Blood groups red cell enzymes and cerumen types of the Ahousat (Nootka) Indians.код для вставкиСкачать
Blood Groups, Red Cell Enzymes, and Cerumen Types of the Ahousat (Nootka) Indians BRAXTON M. ALFRED, T. D. STOUT, JOHN BIRKBECK, MELVIN LEE AND NICHOLAS L. PETRAKIS Department of Anthropology and Sociology, University of British Columbia; Canadian Red Cross, Vancouver, B. C.; School of Home Economics, University of British Columbia; Department of Epidemiology and International Health, University of California, San Francisco, California A survey of the blood groups of a Nootka band produced frequencies ABSTRACT characteristic of North American Indians for the ABO system (0.99 for 0, 0.0 for B, and 0.01 for A), Rhesus (0.822 for cDE, 0.011 for cde, 0.023 for cDe), Lutheran (1.00 for Lu(a-)), Duffy (0.505 for F y f a f ) ) and Diego (0.039 for Di(a+)). K is not absent though the frequency is not great (0.028). Surprising results were obtained for the MN locus (0.399 for M, 0.601 for N ) , P (0.209 for PI), and Lewis (0.568 for Le(o+)). A frequency of phosphoglucomutase type P G M I ~of 0.890 was found; all hemoglobins were type AA; n o G-6-PD deficiency was found a n all were type B positive; the frequency of the dry cerumen allele was found to be 0.323. The Ahousat are a Central Nootkan group currently living on Flores Island which is off the west coast of Vancouver Island somewhat north of Barclay Sound (fig. 1). Earlier their primary concentration was on the mainland near what is now called Chetarpe with a subsidiary location at Ahous Point on Vargas Island. They came by their present location after a long and bloody war with the Otsosat early in the nineteenth Century. In 1774 a Spanish vessel put into Nootka Sound; Cook arrived in 1778 and his visit was responsible for beinning the lucrative sea otter fur trade with China. This contact brought to the Nootka iron, copper, brass, muskets, cloth, rum and disease. Small pox epidemics ravaged the population periodically with a particularly severe outbreak in 1852. Also measles, influenza, tuberculosis, venereal disease and alcohol were newly available means of death. Aboriginally the west coast of Vancouver Island supported one of the greatest population densities in the New World; the impact of contagious diseases was magnified correspondingly. The social structure was greatly affected because “Decrease of population meant that chiefs died without heirs in the direct line.” (Drucker, ’51: 12). AM. J. PHYS. ANTHROP.,31: 391-398. In the 1850’s the dogfish oil trade arose with the nascent lumbering industry. In 1860 the town of Alberni was established at the head of the Alberni Canal in the region of the Sproat Lake Nootkan groups; in 1875 Father Brabant’s mission was established at Hesquiat. The fur seal trade blossomed in the 1880’s and some Nootka men, shipping as hunters, made visits to Japan, China and San Francisco. Canneries began to appear and the town of Tofino was established around the turn of the century.2 Reasonably good population counts have been made since about 1880. Figure 2 presents the population curve for the Ahousat band since 1883. The curve drawn in is not fitted; it is to be used only as a guide to the likely underlying trend. Between 1965 and 1968 the population of registered Indians at Ahousat increased by 8.05% or roughly 4% each year. The shape of the population curve at Ahousat is very similar to that reported by Duff (’65: 44) for the total provincial Indian population. We are, then, considering a group of people having survived 200 years of white 1 We wish to thank Dr. Bruce Chown, Rh Laboratory Winnipeg, Manitoba for reading and commenting on’ an earlier draft. 2 This account is drawn heavily from Drucker (’51) and Duff (’64). 391 392 ALFRED, STOUT, BIRK3ECK, LEE AND PETRAKIS \\ COURTENA cL*yoQfio~ C O < Figure 1 .- Kelienat lJdgOmOied Z 100 1880 ' 1890 1900 1910 1920 1930 1940 ' L 1950 1960 1' '0 Y E A R Figure. 