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  • 1
    Electronic Resource
    Electronic Resource
    ANGIOTENSIN-CONVERTING ENZYME AND REGULATION OF BLOOD PRESSURE IN A LARGE AUSTRALIAN FAMILY (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Animal studies have implicated the angiotensin-converting enzyme (ACE) gene as an inherited risk factor contributing towards elevation of blood pressure.2. A polymorphism of the ACE gene, involving the presence or absence of a 287 base pair (bp) segment within the gene region, was assessed for association with high blood pressure in a large, multigeneration Australian family. The association of these alleles with hypertension in unrelated individuals was also examined.3. There was no evidence to link the ACE gene and high blood pressure in the large family. Similarly, there was no significant association between this gene and high blood pressure in the population tested. As has been reported previously, plasma levels of the enzyme were associated with genotype. These results suggest that this gene is unlikely to be a major risk factor for hypertension in this group.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01694.x
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  • 2
    Electronic Resource
    Electronic Resource
    POLYMORPHISMS OF CANDIDATE GENES IN ESSENTIAL HYPERTENSION (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Family and population studies have reported that blood pressure has a heritability of 30–50%, but simple genetic models do not readily explain the patterns of inheritance of hypertension.2. Restriction fragment length polymorphisms were used to study allele frequencies of a selection of candidate genes that may be important in determining the genetic component of hypertension. These included the genes for renin, haptoglobin, neuropeptide Y and cardiac myosin β heavy chain.3. There was no significant association between alleles at any of these loci and the presence of hypertension in this population, suggesting that the contribution of variation at these loci to the genetic component of the variance in hypertension may be quite small.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00461.x
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  • 3
    Electronic Resource
    Electronic Resource
    ANGIOTENSIN-CONVERTING ENZYME AND ANGIOTENSINOGEN GENES IN PATTERNS OF LEFT VENTRICULAR HYPERTROPHY AND IN DIASTOLIC DYSFUNCTION (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The association of different patterns of left ventricular hypertrophy and diastolic dysfunction with angiotensin converting enzyme (ACE) genotypes or angiotensinogen dinucleotide repeat alleles were studied in human subjects.2. Three abnormal patterns of hypertrophy (remodelled, eccentric and concentric) were associated with a history of hypertension. The presence of remodelled or concentric hypertrophy was associated with diastolic dysfunction.3. There was no difference between the frequencies of the ACE genotypes in normotensive and hypertensive subjects, in subjects with normal ventricles and those with different patterns of left ventricular hypertrophy, nor in subjects with normal and abnormal diastolic function. Similarly, there was no difference between the relative frequencies of AGT alleles in the same clinical subgroups.4. We conclude that in this population of hospital patients, variants of the ACE and AGT genes do not contribute to the presence of different patterns of hypertrophy or to diastolic dysfunction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb02036.x
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  • 4
    Electronic Resource
    Electronic Resource
    RENIN AND ANGIOTENSIN-CONVERTING ENZYME GENOTYPES IN PATIENTS WITH ESSENTIAL HYPERTENSION AND LEFT VENTRICULAR HYPERTROPHY (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The associations between left ventricular hypertrophy (LVH) and specific alleles of the renin and angiotensin-converting enzyme (ACE) genes were studied in patients with essential hypertension and normal blood pressure.2. LVH was present in 42% of those with essential hypertension (n= 72) and 17% of those with normal blood pressure (n= 44).3. The frequency of each renin allele was the same in hypertensive and in normotensive patients. Renin allele frequencies were also the same for those with LVH and those with normal cardiac mass. When only hypertensives were considered, renin alleles were in the same proportion for the groups with and without LVH. Similarly, ACE alleles were not associated with essential hypertension nor with elevated cardiac mass.4. We conclude that, in this population, variations in the renin or ACE genes do not contribute significantly to the development of LVH or to essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02497.x
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  • 5
    Electronic Resource
    Electronic Resource
    α°- and β°- Thalassemia in a Thai family: unusually mild homozygous β°-thalassemia without α-globin gene deletion (1985)
    Springer
    Human genetics 〈Berlin〉 69 (1985), S. 375-377 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Alpha-globin genes were analyzed by the direct method of DNA mapping using α- and ζ-globin specific probes in a Thai family in which the proposita was an unusually mild β°-thalessemia homozygote. α°-Thalessemia was found to be segregating in the family, inherited from the proposita's father by one of her younger sisters. However, α°-thatlessemia was not detected by this DNA mapping in the proposita. The mild homozygous β°-thalessemia in this family may result from interactions of a non-deletion α-thalassemia, a gene responsible for high proteolytic activity permitting more balanced globin-chain levels, or from an unusually active hemoglobin F production in the proposita.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00291658
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  • 6
    Electronic Resource
    Electronic Resource
    Alpha-thalassemia in Papua New Guinea (1986)
    Springer
    Human genetics 〈Berlin〉 74 (1986), S. 432-437 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary A study of the distribution of α-thalassemia in Papua New Guinea (PNG) was carried out by DNA analysis. A total of 664 DNA samples were screened for α-thalassemia 2 and α-thalassemia 1 caused respectively by either deletion of one or both of the duplicated α-globin genes. α-Thalassemia 2 was detected in high frequencies in coastal and lowland regions where malaria has been holo- to hyperendemic but in low frequencies in non-malarious highland regions. The highest frequency was observed in the north coast of PNG. The distribution of α-thalassemia 2 seems to be in accordance with other conditions such as ovalocytosis and G6PD deficiency which are also prevalent in this population, suggesting that they may interact in protection against malaria. However, it appears to be negatively correlated with β-thalassemia and α-thalassemia 1, the latter being extremely rare in this population. Analysis of the types and subtypes of the single α-globin gene deletion revealed a predominance of the −α4.2 type in general, except in some regions in the south where the −α3.7 type is prevalent. The −α3.7 I subtype is the common form of the −α3.7 deletion in the PNG mainland. The −α3.7 III subtype, previously reported to be unique in Melanesians and Polynesians, was detected in an offshore island of PNG. However, this subtype is very rare in Melanesians from the PNG mainland.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00280500
