Displaying publications 1 - 20 of 8030 in total

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  1. Searle AG
    Ann. Hum. Genet., 1959;23:279-288.
    DOI: 10.1111/j.1469-1809.1959.tb01471.x
    1. The incidence of anencephaly in Singapore was determined from hospital records for 1953–56 inclusive. Sixty‐eight cases were found in 88,069 births, or 0.77 per thousand. 2. Analysis of data according to maternal community revealed great heterogeneity (Table 1), with frequencies ranging from 0.0 per thousand in the Hakka group of Chinese to 6.5 per thousand in Sikhs. 3. 48.4 % of anencephalics were males. This unusually high proportion may be connected with the low frequency of primiparity in Singapore and high average birth weight of affected infants, compared with records from elsewhere. Neither maternal age nor parity had a significant effect on the incidence. 4. The causes of anencephaly are discussed. It is suggested that properties of the local external environment (such as type of water supply) are of less importance than dietary and other customs peculiar to different communities, as well as genetical differences. 5. Several reasons are given why anencephaly, and other congenital malformations of the central nervous system, should be regarded as quasi‐continuous variables, due to a threshold effect. A comparison with the ‘curly‐tail’ mutant in the mouse supports this view and also emphasizes the close causal connexion between anencephaly and spina bifida. I am very grateful to Prof. L. S. Penrose, F.R.S., for arousing my interest in this subject and for invaluable advice. I should like to thank Prof. B. H. Sheares, Head of the University of Malaya's Unit at Kandang Kerbau Hospital, and Dr A. Arulanandam, Medical Superintendent, for arranging that I should have access to hospital records. I am greatly indebted to my wife for considerable help in the task of searching through these records. Copyright © 1959, Wiley Blackwell. All rights reserved
    Matched MeSH terms: Genetics
  2. Steinberg AG, Lai LYC, Vos GH, Singh RB, Lim TW
    Am J Hum Genet, 1961 Dec;13:355-71.
    PMID: 13916666
    The ABO, MN and Rh blood types, and the Hp, Tf, and Gm [Gm (a), Gm (x), Gm(b), and Gm-like] factors were determined for 128 unrelated Indians (parents of families, 63 with two parents tested and two with one parent tested), and 90 unrelated Chinese (parents of 46 families, 44 with two parents tested and two with one parent tested), and for the offspring from these families. The frequencies of the several blood types are presented. They were done primarily to aid in paternity testing. They compare favorably with the findings of previous studies. The allele Hp1 is rare in the Indian population (.09) and relatively infrequent in the Chinese (.29). Unfortunately, the data shed no light on the problem of the inheritance of the phenotype Hp O. Only Tf C was found among the Indians. About four per cent of the Chinese were heterozygous for Tf CD,, all other were Tf CC. The Indians have a high frequency of Gm(a) and of Gm (x), and a low frequency of Gm (b). They appear to have alleles Gma, Gmax, and Gmb in the following frequencies: .535, .234(5), and .230(5), respectively. Three families appear to have a GMxb allele, providing the offspring are not extra-marital. The Chinese appear to have the alleles Gm^ab, Gm^a, and Gm^ax in the following frequencies: .741, .231, and .028, respectively.
    Matched MeSH terms: Blood Group Antigens/genetics*; Genetics, Population*
  3. TI TS
    Med J Malaya, 1962 Mar;16:214-8.
    PMID: 13921142
    Matched MeSH terms: Anemia, Hemolytic/genetics*
  4. CHIN J
    Nature, 1964 Mar 07;201:1039.
    PMID: 14191583
    Matched MeSH terms: Genetics, Medical*
  5. Pettit JHS, Chin J
    Lepr Rev, 1964 Jul;35(4):149-56.
    PMID: 14177689
    In a survey of over 1,000 patients with leprosy, 47 cases ( 4.4 per cent) were found to have glucose-6-phosphate dehydrogenase deficiency. A controlled clinical study suggests that such a deficiency does not modify the overall response to therapy but may predispose to a greater tendency to leprosy reactions. All patients were receiving 600 to 800 mgm. of sulphone per week and none had a frank haemolytic anaemia.
    Matched MeSH terms: Genetics*
  6. CHIN J
    Med J Malaysia, 1964 Sep;19:71-2.
    PMID: 14240067
    Matched MeSH terms: Genetics, Medical*
  7. Kim CK, Durham NA
    Med J Malaya, 1965 Mar;19(3):172-83.
