The extent of variability in the number of human hemoglobin (Hb) Incompatibilities between our results and current concepts of a-thalassemia are discussed in the context of differences between Black compared with Oriental and Italian forms of Hb H disease.

C e l l s cultured from amniotic f l u i d (AF) specimens obtained a t 15-18 weeks of gestation f o r a n t e n a t a l detection of chromosomal abnormalities have been typed f o r HL-A antigens by t h e fluorochromasia microcytotoxicity t e s t . Fibroblasts growing i n four AF c u l t u r e s were t e s t e d f o r 31 antigens with 100 a n t is e r a . I n each c u l t u r e , one maternal and one paternal haplotype was detected on AF f i b r o b l a s t s , indicating t h a t these are of f e t a l o r i g i n . The HL-A phenotype of t h e c e l l s dividing i n AF c u l t u r e is s t a b l e a s shown by concordance of antigenic s p e c i f i c i t i e s of t h e same c u l t u r e t e s t e d a t d i f f e r e n t t i s s u e c u l t u r e generations. I n one of t h e four c u l t u r e s , s p e c i f i c it i e s determined by both maternal haplotypes were detected. This finding might i n d i c a t e contamination of t h e AF c u l t u r e with maternal c e l l s , but r e l a t i v e l y weak serological reactions and t h e e x t r a s p e c i f i c i t y involved suggest t h a t cross reaction is the more l i k e l y explanation.HL-A typing can c l e a r l y demonstrate t h e f e t a l o r i g i n of cells dividing i n AF c u l t u r e , a useful observation when there i s concern about contamination by maternal c e l l s . Determination of t h e f e t a l HL-A phenotype provides a p o t e n t i a l method f o r a n t e n a t a l detection of an autosomal dominant disorder by synt e n i c r e l a t i o n s h i p s . This method w i l l be realized when l o c i of genes determining such disorders a r e found t o be c l o s e l y linked t o the HL-A region.A NEW VARlAllT OF GALACTOSEMIA. Claramma il. Chacko* Brandt, Rebecca S. 'rlaopner* and Henry L . !iadler. Northwestern and Indiana Univs., Dept. Peds., Chicago and Indianapolis.Galactosemia i s an autosomal recessive defect i n which the enzyme gal -I-P uridy l transferase ( t ransferase) i s decreased o r absent in several t i s s u e s . Several variants of t h i s enzyme have previously been described. W e report here a family i n which the proband CS has a new variant of transferase. C3 developed anorexia and jaundice s h o r t l y ' a f t e r bcinq placed on Similac. The diagnosis of galactosemia was considered when the Beutler fluorescence screening t e s t revealed no detectable t r a n s f e r a s e a c t i v i t y . Studies of transferase properties; i . e . a c t i v i t y , heat s t a b i l i t y a t 50O C, and starch gel e l e c t r ophoretic m b i l i t y of family ~nembers revealed the fol lowing. + !lorma1 These data suggest that a t l e a s t three a l l e l e s are present a t the t r a n s f e r a s e loci in t h i s fami ly. The mother i s a c l a s s i c heterozygote; the f a t h e r i s a double heterozygote f o r the f a s t -m v i n ? and unstable t r a n s f e r a s e ; and the p a t i e n t i s a double heterozygote f o r the fast-moving and c l a s s i c galactosemia transferase.Baylor Col. of Med., Hou., Tx. 77025. A 17 year...