Hoylenoonan5650

By separating these two components (microbial community and abiotic environment), we found taxonomic composition played a crucial role in suppressing invasion, but this depended critically on local abiotic conditions (adapted communities were more suppressive in nutrient-depleted conditions). This helps predict when resident communities will be most susceptible to invasion, with implications for optimizing treatments based on microbiota management.An epidemic can be characterized by its strength (i.e., the reproductive number [Formula see text]) and speed (i.e., the exponential growth rate r). Disease modellers have historically placed much more emphasis on strength, in part because the effectiveness of an intervention strategy is typically evaluated on this scale. Transmembrane Transporters inhibitor Here, we develop a mathematical framework for the classic, strength-based paradigm and show that there is a dual speed-based paradigm which can provide complementary insights. In particular, we note that r = 0 is a threshold for disease spread, just like [Formula see text] [ 1], and show that we can measure the strength and speed of an intervention on the same scale as the strength and speed of an epidemic, respectively. We argue that, while the strength-based paradigm provides the clearest insight into certain questions, the speed-based paradigm provides the clearest view in other cases. As an example, we show that evaluating the prospects of 'test-and-treat' interventions against the human immunodeficiency virus (HIV) can be done more clearly on the speed than strength scale, given uncertainty in the proportion of HIV spread that happens early in the course of infection. We also discuss evaluating the effects of the importance of pre-symptomatic transmission of the SARS-CoV-2 virus. We suggest that disease modellers should avoid over-emphasizing the reproductive number at the expense of the exponential growth rate, but instead look at these as complementary measures.Allee effects play an important role in the dynamics of many populations and can increase the risk of local extinction. However, some authors have questioned the weight of evidence for Allee effects in wild populations. We therefore exploited a natural experiment provided by two adjacent breeding colonies of contrasting density to investigate the potential for Allee effects in an Antarctic fur seal (Arctocephalus gazella) population that is declining in response to climate change-induced reductions in food availability. Biometric time-series data were collected from 25 pups per colony during two consecutive breeding seasons, the first of which was among the worst on record in terms of breeding female numbers, pup birth weights and foraging trip durations. In previous decades when population densities were higher, pup mortality was consistently negatively density dependent, with rates of trauma and starvation scaling positively with density. However, we found the opposite, with higher pup mortality at low density and the majority of deaths attributable to predation. In parallel, body condition was depressed at low density, particularly in the poor-quality season. Our findings shed light on Allee effects in wild populations and highlight a potential emerging role of predators in the ongoing decline of a pinniped species.Chimeric antigen receptor (CAR) T cell therapy is a remarkably effective immunotherapy that relies on in vivo expansion of engineered CAR T cells, after lymphodepletion (LD) by chemotherapy. The quantitative laws underlying this expansion and subsequent tumour eradication remain unknown. We develop a mathematical model of T cell-tumour cell interactions and demonstrate that expansion can be explained by immune reconstitution dynamics after LD and competition among T cells. CAR T cells rapidly grow and engage tumour cells but experience an emerging growth rate disadvantage compared to normal T cells. Since tumour eradication is deterministically unstable in our model, we define cure as a stochastic event, which, even when likely, can occur at variable times. However, we show that variability in timing is largely determined by patient variability. While cure events impacted by these fluctuations occur early and are narrowly distributed, progression events occur late and are more widely distributed in time. We parameterized our model using population-level CAR T cell and tumour data over time and compare our predictions with progression-free survival rates. We find that therapy could be improved by optimizing the tumour-killing rate and the CAR T cells' ability to adapt, as quantified by their carrying capacity. Our tumour extinction model can be leveraged to examine why therapy works in some patients but not others, and to better understand the interplay of deterministic and stochastic effects on outcomes. For example, our model implies that LD before a second CAR T injection is necessary.The scaling relationship observed between species richness and the geographical area sampled (i.e. the species-area relationship (SAR)) is a widely recognized macroecological relationship. Recently, this theory has been extended to trophic interactions, suggesting that geographical area may influence the structure of species interaction networks (i.e. network-area relationships (NARs)). Here, we use a global dataset of host-helminth parasite interactions to test existing predictions from macroecological theory. Scaling between single locations to the global host-helminth network by sequentially adding networks together, we find support that geographical area influences species richness and the number of species interactions in host-helminth