Among 80 Black patients with sarcoidosis, 11 families were identified as containing multiple cases. Monogenic modes of inheritance were reasonably excluded by informal inspection of pedigree patterns and by poor fit of corrected ratios within sibships to the expected ratio for all sibships at risk. The observed familial distribution conforms in several respects to properties that are descriptive of multigenic traits. Additionally, heritability based only on female probands was estimated to be between 60% and 70%. A larger sample size should permit analysis of additional multigenic properties.

In this exploratory study, we investigated total erythrocyte carbonic anhydrase (CA) estrase activity as well as CA I isozyme concentration in patients with diabetes mellitus type II (DM) and healthy individuals of Howard University Hospital community. Total estrase activity of CA was measured spectrophotometrically using p-nitrophenol acetate before and after inhibition with acetazolamide. CA I isozyme was measured by radial immunodiffusion using monoclonal antibody (CA I) in agarose plates. The study involved 20 consented participants; 10 normal (N) and 10 (DM), 21 to 84 years of age. The study was approved by the Howard University Institution Review Board. The CA activity was measured following lysis of cells as U/min/mL and CA I concentration as mg/l. We observed CA activity as 46.3+/-4(N) and 25+/-2.1 (DM) whereas CA I concentration as 1896+/-125 (N) and 1104 +/-63 (DM). We speculate that the change in the CA activity may of fundamental importance in the regulation of intracellular; pH(i) for the basic control of metabolism in diabetes mellitus. Further, we propose that CA activity is a good candidate for a biomarker of diabetes mellitus for the early detection of insulin resistance because the CA activity variation was proportional to the severity of the diabetes.

The electrophoretic phenotypes of the two isozymes of red cell carbonic anhydrase, CA I and CA II, are described in nine species of macaque monkeys from southeast Asia and Japan. Twelve phenotypes of CA I, apparently under the control of seven alleles, and five phenotypes of CA II, under the control of three alleles, were found in the different macaque populations studied. Extensive electrophoretic polymorphisms of CA 1 were found in three species (Macaca nemestrina, Macaca speciosa, and Macaca fuscata), and polymorphisms at the CA II locus were found in Macaca irus, Macaca mulatta, and M. nemestrina. In addition to the electrophoretic polymorphisms at the CA I locus in M. nemestrina, an inherited deficiency of CA I was also discovered in which approximately 30 % of the individuals in all populations of M. nemestrina tested showed the deficient phenotype. Although the recessive gene controlling this deficiency appears to be an allele of the CA I locus, it is postulated that the CA I defieieney eould also be under the control of a closely linked gene. The comparative data on the extent of genetic variation observed in the two isozymes of red cell carbonic anhydrase in macaques appear to support the concept that CA I has evolved more rapidly than CA H in mammals.

Analyses were made of total sodium, potassium and chloride content and of inulin space in dog carotid artery. The Ki/Ko gradient was found to be 125/4. Sodium space calculated from these analyses is larger than total hydration, thus precluding calculation of the Nai/No gradient. It is postulated that the excess sodium is associated with the mucopolysaccharides present in the interstitial spaces of the artery wall media. This associated sodium is readily replaced during 3-minute incubation of the artery wall media in Krebs' solution in which either the hydrogen or the potassium concentration is increased. It appears improbable that the majority of the excess sodium can be attributed to a Donna equilibrium since chloride concentration in the incubated tissue is much greater than that calculated to be required for this equilibrium.

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