[Low protection against this winter's influenza. A repeat performance of last season's subtype A?].
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Biomedical subjects
Publications and source records attributed to A Nordén.
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Structural chromosome aberrations were analyzed in peripheral lymphocytes of eight monozygotic (MZ) and seven dizygotic (DZ) pairs of male twins. There was no significant intrapair difference in the variance of aberration frequencies among the MZ and DZ twins. Thus, there was no evidence of a major genetic influence on the development of structural chromosome aberrations. Although a genetic component could not be excluded, it was concluded that any chromosome aberrations observed were probably due mainly to environmental influences.
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Sister chromatid exchanges (SCEs) were analyzed in peripheral lymphocytes obtained from nine healthy monozygotic (MZ) and nine healthy dizygotic (DZ) pairs of male twins. In addition, increases in SCE rates following in vitro treatment of whole blood with 100 microM N-acetoxy-2-acethylaminofluorene (NA-AAF), and after an 18-h DNA repair incubation period, were analyzed in the same twins. There was no significant intrapair difference in the variance of SCE frequencies among MZ and DZ twins at the baseline level, after NA-AAF treatment, or after a DNA repair incubation period. It was concluded that genetic factors probably do not contribute significantly to the individual variation that has been observed in baseline or NA-AAF-induced SCE rates. Thus, any observed alterations in SCE frequencies are probably caused by environmental influences.
The occupations, as given in the national public census 1975, of 124 adult patients with non-systemic glomerulonephritis were compared with those of the general population in the catchment area of the hospital. Occupations assumed to be linked with exposure to organic solvents or fuels were commoner among patients than in the general population. The finding supports the idea that such exposure is causal in glomerulonephritis.
The level of N-acetoxy-2-acetylaminofluorene (NA-AAF)-induced unscheduled DNA synthesis and the level of covalent binding of NA-AAF to DNA were determined in the mononuclear leukocytes of monozygotic and diazygotic twin pairs (n = 16 for each type). A statistically significant high degree of heritability was calculated for both parameters which, in turn, indicate genetic control of individual levels of induced DNA damage by NA-AAF.
A strict vegetarian diet [vegan diet (VD)] was investigated. Six middle-aged vegans (three men and three women) collected copies of 24-h diets using the duplicate portion sampling technique. By chemical analyses, the nutrient composition was determined in detail and compared with corresponding figures of a normal mixed Swedish diet. In the VD 30% of the energy originated from fat compared with 40% in normal Swedish mixed diet (MD). Linoleic acid was the dominant fatty acid (60% of total fat in VD versus 8% in MD). The VD contained 24 g protein/1000 kcal compared to 30 g/1000 kcal in MD, but the intake of essential amino acids by the vegans exceeded the recommendations. Dietary fiber was about 5 times higher in the vegan diet (29 versus 6 g/1000 kcal) and sucrose similar to MD (18 versus 21 g/1000 kcal). Among the inorganic nutrients the concentration of calcium (351 versus 391 mg/1000 kcal) and sodium (53 versus 49 mmol/1000 kcal) were similar in both types of diets but the amount of potassium (56 versus 30 mmol/1000 kcal, magnesium (300 versus 110 mg/1000 kcal), iron (9 versus 6.5 mg/1000 kcal), zinc (6.5 versus 4.7 mg/1000 kcal), and copper (2 versus 0.7 mg/1000 kcal) were nearly doubled. Iodine (39 versus 156 micrograms/1000 kcal and selenium (5 versus 17 micrograms/1000 kcal) were much lower in the VD, selenium even being undetectable in several 24-h diets. The VD was rich in folic acid (301 versus 90 micrograms/1000 kcal in MD) but the intake of vitamin B12 was only 0.3 to 0.4 microgram/day (MD: 3 to 4 micrograms/day). No clinical signs of nutritional deficiency were observed in the vegans. Serum protein levels of the vegans as well as their serum lipoproteins were near the lower range of the reference group. In addition, none of the vegans was overweight and their blood pressures were low for their age.
