Release Of Neutrophil Chemotactic Factor Research Articles

Surfactant Protein A Stimulates Release of Neutrophil Chemotactic Factors by Alveolar Type II Pneumocytes

Mucosal immunity is an important mechanism in the response to injury. Our hypothesis is that surfactant protein A (SP-A) is an autocrine factor that stimulates alveolar type II epithelial cell release of neutrophil chemotactic factors by binding to the SP-A receptor expressed by these cells. We examined (1) the effect of SP-A (20 μg/ml) or IL-1β (10 ng/ml) on release of neutrophil chemotactic factors by primary cultures of type II cells or alveolar macrophages, and (2) the effect of intratracheal instillation of the blocking antibody to the SP-A receptor on the response to oleic acid-induced lung injury in vivo. All media and cell culture supernates were assayed for neutrophil chemotactic activity, and bronchoalveolar lavage fluid from the in vivo experiments was analyzed for inflammatory cell counts. While SP-A and media used for the cell cultures has no intrinsic neutrophil chemotactic activity, supernates from primary cultures of type II cells incubated in either SP-A or IL-1β had twofold higher neutrophil chemotactic factor activity compared to supernates from controls. SP-A had no effect on release of neutrophil chemotactic factor by alveolar macrophages. Oleic acid-induced lung injury resulted in a marked influx of neutrophils into BAL, and this influx was reduced by 70% by pretreatment with the antibody to SP-A receptor. We conclude that SP-A stimulates the release of neutrophil chemotactic factor by alveolar type II cells, and this effect is mediated by the receptor for SP-A specifically expressed by these cells.

Mineral trioxide aggregate stimulates macrophages and mast cells to release neutrophil chemotactic factors: role of IL-1β, MIP-2 and LTB 4

In the present study, the role of macrophages and mast cells in mineral trioxide aggregate (MTA)-induced release of neutrophil chemotactic factor was investigated. MTA suspension (50 mg/mL) was plated over inserts on macrophages or mast cells for 90 minutes. Untreated cells served as controls. Cells were washed and cultured for 90 minutes in RPMI without the stimuli. Macrophages and mast cell supernatants were injected intraperitoneally (0.5 mL/cavity), and neutrophil migration was assessed 6 hours later. In some experiments, cells were incubated for 30 minutes with dexamethasone (DEX, 10 muM/well), BWA4C (BW, 100 muM/well) or U75302 (U75, 10 muM/well). The concentration of Leukotriene B(4) (LTB(4)) in the cell-free supernatant from mast cells and macrophage culture was measured by ELISA. Supernatants from MTA-stimulated macrophages and mast cells caused neutrophil migration. The release of neutrophil chemotactic factor by macrophages and mast cells was significantly inhibited by DEX, BW, or U75. Macrophages and mast cells expressed mRNA for interleukin-1 (IL-1)beta and macrophage inflammatory protein-2 (MIP-2) and the pretreatment of macrophages and mast cells with DEX, BW, or U75 significantly altered IL-1beta and MIP-2 mRNA expression. LTB(4) was detected in the MTA-stimulated macrophage supernatant but not mast cells. MTA-induces the release of neutrophil chemotactic factor substances from macrophages and mast cells with participation of IL-1beta, MIP-2, and LTB(4).

Role of alveolar macrophages and neutrophils in the defense system against infection of Pseudomonas aeruginosa in the respiratory tract and the effect of derivative of muramyl dipeptide

We investigated the role of alveolar macrophages and neutrophils on the defense system against infection of Pseudomonas aeruginosa (P. aeruginosa) in the lower respiratory tracts of rats. Intratracheal inoculation of formalin-inactivated P. aeruginosa to normal rats showed an increased number of neutrophils in bronchoalveolar lavage (BAL) fluid obtained at 24 hours after the inoculation. This response of neutrophils was induced by intravenous administration of MDP-Lys, which is muramyl dipeptide. Phagocytic activity of neutrophils for P. aeruginosa was higher than that of alveolar macrophages, indicating that neutrophils are essential phagocytes in the defense system against P. aeruginosa infection in the lower respiratory tract. Alveolar macrophages released neutrophil chemotactic factor after phagocytosis of P. aeruginosa. This function of alveolar macrophages was increased by MDP-Lys administration. These results indicated that alveolar macrophages play an important role in neutrophil accumulation by release of neutrophil chemotactic factor after the P. aeruginosa phagocytosis in the lower respiratory tract. Moreover MDP-Lys can amplify the neutrophil-dependent defense system against P. aeruginosa by activation of the alveolar macrophage function in vivo.

