Connectionist natural language parsing

The key developments of two decades of connectionist parsing are reviewed. Connectionist parsers are assessed according to their ability to learn to represent syntactic structures from examples automatically, without being presented with symbolic grammar rules. This review also considers the extent to which connectionist parsers offer computational models of human sentence processing and provide plausible accounts of psycholinguistic data. In considering these issues, special attention is paid to the level of realism, the nature of the modularity, and the type of processing that is to be found in a wide range of parsers

Relapse after severe acute malnutrition: A systematic literature review and secondary data analysis.

The objectives of most treatment programs for severe acute malnutrition (SAM) in children focus on initial recovery only, leaving post-discharge outcomes, such as relapse, poorly understood and undefined. This study aimed to systematically review current literature and conduct secondary data analyses of studies that captured relapse rates, up to 18-month post-discharge, in children following recovery from SAM treatment. The literature search (including PubMed and Google Scholar) built upon two recent reviews to identify a variety of up-to-date published studies and grey literature. This search yielded 26 articles and programme reports that provided information on relapse. The proportion of children who relapsed after SAM treatment varied greatly from 0% to 37% across varying lengths of time following discharge. The lack of a standard definition of relapse limited comparability even among the few studies that have quantified post-discharge relapse. Inconsistent treatment protocols and poor adherence to protocols likely add to the wide range of relapse reported. Secondary analysis of a database from Malawi found no significant association between potential individual risk factors at admission and discharge, except being an orphan, which resulted in five times greater odds of relapse at 6 months post-discharge (95% CI [1.7, 12.4], P = 0.003). The development of a standard definition of relapse is needed for programme implementers and researchers. This will allow for assessment of programme quality regarding sustained recovery and better understanding of the contribution of relapse to local and global burden of SAM

Correction to: Cluster identification, selection, and description in Cluster randomized crossover trials: the PREP-IT trials

An amendment to this paper has been published and can be accessed via the original article

Natural Behaviours of Echolocators, with an Emphasis on Vespertilionid Bats

Here I report on two experimental studies and one observational analysis addressing the flexibility and ecological limitations of sensorimotor integration in echolocating mammals, as they relate to sensory ecology and foraging behaviour. In chapter two, I use acoustic data to comparatively assess echolocation and motor activities of bats and toothed whales to test (i) how the presence of a conspecific influences the spectral and temporal content of echolocation signals and (ii) whether these species behave similarly when foraging with a conspecific. The results suggest that in the presence of conspecifics (i) both bats and toothed whales exhibit the Lombard effect, and (ii) bats additionally employ subsets of both a Jamming Avoidance Response and a clutter response. Behaviourally, only porpoises appear to modify their beam direction. In chapter three, I use acoustic, photo, and video data to compare the developmental trajectories of (i) flight attempts, (ii) wing morphology, and (iii) vocalizations of big brown bat pups in the context of landing behavior, specifically with respect to landing buzz production. The results (i) clarified previous studies exploring pup vocal and flight ontogeny and (ii) identified developmental relationships between wing morphology (RWL) and flight milestones. In chapter four, I comparatively assess acoustic recordings of bat activity before and after the introduction of white-nose syndrome (WNS) to South Eastern Ontario to explore the effects of WNS on (i) species abundance and (ii) habitat use. I also explore (iii) the possibility of niche release and realized niche expansion due to reduced interspecific competition resulting from species-specific WNS susceptibility. The results confirm that (i) endangered species are detected less often foraging in open field habitats since the introduction of WNS, and that (ii) relatively unaffected species have increased their presence (but not active foraging) in clutter/edge and open field habitats. The results also indicate that (iii) over water habitats showed no difference between pre- and post-WNS bat activity, suggesting that niche expansion for relatively unaffected species may be limited to some habitats and not others.Ph.D

