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Background: Overall, there is conflicting evidence regarding the beneficial effects of optimal lifestyle modification, particularly weight loss interventions, with nonalcoholic fatty liver disease (non‐alcoholic fatty liver disease (NAFLD)). Therefore, this study investigated the effects of weight loss interventions on laboratory and clinical parameters in children and adolescents with NAFLD. Methods: Original databases (PubMed/MEDLINE, Web of Science, SCOPUS, and Embase) were searched using standard keywords to identify all controlled trials investigating the effects of weight loss interventions among NAFLD children and adolescents. Pooled weighted mean difference and 95% confidence intervals were achieved by random‐effects model analysis. Results: Eighteen eligible clinical trials were included in this systematic review and meta‐analysis. The pooled findings showed that especially more intense weight loss interventions significantly reduced the glucose (p = 0.007), insulin (p = 0.002), homeostatic model assessment‐insulin resistance (HOMA‐IR) (p = 0.003), weight (p = 0.025), body mass index (BMI) (p = 0.003), BMI z‐score (p < 0.001), waist circumference (WC) (p = 0.013), triglyceride (TG) (p = 0.001), and aspartate transaminase (AST) (p = 0.027). However, no significant changes were found in total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), high‐density lipoprotein cholesterol (HDL‐C), alanine transaminase (ALT), and hepatic steatosis grades (all p > 0.05) following weight loss interventions. Conclusions: Weight loss interventions had significant effects on NAFLD‐related parameters including glucose, insulin, HOMA‐IR, weight, BMI, BMI z‐score, WC, TG, and AST. [ABSTRACT FROM AUTHOR]

Background: Considering the conflicting effects of bupropion on parameters related to metabolic syndrome including glucose metabolism and lipid profile, in this meta‐analysis study, we investigated the effects of this drug alone or in combination with naltrexone on glucose metabolism and lipid profile. Methods: Scopus, PubMed/Medline, Web of Science and Embase databases were searched using standard keywords to identify all controlled trials investigating effects of bupropion alone and combined with naltrexone on the glucose and lipid profile. Pooled weighted mean difference and 95% confidence intervals were achieved by random‐effects model. Results: Twelve studies with 5152 participants' were included in this article. The pooled findings showed that bupropion alone or in combination with naltrexone would significantly reduce glucose (weighted mean difference (WMD): −2.25 mg/dL, 95% confidence interval (CI): −4.10, −0.40), insulin (WMD: −4.06 μU/mL, 95% CI: −6.09, −2.03), homeostatic model assessment for insulin resistance (HOMA‐IR) (WMD: −0.58, 95% CI: −0.98, −0.19), triglyceride (TG) (WMD: −11.78 mg/dL, 95% CI: −14.48 to −9.08) and increase high‐density lipoprotein (HDL) (WMD: 2.68 mg/dL, 95% CI: 2.13 to 3.24). A Greater reduction in glucose levels was observed with duration >26 weeks. Dose of bupropion intake ≤360 mg and intervention for more than 26 weeks decreased insulin level significantly. With regard to lipid profile, reduction of triglycerides is more significant with dose of bupropion greater than 360 mg and a shorter intervention length equal to 26 weeks. Conclusions: The addition of combination therapies such as bupropion and naltrexone to lifestyle modification can significantly improve glucose metabolism and some lipid parameters. [ABSTRACT FROM AUTHOR]

Fisheries and aquaculture provide food and economic security, especially in the developing world, but both face challenges from infectious disease. Here, we consider management of disease issues from a structured decision‐making perspective to examine how infectious disease can threaten seafood production and influence management decisions. For both wild fisheries and aquaculture, disease‐management objectives generally aim to mitigate the severity and economic burden of outbreaks. General management strategies include manipulating host densities, reducing system connectivity, conserving or improving habitat, and implementing direct treatments or some other biological interventions. To inform decisions, mathematical models can be used to explore disease dynamics and to forecast the potential effectiveness of alternative management actions. Developing and implementing disease‐management strategies also involve considering uncertainties and balancing competing stakeholder interests and risk tolerances. We conclude by outlining several steps for applying structured decision making that are broadly useful to decision makers facing issues related to disease. [ABSTRACT FROM AUTHOR]

