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Cited by 507

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Complement-Induced Granulocyte Aggregation: An Unsuspected Mechanism of Disease

Bleich, Howard L., Moore, Mary Jean, Jacob, Harry S., Craddock, Philip R., Hammerschmidt, Dale E., Moldow, Charles F.·1980·New England Journal of Medicine

Abstract

The capacity of blood cells to aggregate, best exemplified by the response of platelets to vascular injury, is generally thought to be beneficial. However, if aggregation occurs inappropriately—that is, in a manner irrelevant to hemostasis — ischemic syndromes may result. The myocardial ischemia of Prinzmetal's angina pectoris, for example, may reflect platelet aggregation in coronary arteries. This article presents evidence that granulocytes as well as platelets can aggregate intravascularly, and that the resultant and previously unsuspected phenomenon of leukoembolization may underlie tissue damage in such diverse clinical situations as pulmonary dysfunction in hemodialyzed patients, sudden blindness with retinal infarction after . . .

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Metadata

Authors
Bleich, H. L., Moore, M. J., Jacob, H. S., Craddock, P. R., Hammerschmidt, D. E., & Moldow, C. F.
Venue
New England Journal of Medicine
Published
1980-04-03
Volume
302
Issue
14
Pages
789-794
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W2090763136
Cited by
507
References
0
FWCI
15.16
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Complement-Induced Granulocyte Aggregation: An Unsuspected Mechanism of Disease. https://app.cochat.ai/papers/10.1056/nejm198004033021407
The paper
Bleich, H. L., Moore, M. J., Jacob, H. S., Craddock, P. R., Hammerschmidt, D. E., & Moldow, C. F. (1980). Complement-Induced Granulocyte Aggregation: An Unsuspected Mechanism of Disease. New England Journal of Medicine. https://doi.org/10.1056/nejm198004033021407

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.