Macrophages and Mast Cells Control the Neutrophil Migration Induced by Dentin Proteins

Dentin sialoprotein (DSP) and dentin phosphoprotein (DPP), the major dentin proteins, have been shown to induce neutrophil migration through release of IL-1beta, TNF-alpha, MIP-2, and KC. However, the sources of these mediators were not determined. Here, the roles of macrophages and mast cells (MC) in dentin-induced neutrophil accumulation were investigated. Peritoneal MC depletion or the enhancement of macrophage population increased DSP- and DPP-induced neutrophil extravasation. Moreover, supernatants from DSP- and DPP-stimulated macrophages caused neutrophil migration. The release of neutrophil chemotactic factor by macrophages was inhibited by dexamethasone or the supernatant of DSP-treated MC. Consistently, dexamethasone and the MC supernatant inhibited the production of IL-1beta, TNF-alpha, and MIP-2 by macrophages. This inhibitory activity of the DSP-stimulated MC was neutralized by anti-IL-4 and anti-IL-10 antibodies. These results indicate that dentin induces the release of the neutrophil chemotactic substance(s) by macrophages, which are down-modulated by MC-derived IL-4 and IL-10.

Neutrophil migration induced by IL-8-activated mast cells is mediated by CINC-1.

The aim of this study was to characterize the mediators released by mast cells responsible for IL-8-induced neutrophil migration. It was observed that IL-8 induces a dose-dependent neutrophil migration into peritoneal cavity of rats, but not into air-pouch cavity in which resident mast cells are not present. The transference of peritoneal mast cells to the air-pouch renders this cavity responsive to IL-8. The neutrophil migration induced by IL-8 into the peritoneal cavity was not observed when the peritoneal-resident mast cells were depleted by compound 48/80 or distilled water treatment. Confirming the importance of mast cells, IL-8-stimulated mast cells supernatant induced significant neutrophil migration when injected into peritoneal and air-pouch cavities. The IL-8-induced neutrophil migration was observed not to be dependent on LTB(4), prostaglandins or TNF-alpha, since MK886, indomethacin or thalidomide were unable to block the IL-8-induced neutrophil accumulation 'in vivo' or the release of neutrophil chemotactic factor "in vitro" by IL-8-stimulated mast cells. However, dexamethasone, an inhibitor of the synthesis of pro-inflammatory cytokines, blocked the neutrophil migration induced by IL-8 "in vivo" and also inhibited the release of the neutrophil chemotactic factor by IL-8-stimulated mast cells. Moreover, the incubation of IL-8-stimulated mast cells supernatant with antibody against cytokine-induced neutrophil chemoattractant 1 (CINC-1), but not against TNF-alpha or IL-1beta, inhibited its neutrophil chemotactic activity. Furthermore, we found a significant amount of CINC-1 in this supernatant. In conclusion, we demonstrated that the neutrophil migration induced by IL-8 is dependent on CINC-1 release from mast cells.

Early release of neutrophil chemotactic factor from isolated rat heart subjected to regional ischaemia followed by reperfusion.

The study was designed to demonstrate the time course of neutrophil chemotactic factor (NCF) release from blood-free isolated rat hearts and to clarify the characteristics of NCF in order to facilitate its identification. Coronary effluents were collected every minute from Langendorff perfused rat hearts during ligation of the left coronary artery for 40 min and reperfusion for 60 min. The neutrophil chemotactic activity in the effluents was assayed using modified Boyden's chambers with rat neutrophils isolated from peripheral blood as the indicator cells. The NCF release started at 10 min of coronary artery occlusion. During the reperfusion period, NCF release peaked at 5 min (230% of preischaemic value). To clarify the characteristics of NCF, the changes in chemotactic activity were examined using various inhibitors and inactivators of possible NCF candidates (LTB4, PAF, 5-lipoxygenase, and thromboxane synthase). The heat stability of NCF was also examined to exclude heat labile molecules such as adenosine or complements appearing as NCF. Among the various substances examined, only PAF antagonists (CV-6209 and TCV-309 at concentrations of 10(-6) M and 10(-5) M respectively) abolished the chemotactic activity. However direct measurement of PAF in the effluents was unsuccessful. NCF is released from the heart early after ischaemic insult, with the highest peak occurring at 5 min of reperfusion. PAF related substances might be the primary NCF in the effluent but this remains to be determined.