Summary: Background: There is evidence of inconsistency in sequelae of exclusive enteral nutrition (EEN) as induction therapy in paediatric patients with Crohn's disease (CD). Aim: To investigate the potential effects of EEN on paediatric Crohn's disease activity index (PCDAI), inflammation and biochemical parameters in paediatric patients with CD. Methods: We performed a comprehensive systematic search of PubMed/MEDLINE, Web of Science, SCOPUS and Embase until 8 January 2022 regardless of the time of publication or language. Random‐effects model was applied to combine the datasets. The main outcomes were analysed through mean difference (MD) and its 95% confidence interval (CI). Results: Forty six studies met eligibility criteria and were included in the meta‐analysis. Pooled findings indicated that PCDAI score (MD of −27.24; 95% CI −31.84 to −22.64), calprotectin (MD of −842.83 mg/kg; CI −1018.24 to −667.42), CRP (pooled MD of −2.36 mg/dl; CI −2.68 to −2.03), and ESR (MD of −21.09 mm/h; CI −23.79 to −18.38), albumin (MD of 0.65 g/dl; CI 0.58 to 0.72), haemoglobin (MD of 1.12 g/dl; CI 0.87 to 1.37), weight (MD of 4.30 kg; CI 3.39 to 5.22), and height (MD of 0.98 cm; CI 0.35 to 1.62) improved significantly with EEN. Conclusions: Adherence to EEN can have significant, beneficial effects as induction therapy in paediatric patients with CD. [ABSTRACT FROM AUTHOR]

The ongoing explosion of fine‐resolution movement data in animal systems provides a unique opportunity to empirically quantify spatial, temporal and individual variation in transmission risk and improve our ability to forecast disease outbreaks. However, we lack a generalizable model that can leverage movement data to quantify transmission risk and how it affects pathogen invasion and persistence on heterogeneous landscapes. We developed a flexible model 'Movement‐driven modelling of spatio‐temporal infection risk' (MoveSTIR) that leverages diverse data on animal movement to derive metrics of direct and indirect contact by decomposing transmission into constituent processes of contact formation and duration and pathogen deposition and acquisition. We use MoveSTIR to demonstrate that ignoring fine‐scale animal movements on actual landscapes can mis‐characterize transmission risk and epidemiological dynamics. MoveSTIR unifies previous work on epidemiological contact networks and can address applied and theoretical questions at the nexus of movement and disease ecology. [ABSTRACT FROM AUTHOR]

Pathogen transport by biotic or abiotic processes (e.g. mechanical vectors, wind, rain) can increase disease transmission by creating more opportunities for host exposure. But transport without replication has an inherent trade‐off, that creating new venues for exposure decreases the average pathogen abundance at each venue. The host dose‐response relationship is therefore required to correctly assess infection risk. We model and analyse two examples—biotic mechanical vectors in plant–pollinator networks, and abiotic‐facilitated long‐distance pathogen dispersal—to illustrate how oversimplifying the dose‐response relationship can lead to incorrect epidemiological predictions. When the minimum infective dose is high, mechanical vectors amplify disease transmission less than suggested by simple compartment models, and may even dilute transmission. When long‐distance dispersal leads to infrequent large exposures, models that assume a linear force of infection can substantially under‐predict the speed of epidemic spread. Our work highlights an important general interplay between dose‐response relationships and pathogen transport. [ABSTRACT FROM AUTHOR]

Novel pathogen introduction can have drastic consequences for naive host populations, and outcomes can be difficult to predict. Evolutionary rescue (ER) provides a foundation for understanding whether hosts are driven to extinction or survive via adaptation. Currently, patterns of host population dynamics alongside evidence of adaptation are used to infer ER. However, the gap between established ER theory and complexity inherent in natural systems makes interpreting empirical patterns difficult because they can be confounded with ecological drivers of survival under current theory. To bridge this gap, we expand ER theory to include biological selective agents, such as pathogens. We find birth processes to be more important than previously theorised in determining ER potential. We employ a novel framework evaluating ER potential within natural systems and gain ability to identify system characteristics that make ER possible. Identifying these characteristics allows a shift from retrospective observation to a predictive mindset, and our findings suggest that ER occurrence may be more limited than previously thought. We use the plague system of Yersinia pestis infecting Cynomys ludovicianus (black‐tailed prairie dogs) and Spermophilus beecheyi (California ground squirrels) as a case study. [ABSTRACT FROM AUTHOR]

