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High dietary fat intake leads to insulin resistance in skeletal muscle, and this represents a major risk factor for type 2 diabetes and cardiovascular disease. Mitochondrial dysfunction and oxidative stress have been implicated in the disease process, but the underlying mechanisms are still unknown. Here we show that in skeletal muscle of both rodents and humans, a diet high in fat increases the H(2)O(2)-emitting potential of mitochondria, shifts the cellular redox environment to a more oxidized state, and decreases the redox-buffering capacity in the absence of any change in mitochondrial respiratory function. Furthermore, we show that attenuating mitochondrial H(2)O(2) emission, either by treating rats with a mitochondrial-targeted antioxidant or by genetically engineering the overexpression of catalase in mitochondria of muscle in mice, completely preserves insulin sensitivity despite a high-fat diet. These findings place the etiology of insulin resistance in the context of mitochondrial bioenergetics by demonstrating that mitochondrial H(2)O(2) emission serves as both a gauge of energy balance and a regulator of cellular redox environment, linking intracellular metabolic balance to the control of insulin sensitivity.

Lassa fever (LF) is a zoonotic disease that is widespread in West Africa and involves animal-to-human and human-to-human transmission. Animal-to-human transmission occurs upon exposure to rodent excreta and secretions, i.e. urine and saliva, and human-to-human transmission occurs via the bodily fluids of an infected person. To elucidate the seasonal drivers of LF epidemics, we employed a mathematical model to analyse the datasets of human infection, rodent population dynamics and climatological variations and capture the underlying transmission dynamics. The surveillance-based incidence data of human cases in Nigeria were explored, and moreover, a mathematical model was used for describing the transmission dynamics of LF in rodent populations. While quantifying the case fatality risk and the rate of exposure of humans to animals, we explicitly estimated the corresponding contact rate of humans with infected rodents, accounting for the seasonal population dynamics of rodents. Our findings reveal that seasonal migratory dynamics of rodents play a key role in regulating the cyclical pattern of LF epidemics. The estimated timing of high exposure of humans to animals coincides with the time shortly after the start of the dry season and can be associated with the breeding season of rodents in Nigeria. This article is part of the theme issue ‘Modelling infectious disease outbreaks in humans, animals and plants: approaches and important themes’. This issue is linked with the subsequent theme issue ‘Modelling infectious disease outbreaks in humans, animals and plants: epidemic forecasting and control’.

Because the white matter of the cerebral cortex contains axons that connect distant neurons in the cortical gray matter, the relationship between the volumes of the 2 cortical compartments is key for information transmission in the brain. It has been suggested that the volume of the white matter scales universally as a function of the volume of the gray matter across mammalian species, as would be expected if a global principle of wiring minimization applied. Using a systematic analysis across several mammalian clades, here we show that the volume of the white matter does not scale universally with the volume of the gray matter across mammals and is not optimized for wiring minimization. Instead, the ratio between volumes of gray and white matter is universally predicted by the same equation that predicts the degree of folding of the cerebral cortex, given the clade-specific scaling of cortical thickness, such that the volume of the gray matter (or the ratio of gray to total cortical volumes) divided by the square root of cortical thickness is a universal function of total cortical volume, regardless of the number of cortical neurons. Thus, the very mechanism that we propose to generate cortical folding also results in compactness of the white matter to a predictable degree across a wide variety of mammalian species.

Altered disturbance regimes, increasing atmospheric CO2, and other processes have increased woody cover and homogenized vegetation in savannas across the planet. African savannas with extensive versus minimal woody cover often have vastly different animal communities. However, we lack a clear mechanistic understanding of why animal communities are changing with vegetation structure. Our goal for this study was to understand how vegetation structure in an African savanna shaped the perceived predation risk of small mammals, hence affecting their activity. Using a reciprocal measure of standard giving-up-densities, amount of food eaten, we found sharp declines in rodents’ perceived predation risk and increased rodent activity underneath shrub cover. This response was consistent across species; however, species showed subtle differences in their responses to grassy vegetation. Our findings suggest that areas of minimal or extensive shrub cover (shrub encroachment) may be homogenizing rodents’ perceptions of predation risk and thus shaping their use of space.

