Biomedical subjects

Richard L Lewis

Publications and source records attributed to Richard L Lewis.

4 recordsLinked to original sources

PubMed2006

Computational principles of working memory in sentence comprehension.

Understanding a sentence requires a working memory of the partial products of comprehension, so that linguistic relations between temporally distal parts of the sentence can be rapidly computed. We describe an emerging theoretical framework for this working memory system that incorporates several independently motivated principles of memory: a sharply limited attentional focus, rapid retrieval of item (but not order) information subject to interference from similar items, and activation decay (forgetting over time). A computational model embodying these principles provides an explanation of the functional capacities and severe limitations of human processing, as well as accounts of reading times. The broad implication is that the detailed nature of cross-linguistic sentence processing emerges from the interaction of general principles of human memory with the specialized task of language comprehension.

Attention↗

PubMed2005

Mechanisms involved in the swelling of erythrocytes caused by Pacific and Caribbean ciguatoxins.

The mechanisms underlying the swelling of frog red blood cells (RBC), induced by Pacific (P-CTX-1) and Caribbean (C-CTX-1) ciguatoxins (CTXs), were investigated by measuring the length, width and surface of their elliptic shape. P-CTX-1 (0.5 to 5 nM) and C-CTX-1 (1 nM) induced RBC swelling within 60 min. The CTXs-induced RBC swelling was blocked by apamin (1 microM) and by Sr(2+) (1 mM). P-CTX-1-induced RBC swelling was prevented and inhibited by H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (27 microM), an inhibitor of soluble guanylate cyclase (sGC), and NOS blockade by NG methyl-l-arginine (l-NMA; 10 microM). Cytochalasin D (cytD, 10 microM) increased RBC surface and mimicked CTX effect but did not prevent the P-CTX-1-induced l-NMA-sensitive extra increase. Calculations revealed that P-CTX-1 and cytD increase RBC total surface envelop and volume. These data strongly suggest that the molecular mechanisms underlying CTXs-induced RBC swelling involve the NO pathway by an activation of the inducible NOS, leading to sGC activation which modulates intracellular cGMP and regulates L-type Ca(2+) channels. The resulting increase in intracellular Ca(2+) content, in turn, disrupts the actin cytoskeleton, which causes a water influx and triggers a Ca(2+)-activated K(+) current through SK2 isoform channels.

Actins↗

PubMed2005

Dual-route processing of complex words: new fMRI evidence from derivational suffixation.

Many behavioral models of the comprehension of suffixed words assume a dual-route mechanism in which these words are accessed sometimes from the mental lexicon as whole units and sometimes in terms of their component morphemes (such as happi+ness). In related neuropsychological work, Ullman et al. (1997) proposed a dual-route model for past tense processing, in which the lexicon (used for access to irregularly inflected forms) corresponds to declarative memory and a medial temporal/ parietal circuit, and the rule system (used for computation of regularly inflected forms) corresponds to procedural memory and a frontal (including Broca's area)/basal ganglia circuit. We used functional MRI and a memory encoding task to test this model for derivationally suffixed words, comparing those words that show evidence of decompositional processing in behavioral studies (-ness, -less, and -able words) with derived words that do not show decomposition effects (-ity and -ation words). By examining Broca's area and the basal ganglia as regions of interest, we found that "decomposable" derived and inflected words showed increases in activity relative to nondecomposable suffixed words. Results support a dual-route model of lexical access of complex words that is consistent with the Ullman et al. proposal.

Adolescent↗

PubMed2002

A computational approach to control in complex cognition.

Cognitive deficits associated with dorsolateral prefrontal cortex (DLPFC) damage are often most apparent in higher cognitive tasks that involve problem solving and managing multiple goals. However, computational models of prefrontal deficits on such tasks are difficult to construct. Problem solving is most naturally modeled with symbolic systems (e.g. production systems), but the effects of lesions are most naturally modeled with subsymbolic systems (neural networks). We show that when we adopt a simple and plausible model of neural computation, there is a natural and explicit mapping from symbolic, goal-driven cognition onto neural computation. We exploit this mapping to construct a neural network model that is capable of solving complex problems in the Tower of London task. The model leads to a specific hypothesis about the role of DLPFC in such tasks, namely, that DLPFC represents internally generated subgoals that modulate competition among posterior representations. When intact, the model accurately simulates the behavior of college students even on the most difficult problems. Furthermore, when the subgoal component is lesioned, it accurately simulates the behavior of prefrontal patients, including the fact that their deficits are most apparent on the most difficult tasks and that they have special difficulty with tasks that require inhibiting a prepotent response.

Cognition↗