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B R Nagy

Publications and source records attributed to B R Nagy.

10 recordsLinked to original sources

Secretory component-dependent hepatic transport of IgA antibody-antigen complexes.

The ability of the liver to transport antigen-antibody complexes containing polymeric IgA was tested in a model system using the isolated perfused rat liver and soluble complexes formed between trinitrophenylated (TNP) antigens and MOPC 315, a polymeric mouse IgA protein with anti-TNP activity. A double-label strategy (125I and 131I) was used to separately follow antigen and antibody during isolation and transport by the isolated perfused liver. Complexes formed in antigen excess and isolated by gel filtration were added to the perfusate. The quantity of antigen or antibody transported was determined by counting the radioactivity in collected bile fractions. TNP-human albumin (TNP-HSA) complexed to polymeric IgA antibody was transported from blood to bile while the same antigen complexed to IgG antibody was not. The transport of IgA-(TNP-HSA) complexes was inhibited by preincubation with human secretory component (SC), which indicated that transport of such complexes proceeds though an SC-dependent mechanism previously described for uncomplexed polymeric IgA antibody. Complexes (m.w. congruent to 970,000) of trinitrophenylated bovine thyroglobulin (TNP-TG) and polymeric IgA were transported less well than IgA-(TNP-HSA) complexes (m.w. less than or equal to 460,000), even though both types of complexes bound SC. The possibility that the poor transport of IgA-(TNP-TG) complexes reflected a size restriction on hepatic transport from blood to bile is discussed.

Animals↗

Monitored Antabuse in the emergency room.

The Southern Tier Alcoholism Rehabilitation Service (STARS), a full-service treatment program, has for some time offered monitored antabuse to a few selected patients. This is given daily on an outpatient basis in the emergency room of the general hospital in which we are located. Over 100 patients have been served. This has been helpful for two kinds of patients: 1) those self-motivated voluntary patients making use of this on a short-term basis to extend structure, reassurance, support, and other rehabilitation services following a period of inpatient detoxification, or to get "realigned" following a brief slip, and 2) those poorly motivated patients using this on a long-term basis at the direction of the courts. About half of this latter group have been unsuccessful alumni of 30-day treatment programs outside the community. The program ensures a long-term (several months) period of sobriety in the patient's home setting, offering a chance to develop new life styles, support systems, and respect which can eventually become self-sustaining. It is unlikely that these changes would come about while the patient continued actively drinking. Specific procedures of administration, record keeping, confidentiality, and payment are discussed. The cost-effectiveness to motivated patients and cost-avoidance to taxpayers and third-party payers while providing effective therapy to long-term patients are significant advantages of the program.

Alcoholics Anonymous↗

Effects of iodoacetate and fluoride on islate respiration and insulin biosynthesis.

Fluoride and iodoacetate inhibited the oxidation of glucose by islets of Langerhans isolated from the rat pancreas. Fifty % inhibition occurred with either 17 mM fluoride or 0.5 mM iodoacetate. The rate of insulin biosynthesis was more strongly inhibited by these inhibitors, especially fluoride. Fifty % inhibition occurred with approximately 1.5 mM fluoride. At high concentrations of iodoacetate and fluoride, the inhibitory effect on insulin synthesis was not reversed to a significant degree by the addition of pyruvate in the incubation medium. In addition to inhibiting the glycolysis and depriving islets of energy essential for the biosynthesis of insulin, fluoride probably exerts a direct inhibitory influence on the biosynthetic mechanism. A separate experiment with [6-14C]glucose indicated that 0.2 mM iodoacetate does not inhibit glycolysis completely.

Animals↗