Impacts of Man-Made Structures on Avian Community Metrics in 4 State Parks in Northwestern Arkansas

Avian community metrics often differ between areas with no human disturbance and areas with high levels of human disturbance. However, the relationships between avian community metrics and smaller-scale disturbances are not as clear. Our goal was to investigate if avian abundance, richness, evenness, and diversity differed in areas with and without small-scale human developments. We used fixed-radius 50-m avian point counts to compare points which contained a man-made structure (n = 47), such as a picnic area, road, or campsite to those that did not contain a man-made structure (n = 181) at 4 state parks in Arkansas during 18 May – 7 August 2015. We used paired t-tests to compare points at the park scale and one-way ANOVAs or Kruskal-Wallis tests to investigate differences among the hiking and biking trails within parks. At the park scale, avian abundance (t₃ = -1.44, P = 0.246), richness (t₃ = ˗0.86, P = 0.453), diversity (t₃= 2.02, P = 0.137), and evenness (t₃ =˗0.37, P = 0.733) did not differ between points containing man-made structures and points without man-made structures. Species richness (F1,11 = 5.03, P= 0.047) and diversity (X^2₁ = 4.20, P = 0.040) were higher at points with man-made structures (Simpson’s D mean = 0.13 ± 0.01SE; S mean = 8.99 ± 0.70SE) at Pinnacle Mountain than points without man-made structures (Simpson’s D mean = 0.18 ± 0.03SE; S mean = 7.17 ± 0.47SE); abundance (F₁, ₁₁ = 1.43, P =0.257) and evenness (F₁, ₁₁ = 0.16, P = 0.695) did not differ among points. Within the 3 remaining parks, abundance (F₁,7-9 = 0.11 – 2.59, P = 0.152 – 0.748), richness (χ^2 ₁ = 0.300 – 1.68, P = 0.195 – 0.584), diversity (χ2 = 0.300 – 1.05, P = 0.305 – 0.584; F₁,7 =1.82, P = 0.219) and evenness (F₁,7-9 = 0.35 – 4.28, P =0.077 – 0.570) did not differ between points with and without man-made structures. Given the results of our analyses both at the park scale and within parks, it appears that small-scale man-made disturbances may have limited or no impact on avian community metrics

Geophysics

Contains reports on three research projects

Scalar on time-by-distribution regression and its application for modelling associations between daily-living physical activity and cognitive functions in Alzheimer's Disease

Wearable data is a rich source of information that can provide deeper understanding of links between human behaviours and human health. Existing modelling approaches use wearable data summarized at subject level via scalar summaries using regression techniques, temporal (time-of-day) curves using functional data analysis (FDA), and distributions using distributional data analysis (DDA). We propose to capture temporally local distributional information in wearable data using subject-specific time-by-distribution (TD) data objects. Specifically, we propose scalar on time-by-distribution regression (SOTDR) to model associations between scalar response of interest such as health outcomes or disease status and TD predictors. We show that TD data objects can be parsimoniously represented via a collection of time-varying L-moments that capture distributional changes over the time-of-day. The proposed method is applied to the accelerometry study of mild Alzheimer's disease (AD). Mild AD is found to be significantly associated with reduced maximal level of physical activity, particularly during morning hours. It is also demonstrated that TD predictors attain much stronger associations with clinical cognitive scales of attention, verbal memory, and executive function when compared to predictors summarized via scalar total activity counts, temporal functional curves, and quantile functions. Taken together, the present results suggest that the SOTDR analysis provides novel insights into cognitive function and AD

Geophysics

Contains research objectives and reports on three research projects

LC3 and STRAP regulate actin filament assembly by JMY during autophagosome formation.

During autophagy, actin filament networks move and remodel cellular membranes to form autophagosomes that enclose and metabolize cytoplasmic contents. Two actin regulators, WHAMM and JMY, participate in autophagosome formation, but the signals linking autophagy to actin assembly are poorly understood. We show that, in nonstarved cells, cytoplasmic JMY colocalizes with STRAP, a regulator of JMY's nuclear functions, on nonmotile vesicles with no associated actin networks. Upon starvation, JMY shifts to motile, LC3-containing membranes that move on actin comet tails. LC3 enhances JMY's de novo actin nucleation activity via a cryptic actin-binding sequence near JMY's N terminus, and STRAP inhibits JMY's ability to nucleate actin and activate the Arp2/3 complex. Cytoplasmic STRAP negatively regulates autophagy. Finally, we use purified proteins to reconstitute LC3- and JMY-dependent actin network formation on membranes and inhibition of network formation by STRAP. We conclude that LC3 and STRAP regulate JMY's actin assembly activities in trans during autophagy

The position of graptolites within Lower Palaeozoic planktic ecosystems.

An integrated approach has been used to assess the palaeoecology of graptolites both as a discrete group and also as a part of the biota present within Ordovician and Silurian planktic realms. Study of the functional morphology of graptolites and comparisons with recent ecological analogues demonstrates that graptolites most probably filled a variety of niches as primary consumers, with modes of life related to the colony morphotype. Graptolite coloniality was extremely ordered, lacking any close morphological analogues in Recent faunas. To obtain maximum functional efficiency, graptolites would have needed varying degrees of coordinated automobility. A change in lifestyle related to ontogenetic changes was prevalent within many graptolite groups. Differing lifestyle was reflected by differing reproductive strategies, with synrhabdosomes most likely being a method for rapid asexual reproduction. Direct evidence in the form of graptolithophage 'coprolitic' bodies, as well as indirect evidence in the form of probable defensive adaptations, indicate that graptolites comprised a food item for a variety of predators. Graptolites were also hosts to a variety of parasitic organisms and provided an important nutrient source for scavenging organisms

Chronic exposure to low dose of bisphenol A impacts on the first round of spermatogenesis via SIRT1 modulation.

