scholarly journals Antibody Titers of an Human Immunoglobulin Preparation against Group B Streptococci

1993 ◽  
Vol 67 (12) ◽  
pp. 1233-1234
Author(s):  
Shuji MIURA ◽  
Toshihiko ARAI
1990 ◽  
Vol 58 (6) ◽  
pp. 1789-1795 ◽  
Author(s):  
B F Anthony ◽  
N F Concepcion ◽  
S M Puentes ◽  
N R Payne

1985 ◽  
Vol 17 (2) ◽  
pp. 191-193
Author(s):  
Chris Mulder ◽  
Pieter Bol ◽  
Arjan Nabbe ◽  
Bob Zanen

1999 ◽  
Vol 86 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Richard M. Whitehurst ◽  
Rachel Laskey ◽  
Ronald N. Goldberg ◽  
Donald Herbert ◽  
Cornelius Van Breemen

To study whether a sepsis-induced increase in des-Arg9-bradykinin (des-Arg9-BK) and bradykinin (BK) B1-receptor activity participates in the observed increase in pulmonary vascular resistance in neonatal group B streptococcal sepsis (GBS), isometric force bioassays of pulmonary artery (PA) rings were studied, after 4-h exposure to either Krebs or GBS, by using the following protocols: 1) BK dose-response curve, 2) vascular response to BK with N G-nitro-l-arginine methyl ester (l-NAME), and 3) response to des-Arg9-BK (BK metabolite and B1 agonist). PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group ( P = 0.034) at a concentration of 10−5 M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls ( P < 0.001). BK (10−6 M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls ( P < 0.001), and preincubation withl-NAME decreased relaxation in both. These results suggest that GBS decreased endothelium-dependent BK relaxation and increased contractile response to des-Arg9-BK. We speculate that this occurs secondary to upregulation of B1 receptors reflected by B1-agonist-mediated PA contraction.


1977 ◽  
Vol 2 (15) ◽  
pp. 500-501 ◽  
Author(s):  
Leslie R. Ashdown ◽  
P. H. Hewson ◽  
S. K. Suleman
Keyword(s):  

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