2 Population trend at Ahousat BLOOD FACTORS AND CERUMEN TYPES OF contact. Northwest coast warfare often involved taking women and children as slaves. This, plus the pressure of band exogamy should have resulted in genetic mixing sufficient to obscure any local effects of white contact; that is local effects have either diffused through the region or have been cancelled. In March 1968 a survey of nutrition and health was conducted at Ahousat under the direction of Dr. Melvin Lee, University of British Columbia School of Home Economics. Blood was drawn routinely and typing carried out by the Candian Red Cross. The blood was also studied for hemoglobin, glucose-6-phosphate dehydrogenase (G-6-PD) and phosphoglucomutase (PGM) polymorphisms. In addition the subjects were classified as to cerumen type, a recently described genetic polymorphism. METHODS A. Sampling Subjects were not randomly drawn and no attempt was made to exclude relatives. Of the 669 registered Indians on the Ahousat band list, 310 were living on the Reserve at the time of the survey, Blood samples were obtained on 198, 64% of those in residence. Pedigrees3 were constructed; from these we estimate that three of our subjects are not related closely (i.e. as sibling or as parent/child) to another member of the sample. (No first cousin marriages appear.) The amount of relatedness in the sample is not serious concern since this characterizes the (finite) population for which genetic parameters are to be estimated. The sampling technique, however, may be a serious deficiency although intuitively it does not seem that it should be. In random sampling from a finite population without replacement, at the kth draw there are N - k 1 items remaining; therefore, each must have probability 1/N - k 1 of being included. When subjects are selfselected, which was true of this survey and probably of nearly all such surveys, this probability does not obtain. For the present we will make the assumption that our sample is the equivalent of a random sample. + 393 THE NOOTKA From figure 3, which presents the age by sex distributions for the Ahousat band list, and the current sample, one may see that the sample is fairly representative of the population with regard to these two attributes. B. LaboTatoy All blood specimens were collected in heparin. Most of the serum was removed from each specimen for biochemical studies and ACD was then added to the cells. This was done within 24 hours of collection. The ACD specimens were then refrigerated and shipped to the Red Cross Blood Transfusion Senice in Vancouver. The cells were grouped during the next four days4 There was no appreciable hemolgsis during the test period. The anti-sera and grouping techniques are given in table 1. A number of cells were retested as follows: Nine e-negative specimens were checked with two anti-e sera by three methods and Y t R FEMALE &*NO , SAMPLFI-J + Fig. 3 Age, sex population tree. SWe wish to express our gratitude to Mr. George Pettifer Public Health Nurse, Medical Services, of Tofino $or providing much of the information necessary to complete and correct pedigrees. 4Typing was carried out by Mrs. Isabella Horvath, R.T. and Mrs. Judith Decker, R.T. of the Red Cross Elood Transfusion Service, Vancouver, B.C. 394 ALFRED, STOUT, BIRKBECK, LEE AND PETRAKIS TABLE 1 Anti-sera and grouping techniques Anti-sera Anti-A1 Anti-A Anti-B Anti-A & B Anti-D Anti-C Anti-E Anti-? Antie' Anti-M Anti-N Anti-S Anti2 Anti-P Anti-Lua An ti-Lub An ti-Lea Anti-Leb Anti-Kell Anti-k Anti-Fya Anti-Fyb AntiJKa Anti-JKb Anti-WP Anti-Wr" Anti-Di" Anti-Vel An ti-Vel Anti-Human Globulin 30% Bovine Alb. Source Sal. Sal. Sal. Sal. Sal. Sal. Sal. Inc. Sal. Sal. Sal. Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Ortho Pharmaceutical Corporation Ortho Pharmaceutical Corporation Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Blood Grouping Labs., Boston Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Dr. M. N. Crawford Can. Red Cross B.T.S. Vancouver Can. Red Cross B.T.S. Vancouver Can. Red Cross B.T.S. Vancouver Can. Red Cross B.T.S. Vancouver Can. Red Cross B.T.S. Vancouver Dade (Dried) Can. Red Cross B.T.S. Vancouver Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Vancouver Dr. Bruce Chown, Winnipeg Can. Red Cross B.T.S. Toronto Can. Red Cross B.T.S. Vancouver Pfizer Pentex Test Capillary Capillary Capillary Capillary Capillary Capillary Capillary Lows Pap. Capillary Lows Pap. Capillary Lows Pap. Capillary Lows Pap. Capillary Ind. Coombs. Cap. Ind. Coombs. Cap. Capillary Capillary Lows Pap. Ind. Coombs Capillary Saline Tube Capillary Lows Pap. Capillary Lows Pap. Ind. Coombs Cap. Ind. Coombs Cap. Ind. Coombs Cap. Sal. Ind. Coombs. Cap. Ind. Coombs Cap. Method for re-check neg. results I.C. Tube I.C. Tube Sal. Tube Sal. Tube Sal. Tube I.C. I.C. I.C. I.C. Tube Tube Tube Tube Ind. Coombs. Cap. Ind. Coombs. Cap. Capillary Capillary I.C. Tube Tube One hundred fifty-four blood samples including two positive controls, one of which was an Ahousate positive specimen. were analyzed electrophoretically for heThis was done to establish that the anti-e moglobin, G-6-PD, and phosphoglucomutase types employing methods described by was working properly. Because of the unusual MN findings Briere et al. ( ' 6 5 ) , Kirkman and Hendrickthirty secimens were sent to the National son ( ' 6 3 ) , and Spencer et al. ('64), reLaboratory, Canandian Red Cross Blood spectively. Cerumen type was determined by visual Transfusion Service, Toronto. The results in the National Laboratory were identical inspection employing an otoscope accordwith those in Vancouver. The National ing to the criteria given by Petrakis ('67). Laboratory also tested 5 M M and 5 N N RESULTS cells of this group with anti-Mc, anti-Mur In table 2 are presented allele and pheand anti-Mi". All 10 cells were negative notype frequencies. There are no large with these three antisera. All P negative cells were retested with departures from expectation. Consequently, anti-PI to check as to whether any weakly it appears that the mating pattern of the reacting P cells had been missed. There population results in the stochastically independent union of genes at all loci obwere no discrepancies. The three group A individuals were served. In table 3 are presented the Rh and tested with anti-Al and were all AI. The six (Le(a-,b-) cells were re- MNSs chromosone frequencies; the former checked using saline tube test and found were computed by an iterative procedure which will be described elsewhere. to be correct. BLOOD FACTORS AND C E R U M E N TYPES O F 395 THE NOOTKA TABLE 2 Blood group phenotype and gene frequencies System ABO P Phenotype A B AB 0 Pi Pz Kell Diego 2 Duffy a Kidd Lewis 5 MNSs Rhesus kk Kk KK Di( a + ) Di(a-) FY(a+ ) Ma-) Jk( a+ 1 Jk( a- 1 W a f ) Le(a-) MMSS MMSs MMss MNSS MNSs MNss NNSS NNSs NNss CcDEe CcDEE ccDEe ccDEE ccDee CcDee Observed phenotype frequency Allele 3 (0.015) o (0.000 j 0 (0.000) 195 (0.985) 74 (0.374) 124 (0.626) 187 (0.944) 11 (0.056) 0 (0.000) 12 (0.075) 148 (0.925) 184 (0.929) 14 (0.071) 118 (0.596) 80 (0.404) 113 (0.571) 85 (0.429) 0 (0.000) l(0.005) 24 (0.121) l(0.005) 20 (0.101) 87 (0.439) 0 (0.000) 8 (0.040) 57 (0.288) 27 (0.136) 19 (0.096) 8 (0.040) 140 (0.707) l(0.005) 3 (0.015) Allele frequency A B 0 0.008 0.000 P1 PZ k K 0.209 0.791 0.972 0.028 D1( 0.992 a+) Di(a-) FY(a+ 1 Ma-) Jk(a+) Jk(a-) W a f ) Le(a-) M N S S D C E C e 0.038 0.962 0.734 0.266 0.364 0.636 0.756 0.244 0.399 0.601 0.078 0.922 1 .ooo 0.124 0.891 0.876 0.109 All (3) A positive reactions were to anti-AI, i.e. no A2 was found. No further testing. aAnti-Fy(b) was used on 30 bloods; 10 were Fy(a+,b+), 16 were Fy(a+,b-1, and 4 were Fy(a-.b+). *Anti-Jk(b) was used on 30 bloods; 17 were Jk(a+,b+), 1 was Jk(a+,L+). and 12 were Jkf a--.b4->. - 5 A l l subjects were more than 18 months old, Anti-Le(b) was also used; 113 were Le(a+,b-), 79 were Le(a-,b+), and 6 were Le(a- b-). Additionally 92 were typed for WrigGt and all were Wr--; 195 (all type 0 bloods) were typed for Lutheran and all were Lu(a-,b+); 189 were typed for Vel and all were Vel+. 