Acta Medica ScandinavicaVolume 137, Issue 3 p. 187-197 Variations of the Acid and Alkaline Phosphatase Activity in the Livers of White Rats during the 24-Hours Period HJ. HOLMGREN, HJ. HOLMGREN Department of Experimental Histology, Karolinska Institutet Stockholm.Search for more papers by this authorA. SVANBORG, A. SVANBORG Department of Experimental Histology, Karolinska Institutet Stockholm.Search for more papers by this author HJ. HOLMGREN, HJ. HOLMGREN Department of Experimental Histology, Karolinska Institutet Stockholm.Search for more papers by this authorA. SVANBORG, A. SVANBORG Department of Experimental Histology, Karolinska Institutet Stockholm.Search for more papers by this author First published: January/December 1950 https://doi.org/10.1111/j.0954-6820.1950.tb13187.xCitations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume137, Issue3January/December 1950Pages 187-197 RelatedInformation

Acta Medica ScandinavicaVolume 179, Issue 4 p. 447-452 The Fatty Acid Composition of Mitochondrial Lipids from Musculus Pectoralis Minor in Non-diabetics and Diabetics B. HALLGREN, B. HALLGREN Medical Clinic II (Head: Erik Wassén. M.D.), Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden, and the Research Laboratories, Astra Nutrition AB, Mölndal, SwedenSearch for more papers by this authorC.-G. LUNDQUIST, C.-G. LUNDQUIST Medical Clinic II (Head: Erik Wassén. M.D.), Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden, and the Research Laboratories, Astra Nutrition AB, Mölndal, SwedenSearch for more papers by this authorA. SVANBORG, A. SVANBORG Medical Clinic II (Head: Erik Wassén. M.D.), Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden, and the Research Laboratories, Astra Nutrition AB, Mölndal, SwedenSearch for more papers by this author B. HALLGREN, B. HALLGREN Medical Clinic II (Head: Erik Wassén. M.D.), Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden, and the Research Laboratories, Astra Nutrition AB, Mölndal, SwedenSearch for more papers by this authorC.-G. LUNDQUIST, C.-G. LUNDQUIST Medical Clinic II (Head: Erik Wassén. M.D.), Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden, and the Research Laboratories, Astra Nutrition AB, Mölndal, SwedenSearch for more papers by this authorA. SVANBORG, A. SVANBORG Medical Clinic II (Head: Erik Wassén. M.D.), Sahlgren's Hospital, University of Gothenburg, Gothenburg, Sweden, and the Research Laboratories, Astra Nutrition AB, Mölndal, SwedenSearch for more papers by this author First published: January/December 1966 https://doi.org/10.1111/j.0954-6820.1966.tb05482.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 CARLSTEN, A., HALLGREN, B., JAGENBURG, R., SVANBORG, A. & WERKÖ, L.: Myocardial extraction of plasma free fatty acids in healthy individuals and diabetics. Metabolism 11: 814, 1962. CASPubMedWeb of Science®Google Scholar 2 CHAPPELL, J. B. & PERRY, S. V.: Biochemical and osmotic properties of skeletal muscle mitochondrial. Nature 173: 1094, 1954. 10.1038/1731094a0 CASPubMedWeb of Science®Google Scholar 3 FLEISCHER, S., KLOUWEN, H. & BRIERLY, G.: Studies of the electron transfer system. XXXVIII Lipid composition of purified enzyme preparations derived from beef heart mitochondria. J. biol. Chem. 236: 2936, 1961. CASPubMedWeb of Science®Google Scholar 4 GELLHORN, A. & BENJAMIN, W.: The intracellular localization of an enzymatic defect of lipid metabolism in diabetic rats. Biochim. biophys. Acta (Amst.) 84: 167, 1964. CASPubMedWeb of Science®Google Scholar 5 GETZ, G. S. & BARTLEY, W.: The intracellular distribution of fatty acids in rat liver. The fatty acids of intracellular compartments. Biochem. J. 78: 307, 1961. 10.1042/bj0780307 CASPubMedWeb of Science®Google Scholar 6 GETZ, G. S., BARTLEY, W., STRIPE, F., NOTTON, B. M. & RENSHAW, A.: The lipid composition of rat-liver mitochondria, fluffy layer and microsomes. Biochem. J. 83: 181, 1962. 10.1042/bj0830181 CASPubMedWeb of Science®Google Scholar 7 GIBSON, D. M. & HUBBARD, D. D.: Incorporation of malonyl CoA into fatty acids by liver in starvation and alloxan diabetes. Biochem. biophys. Res. commun. 3: 531, 1960. 10.1016/0006-291X(60)90169-8 CASPubMedWeb of Science®Google Scholar 8 HALL, J. C., SORDAHL, L. A. & STEFKO, P. L.: The effect of insulin on oxidative phosphorylation in normal and diabetic mitochondria. J. biol. Chem. 235: 1536, 1960. CASPubMedWeb of Science®Google Scholar 9 HALLGREN, B., STENHAGEN, S., SVANBORG, A. & SVENNERHOLM, L.: Gas chromatographic analysis of the fatty acid composition of the plasma lipids in normal and diabetic subjects. J. clin. Invest. 39: 1424, 1960. 10.1172/JCI104162 CASPubMedWeb of Science®Google Scholar 10 HOLMAN, R. T. & WIDMER, C.: Polysaturated fatty acids in beef heart mitochondria and derived enzymatically active lipoprotein fractions. J. biol. Chem. 234: 2269, 1959. CASPubMedWeb of Science®Google Scholar 11 LAVGENS, R. & BIANCHI, N.: Fine structure of the liver in human idiopathic diabetes mellitus. I. Parenchymal cell mitochondria. Exp. Molecular Pathology 2: 203, 1963. 10.1016/0014-4800(63)90035-2 CASGoogle Scholar 12 LUNDQUIST, C.-G. & SVANBORG, A.: Respiratory activity of mitochondria from human skeletal muscle before and after insulin administration. Acta med. scand. 176: 1094, 1954. Google Scholar 13 PANGBORN, M. C.: The composition of cardiolipin. J. biol. Chem. 168: 351, 1947. 10.1016/S0021-9258(17)35123-2 CASPubMedWeb of Science®Google Scholar 14 SVANBORG, A. & SVENNERHOLM, L.: Plasma total lipid, cholesterol, triglycerides, phospholipids and free fatty acids in a healthy Scandinavian population. Acta med. scand. 169: 43, 1961. 10.1111/j.0954-6820.1961.tb17091.x CASWeb of Science®Google Scholar Citing Literature Volume179, Issue4January/December 1966Pages 447-452 ReferencesRelatedInformation

