| 41. |
- Nyberg, Lena
(författare)
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Digestion and Absorption of Sphingomyelin from Milk.
- 1998
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Sphingomyelin (SM) is a major component of mammalian cell membranes. Due to its widespread occurrence it is a dietary component, occurring mainly in milk, eggs, meat and fish. In the cell membrane SM was earlier considered to be only a structural element, which interacts with cholesterol and forms a system for bilayer stabilization. In the last decade there has been an increasing interest in sphingolipid metabolism, since hydrolysis products originating from both endogenous and dietary sphingolipids may have important signalling effects and thereby influence cellular functions, such as cell growth, cell differentiation and apoptosis. After some early studies in Lund in the sixties, rather few studies have concerned the digestion and absorption of dietary SM. In this thesis SM isolated from bovine milk was characterized chemically and physically, and used in studies on its intestinal digestion and absorption. SM digestion is extended all over the small intestine and occurs mainly in the middle and lower parts. This coincides with the intestinal distribution of an alkaline sphingomyelinase (SMase), which may be important for digestion. The capacity of SM digestion is limited. Also after administration of small amounts, all of the small intestine and colon are exposed to SM and its metabolites. When rats were fed a mixture of SM and cholesterol, the uptake of both components in the rat intestine was reduced. A novel alkaline SMase has been identified in human bile, with several properties similar to those of the intestinal SMase. In human milk, enzyme activities for the first two steps in the degradation of SM were identified; an acid SMase and an alkaline ceramidase activity. The latter activity was assigned to the bile salt stimulated lipase (BSSL).
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| 42. |
- Rydberg, Lennart, 1944, et al.
(författare)
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An ELISA technique for quantitation of human xenoantibodies binding to pig cells: application in patients with pig kidneys extracorporeally connected to the circulation.
- 1998
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Ingår i: Xenotransplantation. - 0908-665X. ; 5:2, s. 105-10
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Tidskriftsartikel (refereegranskat)abstract
- A quantitative ELISA technique for determination of human anti-pig xenoantibody number in serum samples has been established using pig lymphocytes and pig/rabbit erythrocytes as target cells and a pool of serum from human blood group AB donors. The number of low affinity antibodies binding to the cells was determined by quantitation following the use of aqueous washing of the cells and separation of bound and unbound antibodies with the phthalate oil method. The efficiency of different soluble Gal(alpha)1-3Gal-terminating di- and tri-saccharides to inhibit antibody binding was tested and found to vary between 70-90% at a saccharide concentration of 10 mg/ml. The assay was used to evaluate the antibody changes in two patients who, after plasmapheresis treatments, had pig kidneys extracorporeally connected to their blood circulation. The number of anti-pig IgM/IgG antibodies bound to each pig lymphocyte were reduced from 5,600/13,200 to 1,300/3,100 in patient 1 and from 1,200/6,500 to 500/2,100 in patient 2 by three consecutive daily plasmapheresis treatments. Although the lymphocytotoxic titers were reduced to very low levels, the antibody numbers still present in the blood of patient 1 caused a hyperacute rejection of the pig kidney. However, the antibody levels in patient 2 did not cause rejection of this kidney during 15 min perfusion time. A strong anti-pig antibody response 3 weeks after the perfusion experiment was found in patient 1 as shown by 27,600/245,300 IgM/IgG molecules bound to pig lymphocytes corresponding to an increase of lymphocytotoxic titer from 8 to 512. The second patient showed a much weaker immune response with 1,400/19,800 IgM/IgG antibodies corresponding to a lymphocytotoxic titer increase from 8 to 32. The use of this quantitation technique enables more accurate investigation of antibody binding to xenogenic target cells than conventional titration techniques.
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| 43. |
- Smedman, A E, et al.
(författare)
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Pentadecanoic acid in serum as a marker for intake of milk fat : relations between intake of milk fat and metabolic risk factors.
