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11. |
Apheresis in the pediatric patient |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 91-94
Christina A. Kasprisin,
Duke O. Kasprisin,
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ISSN:0733-2459
DOI:10.1002/jca.2920020114
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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12. |
Intensive plasma exchange in pediatric patients |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 95-97
S. V. Kevy,
M. Fosburg,
L. Wolfe,
M. Dolan,
D. Galacki,
S. Peters,
M. Jacobson,
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ISSN:0733-2459
DOI:10.1002/jca.2920020115
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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13. |
Putative methods for prevention and treatment of neonatal septicemia |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 98-104
Robert D. Christensen,
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摘要:
AbstractThe high mortality rate observed in newborn infants who contract bacterial sepsis within the first days of life has prompted investigators to seek new methods for the prevention and treatment of this disorder. Among the putative measures recommended for prevention are: (1) administration of antimicrobials to all infants at the time of delivery, (2) identification and treatment of pregnant women colonized with those bacteria known to be major neonatal pathogens and (3) immunization of women to major neonatal pathogens. Three other measures, targeted at diminishing the mortality and morbidity in those in whom preventive measures fail, include: (1) granulocyte transfusion, (2) exchange transfusion and (3) administration of antibody.
ISSN:0733-2459
DOI:10.1002/jca.2920020116
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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14. |
Keynote address: The need for randomized control trials |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 105-111
Thomas C. Chalmers,
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ISSN:0733-2459
DOI:10.1002/jca.2920020117
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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15. |
Leukapheresis and pathogenetic mechanisms in rheumatoid arthritis |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 112-118
Ronald L. Wilder,
Daniel G. Malone,
Cheryl H. Yarboro,
Carole Berkebile,
Boulos Haraoui,
Janice B. Allen,
Sharon M. Wahl,
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摘要:
AbstractRheumatoid Arthritis is a chronic, usually progressive inflammatory disorder of joints in which the immune system plays a central role in the pathogenesis. In its classic form, the synovial tissues from severely affected joints are densely infiltrated with HLA‐DR bearing T‐lymphocytes (primarily OKT4+/Leu3+subset) and macrophage‐like cells. Moreover, these tissues, as demonstrated by ex vivo culture, spontaneously produce high levels of a multitude of inflammatory mediators, such as collagenase, PGE2, interleukin 1 and fibroblast activating factors, indicating that the cells infiltrating the synovium are “activated”. The action of these various inflammatory mediators on different target substances or cells (collagen, fibroblasts, chondrocytes, osteoclasts, etc.) most likely produce the characteristic pattern of joint pathology. Recent data indicate that this classic form of synovitis tends to be associated with peripheral anergy and other qualitative and quantitative abnormalities in the peripheral blood mononuclear cells. Repeated leukapheresis can induce substantial, although transient, clinical improvement in patients with these classic features, probably as a consequence of disrupting T‐lymphocyte traffic.Rheumatoid synovitis, however, is highly heterogeneous, but can be categorized into subsets. For example, a subset of patients with highly active clinical rheumatoid arthritis exists which do not exhibit the classic features of disease. Synovial tissues from this patient subset are sparsely infiltrated by T‐lymphocytes but contain mainly macrophages and fibroblasts, as well as prominent lining layer fibrin deposition. Patients with these synovial features do not appear to respond therapeutically to repeated leukapheresis. In view of the wide immunopathologic spectrum in rheumatoid arthritis, assessment of the role, if any, of leukapheresis in therapy remains unclear, but the technique does provide a powerful investigative tool.Rheumatoid arthritis is a chronic, usually progressive, destructive disorder of joints in which effector mechanisms of the immune system appear to play a major role in its pathogenesis. Various types of apheresis have the potential to modulate immune effector mechanisms and, in theory, could have a therapeutic effect in this disorder. In this report, we present an overview of evolving concepts of the immunopathogenesis of rheumatoid arthritis and relate these concepts to our experiences with
ISSN:0733-2459
DOI:10.1002/jca.2920020118
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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16. |
A controlled trial of plasma exchange in rheumatoid arthritis |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 119-126
Alan R. Giles,
Isaac L. Dwosh,
Peter M. Ford,
Joseph L. Pater,
Tassos P. Anastassiades,
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ISSN:0733-2459
DOI:10.1002/jca.2920020119
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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17. |
Lymphapheresis in rheumatoid arthritis |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 127-134
T. W. Bunch,
J. D. O'Duffy,
A. A. Pineda,
A. R. Zinsmeister,
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ISSN:0733-2459
DOI:10.1002/jca.2920020120
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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18. |
Immunosuppressive drug therapy with plasmapheresis in chronic progressive multiple sclerosis: A controlled study |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 135-137
B. O. Khatri,
G. J. Harrington,
D. Schmoll,
M. P. McQuillen,
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ISSN:0733-2459
DOI:10.1002/jca.2920020121
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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19. |
Free communication ‐ scientific session |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 138-150
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ISSN:0733-2459
DOI:10.1002/jca.2920020122
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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20. |
Program committee |
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Journal of Clinical Apheresis,
Volume 2,
Issue 1,
1984,
Page 151-151
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ISSN:0733-2459
DOI:10.1002/jca.2920020123
出版商:John Wiley&Sons, Inc.
年代:1984
数据来源: WILEY
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