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Biomedical subjects

D Lawson

Publications and source records attributed to D Lawson.

At least 109 records · Page 6Linked to original sources
PubMed1989

Neutrophil function in ischemic heart disease.

Neutrophils contribute to the healing of and scar formation in myocardium after ischemic injury. Many recent studies indicate that neutrophils may be involved in the genesis and propagation of myocardial ischemia. To characterize neutrophil function in ischemic heart disease, neutrophil chemotaxis, leukotriene B4 (LTB4) generation, and elastase release in plasma were measured in 20 patients with stable angina, 17 patients with unstable angina or acute myocardial infarction (AMI), and 20 age-matched control subjects. Neutrophils from patients with stable angina exhibited markedly increased chemotactic activity and LTB4 generation as compared with the age-matched control subjects (p less than 0.01). Neutrophils of nine of 17 patients with unstable angina or AMI clumped spontaneously ex vivo and exhibited marked pseudopod formation and granule extrusion on electron microscopy. Subsequent chemotactic activity and LTB4 generation by neutrophils from these patients was less than in patients with stable angina, suggesting previous in vivo activation. Plasma levels of peptide B beta, a product of fibrin degradation by human neutrophil elastase, were approximately 15-fold higher (p less than 0.001) in patients with unstable angina or AMI (588 +/- 171 pmol/l, mean +/- SEM) compared with those in patients with stable angina (37 +/- 25 pmol/l) or control subjects (40 +/- 22 pmol/l), confirming intense in vivo neutrophil activation. Our study shows enhanced neutrophil function in patients with ischemic heart disease. The increased neutrophil chemotactic activity and LTB4 generation may be markers of stable angina pectoris. Intense neutrophil activation in unstable angina or AMI, as manifested by morphologic changes in neutrophils and elastase release, may relate to ongoing in vivo cellular activation.

Chemotaxis, Leukocyte↗
PubMed1989

Reduced myocardial neutrophil accumulation and infarct size following thromboxane synthetase inhibitor or receptor antagonist.

Since thromboxane A2 (TXA2) release may relate to the extension of myocardial injury following coronary ligation, the authors examined the effects of pretreatment with a selective TXA2 synthetase inhibitor U-63,557A, or a TXA2 receptor antagonist SQ-29,548, on myocardial infarct size forty-eight hours following left coronary ligation in rats. Myocardial infarct size (as percent of left ventricle, LV) was decreased from 44 +/- 3% in saline-treated control animals to 34 +/- 4% (P less than 0.05) in U-63,557A-treated animals and to 32 +/- 4% (P less than 0.05) in SQ-29,548 treated animals (U-63,557A-treated vs SQ-29,548-treated, P = NS). LV creatine kinase (CK) was 5.08 +/- 0.42 IU/mg protein in noninfarcted untreated rats and 1.79 +/- 0.21 IU/mg protein in saline-treated infarcted rats. LV CK was 2.86 +/- 0.40 IU/mg protein in U-63,557A-treated rats and 3.11 +/- 0.51 IU/mg protein in SQ-29,548-treated infarcted rats (both P less than 0.05 compared with saline-treated rats). The beneficial effects of U-63,557A and of SQ-29,548 were not accompanied by reduction in indices of myocardial oxygen demand (heart rate and arterial pressure). However, neutrophil accumulation in the infarcted myocardium was markedly decreased by U-63,557A and SQ-29,548 pretreatment. Myocardial myeloperoxidase activity, a specific marker of neutrophil infiltration, was also decreased (P less than 0.02) in U-63,557A- and SQ-29,548-treated animals (0.09 +/- 0.03 and 0.07 +/- 0.02 units/100 mg, respectively) compared with saline-treated infarcted rats (0.19 +/- 0.04 units/100 mg). In vitro incubation of U-63,557A and SQ-29,548 caused a significant and similar reduction in f-MLP-induced neutrophil chemotaxis, and U-63,557A increased prostacyclin formation in whole blood. These data suggest that reduction in the extent of myocardial injury by TXA2 synthetase or receptor inhibitors may, in part, relate to a decrease in neutrophil accumulation in the infarcted tissue. In spite of differences in mechanisms of action of U-63,557A and SQ-29,548, both agents exert a similar protective effect on the extent of myocardial injury following coronary ligation. Reduction in neutrophil accumulation in the infarcted zone, as well as in f-MLP-directed chemotaxis in vitro, suggests that TXA2 inhibition may modulate neutrophil migration.

