Cross-species reactivity of the anti-idiotype anti-OKT3 cascade between mice and humans
The administration of murine mAb specific for the CD3ϵ subunit of the TCR complex (OKT3) has been demonstrated to engender in humans an anti-OKT3 idiotypic cascade. This study used murine-derived anti-OKT3 (Ab2) as a bioreagent to determine whether this Ab2 and polyclonal anti-(anti-OKT3) (Ab3) gene...
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| Veröffentlicht in: | Human immunology 1992-04, Vol.33 (4), p.249-258 |
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| creator | Carreno, Manuel Fuller, Laphalle Zucker, Keith Yang, Wen-Chic Burke, George Nery, Jose Gomez, Carmen Esquenazi, Violet Miller, Joshua |
| description | The administration of murine mAb specific for the CD3ϵ subunit of the TCR complex (OKT3) has been demonstrated to engender in humans an anti-OKT3 idiotypic cascade. This study used murine-derived anti-OKT3 (Ab2) as a bioreagent to determine whether this Ab2 and polyclonal anti-(anti-OKT3) (Ab3) generated in some human kidney transplant patients are idiotypically connected. Two anti-OKT3 mAbs G-880 (IgG1) and M-12 (IgM) were derived by immunizing BALB/c mice with the OKT3-secreting hybridoma. The two mAbs exhibited specificity for OKT3-F(ab)
′
2 idiotypic determinants. Both mAbs were tested for their ability to inhibit OKT3 induced mitogenesis and to block FITC—OKT3 binding to cell surface CD3ϵ chain. The M-12 mAb inhibited OKT3-induced mitogenesis and blocked (≈60%) the binding of OKT3 to peripheral blood (PBL) T-cell CD3ϵ chain in flow cytometry. In contrast, the G-880 mAb did not inhibit mitogenesis and only weakly blocked OKT3 binding to CD3ϵ chain (≈12%). Sera of kidney transplant recipients who received OKT3 antirejection therapy and who developed antiidiotypic anti-OKT3 antibodies could be divided into two subgroups exhibiting anti-OKT3 activity: (a) those who had similar specificity as M-12 and failed to enhance the M-12 inhibition of OKT3 binding to PBL T-cell CD3ϵ chain when added as a third component (
n = 3), and (b) those with anti-OKT3 antibodies with idiotype specificity dissimilar to M-12 and who were able to increase the (maximum 60%) inhibition obtained with M-12 in the OKT3 to T-cell CD3-binding assay (
n = 4). From these observations, we conclude that M-12 had the characteristics of an Ab2β and G-880 that of an Ab2α. Additionally, there was an idiotypic connectivity of mouse-derived M-12 anti-OKT3 (Ab2) and OKT3-engendered human polyclonal anti-(anti-OKT3) (Ab3), in that three of seven patients examined had human serum IgG antibodies that specifically recognized M-12 idiotypic determinants as demonstrated in ELISA. |
| doi_str_mv | 10.1016/0198-8859(92)90332-H |
| format | Article |
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′
2 idiotypic determinants. Both mAbs were tested for their ability to inhibit OKT3 induced mitogenesis and to block FITC—OKT3 binding to cell surface CD3ϵ chain. The M-12 mAb inhibited OKT3-induced mitogenesis and blocked (≈60%) the binding of OKT3 to peripheral blood (PBL) T-cell CD3ϵ chain in flow cytometry. In contrast, the G-880 mAb did not inhibit mitogenesis and only weakly blocked OKT3 binding to CD3ϵ chain (≈12%). Sera of kidney transplant recipients who received OKT3 antirejection therapy and who developed antiidiotypic anti-OKT3 antibodies could be divided into two subgroups exhibiting anti-OKT3 activity: (a) those who had similar specificity as M-12 and failed to enhance the M-12 inhibition of OKT3 binding to PBL T-cell CD3ϵ chain when added as a third component (
n = 3), and (b) those with anti-OKT3 antibodies with idiotype specificity dissimilar to M-12 and who were able to increase the (maximum 60%) inhibition obtained with M-12 in the OKT3 to T-cell CD3-binding assay (
