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Human neutrophil elastase catalyzes the inactivation of antithrombin by a specific and limited proteinolytic cleavage. This inactivation reaction is greatly accelerated by an active anticoagulant heparin subfraction with high binding affinity for antithrombin. A potentially complex reaction mechanism is suggested by the binding of both neutrophil elastase and antithrombin to heparin. The in vitrokinetic behavior of this system was examined under two different conditions: 1) at a constant antithrombin concentration in which the active anticoagulant heparin was varied from catalytic to saturating levels; and 2) at a fixed, saturating heparin concentration and variable antithrombin levels. Under conditions of excess heparin, the inactivation could be continuously monitored by a decrease in the ultraviolet fluorescence emission of the inhibitor. A Kmof approximately 1 µMfor the heparin-antithrombin complex and a turnover number of approximately 200/min was estimated from these analyses. Maximum acceleratory effects of heparin on the inactivation of antithrombin occur at heparin concentrations significantly lower than those required to saturate antithrombin. The divergence in acceleratory effect and antithrombin binding contrasts with the anticoagulant functioning of heparin in promoting the formation of covalent antithrombin-enzyme complexes and is likely to derive from the fact that neutrophil elastase is not consumed in the inactivation reaction. A size dependence was observed for the heparin effect since an anticoagulantly active octasaccharide fragment of heparin, with avid antithrombin binding activity, was without effect on the inactivation of antithrombin by neutrophil elastase. Despite the completely nonfunctional nature of elastase-cleaved antithrombin and the altered physical properties of the inhibitor as indicated by fluorescence and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the inactivated inhibitor exhibited a circulating half-life in rabbits that was indistinguishable from native antithrombin. These results point to an unexpected and apparently contradictory function for heparin which may relate to the properties of the vascular endothelium in pathological situations.

It is the purpose of this paper to present some observations on the relationship of ear disease and nasopharyngeal lymphoid tissue. Interest in pharyngeal lymphoid tissue occurred very early in the history of medicine. Hippocrates referred to swellings and inflammations of the throat in 400 B. C. Celsus described a method for removing the tonsils in 50 A. D. The word adenoid first appeared in the literature during the Roman domination of medicine. Alubucasis published what is perhaps the first account of the indications for tonsillectomy, about 1100 A. D.1 Numerous reports on this subject have been published, but many questions concerning this problem still remain unanswered.Clinical evidence has long supported the assumption that diseases of the Eustachian tube and middle ear are frequently related to changes of the lymphoid tissue of the nasopharynx. The anatomical continuity of the structures of the Eustachian tube and the nasopharynx is

CLINICAL observations indicate that many body changes classified as allergic cannot be explained purely on the basis of antigen-antibody reactions. Autonomic dysfunctions, including psychic changes, vasomotor reactions, and endocrine imbalances, are equally important in the production of this altered reaction known as allergy. The phylogenetic concept of allergy as presented by Williams1 offers a refreshing approach to the scope of allergy. The statement by Forman2 that allergy is the sum total of unfavorable stresses and strains which the environment places upon the individual indicates a broadening of the concept. The appreciation of allergy in the various fields of medicine has altered the diagnosis and treatment in many diseases. This change has been very apparent in otorhinolaryngology.It is the purpose of this presentation to evaluate the role of allergy in otology. The material presented was obtained from a partnership practice limited to otology. The partnership consists of Dr.