Animals↗
PubMed1989

Comparative effects of mezlocillin and carbenicillin on platelet function and thromboxane generation in patients with cancer.

Carbenicillin and mezlocillin are widely used for treatment of Pseudomonas infections in patients with cancer. Carbenicillin has been reported to cause platelet dysfunction and bleeding diathesis in some individuals. We evaluated whether carbenicillin causes deterioration of platelet function in patients with cancer and whether mezlocillin causes similar effects on platelets from normal subjects or from patients with cancer. In these in vitro studies, carbenicillin and mezlocillin decreased ADP and epinephrine-induced platelet aggregation and thromboxane A2 generation similarly, but only in concentrations of 3.2 mg/ml or higher. In contrast, carbenicillin was more potent than mezlocillin in decreasing ristocetin-induced platelet aggregation. We also evaluated effects of these antibiotics on platelet function in 19 patients with cancer who developed fever and neutropenia. These patients received either mezlocillin (10 patients) or carbenicillin (nine patients) in combination with nafcillin and gentamycin. Neither carbenicillin nor mezlocillin had any significant effect on platelet aggregation or thromboxane A2 generation. Lack of effects in vivo was due to defective platelet function in these patients prior to any antibiotics. These defects were most probably related to underlying disease and/or prior chemotherapy. Thus, carbenicillin and mezlocillin can both safely be used in patients with cancer who develop fever and neutropenia, and neither seems to have advantage over the other in terms of platelet function.

Adolescent↗
PubMed1988

Enhancement of human neutrophil function by platelets: effects of indomethacin.

To characterize the influence of presence of platelets on human neutrophil function, neutrophil oxidative burst, chemotaxis, leukotriene B4 and prostacyclin generation were examined in the presence of physiologic concentration of platelets (40: 1). Presence of platelets significantly (P less than or equal to 0.05) increased all these neutrophil functions. To determine if cyclooxygenase products are involved in platelet-neutrophil interaction, neutrophils (+/- platelets) were incubated with indomethacin. Although high concentrations of indomethacin (10 microM) inhibited neutrophil (no platelets) chemotaxis and leukotriene B4 generation, these inhibitory effects of indomethacin were attenuated in the presence of platelets. Thus presence of platelets enhances neutrophil activity and overcomes the inhibitory effects of indomethacin on neutrophils.

Blood Platelets↗
PubMed1988

The primary wave of epinephrine-induced platelet aggregation represents alpha 2-adrenoceptor status.

We examined relationships between epinephrine-induced slope of primary wave of aggregation and the alpha 2-adrenoceptor status on platelets. A concentration (10(-9) to 10(-6]-dependent increase in slope of primary wave with EC50 of epinephrine at 4.5 +/- 0.4 x 10(-7) was observed. In studies on epinephrine binding to alpha 2-adrenoceptors in competition with 3H-yohimbine to platelets, (IC50) of epinephrine was 4.8 +/- 3.4 x 10(-7) M. There was a significant (P less than or equal to 0.02) correlation between EC50 of epinephrine to evoke biological response and IC50 of epinephrine to bind to alpha 2-adrenoceptors (r-0.75). There was no relationship between number of receptor sites or dissociation constant of 3H-yohimbine binding and primary wave of platelet aggregation. These data show that the slope of primary wave in response to epinephrine reflects alpha 2-adrenoceptor binding of the agonist.

Adolescent↗
PubMed1988

Alterations in platelet alpha 2-adrenoceptors by aspirin.

Epinephrine-induced platelet aggregation (mediated through interaction with alpha 2-adrenoceptors) is inhibited by aspirin. To determine if aspirin modulates alpha 2-adrenoceptors, we quantitated dissociation constant (KD) and maximum number of binding sites (Bmax) on isolated platelet membranes using alpha 2-antagonist 3H-yohimbine in normal subjects given 650 mg of aspirin orally. Alpha 2-receptor KD increased from 3.20 +/- 1.80 to 7.32 +/- 3.32 nM (p less than 0.02) and Bmax from 115 +/- 77 to 190 +/- 140 fmol/mg protein. To determine if these alterations in alpha 2-receptors by aspirin were mediated through circulatory or intracellular effects, intact platelets or isolated platelet membranes were incubated with aspirin for 30 minutes in vitro. In these in vitro experiments, alpha 2-receptor KD increased from 2.92 +/- 1.76 to 9.83 +/- 8.55 nM and Bmax from 140 +/- 81 to 191 +/- 129 fmol/mg protein (p less than 0.05). Oral ingestion of aspirin or incubation of aspirin with intact platelets or lysates increased (3 to 10 fold) the concentration of 1-epinephrine required for inhibition of 3H-yohimbine binding by 50% (p less than 0.05). Basal platelet cyclic AMP as well as its elevation with PGE1 or PGI2 and decrease with catecholamines were not influenced by aspirin treatment of platelets. These data indicate that aspirin decreases platelet alpha 2-receptor affinity for agonist as well as antagonist. These effects of aspirin are independent of circulatory or dynamic intraplatelet changes.