    PMID: 4220469
    Matched MeSH terms: Anemia, Sickle Cell/genetics*
  8. Fischer H
    Zentralbl Veterinarmed A, 1966 Jun;13(4):352-5.
    PMID: 4961318
    Matched MeSH terms: Cattle Diseases/genetics*; Spinal Cord Diseases/genetics
  9. Boon WH, Salmon Y, Seng CT
    Med J Malaya, 1966 Sep;21(1):56-62.
    PMID: 4224879
    Matched MeSH terms: Disorders of Sex Development/genetics*
  10. Wiesenfeld SL
    Science, 1967 Sep 08;157(3793):1134-40.
    PMID: 6038684
    The particular agricultural adaptation we have been considering is the ultimate determinant of the presence of malaria parasites in the intracellular environment of the human red blood cell. This change in the cellular environment is deleterious for normal individuals, but individuals with the sickle-cell gene are capable of changing their red-cell environment so that intense parasitism never develops. Normal individuals suffer higher mortality rates and lower fertility rates in a malarious environment than individuals with the sickle-cell trait do, so the latter contribute proportionately more people to succeeding generations.
    Matched MeSH terms: Genetics, Population*
  11. Inwang EE, Khan MA, Brown AW
    Bull World Health Organ, 1967;36(3):409-21.
    PMID: 5299673
    The yellow fever mosquito Aedes aegypti has developed resistance to DDT in the Caribbean region and in South-East Asia, but not in West Africa. Therefore West African strains were compared with South-East Asian strains for their response to laboratory selection with DDT. It was found that West African strains were much slower to respond initially, but eventually could build up a high degree of DDT-resistance. By crossing and backcrossing with a susceptible marker-gene strain, it was found that this resistance was due to a single gene linked with the gene y (yellow) on chromosome 2 at a cross-over distance of approximately 35 units in an Upper Volta strain as in a Bangkok strain; interstrain crosses indicated that the gene was the same as that in a Trinidad strain and in one from Penang. Dieldrin-resistance could be readily induced in the Upper Volta strain and proved to be due to a gene also linked with y but at a crossover distance of approximately 25 units, comparable to that in Caribbean strains previously studied. Material from Karachi, West Pakistan, developed a dieldrin-resistance also showing 25% crossing over with y, and a DDT-resistance also linked with this chromosome-2 marker gene.
    Matched MeSH terms: Genetics
  12. Lie-Injo Luan Eng, Lopez CG, Poey-Oey Hoey Giok
    Am J Hum Genet, 1968 Mar;20(2):101-6.
    PMID: 5643177
    Matched MeSH terms: Genetics, Medical*
  13. Boon WH
    Med J Malaya, 1968 Sep;23(1):61-6.
    PMID: 4237561
    Matched MeSH terms: Hemoglobinopathies/genetics*
  14. Kutty MK, Dutt AK, Lopez G, Ramanathan K, Pillay DR, Omar-Ahmad UD
    Med J Malaya, 1968 Sep;23(1):51-3.
    PMID: 4237557
    Matched MeSH terms: Klinefelter Syndrome/genetics*
  15. Boon WH, Seng CT
    Med J Malaya, 1968 Sep;23(1):20-8.
    PMID: 4237551
    Matched MeSH terms: Turner Syndrome/genetics*
  16. Bolton JM, Lie-Injo Luan Eng
    Med J Malaya, 1969 Sep;24(1):36-40.
    PMID: 4244260
    Matched MeSH terms: Thalassemia/genetics
  17. Lopez CG, Lie-Injo Luan Eng
    Med J Malaya, 1969 Dec;24(2):101-6.
    PMID: 4244132
    Matched MeSH terms: Anemia, Hemolytic/genetics*
  18. Gordon H, Huskisson ID, Torrington M, Pannell A, Zackon D
    Am J Obstet Gynecol, 1970 May 15;107(2):254-62.
    PMID: 5462441
    Matched MeSH terms: Hypertension/genetics*; Pre-Eclampsia/genetics*
  19. Banerjee AK
    Med J Malaya, 1970 Sep;25(1):21-4.
    PMID: 4249489
    Matched MeSH terms: Jaundice, Chronic Idiopathic/genetics*
  20. Tan KL, Thomas MA
    Med J Malaya, 1970 Sep;25(1):46-9.
    PMID: 4249495
    Matched MeSH terms: Abnormalities, Multiple/genetics*; Polycystic Kidney Diseases/genetics*
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