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ABSTRACT Rural shellfish harvesters, including many Alaska Native peoples, require safe access to wild shellfish for subsistence, food security, and cultural practices. However, wild shellfish may be contaminated with paralytic shellfish toxins, leaving harvesters with increased risks of significant illness or death. To manage these risks, the Sitka Tribe of Alaska Environmental Research Lab (STAERL) was established to test shellfish samples sent in by harvesters in the community and to support regular monitoring of select local beaches by tribal governments. Here, we investigated harvester utilization of this shellfish testing service from 2016-2024, comprising 299 samples sent in by local harvesters, and used generalized linear models to examine how annual testing rates varied by year, location, species, and species-based detoxification rates. We pay particular attention to differences that may reflect the influence of risk perceptions and accessibility of harvesting and testing on utilization (DOI: 10.5061/dryad.dfn2z35dr). We find that testing utilization has increased through time (1.278, 95% CI: 1.161, 1.407), testing rates are highest in spring and broadly similar between the other three seasons, testing rates in Sitka are much higher than those outside of it, and neither road accessibility nor species-based detoxification rates strongly affect testing rate ratios. These findings suggest that shellfish testing behavior is consistent despite seasonal variations in risk and convenience, but that the STAERL individual testing program provides a pathway to maintain established subsistence harvest practices while reducing poisoning risks. 

Harmful algal blooms (HABs) are a reoccurring threat to subsistence and recreational shellfish harvest in Southeast Alaska. Recent Tribally led monitoring programs have enhanced understanding of the environmental drivers and toxicokinetics of shellfish toxins in the region; however, there is considerable variability in shellfish toxins in some species, which cannot be easily explained by seasonal bloom dynamics. Persistent concentrations of paralytic shellfish toxins (PSTs) in homogenized butter clam samples (n > 6, Saxidomus gigantea) have been observed in several communities, and relatively large spikes in concentrations are sometimes seen without Alexandrium observations or increased toxin concentrations in other species. In order to investigate potential sources of variability in PST concentrations from this subsistence species, we assessed individual concentrations of PSTs across a size gradient of butter clams during a period of relatively stable PST concentrations. We found that increasing concentrations of PSTs were significantly associated with larger clams using a log-linear model. We then simulated six clams randomly sampled from three size distributions, and we determined large clams had an outsized probability of contributing a significant proportion of the total toxicity in a six-clam homogenized sample. While our results were obtained during a period of low HAB activity and cannot be extrapolated to periods of intoxication or rapid detoxification, they have significant ramifications for both monitoring programs as well as subsistence and recreational harvesters. 

OBJECTIVETo characterize high type 1 diabetes (T1D) genetic risk in a population where type 2 diabetes (T2D) predominates. RESEARCH DESIGN AND METHODSCharacteristics typically associated with T1D were assessed in 109,594 Million Veteran Program participants with adult-onset diabetes, 2011–2021, who had T1D genetic risk scores (GRS) defined as low (0 to <45%), medium (45 to <90%), high (90 to <95%), or highest (≥95%). RESULTST1D characteristics increased progressively with higher genetic risk (P < 0.001 for trend). A GRS ≥ 90% was more common with diabetes diagnoses before age 40 years, but 95% of those participants were diagnosed at age ≥40 years, and they resembled T2D in mean age (64.3 years) and BMI (32.3 kg/m2). Compared with the low risk group, the highest-risk group was more likely to have diabetic ketoacidosis (low 0.9% vs. highest GRS 3.7%), hypoglycemia prompting emergency visits (3.7% vs. 5.8%), outpatient plasma glucose <50 mg/dL (7.5% vs. 13.4%), a shorter median time to start insulin (3.5 vs. 1.4 years), use of a T1D diagnostic code (16.3% vs. 28.1%), low C-peptide levels if tested (1.8% vs. 32.4%), and glutamic acid decarboxylase antibodies (6.9% vs. 45.2%), all P < 0.001. CONCLUSIONSCharacteristics associated with T1D were increased with higher genetic risk, and especially with the top 10% of risk. However, the age and BMI of those participants resemble people with T2D, and a substantial proportion did not have diagnostic testing or use of T1D diagnostic codes. T1D genetic screening could be used to aid identification of adult-onset T1D in settings in which T2D predominates.