The University Press of Florida (UPF) is the scholarly publishing arm of the State University System of Florida, representing Florida's twelve state universities. It is located in Gainesville near the University of Florida, one of the state's major research institutions. It is overseen by the Florida Board of Governors and publishes works from and about the state. Its predecessor was the University of Florida Press..
Complex ecological systems obey universal scaling laws such as the Taylor law, which links population variance to the sample mean. A natural question is whether other complex systems with integrated and segregated functional networks, such as the human brain, follow analogous scaling laws, and how these laws behave under synchronized activity. Addressing this is challenging because neural signals at all measurement scales contain both positive and negative values, whereas the Taylor law was developed for non-negative ecological data. To overcome this limitation, we replace the sample mean with the root mean square (RMS) of detrended neural activity and formulate a generalized spatial scaling law applicable to signed data. This framework extends spatial scaling obeying the Taylor law to neural systems and other complex systems across disciplines and allows examination of how coordinated, synchronized activity shapes these laws. Synchrony is quantified using a dedicated metric of functional coordination. Analytical derivations and numerical simulations using multivariate Poisson, binomial, uniform, and gamma distributions demonstrate that the scaling exponent is inversely related to synchrony. Applying this framework to human fMRI data from three large lifespan cohorts (N=840, ages 18 to 88) reveals distinct age-associated trajectories of the scaling exponent. Healthy aging is characterized by a substantial synchrony-induced reduction in the exponent. The synchrony and scaling relationship is stable during resting-state activity but progressively shifts during naturalistic tasks across the lifespan. Limbic, subcortical, and cerebellar regions show particularly strong synchrony and scaling coupling, indicating preservation at subnetwork levels. Finally, individuals with ADHD exhibit disrupted synchrony and scaling relationships, underscoring the potential clinical utility of this novel metric. ### Competing Interest Statement The authors have declared no competing interest.
Corals (Cnidaria; Anthozoa) play critical roles as habitat-forming species with a wide range, from warm shallow-water tropical coral reefs to cold-water ecosystems. They also represent a complex ecosystem as intricate holobionts made up of microbes from all domains of the Tree of Life that can play significant roles in host health and fitness. The corallicolids are a clade of apicomplexans that infect a wide variety of anthozoans worldwide and can influence the thermal tolerance of habitat-forming corals. Despite their potentially important impacts on reef ecosystems, much of the basic biology and ecology of corallicolids remains unclear. Apicomplexans often have a closed life cycle, with minimal environmental exposure and sometimes multiple hosts. Corallicolids have only been documented in anthozoan hosts, with no known secondary/reservoir hosts or vectors. Here, we show that abundant corallicolid sequences are recovered from bearded fireworms (Hermodice carunculata) in tropical reef habitats off Curaçao and that they are distinct from corallicolids infecting the corals on which the fireworms were feeding at the time of their collection. These data are consistent with a fireworm-specific corallicolid infection, not merely a byproduct of the worms feeding on infected corals. Furthermore, we suggest that H. carunculata is potentially a vector moving corallicolids among coral hosts through its feces. These findings not only expand our understanding of the ecological interactions within coral reef ecosystems but also highlight the potential role of host-associated parasites in shaping the resilience of reef habitats.
Alzheimer's disease (AD) is characterized by a progressive cognitive decline underpinned by disruptions in neural circuit dynamics. Early-stage AD is associated with cortical hyperexcitability, whereas later stages exhibit oscillatory slowing and hypoactivity, a progression observable in electrophysiological spectral characteristics. While previous studies have linked these changes to the dysfunction of fast-spiking parvalbumin-positive (PV) interneurons and neuronal loss associated with amyloid-beta (Abeta) and hyperphosphorylated tau (hptau) pathology, the precise mechanistic relationship between cellular and altered electrophysiology remains unclear. To study this relationship, we employed a Laminar Neural Mass Model that integrates excitatory and inhibitory neural populations within a biophysically informed columnar framework. The connectivity constant from PV cells to pyramidal neurons was gradually reduced to simulate the progressive neurotoxic effects of Abeta oligomers. Other model parameters were systematically varied to compare with existing modeling literature and also to simulate the effects of hptau. All model predictions were compared to empirical M/EEG findings in the literature. Our simulations of PV interneuron dysfunction successfully reproduced the biphasic electrophysiological progression observed in AD: an early phase of hyperexcitability with increased gamma and alpha power, followed by oscillatory slowing and reduced spectral power. Alternative mechanisms and model parameters, such as increased excitatory drive, failed to replicate the observed biomarker trajectory. Additionally, to reconcile the hypoactivity and decreased firing rates observed in advanced AD stages, we combined the PV dysfunction model with a disruption of the pyramidal cell populations that reflects the neurotoxicity induced by hptau. Although this additional mechanism is not necessary to reproduce oscillatory changes in the isolated neural mass, it is crucial for aligning the model with evidence of reduced firing rates, metabolic activity, and cell loss and will enhance its applicability in future whole-brain modeling studies. These results support the hypothesis that at the local level, PV interneuron dysfunction is a primary driver of cortical electrophysiological alterations, while pyramidal neuron loss underlies later-stage severe hypoactivity. Our model provides a mechanistic framework for interpreting excitation-inhibition imbalance across AD progression, demonstrating the value of biophysically constrained models for interpreting electrophysiological biomarkers. ### Competing Interest Statement RST, BM, ELS, MG, and GR work for Neuroelectrics. GR is a co-founder.
Digital replicas (or twins) of the entire planet and of its inhabitants are being actively proposed by the research community for a variety of purposes, with a focus on climate adaptation and mitigation. Since mathematical modelling is at the core of this digital enterprise, we undertake to explore the possible limits of models in creating twins of the Earth by recalling some of the existing visions about the nature and function of mathematical models. We thus discuss what models are, what their function is in relation to the production of knowledge, and how one can question if a model is fair, by keeping the digital twins as the focus of our analysis. This leads us to discuss the way models intervene in the democratic process and orient power toward those who wield the models, and what these artifacts represent in the context of governance of science itself.
Genetic assimilation is a process by which a trait originally driven by the environment becomes independent of the initial cue and is expressed constitutively in a population. More than seven decades have passed since Waddington's pioneering demonstration of the acquisition of morphological traits through genetic assimilation, but the underlying mechanism remains unknown. Here, we address this gap by performing combined genomic analyses of Waddington's genetic assimilation experiments using the ectopic veins (EV) phenocopy in Drosophila as a model. Our study reveals the assimilation of EV in both outbred and inbred fly natural populations, despite their limited genetic diversity. We identified key changes in the expression of developmental genes and pinpointed selected alleles involved in EV assimilation. The assimilation of EV is mainly driven by the selection of regulatory alleles already present in the ancestral populations, including the downregulation of the receptor tyrosine kinase gene Cad96Ca by the insertion of a transposable element in its 3' untranslated region. The genetic variation at this locus in the inbred population is maintained by a large chromosomal inversion. In outbred populations, the evolution of EV results from a polygenic response shaped by the selective environment. Our results support a model in which selection for multiple preexisting alleles in the ancestral population, rather than stress-induced genetic or epigenetic variation, drives the evolution of EV in natural fly populations.