Exploitative parasites are predicted to evolve in highly connected populations or in expanding epidemics. However, many parasites rely on host dispersal to reach new populations, potentially causing conflict between local transmission and global spread. We performed experimental range expansions in interconnected microcosms of the protozoan Paramecium caudatum, allowing natural dispersal of hosts infected with the bacterial parasite Holospora undulata. Parasites from range front treatments facilitated host dispersal and were less virulent, but also invested less in horizontal transmission than parasites from range cores. These differences were consistent with parameter estimates derived from an epidemiological model fitted on population‐level time‐series data. Our results illustrate how dispersal selection can have profound consequences for the evolution of parasite life history and virulence. Decrypting the eco‐evolutionary processes that shape parasite 'dispersal syndromes' may be important for the management of spreading epidemics in changing environments, biological invasions or in other spatial non‐equilibrium settings. [ABSTRACT FROM AUTHOR]

Spatial variation in ecological systems can arise both as a consequence of variation in the quality and availability of resources and as an emergent property of spatially structured interactions. We used a spatially explicit model to simulate populations of herbivore hosts and their parasitoids in landscapes with different levels of variance in plant patch quality and different spatial arrangements of high- and low-quality plant patches. We found that even small variation in patch quality at a fine spatial scale decreased overall herbivore populations, as parasitoid populations on low-quality plant patches were subsidized by those from high-quality neighbors. On landscapes with large, homogeneous regions of high- and low-quality plant patches, herbivore populations increased with variation in patch quality. Overall, our results demonstrate that local variation in resource quality profoundly influences global population dynamics. In particular, fine-scale variation in plant patch quality enhanced biological control of herbivores by parasitoids, suggesting that adding back plant genetic variation into perennial production systems may enhance the biological control of herbivores by their natural enemies. [ABSTRACT FROM AUTHOR]

Biological diversity has long been used to measure ecological health. While evidence exists from many ecosystems that declines in host biodiversity may lead to greater risk of disease emergence, the role of pathogen diversity in the emergence process remains poorly understood. Particularly, because a more diverse pool of pathogen types provides more ways in which evolutionary innovations may arise, we suggest that host-pathogen systems with high pathogen diversity are more prone to disease emergence than systems with relatively homogeneous pathogen communities. We call this prediction the diversity-emergence hypothesis., To show how this hypothesis could be tested, we studied a system comprised of North American shorebirds and their associated low-pathogenicity avian influenza ( LPAI) viruses. These viruses are important as a potential source of genetic innovations in influenza. A theoretical contribution of this study is an expression predicting the rate of viral subtype reassortment to be proportional to both prevalence and Simpson's Index, a formula that has been used traditionally to quantify biodiversity. We then estimated prevalence and subtype diversity in host species at Delaware Bay, a North American AIV hotspot, and used our model to extrapolate from these data., We estimated that 4 to 39 virus subtypes circulated at Delaware Bay each year between 2000 and 2008, and that surveillance coverage (percentage of co-circulating subtypes collected) at Delaware Bay is only about 63·0%. Simpson's Index in the same period varied more than fourfold from 0·22 to 0·93. These measurements together with the model provide an indirect, model-based estimate of the reassortment rate. A proper test of the diversity-emergence hypothesis would require these results to be joined to independent and reliable estimates of reassortment, perhaps obtained through molecular surveillance., These results suggest both that subtype diversity (and therefore reassortment) varies from year to year and that several subtypes contributing to reassortment are going undetected. The similarity between these results and more detailed studies of one host, ruddy turnstone ( Arenaria interpres), further suggests that this species may be the primary host for influenza reassortment at Delaware Bay., Biological diversity has long been quantified using Simpson's Index. Our model links this formula to a mechanistic account of reassortment in multipathogen systems in the form of subtype diversity at Delaware Bay, USA. As a theory of how pathogen diversity may influence the evolution of novel pathogens, this work is a contribution to the larger project of understanding the connections between biodiversity and disease. [ABSTRACT FROM AUTHOR]