OBJECTIVE:To investigate the survival rate in very elderly individuals in relation to Alzheimer disease, vascular dementia, and other mental and physical disorders.DESIGN:A 7-year longitudinal survey.SETTING:Community and institutions in Gothenburg, Sweden.PARTICIPANTS:A representative sample of 494 people aged 85 years.MAIN OUTCOME MEASURES:Results of neuropsychiatric and physical examinations, key informant interview, and computed tomographic scan of the head. Information on mortality was obtained from the parish office.RESULTS:The 7-year survival rate was higher in women (34.5%) than in men (20.3%). Alzheimer disease and vascular dementia predicted 30.7% of deaths in men and 49.7% of deaths in women according to a calculation of population attributable risk (PAR). A regression analysis showed that mortality in men was predicted by the presence of chronic obstructive lung disease (PAR, 18.8), Alzheimer disease (PAR, 16.0), vascular dementia (PAR, 14.7), cancer of the gastrointestinal tract (PAR, 10.2), and skin cancer (PAR, 6.2), and in women by vascular dementia (PAR, 29.4), Alzheimer disease (PAR, 20.3), cerebrovascular disorder (PAR, 12.1), congestive heart failure (PAR, 8.5), hypertension (PAR, 8.0), myocardial infarction (PAR, 6.5), and cancer of the gastrointestinal tract (PAR, 4.3). Life expectancy decreased with severity of dementia, although survival time in individuals with mild Alzheimer disease was not different from that in individuals without dementia.CONCLUSIONS:In extreme old age, Alzheimer disease and vascular dementia influence the mortality rate considerably. However, mild Alzheimer disease does not influence longevity, at least not during the first 7 years. These findings have important public health implications.

Muscles in the limbs change with age, but the aging process of urethral muscles is unknown. Therefore, we compared smooth and striated muscle content in the female rat urethra in young (12 month) and old (32 month) animals, using immunochemical techniques. All the striated skeletal fibers at both ages contain slow myosin. Urethral diameter does not change with age (young, 1.44±0.08 mm; old, 1.46±0.10 mm,n=5), nor does the external sphincter width (young, 0.088±0.016 mm; old, 0.080±0.017 mm,n=5). Neither smooth nor skeletal muscle volume in the urethra is changed with age (skeletal: young, 20.72±2.94%; old, 19.95±2.35%. Smooth: young, 22.26±2.98%; old, 26.75±2.35%,n=5). The external striated sphincter is separate and distinct from the pubococcygeal region of the levator ani muscle, but is closely apposed to another layer of longitudinally oriented fibers into the vaginal musculature. The morphometric analysis shows no difference in urethral architecture in aging female rats.