2 Hemoglobin, G-6-PD, electrophoresis, and cerumen types.'. All hemoglobins were type AA. All samples were type B positive for G-6-PD and no deficiency was found. Phosphoglucomutase (PGM) electrophoresis revealed 79.3% type 1-1 and 20.7% type 2-1 giving allele frequencies f o r PGM: of 0.89 PGMf of 0.11. Eighty-nine of 244 subjects (32.3%) had dry type cerumen giving q = 0.56. The sample was broken into four age groups to determine if there is any obvious trend through time for the frequency o f positive reactions to any of the anti-sera used. The result is presented in table 4. Since all the positive reactions to anti-A are given by subjects under 20 years old (i.e., born after 1948) we may tentatively conclude either that the A antigen is a recent introduction or that selective pressure on this locus has not had time to eradicate it. Intuitively, the former seems more likely as there is no presently known relationship between this antigen and any 5 We gratefully acknowledge the assistance given by Mr. Robert Mossberger and Dr. Luan Eng Lie-Injo in the electrophoretic studies. This part of the work was partially supported by a gift from Viola K. Schroeder i n memory of Walter Schroeder. 396 ALFRED, STOUT, BIRKBECK, L E E AND PETRAKIS TABLE 3 Chromosome frequencies 0.014 0.047 0.023 0.822 0.011 0.003 0.020 0.060 cDE (Rx) Rhesus cde (r) CdE (R,.) cdE ( R ’ ) MS 0.030 0.369 0.049 0.552 MS MNSs WS NS selective agent. As mentioned above, however, all A positive reactions were to type AX and so this is not evidence for white admixture. Except for P and Diego, most proportions seem to be fluctuating randomly. At €’ we note that the proportion with the PI antigen in the total sample is 0.209; among those individuals born before 1908 it is 0.042 (i.e., the proportion o f the PI phenotype is 0.083). Again, however, we cannot know whether there was a large influx of the PI antigen after 1908 or whether some unknown selective pressure is operating. The latter seems less likely because the proportions have apparently stabilized. At Diego a similar kind of conclusion is reached; the proportion with the DIa antigen is 0.03 for those born after 1928 and is 0 for those born before. We do not wish push this discussion of pos- sibilities beyond simply calling attention to them as the numbers on which the proportions are based are too small to warrant anything else (Gajdusek, ’64). DISCUSSION Two previous studies have reported on Nootkan samples not mixed in with other groups. The amount of directly comparable information is small, however. Hulse (’55: 96) reports gene frequencies of (0.02, 0, 0.98) for A, B and 0 respectively for his “Central Nootka” samplc6 Ride (Mourant et al., ’58: 190) got (0.03, 0, 0.97) for the Nootka in 1935. A, is absent in our sample and neither of the two prior studies made the discrimination. At the Rh locus D, neither Hulse nor 6Professor Hulse h a s kindly suppljed us with his original data. Among those he .fyped i n 1955, 14 were carried on the Ahousat band list in Maxch 1968. Of these, 4 appeared jn our sample. There was complete agreement on the ABO typing, but discrepancies arose at the MN and R h loci. First consider the results of Mn: Subject Hulse Ahousat 1 2 3 4 M M N MN M N MN MN In his 1955 paper.Hulse reports only the Rh locus D. In the data he provided to us, however, information is also given on C and E; presumably 3 anti-sera were used. The following comparison is possible: Subjcct Hulse Ahousat I 2 3 cDE CDE CDE CDE CcDE cDE CcDEe CcDEe 4 There i s complete agreement at the D and E loci but discrcpancies at the C locus. TABLE 4 Positive reactions to selected anti-sera by age group Anti-serum 3 Total sample Less t h a n 20 years N = 120 Between 20 and 40 years N = 37 0.015 0.242 0.985 0.197 0.672 0.879 0.152 0.995 0.374 0.571 0.056 0.929 0.596 0.061 0.025 0.233 0.975 0.192 0.633 0.875 0.150 0.000 0.270 1,000 0.216 0.649 N=1871 1.000 0.417 0.600 0.058 0.950 0.642 0.058 This is the total on whom age was available. 