The Role of Semantic Clustering in Optimal Memory Foraging.

Recent studies of semantic memory have investigated two theories of optimal search adopted from the animal foraging literature: Lévy flights and marginal value theorem. Each theory makes different simplifying assumptions and addresses different findings in search behaviors. In this study, an experiment is conducted to test whether clustering in semantic memory may play a role in evidence for both theories. Labeled magnets and a whiteboard were used to elicit spatial representations of semantic knowledge about animals. Category recall sequences from a separate experiment were used to trace search paths over the spatial representations of animal knowledge. Results showed that spatial distances between animal names arranged on the whiteboard were correlated with inter-response intervals (IRIs) during category recall, and distributions of both dependent measures approximated inverse power laws associated with Lévy flights. In addition, IRIs were relatively shorter when paths first entered animal clusters, and longer when they exited clusters, which is consistent with marginal value theorem. In conclusion, area-restricted searches over clustered semantic spaces may account for two different patterns of results interpreted as supporting two different theories of optimal memory foraging.

Angiotensin receptor blockade recovers hepatic UCP2 expression and aconitase and SDH activities and ameliorates hepatic oxidative damage in insulin resistant rats.

Metabolic syndrome (MetS) is commonly associated with elevated renin-angiotensin system, oxidative stress, and steatohepatitis with down-regulation of uncoupling proteins (UCPs). However, the mechanisms linking renin-angiotensin system, steatosis, and UCP2 to hepatic oxidative damage during insulin resistance are not described. To test the hypothesis that angiotensin receptor activation contributes to decreased hepatic UCP2 expression and aconitase activity and to increased oxidative damage after increased glucose intake in a model of MetS, lean and obese Long Evans rats (n = 10/group) were randomly assigned to the following groups: 1) untreated Long Evans Tokushima Otsuka (lean, strain control), 2) untreated Otsuka Long Evans Tokushima Fatty (OLETF) (MetS model), 3) OLETF + angiotensin receptor blocker (ARB) (10 mg olmesartan/kg·d × 6 wk), 4) OLETF + high glucose (HG) (5% in drinking water × 6 wk), and 5) OLETF + ARB + HG (ARB/HG × 6 wk). HG increased body mass (37%), plasma triglycerides (TGs) (35%), plasma glycerol (87%), plasma free fatty acids (28%), and hepatic nitrotyrosine (74%). ARB treatment in HG decreased body mass (12%), plasma TG (15%), plasma glycerol (23%), plasma free fatty acids (14%), and hepatic TG content (42%), suggesting that angiotensin receptor type 1 (AT1) activation and increased adiposity contribute to the development of obesity-related dyslipidemia. ARB in HG also decreased hepatic nitrotyrosine and increased hepatic UCP2 expression (59%) and aconitase activity (40%), as well as antioxidant enzyme activities (50-120%), suggesting that AT1 activation also contributes to protein oxidation, impaired lipid metabolism, and antioxidant metabolism in the liver. Thus, in addition to promoting obesity-related hypertension, AT1 activation may also impair lipid metabolism and antioxidant capacity, resulting in steatosis via decreased UCP2 and tricarboxylic acid cycle activity.