The development of transgenic technologies, coupled with sterile insect techniques (SIT), is being explored in relation to new approaches for the biological control of insect pests. Recent studies have shown that there are often fitness costs associated with transgenic insect strains, but the impact of these costs on their potential use in pest control is poorly understood. In this paper, we explore the impact of an insect fitness cost on two control strategies (classical SIT and transgenic late-acting bisex lethality) using a stage-structured mathematical model, which is parameterized for the mosquito Aedes aegypti. Counter to the majority of studies, we use realistic pulsed release strategies and incorporate a fitness cost, which is manifested as a reduction in male mating competitiveness. For both models we show that the level of control of a pest mosquito population is highly sensitive to the rate at which the transgenic or sterile males are released. Population control is more effective when smaller numbers of sterile/transgenic males are released more frequently than larger and less frequent releases. If the wild-type mosquito population exhibits cycles of peaks and troughs in abundance, as is the case for many insect species, then high frequency releases of transgenic males not only reduce mosquito abundance, but they may dampen future pest outbreaks, whereas the use of SIT alone may have an adverse effect, causing an increase in mosquito abundance. Additionally, the timing of sterile/transgenic male release during the mosquito population cycle is critical in reducing pest outbreak levels. In all cases, the reduced fitness of the sterile/transgenic males causes reductions in control, thus requiring more frequent or greater magnitude releases. Synthesis and applications. The sterile insect technique is considered to be a valuable non-chemical tool for pest management. With the potential application of recent genetic developments to enhance the technique, it is becoming increasingly important to consider the wider ecological implications of this biological control strategy. Predicting the most efficient release strategies will be important in combating pest and vector insects as well as for limiting potential broader ecological effects. Although the focus of our models are based on the mosquito, A. aegypti, which can spread yellow fever, dengue fever and Chikungunya disease, our modelling approach and results can be applied more broadly to other species. [ABSTRACT FROM AUTHOR]

Parasitism can influence many aspects of the host's behaviour and physiology, which in turn can have a profound impact on their population and evolutionary ecology. In many host–parasite interactions there is often a time lag between infection and the death of the host, yet little is known, experimentally or theoretically, about the effects that intra-class competition between parasitised and unparasitised hosts have on the host–parasite population dynamics. In this article we address this gap in our understanding using a stage-structured mathematical model for a host–parasitoid interaction, which has been parameterised for the Plodia–Venturia experimental system. In the case where parasitised larvae do not compete and do not cannibalise unparasitised larvae, our model predicts a wide range of host–parasitoid dynamics, ranging from host–parasitoid generation cycles, to host generation cycles with parasitoid half-generation cycles, to host–parasitoid equilibria, to host generation cycles with parasitoid extinction. However, when parasitised larvae can compete with their unparasitised larvae counterparts, the host–parasitoid population dynamics can dramatically change. In particular, we show that high levels of competition exerted by unparasitised larvae upon parasitised larvae is more likely to lead to parasitoid extinction. In addition, we demonstrate that unparasitised host larvae that are sufficiently susceptible to intra-class competition, or parasitised host larvae that are sufficiently strong competitors, can have a stabilising effect on the host–parasitoid population dynamics. The implications of these theoretical results are discussed in light of our understanding of host–parasitoid interactions and host–parasite systems in general. [ABSTRACT FROM AUTHOR]

1. The patterns of density-dependent resource competition and the mechanisms leading to competitive exclusion in an experimental two-species insect age-structured interaction were investigated. 2. The modes of competition (scramble or contest) and strength of competition (under- to overcompensatory) operating within and between the stages of the two species was found to be influenced by total competitor density, the age structure of the competitor community and whether competition is between stages of single or two species. 3. The effect of imposed resource limitation on survival was found to be asymmetric between stages and species. Environments supporting both dominant and subordinate competitors were found to increase survival of subordinate competitors at lower total competitor densities. Competitive environments during development within individual stage cohorts (i.e. small or large larvae), differed from the competitive environment in lumped age classes (i.e. development from egg→pupae). 4. Competition within mixed-age, stage or species cohorts, when compared with uniform-aged or species cohorts, altered the position of a competitive environment on the scramble-contest spectrum. In some cases the competitive environment switched from undercompensatory contest to overcompensatory scramble competition. 5. Such switching modes of competition suggest that the relative importance of the mechanisms regulating single-species population dynamics (i.e. resource competition) may change when organisms are embedded within a wider community. [ABSTRACT FROM AUTHOR]

It is well established that intraspecific aggregation has the potential to promote coexistence in communities of species competing for patchy ephemeral resources. We developed a simulation model to explore the influence of aggregation on coexistence in such communities when an important assumption of previous studies – that interspecific interactions have only negative effects on the species involved – is relaxed. The model describes a community of competing insect larvae in which an interaction that is equivalent to intraguild predation (IGP) can occur, and is unusual in that it considers species exploiting very small resource patches (carrying capacity=1). Model simulations show that, in the absence of any intraspecific aggregation, variation between species in the way that resource heterogeneity affects survival increases the likelihood of species coexistence. Simulations also show that intraspecific aggregation of the dominant competitor's eggs across resource patches can promote coexistence by reducing the importance of interspecific competition relative to that of intraspecific competition. Crucially, however, this effect is altered if one competitor indulges in IGP. In general, coexistence is only possible when the species that is capable of IGP is less effective at exploiting the shared resource than its competitor. Because it reduces the relative importance of interspecific interactions, intraspecific aggregation of the eggs of a species that is the victim of IGP actually reduces the likelihood of coexistence in parts of parameter space in which the persistence of the other species is dependent on its ability to exploit its competitor. Since resource heterogeneity, intraspecific aggregation and IGP are all common phenomena, these findings shed light on mechanisms that are likely to influence diversity in communities exploiting patchy resources. [ABSTRACT FROM AUTHOR]

