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1. |
Human parotid proline‐rich proteins: Correlation of genetic polymorphisms to dental caries |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page 147-152
Pao‐Lo Yu,
David Bixler,
Patricia A. Goodman,
Edwin A. Azen,
Robert C. Karn,
D. C. Rao,
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摘要:
AbstractParotid saliva contains a variety of proline‐rich proteins. This study found that, among 306 children between the ages of 5 to 15 years, there is a significant increase in the decayed‐missing‐filled tooth surface (DMFS) score of the permanent teeth with age in children with the specific proline‐rich protein phenotypes Pa and Pr. However, the increase in DMFS score of the permanent teeth of children was significantly greater in children with Pa+ and Pr22 than in those with the other phenotypes (Pa– or Pr11 and Pr12). The previously established close correlation between the Pa and Pr phenotypes and the genetic variants of salivary peroxidase (a powerful antibacterial system in the oral cavity) may provide an explanation for the relationship of certain proline‐rich protein phenotypes to de
ISSN:0741-0395
DOI:10.1002/gepi.1370030302
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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2. |
Symptom patterns and causes of somatization in men: I. Differentiation of two discrete disorders |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page 153-169
Soren Sigvardsson,
Michael Bohman,
Anne‐Liis von Knorring,
C. Robert Cloninger,
P. M. Conneally,
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摘要:
AbstractTwo distinct patterns of somatization were identified in 807 Swedish adopted men, using comprehensive lifetime psychiatric and sick‐leave records. “Diversiform” somatizers had a high frequency of brief sickness occasions for a wide diversity of complaints, particularly pain in the head, joints, and abdomen. “Asthenic” somatizers had a lower frequency and diversity of complaints. They recuperate more slowly, however, and were more often disabled by fatigue, weakness, and minor illnesses such as upper respiratory infections. Both types of somatizers had associated psychosocial maladjustment, but they had discrete clinical patterns, with infrequent overlap. Diversiform somatizers had a higher risk of alcohol abuse, psychiatric hospitalization, and substandard income than either asthenic somatizers or non‐somatizers. Asthenic somatizers had a higher risk of divorce than either diversiform somatizers or non‐somatizers. Men with prominent somatization had an excess of psychiatric treatment for alcoholism or anxiety disorders, but, unlike female somatizers, no excess of criminality. These clinical differences suggest that the psychiatric processes associated with somatization may be qualitatively different in men and women. The method used here is generally applicable in genetic epidemiology to identify natural clinical subtypes within a heterogene
ISSN:0741-0395
DOI:10.1002/gepi.1370030303
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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3. |
Symptom patterns and causes of somatization in men: II. Genetic and environmental independence from somatization in women |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page 171-185
C. Robert Cloninger,
Anne‐Liis von Knorring,
Soren Sigvardsson,
Michael Bohman,
P. M. Conneally,
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摘要:
AbstractThe genetic and environmental antecedents of clinically distinct disorders leading to somatization were compared in 807 Swedish men and 859 Swedish women adopted at an early age by non‐relatives. Asthenic somatization, the predominant form in men, was a neurotic disorder associated with a lower incidence of criminality in the somatizers' biological parents than in the biological parents of non‐somatizers of either sex. In contrast, most female somatizers and a minority of men with diversiform somatization had disorders that were associated with a higher incidence of criminality in their biological parents than in other biological parents. Likewise, female somatizers, but not male somatizers, had an excess of alcoholic biological fathers when compared to other adoptees. In addition, different postnatal environmental background factors contributed to the risk for somatization in each sex. These findings support the distinctions among the different types of somatizers and show that the usual causes of somatization are fundamentally different in men and women. This illustrates the utility of the adoption paradigm in resolving genetic and environmental contributions to the familial aggregation of developmentally complex phenoty
ISSN:0741-0395
DOI:10.1002/gepi.1370030304
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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4. |
Log‐linear model analysis of allelic associations |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page 187-194
C. E. Aston,
S. R. Wilson,
D. C. Rao,
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摘要:
AbstractAn approach is outlined for the analysis of nonrandom allelic associations in multilocus systems in a diploid population. The concept of composite link functions in generalised linear model analysis is used to handle the problem of incomplete identification of constituent gametes often encountered in genotypic data for two or more marker loci.
ISSN:0741-0395
DOI:10.1002/gepi.1370030305
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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5. |
Progress toward resolving the possible linkage of multiple endocrine neoplasia type 2A to haptoglobin and group‐specific loci: Use of restriction fragment length polymorphisms extends exclusion region |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page 195-200
K. K. Kidd,
J. R. Kidd,
C. M. Castiglione,
A. J. Pakstis,
R. S. Sparkes,
D. C. Rao,
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摘要:
AbstractIn an earlier paper, positive but nonsignificant lod scores were found in pair‐wise linkage tests between multiple endocrine neoplasia type 2A (MEN‐2A) and both the haptoglobin (HP) locus on chromosome 16 and group‐specific component (GC) locus on chromosome 4. Recently discovered restriction fragment length polymorphisms forHPand for metallothionein 2 processed pseudogene 1 (MT2P1) nearGChave made it possible to carry out a more powerful set of linkage tests with MEN‐2A. This paper reports the results of such linkage analyses employing both pair‐wise and multipoint tests. Close linkage ofHPon chromosome 16 and MEN‐2A is excluded. Linkage of MEN‐2A on chromosome 4 withGCis excluded on theMT2P1side ofGCin a 7‐centimorgan inter
ISSN:0741-0395
DOI:10.1002/gepi.1370030306
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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6. |
Evidence for linkage between Wilson disease and esterase D in three kindreds: Detection of linkage for an autosomal recessive disorder by the family study method |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page 201-209
Batsheva Bonné‐Tamir,
Lindsay A. Farrer,
Moshe Frydman,
H. Kanaaneh,
D. C. Rao,
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摘要:
AbstractWilson disease (WD) is an inherited disorder of copper metabolism that affects the brain, liver, and other organs. Our group recently reported close linkage between the locus for WD and a polymorphic red cell enzyme, esterase D (EsD), in a large inbred Israeli‐Arab lineage. We have subsequently studied two unrelated Druze kindreds in order to confirm this linkage and more precisely define the distance between the two loci. The maximum likelihood estimate of recombination was determined to be zero with lod scores of 1.48 and 1.06 in each Druze family, respectively. The combined maximum lod score based on pooled results from the Israeli‐Arab and Druze kindreds is 5.49 at θ = 0.03.WD is one of a few autosomal recessive disorders that has been mapped by classical family study methods. In this paper, the merits for using large, inbred families in linkage studies of rare recessive disorders are discussed. Major considerations for pedigree selection are size and number of constituent nuclear families, number and distribution of affected individuals, and pedigree structure that may provide information for determination of phase between the disease and marker
ISSN:0741-0395
DOI:10.1002/gepi.1370030307
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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7. |
Announcement |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page 211-211
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ISSN:0741-0395
DOI:10.1002/gepi.1370030308
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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8. |
Masthead |
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Genetic Epidemiology,
Volume 3,
Issue 3,
1986,
Page -
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PDF (91KB)
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ISSN:0741-0395
DOI:10.1002/gepi.1370030301
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1986
数据来源: WILEY
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