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Biomedical subjects

A Danielsson

Publications and source records attributed to A Danielsson.

At least 145 records · Page 8Linked to original sources
PubMed1984

Weight reduction after gastroplasty: the predictive value of surgical, metabolic, and psychological variables.

Twenty-one grossly obese patients (mean body weight 126 kg, range 93-190 kg) were treated with gastroplasty ad modum Gomez. Eighteen months after surgery the average weight loss was 30.4 kg (range 1-71 kg); about 80 per cent of this weight loss represented loss of body fat. Mean weight loss of the entire programme, including preoperative weight reduction was 34.4 kg (range 1-71 kg). Dilation of the pouch and/or channel occurred in 14 patients and was generally discovered 6-12 months after operation. The wide range in weight reduction could not be unequivocally attributed to technical-surgical factors. Although the patients with the least weight reduction had all developed channel dilation, several patients with excellent weight loss also showed dilation of the pouch and/or channel. An extensive psychological investigation performed before surgery demonstrated more signs of sensitivity and denial in the unsuccessful patients; the successful ones were more dependent and tended to live in a supportive social environment. The unsuccessful patients were younger and their estimated alcohol consumption was higher. A number of morphological and biochemical variables including body weight, fat cell size, and variables reflecting thyroid function, lipid and glucose metabolism, and adipose tissue metabolism were not related to subsequent weight loss.

Adaptation, Psychological↗
PubMed1983

Properties of antithrombin-thrombin complex formed in the presence and in the absence of heparin.

Purification of antithrombin-thrombin complex by ion-exchange chromatography on DEAE-agarose resulted in predominantly monomeric complex, whereas purification on matrix-linked heparin produced large amounts of aggregated complex. Monomeric antithrombin-thrombin complexes formed in the presence and in the absence of heparin had similar conformations and heparin affinities. Moreover, the first-order dissociation rate constants, measured by thrombin release, of these complexes were similar, 2.3 X 10(-6)-3.4 X 10(-6)S-1, regardless of whether newly formed or purified complex was analysed. Similar dissociation rate constants were also obtained for purified complex formed with or without heparin, from analyses by dodecyl sulphate/polyacrylamide-gel electrophoresis of the release of modified antithrombin, cleaved at the reactive-site bond. No dissociation of intact antithrombin from the complex was detected by activity measurements or by gel electrophoresis. Aggregation of the complex was found to be accompanied by a decrease in apparent dissociation rate. The similar properties of antithrombin-thrombin complexes formed with or without heparin support the concept of a catalytic role for the polysaccharide in the antithrombin-thrombin reaction. Furthermore, the results indicate that the reaction between enzyme and inhibitor involves the rapid formation of an irreversible, kinetically stable, complex that dissociates into active thrombin and modified, inactive, antithrombin by a first-order process with a half-life of about 3 days. The inhibition thus resembles a normal proteolytic reaction, one intermediate step of which is very slow.

Animals↗
PubMed1983

Effects of selective alpha 1 and alpha 2 adrenoceptor active drugs on 86Rb+ efflux from pieces of rat parotid gland.

Minute pieces of rat parotid gland were used in studies of adrenergic regulation of K+ efflux using 86Rb+ as a probe for K+. Noradrenaline induced a concentration-dependent RB+ efflux, whereas the beta 1-selective agonist prenalterol was without effect. On the other hand, the beta 2-selective drug, terbutaline, at high concentrations displayed a small enhancement of Rb+-secretion. The selective alpha 1-adrenoceptor drug, phenylephrine, was as potent as noradrenaline, whereas the alpha 2-agonist clonidine had only a small effect. The noradrenaline-induced Rb+-efflux was effectively inhibited in the presence of prazosin, an alpha 1-blocker, whereas the alpha 2-antagonist, yohimbine, was roughly 50 times less potent. The results suggest that catecholamine-induced K+-secretion from the rat parotid gland is mediated via activation of post-synaptic alpha-adrenoceptors of the alpha 1-subtype.

Adrenergic alpha-Agonists↗
PubMed1983

Ultrastructural changes in rat parotid acinar cells after selective beta 1-adrenoceptor agonist treatment.

Administration of the selective beta 1-adrenoceptor agonist, prenalterol, affects the acinar cell of the rat parotid in a manner similar to that observed after isoprenaline (IPR) treatment. Sixty minutes after injection of prenalterol, many cells are depleted of their zymogen granules and there is evidence of secretory protein resynthesis. Long term treatment leads to cellular hypertrophy and marked structural changes in the granule population. The cellular alterations are, however, not as pronounced as those observed after IPR injections. This may be due to the combined beta 1- and beta 2-adrenoceptor effect of IPR. With prenalterol, cell damage is obvious in acute experiments. In long term treated animals numerous characteristic autophagic vacuoles are observed, reflecting a reorganization of cytoplasmic components in superstimulated glands. Although prenalterol and IPR give rise to rather similar structural changes in parotid glands, marked differences between effects of the two drugs on gland biochemistry have been noted. It seems evident that different biochemical pathways involved in secretory activity have actions in common with respect to effects on submicroscopical structures.

