Evaluation of biocompatibility of mineral trioxide aggregate with an improved rabbit ear chamber

2005 ◽  
Vol 32 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Y. M. MASUDA ◽  
X. WANG ◽  
M. HOSSAIN ◽  
A. UNNO ◽  
J. A. JAYAWARDENA ◽  
...  
1973 ◽  
Vol 78 (3) ◽  
pp. 167-168
Author(s):  
J. Falk ◽  
K.-E. Arfors ◽  
F. N. McKenzie

1976 ◽  
Vol 21 (1) ◽  
pp. 45-49
Author(s):  
R.A.J. Ireland ◽  
T.A. Robertson ◽  
J.M Papadimitriou

1951 ◽  
Vol 94 (6) ◽  
pp. 521-534 ◽  
Author(s):  
W. Barry Wood ◽  
Mary Ruth Smith ◽  
William D. Perry ◽  
John W. Berry

Evidence has been presented that the introduction of large numbers of bacteria into the blood stream causes a widespread intravascular reaction, characterized by the sticking of leucocytes to the endothelium of capillaries, arterioles, and venules. The adherent granulocytes promptly become motile and thus potentially phagocytic. This intravascular leucocytic response affords a rapid and efficient mobilization of a vast number of active phagocytes within the blood stream. In some of the smaller vessels of both the systemic and pulmonary circulation the reaction is accompanied by the deposition of what appears to be intravascular fibrin. Direct observation by the rabbit ear chamber technique has revealed that leucocytes thus mobilized in small peripheral vessels are capable of phagocyting fully encapsulated Friedländer’s bacilli in the absence of antibody. Ingestion of the encapsulated blood-borne bacteria results from surface phagocytosis and occurs primarily in those vessels in which the flow of blood is either slowed or has temporarily stopped altogether. Leucocytes can be seen to phagocyte the organisms by first trapping them against the walls of the vessels or against adjacent leucocytes. Bacteria caught in the interstices of the intravascular "fibrin" may likewise be immobilized and readily phagocyted. Thus granulocytes, without the aid of opsonins, are able to ingest and destroy encapsulated blood-borne bacteria by the same mechanisms that operate in extravascular tissues. It is concluded from these studies that intravascular surface phagocytosis by polymorphonuclear leucocytes supplements the well known phagocytic activities of the reticulo-endothelial cells and therefore serves as an important defense of the host in acute infections caused by encapsulated bacteria and complicated by bacteriemia.


1966 ◽  
Vol 124 (4) ◽  
pp. 543-556 ◽  
Author(s):  
W. J. Cliff

Responses to injections of various materials into rabbit ear chambers were studied by in vivo microscopy. The acute inflammatory responses provoked by injections of antibody-antigen complexes were both quantitatively and qualitatively different from the responses obtained after injections of either homologous sera or the antigens alone. The sticking of leukocytes to endothelium during these responses occurred only in the venules draining the injection sites and was frequently present only on the sides of the venules towards the injection sites. An explanation of this finding was proposed in terms of absorption by the minute vessels related to the injection sites of postulated mediator(s) with specific activity on venular endothelium. Analysis of the rates and direction of movement of leukocytes during the reactions produced by the antibody-antigen complexes was performed with the aid of time-lapse cinemicroscopy. The leukocytes that were sticking to the venular endothelium frequently exhibited amoeboid locomotion within the vessels. Twice as many of these cells moved against the direction of blood flow as with it. This finding was discussed and an explanation proposed. A method for detecting a drift in the overall population of emigrated leukocytes within the inflamed tissue was described and revealed that four times as many amoeboid cells moved away from the injection sites as towards them. This result was discussed in the light of the in vitro chemotactic properties of antibody-antigen complexes demonstrated for rabbit leukocytes. An alternative explanation was proposed in terms of variation in the population density of these cells and their random movements and collisions. The rates of amoeboid movement of leukocytes during the acute inflammatory reactions produced by antibody-antigen complexes were similar to the rates found during turpentine inflammation and were compared to other published values.


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