Spermatogenesis depends on endocrine, autocrine and paracrine communications along the hypothalamus-pituitary-gonad axis. Bisphenol A (BPA), an estrogen-mimic endocrine disrupting chemical, is an environmental contaminant used to manufacture polycarbonate plastics and epoxy resins with toxic effects for male reproduction. Here we investigated whether the chronic exposure to low BPA doses affects spermatogenesis through the modulation of SIRT1, a NAD+-dependent deacetylase involved in the progression of spermatogenesis, with outcomes on apoptosis, oxidative stress, metabolism and energy homeostasis. BPA exposure via placenta first, and lactation and drinking water later, affected the body weight gain in male offspring at 45 postnatal days and the first round of spermatogenesis, with impairment of blood testis barrier, reactive oxygen species production, DNA damage and decreased expression of SIRT1. The analysis of SIRT1 downstream molecular pathways revealed the increase of acetyl-p53Lys370, γH2AX foci, the decrease of oxidative stress defenses and the higher apoptotic rate in the testis of treated animals, with partial rescue at sex maturation. In conclusion, SIRT1 pathways disruption after BPA exposure can have serious consequences on the first round of spermatogenesis

Bedtime habits in adults with and without type 2 diabetes

This study aimed to identify determinants of objectively-estimated bedtime habits and to determine if these bedtime habits differed between adults with and without type 2 diabetes. Adults with accelerometry data from the National Health and Nutrition Examination Survey 2003-2004 and 2005-2006 cohorts were classified as having no diabetes or type 2 diabetes and matched for age, gender, and BMI across the two groups. Multivariate linear regression models assessed bedtime habits (time-in-bed, early versus late bedtime periods, regularity), chronotype (mid-points), and type 2 diabetes status. While the results indicated no differences in bedtime habits between adults with and without type 2 diabetes, an interesting finding was the support for an association between objectively-estimated earlier bedtime midpoints and greater physical activity

Expression of SMARCD1 interacts with age in association with asthma control on inhaled corticosteroid therapy.

BackgroundGlobal gene expression levels are known to be highly dependent upon gross demographic features including age, yet identification of age-related genomic indicators has yet to be comprehensively undertaken in a disease and treatment-specific context.MethodsWe used gene expression data from CD4+ lymphocytes in the Asthma BioRepository for Integrative Genomic Exploration (Asthma BRIDGE), an open-access collection of subjects participating in genetic studies of asthma with available gene expression data. Replication population participants were Puerto Rico islanders recruited as part of the ongoing Genes environments & Admixture in Latino Americans (GALA II), who provided nasal brushings for transcript sequencing. The main outcome measure was chronic asthma control as derived by questionnaires. Genomic associations were performed using regression of chronic asthma control score on gene expression with age in years as a covariate, including a multiplicative interaction term for gene expression times age.ResultsThe SMARCD1 gene (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily D member 1) interacted with age to influence chronic asthma control on inhaled corticosteroids, with a doubling of expression leading to an increase of 1.3 units of chronic asthma control per year (95% CI [0.86, 1.74], p = 6 × 10- 9), suggesting worsening asthma control with increasing age. This result replicated in GALA II (p = 3.8 × 10- 8). Cellular assays confirmed the role of SMARCD1 in glucocorticoid response in airway epithelial cells.ConclusionFocusing on age-dependent factors may help identify novel indicators of asthma medication response. Age appears to modulate the effect of SMARCD1 on asthma control with inhaled corticosteroids

FTO and MC4R Gene Variants Are Associated with Obesity in Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is the leading cause of anovulatory infertility in women. It is also associated with metabolic disturbances that place women at increased risk for obesity and type 2 diabetes. There is strong evidence for familial clustering of PCOS and a genetic predisposition. However, the gene(s) responsible for the PCOS phenotypes have not been elucidated. This two-phase family-based and case-control genetic study was designed to address the question of whether SNPs identified as susceptibility loci for obesity in genome-wide association studies (GWAS) are also associated with PCOS and elevated BMI. Members of 439 families having at least one offspring with PCOS were genotyped for 15 SNPs previously shown to be associated with obesity. Linkage and association with PCOS was assessed using the transmission/disequilibrium test (TDT). These SNPs were also analyzed in an independent case-control study involving 395 women with PCOS and 176 healthy women with regular menstrual cycles. Only one of these 15 SNPs (rs2815752 in NEGR1) was found to have a nominally significant association with PCOS (χ2 = 6.11, P = 0.013), but this association failed to replicate in the case-control study. While not associated with PCOS itself, five SNPs in FTO and two in MC4R were associated with BMI as assessed with a quantitative-TDT analysis, several of which replicated association with BMI in the case-control cohort. These findings demonstrate that certain SNPs associated with obesity contribute to elevated BMI in PCOS, but do not appear to play a major role in PCOS per se. These findings support the notion that PCOS phenotypes are a consequence of an oligogenic/polygenic mechanism