Insects are subject to attack from a range of natural enemies. Many natural enemies, such as parasitoids, do not immediately, or ever, kill their victims but they are nevertheless important in structuring biological communities. The lag that often occurs between attack and host death results in mixed populations of healthy and parasitised hosts. However, little is understood about how the effects of parasitism during this lag period affect the competitive ability of parasitised hosts and how this, in turn, affects the survival and dynamics of the surviving healthy host populations. Here we investigate the impact of the timing of introduction, and the strength of that introduction, of a parasitoid natural enemy Venturia canescens (Gravenhorst) on the outcome of intraspecific competition between larvae of the Indian meal moth, Plodia interpunctella (Hübner). In contrast to healthy hosts alone, we find reduced survival of healthy larvae with increasing periods of exposure to greater numbers of parasitised conspecifics. This represents indirect mortality of the host, which is in addition to that imposed by parasitism itself. Furthermore, longer periods of exposure to parasitised larvae resulted in an increase in development time of healthy individuals and they were larger when they emerged as adults. These results are relevant to both insect–parasitoid and insect–pathogen systems where there is a lag in host death following infection or attack. [ABSTRACT FROM AUTHOR]

Cyclic dynamics of various periods are pervasive in many insect populations where interactions with natural enemies are known to be important. How stage-structured processes within the host population, such as competition and cannibalism, affect these interactions has received little attention so far. Using the well-studied laboratory host­parasitoid system of Plodia interpunctella and Venturia canescens, we explore a series of host­parasitoid models of increasing complexity. Specifically, we identify the circumstances under which stage-structured processes both within the host and parasitoid populations generate dynamical beha- viour ranging from generation to true consumer­resource (multi-generation) cycles. We find that both within-host interactions (strong competition and egg cannibalism by late instar larvae) and parasitoid recruitment structure (a developmental lag in the parasitism of larvae) can suppress long period cycles and promote host generation cycles. In short, we show that simple stage-structured processes in both host and para- sitoid can modulate the strength of the consumer­resource interaction. For some parameters we find more than one stable cyclic attractor. The presence of multiple attractors means that the same mechanism can give rise to cycles of different periods depending on initial population numbers. Because the host-alone system may exhibit transient dynamics for a substantial period, the timing of a parasitoid invasion can be crucial to the dynamical outcome. We discuss the consequences of using a single descriptor of an ecological time series, the cycle period, to infer properties about the underlying system and its food web interactions. [ABSTRACT FROM AUTHOR]

In recent years, ecologists and epidemiologists have paid increasing attention to the influence of spatial structure in shaping the dynamics and determining the persistence of populations. This is fundamentally affected by the concept of ‘coupling’—the flux of individuals moving between separate populations. In this paper, we contrast how coupling is typically implemented in epidemic models with more detailed approaches. Our aim is to link the popular phenomenological formulations with the results of mechanistic models. By concentrating on the behaviour of simple epidemic systems, we relate explicit movement patterns with observed levels of coupling, validating the standard formulation. The analysis is then extended to include a brief study of how the correlation between stochastic populations is affected by coupling, the underlying deterministic dynamics and the relative population sizes. [ABSTRACT FROM AUTHOR]

1. We present a novel metapopulation model where dispersal is fitness dependent: the strength of migration from a site is dependent on the expected reproductive fitness of individuals there. Furthermore, individuals continue to migrate until they reach a suitable habitat where their expected fitness is above a threshold value. 2. Fitness-dependent dispersal has a very strong stabilizing effect on population dynamics, even when the intrinsic dynamics of populations in the absence of dispersal exhibit complex high-amplitude oscillations. This stabilizing effect is much stronger than that of the density-independent dispersal normally considered in metapopulation models. 3. Even when fitness-dependent dispersal does not stabilize the dynamics in a formal sense, it generally leads to simplification, with complex or even chaotic fluctuations being reduced to simple cycles. 4. This form of dispersal also has a strong tendency to synchronize local population dynamics across the spatial extent of the metapopulation. 5. These conclusions are robust to the addition of strong stochasticity in the migration threshold. [ABSTRACT FROM AUTHOR]