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Biomedical subjects

U Eriksson

Publications and source records attributed to U Eriksson.

At least 127 records · Page 7Linked to original sources
PubMed1984

Cellular retinol-binding protein. Quantitation and distribution.

The distribution of cellular retinol-binding protein was localized in three tissues involved in the transport of vitamin A using the peroxidase-antiperoxidase technique. In addition, a sensitive radioimmunoassay was developed to quantitate cellular retinol-binding protein in various tissues. In liver, the protein was found in the hepatocytes and in the perisinusoidal fat-storing cells. The columnar epithelial cells of the jejunum and the cells of the proximal tubuli also exhibit high concentrations of cellular retinol-binding protein. Estimations of the content of the protein in various tissues from normal and retinol-deficient rats showed that the retinol status did not affect the tissue levels or the subcellular distribution. The appearance of high amounts of this protein in cells involved in the dietary uptake, storage, mobilization, and resorption of vitamin A suggest that one function of the cellular retinol-binding protein is to act as a vehicle in the intracellular transport of retinol through these organs.

Amino Acid Sequence↗
PubMed1984

The three-dimensional structure of retinol-binding protein.

The complex of retinol with its carrier protein, retinol-binding protein (RBP) has been crystallized and its three-dimensional structure determined using X-ray crystallography. Its most striking feature is an eight-stranded up-and-down beta barrel core that completely encapsulates the retinol molecule. The retinol molecule lies along the axis of the barrel with the beta-ionone ring innermost and the tip of the isoprene tail close to the surface.

Animals↗
PubMed1984

Pain as a symptom in depressive disorders and its relationship to platelet monoamine oxidase activity.

144 depressed in-patients were rated by means of the Comprehensive Psychopathological Rating Scale (CPRS) and platelet monoamine oxidase (MAO) was determined. 49 per cent of the patients were found to have pain as a symptom, and 21 per cent were found to have more severe pain. The patients with more severe pain were found to have lower platelet MAO activity than the patients without pain or with slight pain. As platelet MAO activity may reflect the turn-over in the serotinergic systems in CNS it is hypothesized that patients with depressive disorders with pain as a symptom may have more pronounced disturbances in the serotinergic systems than patients without pain as a symptom.

Adult↗
PubMed1983

Subcellular localization in normal and vitamin A-deficient rat liver of vitamin A serum transport proteins, albumin, ceruloplasmin and class I major histocompatibility antigens.

The subcellular localization in rat liver cells of retinol-binding protein (RBP), prealbumin, ceruloplasmin, albumin, and class I transplantation antigen chains was investigated by radioimmunoassay determinations. The concentration of RBP was high in the rough and smooth endoplasmic reticulum (SER). The relative concentrations of prealbumin, ceruloplasmin and albumin were similar in the endoplasmic reticulum fractions and in the Golgi fraction. Neither of the proteins were found in significant amounts in the post-microsomal supernatant nor in the plasma membrane. The concentrations of the class I transplantation antigen chains were higher in the Golgi fraction than in the endoplasmic reticulum fractions. In the rough endoplasmic reticulum (RER) fraction ceruloplasmin and the class I antigens partially interact with high-molecular weight (MW) components, presumably membrane-bound glycosyltransferases. RBP, prealbumin and albumin seemed to be present in free form within the microsomal lumen. In vitamin A deficiency the RBP and to a lesser extent the prealbumin concentrations in the endoplasmic reticulum fractions were significantly increased, as compared to fractions from normal livers. This suggests that the presence of vitamin A is a prerequisite for the transport of RBP from the endoplasmic reticulum to the Golgi complex. The intracellular concentrations of albumin and ceruloplasmin were not significantly altered by vitamin A deficiency. In contrast, the amounts of the class I antigen heavy chains were found to be increased.

Animals↗
PubMed1983

Pain as a symptom in depressive disorders. II. Relationship to personality traits as assessed by means of KSP.

The series included 140 hospitalized patients with depressive disorders, who were rated by means of the Comprehensive Psychopathological Rating Scale (CPRS). Furthermore, a personality inventory, KSP, was completed when the patients had improved markedly. Forty-six per cent of the patients were found to have pain as a symptom. The patients with pain were found to have more somatic anxiety, more muscular tension, more psychasthenia and more inhibition of aggression but no significant differences were found in guilt. Thus pain as a symptom in depressive disorders seems to be linked to muscular tension and the patients seem to have more introjected aggression while no evidence emerges indicating that pain could serve to relieve the feelings of guilt.

Adult↗
PubMed1983

Structure and tissue distribution of some retinoid-binding proteins.

