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Biomedical subjects

U Eriksson

Publications and source records attributed to U Eriksson.

159 records · Page 9Linked to original sources
PubMed1976

Thrombosis following hip arthroplasty. A study using phlebography and 125I-fibrinogen test.

Venous thrombosis after hip arthroplasty was studied using the 125I-fibrinogen test and phlebography. Eight out of ten dextran-treated and six out of ten control patients developed thrombosis. The thrombi were small and most frequently dorsal and dorso-lateral veins were involved. There were no thigh thrombi without concurrent calf thrombi. Half of the thrombi were found within the first postoperative week whereas the remainder occurred later. Preoperative venous pathology predisposed to postoperative thrombosis.

Aged↗
PubMed1976

Indirect immunofluorescence staining of human thyroid by antibodies occurring in Yersinia enterocolitica infections.

In the diagnostic routine for tissue antibodies, using indirect immunofluorescence on cryostat sections of human thyrotoxic thyroid, rat stomach and kidney, ninety-six out of 48,388 sera showed a marginal staining of the membrane region of thyroid epithelial cells but no other reaction. Twenty-six of these sera were from patients with acute Yersinia enterocolitica serotype 3 infection but without signs of thyroid disease. Fifty of sixty-three sera with agglutinins against Y. enterocolitica serotype 3 and three out of four sera with agglutinins against Y. enterocolitica serotype 9 also showed this reaction on thyroid sections. It was due to antibodies, mostly of the IgG class, occurring in low titre, which react with intracytoplasmic antigens in thyroid, as staining of live thyroid epithelial cells was negative. The pattern of immunofluorescence on thyroid sections caused by these antibodies could not be distinguished from that caused by smooth muscle antibodies by appearance only. However, smooth muscle antibodies react also on other tissue sections and extracts of contractile proteins which absorb out these, did not change the reaction on thyroid of Y. enterocolitica sera. Absorption with sonicated Y. enterocolitica 3 and 9 antigens, but not with heat-killed whole bacteria, extinguished the reaction on thyroid. This indicates the presence of a cross-reactivity between antigens in these bacteria, different from the O antigen, and antigens in thyroid epithelial cells. Knowledge of this pattern of immunofluorescence on thyroid sections can be of diagnostic significance.

Agglutination Tests↗
PubMedDate not supplied

Impaired release of vitamin A from liver in primary biliary cirrhosis.

In 44 patients with primary biliary cirrhosis serum levels of vitamin A, retinol-binding protein and transthyretin (prealbumin) were found to be significantly lower than in 25 sex- and age-matched controls. Liver biopsies were available for chemical analyses in 28 of the patients. Their mean liver vitamin A concentration (2.8 +/- 2.0 mumoles per gm wet weight) did not differ significantly from that in 22 cases of sudden death which served as controls (2.0 +/- 1.5 mumoles per gm wet weight). Immunohistochemical investigation showed a normal distribution of serum retinol-binding protein in the patients' livers, whereas the staining pattern of cellular retinol-binding protein, believed to be involved in the intrahepatic transport of vitamin A, was abnormal. Thus, the number size and cellular retinol-binding protein staining intensity of fat-storing (Ito) cells were clearly higher in the patients as compared with controls. The results suggest that the low serum vitamin A levels in primary biliary cirrhosis are not a consequence of vitamin A deficiency but instead reflect a defective mobilization of vitamin A from the liver.

Female↗
PubMedDate not supplied

Flavonoids in grapefruit juice inhibit the in vitro hepatic metabolism of 17 beta-estradiol.

Naringenin, quercetin and kaempferol, which may be found in glycoside form in natural compounds such as grapefruit, are potent inhibitors of cytochrome P-450 metabolism. The influence of these flavonoids on the metabolism of 17 beta-estradiol was investigated in a microsome preparation from human liver. The flavonoids were added in concentrations of 10, 50, 100, 250 and 500 mumol/l to the microsome preparation. The metabolism of 17 beta-estradiol was concentration dependently inhibited by all the flavonoids tested. Addition of the flavonoids to the microsome preparation did not influence estrone formation, while a potent inhibition of estriol formation was observed. At the highest concentrations tested of the respective flavonoid, there was approximately 75-85% inhibition of estriol formation. However, naringenin was a less potent inhibitor of 17 beta-estradiol metabolism as compared to quercetin and kaempferol. The most likely mechanism of action of the flavonoids on 17 beta-estradiol metabolism is inhibition of the cytochrome P-450 IIIA4 enzyme, which catalyzes the reversible hydroxylation of 17 beta-estradiol into estrone and further into estriol. These hydroxylation processes represent the predominant steps of the hepatic metabolic conversion of endogenous as well as exogenous 17 beta-estradiol. This interaction would be expected to inhibit the first-pass metabolism of 17 beta-estradiol, and this has recently been demonstrated after oral administration of 17 beta-estradiol to women.