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The present study found no link between the intake of energy and various nutrients, on the one hand, and high or low blood pressure (BP) in women, on the other. Sixty women not on treatment for hypertension were selected from a defined population and examined, applying the duplicate portion technique, with respect to the relationships between BP and the intake of energy and nutrients. They were selected from above the 95th percentile for BP (group A) and from below the 30th (group B). The two groups were age-matched. The food sampling comprised six days, divided into three periods of two consecutive days within a period of four weeks. Twenty-four hour urine specimens were collected in each period and on two other occasions. The mean values for intake of energy, fat, protein, carbohydrates, minerals and electrolytes did not differ between the two groups despite the large differences in BP and obesity. The mean values for urinary excretion of minerals, electrolytes and nitrogen (calculated as crude protein) did not differ between groups. The present findings for the effect of salt on BP do not justify restriction of the salt intake as a means for decreasing BP in the population.
In a diabetes detection survey carried out between 1962 and 1965, 2477 (1.1%) of 228,883 subjects had Clinistix-positive glucosuria after a carbohydrate-rich luncheon meal. Of these 2477, 578 displayed impaired tolerance to oral glucose without having manifest diabetes. From this group, 267 men were divided into five groups and subjected to the following treatments and controls: (a) diet regulation and 0.5 g tolbutamide t.i.d. (N = 49), annual oral glucose tolerance test (OGTT); (b) diet regulation and one placebo tablet t.i.d. (N = 48), annual OGTT; (c) diet regulation only (N = 50), annual OGTT; (d) no treatment (N = 61), annual OGTT; and (e) no treatment, OGTT at follow-up (N = 59 at follow-up). In addition, a control group was included comprised of men with normal OGTT (N = 52). At follow-up, 29% of those without diet regulation and medication (group e: N = 59) had developed diabetes. Of those on diet regulation, but without active medication (group b plus group c, N = 98), 13% had diabetes. No individual maintaining tolbutamide and diet regulation (N = 23) had progressed to diabetes. In this group, 80% of those later examined (N = 11) had serum tolbutamide concentrations in the therapeutic range. No individual with initially normal OGTT developed diabetes or impaired OGTT. The findings suggest that normal oral glucose tolerance signifies little risk of progress to impaired glucose tolerance and manifest diabetes, whereas impaired glucose tolerance is associated with a high risk of progression to diabetes. In addition, it seems possible that treatment with diet regulation, in combination with tolbutamide, may prevent or postpone progression from impaired glucose tolerance to manifest diabetes.
A two-site immunoradiometric assay for human ferritin has been developed using antibody-coated polystyrene tubes. Serum ferritin was measured in fifty-four men and women aged 73 years. The geometric mean was 166 micrograms/l for thirty-one men and 161 micrograms/l for twenty-two women. One woman was excluded from the statistical calculations. Twenty-eight of the subjects had earlier participated in a study of food consumption by the duplicate portion technique. There was a significant correlation (r = 0.44, P < 0.01) between the food iron intake and the serum ferritin values. A reference material of men and women aged 18-55 years was also analysed. The geometric mean for males was 170 micrograms/l with a 95% confidence range of 46-637 micrograms/l. The female controls were found to have significantly lower values (geometric mean 51 micrograms/l, 95% confidence range 10-260 micrograms/l) than both the older women (P < 0.001) and the male controls (P < 0.001).
The excretion of bile acids in urine from a patient with chronic malabsorption was investigated. Bile acids were separated according to mode of conjugation using a lipophilic anion exchanger, diethylaminohydroxypropyl Sephadex LH-20. Following hydrolysis, individual bile acids were analyzed by computerized GC/MS. In addition, bile acid glucuronides were isolated and their methyl ester trimethylsilyl ether derivatives were directly analyzed by GC/MS. The patient had a normal or slightly increased excretion of bile acids in urine. Bile acids carrying a hydroxyl group at C-6 constituted about 40% of the total. Tetrahydroxylated bile acids were present which have not been found in healthy subjects. Glucuronides of otherwise unconjugated bile acids accounted for 20% of the total. About 90% of these conjugates were 6-hydroxylated, hyodeoxycholic acid being the major bile acid. It is suggested that a specific abnormality of bile acid metabolism is related to the disease in this patient.
