| 1. |
- Andersson, Lena, et al.
(författare)
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Hydrolysis of galactolipids by human pancreatic lipolytic enzymes and duodenal contents
- 1995
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Ingår i: Journal of Lipid Research. - 1539-7262. ; 36:6, s. 1392-1400
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Tidskriftsartikel (refereegranskat)abstract
- Monogalactosyldiacylglycerols (MGDG), digalactosyldiacylglycerols (DGDG) and sulfoquinovosyldiacylglycerols (SQDG) are major lipids in vegetable food. Their digestion and absorption are unknown. This study examines the hydrolysis of galactolipids in vitro with human duodenal contents, pancreatic juice, and purified human pancreatic lipases. Galactolipids were incubated with human duodenal contents, pancreatic juice, pure pancreatic carboxyl ester lipase (CEL), and colipase-dependent lipase with colipase (Lip-Col). Hydrolysis was estimated as release of free fatty acids and by the use of [3H]galactose or [3H]fatty acid-labeled DGDG. Pancreatic juice and duodenal contents hydrolyzed DGDG to fatty acids, digalactosylmonoacylglycerol (DGMG) and water-soluble galactose-containing compounds. The hydrolysis of DGDG was bile salt-dependent and had a pH optimum at 6.5-7.5. Human pancreatic juice released fatty acids from MGDG, DGDG, and SQDG. Purified CEL hydrolyzed all three substrates; the hydrolysis rate was MGDG > SQDG > DGDG. Pure Lip-Col had activity toward MGDG but had little activity against DGDG. Separation of pancreatic juice by Sephadex G100 gel filtration chromatography revealed two peaks with galactolipase activity that coincided with CEL (molecular mass 100 kD) and lipase (molecular mass 50 kD) peaks. In contrast to pure Lip-Col enzymes of the latter peak were as active against DGDG as against MGDG. Thus, DGDG is hydrolyzed both by CEL and by a pancreatic enzyme(s) with a molecular mass of 40-50 kD to fatty acids and lyso DGDG. MGDG, DGDG, and SQDG are all hydrolyzed by human pancreatic juice. Pure CEL hydrolyzed all three substrates.
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| 2. |
- Bengtsson, Hanna, et al.
(författare)
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Destination Baltikum
- 1996
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Rapport (övrigt vetenskapligt/konstnärligt)
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| 3. |
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| 4. |
- Nilsson, Charlotte
(författare)
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A unilateral versus a multilateral carbon dioxide tax : a numerical analysis with the European model GEM-E3
- 1999
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- This paper analyzes and compares the effects of a common reduction of C02 emissions within the European Union to a Swedish unilateral decision to reduce CO2 emissions. For this purpose, a numerical general equilibrium model, GEM-E3, has been used as the analytical tool. The model covers all European Union countries, with production disaggregated into 18 sectors. The 13 consumption goods included are classified into three consumption categories (durable, non-linked non-durable and linked durable goods) to improve the energy allocation description. In addition, the industry exemption of C02 tax is studied. The results indicate that if Sweden unilaterally decides to increase its carbon dioxide tax, the total European Union carbon dioxide emissions will increase, i.e. there will be a "carbon leakage effect". Perhaps more surprising, a European Union multilateral implementation of a carbon dioxide tax rate will induce lower welfare (excluding environmental benefits) in Sweden, as compared to the situation where the same carbon dioxide tax is unilaterally introduced.
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| 5. |
- Nilsson, Charlotte
(författare)
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Studies on the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on vitamin A homeostasis
- 1999
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Vitamin A (retinoids) is needed for normal vision, growth, reproduction, cell differentiation, embryonic development, and immune function. Retinoids exert their functions in the same way as classical hormones, as transcription factors acting via nuclear receptors. In addition, retinoids have been shown to have a key role in several other endocrine systems. It is therefore not surprising that tissue homeostasis of retinoids is well regulated. Dioxins are widespread, highly toxic, environmental pollutants. Their resistance to chemical and biological degradation, together with their lipophilicity, cause dioxins to be accumulated in the food chain. Humans are exposed to these substances mainly via food such as fatty fish, meat, and milk products. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the most potent dioxin congener and also the most studied. The fact that dioxins disturb retinoid homeostasis has been known for quite some time. The aim of this thesis was to clarify the mechanisms behind the effects of TCDD on vitamin A homeostasis in rats, and to establish which effect of TCDD on vitamin A homeostasis is the critical one, resulting in the altered tissue levels of vitamin A and possibly also other effects. The results indicate that TCDD has minor effects on the intestinal absorption and processing of orally administered retinol, and on the hepatic uptake and processing of dietary vitamin A. The lower levels of hepatic retinyl esters in TCDD-treated rats may be due to a combination of increased mobilization of hepatic stores of vitamin A, and a severely decreased LRAT activity in the hepatic stellate cells. The increased mobilization is predicted to be an early as well as a major effect of TCDD, and it occurs even though TCDD does not increase the activity of three investigated hepatic retinyl ester hydrolases. TCDD causes increased protein levels of RBP in the liver, possibly by another mechanism than impaired release of RBP into circulation. The increased renal LRAT activity in TCDD-treated rats may be the cause of the observed increased renal levels of retinyl esters. It is possible that TCDD increases LRAT activity via a retinoic acid receptor-dependent mechanism. The increased retinoic acid levels in serum in TCDD-treated rats indicate the ability of TCDD to affect the homeostasis of this important signaling retinoid. An interference of TCDD with the retinoic acid signaling pathway may have many implications for basic cellular processes, resulting from changed expression of retinoid-responsive genes. Such an effect would be compatible with the hypothesis that at least some of the toxicity of TCDD is due to a perturbation of vitamin A metabolism.
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| 6. |
- Stenman, U H, et al.
(författare)
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Summary report of the TD-3 workshop: characterization of 83 antibodies against prostate-specific antigen
- 1999
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Ingår i: Tumor Biology. - : Springer Science and Business Media LLC. - 1423-0380 .- 1010-4283. ; 20:Suppl. 1, s. 1-12
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Tidskriftsartikel (refereegranskat)abstract
- Twelve research groups participated in the ISOBM TD-3 Workshop in which the reactivity and specificity of 83 antibodies against prostate-specific antigen (PSA) were investigated. Using a variety of techniques including cross-inhibition assays, Western blotting, BIAcore, immunoradiometric assays and immunohistochemistry, the antibodies were categorized into six major groups which formed the basis for mapping onto two- and three-dimensional (2-D and 3-D) models of PSA. The overall findings of the TD-3 Workshop are summarized in this report. In agreement with all participating groups, three main antigenic domains were identified: free PSA-specific epitopes located in or close to amino acids 86-91; discontinuous epitopes specific for PSA without human kallikrein (hK2) cross-reactivity located at or close to amino acids 158-163; and continuous or linear epitopes shared between PSA and hK2 located close to amino acids 3-11. In addition, several minor and partly overlapping domains were also identified. Clearly, the characterization of antibodies from this workshop and the location of their epitopes on the 3-D model of PSA illustrate the importance of selecting appropriate antibody pairs for use in immunoassays. It is hoped that these findings and the epitope nomenclature described in this TD-3 Workshop are used as a standard for future evaluation of anti-PSA antibodies.
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| 7. |
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