Asbestos-Induced Release of a Human Alveolar Macrophage-Derived Neutrophil Chemotactic Factor

Neutrophils accumulate in the alveoli of asbestos-exposed individuals. In determining whether asbestos fibers induce the release of neutrophil chemotactic factor (NCF) from human alveolar macrophages, alveolar macrophages (10(6) cell/mL) obtained by bronchoalveolar lavage from six non-asbestos-exposed control subjects were exposed to crocidolite (0.1 and 1 mg/mL), chrysotile (1 mg/mL), or medium alone for 4 h, and NCF activity was measured in the supernatants in a 48-well microchemotaxis chamber with polycarbonate membrane filters (pore size, 3 microns) and purified human neutrophils. Alveolar macrophages in medium alone released negligible amounts of NCF (4 +/- 1 neutrophils per high-power field [N/HPF]). When macrophages were exposed to crocidolite (0.1 and 1 mg/mL), significant NCF release occurred (43 +/- 9 and 105 +/- 32 N/HPF, respectively; p less than 0.01 for each amount compare to alveolar macrophages cultured in medium alone). Chrysotile (1 mg/mL) induced similar NCF release (96 +/- 14 N/HPF; p less than 0.01 compared to unstimulated alveolar macrophages). Partial characterization of the NCF by Sephadex G-25 fine gel filtration demonstrated a molecular size of less than 1,000 daltons. These results show that human alveolar macrophages release NCF after exposure to asbestos. Release of NCF by alveolar macrophages in asbestos-exposed individuals may play a central role in the pathogenesis of asbestosis.

Role of Alveolar Macrophages in the Neutrophil-dependent Defense System againstPseudomonas aeruginosaInfection in the Lower Respiratory Tract: Amplifying Effect of Muramyl Dipeptide Analog

Alveolar macrophages are thought to be important in immune or inflammatory reactions. We investigated the role of alveolar macrophages in defense against Pseudomonas aeruginosa infection in the lower respiratory tract. Intratracheal inoculation of formalin-inactivated P. aeruginosa (1 x 10(8)-1 x 10(10) organisms) into normal rats resulted in increase in the number of neutrophils in the bronchoalveolar lavage (BAL) fluid obtained 24 h later. The phagocytic activity of neutrophils for P. aeruginosa was higher than that of alveolar macrophages. These findings indicate that neutrophils are essential for phagocytosis of P. aeruginosa in the lower respiratory tract. On incubation with P. aeruginosa, alveolar macrophages released neutrophil chemotactic factor (NCF) dose-dependently. MDP-Lys(L18), a muramyl dipeptide analog, stimulated alveolar macrophages to phagocytize P. aeruginosa and stimulate the release of NCF from alveolar macrophages in vitro and enhanced the neutrophil response to inoculated P. aeruginosa in vivo. These results indicate that alveolar macrophages are important in initiating the neutrophil-dependent defense system against P. aeruginosa by releasing NCF and that MDP-Lys(L18) can amplify the defense system.

Pathological changes following implantation of intramammary devices (imd) and immunological mediator release by cells on recovered imds

Implantation of abraded polyethylene intramammary devices (IMD) for six months in the mammary glands of cows resulted in macroscopic and microscopic pathological changes in udder tissue. These changes were characterised by hyperplasia and metaplasia of the epithelial cells and hypertrophy of the subepithelial connective tissue examined by light and electron microscopy (EM). Quarters containing IMDs also had increased numbers of neutrophils and macrophages in the subepithelial stroma compared with control quarters. IMDs recovered six months after implantation were shown by transmission and scanning EM to be covered with plaque and cells. These cells were mainly macrophages, although other leucocytes were also present. In vitro culture of recovered IMDs in the presence of lipopolysaccharide resulted in the release of neutrophil chemotactic factor, or factors, and interleukin-1. Some quarters with IMDs also had concurrent infections at the time of slaughter. In these cases both the pathological changes seen in the tissues and the release of soluble mediators following in vitro culture of the IMDs were significantly increased compared with sterile quarters containing IMD.

