Human herpesvirus-8 (HHV-8) DNA was identified in kidney allografts in 2 of 3 transplant recipients prior to the development of Kaposi's sarcoma, and increase in viral antibody titer was found in the third. Combined genotypic and serologic analyses could be used to identify patients at risk and suggest that the kidney may be a site of HHV-8 latency.

No abstract

No abstract

The availability of monoclonal antibodies which bind to a specific antigen at distinct and well-defined sites has led to a better understanding of the effects of highly specific enzyme-antibody interactions on enzyme behaviour. By appropriate selection it has been possible to isolate those antibodies that are non-inhibitory to biological activity of the enzyme and bind at strategic locations on the antigen molecule, resulting in a considerable stabilization effect on the enzyme conformation. Moreover, such monoclonal antibodies proved to have a chaperone activity leading to a considerable refolding effect on the enzyme which was already partially heat denatured. Renaturation of carboxypeptidase A after heat denaturation in the presence of selected monoclonal antibodies, was followed by recovery of its enzymatic activity. The refolding effect of anti-CPA monoclonal antibodies on heat-denatured enzyme depends on the degree of denaturation of the enzyme and on the location of the antigenic site of each antibody. The additivity effect of the pairs of monoclonal antibodies on the refolding process of CPA proved to be dependent on the localization of the antigenic sites of the monoclonal antibodies studied.

THE MEASUREMENT of serum en$ zyme activities, particularly those of crea$ tine phosphokinase (CPK), aldolase, and glutamic oxaloacetic transaminase (SGOT), is an important adjunct in the diagnosis of primary muscle disease.1-4 Elevations have been found in patients with muscular dystrophy and polymyositis,5-7 whereas patients with neurogenic atrophy generally have had normal levels.8Altered potassium metabolism has long been associated with muscle dysfunction,9 but only a few references have appeared linking hypokalemia, myopathy, and serum enzyme elevation.10-12 Three patients with hypokalemia and severe muscle weakness were studied; all had marked alterations in their serum enzymes, particularly CPK. MethodsCreatine phosphokinase determinations were done using the method of Nielsen and Ludvigsen.13 The normal range is 0\g=m\Uto 18\g=m\U per milliliter.Glutamic oxaloacetic transaminase determinations were performed using a modification of the method of Henry and co-workers.14 The normal values are in the range of 10\g=m\Uto 35\g=m\U per milliliter. Aldolase determinations were based on the method of Beisenherz and co-workers15 and the normal values are 3/iU to 8µ per milliliter.Serum potassium values were determined by flame photometry. Normal range is 3.9 to 5.2 mEq/liter ± 0.2 mEq/liter. Muscle strength was evaluated daily by one, and often by two, of the authors. Strength was graded according to the method used by Smith et al16 where 5 is normal and 0 represents no observed activity.