The evidence that diel patterns of physiology and behaviour in mammals are governed by circadian ‘clocks’ is based almost entirely on studies of nocturnal rodents. The emergent circadian paradigm, however, neglects the roles of energy metabolism and alimentary function (feeding and digestion) as determinants of activity pattern. The temporal control of activity varies widely across taxa, and ungulates, microtine rodents, and insectivores provide examples in which circadian timekeeping is vestigial. The nocturnal rodent/human paradigm of circadian organisation is unhelpful when considering the broader manifestation of activity patterns in mammals.

Ecosystem engineers can increase biodiversity by creating novel habitat supporting species that would otherwise be absent. Their more routine activities further influence the biota occupying engineered habitats. Beavers are well-known for transforming ecosystems through dam building and are therefore increasingly being used for habitat restoration, adaptation to climate extremes and in long-term rewilding. Abandoned beaver ponds (BP) develop into meadows or forested wetlands that differ fundamentally from other terrestrial habitats and thus increase landscape diversity. Active BP, by contrast, are superficially similar to other non-engineered shallow wetlands, but ongoing use and maintenance might affect how BP contribute to aquatic biodiversity. We explored the ‘within-habitat’ effect of an ecosystem engineer by comparing active BP in southern Sweden with coexisting other wetlands (OW), using sedentary (plants) and mobile (water beetles) organisms as indicators. BP differed predictably from OW in environmental characteristics and were more heterogeneous. BP supported more plant species at plot (+15%) and site (+33%) scales, and plant beta diversity, based on turnover between plots, was 17% higher than in OW, contributing to a significantly larger species pool in BP (+17%). Beetles were not differentiated between BP and OW based on diversity measures but were 26% more abundant in BP. Independent of habitat creation beaver are thus significant agents of within-habitat heterogeneity that differentiates BP from other standing water habitat; as an integral component of the rewilding of wetlands re-establishing beaver should benefit aquatic biodiversity across multiple scales. This article is part of the theme issue ‘Trophic rewilding: consequences for ecosystems under global change’.

The semicircular canals (SCs) of the inner ear detect angular acceleration and are located in the bony labyrinth of the petrosal bone. Based on high-resolution computed tomography, we created a size-independent database of the bony labyrinth of 50 mammalian species especially rodents of the squirrel-related clade comprising taxa with fossorial, arboreal and gliding adaptations. Our sampling also includes gliding marsupials, actively flying bats, the arboreal tree shrew and subterranean species. The morphometric anatomy of the SCs was correlated to the locomotion mode. Even if the phylogenetic signal cannot entirely be excluded, the main significance for functional morphological studies has been found in the diameter of the SCs, whereas the radius of curvature is of minor interest. Additionally, we found clear differences in the bias angle of the canals between subterranean and gliding taxa, but also between sciurids and glirids. The sensitivity of the inner ear correlates with the locomotion mode, with a higher sensitivity of the SCs in fossorial species than in flying taxa. We conclude that the inner ear of flying and gliding mammals is less sensitive due to the large information flow into this sense organ during locomotion.

In modern eutherian (placental) mammals, brown adipose tissue (BAT) evolved as a specialized thermogenic organ that is responsible for adaptive non-shivering thermogenesis (NST). For NST, energy metabolism of BAT mitochondria is increased by activation of uncoupling protein 1 (UCP1), which dissipates the proton motive force as heat. Despite the presence of UCP1 orthologues prior to the divergence of teleost fish and mammalian lineages, UCP1’s significance for thermogenic adipose tissue emerged at later evolutionary stages. Recent studies on the presence of BAT in metatherians (marsupials) and eutherians of the afrotherian clade provide novel insights into the evolution of adaptive NST in mammals. In particular studies on the ‘protoendothermic’ lesser hedgehog tenrec (Afrotheria) suggest an evolutionary scenario linking BAT to the onset of eutherian endothermy. Here, we review the physiological function and distribution of BAT in an evolutionary context by focusing on the latest research on phylogenetically distinct species.