0.865 0.162 1.000 0.297 0.459 0.054 0.892 0.541 0.081 Between 40 and 60 More t h a n 60 years N = 12 0.000 0.222 1.000 0.111 0.833 0.889 0.167 1.000 0.444 0.611 0.056 1.000 0.500 0.000 0.000 0.167 years N = 38 1.000 0.167 0.750 0.750 0.167 0.917 0.083 0.667 0.083 0.833 0.750 0.000 BLOOD FACTORS AND CERUMEN TYPES OF THE NOOTKA the present study observed any cases of the genotype dd. Neel and Salzano ('64: 87) listed "Some Distinctive Genetic Features of the American Indian" as follows: System High frequency of 0 High frequency of M Rh The frequency of cDE is higher than any where else in the world; cde and cDe low or absent. Kcll K may have been absent in pre-Columbian Indians Duffy High frequency of F7a Diego High frequency of D,a Lewis Almost all populations show Le(a-) only Luthernn Almost all populations show Lu(a-) ABO MN only (Some notational changes have been introduced.) To this list might be added that North American Indians have very high frequencies of the allele for dry type cerumen (Petrakis et al., '67; Petrakis, '69). The blood group allele frequenices at Ahousat are ambiguous. On the one hand, the frequencies of the 0 and A, antigens, the Rh pattern, and the uniformly Lu( a-) traits are aboriginal Indian indicating little, ii any, white admixture. But the MNSs system frequencies stand in direct contradiction to, not only the Neel and Salzano criteria, but also to every other study of the Northwest Coast known to us. Further, the pattern bears little resemblance to the English or Candian pattern as is seen below. English 1 Canadian 1 Ahousat 1 MS 0.247 0.255 0.030 Ms 0.283 0.304 0.369 NS 0.080 0.061 0.049 Ns 0.390 0.380 0.552 (Race and Sanger, '68: 91) Chown and Lewis (Montagu, '60: 347) report the following phenotypic proportions for "British Columbia Indians :" M N S S Phenotgpic Frequencies Chown Lewisand MMSS, n'6MSs MMss MNSS, MNSs MNSS NNSS. NNS5 NNss 0,227 0.370 0.090 0.257 0.010 0 047 Ahousat 0.005 0.121 0.106 0.439 0.040 0.288 ~- Chown and Lewis used anti-sera M, N, S while the Ahousat study used M, N. S and s. 397 At the locus P the frequency of the Pi phenotype is 0.374, giving a gene frequency of 0.209. Montagu ('60. 356) reports phenotypic frequencies this low or lower in Australia (0.23), Thailand (0.30) and New Britain (0.35); Caucasian frequencies are around 0.78 for the Pi antigen (Race and Sanger, '68: 159). Doeblin and IClohn ('67: 706) report a frequency for the Pi phenotype of 0.896 among the Seneca, and Thomas et al. ('64: 192) report 0.637 and 0.582 at Masset and Skidegate respectively in the Queen Charlotte Islands. The Caucasian frequency for the Kf phenotype seems to lie between about 0.05 to 0.09 (Race and Sanger, '68 : 266; Chown et al., '63: 379). This may be compared with 0.056 at Ahousat, which is intermediate among the range of studies reported by Montagu ('60: 357) but considerably higher than most other North American Indians (e.g. Thomas et al., '64; Doeblin and Mohn, '67). Comparing the Diego locus with the Indian samples reported by Laryisse ('58: 177, 182) it is seen that the Ahousat sample is clearly more typical of North than of South American Indians in general. But the Haida have a frequency for the D," antigen of 0.007 (Thomas et al., '65: 192), and the geographically nearest comparable frequency occurs among the Blackfoot of Alberta (Doeblin and Mohn, '67: 706), an Algonkian speaking group; next are the Southwest Athapaskans, i.e., Apache 0.041, Navaho 0.047. Similarities with the Apache end, however, with this Diego frequency (Gershowitz, '51 : 197). Apparently there are no similar frequencies to the north, e.g. Alaskan Athapaskan, 0.005, Tlingit, 0.000, Kutchin, 0.000 (Doeblin and Mohn, '67). Finally, a very striking frequency was obtained at Lewis. The Ahousat frequency for the Le ( a + ) phenotype is 0.571. With the exception of a Central Australian group, which was 100% Le(a+), reported by Simmons et al. (Montagu, '60: 361) this is the highest frequency known to us. Thomas et al. ('64: 192) found 0.239 and 0.232 at their two sites, Doeblin and Mohn ('67: 706) found 0.208 among the Seneca. The only region that seems to have 398 ALFRED, STOUT, BIRKRECK, LEE AND PETKAKIS Negroes; Blood Types of Asiatic Indians and frequencies of this phenotype in the range Apaches. Am. J. Phys. Anthrop. 