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Biomedical subjects

W J Turner

Publications and source records attributed to W J Turner.

At least 37 records · Page 2Linked to original sources
PubMed1983

BPD2. An autosomal dominant form of bipolar affective disorder.

Seven pedigrees with bipolar affective disorder (BPD2) have been found to show a pattern consistent with autosomal dominant genetic inheritance in linkage with, but distal to, HLA on the short arm of chromosome 6. Segregation analysis of subjects by narrow criteria yielded lod score 8.02 at theta = 0.15. Four pedigrees of three to five generations contributed most to the total score. Note is made of high concordance of marker HLA haplotype in affected sibs.

Adult↗
PubMed1982

The effects of requisite assumptions on linkage analyses of manic-depressive illness with HLA.

Two large pedigrees with a bipolar proband were selected on the basis of compatibility with the hypothesis of autosomal dominant inheritance of a depressive taxon. We compared the results of linkage analyses of the depressive taxon with HLA and GLO in these pedigrees when penetrance function, diagnostic classification, and HLA haplotype frequencies were varied. The analyses show that all three types of assumptions affect the lod scores and likelihoods obtained. Using the most favorable assumptions, we obtain a lod score of 3.901 at theta = 0.10 for HLA with the depressive taxon. This lod score would conventionally be considered strong evidence of linkage of a subtype of manic-depressive illness with HLA but the dependence of these results on several untested assumptions suggests more cautious interpretation. Nonetheless, we feel it does represent evidence in favor of linkage because this high a lod score cannot readily be dismissed as statistical artifact. The results point out the importance of careful delineation of the assumptions made in linkage analyses of complex disorders, including the diagnostic criteria, marker allele frequencies, and age-of-onset function used.

Adolescent↗
PubMed1981

Two genetically distinct forms of bipolar affective disorder?

In five pedigrees in which bipolar affective illness (BPD) can be traced through three generations with no father-son transmission, no linkage to HLA could be established. This group was evidently dependent on a single dominant gene (X-linked?), for which the noncommittal designation BPD1 was proposed. Two pedigrees of BPD, in which father-son transmission occurred at least twice, showed highly suggestive linkage to HLA (lod = 2.61 at theta = 0.15). BPD2 was proposed as the designation for this gene. Loss of BPD in one HLA-A/B cross-over suggests that a single dominant gene in this group has a locus in p2-pter region of chromosome 6.

Bipolar Disorder↗
PubMed1979

Genetic markers for schizotaxia.

Evidence is presented for the occurrence of a locus for schizotaxia on the short arm of chromosome 6. This derives from study of 63 informative members of seven pedigrees in which the proband and a parent (or a sib of parent) suffered with schizophrenia and other kin were either normal or fell within a spectrum of conditions related to schizophrenia. For linkage of HLA and schizotaxia a Lod score, 2.57, at recombination frequency 0.15 is reported, which gives p = 0.008. This is in contrast to data on 54 informative members of six pedigrees with atypical (schizo-affective or mixed) psychoses in two generations. Glyoxalase isoenzymes were of value in linkage analysis in two pedigrees. No evidence for linkage was found for any erythrocyte surface antigen nor for 15 other genetic markers. Details for each pedigree are provided.

Adult↗
PubMed1978

Celiac disease.

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Celiac Disease↗
PubMed1976

HLA antigen frequencies in paralytic dementia.

HLA typing was performed on 75 caucasian and 58 black patients with paralytic dementia hospitalized at 2 state mental institutions in New York. Serological testing was performed to confirm previous infection with T. pallidum. The caucasian patients showed an increase in B18(18.7% vs. 9.6% in controls). The black patients showed an increase in A2 (48.3% vs. 28.7% in controls) and an increase in B7 (27.6% vs. 15.7% in controls.

Black People↗
PubMed1976

Metabolic response of humans to ingestion of nicotinic acid and nicotinamide.

The identification of nicotinamide-N1-oxide as a metabolite in the urine of a schizophrenic patient prompted a study of the relative metabolism of nicotinic acid and nicotinamide in mental patients and healthy volunteers. Metabolites quantified included N1-methyl-2-pyridone-5-carboxamide, N1-methyl-4-pyridone-3-carboxamide, N1-methylnicotinamide, nicotinuric acid, and nicotinamide-N1-oxide. More of most of these metabolites evidently was excreted after nicotinamide ingestion than after nicotinic acid. At the highest doses (3000 mg/day), the relative proportions of these metabolites in the urine were changed. There were only slight difference between healthy individuals and mental patients in the quantities of metabolites excreted, and no statistically significant trends were noted.

Adult↗
PubMed1975

Total body potassium and 24-hour creatinine excretion in healthy males.

Total body potassium may be predicted from height, weight, and age by TBKmmol = 30.83 Hcm + 18.05 Wkg - 11 (ageyr - 20) - 3034. This equation, based on measurements of 31 men, has been compared with others in the literature. Prediction of 24-hr creatinine (CR), excretion derived from 33 control adults whose excretion rates gave a coefficient of variation less than 13%, may be made from the equation: CRgm = 0.0143 Hcm + 0.00975 Wkg - 0.00734 (ageyr -20) -1.391. For 31 chronic schizophrenics, the corresponding equation CRgm = 0.0122 Hcm + 0.0145 Wkg - 1.611 contained no age correction. The relationship between CR and TBK is expressed by CRgm = 0.000403 TBKmmol + 0.278. Discussion of significance of these equations in the light of extensive literature suggests that about half of the error variance in predicting CR may be explained by the lack of suitable data on somatotype and much of the residual variance, including the day-to-day variation in CR, relate to factors altering basal O2 consumption. The predictors given should prove generally satisfactory for many metabolic and drug studies.

Adult↗