| 1. |
- Berggård, T, et al.
(author)
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Alpha1-microglobulin chromophores are located to three lysine residues semiburied in the lipocalin pocket and associated with a novel lipophilic compound
- 1999
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In: Protein Science. - : Wiley. - 0961-8368. ; 8:12, s. 20-2611
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Journal article (peer-reviewed)abstract
- Alpha1-microglobulin (alpha1m) is an electrophoretically heterogeneous plasma protein. It belongs to the lipocalin superfamily, a group of proteins with a three-dimensional (3D) structure that forms an internal hydrophobic ligand-binding pocket. Alpha1m carries a covalently linked unidentified chromophore that gives the protein a characteristic brown color and extremely heterogeneous optical properties. Twenty-one different colored tryptic peptides corresponding to residues 88-94, 118-121, and 122-134 of human alpha1m were purified. In these peptides, the side chains of Lys92, Lys118, and Lys130 carried size heterogeneous, covalently attached, unidentified chromophores with molecular masses between 122 and 282 atomic mass units (amu). In addition, a previously unknown uncolored lipophilic 282 amu compound was found strongly, but noncovalently associated with the colored peptides. Uncolored tryptic peptides containing the same Lys residues were also purified. These peptides did not carry any additional mass (i.e., chromophore) suggesting that only a fraction of the Lys92, Lys118, and Lys130 are modified. The results can explain the size, charge, and optical heterogeneity of alpha1m. A 3D model of alpha1m, based on the structure of rat epididymal retinoic acid-binding protein (ERABP), suggests that Lys92, Lys118, and Lys130 are semiburied near the entrance of the lipocalin pocket. This was supported by the fluorescence spectra of alpha1m under native and denatured conditions, which indicated that the chromophores are buried, or semiburied, in the interior of the protein. In human plasma, approximately 50% of alpha1m is complex bound to IgA. Only the free alpha1m carried colored groups, whereas alpha1m linked to IgA was uncolored.
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| 2. |
- Abrahamsson, Kate, 1959, et al.
(author)
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Pivalic acid-induced carnitine deficiency and physical exercise in humans.
- 1996
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In: Metabolism: clinical and experimental. - : Elsevier BV. - 0026-0495. ; 45:12, s. 1501-7
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Journal article (peer-reviewed)abstract
- To study the effect of carnitine depletion on physical working capacity, healthy subjects were administered pivaloyl-conjugated antibiotics for 54 days. The mean carnitine concentration in serum decreased from 35.0 to 3.5 mmicromol/L, and in muscle from 10 to 4.3 micromol/g noncollagen protein (NCP). Exercise tests were performed before and after 54 days' administration of the drug. At submaximal exercise, there was a slight increase in the concentration of 3-hydroxybutyrate in serum, presumably caused by decreased fatty acid oxidation in the liver. There was also a decreased consumption of muscle glycogen, indicating decreased glycolysis in the skeletal muscle. The muscle presumably had enough energy available, since there was no significant decrease in the concentration of adenosine triphosphate (ATP) and creatine phosphate during exercise. The work at maximal oxygen uptake (VO2max) and the maximal heart rate were reduced. Since VO2max is considered dependent on heart function, carnitine depletion seemed to affect cardiac function.
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| 3. |
- Abrahamsson, Kate, 1959, et al.
(author)
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Transient reduction of human left ventricular mass in carnitine depletion induced by antibiotics containing pivalic acid.
- 1995
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In: British heart journal. - : BMJ. - 0007-0769. ; 74:6, s. 656-9
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Journal article (peer-reviewed)abstract
- To study the effect of induced carnitine depletion on myocardial structure and function.7 healthy adult volunteers given 1200 mg pivmecillinam per day for 7-8 weeks were studied by echocardiography before and after 7-8 weeks of treatment and a 15 months follow up after the treatment period.Teaching hospital.Carnitine concentration in serum, urine, and muscle and echocardiographic measurements.After 7-8 weeks of treatment the median free serum carnitine concentration was reduced to 7% and the median total muscle carnitine concentration to 46% of the pretreatment levels. The median diastolic interventricular septum thickness decreased by 14% (mean 26%, P = 0.028) and the median left ventricular mass by 10% (mean 20%, P = 0.018). Fifteen months later these dimensions had increased but not completely returned to pretreatment values.Extended treatment with pivalic acid containing antibiotics causes carnitine depletion which may lead to changes in cardiac structure.