Morphological, olfactory, and vocal development in big brown bats

Using a within subjects design, we documented morphological, bioacoustical and behavioral developmental changes in big brown bats. Eptesicus fuscus pups are born naked and blind but assume an adult-like appearance by post-natal day (PND) 45 and flight by PND 30. Adult females use spatial memory, acoustic and olfactory cues to reunite with offspring, but it is unclear if pups can recognize maternal scents. We tested the olfactory discrimination abilities of young E. fuscus pups and found they exhibited no odor preferences. Pups also emit distinct vocalizations called isolation calls (i-calls) that facilitate mother-offspring reunions, but how pups shift their vocalizations from i-calls to downward frequency modulated (FM) sweeps used in echolocation remains unclear. Between PND 0–9, pups emitted mainly long duration, tonal i-calls rich in harmonics, but after they switched to short duration, downward FM sweeps with fewer harmonics. Call maximum frequency and repetition rate showed minor changes across development. Signal duration, bandwidth, and number of harmonics decreased, whereas the maximum, minimum and bandwidth of the fundamental, and peak spectral frequency all increased. We recorded vocalizations during prolonged maternal separation and found that isolated pups called longer and at a faster rate, presumably to signal for maternal assistance. To assess how PND 13 pups alter their signals during interactions with humans we compared spontaneous and provoked vocalizations and found that provoked calls were spectrally and temporally more similar to those of younger bats suggesting that pups in distress emit signals that sound like younger bats to promote maternal assistance

White-nose syndrome increases torpid metabolic rate and evaporative water loss in hibernating bats

Fungal diseases of wildlife typically manifest as superficial skin infections but can have devastating consequences for host physiology and survival. White-nose syndrome (WNS) is a fungal skin disease that has killed millions of hibernating bats in North America since 2007. Infection with the fungus Pseudogymnoascus destructans causes bats to rewarm too often during hibernation, but the cause of increased arousal rates remains unknown. On the basis of data from studies of captive and free-living bats, two mechanistic models have been proposed to explain disease processes in WNS. Key predictions of both models are that WNS-affected bats will show 1) higher metabolic rates during torpor (TMR) and 2) higher rates of evaporative water loss (EWL). We collected bats from a WNS-negative hibernaculum, inoculated one group with P. destructans, and sham-inoculated a second group as controls. After 4 mo of hibernation, TMR and EWL were measured using respirometry. Both predictions were supported, and our data suggest that infected bats were more affected by variation in ambient humidity than controls. Furthermore, disease severity, as indicated by the area of the wing with UV fluorescence, was positively correlated with EWL, but not TMR. Our results provide the first direct evidence that heightened energy expenditure during torpor and higher EWL independently contribute to WNS pathophysiology, with implications for the design of potential treatments for the disease. fungal diseases of wildlife are on the rise worldwide (13). In contrast to viral and bacterial pathogens, which often lead to systemic infections, fungal pathogens of animals often manifest as superficial skin infections, especially among poikilothermic species. Although typically limited to infecting skin, fungal pathogens can lead to devastating physiological impacts and fatal disease across a range of taxa (1, 4, 5, 35, 36). A mechanistic understanding of pathogenesis in fungal diseases of wildlife is critical for understanding and predicting population-level impacts and developing safe and effective mitigation and management strategies. White-nose syndrome (WNS), caused by the fungus Pseudogymnoascus destructans, is a recently emerged disease of hibernating bats (5) (25, 42). Since its discovery in 2007, millions of bats have been killed in eastern and central North America, leading to dramatic population declines (16) and the possibility of regional extinctions (15). Recent reviews have summarized our understanding of disease mechanisms in WNS (17, 45). A number of putative virulence factors have now been identified (14, 29), and studies of both captive (42) and free-living (33) bats indicate that the disease causes increased frequency of arousals from torpor during hibernation, emaciation, and death. Infected bats also exhibit signs of altered fluid, electrolyte, and pH balance (10, 11, 26, 41, 43), leading to development of two complementary mechanistic models of WNS pathophysiology (41, 43). Symptoms of WNS develop in a progressive manner (26), and the most pronounced symptoms are only apparent relatively late in hibernation (41, 43). Increased arousal frequency and arousal cascades that may reflect conspecific disturbances (40) in later stages of infection lead to dramatic increases in energy expenditure and are thought to be a primary cause of emaciation (43). This pattern is described in a pathophysiological model proposed by Warnecke et al. (43). The model proposes that lesions in wing tissue, which occur in later stages of fungal infection, lead to altered blood chemistry and hematology and increased water loss, respiratory rate, and energy consumption. More recently, however, Verant et al. (41) found evidence of increased energy turnover at an earlier stage of disease, before a detectable increase in arousal frequency was observed. They proposed a model of earlier-stage disease based on these findings. Their model suggests that increased metabolic rate following initial tissue invasion, combined with reduced excretion of CO2, initiates the cascade of physiological responses observed by Warnecke et al. (15) in the final stages of WNS (16). Two key elements of both models are increased energy expenditure and disruption of osmotic homeostasis (41, 43). Although the cause of increased arousal frequency is unknown, observations of electrolyte and fluid depletion (10) led to the dehydration hypothesis (11, 46) that fluid loss across fungal lesions on the skin increases rates of water loss, resulting in increased arousal frequency and energy depletion. In healthy hibernators, ambient humidity and evaporative water loss (EWL) affect torpor bout duration (3, 38), which suggests that increased EWL due to wing damage could trigger increased arousal frequency and mortality in WNS (46). Thus, understanding the impacts of WNS on energy expenditure and water loss, as predicted by both pathophysiological models of WNS published to date, is a critical step in understanding the mechanism by which fungal infection leads to bat mortality. We conducted an experimental inoculation to test the hypothesis that WNS causes increased energy expenditure and EWL during torpor bouts, as predicted by mechanistic models of WNS (41, 43). Specifically, we predicted that bats inoculated with P. destructans would have 1) higher torpid metabolic rate (TMR) and 2) increased EWL compared with healthy controls. We also measured TMR and EWL in both dry and humidified air to assess the impact of environmental conditions on WNS pathophysiology