Vitamin A has, apart from its function in the visual pigments, general effects on several organs. Early signs of vitamin A deficiency include keratinization of epithelia and hyperkeratosis of the skin. To elucidate a generalized function for vitamin A, we have taken the approach of tracing the vitamin from its storage site in the liver via its blood transport by the retinol-binding protein (RBP) to its uptake by susceptible cells. We have also examined the intracellular occurrence of vitamin A as regards its binding to specific receptor proteins. Here we summarize data on the amino acid sequences of several vitamin A-binding proteins. The finding that CRBP and CRABP, the two intracellular proteins, are homologous to each other, to a myelin protein, and to a fatty acid-binding protein may shed light on the functions of these proteins. Retinoic acid, which binds to CRABP but not CRBP, induces differentiation of teratocarcinoma cells. This is accompanied by a lowering of the CRABP concentration, an increase of the CRBP level, and an increase in the uptake of retinol from RBP. The epidermis contains both CRBP and CRABP, and their distributions are rather similar. However, in contrast to CRBP, CRABP is most abundant in cells lining the hair follicles. CRBP occurs in greatest relative amounts in the outer layers of the epidermis. Since techniques have been developed to measure CRBP and CRABP, normal and disease-affected skin may now be explored as to quantity and cellular distribution of the retinoid-binding proteins.

Amino Acid Sequence↗
PubMed1983

Estimation of fetal maturity by amniotic fluid cytology, creatinine, lecithin/sphingomyelin ratio and phosphatidylglycerol.

The value of four amniotic fluid tests--the lecithin/sphingomyelin ratio, the presence of phosphatidylglycerol, amniotic fluid cytology and the creatinine concentration--in the prediction of fetal lung maturity was investigated. The sensitivity was high for all tests except for amniotic fluid cytology, which had a higher specificity. The overall outcome, particularly the value for predicting immaturity, was improved by various combinations of tests. The combination of amniotic fluid cytology and creatinine proved useful in predicting the gestational age. A diagram for estimation of gestational age is presented.

Amniotic Fluid↗
PubMed1983

Effect of a hypoglycaemic sulphonylurea (HB419) and a non-metabolizable amino acid (BCH) on the insulin release and endogenous substrate metabolism of rat pancreatic islets.

The effects of the hypoglycaemia sulphonylurea glibenclamide (HB419) and the non-metabolizable leucine analogue beta-2-aminobicyclo(2.2.1)heptane-2-carboxylic acid (BCH) on insulin release and endogenous substrate metabolism were studied in isolated rat islets. Pre-labelling of the endogenous islet substrate was performed with [14C]glucose (20 mM) or [14C]glutamine (10 mM) during a 24 h tissue culture period before measurements of insulin release or 14CO2 production in short-term incubations. Both HB419 and BCH stimulated the insulin release of the cultured islets, although BCH only after culture of islets with glutamine. The rate of labelling of the islets with [14C]glucose reached an apparent plateau after 16 h in culture and the total islet accumulation of glucose carbon over the 24 h period averaged 12.9 +/- 3.0 nmol/25 islets. Less than 0.5% of the glucose residues was converted to glycogen whereas lipids represented about 2.5%. Fractionation of lipids showed 67% phospholipids, 18% triacylglycerols, 11% diacylglycerols and 6% non-esterified fatty acid. The islet accumulation of glutamine during 24 h corresponded to 11.5 +/- 1.5 nmol/25 islets. After pre-labelling of islets with [14C]glucose there was no effect on the 14CO2-evolution over a 30 min incubation period of either HB419 or BCH. There was also no effect of HB419 after pre-labelling with [14C]glutamine, whereas, in this latter situation, a significant stimulation was observed with BCH. It is concluded that the effects on the pancreatic B-cells by antidiabetic sulphonylureas are not mediated via nutrient receptors.

Amino Acids↗
PubMed1983

Increased platelet volume in manifest diabetic rats.

Platelet function, evaluated as in vitro aggregability, has been reported to be disturbed in diabetes, both in humans and animals. Platelet number and mean volume greatly influence these aggregation tests. The present study was designed to evaluate the impact of two different degrees of experimentally induced glucose intolerance on platelet number and mean volume. For this purpose, we used manifest diabetic and chemically diabetic rats. In the control group, the female rats showed a significantly lower number of platelets compared to the males. The chemically diabetic rats exhibited a tendency towards increased mean platelet volume, whereas the platelet volume of the manifest diabetic females was significantly greater than all other groups. This increase was found to be mainly due to a general shift towards larger volumes of the individual platelets of the manifest diabetic females. It is suggested, that the enlargement of the mean platelet volume induced by increased severity of the diabetic state may reflect decreased mean age of the circulating platelets. This implies shorter survival time and an increased turnover of the platelet population in diabetes mellitus.

Animals↗
PubMed1983

Glycogen content and lipid biosynthesis in the lungs of fetuses of diabetic rats.

