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Biomedical subjects

L E Crawford

Publications and source records attributed to L E Crawford.

15 recordsLinked to original sources

Linguistic and non-linguistic spatial categorization.

Three experiments examine the relation between linguistic and non-linguistic categorization of spatial relations. We compare linguistic and non-linguistic responses to the same spatial stimuli. Contrary to earlier claims in the literature (Hayward, W. G. & Tarr, M. J. (1995). Spatial language and spatial representation. Cognition, 55, 39-84), we find that linguistic and non-linguistic spatial categories do not correspond. Rather, they appear to have an inverse relation such that the prototypes of linguistic categories, such as 'above', are boundaries in non-linguistic spatial categorization. Evidence for this inverse relation comes from linguistic acceptability judgments and the pattern of bias in participants' reproductions of location. Our findings suggest that while linguistic and non-linguistic spatial organization rely on a common underlying structure, that structure may play different roles in the two organizational systems.

Cognition↗

Category effects on estimates of stimuli: perception or reconstruction?

The present study examined a common category effect that has been reported in the literature: the tendency for estimates of individual stimuli to be biased toward the central value of the presented set of stimuli. Both encoding and reconstruction accounts of this central-tendency effect are considered. Plain vertical lines and vertical lines embedded in the Müller-Lyer illusion were estimated while still in view or from memory. Although bias due to the Müller-Lyer illusion remained constant across the two conditions, bias due to the context set (category) occurred only when stimuli were estimated from memory. The results suggest that the category bias occurs at a later stage of processing than the Müller-Lyer effect and offer support for a reconstruction account of category effects on stimulus estimation.

Adult↗

Enhanced external counterpulsation in the management of patients with cardiovascular disease.

Studies over the past several decades support the hypothesis that enhanced external counterpulsation (EECP) can provide long-term benefits in patients with angina secondary to chronic coronary disease. Numerous non-sham controlled trials have recently been substantiated by a multicenter, randomized trial. Although the mechanism by which this mechanical treatment effects an alteration in cellular processes within the myocardium remains unclear, recent scientific investigations suggest that shear stress induced by chronic exposure to EECP might result in the release of a variety of growth factors and the subsequent stimulation of angiogenesis in the coronary beds. Ongoing clinical trials in patients with significant left ventricular dysfunction, an international registry, and additional clinical trials may help to elucidate further the role of this novel and unique therapy in our clinical armamentarium.

Angina Pectoris↗

Superoxide-mediated actin response in post-hypoxic endothelial cells.

The mechanism leading to changes in the superstructure of endothelial cells exposed to ischemia and reperfusion remains uncharacterized. We show that in post-hypoxic endothelial cells, the simple re-addition of oxygen induces a profound reorganization of the actin cytoskeleton. The total filamentous actin pool increases by 41% and translocation of actin filaments to the submembranous network is observed. Concurrent with the actin polymerization, increased tyrosine phosphorylation of endothelial cell substrates is detected on Western blots. Overexpression of superoxide dismutase using replication incompetent adenovirus inhibits the actin and tyrosine phosphorylation responses to reoxygenation. Inhibition of tyrosine kinases with the isoflavone genistein also suppressed the actin polymerization response to reoxygenation, but unlike superoxide dismutase, genistein also induced the collapse of the superstructure of endothelial cells upon reoxygenation. These experiments support the concept that reoxygenation following a period of hypoxia can induce the remodeling of the actin cytoskeleton in endothelial cells. Such a response requires the intact coupling of superoxide producing pathway(s) with tyrosine kinase pathway(s).

Actins↗

EJ-Ras inhibits phospholipase C gamma 1 but not actin polymerization induced by platelet-derived growth factor-BB via phosphatidylinositol 3-kinase.

Transformation of fibroblast-like cells (NIH 3T3) by a constitutively activated GTP-bound isoform of p21ras (EJ-Ras) produces morphogenic changes characterized by decreased attachment to the substratum, with retraction and rounding of the cell body. Transformed fibroblasts lose their "stressed" conformation and adopt a "relaxed" morphology. The specific molecular mechanisms responsible for these changes remain uncharacterized. We found that EJ-Ras transformation of NIH 3T3 cells decreased the cellular content of polymerized actin, particularly at the expense of actin stress fibers, but induced the accumulation of actin filaments in peripheral ruffling membranes. Polymerization of actin could be induced in EJ-Ras-transformed cells by exposure to platelet-derived growth factor (PDGF)-BB to an extent similar to that observed in wild-type NIH 3T3 cells. In EJ-Ras cells, actin polymerization was independent of phospholipase C gamma 1 (PLC gamma 1) activity, because inositol tris-phosphate (IP3) production observed in control NIH 3T3 cells in response to PDGF-BB was absent. Although PDGF-BB did stimulate tyrosine phosphorylation of PLC gamma 1, the phospholipase was strongly inhibited by an inhibitory factor present in the cytoplasm of EJ-Ras-transformed cells. In addition, cytoplasmic extracts of EJ-Ras, but not of control cells, inhibited phosphatidylinositol 4,5-diphosphate (PIP2) hydrolysis catalyzed by a recombinant PLC gamma 1 in vitro. Although PIP2 hydrolysis could not contribute to the reorganization of the actin cytoskeleton induced by PDGF-BB in EJ-Ras-transformed cells, phosphatidylinositol 3-kinase (PI3-K) was necessary for actin polymerization. Wortmannin, a specific PI3-K inhibitor, not only blocked actin polymerization in both control and EJ-Ras-transformed cells but actually led to rapid actin depolymerization when these cells were exposed to PDGF-BB. Thus, in EJ-Ras-transformed cells, cell morphogenic changes in response to PDGF-BB rely importantly on PI3-K and can occur in the complete absence of IP3 production despite tyrosine phosphorylation of PLC gamma 1.

3T3 Cells↗

Clinical efficacy of valproic acid in relation to plasma levels.

Valproic acid is a new antiepileptic drug recently introduced in the United States for the treatment of absence seizures. In this study on patients with absence and other seizure types, the majority of patients achieved optimal control within four weeks of therapy. No patient responded to valproic acid who did not show an initial clinical response by four weeks of active therapy. Optimal response was generally achieved when plasma levels were greater than 55 microgram/ml. Excellent clinical response was observed in the treatment of absence and myoclonic seizures. Twenty-two patients continued in a long term study have maintained the same degree of seizure control as observed at the time of optimal control.

Adolescent↗

Hospital "de-ministration" experiences in six teaching hospitals.

An experimental management programme at Sydney Hospital, first reported in this Journal in 1971, has now been repeated in five other teaching hospitals. These programmes confirm that when professional staff members are encouraged to participate in managing their hospital, they do so very effectively. Results include: better patient care, more patients treated, lower cost per patient, improved morale and flexibility in outlook. The benefits potentially available from the widespread introduction of this approach to managing hospitals are tremendous but to realize them requires radical changes in the way public hospitals are controlled by health authorities.

Accounting↗