Effects of in vitro exposure to nitrogen dioxide on human alveolar macrophage release of neutrophil chemotactic factor and interleukin-1

To evaluate the potential toxic and immunologic effects of nitrogen dioxide (NO2) exposure on cells from the lower respiratory tract, normal human alveolar macrophages obtained by bronchoalveolar lavage were exposed to increasing concentrations of NO2 using an in vitro exposure system. Alveolar macrophages exposed to 5, 10, or 15 ppm NO2 for 3 hr showed no difference in cell viability when compared to air-exposed macrophages. In addition, the spontaneous release of neutrophil chemotactic factor (NCF) was not changed by NO2 exposure, nor was there any effect on the ability of alveolar macrophages to release increased amounts of NCF following stimulation with activated zymosan. Furthermore, alveolar macrophages did not spontaneously release interleukin-1 (IL-1) following air or NO2 exposure. When stimulated with influenza virus both air- and NO2-exposed cells released increased amount of IL-1, but was no significant difference in the amount of IL-1 released by air- and NO2-exposed alveolar macrophages. Thus, although NO2 exposure is known to incite an inflammatory response in the lower respiratory tract, using the in vitro exposure system described in this study we were unable to demonstrate a direct toxic effect of NO2 on viability or any NO2-induced change in the release of the immunoregulatory molecules NCF and IL-1.

Neutrophil Chemotactic Factor Release and Neutrophil Alveolitis in Asbestos-Exposed Individuals

Alveolar neutrophil accumulation occurs in asbestosis. To evaluate a possible role for release of neutrophil chemotactic factor (NCF) in the pathogenesis of asbestosis, spontaneous NCF release from alveolar macrophages obtained by bronchoalveolar lavage (BAL) in eight individuals with asbestosis, 13 asbestos-exposed individuals without asbestosis, and five control subjects has been studied. Alveolar macrophages were incubated in medium (four hours; 37 degrees C), and neutrophil responses to the supernatants were assayed in a microchemotaxis chamber. Alveolar macrophages from subjects with asbestosis released more NCF (97 +/- 19 neutrophils per high-power field [N/HPF]) than controls (3 +/- 1 N/HPF; p less than 0.01). Alveolar macrophages from individuals with asbestos exposure and increased BAL neutrophil proportions (n = 7) released more NCF (93 +/- 24 N/HPF) than individuals with asbestos exposure and normal BAL neutrophil proportions (n = 6; 11 +/- 6 N/HPF; p less than 0.02). The results show that spontaneous NCF release occurs in asbestosis and that NCF release is associated with neutrophil alveolitis in asbestos-exposed individuals without asbestosis, suggesting a pathogenic role for NCF in mediating this neutrophil alveolitis. The results of the study also suggest that the presence of crackles is a better predictor of the presence of neutrophil alveolitis than is an abnormal chest x-ray film.

Effect of disodium cromoglycate on inflammatory cells bearing the Fc epsilon receptor type II (Fc ϵRII)

Disodium cromoglycate (DSCG) has well-established stabilizing properties on mast cells and basophils. However, the potential inhibitory effect of DSCG has been little demonstrated on the IgE stimulation of cell populations expressing epsilon receptors type II, (Fc ϵRII), such as mononuclear phagocytes, eosinophils or platelets. Therefore, using various parameters of IgE-mediated triggering, we demonstrated the inhibitory role of DSCG on: (i) the release of neutrophil chemotactic factor by human alveolar macrophages, (ii) the oxygen metabolite-dependent chemiluminescence of human alveolar macrophages, rat peritonal macrophages, human eosinophils, human and rat platelets, and (iii) the β-glucuronidase release and synthesis by human alveolar macrophages. The inhibition of IgE-dependent stimulation ranged from 60% to 80%, according to the cells and to the measured parameter. It could therefore be considered that the action of DSCG was not restricted to its effects on mast cells and basophils, but also on other cells expressing Fc ϵR leading to a potential reduction of the physiopathological consequences of allergic asthma and, possibly, of the late phase reaction sometimes associated with the disease, insofar as these cells are involved.

Identification and characterization of neutrophil chemotactic activity in aspirin-induced asthma.

