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G L Shaw

Publications and source records attributed to G L Shaw.

62 records · Page 4Linked to original sources
PubMed1979

Dendritic bundles: survey of anatomical experiments and physiological theories.

Dendritic bundles have been found throughout the mammalian brain. Unquestionably, these bundles must serve one or more important, fundamental roles in the brain's functioning. However, no physiological experiments to determine their function have been performed on these well-established anatomical units. We survey the numerous anatomical reports of bundling. In addition, we discuss several physiological possibilities for the functional significance of bundles.

Animals↗
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Space-time correlations of neuronal firing related to memory storage capacity.

Most viable theories of memory require some form of synaptic modification dependent on the correlation of pre- and postsynaptic neuronal firing (which we will denote as the Hebb hypothesis). We show here that a possible consequence of this hypothesis is that the storage capacity of a network of highly interconnected neurons is related to the number of synapses and that this implies that the network can be excited into many different time sequence of firing patterns of assemblies of neurons. The important role played by the assembly (as defined by E. R. John) is discussed in detail. A modified Hebb hypothesis is proposed. The crucial experiments to test the model involve the use of two (or more) extracellular microelectrodes to record, simultaneously, the firing activity of several neurons and thus determine the spatial and temporal cross correlations after presenting a mature animal with a variety of stimuli.

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Learning by selection in the trion model of cortical organization.

The basic issue of whether mammalian learning in cortex proceeds via a selection principle, as stressed by Edelman, versus an instructional one is of major importance. We present here a realization of selection learning in the trion model, which is based on the Mountcastle columnar organizational principle of cortex. We suggest that mammalian cortex starts out with an a priori connectivity between minicolumns that is highly structured in time and in space, competing between excitation and inhibition. This provides a "naive" repertoire of spatial-temporal firing patterns that stimuli and internal processing map onto. These patterns can be learned with small modifications to the connectivity strengths determined by a Hebbian learning rule. As various patterns are learned, the repertoire changes somewhat in order to respond properly to various stimuli, but the majority of all possible stimuli still map onto spatial-temporal firing patterns of the original repertoire. In order to show that the example presented here is showing true selectivity and is not an artifact of more stimuli evolving into the learned pattern, we develop a selectivity measure. We suggest that some form of instructional learning (in which connectivities are finely tuned) is present for difficult tasks requiring many trials, whereas very rapid learning involves selectional learning. Both types of learning must be considered to understand behavior.

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Changing patterns of lung cancer incidence by histological type.

Using data from five registries covering 7% of the U.S. population, we investigated lung carcinoma incidence trends from 1969-86 by histological type, sex, race, age, calendar time period, and cohort year of birth. Among white men, squamous cell carcinoma was the most frequent histological type, but by the mid-1980s the age-adjusted rates were decreasing while rates of adenocarcinoma and small (oat) cell carcinoma continued to rise. Among white women, adenocarcinoma was the most frequent type, followed by small cell carcinoma, with rates of all histological types rising over the entire study period. Similar time trends were seen among blacks. Rates for squamous cell carcinoma among both sexes and adenocarcinoma among men, however, were considerably higher for blacks than whites, whereas no racial disparity was seen for small cell carcinomas. Rates for each histological type were higher among men than women, although male-female sex ratios diminished over time. Age-specific rates varied considerably by cohort year of birth; incidence of squamous cell carcinoma among men increased steadily among those born from the late 1800s to the first quarter of this century before declining among those born thereafter. Cohort peaks were also reached, although about 10 to 20 years later, for small cell carcinoma and adenocarcinoma, suggesting an eventual reduction in incidence in these histological types as well. For each type, the peak incidence occurred earlier for men than women. These differing incidence patterns add to the evidence that the mechanisms of lung carcinogenesis may vary by histological type.

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Debrisoquine metabolism and lung cancer risk.

Previous reports of the association between the debrisoquine metabolic polymorphism and lung cancer risk have been conflicting. We examined the hypothesis that the genetically determined ability to metabolize debrisoquine identifies individuals at increased risk for lung cancer in a study designed to address some of the methodological criticisms of previous studies. A case-control study of 335 incident Caucasian lung cancer patients and 373 controls matched for age, race, sex, and hospital, was conducted at the National Naval Medical Center (Bethesda, MD) and at the Laval Hospital (Sainte-Foy, Quebec, Canada). Debrisoquine metabolic phenotype was determined by debrisoquine administration and analysis of debrisoquine and 4-hydroxydebrisoquine in the subsequent 8-h urine collected. Stratified and logistic regression analyses were used to evaluate the association between extensive or intermediate debrisoquine metabolism and lung cancer risk. We found no increased risk among extensive or intermediate metabolizers (odds ratio, 0.6; 95% confidence interval, 0.3-1.2). The lack of an association was not confounded by control diagnoses, medications used within 1 month of debrisoquine administration, smoking, stage, or histology of lung cancer. No relationship was found among either heavy smokers or light and nonsmokers. Our results do not support the role of debrisoquine metabolism as a marker for lung cancer risk. While the concept that polymorphisms of metabolism may account for differential susceptibility to lung cancer is sound, debrisoquine metabolic phenotype was not associated with lung cancer risk in these data.

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