n = 4). From these observations, we conclude that M-12 had the characteristics of an Ab2β and G-880 that of an Ab2α. Additionally, there was an idiotypic connectivity of mouse-derived M-12 anti-OKT3 (Ab2) and OKT3-engendered human polyclonal anti-(anti-OKT3) (Ab3), in that three of seven patients examined had human serum IgG antibodies that specifically recognized M-12 idiotypic determinants as demonstrated in ELISA.</description><identifier>ISSN: 0198-8859</identifier><identifier>EISSN: 1879-1166</identifier><identifier>DOI: 10.1016/0198-8859(92)90332-H</identifier><identifier>PMID: 1386353</identifier><identifier>CODEN: HUIMDQ</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Analysis of the immune response. Humoral and cellular immunity ; Animals ; Antibodies, Anti-Idiotypic - biosynthesis ; Antibodies, Anti-Idiotypic - blood ; Antibodies, Anti-Idiotypic - immunology ; Antibody production ; Antibody Specificity - immunology ; Antigens, Differentiation, T-Lymphocyte - immunology ; Binding Sites, Antibody ; Binding, Competitive ; Biological and medical sciences ; CD3 Complex ; Cross Reactions - genetics ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Humans ; Immunobiology ; Kidney Transplantation - immunology ; Mice ; Mice, Inbred BALB C ; Muromonab-CD3 - immunology ; Muromonab-CD3 - physiology ; Receptors, Antigen, T-Cell - immunology ; Species Specificity ; T-Lymphocytes - immunology</subject><ispartof>Human immunology, 1992-04, Vol.33 (4), p.249-258</ispartof><rights>1992</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-c6172a963aa6247814c772d8ab5ff9d17c96b7f0bc7582a7881b53468ea81fae3</citedby><cites>FETCH-LOGICAL-c332t-c6172a963aa6247814c772d8ab5ff9d17c96b7f0bc7582a7881b53468ea81fae3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0198-8859(92)90332-H$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5402115$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1386353$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Carreno, Manuel</creatorcontrib><creatorcontrib>Fuller, Laphalle</creatorcontrib><creatorcontrib>Zucker, Keith</creatorcontrib><creatorcontrib>Yang, Wen-Chic</creatorcontrib><creatorcontrib>Burke, George</creatorcontrib><creatorcontrib>Nery, Jose</creatorcontrib><creatorcontrib>Gomez, Carmen</creatorcontrib><creatorcontrib>Esquenazi, Violet</creatorcontrib><creatorcontrib>Miller, Joshua</creatorcontrib><title>Cross-species reactivity of the anti-idiotype anti-OKT3 cascade between mice and humans</title><title>Human immunology</title><addtitle>Hum Immunol</addtitle><description>The administration of murine mAb specific for the CD3ϵ subunit of the TCR complex (OKT3) has been demonstrated to engender in humans an anti-OKT3 idiotypic cascade. This study used murine-derived anti-OKT3 (Ab2) as a bioreagent to determine whether this Ab2 and polyclonal anti-(anti-OKT3) (Ab3) generated in some human kidney transplant patients are idiotypically connected. Two anti-OKT3 mAbs G-880 (IgG1) and M-12 (IgM) were derived by immunizing BALB/c mice with the OKT3-secreting hybridoma. The two mAbs exhibited specificity for OKT3-F(ab)
′
2 idiotypic determinants. Both mAbs were tested for their ability to inhibit OKT3 induced mitogenesis and to block FITC—OKT3 binding to cell surface CD3ϵ chain. The M-12 mAb inhibited OKT3-induced mitogenesis and blocked (≈60%) the binding of OKT3 to peripheral blood (PBL) T-cell CD3ϵ chain in flow cytometry. In contrast, the G-880 mAb did not inhibit mitogenesis and only weakly blocked OKT3 binding to CD3ϵ chain (≈12%). Sera of kidney transplant recipients who received OKT3 antirejection therapy and who developed antiidiotypic anti-OKT3 antibodies could be divided into two subgroups exhibiting anti-OKT3 activity: (a) those who had similar specificity as M-12 and failed to enhance the M-12 inhibition of OKT3 binding to PBL T-cell CD3ϵ chain when added as a third component (
n = 3), and (b) those with anti-OKT3 antibodies with idiotype specificity dissimilar to M-12 and who were able to increase the (maximum 60%) inhibition obtained with M-12 in the OKT3 to T-cell CD3-binding assay (