Functional performance, i.e. personal and instrumental activities of daily living (P-ADL, I-ADL), was studied in a population of 70-year-old persons followed to the age of 76, and with an intervention period included between the ages of 70 and 73. At age 70 (n = 617), 83% were independent, 13% were dependent in I-ADL and 4% dependent in I+P-ADL. Among the independent subjects, the 6-year outcome in mortality was 13%. Dependence at 70 predicted mortality as well as institutionalization, and the risk was higher for those dependent in P+I-ADL than for persons dependent in I-ADL only. Of participant survivors the incidence of disability was 30% (8% between 70 and 73, 26% between 73 and 76 years of age) and was dominated by dependence in I-ADLs. The intervention did not lead to less dependence in ADL at age 76. Gender differences were found at age 76 in cooking, bathing and dressing, males being more dependent in such activities. At 70, 73 and 76 years of age, assistance given by relatives dominated.

Background Vascular causes of dementia may be more common than supposed. Vascular factors may also have a role in late-onset Alzheimer's disease, but the role of hypertension in the development of dementia is unclear.Methods As part of the Longitudinal Population Study of 70-year-olds in Goteborg, Sweden, we analysed the relation between blood pressure and the development of dementia in the age intervals 70-75, 75-79, and 79-85 years in those non-demented at age 70 (n=382). The sample was followed up for 15 years and examined repeatedly with a comprehensive investigation, including a psychiatric and physical examination.Findings Participants who developed dementia at age 79-85 had higher systolic blood pressure at age 70 (mean 178 vs 164 mm Hg, p=0.034) and higher diastolic blood pressure at ages 70 (101 vs 92, p=0.004) and 75 (97 vs 90, p=0.022) than those who did not develop dementia, For subtypes of dementia, higher diastolic blood pressure was recorded at age 70 (101, p=0.019) for those developing Alzheimer's disease and at age 75 (101, p=0.015) for those developing vascular dementia than for those who did not develop dementia. Participants with white-matter lesions on computed tomography at age 85 had higher blood pressure at age 70 than those without such lesions. Blood pressure declined in the years before dementia onset and was then similar to or lower than that in non-demented individuals.Interpretation Previously increased blood pressure may increase the risk for dementia by inducing small-vessel disease and white-matter lesions. To what extent the decline in blood pressure before dementia onset is a consequence or a cause of the brain disease remains to be elucidated.

Joint complaints were studied in two cohorts longitudinally followed at 4-5 year intervals between the ages of 70 and 79, representative of the elderly population of Goteborg, Sweden. Joint complaints were reported by 30-43% of the women and by 15-25 of the men. A significant increase of joint complaints was found in both sexes between the ages of 70 and 75 but not thereafter. The knee joints were the most common site of complaints in both sexes. Complaints were not consistently reported by the probands at all examinations, however, and a 'disappearance' of complaints with age was found. Complaints on all three occasions were reported by 15% of the women and 3% of the men. An association was observed between repeatedly reported complaints and radiographic osteoarthritis as well as with self-reported rheumatoid arthritis.

The prevalence of joint complaints and clinical and radiological findings of osteoarthritis in wrist, hand, and knee joints was studied in representative population subsamples of 79 and 85 year olds. Joint complaints, clinical findings of osteoarthritis, and radiographic osteoarthritis were more common in women. Age related differences in the prevalence of osteoarthritis were not found. Although there was a correlation between clinical signs of osteoarthritis and radiographic osteoarthritis, clinical signs were often present without radiographic evidence and moderate and severe radiographic osteoarthritis was often present without clinical signs.

Selected factors potentially associated with radiographic osteoarthritis (OA) were studied in 2 subsamples of 79-year-olds, within the longitudinal prospective study 70-year-old People in Göteborg. A very significant (p less than 0.01 in men, p less than 0.001 in women) association was found between radiographic knee OA and body mass index (BMI), and a significant (p less than 0.05) association was also observed between radiographic hand OA and BMI in men. Smoking correlated negatively (p less than 0.01) to radiographic knee OA in both sexes, even after adjusting for BMI. Other factors, including diabetes, ischemic heart disease, hypertension, physical activity, education, vocational training, marital status, serum uric acid, triglycerides, cholesterol and blood glucose levels did not correlate to radiographic OA. Finally, no correlation was found between either decreased bone mineral content or the presence of previous fragility fractures.

