Search PubMed⌕ Search

Biomedical subjects

N Okazaki

Publications and source records attributed to N Okazaki.

202 records · Page 12Linked to original sources
PubMedDate not supplied

Selective induction of macrophages in the middle ear.

A method is described for inducing an influx primarily of macrophages into the middle ears of chinchillas using keyhole limpet hemocyanin (KLH, a strong immunogen) and mineral oil (a nonimmunogen) to provide adequate numbers of these cells for study. Although KLH and mineral oil both induced sterile otitis media in which macrophages were the predominant cell type present in the middle ear, the cytological and histological responses of the middle ears to these substances differed. KLH proved to be a much stronger inducer of actively phagocytic macrophages and also produced serous effusions in about 11% of the experimental animals. This experimental model provides an opportunity for the in vitro and in vivo study of the role of macrophages, the predominant cell type associated with human chronic otitis media with effusion, in the defense system of the middle ear.

Animals↗
PubMedDate not supplied

Experimental otitis media with effusion following middle ear inoculation of nonviable H influenzae.

In order to test the hypothesis that nonviable bacteria can induce middle ear inflammation leading to persistent middle ear effusion (MEE), we conducted an animal experiment using formalin-killed Hemophilus influenzae, the bacterium reported to be the most common pathogen isolated from chronic MEEs. Over 70% of the chinchillas injected with formalin-killed H influenzae type b or a nontypeable isolate developed sterile, straw-colored serous MEEs, and exhibited histological evidence of extensive inflammatory changes of the middle ear mucosal connective tissue and epithelium. Control animals injected with pyrogen-free sterile saline did not exhibit any inflammatory changes or effusions in the middle ears. Our data suggest that endotoxin on the surface of H influenzae, a gram-negative bacterium, may be responsible for the induction of the otitis media with effusion. It is suggested that endotoxin (even when the organisms are no longer viable) may be responsible for the production of serous MEE and inflammatory changes in the middle ear.

Animals↗
PubMedDate not supplied

Experimental study of the Eustachian tube function with regard to its related muscles.

Utilizing electromyography and electrical muscle stimulation, the muscle responsible for opening the Eustachian tube was examined im 12 dogs. Different time values for tubal opening and levator activity indicate little contribution of the levator in the functioning of the tube. By relatively low stimulation of the tensor, the tube opened consistently, while the levator failed to produce any dilation of the tube, regardless of the amount of stimulation, in 6 dogs. Thus, it is concluded that the sole muscle responsible for tubal opening is the tensor, while the levator does not participate in the functioning of the tube.

Animals↗