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Five out of 74 patients with adult coeliac disease (ACD) diagnosed from 1965 through 1977 developed intestinal lymphoma. The age at diagnosis of ACD was 54-63 years (mean 58) and in all patients an initial improvement was noted on a gluten-free diet. The interval between the diagnoses of ACD and lymphoma was 0.5-6 years (mean 3). In 4 patients the diagnosis of lymphoma was preceded by relapse of diarrhoea and loss of weight despite an adequate diet; 2 patients developed perforation of the bowel. In all patients who subsequently developed lymphoma a pronounced lymphocytopenia, 0.4-1.3 X 10(9)/l, was found at the diagnosis of ACD. It is suggested that ACD patients over 40 who have relapse of malabsorption symptoms despite an adequate diet should be investigated for the presence of an intestinal lymphoma. The suspicion of a malignant transformation may be especially strong if a previous, pronounced lymphocytopenia has been recorded. Three patients died 1-12 months after the diagnosis of lymphoma. However, 2 patients are in good condition 14 and 20 months, respectively, after laparotomy and removal of the tumour, indicating that an early diagnosis and treatment may have a reasonably palliative effect in some cases.
Quantitative analyses of plasma concentrations of retinol binding protein (RBP), prealbumin and total proteins were performed in normal subjects and in forty-two patients suffering from diseases of the intestine and liver. The visual dark adaptation ability (DAA) was also assessed. Reduction of DAA and of RBP and prealbumin levels was noted in patients with chronic liver disease and fat malabsorption. In sixty-eight patients with intestinal diseases the RBP concentration seemed to be reduced in relation to the degree and duration of steatorrhoea. Furthermore, inflammatory activity, as revealed by laborabory tests, markedly reduced the RBP level. Treatment with vitamin A increased the RBP and prealbumin concentrations and restored the DAA to normal in patients with malabsorption but normal liver function. In patients with liver disease reduced DAA and serum RBP values were not affected by vitamin A therapy. Only at RBP concentrations below half the normal was impairment of the dark adaptation observed, suggesting that serum RBP is a more sensitive indicator of vitamin A deficiency than measurement of dark adaptation.
In an attempt to determine the frequency of liver injury in adult coeliac disease (A.C.D.) the case records of 74 consecutive patients were examined. In 13 cases histological sections of the liver were available and in 5 of these there were signs of reactive hepatitis. Histological signs of distinct hepatic injury with cirrhosis and/or chronic active hepatitis were found in 7 other patients. In 5 of these serum-IgA was normal, whereas 16 out of 20 control patients with liver cirrhosis not associated with A.C.D. had raised serum-IgA. Serum-aspartate-aminotransferase and serum-alanine-aminotransferase were determined in 53 patients; 29 had raised concentrations. In 19 patients serum-aminotransferases were repeatedly determined before and during the dietary regimen and there was a significant reduction in enzyme concentrations during treatment. The median concentration of serum-alkaline-phosphatase was also reduced during treatment but not significantly. The histological evidence of liver injury in 16% and the abnormal liver-function tests in 39% of the patients indicate that hepatic injury is common in A.C.D. Since liver-function tests or liver biopsy specimens were available for only about two-thirds of the patients, liver damage in A.C.D. may be more common than indicated by these results. The effect of a gluten-free diet on aminotransferase concentrations indicates that the liver injury may be reversible and suggests that in some A.C.D. patients progressive liver damage may be prevented by suitable treatment. Since A.C.D. is not always recognised, the diagnosis should be considered in patients with liver disease of unknown aetiology.