n = 4). From these observations, we conclude that M-12 had the characteristics of an Ab2β and G-880 that of an Ab2α. Additionally, there was an idiotypic connectivity of mouse-derived M-12 anti-OKT3 (Ab2) and OKT3-engendered human polyclonal anti-(anti-OKT3) (Ab3), in that three of seven patients examined had human serum IgG antibodies that specifically recognized M-12 idiotypic determinants as demonstrated in ELISA.</description><subject>Analysis of the immune response. Humoral and cellular immunity</subject><subject>Animals</subject><subject>Antibodies, Anti-Idiotypic - biosynthesis</subject><subject>Antibodies, Anti-Idiotypic - blood</subject><subject>Antibodies, Anti-Idiotypic - immunology</subject><subject>Antibody production</subject><subject>Antibody Specificity - immunology</subject><subject>Antigens, Differentiation, T-Lymphocyte - immunology</subject><subject>Binding Sites, Antibody</subject><subject>Binding, Competitive</subject><subject>Biological and medical sciences</subject><subject>CD3 Complex</subject><subject>Cross Reactions - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Humans</subject><subject>Immunobiology</subject><subject>Kidney Transplantation - immunology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Muromonab-CD3 - immunology</subject><subject>Muromonab-CD3 - physiology</subject><subject>Receptors, Antigen, T-Cell - immunology</subject><subject>Species Specificity</subject><subject>T-Lymphocytes - immunology</subject><issn>0198-8859</issn><issn>1879-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV1r2zAUhsVoSdNu_2ADX5TRXnjTkWx93AxGaJvSQG4ydilk-ZhoxHYqKS3597OXkN21VwfxPueDR4R8BvoNKIjvFLTKlSr1jWa3mnLO8vkHMgUldQ4gxBmZnpALchnjH0qppLKYkAlwJXjJp-T3LPQx5nGLzmPMAlqX_ItP-6xvsrTGzHbJ5772fdpvj6_l04pnzkZna8wqTK-IXdZ6N8Z1tt61tosfyXljNxE_HesV-XV_t5rN88Xy4XH2c5G74d6UOwGSWS24tYIVUkHhpGS1slXZNLoG6bSoZEMrJ0vFrFQKqpIXQqFV0FjkV-TrYe429M87jMm0PjrcbGyH_S4ayanWWrB3QRj2U83kABYH0I1mAjZmG3xrw94ANaN4M1o1o1Wjmfkn3syHti_H-buqxfp_08H0kF8f81Hcpgm2cz6esLKgDKAcsB8HDAdpLx6DicPHdA5rH9AlU_f-7Tv-AlCJnlA</recordid><startdate>199204</startdate><enddate>199204</enddate><creator>Carreno, Manuel</creator><creator>Fuller, Laphalle</creator><creator>Zucker, Keith</creator><creator>Yang, Wen-Chic</creator><creator>Burke, George</creator><creator>Nery, Jose</creator><creator>Gomez, Carmen</creator><creator>Esquenazi, Violet</creator><creator>Miller, Joshua</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>199204</creationdate><title>Cross-species reactivity of the anti-idiotype anti-OKT3 cascade between mice and humans</title><author>Carreno, Manuel ; Fuller, Laphalle ; Zucker, Keith ; Yang, Wen-Chic ; Burke, George ; Nery, Jose ; Gomez, Carmen ; Esquenazi, Violet ; Miller, Joshua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-c6172a963aa6247814c772d8ab5ff9d17c96b7f0bc7582a7881b53468ea81fae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Analysis of the immune response. Humoral and cellular immunity</topic><topic>Animals</topic><topic>Antibodies, Anti-Idiotypic - biosynthesis</topic><topic>Antibodies, Anti-Idiotypic - blood</topic><topic>Antibodies, Anti-Idiotypic - immunology</topic><topic>Antibody production</topic><topic>Antibody Specificity - immunology</topic><topic>Antigens, Differentiation, T-Lymphocyte - immunology</topic><topic>Binding Sites, Antibody</topic><topic>Binding, Competitive</topic><topic>Biological and medical sciences</topic><topic>CD3 Complex</topic><topic>Cross Reactions - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Humans</topic><topic>Immunobiology</topic><topic>Kidney Transplantation - immunology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Muromonab-CD3 - immunology</topic><topic>Muromonab-CD3 - physiology</topic><topic>Receptors, Antigen, T-Cell - immunology</topic><topic>Species Specificity</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carreno, Manuel</creatorcontrib><creatorcontrib>Fuller, Laphalle</creatorcontrib><creatorcontrib>Zucker, Keith</creatorcontrib><creatorcontrib>Yang, Wen-Chic</creatorcontrib><creatorcontrib>Burke, George</creatorcontrib><creatorcontrib>Nery, Jose</creatorcontrib><creatorcontrib>Gomez, Carmen</creatorcontrib><creatorcontrib>Esquenazi, Violet</creatorcontrib><creatorcontrib>Miller, Joshua</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Human immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carreno, Manuel</au><au>Fuller, Laphalle</au><au>Zucker, Keith</au><au>Yang, Wen-Chic</au><au>Burke, George</au><au>Nery, Jose</au><au>Gomez, Carmen</au><au>Esquenazi, Violet</au><au>Miller, Joshua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cross-species reactivity of the anti-idiotype anti-OKT3 cascade between mice and humans</atitle><jtitle>Human immunology</jtitle><addtitle>Hum Immunol</addtitle><date>1992-04</date><risdate>1992</risdate><volume>33</volume><issue>4</issue><spage>249</spage><epage>258</epage><pages>249-258</pages><issn>0198-8859</issn><eissn>1879-1166</eissn><coden>HUIMDQ</coden><abstract>The administration of murine mAb specific for the CD3ϵ subunit of the TCR complex (OKT3) has been demonstrated to engender in humans an anti-OKT3 idiotypic cascade. This study used murine-derived anti-OKT3 (Ab2) as a bioreagent to determine whether this Ab2 and polyclonal anti-(anti-OKT3) (Ab3) generated in some human kidney transplant patients are idiotypically connected. Two anti-OKT3 mAbs G-880 (IgG1) and M-12 (IgM) were derived by immunizing BALB/c mice with the OKT3-secreting hybridoma. The two mAbs exhibited specificity for OKT3-F(ab)
′
2 idiotypic determinants. Both mAbs were tested for their ability to inhibit OKT3 induced mitogenesis and to block FITC—OKT3 binding to cell surface CD3ϵ chain. The M-12 mAb inhibited OKT3-induced mitogenesis and blocked (≈60%) the binding of OKT3 to peripheral blood (PBL) T-cell CD3ϵ chain in flow cytometry. In contrast, the G-880 mAb did not inhibit mitogenesis and only weakly blocked OKT3 binding to CD3ϵ chain (≈12%). Sera of kidney transplant recipients who received OKT3 antirejection therapy and who developed antiidiotypic anti-OKT3 antibodies could be divided into two subgroups exhibiting anti-OKT3 activity: (a) those who had similar specificity as M-12 and failed to enhance the M-12 inhibition of OKT3 binding to PBL T-cell CD3ϵ chain when added as a third component (
n = 3), and (b) those with anti-OKT3 antibodies with idiotype specificity dissimilar to M-12 and who were able to increase the (maximum 60%) inhibition obtained with M-12 in the OKT3 to T-cell CD3-binding assay (
n = 4). From these observations, we conclude that M-12 had the characteristics of an Ab2β and G-880 that of an Ab2α. Additionally, there was an idiotypic connectivity of mouse-derived M-12 anti-OKT3 (Ab2) and OKT3-engendered human polyclonal anti-(anti-OKT3) (Ab3), in that three of seven patients examined had human serum IgG antibodies that specifically recognized M-12 idiotypic determinants as demonstrated in ELISA.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>1386353</pmid><doi>10.1016/0198-8859(92)90332-H</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Human immunology, 1992-04, Vol.33 (4), p.249-258 |
| issn | 0198-8859 1879-1166 |
| language | eng |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Analysis of the immune response. Humoral and cellular immunity Animals Antibodies, Anti-Idiotypic - biosynthesis Antibodies, Anti-Idiotypic - blood Antibodies, Anti-Idiotypic - immunology Antibody production Antibody Specificity - immunology Antigens, Differentiation, T-Lymphocyte - immunology Binding Sites, Antibody Binding, Competitive Biological and medical sciences CD3 Complex Cross Reactions - genetics Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Immunobiology Kidney Transplantation - immunology Mice Mice, Inbred BALB C Muromonab-CD3 - immunology Muromonab-CD3 - physiology Receptors, Antigen, T-Cell - immunology Species Specificity T-Lymphocytes - immunology |
| title | Cross-species reactivity of the anti-idiotype anti-OKT3 cascade between mice and humans |
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