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Habitat compression and ecosystem shifts as potential links between marine heatwave and record whale entanglements
Climate change and increased variability and intensity of climate events, in combination with recovering protected species populations and highly capitalized fisheries, are posing new challenges for fisheries management. We examine socio-ecological features of the unprecedented 2014–2016 northeast Pacific marine heatwave to understand the potential causes for record numbers of whale entanglements in the central California Current crab fishery. We observed habitat compression of coastal upwelling, changes in availability of forage species (krill and anchovy), and shoreward distribution shift of foraging whales. We propose that these ecosystem changes, combined with recovering whale populations, contributed to the exacerbation of entanglements throughout the marine heatwave. In 2016, domoic acid contamination prompted an unprecedented delay in the opening of California’s Dungeness crab fishery that inadvertently intensified the spatial overlap between whales and crab fishery gear. We present a retroactive assessment of entanglements to demonstrate that cooperation of fishers, resource managers, and scientists could mitigate future entanglement risk by developing climate-ready fisheries approaches, while supporting thriving fishing communities.
Climate-driven extreme events may have strong local impacts on marine organisms and fisheries. Here the authors report increased whale entanglements in the northeast Pacific following a marine heatwave, and propose compression of coastal upwelling habitat as the potential driver.
Journal Article
The village that almost vanished
Samantha Archer, also known as Sam, couldn't be more excited about her class trip to Scrub Brush, the cool frontier town. But from the second they arrive at the historic village, it's clear someone's trying to make the whole town disappear.
Book
Influence of a Locomotor Training Approach on Walking Speed and Distance in People With Chronic Spinal Cord Injury: A Randomized Clinical Trial
Impaired walking limits function after spinal cord injury (SCI), but training-related improvements are possible even in people with chronic motor incomplete SCI.
The objective of this study was to compare changes in walking speed and distance associated with 4 locomotor training approaches.
This study was a single-blind, randomized clinical trial.
This study was conducted in a rehabilitation research laboratory.
Participants were people with minimal walking function due to chronic SCI.
Participants (n=74) trained 5 days per week for 12 weeks with the following approaches: treadmill-based training with manual assistance (TM), treadmill-based training with stimulation (TS), overground training with stimulation (OG), and treadmill-based training with robotic assistance (LR).
Overground walking speed and distance were the primary outcome measures.
In participants who completed the training (n=64), there were overall effects for speed (effect size index [d]=0.33) and distance (d=0.35). For speed, there were no significant between-group differences; however, distance gains were greatest with OG. Effect sizes for speed and distance were largest with OG (d=0.43 and d=0.40, respectively). Effect sizes for speed were the same for TM and TS (d=0.28); there was no effect for LR. The effect size for distance was greater with TS (d=0.16) than with TM or LR, for which there was no effect. Ten participants who improved with training were retested at least 6 months after training; walking speed at this time was slower than that at the conclusion of training but remained faster than before training.
It is unknown whether the training dosage and the emphasis on training speed were optimal. Robotic training that requires active participation would likely yield different results.
In people with chronic motor incomplete SCI, walking speed improved with both overground training and treadmill-based training; however, walking distance improved to a greater extent with overground training.
Journal Article
Coadministration of Glucagon-Like Peptide-1 During Glucagon Infusion in Humans Results in Increased Energy Expenditure and Amelioration of Hyperglycemia
Glucagon and glucagon-like peptide (GLP)-1 are the primary products of proglucagon processing from the pancreas and gut, respectively. Giving dual agonists with glucagon and GLP-1 activity to diabetic, obese mice causes enhanced weight loss and improves glucose tolerance by reduction of food intake and by increase in energy expenditure (EE). We aimed to observe the effect of a combination of glucagon and GLP-1 on resting EE and glycemia in healthy human volunteers. In a randomized, double-blinded crossover study, 10 overweight or obese volunteers without diabetes received placebo infusion, GLP-1 alone, glucagon alone, and GLP-1 plus glucagon simultaneously. Resting EE—measured using indirect calorimetry—was not affected by GLP-1 infusion but rose significantly with glucagon alone and to a similar degree with glucagon and GLP-1 together. Glucagon infusion was accompanied by a rise in plasma glucose levels, but addition of GLP-1 to glucagon rapidly reduced this excursion, due to a synergistic insulinotropic effect. The data indicate that drugs with glucagon and GLP-1 agonist activity may represent a useful treatment for type 2 diabetes and obesity. Long-term studies are required to demonstrate that this combination will reduce weight and improve glycemia in patients.
Journal Article
The teacher who forgot too much
Catalina \"Cat\" Duran and her class are off to the recycling center for what seems like the worst field trip ever. But when they arrive, they find out that the recycling plant has been sabotaged! Only Cat and her friends can save the day (and help save the Earth, too!).
Book
Monoallelic expression and epigenetic inheritance sustained by a Trypanosoma brucei variant surface glycoprotein exclusion complex
The largest gene families in eukaryotes are subject to allelic exclusion, but mechanisms underpinning single allele selection and inheritance remain unclear. Here, we describe a protein complex sustaining variant surface glycoprotein (
VSG
) allelic exclusion and antigenic variation in
Trypanosoma brucei
parasites. The
VSG-
exclusion-1 (VEX1) protein binds both telomeric
VSG
-associated chromatin and VEX2, an ortholog of nonsense-mediated-decay helicase, UPF1. VEX1 and VEX2 assemble in an RNA polymerase-I transcription-dependent manner and sustain the active, subtelomeric
VSG
-associated transcription compartment.
VSG
transcripts and VSG coats become highly heterogeneous when VEX proteins are depleted. Further, the DNA replication-associated chromatin assembly factor, CAF-1, binds to and specifically maintains VEX1 compartmentalisation following DNA replication. Thus, the VEX-complex controls
VSG
-exclusion, while CAF-1 sustains VEX-complex inheritance in association with the active-
VSG
. Notably, the VEX2-orthologue and CAF-1 in mammals are also implicated in exclusion and inheritance functions. In trypanosomes, these factors sustain a highly effective and paradigmatic immune evasion strategy.
Monoallelic expression of variant surface glycoprotein genes (
VSGs
) is essential for immune evasion by
Trypanosoma brucei
. Here, Faria
et al
. show that the VEX protein complex controls
VSG
allelic exclusion, and that CAF‐1 sustains inheritance of the VEX‐complex in association with the active
VSG
.
Journal Article