Influence of Manatees' Diving on Their Risk of Collision with Watercraft

Watercraft pose a threat to endangered Florida manatees (Trichechus manatus latirostris). Mortality from watercraft collisions has adversely impacted the manatee population’s growth rate, therefore reducing this threat is an important management goal. To assess factors that contribute to the risk of watercraft strikes to manatees, we studied the diving behavior of nine manatees carrying GPS tags and time–depth recorders in Tampa Bay, Florida, during winters 2002–2006. We applied a Bayesian formulation of generalized linear mixed models to depth data to model the probability (P_t) that manatees would be no deeper than 1.25 m from the water’s surface as a function of behavioral and habitat covariates. Manatees above this threshold were considered to be within striking depth of a watercraft. Seventy-eight percent of depth records (individual range 62–86%) were within striking depth (mean = 1.09 m, max = 16.20 m), illustrating how vulnerable manatees are to strikes. In some circumstances manatees made consecutive dives to the bottom while traveling, even in areas >14 m, possibly to conserve energy. This is the first documentation of potential cost-efficient diving behavior in manatees. Manatees were at higher risk of being within striking depth in shallow water (<0.91 m), over seagrass, at night, and while stationary or moving slowly; they were less likely to be within striking depth when ≤50 m from a charted waterway. In shallow water the probability of a manatee being within striking depth was 0.96 (CI = 0.93–0.98) and decreased as water depth increased. The probability was greater over seagrass (P_t = 0.96, CI = 0.93–0.98) than over other substrates (P_t = 0.73, CI = 0.58–0.84). Quantitative approaches to assessing risk can improve the effectiveness of manatee conservation measures by helping identify areas for protection.     

Muscle Logic: New Knowledge Resource for Anatomy Enables Comprehensive Searches of the Literature on the Feeding Muscles of Mammals

Background

In recent years large bibliographic databases have made much of the published literature of biology available for searches. However, the capabilities of the search engines integrated into these databases for text-based bibliographic searches are limited. To enable searches that deliver the results expected by comparative anatomists, an underlying logical structure known as an ontology is required.

Development and Testing of the Ontology

Here we present the Mammalian Feeding Muscle Ontology (MFMO), a multi-species ontology focused on anatomical structures that participate in feeding and other oral/pharyngeal behaviors. A unique feature of the MFMO is that a simple, computable, definition of each muscle, which includes its attachments and innervation, is true across mammals. This construction mirrors the logical foundation of comparative anatomy and permits searches using language familiar to biologists. Further, it provides a template for muscles that will be useful in extending any anatomy ontology. The MFMO is developed to support the Feeding Experiments End-User Database Project (FEED, https://feedexp.org/), a publicly-available, online repository for physiological data collected from in vivo studies of feeding (e.g., mastication, biting, swallowing) in mammals. Currently the MFMO is integrated into FEED and also into two literature-specific implementations of Textpresso, a text-mining system that facilitates powerful searches of a corpus of scientific publications. We evaluate the MFMO by asking questions that test the ability of the ontology to return appropriate answers (competency questions). We compare the results of queries of the MFMO to results from similar searches in PubMed and Google Scholar.

Results and Significance

Our tests demonstrate that the MFMO is competent to answer queries formed in the common language of comparative anatomy, but PubMed and Google Scholar are not. Overall, our results show that by incorporating anatomical ontologies into searches, an expanded and anatomically comprehensive set of results can be obtained. The broader scientific and publishing communities should consider taking up the challenge of semantically enabled search capabilities.     

Tree diversity,tree height and environmental harshness in eastern and western North America

Does variation in environmental harshness explain local and regional species diversity gradients? We hypothesise that for a given life form like trees, greater harshness leads to a smaller range of traits that are viable and thereby also to lower species diversity. On the basis of a strong dependence of maximum tree height on site productivity and other measures of site quality, we propose maximum tree height as an inverse measure of environmental harshness for trees. Our results show that tree species richness is strongly positively correlated with maximum tree height across multiple spatial scales in forests of both eastern and western North America. Maximum tree height co‐varied with species richness along gradients from benign to harsh environmental conditions, which supports the hypothesis that harshness may be a general mechanism limiting local diversity and explaining diversity gradients within a biogeographic region.     