Aspirin↗
PubMed1988

Reduction in plasminogen activator inhibitor-1 (PAI-1) with omega-3 polyunsaturated fatty acid (PUFA) intake.

Activity of plasminogen activator inhibitor-1 (PAI-1) in human blood correlates with thrombotic tendency and with serum triglyceride concentrations. Since intake of fish-derived omega-3 polyunsaturated fatty acids (PUFA) decreases serum triglycerides, we examined the effects of omega-3 PUFA maximum eicosapentaenoic acid (Max EPA) intake on PAI-1 levels in eight patients with coronary artery disease and in four normal subjects. After 4 weeks of Max-EPA intake by coronary artery disease patients, serum triglyceride concentrations and PAI-1 levels decreased 43 +/- 8% and 21 +/- 5%, respectively (both p less than or equal to 0.01) without any change in tissue plasminogen activator (TPA) levels. No changes were noted at 1 week of Max EPA intake in normal subjects, but at 3 weeks serum triglyceride concentrations and PAI-1 levels decreased 32 +/- 13% and 22 +/- 4%, respectively (p less than or equal to 0.01) without any change in tissue plasminogen activator (TPA) levels. No changes were noted at 1 week of Max EPA intake in normal subjects, but at 3 weeks serum triglyceride concentrations and PAI-1 levels decreased 32 +/- 13% and 22 +/- 4%, respectively (p less than or equal to 0.02) without change in TPA. The magnitude of reduction in triglycerides was dependent on the initial serum concentration (r = 0.68, p less than or equal to 0.01). In addition, decrease in PAI-1 levels correlated with reduction in serum triglycerides (r = 0.79, p less than or equal to 0.01). This study shows that omega-3 PUFA intake reduces PAI-1 levels without change in TPA antigen. These observations may relate to decrease in thrombotic activity upon consumption of large amounts of fish or fish-derived products.

Aged↗
PubMed1988

Dietary supplementation with omega-3 polyunsaturated fatty acids in patients with stable coronary heart disease. Effects on indices of platelet and neutrophil function and exercise performance.

It has been suggested that omega-3 polyunsaturated fatty acids (PUFAs) may alter the course of coronary artery disease by influencing platelet and neutrophil function, arachidonic acid metabolism, and circulating lipid concentrations. To examine this hypothesis, placebo or omega-3 PUFAs as Max-EPA (equivalent to 3.2 g of eicosapentaenoic acid and 2.2 g of docosahexaenoic acid daily) was administered to eight patients with stable coronary artery disease and positive exercise stress test results in a randomized, double-blind, crossover fashion over a 12-week period. With Max-EPA administration, platelet aggregation threshold to epinephrine was increased in only two patients, but neutrophil aggregation and chemotaxic functions decreased consistently (both p less than or equal to 0.01 compared with preceding placebo phase) in all eight. Serum and platelet-rich plasma thromboxane B2 concentrations decreased 40 percent and 28 percent, respectively (both p less than or equal to 0.05). Neutrophil leukotriene B4 formation decreased 23 percent (p less than or equal to 0.01) and synthesis of leukotriene B5 became apparent in all subjects. Serum triglyceride concentrations fell 52 percent (p less than or equal to 0.05) without significant change in total cholesterol, high-density lipoprotein-cholesterol, or low-density lipoprotein-cholesterol concentrations. Systolic blood pressure and the double product (heart rate X systolic blood pressure) were lower (p less than or equal to 0.05) at the end of the Max-EPA phase than in the preceding placebo phase. Heart rate, systolic blood pressure, and the double product were also lower (p less than or equal to 0.05) at three as well as at six minutes of an exercise stress test, indicating a significant reduction in myocardial oxygen demand. Despite these alterations in platelet and neutrophil function, arachidonic acid metabolism, serum triglyceride concentrations, and myocardial oxygen demand, there were no significant changes in subjective parameters of coronary artery disease during the Max-EPA phase (angina frequency 3.7 versus 2.8 episodes per week, nitroglycerin consumption 3.0 versus 1.9 tablets per week, both p = NS). Similarly, exercise times to ST-segment depression (6.5 versus 4.1 minutes) and to onset of angina (5.4 versus 5.0 minutes) were not altered by administration of Max-EPA. Thus, short-term dietary supplementation with omega-3 PUFAs to patients with stable coronary artery disease does not appear to alter subjective or objective parameters of myocardial ischemia.