In order to determine if mast cell mediators are released during aspirin challenge in aspirin-sensitive asthmatics, we measured neutrophil chemotactic activity, which has been shown to be an indicator of mast cell degranulation. Four aspirin-sensitive asthmatic subjects were given doses of aspirin (60 to 325 mg) previously determined to cause a 20 to 30% fall in forced expiratory volume in one second (FEV1); pulmonary function was followed by serial spirograms and body plethysmography. Serum was obtained before and at 30, 60, 90, 120, 180, and 240 min after challenge, corresponding to the times of pulmonary function measurements. Neutrophil chemotactic activity was measured using a modified Boyden chamber assay. Maximal bronchoconstriction occurred 60 to 120 min after aspirin ingestion. An increase in neutrophil chemotactic activity of 300 to 600% over baseline was detected in all subjects. In 3 subjects, neutrophil chemotactic activity release paralleled bronchoconstriction, and in 1 subject, it followed onset of bronchoconstriction. Physicochemical analysis showed that the neutrophil chemotactic activity eluted in the void volume of a Sephadex G-200 column (greater than or equal to 250,000 daltons) and from Sephadex QAE anion exchange chromatography in a region corresponding to 0.2 to 0.3 M NaCl. Its isoelectric point was in the pH range 6.5 to 7.5. These characteristics are compatible with neutrophil chemotactic factor of mast cell origin. Pretreatment with sodium cromolyn (40 mg) completely eliminated neutrophil chemotactic factor release, but only partially suppressed the fall in FEV1 in 2 subjects and had no effect on FEV1 fall in a third.(ABSTRACT TRUNCATED AT 250 WORDS)

Mediators in exercise-induced asthma

Circulating concentrations of the mast cell-associated mediators, histamine and neutrophil chemotactic factor (NCF) of high molecular weight, were measured in atopic and nonatopic asthmatics after treadmill exercise. Elevations in the concentrations of both mediators accompanied the development of exercise-induced asthma (EIA). Normal individuals did not release mediators or develop bronchoconstriction after an identical exercise. The elaboration of mediators was not due to the onset of airflow obstruction, the postexercise basophilia, or the exercise task per se. A treadmill exercise undertaken while inhaling fully conditioned air inhibited EIA and NCF release; in contrast the same exercise undertaken while breathing cold, dry air elicited EIA and the production of mediators. This suggests that the stimulus for EIA and mediator release may be identical. Late-phase asthmatic reactions occur 3 to 9 hr after exercise in some asthmatics and are accompanied by the appearance of circulating NCF, as previously reported in allergen-induced late responses. In addition to the contribution of mediators to the spasmogenic reaction in EIA, mediators may contribute to bronchial inflammation by activating circulating leukocytes. There was a kinetic increase in the expression of neutrophil C3b receptors in EIA (+) asthmatics for up to 60 min after treadmill exercise. The enhancement of C3b receptors, as evidence of neutrophil activation, was preceded by release of NCF and reductions in peak expiratory flow rates. The prior administration of cromolyn inhibited EIA, NCF release, and enhancement of C3b receptors. These changes were not observed in EIA (−) asthmatics after an identical exercise task. These findings support the view that mediators are released in EIA and may play an important role in its pathogenesis.

Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure.

After intratracheal injection of short chrysotile asbestos fibres in guinea-pigs an intense neutrophil alveolitis was observed within three days. Evaluation by bronchoalveolar lavage of the inflammatory and immune effector cells producing the alveolitis by three days showed an increased proportion of polymorphonuclear leucocytes, which comprised 21% +/- 3% of the total leucocytes compared with 9% +/- 2% for the controls (p less than 0.05), persisting for at least six weeks (after which time the polymorphonuclear leucocytes comprised 28% +/- 2% compared with 7% +/- 1% for the controls: p less than 0.05). One mechanism by which asbestos fibres may cause polymorphonuclear leucocytes to be attracted to the alveolar structures is by induced release of neutrophil chemotactic factor by alveolar macrophages. When exposed in vitro to short or intermediate chrysotile fibres or amosite or crocidolite fibres guinea-pig alveolar macrophages released appreciable amounts of neutrophil chemotactic factor. The release of this chemotactic factor was augmented when the asbestos fibres had been previously exposed to normal serum. The chemotactic factor was lipid soluble, and was similar to the neutrophil chemotactic factor spontaneously released by alveolar macrophages recovered from guinea-pigs exposed in vivo to short chrysotile fibres. These observations suggest that alveolar macrophages may play an important part in the early stages of asbestosis by modulating the migration of neutrophils to the lung.

