Football players\' decision-making behaviours near the scoring target (finishing situations) emerge from the evolving spatiotemporal information directly perceived in the game\'s landscape. In finishing situations, the ball carrier\'s decision-making about shooting or passing is not an individual decision-making process, but a collective decision that is guided by players\' perceptions of match affordances. To sustain this idea, we collected spatiotemporal information and built a model to quantify the \"Finishing Space Value\" (FSV) that results from players\' perceived affordances about two main questions: (a) is the opponent\'s target successfully reachable from a given pitch location?; and (b) from each given pitch location, the opposition context will allow enough space to shoot (low adversaries\' interference)? The FSV was calculated with positional data from high-performance football matches, combining information extracted from Voronoi diagrams (VD) with distances and angles to the goal line. FSV was tested using as a reference the opinion of a \"panel of expert\" (PE), composed by football coaches, about a questionnaire presenting 50 finishing situations. Results showed a strong association between the subjective perception scale used by the PE to assess how probable a shot made by the ball carrier could result in a goal and FSV calculated for that same situation (R2=0.6706). Moreover, we demonstrate the accuracy of the FSV quantification model in predicting coaches\' opinions about what should be the \"best option\" to finish the play. Overall, results indicated that the FSV is a promising model to capture the affordances of the shooting circumstances for the ball carrier\'s decision-making in high-performance football. FSV might be useful for more precise match analysis and informing coaches in the design of representative practice tasks.

Complex systems are neither fully determined nor completely random. Biological complex systems, including single neurons, manifest intermediate regimes of randomness that recruit integration of specific combinations of functionally segregated subsystems. Such emergence of biological function provides the substrate for the expression of degeneracy, the ability of disparate combinations of subsystems to yield similar function. Here, we present evidence for the expression of degeneracy in morphologically realistic models of dentate gyrus granule cells (GC) through functional integration of disparate ion-channel combinations. We performed a 45-parameter randomized search spanning 16 active and passive ion channels, each biophysically constrained by their gating kinetics and localization profiles, to search for valid GC models. Valid models were those that satisfied 17 sub- and supra-threshold cellular-scale electrophysiological measurements from rat GCs. A vast majority (>99%) of the 15,000 random models were not electrophysiologically valid, demonstrating that arbitrarily random ion-channel combinations wouldn\'t yield GC functions. The 141 valid models (0.94% of 15,000) manifested heterogeneities in and cross-dependencies across local and propagating electrophysiological measurements, which matched with their respective biological counterparts. Importantly, these valid models were widespread throughout the parametric space and manifested weak cross-dependencies across different parameters. These observations together showed that GC physiology could neither be obtained by entirely random ion-channel combinations nor is there an entirely determined single parametric combination that satisfied all constraints. The complexity, the heterogeneities in measurement and parametric spaces, and degeneracy associated with GC physiology should be rigorously accounted for, while assessing GCs and their robustness under physiological and pathological conditions.

Maintaining balance is a complex motor problem that requires coordinated contributions from multiple biological systems. Aging inevitably lessens the fidelity of biological systems, which can result in an increased risk of falling, and associated injuries. It is advantageous to land safely, but falls manifest in diverse ways, so different motor solutions are required to land safely. However, without considerable practice, it is difficult to recall the appropriate motor solution for a fall and then apply it effectively in the brief duration before hitting the ground. A complex systems perspective provides a lens through which to view the problem of safe-landing. It may be possible to use motor analogies to promote degeneracy within the perceptual-motor system so that, regardless of the direction in which an older person falls, their body self-organizes to land with less likelihood of injury.

Degeneracy and symmetry have a profound relation in quantum systems. Here, we report gate-tunable subband degeneracy in PbTe nanowires with a nearly symmetric cross-sectional shape. The degeneracy is revealed in electron transport by the absence of a quantized plateau. Utilizing a dual gate design, we can apply an electric field to lift the degeneracy, reflected as emergence of the plateau. This degeneracy and its tunable lifting were challenging to observe in previous nanowire experiments, possibly due to disorder. Numerical simulations can qualitatively capture our observation, shedding light on device parameters for future applications.

Concepts from network science and graph theory, including the framework of network motifs, have been frequently applied in studying neuronal networks and other biological complex systems. Network-based approaches can also be used to study the functions of individual neurons, where cellular elements such as ion channels and membrane voltage are conceptualized as nodes within a network, and their interactions are denoted by edges. Network motifs in this context provide functional building blocks that help to illuminate the principles of cellular neurophysiology. In this review we build a case that network motifs operating within neurons provide tools for defining the functional architecture of single-neuron physiology and neuronal adaptations. We highlight the presence of such computational motifs in the cellular mechanisms underlying action potential generation, neuronal oscillations, dendritic integration, and neuronal plasticity. Future work applying the network motifs perspective may help to decipher the functional complexities of neurons and their adaptation during health and disease.

Nociceptive sensory neurons convey pain-related signals to the CNS using action potentials. Loss-of-function mutations in the voltage-gated sodium channel NaV1.7 cause insensitivity to pain (presumably by reducing nociceptor excitability) but clinical trials seeking to treat pain by inhibiting NaV1.7 pharmacologically have struggled. This may reflect the variable contribution of NaV1.7 to nociceptor excitability. Contrary to claims that NaV1.7 is necessary for nociceptors to initiate action potentials, we show that nociceptors can achieve similar excitability using different combinations of NaV1.3, NaV1.7, and NaV1.8. Selectively blocking one of those NaV subtypes reduces nociceptor excitability only if the other subtypes are weakly expressed. For example, excitability relies on NaV1.8 in acutely dissociated nociceptors but responsibility shifts to NaV1.7 and NaV1.3 by the fourth day in culture. A similar shift in NaV dependence occurs in vivo after inflammation, impacting ability of the NaV1.7-selective inhibitor PF-05089771 to reduce pain in behavioral tests. Flexible use of different NaV subtypes exemplifies degeneracy - achieving similar function using different components - and compromises reliable modulation of nociceptor excitability by subtype-selective inhibitors. Identifying the dominant NaV subtype to predict drug efficacy is not trivial. Degeneracy at the cellular level must be considered when choosing drug targets at the molecular level.