networks. However, species-area slopes were larger for host species relative to their helminth parasites, counter to theoretical predictions. Lastly, host-helminth network modularity-capturing the tendency of the network to form into separate subcommunities-decreased with increasing area, also counter to theoretical predictions. Reconciling this disconnect between existing theory and observed SAR and NAR will provide insight into the spatial structuring of ecological networks, and help to refine theory to highlight the effects of network type, species distributional overlap, and the specificity of trophic interactions on NARs.Many comparative neurobiological studies seek to connect sensory or behavioural attributes across taxa with differences in their brain composition. Recent studies in vertebrates suggest cell number and density may be better correlated with behavioural ability than brain mass or volume, but few estimates of such figures exist for insects. Here, we use the isotropic fractionator (IF) method to estimate total brain cell numbers for 32 species of Hymenoptera spanning seven subfamilies. We find estimates from using this method are comparable to traditional, whole-brain cell counts of two species and to published estimates from established stereological methods. We present allometric scaling relationships between body and brain mass, brain mass and nuclei number, and body mass and cell density and find that ants stand out from bees and wasps as having particularly small brains by measures of mass and cell number. We find that Hymenoptera follow the general trend of smaller animals having proportionally larger brains. Smaller Hymenoptera also feature higher brain cell densities than the larger ones, as is the case in most vertebrates, but in contrast with primates, in which neuron density remains rather constant across changes in brain mass. Overall, our findings establish the IF as a useful method for comparative studies of brain size evolution in insects.Sensorimotor coordination is thought to rely on cerebellar-based internal models for state estimation, but the underlying neural mechanisms and specific contribution of the cerebellar components is unknown. A central aspect of any inferential process is the representation of uncertainty or conversely precision characterizing the ensuing estimates. Here, we discuss the possible contribution of inhibition to the encoding of precision of neural representations in the granular layer of the cerebellar cortex. Within this layer, Golgi cells influence excitatory granule cells, and their action is critical in shaping information transmission downstream to Purkinje cells. In this review, we equate the ensuing excitation-inhibition balance in the granular layer with the outcome of a precision-weighted inferential process, and highlight the physiological characteristics of Golgi cell inhibition that are consistent with such computations.Emerging infectious diseases (EIDs) present global health threats, and their emergences are often linked to anthropogenic change. Artificial light at night (ALAN) is one form of anthropogenic change that spans beyond urban boundaries and may be relevant to EIDs through its influence on the behaviour and physiology of hosts and/or vectors. Although West Nile virus (WNV) emergence has been described as peri-urban, we hypothesized that exposure risk could also be influenced by ALAN in particular, which is testable by comparing the effects of ALAN on prevalence while controlling for other aspects of urbanization. By modelling WNV exposure among sentinel chickens in Florida, we found strong support for a nonlinear relationship between ALAN and WNV exposure risk in chickens with peak WNV risk occurring at low ALAN levels. Although our goal was not to discern how ALAN affected WNV relative to other factors, effects of ALAN on WNV exposure were stronger than other known drivers of risk (i.e. impervious surface, human population density). Ambient temperature in the month prior to sampling, but no other considered variables, strongly influenced WNV risk. These results indicate that ALAN may contribute to spatio-temporal changes in WNV risk, justifying future investigations of ALAN on other vector-borne parasites.Recent theory has suggested that dosage compensation mediates sexual antagonism over X-linked genes. This process relies on the assumption that dosage compensation scales phenotypic effects between the sexes, which is largely untested. We evaluated this by quantifying transcriptome variation associated with a recently arisen, male-beneficial, X-linked mutation across tissues of the field cricket Teleogryllus oceanicus, and testing the relationship between the completeness of dosage compensation and female phenotypic effects at the level of gene expression. Dosage compensation in T. oceanicus was variable across tissues but usually incomplete, such that relative expression of X-linked genes was typically greater in females. Supporting the assumption that dosage compensation scales phenotypic effects between the sexes, we found tissues with incomplete dosage compensation tended to show female-skewed effects of the X-linked allele. In gonads, where expression of X-linked genes was most strongly female-biased, ovaries-limited genes were much more likely to be X-linked than were testes-limited genes, supporting the view that incomplete dosage compensation favours feminization of the X. Our results support the expectation that sex chromosome dosage compensation scales phenotypic effects of X-linked genes between sexes, substantiating a key assumption underlying the theoretical role of dosage compensation in determining the dynamics of sexual antagonism on the X.