Aged↗
PubMed1988

Modulation of human neutrophil superoxide production by selective thromboxane synthetase inhibitor U63,557A.

Prostaglandin I2 and prostaglandins of E series have been known to inhibit human neutrophil superoxide production. To examine the effects of selective thromboxane synthetase inhibition on human neutrophil superoxide production (with or without platelets), neutrophils were incubated with U63,557A and stimulated with f-MLP, serum-activated zymosan or calcium ionophore A23187. U63,557A had no significant direct inhibitory effect on neutrophil superoxide production. On the other hand, in the presence of platelets in neutrophil suspension, U63,557A significantly reduced neutrophil superoxide production and increased prostaglandin I2 release. These data suggest that selective thromboxane synthetase inhibition may reduce neutrophil superoxide generation, most likely via increase in prostaglandin I2.

Benzofurans↗
PubMed1988

Reduction in coronary vasodilator reserve following coronary occlusion and reperfusion in anesthetized dog: role of endothelium-derived relaxing factor, myocardial neutrophil infiltration and prostaglandins.

To examine the effects of acute myocardial ischemia and reperfusion on regional coronary vasodilator (or flow) reserve, peak reactive hyperemic blood flow following a 10 s occlusion was obtained in dogs subjected to circumflex (Cx) coronary artery occlusion for 1 h followed by reperfusion for 1 h. Acute myocardial ischemia resulting from Cx artery occlusion-reperfusion caused an attenuation in peak reactive hyperemic Cx flow (mean +/- S.E., from 215 +/- 29% to 87 +/- 17%, P less than or equal to 0.001). Acetylcholine-induced increase in Cx flow was also significantly (P less than or equal to 0.01) attenuated following Cx occlusion-reperfusion. These alterations were not observed in the left anterior descending (LAD) coronary artery, which was not subjected to occlusion. Pre-treatment of four dogs with indomethacin inhibited prostaglandin release (P less than or equal to 0.01), but did not affect peak reactive hyperemic coronary flow or acetylcholine-induced increase in coronary flow before or after occlusion-reperfusion. Histopathology revealed extensive myocardial neutrophil infiltration in the Cx-supplied region compared to the LAD-supplied region. Myocardial myeloperoxidase activity, an index of neutrophil infiltration, was also increased in the Cx compared to the LAD region (P less than or equal to 0.02). Myocardial neutrophil accumulation and myeloperoxidase activity were similar in the control and indomethacin-treated animals. These observations suggest that acute myocardial ischemia resulting from coronary artery occlusion-reperfusion impairs coronary vasodilator reserve in anesthetized dogs. This impairment, which was not modified by prostaglandin inhibition, may be related to the loss of endothelium-derived relaxing factor and/or decreased microvascular cross-sectional area resulting from capillary plugging by neutrophils.

Acetylcholine↗
PubMed1988

Relative effectiveness of alternative androgen withdrawal therapies in initiating regression of rat prostate.