Key Points Environmental enrichment has been shown to have various effects on wild-type mice and rats, from behavioural to cellular and molecular alterations. There is no consensus on which environmental enrichment paradigms are ideal with respect to beneficial effects on brain and behaviour. However, key aspects seem to be environmental complexity, novelty and the age at which enrichment commences, as well as the duration of exposure to enriched environments. Genetic and pharmacological parameters that modulate brain function and dysfunction have been explored in detail, but environmental parameters have received far less attention. The large number of uncontrolled variables that impinge on human epidemiological studies, which limits their ability to demonstrate the involvement of specific environmental factors in particular brain disorders, has meant that animal models have proved crucial in exploring gene–environment interactions. During the last decade, enrichment studies using mouse models of Huntington's disease and Alzheimer's disease have opened the way for the exploration of gene–environment interactions in neurodegeneration. In a transgenic mouse model of Huntington's disease, environmental enrichment has been shown to delay the onset and progression of motor symptoms. Using transgenic models of Alzheimer's disease, studies have also shown that enrichment can enhance learning and memory. However, there are contradictory results regarding its effects on amyloid levels. Effects of environmental enrichment have also recently been identified in other brain disorders such as Parkinson's disease, amyotrophic lateral sclerosis, fragile X syndrome, Down syndrome and various other forms of brain injury. Although enrichment experiments could provide novel insights into each disorder, common effects across disorders point towards general mechanisms of experience-dependent plasticity. Studies on the effect of environmental factors, such as enrichment, on a wide range of CNS disorders have implications for clinical occupational therapies and related approaches. In addition, these environmental manipulations can provide powerful tools to dissect cause and effect among molecular and cellular correlates of pathogenesis, and so identify novel targets for the future development of therapeutics. Enhanced novelty and complexity in the environment can have impressive effects on experience-dependent plasticity under normal conditions. Moreover, such enriched environments can delay the onset and progression of a range of CNS disorders, with important implications for therapeutic strategies. Behavioural, cellular and molecular studies have revealed significant effects of enriched environments on rodents and other species, and provided new insights into mechanisms of experience-dependent plasticity, including adult neurogenesis and synaptic plasticity. The demonstration that the onset and progression of Huntington's disease in transgenic mice is delayed by environmental enrichment has emphasized the importance of understanding both genetic and environmental factors in nervous system disorders, including those with Mendelian inheritance patterns. A range of rodent models of other brain disorders, including Alzheimer's disease and Parkinson's disease, fragile X and Down syndrome, as well as various forms of brain injury, have now been compared under enriched and standard housing conditions. Here, we review these findings on the environmental modulators of pathogenesis and gene–environment interactions in CNS disorders, and discuss their therapeutic implications.

Rodents' ultrasonic vocalizations (USVs) provide useful information for assessing their social behaviors. Despite previous efforts in classifying subcategories of time-frequency patterns of USV syllables to study their functional relevance, methods for detecting vocal elements from continuously recorded data have remained sub-optimal. Here, we propose a novel procedure for detecting USV segments in continuous sound data containing background noise recorded during the observation of social behavior. The proposed procedure utilizes a stable version of the sound spectrogram and additional signal processing for better separation of vocal signals by reducing the variation of the background noise. Our procedure also provides precise time tracking of spectral peaks within each syllable. We demonstrated that this procedure can be applied to a variety of USVs obtained from several rodent species. Performance tests showed this method had greater accuracy in detecting USV syllables than conventional detection methods.