Body temperatures of hibernating little brown bats reveal pronounced behavioural activity during deep torpor and suggest a fever response during white-nose syndrome

Hibernating animals use torpor [reduced body temperature (T b) and metabolic rate] to reduce energy expenditure during winter. Periodic arousals to normal T b are energetically expensive, so hibernators trade off arousal benefits against energetic costs. This is especially important for bats with white-nose syndrome (WNS), a fungal disease causing increased arousal frequency. Little brown bats (Myotis lucifugus) with WNS show upregulation of endogenous pyrogens and sickness behaviour. Therefore, we hypothesized that WNS should cause a fever response characterized by elevated T b. Hibernators could also accrue some benefits of arousals with minimal T b increase, thus avoiding full arousal costs. We compared skin temperature (T sk) of captive Myotis lucifugus inoculated with the WNS-causing fungus to T sk of sham-inoculated controls. Infected bats re-warmed to higher T sk during arousals which is consistent with a fever response. Torpid T sk did not differ. During what we term “cold arousals”, bats exhibited movement following T sk increases of only 2.2 ± 0.3 °C, compared to \u3e20 °C increases during normal arousals. Cold arousals occurred in both infected and control bats, suggesting they are not a pathophysiological consequence of WNS. Fever responses are energetically costly and could exacerbate energy limitation and premature fat depletion for bats with WNS. Cold arousals could represent an energy-saving mechanism for both healthy and WNS-affected bats when complete arousals are unnecessary or too costly. A few cold arousals were observed mid-hibernation, typically in response to disturbances. Cold arousals may, therefore, represent a voluntary restriction of arousal temperature instead of loss of thermoregulatory control

Potential foraging niche release in insectivorous bat species relatively unaffected by white-nose syndrome?

White-nose syndrome (WNS) has rendered four of Ontario’s species endangered, while leaving the other four species relatively unaffected. The causes and extent of the declines have been widely studied. The influence on remaining bat species has not. Comparing acoustic data recorded ∼10 years apart, we evaluated how species in southeastern Ontario, Canada, use different foraging habitats pre- and post-WNS detection. We observed activity declines in now-endangered species over open fields (small-footed myotis, Myotis leibii (Audubon and Bachman, 1842); little brown bat, Myotis lucifugus (Le Conte, 1831); northern myotis, Myotis septentrionalis (Trouessart, 1897); tricolored bat, Perimyotis subflavus (F. Cuvier, 1832)) and speculate that the reduction of the once most common species (M. lucifugus) may have resulted in other species searching for prey in habitat once dominated by M. lucifugus. That is, these changes may have allowed greater presence in open field and clutter or edge environments by the big brown bat (Eptesicus fuscus (Palisot de Beauvois, 1796)) and three migratory species (silver-haired bat, Lasionycteris noctivagans (Le Conte, 1831); red bat, Lasiurus borealis (Müller, 1776); hoary bat, Lasiurus cinereus (Palisot de Beauvois, 1796)). However, our results also suggest that (i) while the decline of most resident bat species due to WNS may have relaxed competition for relatively unaffected species in some, but not all habitats, that (ii) sensory and biomechanical constraints may limit prey exploitation by these less-affected bat species in these habitats.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

White-nose syndrome increases torpid metabolic rate and evaporative water loss in hibernating bats