In a representative population sample of 619 70-year-old people, 26% were taking antihypertensive treatment. Twenty per cent (n = 32) of them showed no signs of cardiovascular disease and had a blood pressure of less than 175/95 mmHg. Treatment was withdrawn in 25 of the 32 patients. Casual blood pressure, blood pressure during isometric exercise and left ventricular morphology and function were studied repeatedly over 2 years, using non-invasive methods. A significant increase in mean systolic and diastolic blood pressures was observed in the 14 patients who completed the study. No change was observed with respect to left ventricular morphology and left ventricular diastolic function. A statistically significant decrease in left ventricular fractional shortening, but no clinical signs of congestive heart failure were observed. Withdrawal of antihypertensive treatment in elderly patients free from signs of cardiovascular disease may thus be attempted without harmful effects on cardiovascular function.

In a population study of 70-year-old people in Göteborg, Sweden, a representative sample of 449 men and 524 women was followed for nine years. The prevalence of coronary heart disease (CHD) at age 70 was about 30% in both sexes and did not change up to age 79. Myocardial infarction appeared twice as often in men as in women at age 70 but angina pectoris and ST-T changes on ECG showed no sex difference. Myocardial infarction and probable ischaemia on ECG increased significantly between ages 70 and 79 in both sexes. Half of the men with angina pectoris had a history of myocardial infarction and/or probable ischaemia on ECG criteria compared with 23% of the women. The mortality rate was twice as high in men as in women irrespective of CHD. When CHD was present at age 70 the nine-year mortality was doubled. CHD was shown to be a strong independent risk factor for death also in this age group.

An intervention trial using oral oestriol to treat urinary incontinence was performed in a number of patients taken from a representative sample of 562 women aged 75 yr. The clinical series consisted of 34 patients who took part in a double-blind crossover study of the possible effects of oestriol, given in a single daily dose of 3 mg, and of a placebo over a period of 3 mth. The clinical examinations included bacteriological cultures and an assessment of the degree of atrophy of the surface membranes in the vagina. In most patients, oestriol was effective in reversing the atrophy. The clinical effect was excellent in urgency and mixed incontinence, but not in stress incontinence.

Relationships between an index of gonadal steroid hormone function and personality as well as sexual activity were studied in a sample representative for 70-year-olds in Gotenburg, Sweden. Personality was described by means of inventories, sexual activity through a systematic interview and the balance between androgen and oestrogen activity by the quotient between lecithin and lysolecithin in plasma. Men with a relative dominance of oestrogen activity reported a lower frequency of sexual intercourse than other men. Women with a relative dominance of oestrogen activity described themselves as more resourceful, active, confident, unconcerned with the opinion of others, and able to take care of themselves than other women. There were no associations in women between the hormonal balance and the frequency of sexual intercourse.

Norethisterone acetate (NET), levonorgestrel (NORG) and medroxyprogesterone acetate (MPA) were administered to oophorectomized women to evaluate the effects on individual serum phospholipids as well as serum lecithin and cholesterol ester fatty acid composition. Blood samples were drawn after a 3-week period without hormonal replacement therapy and after 3 weeks on each progestogen. NORG reduced cepahlin and lecithin with a concomitant increase in lysolecithin. This shift in individual phospholipids has previously been induced by exogenous androgens. The 17C-alkylated synthetic progestogens NET and NORG but not the non-alkylated MPA caused a redistribution among the 1-position fatty acids of serum lecithin with an increase in palmitic concomitant with a decrease in stearic acid. These findings indicate differences between 19-nortestosterone derivatives and 17-hydroxyprogesterone derivatives in effect on individual serum phospholipids and in influence on liver lecithin synthesis as judged from serum lecithin fatty acid composition.

In a study of two representative population samples of 70-year-olds, one of which was followed up at 75 years of age, digitalis treatment was associated with oestrogen-like metabolic effects, indicated by changes in the composition of the plasma phospholipid fraction. Digitalis treatment, at least at these ages, is related to metabolic effects even in patients lacking more obvious clinical signs such as gynaecomastia. The results suggest that digitalis treatment may have other oestrogenic effects, e.g. on the water and sodium balance, counteracting the cardiotropic effects of this drug.