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  • 7
    Electronic Resource
    Electronic Resource
    Fine mapping of a human chromosome 6 ferritin heavy chain pseudogene: relevance to haemochromatosis (1991)
    Springer
    Human genetics 〈Berlin〉 88 (1991), S. 175-178 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary We have used a somatic cell hybrid regional mapping panel for the short arm of chromosome 6, linkage analysis and a population study to map in detail a previously described ferritin heavy chain pseudogene sequence on chromosome 6. Our results show that this sequence maps to the short arm of chromosome 6 centromeric to the glyoxylase locus. The ferritin pseudogene locus is thus distant from the locus for the iron storage disease haemochromatosis, confirming previous evidence that this sequence is not a candidate for the haemochromatosis gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00206067
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  • 8
    Electronic Resource
    Electronic Resource
    Functions of the white and topaz loci of Lucilia cuprina in the production of the eye pigment xanthommatin (1980)
    Springer
    Biochemical genetics 18 (1980), S. 643-653 
    Details
    ISSN: 1573-4927
    Keywords: Xanthommatin synthesis ; transport mutants ; Lucilia cuprina ; eye color mutants
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The white and topaz eye color mutants of L. cuprina are defective in the production of the brown screening pigment xanthommatin. Both white and topaz mutants were found to be unable to accumulate xanthommatin precursors in the larval malpighian tubules, correlating with their reduced early pupal level of this metabolite. In addition, white mutants showed reduced rates of accumulation of kynurenine and 3-hydroxykynurenine in the adult eyes. Another mutant strain, grape, was also defective in its ability to accumulate these xanthommatin precursors in the eyes, although accumulation was normal in the larval tubules. In contrast, the topaz mutants were found to be normal in eye accumulation, although tubule accumulation was markedly abnormal. These properties of the white and topaz mutants of L. cuprina are compared with those of the white and scarlet mutants of D. melanogaster, and it seems likely that in the two species these genes are involved with the uptake or storage of xanthommatin precursors in specific tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00484582
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  • 9
    Electronic Resource
    Electronic Resource
    Xanthommatin biosynthesis in wild-type and mutant strains of the Australian sheep blowfly Lucilia cuprina (1978)
    Springer
    Biochemical genetics 16 (1978), S. 1153-1163 
    Details
    ISSN: 1573-4927
    Keywords: xanthommatin synthesis ; eye color mutants ; Lucilia cuprina ; development
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The synthesis of eye pigments has been studied in the seven eye color mutants of the Australian sheep blowfly, Lucilia cuprina. Six appear to be affected primarily in the synthesis of xanthommatin. In wild type, the onset of xanthommatin biosynthesis occurs midway through metamorphosis. Developmental patterns of accumulation of the xanthommatin precursors tryptophan, kynurenine, and 3-hydroxykynurenine have also been established for wild type. By determining the levels of these precursors in late pupae of the mutants, it has been shown that the mutant yellowish accumulates excess tryptophan and the mutant yellow accumulates excess kynurenine. The implications of these results—that yellowish lacks tryptophan oxygenase, thus failing to convert tryptophan to kynurenine, and that yellow lacks kynurenine hydroxylase (blocked in the conversion of kynurenine to 3-hydroxykynurenine)—have been confirmed. This has involved in vitro assays of tryphophan oxygenase and precursor feeding experiments. The precursor accumulation patterns are less clear for the other mutants.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00484536
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  • 10
    Electronic Resource
    Electronic Resource
    Developmental patterns of 3-hydroxykynurenine accumulation in white and various other eye color mutants of Drosophila melanogaster (1977)
    Springer
    Biochemical genetics 15 (1977), S. 1049-1059 
    Details
    ISSN: 1573-4927
    Keywords: Drosophila ; eye pigmentation ; 3-hydroxykynurenine accumulation ; white mutants
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Several points of biochemical similarity between white and scarlet mutants suggest that both are defective in the transport of xanthommatin precursors. In both, accumulation of 3-hydroxykynurenine is negligible during larval life and occurs at only a slow rate during adult development. Larvae of both mutants also excrete 3H-3-hydroxykynurenine and 3H-kynurenine rapidly, which probably accounts for the normal levels of kynurenine during larval life. 3-Hydroxykynurenine levels are abnormal in all white mutants which were studied, although in two alleles which are strongly pigmented (w sat and w col) accumulation is enhanced rather than diminished. In w a, larval accumulation is normal but accumulation during adult development is greatly diminished, suggesting that this mutation has a tissue-specific effect. Similar levels were found in zeste females. Of the 11 other eye color mutants tested, abnormal levels of 3-hydroxykynurenine were found in eight. In four of these (claret, light, lightoid, and pink), larval accumulation is negligible, suggesting that these have defects in the kynurenine transport system like scarlet and white. In three others, however (brown, karmoisin, and rosy), accumulation during larval life is enhanced. In cardinal accumulation is normal during larval life but is excessive during adult development. This evidence supports the suggestion that the cd mutation blocks the final step of xanthommatin synthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00484496
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