No abstract

Previous investigations have indicated that the first of the four recognized components of complement exists in serum as a proesterase which may be activated by antigen-antibody aggregates (1-3), by plasmin (1), or, in the partially purified state, by adjustment of physico-chemical conditions (4).The active esterase hydrolyzed certain synthetic amino acid esters, among which N-acetyl-L-tyrosine ethyl ester was most susceptible (3-5). This substrate was hydrolyzedmaximally between pH 7.5 and 8.2 and at 41°C. The esterase was inhibited by a heat-labile factor in human serum which did not appear to be related to any of the known components of complement, and by certain sulfbydryl-containing reducing agents. The esterase could not be identified with other known hydrolytic enzymes of serum (5) The possible role of the first component of complement (CPl) as a proenzyme was first suggested by studies of the mechanism of inactivation of human complement by plasmin and by antigen-antibody aggregates (1, 2). Subsequently, two independent lines of evidence appeared to substantiate this hypothesis. In the first approach (3), an esterasewith complement-inactivating activity could be eluted from antigen-antibody aggregates which had been treated with CJl-containing serum reagents. In the second approach (4), with which the present report is further concerned, C~I was partially purified at pH 5.5 and at low temperatures and was brought into the soluble phase only at relatively high ionic strengths. Under these conditions, the preparation retained its hemolytic activity in the presence of the second, third, and fourth components of complement provided that it was maintained at pH 5.5, ionic strength 0.30

We describe a patient with granulomatous mastitis due to Mycobacterium abscessus that presented as a mass lesion and was associated with a pierced nipple. To our knowledge, this is the first reported case of mastitis due to M. abscessus and the first association of this organism with body piercing.

Variations in cognitive performance across clinical or other populations may stem from one or a combination of sources. Such variation usually comprises systematic differences in duration, correctness of task performance across multiple trials, or both. Factors affecting these response properties may have to do with architecture of the cognitive system executing the

No abstract