Norethisterone acetate (NET) was administered to 11 oophorectomized women, primed with either 17-C-alkylated ethinylestradiol (EE) or the non-alkylated estrogen, estradiol valerate (E2V), to evaluate the effects on lipid metabolism. Blood samples were drawn after a period without hormonel replacement therapy and after 6 weeks on each estrogen and estrogen-progestogen combination. Serum and lipoprotein lipids were followed and an oral glucose tolerance test was performed with blood glucose and plasma insulin determinations.

Norethisterone acetate, medroxyprogesterone acetate and levonorgestrel were administered to oophorectomised women to evaluate the effects they have on lipid metabolism. Blood samples were drawn after a 3 wk period without hormone therapy and after 3 wk on each progestogen. Serum and lipoprotein lipids were followed and an oral glucose tolerance test with blood glucose and plasma insulin determinations were performed.

Abstract. Norethisterone acetate (NET) was administered to 11 oophorectomized women (mean age 34.5 ± 5.9 years) primed with the 17-C-alkylated ethinyl oestradiol (EOe) and the non-alkylated oestrogen, oestradiol valerate (Oe2V) in separate periods. Blood samples were drawn after 4 weeks without hormonal replacement therapy, after 6 weeks on each oestrogen and after 6 weeks on each oestrogen-progestogen combination. Routine liver function tests were carried out, assessment of individual phosholipids i.e. cephalin, lecithin, lysolecithin and sphingomyelin was done after thin layer chromatography. The relative fatty acid composition of serum and high density lipoprotein lecithin and serum cholesterol ester was determined by gas liquid chromatography. The redistribution of serum individual phospholipids (increase in lecithin and decrease in lysolecithin) induced by both oestrogens was reversed by the addition of NET. This lecithin-lysolecithin shift seen after NET administration could depend on a stimulation of the hepatic lipase with its phospholipase Al-activity. The 17-C-alkylated EOe, but not the non-alkylated Oe2V, caused an increase in palmitic and a decrease in stearic acid in the 1-position of serum lecithin. When NET (like EOe, 17-C-alkylated) was added to EOe, this palmitic-stearic acid shift was further accentuated, and it also appeared when NET was added to Oe2V. It is suggested that the shift in 1-position fatty acids of serum lecithin induced by EOe and NET is a non-hormonal 'drug-effect' linked to their 17-C-alkylation and liver toxicity. The reduction in arachidonic acid of serum lecithin and serum cholesterol ester seen after NET administration is interpreted as an anti-oestrogenic effect which could be mediated by a decreased transformation of linoleic to arachidonic acid in the liver.

Eleven oophorectomized women (mean age 34.5 +/- 5.9) received two treatment cycles, one of the 17-C-alkylated ethinyl estradiol 20 microgram per day, and the second of the non-alkylated estrogen, estradiol valerate 2 mg per day for six weeks in separate periods preceded by six weeks without hormonal replacement therapy. Blood samples were drawn before and after six weeks on each estrogen. The samples were assayed for individual phospholipids i.e. cephalin, lecithin, lysolecithin and sphingomyelin after separation of these lipids by thin layer chromatography. The relative fatty acid composition of serum and high density lipoprotein lecithin and serum cholesterol ester was determined by gas liquid chromatography. Both estrogens reversed the symptoms of estrogen deficiency and had similar effects on serum individual phospholipids i.e. causing an increase in lecithin concomitant with a decrease in lysolecithin. It is suggested that this lecithin-lysolecithin shift could depend on an inhibition of the hepatic lipase and its phospholipase A1-activity. Both estrogens increased serum lecithin arachidonic acid without causing any change in linoleic acid (the major essential fatty acid), which indicates that this increase in arachidonic acid could be an estrogenic effect independent of dietary factors. Ethinyl estradiol caused an increase in palmitic and a decrease in stearic acid in the 1-position of serum lecithin while estradiol valerate did not influence these fatty acids at all. This palmitic-stearic acid shift induced by ethinyl estradiol is interpreted as a non-hormonal "drug-effect" linked to the liver toxicity of 17-C-alkylated steroids in spite of the lack of influence on routine liver function tests.

During long-term treatment with L-dopa in Parkinson's syndrome “on-off” phenomenon develops in many cases, often entailing considerable therapeutic problems. Decreased sensitivity in postsynaptic striatal dopamine (DA) receptors has been shown to occur in parkinsonian patients during long-term treatment with L-dopa. This has been suggested as one possible mechanism for development of the “on-off” phenomenon. In contrast to L-dopa treatment electroconvulsions have been shown to increase sensitivity in the DA receptors, when administered to animals.