Cognitive functioning was assessed in diabetic patients during hypoglycemia (60 mg/dl), euglycemia/control (110 mg/dl), and hyperglycemia (300 mg/dl). Blood glucose levels were set and maintained to within 4% of targeted levels by an artificial insulin/glucose infusion system (Biostator). Attention and fine motor skills, assessed by visual reaction time, was slowed at altered glucose levels. Performance was less impaired during hyperglycemia than hypoglycemia when a longer interstimulus interval was used, although it was still slower than normal. The time required to solve simple addition problems was increased during hypoglycemia, although reading comprehension was not affected. The possibility that some automatic brain skills are disrupted at altered glucose concentrations is discussed, while associative or inferential skills may be less affected.

Over the last two years (2008-2010) we performed a monitoring project to update the Spanish freshwater fish fauna. We have collected in 785 sampling localities homogeneously distributed throughout Spain each year. We find as the most important result of this study the occurrence of several species that constitute new records for some rivers or basins in Spain: Lampetra planeri, Petromyzon marinus, Barbus haasi, Iberochondrostoma lemmingii, Squalius alburnoides, Squalius carolitertii, Squalius malacitanus, Cobitis calderoni, Cobitis paludica, and Salaria fluviatilis. Finally we corroborate the existence of Barbatula barbatula in the Duero basin and the assignation of the northeastern populations of this genus to B. quignardi.

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Naltrexone is an approved drug for management of alcohol use disorder (AUD), but data in patients with liver disease (LD) are limited. We aimed to evaluate the safety of naltrexone in those with LD. This is a retrospective cohort of adults with and without LD who were prescribed naltrexone for AUD from 2015 to 2019 in a safety‐net setting. Naltrexone hepatic safety was determined by liver enzyme changes during and after compared to before naltrexone prescription as well as rates of subsequent hospitalization and death by Kaplan‐Meier methods. Factors associated with hospitalization were examined by Cox regression. Of 160 patients prescribed naltrexone for AUD, 100 (63%) had LD and 47 (47%) of those with LD had cirrhosis (47% decompensated). The total cohort, LD, and cirrhosis groups had lower adjusted mean aspartate aminotransferase and alanine aminotransferase levels after versus before naltrexone prescription (p < 0.001). Two‐year survival was 97.7% (95% confidence interval [CI], 84.6–99.7), 95.4% (95% CI, 82.8–98.8), 90.8% (95% CI, 73.5–97.0), and 81.3% (95% CI, 41.2–93.8) in those without LD, LD without cirrhosis, cirrhosis, and decompensated cirrhosis groups (p = 0.46), respectively. Alcohol‐related 2‐year hospitalization rates were 8.2% (95% CI, 2.7–24), 27.7% (95% CI, 16.6–44.0), 40.5% (95% CI, 24.8–61.6), and 41.7% (95% CI, 23.3–66.6) for the groups without LD, LD without cirrhosis, cirrhosis, and decompensated cirrhosis (p = 0.007), respectively. Independent predictors of subsequent hospitalization were LD, (hazard ratio [HR], 3.70; 95% CI, 1.19–11.51; p = 0.02), cirrhosis (HR, 5.16; 95% CI, 1.69–15.75), and shorter duration (≤30 days) of naltrexone prescription (HR, 2.50; 95% CI, 1.l2–5.20; p = 0.01). Conclusion: Naltrexone is safe to use in patients with underlying LD, including those with compensated cirrhosis. Although encouraging, more safety data are needed for those with decompensated cirrhosis.

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