Adult↗
PubMedDate not supplied

Retinoid binding proteins-expression patterns in the human placenta.

The present study examined the expression and occurrence of different retinoid binding proteins in human first trimester and term placenta. At both stages, messenger RNA for the serum transport vehicle for retinol, retinol-binding protein (RBP), was detected only in decidual cells of the basal plate. In contrast, immunoreactive RBP (irRBP) was present in syncytiotrophoblast, core mesenchyme and lumen of vessels in placental villi and in mesenchyme and decidual cells of the basal plate. In villi of term placentae, however, staining for irRBP was lost in syncytiotrophoblasts and villous core mesenchyme. A putative placental RBP-receptor, approx 60-65kDa, was detected in the villous syncytiotrophoblast of both stages investigated. Immunoreactivity for the cellular retinol binding protein type I (CRBP I), was found in villous stromal cells and in decidual cells of the basal plate in sections of first trimester and term placenta. These results may suggest that maternal RBP-retinol is transferred across the chorionic villi to the fetal/villous circulation and that villous absorption of the complex is mediated via a placental RBP-receptor. Moreover, binding and possibly also metabolism of retinol may occur in the CRBP I positive villous stromal cells and decidual cells of the basal plate. In the latter, release of placental RBP-retinol may also be anticipated.

Allantois↗
PubMedDate not supplied

Polychlorinated biphenyls, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (p,p'-DDT) and 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE) in human plasma related to fish consumption.

Fatty fish species, e.g., salmon and herring, in the Baltic Sea have high levels of polychlorinated biphenyls (PCBs) and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (p,p'-DDT), and its main metabolite: 1,1-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE). We determined levels of 10 different PCB congeners, including non- and mono-ortho-PCBs, as well as DDT and DDE, in human blood plasma from 37 subjects with varying intake of fish (0-1 750 g/wk) from the Baltic Sea. With respect to all of the PCB congeners we investigated, as well as for DDT and DDE, there were statistically significant associations with fish intake. Thus, fish from the Baltic Sea is a major source of exposure to these compounds in Swedes. Polychlorinated dibenzo-p-dioxins (PCDD) and dibenzofurans (PCDF) had been determined earlier in 29 of the subjects. The PCB contribution to "dioxin-like" effects among high consumers of fish (calculated as Nordic TCDD equivalents) was almost 80%, whereas that from PCDD and PCDF was only 20%.

Adult↗
PubMedDate not supplied

Retinoid-binding proteins in craniofacial development.

Cephalic neural crest cells are known to form the frontonasal mesenchyme and contribute to the mesenchyme of the visceral arches. Retinoids affect neural crest cells and their derivatives during development, and thus cause craniofacial, thymus, and conotruncal heart malformations. In addition, retinoids induce malformations of the central nervous system (CNS). Retinoic acid (RA) and its congeners accumulate in a saturable manner in neural crest and neural crest-derived cells, in the hindbrain, and the spinal cord of mouse embryos. Cellular retinoic acid-binding protein (CRABP) was localized by immunohistochemistry in the same areas as were the labelled RA congeners. Thus, CRABP and RA congeners were found in the transitional zone between surface ectoderm and neuropeithelium, from where neural crest cells are known to emanate (day 8 1/2). Later, specific labelling was found in the frontonasal mesenchyme and in the visceral arches. Also in the trunk, neural crest cells were labelled. In CNS, strong staining was seen in the rhombomeres (especially numbers 4-6) of the hindbrain and in the spinal cord. Retinol and cellular retinol-binding protein (CRBP) were more evenly distributed, with exception of surface ectoderm, epithelium of gut, and myocardium, where CRBP was specifically expressed. These findings are discussed in relation to the differential expression of nuclear RA receptors and homeobox genes in the craniofacial region and in the hindbrain. It is possible that RA is important for the normal pattern formation in these regions and acts as a morphogen as previously proposed in limb development.

Animals↗