense of milkweeds against its chewing herbivores. Here we report on new experiments on the heritability and inducibility of latex in several milkweed species. In addition, we review what is known about the genetic and environmental determinants of latex exudation, hormonal regulation, evolution within and among species, and the role and frequency of latex in agricultural crops. We first evaluated genotype-by-environment interactions using ~20 full-sibling genetic families in each of seven Asclepias species treated as controls or attacked by monarch butterfly caterpillars. All species showed substantial genetic variation for latex exudation and six of seven species responded to monarch herbivory (two species increased latex, two species decreased, and two showed variation among genetic families). Exogenous application of jasmonic acid (JA) to three species induced a consistent increase in latex (including species which showed a decline following caterpillar herbivory). We next evaluated three hypotheses for what determines genetic variation for induced latex in A. syriaca: 1) a trade-off with constitutive investment, 2) differential endogenous JA induction, or 3) variation in responsiveness to JA. We only found support for the second hypothesis: genetic families with a stronger JA-burst showed the greatest latex exudation following herbivory. We conclude that most species exhibit a genetic and inducible basis for latex, although genetic variation in inducibility is not pervasive. Finally, we summarized studies across 22 species of Asclepias and found that neither a species\' latitude nor its phylogenetic position predicted latex inducibility. Nonetheless, a negative association between constitutive and induced latex across species indicates a macroevolutionary trade-off in allocation to this defense. Our review indicates that jasmonic acid is a key regulator of latex exudation, laticifer morphology, and defensive metabolites within latex. Biotic and abiotic factors strongly modulate latex expression. A survey of latex in food crops revealed that latex and analogous exudates (gums, resins, mucilage) are more common than expected based on their distribution across all plants. In conclusion, despite its widespread occurrence, the literature on latex is currently dominated by rubber trees and milkweeds, and we look forward to the broadening of ecological, agricultural, and mechanistic research into other systems.

Plants can solve amazingly difficult tasks while adjusting their growth and development to the environment. They can explore and exploit several resources simultaneously, even when the distributions of these vary in space and time. The systematic study of plant behaviour goes back to Darwin\'s book The power of movement in plants. Current research has highlighted that modularity is a key to understanding plant behaviour, as the production, functional specialization and death of modules enable the plant to adjust its movement to the environment. The adjustment is assisted by a flow of information and resources among the modules. Experiments have yielded many results about these processes in various plant species. Theoretical research, however, has lagged behind the empirical studies, possibly owing to the lack of a proper modelling framework that could encompass the high number of components and interactions. In this paper, I propose such a framework on the basis of network theory, viewing the plant as a group of connected, semi-autonomous agents. I review some characteristic plant responses to the environment through changing the states of agents and/or links. I also point out some unexplored areas, in which a dialogue between plant science and network theory could be mutually inspiring. This article is part of the theme issue \'Liquid brains, solid brains: How distributed cognitive architectures process information\'.

Developmental stressors are increasingly recognised for their pervasive influence on the ecology and evolution of animals. In particular, many studies have focused on how developmental stress can give rise to variation in adult behaviour, physiology, and performance. However, there remains a poor understanding of whether general patterns exist in the effects and magnitude of phenotypic responses across taxonomic groups. Furthermore, given the extensive phenotypic variation that arises from developmental stressors, it remains important to ascertain how multiple processes may explain these responses. We compiled data from 111 studies to examine and quantify the effect of developmental stress on animal phenotype and performance from juveniles to adulthood, including studies from birds, reptiles, fish, mammals, insects, arachnids, and amphibians. Using meta-analytic approaches, we show that across all studies there is, on average, a moderate to large negative effect of developmental stress exposure (posterior mean effect: |d| = -0.51) on animal phenotype or performance. Additionally, we demonstrate that interactive effects of timing of stressor onset and the duration of exposure to stressors best explained variation in developmental stress responses. Animals exposed to stressors earlier in development had more-positive responses than those with later onset, whereas longer duration of exposure to a stressor caused responses to be stronger in magnitude. However, the high amount of heterogeneity in our results, and the low degree of variance explained by fixed effects in both the meta-analysis (R2 = 0.034) and top-ranked meta-regression model (R2 = 0.02), indicate that phenotypic responses to developmental stressors are likely highly idiosyncratic in nature and difficult to predict. Despite this, our analyses address a critical knowledge gap in understanding what effect developmental stress has on phenotypic variation in animals. Additionally, our results highlight important environmental and proximate factors that may influence phenotypic responses to developmental stressors.