Fungal diseases of wildlife typically manifest as superficial skin infections but can have devastating consequences for host physiology and survival. White-nose syndrome (WNS) is a fungal skin disease that has killed millions of hibernating bats in North America since 2007. Infection with the fungus Pseudogymnoascus destructans causes bats to rewarm too often during hibernation, but the cause of increased arousal rates remains unknown. On the basis of data from studies of captive and free-living bats, two mechanistic models have been proposed to explain disease processes in WNS. Key predictions of both models are that WNS-affected bats will show 1) higher metabolic rates during torpor (TMR) and 2) higher rates of evaporative water loss (EWL). We collected bats from a WNS-negative hibernaculum, inoculated one group with P. destructans, and sham-inoculated a second group as controls. After 4 mo of hibernation, TMR and EWL were measured using respirometry. Both predictions were supported, and our data suggest that infected bats were more affected by variation in ambient humidity than controls. Furthermore, disease severity, as indicated by the area of the wing with UV fluorescence, was positively correlated with EWL, but not TMR. Our results provide the first direct evidence that heightened energy expenditure during torpor and higher EWL independently contribute to WNS pathophysiology, with implications for the design of potential treatments for the disease. fungal diseases of wildlife are on the rise worldwide (13). In contrast to viral and bacterial pathogens, which often lead to systemic infections, fungal pathogens of animals often manifest as superficial skin infections, especially among poikilothermic species. Although typically limited to infecting skin, fungal pathogens can lead to devastating physiological impacts and fatal disease across a range of taxa (1, 4, 5, 35, 36). A mechanistic understanding of pathogenesis in fungal diseases of wildlife is critical for understanding and predicting population-level impacts and developing safe and effective mitigation and management strategies. White-nose syndrome (WNS), caused by the fungus Pseudogymnoascus destructans, is a recently emerged disease of hibernating bats (5) (25, 42). Since its discovery in 2007, millions of bats have been killed in eastern and central North America, leading to dramatic population declines (16) and the possibility of regional extinctions (15). Recent reviews have summarized our understanding of disease mechanisms in WNS (17, 45). A number of putative virulence factors have now been identified (14, 29), and studies of both captive (42) and free-living (33) bats indicate that the disease causes increased frequency of arousals from torpor during hibernation, emaciation, and death. Infected bats also exhibit signs of altered fluid, electrolyte, and pH balance (10, 11, 26, 41, 43), leading to development of two complementary mechanistic models of WNS pathophysiology (41, 43). Symptoms of WNS develop in a progressive manner (26), and the most pronounced symptoms are only apparent relatively late in hibernation (41, 43). Increased arousal frequency and arousal cascades that may reflect conspecific disturbances (40) in later stages of infection lead to dramatic increases in energy expenditure and are thought to be a primary cause of emaciation (43). This pattern is described in a pathophysiological model proposed by Warnecke et al. (43). The model proposes that lesions in wing tissue, which occur in later stages of fungal infection, lead to altered blood chemistry and hematology and increased water loss, respiratory rate, and energy consumption. More recently, however, Verant et al. (41) found evidence of increased energy turnover at an earlier stage of disease, before a detectable increase in arousal frequency was observed. They proposed a model of earlier-stage disease based on these findings. Their model suggests that increased metabolic rate following initial tissue invasion, combined with reduced excretion of CO2, initiates the cascade of physiological responses observed by Warnecke et al. (15) in the final stages of WNS (16). Two key elements of both models are increased energy expenditure and disruption of osmotic homeostasis (41, 43). Although the cause of increased arousal frequency is unknown, observations of electrolyte and fluid depletion (10) led to the dehydration hypothesis (11, 46) that fluid loss across fungal lesions on the skin increases rates of water loss, resulting in increased arousal frequency and energy depletion. In healthy hibernators, ambient humidity and evaporative water loss (EWL) affect torpor bout duration (3, 38), which suggests that increased EWL due to wing damage could trigger increased arousal frequency and mortality in WNS (46). Thus, understanding the impacts of WNS on energy expenditure and water loss, as predicted by both pathophysiological models of WNS published to date, is a critical step in understanding the mechanism by which fungal infection leads to bat mortality. We conducted an experimental inoculation to test the hypothesis that WNS causes increased energy expenditure and EWL during torpor bouts, as predicted by mechanistic models of WNS (41, 43). Specifically, we predicted that bats inoculated with P. destructans would have 1) higher torpid metabolic rate (TMR) and 2) increased EWL compared with healthy controls. We also measured TMR and EWL in both dry and humidified air to assess the impact of environmental conditions on WNS pathophysiology