Bronchial asthma and the neutrophil chemotactic factor.

Neutrophil chemotactic factor (NCF) is a slight acidic macromolecule which is released into the circulation of asthmatic individuals following antigen provocation and an exercise task. It also appears in late asthmatic reactions with a time course of appearance which precedes the second fall in FEV1. The release of NCF was inhibited by prior administration of disodium cromoglycate (DSCG) suggesting its possible mast cell origin.

Exercise-induced release of histamine and neutrophil chemotactic factor in atopic asthmatics

Concentrations of plasma histamine and serum neutrophil chemotactic factor (NCF) were measured in seven atopic asthmatics who developed exercise-induced asthma (EIA) after a treadmill task. The results were compared with those obtained after inhalation of specific antigen or methacholine. Plasma histamine concentrations were measured with a novel double-isotope radiometric assay, and NCF was identified by its elution in the void volume fractions of Sephadex G-200 and as a single peak of activity at approximately 0.20 molar NaCl after anion exchange chromatography on diethylaminoethyl-Sephacel (pH 7.8). After exercise or antigen challenge, the time courses of appearance of both mediators were virtually identical and accompanied the increase in airways obstruction. There was a statistically significant correlation between the concentrations of histamine or NCF and the magnitude of airflow obstruction after exercise and antigen challenge. This suggested that there may be a direct association between mediator release and EIA or antigen-induced bronchoconstriction. In contrast, there were no significant elevations in circulating histamine and NC'F after inhalation of methacholine, at concentrations giving a fall in FEV 1 comparable to that induced by exercise or antigen. The prior administration of cromolyn to three asthmatics inhibited both their EIA and the release of histamine and NCF. When four asthmatics were exercised for periods of 1, 3, and 6 min, the release of NCF and fall in peak expiratory flow rate were directly related to the duration of the exercise. The rise of NCF activity in subjects with EIA was fivefold greater than that observed in asthmatics who did not experience airways obstruction when subjected to the same exercise task. These results provide further evidence that mediators of hypersensitivity are released during EIA.

Modulation of release of neutrophil chemotactic factor (NCF).

Clinical & Experimental AllergyVolume 10, Issue s1 p. 491-496 Modulation of release of neutrophil chemotactic factor (NCF) T. S. C. ORR, Corresponding Author T. S. C. ORR Fisons Pharmaceutical Division, Research Group, Loughborough, LeicestershireDr T. S. C. Orr, Fisons Pharmaceutical Division, Research Group, Loughborough, Leicestershire.Search for more papers by this authorE. V. ELLIOTT, E. V. ELLIOTT Fisons Pharmaceutical Division, Research Group, Loughborough, LeicestershireSearch for more papers by this authorR. E. C. ALTOUNYAN, R. E. C. ALTOUNYAN Fisons Pharmaceutical Division, Research Group, Loughborough, LeicestershireSearch for more papers by this authorM. A. STERN, M. A. STERN Consultant Clinical Immunologist, General Hospital, LeicesterSearch for more papers by this author T. S. C. ORR, Corresponding Author T. S. C. ORR Fisons Pharmaceutical Division, Research Group, Loughborough, LeicestershireDr T. S. C. Orr, Fisons Pharmaceutical Division, Research Group, Loughborough, Leicestershire.Search for more papers by this authorE. V. ELLIOTT, E. V. ELLIOTT Fisons Pharmaceutical Division, Research Group, Loughborough, LeicestershireSearch for more papers by this authorR. E. C. ALTOUNYAN, R. E. C. ALTOUNYAN Fisons Pharmaceutical Division, Research Group, Loughborough, LeicestershireSearch for more papers by this authorM. A. STERN, M. A. STERN Consultant Clinical Immunologist, General Hospital, LeicesterSearch for more papers by this author First published: July 1980 https://doi.org/10.1111/j.1365-2222.1980.tb02163.xCitations: 10AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume10, Issues1July 1980Pages 491-496 RelatedInformation