Most, if not all, organisms possess the ability to alter their phenotype in direct response to changes in their environment, a phenomenon known as phenotypic plasticity. Selection can break this environmental sensitivity, however, and cause a formerly environmentally induced trait to evolve to become fixed through a process called genetic assimilation. Essentially, genetic assimilation can be viewed as the evolution of environmental robustness in what was formerly an environmentally sensitive trait. Because genetic assimilation has long been suggested to play a key role in the origins of phenotypic novelty and possibly even new species, identifying and characterizing the proximate mechanisms that underlie genetic assimilation may advance our basic understanding of how novel traits and species evolve.
This review begins by discussing how the evolution of phenotypic plasticity, followed by genetic assimilation, might promote the origins of new traits and possibly fuel speciation and adaptive radiation. The evidence implicating genetic assimilation in evolutionary innovation and diversification is then briefly considered. Next, the potential causes of phenotypic plasticity generally and genetic assimilation specifically are examined at the genetic, molecular and physiological levels and approaches that can improve our understanding of these mechanisms are described. The review concludes by outlining major challenges for future work.
Identifying and characterizing the proximate mechanisms involved in phenotypic plasticity and genetic assimilation promises to help advance our basic understanding of evolutionary innovation and diversification.

Optimality models predict that diet-induced bivariate reaction norms for age and size at maturity can have diverse shapes, with the slope varying from negative to positive. To evaluate these predictions, we perform a quantitative review of relevant data, using a literature-derived database of body sizes and development times for over 200 insect species. We show that bivariate reaction norms with a negative slope prevail in nearly all taxonomic and ecological categories of insects as well as in some other ectotherm taxa with comparable life histories (arachnids and amphibians). In insects, positive slopes are largely limited to species, which feed on discrete resource items, parasitoids in particular. By contrast, with virtually no meaningful exceptions, herbivorous and predatory insects display reaction norms with a negative slope. This is consistent with the idea that predictable resource depletion, a scenario selecting for positively sloped reaction norms, is not frequent for these insects. Another source of such selection-a positive correlation between resource levels and juvenile mortality rates-should similarly be rare among insects. Positive slopes can also be predicted by models which integrate life-history evolution and population dynamics. As bottom-up regulation is not common in most insect groups, such models may not be most appropriate for insects.

Digestive flexibility is important because it allows an animal to maximize energy and nutrient return from the diet consumed, and also to reduce the maintenance costs associated with one of the body\'s most expensive systems in terms of energy and protein requirements. Two different patterns of digestive flexibility have been described for vertebrates, one for species in which metabolic costs of homeostasis are relatively high and the gut is rarely empty (e.g., mammals and birds), and one for species in which metabolic costs of homeostasis are relatively low and the gut usually spends long periods of time empty (e.g., amphibians and reptiles). In this review we analyze the information on digestive tract down-regulation during fasting in fish, in order to evaluate the extent to which digestive flexibility in fish conforms to that in other species. We found that: (1) gut size decay during long-term fasting in fish appears to be almost linear with time, even for very long fasting periods. Thus, gut size temporal dynamics in fish during long-term fasting resemble those observed in some mammals species; (2) by contrast, histological changes during fasting in fish are more similar to those described for amphibians and reptiles; and (3) data on enterocyte turnover rates indicate that cell turnover times in fish are relatively short, and although longer than those observed in mammals, they are not very different from those reported for birds. In conclusion, current data suggest that both mechanisms, cell turnover rates and change in epithelial configuration, probably are involved in digestive tract regulation in fish.