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4 result(s) for "Arrigo, Nicole C."
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A Strategy To Estimate Unknown Viral Diversity in Mammals
The majority of emerging zoonoses originate in wildlife, and many are caused by viruses. However, there are no rigorous estimates of total viral diversity (here termed “virodiversity”) for any wildlife species, despite the utility of this to future surveillance and control of emerging zoonoses. In this case study, we repeatedly sampled a mammalian wildlife host known to harbor emerging zoonotic pathogens (the Indian Flying Fox, Pteropus giganteus ) and used PCR with degenerate viral family-level primers to discover and analyze the occurrence patterns of 55 viruses from nine viral families. We then adapted statistical techniques used to estimate biodiversity in vertebrates and plants and estimated the total viral richness of these nine families in P. giganteus to be 58 viruses. Our analyses demonstrate proof-of-concept of a strategy for estimating viral richness and provide the first statistically supported estimate of the number of undiscovered viruses in a mammalian host. We used a simple extrapolation to estimate that there are a minimum of 320,000 mammalian viruses awaiting discovery within these nine families, assuming all species harbor a similar number of viruses, with minimal turnover between host species. We estimate the cost of discovering these viruses to be ~ $6.3 billion (or ~$ 1.4 billion for 85% of the total diversity), which if annualized over a 10-year study time frame would represent a small fraction of the cost of many pandemic zoonoses. IMPORTANCE Recent years have seen a dramatic increase in viral discovery efforts. However, most lack rigorous systematic design, which limits our ability to understand viral diversity and its ecological drivers and reduces their value to public health intervention. Here, we present a new framework for the discovery of novel viruses in wildlife and use it to make the first-ever estimate of the number of viruses that exist in a mammalian host. As pathogens continue to emerge from wildlife, this estimate allows us to put preliminary bounds around the potential size of the total zoonotic pool and facilitates a better understanding of where best to allocate resources for the subsequent discovery of global viral diversity. Recent years have seen a dramatic increase in viral discovery efforts. However, most lack rigorous systematic design, which limits our ability to understand viral diversity and its ecological drivers and reduces their value to public health intervention. Here, we present a new framework for the discovery of novel viruses in wildlife and use it to make the first-ever estimate of the number of viruses that exist in a mammalian host. As pathogens continue to emerge from wildlife, this estimate allows us to put preliminary bounds around the potential size of the total zoonotic pool and facilitates a better understanding of where best to allocate resources for the subsequent discovery of global viral diversity.
Long-read genome assemblies for the study of chromosome expansion: Drosophila kikkawai, Drosophila takahashii, Drosophila bipectinata, and Drosophila ananassae
Flow cytometry estimates of genome sizes among species of Drosophila show a 3-fold variation, ranging from ∼127 Mb in Drosophila mercatorum to ∼400 Mb in Drosophila cyrtoloma. However, the assembled portion of the Muller F element (orthologous to the fourth chromosome in Drosophila melanogaster) shows a nearly 14-fold variation in size, ranging from ∼1.3 Mb to >18 Mb. Here, we present chromosome-level long-read genome assemblies for 4 Drosophila species with expanded F elements ranging in size from 2.3 to 20.5 Mb. Each Muller element is present as a single scaffold in each assembly. These assemblies will enable new insights into the evolutionary causes and consequences of chromosome size expansion.
Long-read genome assemblies for the study of chromosome expansion: Drosophila kikkawai , Drosophila takahashii , Drosophila bipectinata , and Drosophila ananassae
Flow cytometry estimates of genome sizes among species of show a 3-fold variation, ranging from ∼127 Mb in to ∼400 Mb in . However, the assembled portion of the Muller F Element (orthologous to the fourth chromosome in ) shows a nearly 14-fold variation in size, ranging from ∼1.3 Mb to > 18 Mb. Here, we present chromosome-level long read genome assemblies for four species with expanded F Elements ranging in size from 2.3 Mb to 20.5 Mb. Each Muller Element is present as a single scaffold in each assembly. These assemblies will enable new insights into the evolutionary causes and consequences of chromosome size expansion.
Association Between Physical Activity and Sleep in Adults With Chronic Pain: A Momentary, Within-Person Perspective
Individuals with chronic pain consider improved sleep to be one of the most important outcomes of treatment. Physical activity has been shown to have beneficial effects on sleep in the general population. Despite these findings, the physical activity-sleep relationship has not been directly examined in a sample of people with chronic pain. This study aimed to examine the association between objective daytime physical activity and subsequent objective sleep for individuals with chronic pain while controlling for pain and psychosocial variables. An observational, prospective, within-person study design was used. A clinical sample of 50 adults with chronic pain was recruited. Participation involved completing a demographic questionnaire followed by 5 days of data collection. Over this period, participants wore a triaxial accelerometer to monitor their daytime activity and sleep. Participants also carried a handheld computer that administered a questionnaire measuring pain, mood, catastrophizing, and stress 6 times throughout the day. The results demonstrated that higher fluctuations in daytime activity significantly predicted shorter sleep duration. Furthermore, higher mean daytime activity levels and a greater number of pain sites contributed significantly to the prediction of longer periods of wakefulness at night. The small sample size used in this study limits the generalizability of the findings. Missing data may have led to overestimations or underestimations of effect sizes, and additional factors that may be associated with sleep (eg, medication usage, environmental factors) were not measured. The results of this study suggest that engagement in high-intensity activity and high fluctuations in activity are associated with poorer sleep at night; hence, activity modulation may be a key treatment strategy to address sleep complaints in individuals with chronic pain.