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| 4. |
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| 5. |
- Brinck, J, et al.
(author)
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Influence of long-chain alcohols on the adsorption of nonionic surfactants to silica
- 1999
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In: Langmuir. - 0743-7463 .- 1520-5827. ; 15, s. 7719-7724
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Journal article (peer-reviewed)abstract
- The adsorption of surfactant-alcohol mixtures at the silica-water interface was studied by means of ellipsometry. The results show that addition of even small amounts of alcohol can have large effects on the characteristics of the adsorbed layer. For example, a 20% replacement of the octa(ethylene glycol) dodecyl (C12E8) surfactants by dodecanol results in an increase in the total surface excess of 80%. The thickness of the adsorbed layer, on the other hand, is virtually unaffected by the alcohol being added. Hence, as the alcohol content increases, the adsorbed surfactant aggregates at the silica-water interface mainly grow in the surface plane. A surfactant such as C12E5, which forms relatively large surface aggregates from the start, can only solubilize a small fraction of the long-chain alcohols before the system phase separates. This fraction was found not to result in any major structural changes in the surface layer. These findings are discussed in terms of surfactant packing and in relation to observations in bulk solutions reported earlier. Our study also includes measurements of adsorption and desorption kinetics for both the surfactant and the surfactant-alcohol systems. The main finding is that the effect of alcohol is most obvious in the desorption kinetics. We conclude that the effects observed are due to differences between the surfactant and the alcohol in monomer solubility.
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| 6. |
- Brinck, J, et al.
(author)
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Kinetics of nonionic surfactant adsorption and desorption at the silica-water interface: Binary systems
- 1998
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In: Langmuir. - 0743-7463 .- 1520-5827. ; 14, s. 5863-5876
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Journal article (peer-reviewed)abstract
- This paper is the second of two dealing with the adsorption and desorption kinetics of nonionic surfactants at a solid-liquid interface. The first paper described a model of the kinetics of single nonionic surfactant adsorption.1 This work is now being completed by extending the theoretical model to cover binary surfactant systems. The evolution of the total surface excess during the adsorption and desorption has been modeled and compared with experimental results obtained by in situ null ellipsometry. In this comparison, the surface behavior of the two nonionic surfactant pairs C14E6-C10E6 and C12E5-C12E8 at a planar silica-water interface was studied. These binary systems represent two different types of polydispersity: different lengths of the hydrocarbon chains and unequal numbers of ethylene oxide groups in the hydrophilic headgroups. The critical micelle concentrations (cmcs) of the surfactants in the former pair therefore differ a great deal, whereas those of the surfactants in the latter pair are similar. A comparison between experiments and simulations showed good agreement. In an attempt to further analyze the experimental results, individual amounts adsorbed and concentration profiles were calculated. The results of these simulations showed that each surfactant in a given pair has a characteristic adsorption and desorption path. According to the model, this path is determined mainly by the mutual relationship between their cmcs.
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| 7. |
- Brinck, J, et al.
(author)
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Kinetics of nonionic surfactant adsorption and desorption at the silica-water interface: One component
- 1998
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In: Langmuir. - 0743-7463 .- 1520-5827. ; 14, s. 1058-1071
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Journal article (peer-reviewed)abstract
- In this paper we present a theoretical model which describes the kinetics of adsorption and desorption from a micellar solution of nonionic surfactants at a silica surface. Numerical calculations based on this model have been compared with experimental results of CnEm surfactant adsorption, obtained by ellipsometry, and show good agreement. The aim of this work was to develop a model for adsorption through a stagnant layer onto a solid, hydrophilic surface. The surface is considered to be planar and homogeneous. Outside the surface there is a micellar solution of a pure nonionic surfactant. Both monomers and micelles are considered to be able to adsorb. To facilitate the evaluation of the model, a computer program was written which solves the mathematical equations numerically. The course of adsorption and desorption of a number of short-chain CnEm surfactants has been simulated with this program. The results obtained, in terms of amounts adsorbed as a function of time, were compared with experimental data determined by time-resolved null ellipsometry. The same program was used to calculate concentration profiles outside the silica surface. Not only has this model made it possible for us to explain and better understand experimental results, but it has also allowed us to gain an understanding of how the course of adsorption and desorption is affected by parameters which are difficult to vary experimentally in a controlled way. Two examples of this, which will be discussed in this paper, are the effects of stagnant layer thickness and the relation between critical surface aggregation concentration (csac) and critical micelle concentration (cmc).
