Automated identification system for ships data as a proxy for marine vessel related stressors.

An increasing number of marine conservation initiatives rely on data from Automatic Identification System (AIS) to inform marine vessel traffic associated impact assessments and mitigation policy. However, a considerable proportion of vessel traffic is not captured by AIS in many regions of the world. Here we introduce two complementary techniques for collecting traffic data in the Canadian Salish Sea that rely on optical imagery. Vessel data pulled from imagery captured using a shore-based autonomous camera system ("Photobot") were used for temporal analyses, and data from imagery collected by the National Aerial Surveillance Program (NASP) were used for spatial analyses. The photobot imagery captured vessel passages through Boundary Pass every minute (Jan-Dec 2017), and NASP data collection occurred opportunistically across most of the Canadian Salish Sea (2017-2018). Based on photobot imagery data, we found that up to 72 % of total vessel passages through Boundary Pass were not broadcasting AIS, and in some vessel categories this proportion was much higher (i.e., 96 %). We fit negative binomial General Linearized Models to our photobot data and found a strong seasonal variation in non-AIS, and a weekend/weekday component that also varied by season (interaction term p < 0.0001). Non-AIS traffic was much higher during the summer (Apr-Sep) and during the weekend (Sat-Sun), reflecting patterns in recreational vessel traffic not obligated to broadcast AIS. Negative binomial General Additive Models based on the NASP data revealed strong spatial associations with distance from shore (up to 10 km) and non-AIS vessel traffic for both summer and winter seasons. There were also associations between non-AIS vessels and marina and anchorage densities, particularly during the winter, which again reflect seasonal recreational vessel traffic patterns. Overall, our GAMs explained 20-37 % of all vessel traffic during the summer and winter, and highlighted subregions where vessel traffic is under represented by AIS.

Normal Growth and Essential Fatty Acid Status in Children With Intestinal Failure on Lipid Limitation.

OBJECTIVES: Lipid limitation, that is, ≤1 g · kg⁻¹ · day⁻¹ of soy oil lipid emulsion (SOLE), has been suggested as a method to reduce the risk of intestinal failure (IF)-associated liver disease (IFALD). There are limited data as to the effects of this strategy on growth and essential fatty acid (EFA) status. The aim of the study was to assess growth, prevalence of cholestasis, and EFA deficiency in patients with IF who were provided daily SOLE at a dose ≤1 g · kg⁻¹ · day⁻¹. METHODS: Medical records were retrospectively reviewed from 9 patients age 16 months to 8 years who had IF requiring parenteral nutrition support for >12 months. Parenteral nutrition supplied a mean of 53% of total energy (range 24%-86%). RESULTS: Mean SOLE dose was 0.61 g · kg⁻¹ · day⁻¹ (range 0.4-0.81 g · kg⁻¹ · day⁻¹). After 1 month of lipid limitation between 2011 and 2014, no patient developed IFALD as defined by a direct bilirubin >2 mg/dL. The median direct bilirubin was 0.1 mg/dL (range 0.075-0.85 mg/dL). No patient developed EFA deficiency as defined by a triene-to-tetraene ratio >0.2 (median 0.026, range 0.017-0.076). Height z scores increased from mean of -2.568 (range -10.8 to 0.878) to -0.484 (range -3.546 to 0.822). Weight z scores increased from mean of -1.412 (range -5.871 to 0.906) to -0.595 (range -2.178 to 0.926). CONCLUSIONS: In this case series, lipid limitation allowed normal growth while preventing the development of cholestasis and EFA deficiency.

The effect of three inhaled anesthetics in mice harboring mutations in the GluR6 (kainate) receptor gene.

Combinations of GluR5-GluR7, KA1, and KA2 subunits form kainate receptors, a subtype of excitatory ionotropic glutamate receptors. Isoflurane enhances the action of kainate receptors comprising GluR6 subunits expressed in oocytes. To test whether alterations of the GluR6 subunit gene affect the actions of inhaled anesthetics in vivo, we measured the minimum alveolar concentration of desflurane, isoflurane, and halothane in mice lacking the kainate receptor subunit GluR6 (GluR6 knockout mice) and mice with a dominant negative glutamine/arginine (Q/R) editing mutation in membrane domain 2 of the GluR6 receptor (GluR6 editing mutants), which increases the calcium permeability of kainate receptors containing GluR6Q. We also measured the capacity of isoflurane to interfere with Pavlovian fear conditioning to a tone and to context. Absence of the GluR6 subunit did not change the minimum alveolar concentration of isoflurane, desflurane, or halothane. Possibly, kainate receptors assembled from the remaining kainate receptor subunits compensate for the absent subunits and thereby produce a normal minimum alveolar concentration. A Q/R mutation that dominantly affects kainate receptors containing the GluR6 subunit in mice increased isoflurane minimum alveolar concentration (by 12%; P < 0.01), decreased desflurane minimum alveolar concentration (by 18%; P < 0.001), and did not change halothane minimum alveolar concentration (P = 0.25). These data may indicate that kainate receptors containing GluR6Q subunits differently modulate, directly or indirectly, the mechanism by which inhaled anesthetics cause immobility. The mutations of GluR6 that were studied did not affect the capacity of isoflurane to interfere with fear conditioning.

Effects of isoflurane on gamma-aminobutyric acid type A receptors activated by full and partial agonists.

BACKGROUND: Volatile anesthetics prolong inhibitory postsynaptic potentials in central neurons an allosteric action on the gamma-aminobutyric acid type A (GABA(A)) receptor, an effect that may underlie the hypnotic actions of these agents. Inhaled anesthetics such as isoflurane act to enhance responses to submaximal concentrations of GABA, but it is not clear whether their effect is mediated by an increase in the binding of the agonist or by changes in receptor gating behavior. To address this question, the authors studied the effects of isoflurane on a mutant GABA(A) receptor with a gating defect that decreases receptor sensitivity by lowering agonist efficacy. They then compared the effects of clinically relevant concentrations of isoflurane on the actions of GABA and piperidine-4-sulfonic acid (P4S), a partial agonist at the GABA(A) receptor. METHODS: The authors created a mutant of the GABA receptor alpha subunit (L277A) by site-directed mutagenesis. The mutant subunit was coexpressed with beta(2) and gamma(2S) subunits in HEK293 cells, and responses to GABA and P4S were recorded using the whole-cell patch clamp technique. EC values were determined for the full agonist GABA and the partial agonist P4S. The authors also determined the relative efficacy (epsilon) of P4S. These measurements were then repeated in the presence of isoflurane. RESULTS: The concentration-response curve for GABA was shifted to the right (EC(50) = 278 microm) in the alpha(1)(L277A)beta(2)gamma(2S) mutant receptor, compared with the corresponding wild-type alpha(1)beta(2)gamma(2S) GABA(A) receptor (EC(50) = 16 microm). P4S is a partial agonist at both receptors, with a dramatically decreased relative efficacy at the mutant receptor (epsilon = 0.24). When the mutant receptor was studied in the presence of isoflurane, the concentration-response curves for both GABA and P4S were shifted to the left (EC(50) for GABA = 78 microm); the efficacy of P4S also increased significantly (epsilon = 0.40). CONCLUSION: By studying a mutant GABA receptor with impaired gating, the authors were able to demonstrate clearly that isoflurane can increase the efficacy of a partial agonist, as well as increase agonist potency. These data suggest that the volatile anesthetic isoflurane exerts at least some of its effects on the GABA(A) receptor via alterations in gating rather than simply changing binding or unbinding of the agonist.