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Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. III. Demonstration of abnormal clot structure by electron microscopy.

作者信息

BANG N U, FLETCHER A P, ALKJAERSIG N, SHERRY S

出版信息

J Clin Invest. 1962 Apr;41(4):935-48. doi: 10.1172/JCI104548.

DOI:10.1172/JCI104548
PMID:13864646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC290993/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/d1d991cc9acc/jcinvest00313-0289-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/c69131a9d21c/jcinvest00313-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/6cfa8dd84a60/jcinvest00313-0283-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/d1717ef4cbed/jcinvest00313-0283-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/d1049bba90d4/jcinvest00313-0284-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/6efdc3e7f0d9/jcinvest00313-0285-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/af4c33d0c272/jcinvest00313-0286-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/0cae59eb630a/jcinvest00313-0287-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/f8acba28cb44/jcinvest00313-0288-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/d1d991cc9acc/jcinvest00313-0289-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/c69131a9d21c/jcinvest00313-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/6cfa8dd84a60/jcinvest00313-0283-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/d1717ef4cbed/jcinvest00313-0283-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/d1049bba90d4/jcinvest00313-0284-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/6efdc3e7f0d9/jcinvest00313-0285-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/af4c33d0c272/jcinvest00313-0286-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/0cae59eb630a/jcinvest00313-0287-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/f8acba28cb44/jcinvest00313-0288-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14fc/290993/d1d991cc9acc/jcinvest00313-0289-a.jpg

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Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. III. Demonstration of abnormal clot structure by electron microscopy.病理性血浆蛋白水解（“纤维蛋白溶解”）状态下发生的凝血缺陷的发病机制。III. 用电镜显示异常凝块结构
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2
THE FIBRINOLYTIC MECHANISM IN HAEMOSTASIS: A REVIEW.止血中的纤维蛋白溶解机制：综述
J Clin Pathol. 1964 Sep;17(5):520-30. doi: 10.1136/jcp.17.5.520.
3
ULTRAMICROSCOPIC STRUCTURE OF THE RHEUMATOID NODULE.类风湿结节的超微结构

本文引用的文献

1
A study of fixation for electron microscopy.电子显微镜固定研究。
J Exp Med. 1952 Mar;95(3):285-98. doi: 10.1084/jem.95.3.285.
2
Effects of ions and neutral molecules on fibrin clotting.离子和中性分子对纤维蛋白凝血的影响。
J Biol Chem. 1951 Aug;191(2):735-56.
3
A new method for the determination of fibrinogen in small samples of plasma.一种测定少量血浆样本中纤维蛋白原的新方法。
Ann Rheum Dis. 1964 Sep;23(5):345-63. doi: 10.1136/ard.23.5.345.
4
[THE SIGNIFICANCE OF PROTEOLYSIS IN OBSTETRICAL DEFIBRINATION HEMORRHAGES AND THERAPY WITH TRASYLOL].[蛋白酶解在产科去纤维蛋白性出血中的意义及抑肽酶治疗]
Arch Gynakol. 1964 Apr 14;199:475-95. doi: 10.1007/BF00669775.
5
[ELECTRON MICROSCOPIC STUDIES ON FIBRIN DECOMPOSITION BY STREPTOKINASE].[链激酶对纤维蛋白分解作用的电子显微镜研究]
Klin Wochenschr. 1964 Feb 15;42:196-8. doi: 10.1007/BF01482623.
6
ABNORMAL PLASMINOGEN-PLASMIN SYSTEM ACTIVITY (FIBRINOLYSIS) IN PATIENTS WITH HEPATIC CIRRHOSIS: ITS CAUSE AND CONSEQUENCES.肝硬化患者纤溶酶原-纤溶酶系统活性异常（纤维蛋白溶解）：其原因及后果
J Clin Invest. 1964 Apr;43(4):681-95. doi: 10.1172/JCI104953.
7
Thrombolytic therapy.溶栓治疗。
Proc R Soc Med. 1963 May;56(5):414-8. doi: 10.1177/003591576305600536.
8
Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. II. The significance, mechanism and consequences of defective fibrin polymerization.病理性血浆蛋白水解（“纤维蛋白溶解”）状态下凝血缺陷的发病机制。II. 纤维蛋白聚合缺陷的意义、机制及后果。
J Clin Invest. 1962 Apr;41(4):917-34. doi: 10.1172/JCI104547.
9
Adsorptive endocytosis of fibrin monomer by macrophages: evidence of a receptor for the amino terminus of the fibrin alpha chain.巨噬细胞对纤维蛋白单体的吸附性胞吞作用：纤维蛋白α链氨基末端受体的证据。
Proc Natl Acad Sci U S A. 1982 Aug;79(15):4565-9. doi: 10.1073/pnas.79.15.4565.
10
[On the demonstration and occurrence and the importance of the intracorporeal origin of fibrinogen breakdown products with special consideration of the demonstration of high molecular fibrin breakdown products in menstrual blood].[关于纤维蛋白原降解产物的体内起源的证明、发生及重要性，特别考虑月经血中高分子纤维蛋白降解产物的证明]
Blut. 1965 Oct;12(1):22-6. doi: 10.1007/BF01631200.
J Lab Clin Med. 1951 Feb;37(2):316-20.
4
Studies on the thrombolytic activity of human plasma.人体血浆溶栓活性的研究。
J Clin Invest. 1960 Feb;39(2):426-34. doi: 10.1172/JCI104054.
5
Fractionation of polypeptides and proteins on dextran gels.葡聚糖凝胶上多肽和蛋白质的分级分离
Clin Chim Acta. 1959 Nov;4:776-8. doi: 10.1016/0009-8981(59)90026-9.
6
Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. I. The significance of fibrinogen proteolysis and circulating fibrinogen breakdown products.病理性血浆蛋白水解（“纤维蛋白溶解”）状态下发生的凝血缺陷的发病机制。I. 纤维蛋白原蛋白水解和循环纤维蛋白原降解产物的意义。
J Clin Invest. 1962 Apr;41(4):896-916. doi: 10.1172/JCI104546.
7
Pathogenesis of the coagulation defect developing during pathological plasma proteolytic ("fibrinolytic") states. II. The significance, mechanism and consequences of defective fibrin polymerization.病理性血浆蛋白水解（“纤维蛋白溶解”）状态下凝血缺陷的发病机制。II. 纤维蛋白聚合缺陷的意义、机制及后果。
J Clin Invest. 1962 Apr;41(4):917-34. doi: 10.1172/JCI104547.
8
The maintenance of a sustained thrombolytic state in man. I. Induction and effects.人体持续溶栓状态的维持。I. 诱导与效果。
J Clin Invest. 1959 Jul;38(7):1096-110. doi: 10.1172/JCI103886.
9
The mechanism of clot dissolution by plasmin.纤溶酶溶解血栓的机制。
J Clin Invest. 1959 Jul;38(7):1086-95. doi: 10.1172/JCI103885.
10
xi-Aminocaproic acid: an inhibitor of plasminogen activation.ε-氨基己酸：一种纤溶酶原激活抑制剂。
J Biol Chem. 1959 Apr;234(4):832-7.