Adrenergic beta-Agonists↗
PubMed1982

Mechanism of inactivation of trypsin by antithrombin.

General aspects of the mechanism of antithrombin action were elucidated by a comparison of the inactivation of trypsin by antithrombin with the inactivation of coagulation proteinases by the inhibitor. Bovine antithrombin and bovine trypsin were shown to form an inactive equimolar complex. A non-complexed, proteolytically modified form of antithrombin, electrophoretically identical with that formed in the reaction with coagulation proteinases, was also produced in the reaction with trypsin. In the absence of heparin, the inactivation of trypsin by antithrombin was 20 times faster than the inactivation of thrombin; the second-order rate constant was 1.5 x 10(5)m(-1).s(-1) at 25 degrees C and pH 7.4. However, the inhibition of thrombin was accelerated about 30 times more efficiently by small amounts of heparin than was trypsin inhibition. Dissociation of the antithrombin-trypsin complex at pH 7.4 followed first-order kinetics with a half-life for the complex of about 80h at 25 degrees C. The complex was rapidly and quantitatively dissociated at pH 11, resulting in the liberation of a modified two-chain form of the inhibitor, cleaved at the same Arg-Ser bond as in modified antithrombin released from complexes with thrombin, Factor Xa and Factor IXa. This supports the previous proposal that this bond is the active-site bond of antithrombin. Antisera specific for thrombin-modified antithrombin reacted with purified antithrombin-trypsin complex, indicating that the inhibitor was present in the complex in a form immunologically identical with thrombin-modified antithrombin. The results thus suggest a common mechanism, but different kinetics, for the inhibition of trypsin and coagulation proteinases by antithrombin.

Amino Acid Sequence↗
PubMed1982

Effects of neonatal sympathetic denervation on amylase secretion in the adult rat parotid gland: difference in beta 1- and beta 2-adrenoceptor response.

Changes in amylase secretion and cyclic AMP accumulation in response to various secretagogues were studied in parotid glands of adult rats subjected to neonatal sympathetic denervation by unilateral excision of the superior cervical ganglion. Denervation decreased the gland content of amylase and both basal and the stimulated levels of cyclic AMP were elevated. The secretory cells of neonatally denervated glands exhibited enhanced maximal enzyme discharge in response to beta-adrenoceptor agonists. However, the selective beta 1-agonist, prenalterol was not effective in this respect whereas an enhanced maximal secretory response to the beta 2-selective agonist, terbutaline, was particularly prominent. DBcAMP was also more efficient in inducing amylase release from the denervated gland. The result of the present study demonstrate that the usual dominance of the beta 1-adrenoceptor subtype in eliciting amylase release is lost, implying that the differentiation of the beta-adrenoceptor into its subtypes is altered by neonatal sympathetic denervation.

Amylases↗
PubMed1982

Dissociation of beta-adrenoceptor-induced effects on amylase secretion and cyclic adenosine 3', 5' monophosphate accumulation.

By using a multi-channel microperifusion system the effects of noradrenaline, the beta1-adrenoceptor agonist prenalterol, and the beta2-selective agonist terbutaline were studied on amylase pig submandibular glands. 2 Noradrenaline caused significant amylase discharge and cyclic AMP accumulation. 3 Prenalterol was as effective as noradrenaline in causing amylase release but did not significantly affect the cyclic AMP content. 4 Terbutaline stimulated cyclic AMP accumulation, but had little effect on amylase secretion. 5 The present study reveals that there is a dissociation of the beta-adrenoceptor-induced amylase release and cyclic AMP formation, and that this dissociation may be due to different beta-adrenoceptor subtypes.

Amylases↗
PubMed1982

Intestinal absorption and 25-hydroxylation of vitamin D in patients with primary biliary cirrhosis.

