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In a family with a large pericentric inversion in one chromosome No. 6 (Inv(6)(p+q–)), HL-A was shown to have segregated with this chromosome in seven of seven cases. This raises the probability for the localization of HL-A to chromosome No. 6 from a prior 6 to 49 % and confirms the same assignment reported from cell hybridization work. The HL-A locus is most likely to be a little distal to the midpoint of either the short or the long arm of chromosome No. 6.

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A total of 973 unrelated Danes and Norwegians have been typed for a number of HL-A iso-antigens, and so have 150 Danish and Norwegian families with a total of 480 children. Two series of HL-A iso-antigens were investigated: the LA series with the antigens HL-Al, 2,3, Ba *, ILN * and LA4, and the Four series with the antigens HL-A5,7,8, T12, R *, HN, FJH and BB. These antigens were inherited as co-dominant characters with the exception of Ba *, ILN *, and R *, which were operationally recessive to HL-A2, 3 and 5, respectively, but co-dominant in respect of the other factors. No individuals carried more than two antigens from each series, and the family analysis yielded no evidence against the assumption that the antigens within each series are controlled by mutually exclusive genetic determinants: The LA and Four series represent two mutational sites within the HL-A chromosomal region. No recombinations between these series were observed in this study, and the estimated upper limit of the recombination frequency between the corresponding sites was 0.84%. A total of 345 parental haplotypes could be unequivocally deduced; two of these, HL-A (1, 8) and HL-A (3, 7), occurred much oftener than should have been expected from the frequencies of the corresponding determinants, and there is thus linkage disequilibrium between the LA and Four series.In 1965, DAUSSET et al. [7] postulated on the basis of population data that most human leukocyte iso-antigens belong to one system. Family data supporting this assumption was presented by VAN ROOD et al. in 1966 [20b], and in 1967 the final proof was obtained [l, 4, 5,8,211. This system,, is one of the most complex immunogenetic systems known t o exist in man. At the present time, our knowledge of the chromosomal arrangement of its many genetic determinants is increasing rapidly. PAYNE, BODMER and their coworkers [19] had already in 1964 defined two leukocyte antigens, LA1 (HL-A1) and LA2 (HL-A2), which are controlled by alleles, and two years later they [2] added a new allele, LA3 (HL-A3), to 98 SVEJCAARD et al. Genetics of the HL-A System this series, which we now call the LA series (= '1st sublocus' of DAUSSET et al. [9]). These observations were confirmed in 1967 by DAUSSET et al. [8] and CEPPELLINI et al. [4]. The latter authors also found evidence in favour of the existence within the HL-A system of another series (Four = '2nd sublocus' of DAUSSET et al. [9]) of mutually exclusive genetic determinants : To5 (HL-AS), To7 (HL-A8) and Toll ( K N -T l 2 ) ; DAUSSET et al. [7] had previously observed that none of 133 individuals carried more than two of three antigens corresponding t o these Torino determinants, and two antigens from the 7-series of VAN ROOD et al. [20a], 6C = 7C (HL-A7) and 7D (HL-A8), belong also to the Four series. During 1968-69, several reports [9,11,12,22,29,31] confirmed and extended the findings O f CEPPELLINI et al. [4], and evidence was presented [ll, 12,291 that each of the highfrequency antigens 4A and 4B of VAN ROOD et al. [21] consists of narrowe...

SYNOPSIS Platelet survival was determined using untreated and siliconed glass bottles and plastic bags (Fenwal) for collecting and storing blood. The platelets were tagged in vivo with p32 in six polycythaemic patients undergoing treatment with P32. The results showed that fresh ACD blood collected in untreated glass, siliconed glass, and plastic gave the same recovery of platelets in the recipients. The use of EDTA (Fenwal formula) as anticoagulant gave results inferior to those obtained with blood using ACD as anticoagulant. Even after storage up to 24 hours in untreated glass bottles (ordinary bank blood) a satisfactory recovery of platelets was observed. After storage for 72 hours the recovery was less but not negligible.We have tried to solve part of the problem of preserving platelets for subsequent transfusion and for use in extracorporeal circulation by determining the survival of platelets in blood delivered in different containers, using ACD and EDTA as anticoagulant and storing the blood for periods of varying length before transfusion. It is difficult to determine the survival of thrombocytes but it is possible by using platelets tagged with various isotopes. A survey of the methods used was recently published by Aas and Gardner (1958). Tagging is usually performed in vitro, and the rather rough treatment to which the platelets are exposed during tagging has some influence on the results obtained, consequently labelling in vitro is not ideal for an investigation in which a relatively small difference in survival time might indicate superiority or inferiority of one container compared with another. We therefore used platelets tagged in vivo with p32. We used blood from patients with polycythaemia who were treated with p32. The technique employed is very similar to that used by Adelson, Rheingold, and Crosby (1957) in dogs and human beings. It is well known that tagging is maximal in about a week after the administration of the drug (Adelson et al., 1957). Using blood from patients with polycythaemia gives another advantage, namely, the possibility of drawing several pints of blood from the same donor at very short intervals. The various 'pints' drawn from the same donor contain the 'same' platelets marked in exactly the same way in vivo, thus affording an ideal opportunity for comparing the effect of storage on platelets in various containers before transfusion. MATERIALS AND METHODSDONORS Patients with polycythaemia undergoing treatment with P32 were used as donors. They were given about 5 'a. P32 by mouth and after an interval of five to seven days bleedings were started, 500 ml. of blood being drawn on each occasion, and the bleedings were continued daily for three to six days, depending on the clinical and haematological condition of the patients. Six

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