From a large number of potentially effective androgen withdrawal regimens including bilateral orchiectomy, estrogens, antiandrogens and LHRH agonists alone or in combinations, we compared the ability of 12 different treatment options to mimic the acute results of surgical castration on the rat prostate. Agents were administered s.c. in clinical doses to groups of male rats daily for three days. On day 4 the prostatic tissue was removed and analyzed by conventional methods for whole-tissue and nuclear concentrations of dihydrotestosterone, nuclear androgen receptor and cytoplasmic androgen receptor. Castration-like changes were most pronounced with the synergistic combinations of cyproterone acetate + low-dose diethylstilbestrol, and megestrol acetate + low-dose diethylstilbestrol. Comparing the effectiveness of single agents, low-dose diethylstilbestrol was superior to cyproterone acetate, megestrol acetate, flutamide, leuprolide and RU23908. Leuprolide combined with flutamide was superior to leuprolide + cyproterone acetate, leuprolide + cyproterone acetate + low-dose diethylstilbestrol or leuprolide + RU23908 after three days of administration; however, this advantage disappeared when the treatments were extended to seven days. The observations indicate that the most potent androgen withdrawal therapies such as cyproterone acetate + low-dose diethylstilbestrol and megestrol acetate + low-dose diethylstilbestrol at best approximate but do not surpass the early effects of surgical castration. During the same time course, other regimens are characterized by a slower onset of action and a lesser degree of suppression of androgenic mechanisms within the cell.

Anilides↗
PubMed1988

Increased prostacyclin and thromboxane A2 biosynthesis in atherosclerosis.

It has been proposed that atherosclerotic arteries produce less prostacyclin (PGI2) than nonatherosclerotic arteries do, thereby predisposing arteries to vasospasm and thrombosis in vivo. We reexamined this concept by measuring spontaneous as well as arachidonate-induced PGI2 biosynthesis in aortic segments from nonatherosclerotic and cholesterol-fed atherosclerotic New Zealand White rabbits. Thromboxane A2 (TXA2) generation was also measured. Formation of PGI2, as well as TXA2, as measured by radioimmunoassay (RIA) of their metabolites, was increased in atherosclerotic aortic segments relative to nonatherosclerotic segments (P less than or equal to 0.05) at 0, 5, 10, 15, and 30 min of incubation with arachidonate. Pretreatment of arterial segments with indomethacin inhibited PGI2 as well as TXA2 formation, whereas pretreatment with the selective TXA2 inhibitor OKY-046 inhibited only TXA2 release, thus confirming the identity of icosanoids. To confirm the RIA data, aortic segments were incubated with [14C]arachidonate prior to stimulation with unlabeled arachidonate. The uptake of arachidonate was similar, but the release of incorporated [14C]arachidonate was significantly (P less than or equal to 0.05) greater in atherosclerotic segments than in nonatherosclerotic ones. Conversions of released [14C]arachidonate to 6-keto[14C]prostaglandin F1 alpha and [14C]thromboxane B2 were similar in the two types of aortic segments. Thus, synthesis of PGI2 as well as TXA2 is increased in atherosclerosis, and this alteration in arachidonate metabolism is related to increased release of arachidonate.

Animals↗
PubMed1988

Cytoskeleton-associated plectin: in situ localization, in vitro reconstitution, and binding to immobilized intermediate filament proteins.

The association and interaction of plectin (Mr 300,000) with intermediate filaments and filament subunit proteins were studied. Immunoelectron microscopy of whole mount cytoskeletons from various cultured cell lines (rat glioma C6, mouse BALB/c 3T3, and Chinese hamster ovary) and quick-frozen, deep-etched replicas of Triton X-100-extracted rat embryo fibroblast cells revealed that plectin was primarily located at junction sites and branching points of intermediate filaments. These results were corroborated by in vitro recombination studies using vimentin and plectin purified from C6 cells. Filaments assembled from mixtures of both proteins were extensively crosslinked by oligomeric plectin structures, as demonstrated by electron microscopy of negatively stained and rotary-shadowed specimens as well as by immunoelectron microscopy; the binding of plectin structures on the surface of filaments and cross-link formation occurred without apparent periodicity. Plectin's cross-linking of reconstituted filaments was also shown by ultracentrifugation experiments. As revealed by the rotary-shadowing technique, filament-bound plectin structures were oligomeric and predominantly consisted of a central globular core region of 30-50 nm with extending filaments or filamentous loops. Solid-phase binding to proteolytically degraded vimentin fragments suggested that plectin interacts with the helical rod domain of vimentin, a highly conserved structural element of all intermediate filament proteins. Accordingly, plectin was found to bind to the glial fibrillar acidic protein, the three neurofilament polypeptides, and skin keratins. These results suggest that plectin is a cross-linker of vimentin filaments and possibly also of other intermediate filament types.

Animals↗
PubMed1988

Identification of new actin-associated polypeptides that are modified by viral transformation and changes in cell shape.