The absorption, metabolism, and excretion of vitamin D3 was studied in eight women with an established diagnosis of primary biliary cirrhosis (PBC), and the results were compared with those obtained from eight healthy women of a similar age. Four patients had hyperbilirubinemia, low serum calcium levels, and a reduced mineral content of the bone, whereas the other four were presymptomatic with respect to bone disease. Vitamin D absorption was studied after oral administration of tritiated vitamin D, and the appearance of serum radioactivity was recorded. After this, the liver 25-hydroxylation of vitamin D was studied by administering an intravenous dose of tritiated vitamin D and then chromatographing serum samples to determine the radioactivity of the 25-OH D fraction. All PBC patients had normal 25-hydroxylation capacity of the vitamin, and there was no difference in the urinary excretion of radioactivity. On the other hand, the intestinal absorption of vitamin D was severely impaired both in the symptomatic and asymptomatic patients. The absorption of the vitamin was negatively correlated to the amount of fecal fat, and the results suggest that low serum levels of 25-OH D in symptomatic PBC seem to be caused by the steatorrhea, whereas hepatic conversion of vitamin D into 25-OH D seems to be well preserved even in patients with hyperbilirubinemia and signs of osteomalacia. The absorption-metabolism test may be a valuable tool in the study of patients with cholestatic liver disease for determining the nature of the vitamin D deficiency and the logical form of substitution therapy.

Adult↗
PubMed1982

Normal hepatic vitamin-D metabolism in icteric primary biliary cirrhosis associated with pronounced vitamin-D deficiency symptoms.

The intestinal absorption and hepatic metabolism of vitamin D were studied in a woman with icteric primary biliary cirrhosis (PBC) complicated by pronounced bone pain and muscle weakness due to vitamin-D deficiency. The patient had a markedly reduced intestinal absorption of vitamin D, while the 25-hydroxylation of this vitamin was found to be normal despite the presence of longstanding icterus. The malabsorption of fat-soluble compounds secondary to the cholestasis was probably further impaired by several years of cholestyramine treatment. Administration of 1.25-(OH)2D3 increased intestinal calcium absorption, normalized serum calcium and increased bone mineral content of the proximal tibia. Furthermore, drastic improvement of muscle weakness and relief of bone pain were observed. It is recommended that repeated measurements of serum 25-(OH)D should be carried out in patients with PBC, and especially in those treated with cholestyramine. In certain vitamin D deficient patients, studies using radio-labelled vitamin D may provide clinically valuable information as to the exact site of the underlying disturbances.

Cholestyramine Resin↗
PubMed1981

Binding to antithrombin of heparin fractions with different molecular weights.

The interaction between bovine antithrombin, a plasma proteinase inhibitor, and heparin species of different molecular weights was studied. A commercial heparin preparation was divided by gel chromatography into a number of fractions with average molecular weights ranging from 6000 to 34700. Each of these fractions was further fractionated by affinity chromatography on matrix-bound antithrombin. In the latter procedure, those heparin fractions that had molecular weights lower than about 14000 were separated into three peaks. The material in the first of these was not adsorbed on the column, and the other two peaks corresponded to the low-affinity and high-affinity peaks described previously. In contrast, high-molecular-weight heparin samples gave only the low-affinity and high-affinity fractions. U.v. difference absorption studies showed that the non-adsorbed heparin fraction bound to antithrombin in solution with a binding constant at physiological ionic strength only slightly lower than that of low-affinity heparin. The division between the two fractions thus is arbitrary and only dependent on the conditions selected for the affinity-chromatography experiment. Stoicheiometries and binding constants for the binding of several high-affinity heparin species to antithrombin were determined by fluorescence titrations. High-affinity heparin fractions of equal elution positions in the beginning of the peaks of the affinity chromatographies, but with different molecular weights, showed stoicheiometries that were not experimentally distinguishable from 1:1 and also had no appreciable differences in binding constants. However, the anticoagulant activities, calculated on a molar basis, of these fractions increased markedly with molecular weight, a behaviour that thus cannot be explained by differences in the binding of the fractions to antithrombin. In contrast, high-affinity samples of similar molecular weights, which were eluted at increasing ionic strengths from matrix-linked antithrombin, were found to have an increasing proportion of chains with two binding sites for antithrombin and also to have progressively higher binding constants. These binding properties at least partly explain the increasing anticoagulant activities that were observed for these fractions.

Antithrombins↗
PubMed1981

Trophic effect of the sympathetic nervous system on the early development of the rat parotid gland: a quantitative ultrastructural study.

Rats were sympathetically denervated on one side by avulsion of the superior cervical ganglion either immediately after birth (within 4 hr) or when the salivary glands were fully developed. Nine weeks after ganglionectomy the parotid glands were subjects to microscopical studies. As shown by the lack of specific fluorescence, sympathetic denervation caused an almost total depletion of catecholamines in the acini. This was further substantiated at the electron microscopic level using KMnO4 as fixative. No alterations in either gland weight or in acinar cell size were noticeable after adult sympathectomy. On the other hand, neonatal denervation caused a decrease in gland weight as well as ascinar cell hypotrophy. The mean volume of individual acinar cells was reduced by roughly 25% and the granule volume density by about 50%. Also the mean volume of individual granules was decreased. These findings indicate an important role for the sympathetic nerve system in the maturation of the rat parotid gland.

Age Factors↗