- 1999
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 69:1, s. 22-9
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The fatty acid composition of the diet is known to be partially reflected by the fatty acid composition of serum lipids.OBJECTIVE: We examined whether pentadecanoic acid (15:0) in serum lipids can be used as a marker for intake of milk fat, the major dietary source of 15:0. We also investigated the relations between intake of milk fat and cardiovascular disease risk factors.DESIGN: Sixty-two 70-y-old men completed 7-d dietary records. The intake of milk products was studied in relation to the proportions of 15:0 in serum cholesterol esters and phospholipids, as well as to the clinical characteristics of these men, by using Spearman's rank correlation.RESULTS: The proportions of 15:0 in serum cholesterol esters were positively related to butter intake (r = 0.36. P = 0.004) and to the total amount of fat from milk products (r = 0.46, P < 0.0001): 15:0 in phospholipids was related to the amount of fat from milk and cream (r = 0.34, P = 0.008) and to the total amount of fat from milk products (r = 0.34, P = 0.008). Inverse associations were found between intake of milk products and body mass index, waist circumference, LDL-HDL ratio, HDL triacylglycerols, and fasting plasma glucose, whereas relations to HDL cholesterol and apolipoprotein A-I tended to be positive.CONCLUSIONS: The results suggest that 15:0 in serum can be used as a marker for intake of milk fat. The explanation for the inverse associations between the intake of milk products and certain cardiovascular risk factors is not known.
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| 44. |
- Verbaan, Hans
(författare)
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Chronic hepatitis C infection. With special reference to prevalence, aggravating factors and longterm outcome
- 1997
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Since the discovery of hepatitis C virus (HCV) in 1989, it has proved to be a formidable health problem with a major impact on morbidity and mortality throughout the world. In this investigation, patients with chronic hepatitis C infection have been studied with special reference to prevalence, aggravating factors and longterm outcome. The prevalence of HCV infection was high (approximately 10 %) among patients assessed because of chronic liver disease. Although most patients were asymptomatic at entry, the majority of liver biopsied patients with HCV infection manifested histological changes such as CPH, CAH and cirrhosis. A parenteral route of HCV transmission was established in the majority of antiHCV positive patients, and the frequency of community acquired chronic hepatitis C was low. Non-invasive assessment to predict histological grade and stage appears to be of limited value. Individual test results were characterized by considerable overlap between the histological groups, and PIIIP, CLIV and IgG seem to be nonspecific correlates of histological activity. The rate of development of severe liver disease among HCV positive patients appears to be dependent both on endogenous and exogenous factors. Alcohol abuse and ACT deficiency were both independent risk factors for the development of cirrhosis. A high proportion of HCV infected individuals are at serious longterm risk of severe or fatal illness. During a median followup time of 10 years, more than 60 % of the deceased HCV positive patients developed cirrhosis, and approximately 30 % had concomitant HCC.
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| 45. |
- Zhou, Li
(författare)
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Sources of Arachidonic Acid in Platelets, Bone, Marrow and Gastrointestinal Tract
- 1999
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- This study investigates pathways by which the eicosanoid precursor pools in the platelets, bone marrow and the gastrointestinal (GI) mucosa are acquired and regulated, and in this context some aspects on the interaction between triglyceride (TG)-rich lipoproteins and platelets. 1. Platelets take up chylomicrons (CM) in vitro, the main part being sequestered in open canalicular system and not degraded, but do not exhibit any receptor mediated uptake and degradation of chylomicron remnants (CMR). Although CM, CMR and Intralipid affect agonist-induced platelet aggregation in vitro, CMs and CMRs are not an arachidonic acid (AA) source for platelets. The binding of prothrombin and protein S to postprandial TG-rich lipoproteins increased more after a meal rich in saturated fat than after a linoleate (LA) rich meal, which might increase platelet induced activation of these factors. 2. In rats plasma 2-arachidonyl-lysophosphatidylcholine (2-AA-LPC) supplies AA to several extrahepatic tissues, the quantitative importance being large in case of the small intestine. In guinea pigs, local desaturation-elongation of LA taken up as plasma free fatty acids (LA-FFA) is a major AA source. Bone marrow cells including megakaryocytes and the mucosa of GI tract produce much more AA than is exported from the liver. Therefore, we suggest that uptake and local interconversion of plasma LA-FFA and uptake of plasma 2-AA-LPC are two important alternative pathways for the supply of AA to extrahepatic tissues. Since platelets do not convert LA to d6-desaturase products, it is suggested that the build up of AA pools may be an integral part of the platelet formation in the bone marrow. 3. Fasting increases the rate of uptake and interconversion of plasma LA-FFA in both liver and extrahepatic tissues. The increase of plasma FFA concentration enhances the tissue uptake and this is linked to an increased rate of local interconversion of plasma LA-FFA. The concentration and composition of the plasma FFA pool as well as the regulation of desaturases activity in extrahepatic tissues during fasting is important determinants of eicosanoid precursor formation. 4. Our results challenge the common view that the liver is the main site of formation of AA which is then transported to other tissues mainly by lipoproteins. Our animal model can be used to study the rates of fatty acid desaturation and acylation in relation to enzyme activities and substrate availability in vivo.
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