By using a monoclonal antibody we have identified a new polypeptide doublet (C4h and C4l) of Mr approximately 21 kD and pI 8 and 7, respectively, that is associated with and (at the immunofluorescence level) uniformly distributed on actin filament bundles in rat, mouse, and other vertebrate species. C4 is absent in neurones, erythrocytes, and skeletal muscle but the epitope is evolutionarily conserved as it is present in invertebrates such as molluscs and crustaceans. C4h is not found in cells such as lymphocytes and oncogenically transformed mesenchymal cells where actin stress fiber bundles are reduced in number or absent. C4l, on the other hand, is always present. C4h expression can also be blocked by switching normal nontransformed mesenchymal cells from adherent to suspension culture. Reexpression of C4h occurs 24 h after these cells are returned to normal adherent culture conditions, but can be blocked by either actinomycin D or cycloheximide, suggesting that the expression of this epitope is regulated at the transcriptional level.

Actin Cytoskeleton↗
PubMed1987

Ethanol stimulates prostacyclin biosynthesis by human neutrophils and potentiates anti-platelet aggregatory effects of prostacyclin.

Previous reports on the direct effects of ethanol on human platelet aggregation function have been inconsistent. Ethanol ingestion produces vasodilation and raises intracellular cyclic AMP concentrations, effects similar to those of prostacyclin. We, therefore, hypothesized that ethanol may influence biosynthesis and/or bioactivity of prostacyclin. In our experiments, ethanol in concentrations up to 400 mg% had no consistent inhibitory effect on platelet aggregation in response to epinephrine, ADP, or combination of subthreshold concentrations of epinephrine plus ADP. However, ethanol in concentrations as low as 10 mg% potentiated the platelet aggregation inhibitory effects of prostacyclin. In addition, ethanol (20 mg%) decreased formation of thromboxane A2 in whole blood by 41% and stimulated formation of prostacyclin by 160% (both P less than 0.01). Additional studies using isolated human cells demonstrated synthesis of prostacyclin by neutrophils in the presence of platelets, and this neutrophil prostacyclin formation was enhanced in the presence of ethanol. These effects of alcohol in concentrations achieved after moderate intake may relate to the hemodynamic, biochemical, and cardioprotective effects of ethanol.

Drug Synergism↗
PubMed1987

Effect of human tumor cells on platelet aggregation: potential relevance to pattern of metastasis.

Tumor metastasis may be facilitated by interaction of tumor cells with platelets. It is not known, however, whether solid tumors which have predisposition to pulmonary metastasis affect platelets differently than lymphoid tumors, which rarely spread to lungs. We therefore examined the effects of cultured osteogenic sarcoma (MG-63, U2-OS), as well as leukemia (NALM-16, LAZ-221, K-562) and lymphoma (RAJI, MOlt 4) cells, on human platelet aggregation. Human osteogenic sarcoma (MG-63) cells alone induced platelet aggregation, whereas U2-OS cells induced platelet aggregation only after preincubation of platelets with subthreshold concentrations of epinephrine. In contrast, neither leukemia nor lymphoma cells affected platelet aggregation. These observations suggest that the platelet proaggregatory potential of tumor cells is variable and that the platelet stimulatory effects of osteogenic sarcoma cells may relate to their high risk of pulmonary metastasis.

Adenosine Diphosphate↗
PubMed1987

Attention to central and peripheral visual space in a movement detection task: an event-related potential and behavioral study. I. Normal hearing adults.

The effects of focussed attention to peripherally and centrally located visual stimuli were compared via an analysis of event-related brain potentials (ERPs) while subjects detected the direction of motion of a white square in a specified location. While attention to both peripheral and foveal stimuli produced enhancements of the early ERP components, the distribution over the scalp of the attention-related changes varied according to stimulus location. The attention-related increase in the amplitude of the N1 wave (157 ms) to the peripheral stimuli was greater over the parietal region of the hemisphere contralateral to the attended visual field. By contrast, the largest effects of foveally directed attention occurred over the occipital regions where the increase was bilaterally symmetrical. Additionally, the effects of attention on the ERPs were significantly larger for moving than for stationary stimuli, and this effect was greater for peripheral than for central attention. A long-latency positive displacement component (300-600 ms) was larger over the right than the left hemisphere during attention to the lateral visual fields, but was symmetrical in amplitude when central stimuli were attended. These results suggest that different pathways are modulated when attention is deployed to different regions of the visual fields. Further, they suggest that the special role of the right hemisphere in spatial attention may be limited to analysis of information in the visual periphery.

Adolescent↗