Circulating ceramides are inversely associated with cardiorespiratory fitness in participants aged 54–96 years from the Baltimore Longitudinal Study of Aging

Cardiorespiratory fitness (VO₂ peak) declines with age and is an independent risk factor for morbidity and mortality in older adults. Identifying biomarkers of low fitness may provide insight for why some individuals experience an accelerated decline of aerobic capacity and may serve as clinically valuable prognostic indicators of cardiovascular health. We investigated the relationship between circulating ceramides and VO₂ peak in 443 men and women (mean age of 69) enrolled in the Baltimore Longitudinal Study of Aging (BLSA). Individual species of ceramide were quantified by HPLC–tandem mass spectrometry. VO₂ peak was measured by a graded treadmill test. We applied multiple regression models to test the associations between ceramide species and VO₂ peak, while adjusting for age, sex, blood pressure, serum LDL, HDL, triglycerides, and other covariates. We found that higher levels of circulating C18:0, C20:0, C24:1 ceramides and C20:0 dihydroceramides were strongly associated with lower aerobic capacity (P < 0.001, P < 0.001, P = 0.018, and P < 0.001, respectively). The associations held true for both sexes (with men having a stronger association than women, P value for sex interaction <0.05) and were unchanged after adjusting for confounders and multiple comparison correction. Interestingly, no significant association was found for C16:0, C22:0, C24:0, C26:0, and C22:1 ceramide species, C24:0 dihydroceramide, or total ceramides. Our analysis reveals that specific long‐chain ceramides strongly associate with low cardiovascular fitness in older adults and may be implicated in the pathogenesis of low fitness with aging. Longitudinal studies are needed to further validate these associations and investigate the relationship between ceramides and health outcomes.     

Blimp-1-Dependent IL-10 Production by Tr1 Cells Regulates TNF-Mediated Tissue Pathology

Tumor necrosis factor (TNF) is critical for controlling many intracellular infections, but can also contribute to inflammation. It can promote the destruction of important cell populations and trigger dramatic tissue remodeling following establishment of chronic disease. Therefore, a better understanding of TNF regulation is needed to allow pathogen control without causing or exacerbating disease. IL-10 is an important regulatory cytokine with broad activities, including the suppression of inflammation. IL-10 is produced by different immune cells; however, its regulation and function appears to be cell-specific and context-dependent. Recently, IL-10 produced by Th1 (Tr1) cells was shown to protect host tissues from inflammation induced following infection. Here, we identify a novel pathway of TNF regulation by IL-10 from Tr1 cells during parasitic infection. We report elevated Blimp-1 mRNA levels in CD4⁺ T cells from visceral leishmaniasis (VL) patients, and demonstrate IL-12 was essential for Blimp-1 expression and Tr1 cell development in experimental VL. Critically, we show Blimp-1-dependent IL-10 production by Tr1 cells prevents tissue damage caused by IFNγ-dependent TNF production. Therefore, we identify Blimp-1-dependent IL-10 produced by Tr1 cells as a key regulator of TNF-mediated pathology and identify Tr1 cells as potential therapeutic tools to control inflammation.     

Scavenging of extracellular H2O2 by catalase inhibits the proliferation of HER-2/Neu-transformed rat-1 fibroblasts through the induction of a stress response

High levels of reactive oxygen species (ROS) are associated with cytotoxicity. Alternatively, nontoxic levels of ROS like hydrogen peroxide (H(2)O(2)) can mediate the transmission of many intracellular signals, including those involved in growth and transformation. To identify pathways downstream of endogenous cellular H(2)O(2) production, the response of Rat-1 fibroblasts exhibiting differential HER-2/Neu receptor tyrosine kinase activity to removal of physiological H(2)O(2) concentrations was investigated. The proliferation of all cells was abolished by addition of the H(2)O(2) scavenger catalase to the culture medium. HER-2/Neu activity was not significantly affected by catalase treatment, suggesting that the target(s) of the H(2)O(2) signal lie downstream of the receptor in our model. ERK1/2 phosphorylation was blocked by catalase in fibroblasts expressing wild type Neu, however such a response did not occur in cells possessing activated mutant Neu. This indicates that the ERK1/2 response contributes little to the growth inhibition observed. By contrast, JNK1 activity increased following the addition of catalase or H(2)O(2), regardless of Neu activity or level of cell transformation. Phosphorylation of p38 MAPK was induced by H(2)O(2) but not by catalase. These observations suggest that scavenging of H(2)O(2) from the cellular environment blocks Rat-1 proliferation primarily through the activation of stress pathways.