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| 8. |
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| 9. |
- Jönsson, Anders, 1959, et al.
(author)
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Local anesthetics improve dermal perfusion after burn injury.
- 1998
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In: The Journal of burn care & rehabilitation. - 0273-8481. ; 19:1 Pt 1, s. 50-6
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Journal article (peer-reviewed)abstract
- Deep partial-thickness burn injury was induced in the abdominal skin of anesthetized rats. Dermal perfusion was assessed by laser Doppler flowmetry. In the first set of experiments, one group of rats (n = 15) was topically treated with a lidocaine-prilocaine cream 5% (25 mg of each in 1 g) for 6 hours, starting 5 minutes after inducing the burn injury. In one control group (n = 14), the thermal injury was treated with placebo cream. Results showed a markedly reduced perfusion in the skin of the control animals within the first hour after burn injury, with further decrease during the following 5 hours of observation. In animals treated with the lidocaine-prilocaine cream, skin perfusion in the burned area was significantly increased during the first 30 minutes after the burn injury compared to before the burn (p < 0.01), followed by a decrease to a level below the preburn stage but significantly higher than that of control animals during the first hour after burn injury (p < 0.05). As opposed to burned control animals, skin perfusion gradually recovered toward preburn levels at the end of the experiment in local anesthetic-treated animals. In the second experimental set, four groups of animals were burned and subsequently treated with a bolus dose of lidocaine intravenously (2 mg/kg), followed by continuous intravenous lidocaine infusions at a rate of 50 (n = 10), 100 (n = 11), or 150 (n = 10) micrograms.kg-1.min-1. The infusions were started 5 minutes after the burn injury and lasted for 6 hours. Corresponding volumes of saline solution were given to burned control animals (n = 10). Results showed a significantly improved skin perfusion in the lidocaine-treated group in a dose-response fashion as compared to control animals. A maximum improvement of dermal perfusion in the burned area was induced by intravenous lidocaine at an infusion rate of 150 micrograms.kg-1.min-1 as compared to burned controls treated with isotonic saline solution infusions (p < 0.01). Results showed that topical or systemic administration of local anesthetics can prevent progressive dermal ischemia after thermal injury.
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| 10. |
- Jönsson, B, et al.
(author)
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Cost-effectiveness of Fracture Prevention in Established Osteoporosis
- 1996
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In: Scandinavian Journal of Rheumatology. Supplement. - : Taylor & Francis. - 0301-3847 .- 1502-7740 .- 0300-9742 .- 1502-7732. ; 25:Suppl. 103, s. 30-38
-
Journal article (peer-reviewed)abstract
- This study presents the results of a computer simulation model for calculating the cost-effectiveness and cost-utility of treating patients with established osteoporosis in order to reduce the risk of fractures. The results are based on Swedish data for risk of fracture and costs. The treatment intervention modelled is based on treatment of a 62-year-old woman with established osteoporosis. The cost per hip fracture avoided is 350,000 SEK, assuming a 50% reduction in the risk of fracture due to 5 years of treatment. A sensitivity analysis for changes in the cost and effectiveness of treatment, the risk of fracture and the discount rate is performed. The cost per life-year gained and the cost per quality-adjusted life-year (QALY) gained is presented to enable comparison of the cost-effectiveness of treating osteoporosis with that of other health care interventions. A comparison between treating the same woman for osteoporosis and mild hypertension shows a cost per life-year gained of 220,000 SEK and 128,000 SEK respectively. Cost per QALY gained is very similar for the two interventions: 105,000 SEK and 103,000 SEK respectively. This model provides a tool to enable clinicians, administrators and health policy makers to analyze and understand the economic aspects of a major health policy issue.
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