17 (3): 195observed at Ahousat is Polynesia (Montagu, 200. '60: 361). Giblett, E. R. 1967 Variant Phenotypes: HaptoAnalysis of phosphoglucomutase (PGM) gobin, Transferrin, and Red Cell Enzymes. In: Advances in Immunogenetics. T. J. Greenwalt, types demonstrated a high frequency of the ed. J. B. Lippincott. PGM: (0.89), which is similar to that found in Athapaskan and Aleut Indians of Hulse, F. S. 1955 Blood-types and Mating Patterns Among Northwest Coast Indians. SouthAlaska, Scott et al. ('66), and in the Ainu west J. Anthrop., 11: 93-104. in Hokkaido, Giblett ('67), and distinctly Kirkman, N. H., and E. Af. Hendrickson 1963 higher than the frequencies reported for Scx-linked electrophoretic difference in glucoseF-phosphate dehydrogenase. Am. J. Hum. Gen., Orientals, Caucasions and Negroes, 15: 241-258. Spencer et al. ('64). It has been previously M. 1958 Anthropological considerasuggested by one of us (N.L.P.) that in- Layrissc, tions of the Diego (Dia) Antigen. Am. J. Phys. creased frequency of the wet (sticky) Anthrop., 16 ( 1 ) : 173-186. type of cerumen present in Indian tribes Matsunaga, E. 1962 The dimorphism i n human normal cerumen. Annals of Human Gemight be indicative of admixture with netics, 25: 273-286. Caucasians, since Indian tribes known hisM. F. A. 1960 Introduction to Phystorically to be unmixed have higher fre- Montagu, ical Anthropology. Charles C Thomas, Springquencies of the dry allele than found in field, Illinois, this study. Our present findings on blood Mourant, A. E., A. C. Kopec and K. DomaniewskaSobczak 1958 The ABO Blood Groups. Blackgroups and PGM types of the Ahousat do well Scientific Publications, Oxford. not lend support to this hypothesis. Possibly the somewhat low dry allele fre- Mourant, A. E. 1954 The distribution of the human blood groups. Blackwell ScientSc Publiquency in Ahousat represents the results cations, Oxford. of genetic drift or the action of unknown Neel, J. V., and F. M. Salzano 1964 A proselective forces. spectus for genetic studies of the American InLITERATURE CITED Briere, R. O., T. Golias and J. G. Batsakis 1965 Rapid Qualitative Hemoglobin Fractionation. Am. J. Clin. Path., 44: 695-701. Chown, B., &I. Lewis, H. Kaita and S. Philipps 1963 Some BIood Group Frequencies in a Caucasian Population. Vox Sang., 8: 378-381. Doeblin, T. D., and J. F. Mohn 1967 The Blood Groups of the Seneca Indians. Am. J. Hum. Gen., 1 9 ( 6 ) : 7OC-712. Drucker, P. 1951 The Northern and Central Nootkan Tribes. Bureau of American Ethnology, Bulletin 144. Duff, W. 1964 The Indian History of British Columbia, Vol. 1. Anthropology in British Columbia, Memoir No. 5, Provincial Museum of British Columbia, Victoria. Gajdusek, D. C. 1964 Factors Governing the Genetics of Primitive Human Populations. Cold Spring Harbor Laboratory of Quantitative Biology, 29: 121-135. Gershowitz, H. 1959 The Diego Factor Among Asiatic Indians Apaches and West African dian. Cold Springs Harbor Laboratory of Quantitative Biology, 29: 80-98. Petrakis, N. L. 1969 Dry cerumen - a prevalent genetic trait among American Indians. Nature, 222: 1080-1081. Petrakis, K. T. Molohon and D. J. Teppcr 1967 Cerumen in American Indians: Genetic implications of sticky and dry types. Science, 158: 1192-1193. Race, R. R., and R. Sanger 1968 Blood Groups in Man. Blackwell Scientific Publications, Oxford. Scott, E. M., I. W. Duncan, B. Ekstrand and R. C. Wright 1956 Frequency of Polymorhpism Types of Red Cell Enzyme and Serum Fractions in Alaskan Eskimos and Indians. Am. J. Hum. Gen., 18: 408411. Spencer, N., D. A. Hopkinson and H. Narris 1964 Phosphoylucomutase Polymorphis in Man. Nature, 204: 724. Thomas, J. W.,M. A. Stuckey, H. S . Robinson, J. P. Goffon, D. 0. Anderson and J. N. Bell 1964 Blood Groups of the Haida Indians. Am. J. Phys. Anthrop., 22: 189-192.