Synonymous mutations result from the degeneracy of the genetic code. Most amino acids are encoded by two or more codons, and mutations that change a codon to another synonymous codon do not change the amino acid in the gene product. Historically, such mutations have been considered silent because they were assumed to have no to very little impact. However, research in the last few decades has produced several examples where synonymous mutations play important roles. These include optimizing expression by enhancing translation initiation and accelerating or decelerating translation elongation via codon usage and mRNA secondary structures, stabilizing mRNA molecules and preventing their breakdown before translation, and faulty protein folding or increased degradation due to enhanced ubiquitination and suboptimal secretion of proteins into the appropriate cell compartments. Some consequences of synonymous mutations, such as mRNA stability, can lead to different outcomes in prokaryotes and eukaryotes. Despite these examples, the significance of synonymous mutations in evolution and in causing disease in comparison to nonsynonymous mutations that do change amino acid residues in proteins remains controversial. Whether the molecular mechanisms described by which synonymous mutations affect organisms can be generalized remains poorly understood and warrants future research in this area.

The long 19th century was a period of many developments and technical innovations in agriculture and animal biology, during which actors sought to incorporate new practices in light of new information. By the middle of the century, however, while heredity steadily became the dominant concept in animal husbandry, some policies related to livestock improvement in Brazil seemed to have been tailored following a climate-deterministic concept established in the mid-18th century by the French naturalist Georges-Louis Leclerc, the Comte de Buffon. His theory of animal degeneration posited, among other things, the necessity of recurrent crossbreeding to preserve animal species living in nonnative environments from climate-induced degeneration. Although largely discredited by the early 19th century, the teachings of the French naturalist seem to have found supporters in a Brazilian program to modernize national agriculture through the application of the natural sciences. Herein I examine the revival of Buffon\'s theories in that government-sponsored program to improve animal husbandry and breeding techniques, including actual applications of this theory in the real world. Ultimately, I argue that Buffon\'s theory of degeneration was used to tailor public policies and funding for the improvement of domesticated animals in Brazil between 1856 and 1860.

UNASSIGNED: At the cellular level, acute temperature changes alter ionic conductances, ion channel kinetics, and the activity of entire neuronal circuits. This can result in severe consequences for neural function, animal behavior and survival. In poikilothermic animals, and particularly in aquatic species whose core temperature equals the surrounding water temperature, neurons experience rather rapid and wide-ranging temperature fluctuations. Recent work on pattern generating neural circuits in the crustacean stomatogastric nervous system have demonstrated that neuronal circuits can exhibit an intrinsic robustness to temperature fluctuations. However, considering the increased warming of the oceans and recurring heatwaves due to climate change, the question arises whether this intrinsic robustness can acclimate to changing environmental conditions, and whether it differs between species and ocean habitats.
UNASSIGNED: We address these questions using the pyloric pattern generating circuits in the stomatogastric nervous system of two crab species, Hemigrapsus sanguineus and Carcinus maenas that have seen a worldwide expansion in recent decades.
UNASSIGNED: Consistent with their history as invasive species, we find that pyloric activity showed a broad temperature robustness (>30°C). Moreover, the temperature-robust range was dependent on habitat temperature in both species. Warm-acclimating animals shifted the critical temperature at which circuit activity breaks down to higher temperatures. This came at the cost of robustness against cold stimuli in H. sanguineus, but not in C. maenas. Comparing the temperature responses of C. maenas from a cold latitude (the North Sea) to those from a warm latitude (Spain) demonstrated that similar shifts in robustness occurred in natural environments. Our results thus demonstrate that neuronal temperature robustness correlates with, and responds to, environmental temperature conditions, potentially preparing animals for changing ecological conditions and shifting habitats.

How do neurons that implement cell-autonomous self-regulation of calcium react to knockout of individual ion-channel conductances? To address this question, we used a heterogeneous population of 78 conductance-based models of hippocampal pyramidal neurons that maintained cell-autonomous calcium homeostasis while receiving theta-frequency inputs. At calcium steady-state, we individually deleted each of the 11 active ion-channel conductances from each model. We measured the acute impact of deleting each conductance (one at a time) by comparing intrinsic electrophysiological properties before and immediately after channel deletion. The acute impact of deleting individual conductances on physiological properties (including calcium homeostasis) was heterogeneous, depending on the property, the specific model, and the deleted channel. The underlying many-to-many mapping between ion channels and properties pointed to ion-channel degeneracy. Next, we allowed the other conductances (barring the deleted conductance) to evolve towards achieving calcium homeostasis during theta-frequency activity. When calcium homeostasis was perturbed by ion-channel deletion, post-knockout plasticity in other conductances ensured resilience of calcium homeostasis to ion-channel deletion. These results demonstrate degeneracy in calcium homeostasis, as calcium homeostasis in knockout models was implemented in the absence of a channel that was earlier involved in the homeostatic process. Importantly, in reacquiring homeostasis, ion-channel conductances and physiological properties underwent heterogenous plasticity (dependent on the model, the property, and the deleted channel), even introducing changes in properties that were not directly connected to the deleted channel. Together, post-knockout plasticity geared towards maintaining homeostasis introduced heterogenous off-target effects on several channels and properties, suggesting that extreme caution be exercised in interpreting experimental outcomes involving channel knockouts.