The fetal pulmonary glycogen content and the pulmonary biosynthesis of neutral lipids and phospholipids were estimated at gestational days 18, 20, and 22 in the offspring of normal, manifest diabetic, and insulin-treated diabetic rats. In all groups the fetal pulmonary glycogen concentration was highest on gestational day 20 and decreased during the subsequent 2 days. At the same time the biosynthesis of neutral lipids and phospholipids increased in the fetal lungs. The fetuses of the manifest diabetic rats showed an increased glycogen concentration and decreased total lipid biosynthesis compared with the other two groups. Insulin treatment of the rat mothers largely normalized the pulmonary lipid biosynthesis and glycogen accumulation in their fetuses. These data suggest that the diabetic maternal environment induces a transient block in the fetal utilization of pulmonary glycogen for the biosynthesis of lipids, in particular for the production of surfactant phospholipids.

Animals↗
PubMed1982

Diabetes in pregnancy: islet cell proliferation in the fetal rat pancreas.

Since it has not been possible to reproduce, in the rat, the hyperplasia of the islets of Langerhans observed in the fetus in human diabetic pregnancy, the rate of proliferation of the endocrine pancreas of fetuses of manifest diabetic rats has been studied. Rats were rendered diabetic by streptozotocin injections before mating. At days 20 or 22 of gestation the pregnant rats were injected with colchicine and sacrificed at 1-h intervals. The mitotic indices of the fetal endocrine pancreas were determined and plotted against the time after colchicine injection. The production of new cells (i.e. the cell birth rate) was estimated from the slopes of the regression lines. On both days 20 and 22 of gestation, the cell birth rates of the endocrine pancreas of the fetuses of manifest diabetic mothers were only one-third of the control values obtained in normal, age-matched fetal pancreas (daily cell birth rate = 10%). This finding corresponds to the previous observation of a low B cell mass in the offspring of diabetic rats. The results indicate that the growth and development of the fetal endocrine pancreas is retarded in manifest diabetic pregnancy in the rat.

Animals↗
PubMed1982

Diabetes in pregnancy: growth of the fetal pancreatic B cells in the rat.

The development of the pancreatic B cells in the offspring of normal (N), subdiabetic (SD), manifest diabetic (MD) and insulin-treated diabetic (MDI) rats was studied with the aid of immunocytochemical staining for insulin. Morphometric evaluation of the B-cell volume density and weight was made by point sampling. The offspring were studied on gestational days 20 and 22 and in the newborn state. In the N offspring the weight of the B-cell parenchyma doubled during the last 2 days of gestation. This rapid increase may be ascribed not only to high mitotic activity but also to differentiation of putative percursor cells to B cells. The mild glucose intolerance of the SD mothers had no major effects on the fetal B-cell development. In the MD group both the volume density and the weight of the B cells were considerably lower than in the N and SD groups at all ages studied. Despite prolonged gestation, the weight of the fetal B cells in the MD newborns was not greater than that in the 20-day-old fetuses of the N group. Insulin treatment of the MD mothers restored the fetal B-cell development towards normal. This study indicates that manifest maternal diabetes in the rat retards the development of the fetal B cells. This is in obvious contrast to the corresponding situation in human diabetic pregnancy, in which hyperinsulinism represents a striking feature of diabetic fetopathy. It is suggested that a milder form of maternal glucose intolerance together with the relatively longer gestational period in man, compared with the rat, may create conditions that favour fetal B-cell hyperplasia.

Animals↗
PubMed1982

Increased incidence of congenital malformations in the offspring of diabetic rats and their prevention by maternal insulin therapy.

Intensive care of the pregnant mother with diabetes has dramatically decreased the incidence of diabetic fetopathy. The persistently high rate of fetal and neonatal mortality in diabetic pregnancies is nowadays mainly due to the increased incidence of serious congenital malformations. However, attempts to elucidate the precise teratogenic mechanisms have been sparse, presumably because of a lack of relevant animal models. In the present study we recorded the incidence and types of skeletal malformations in live offspring of normal rats and in rats made diabetic with the B-cytotoxic agent streptozotocin (SZ) at least 2 wk before conception. In some of the diabetic animals insulin treatment was begun 1 wk after the SZ injection and continued throughout pregnancy. In addition, the fetal development was followed by assessing the calcification of the skeleton on gestational days 20 and 22 with the aid of Alazarin Red S staining. Manifest diabetes in the pregnant rat induced a decrease in fetal weight and viability and marked retardation of skeletal maturation. In addition, about 20% of 135 viable fetuses showed skeletal malformations comprising either micrognathia or caudal dysgenesis. These defects were not found in 314 offspring of the control rats. Only two cases of caudal dysgenesis and none of micrognathia were detected among 233 offspring of the insulin-treated rats. The present data underscore the importance of a strict differentiation in the offspring of the diabetic rat between transient development retardations and true malformations. They also demonstrate that correction of the maternal glucose intolerance is crucial for preventing the fetus from developing skeletal malformations. Altogether the data suggest that fetal malformations in the diabetic rat are attributable either to the hyperglycemia as such or to some accompanying metabolic consequence of insulin deficiency.

Animals↗