| 1. |
- Larsson, K, et al.
(författare)
-
Genetic and perinatal factors as risk for childhood type 1 diabetes
- 2004
-
Ingår i: Diabetes/Metabolism Research & Reviews. - : Wiley. - 1520-7552. ; 20:6, s. 429-437
-
Forskningsöversikt (refereegranskat)abstract
- The mechanisms by which gestational infections, blood incompatibility, birth weight, mother's age and other prenatal or neonatal events increase the risk for type 1 diabetes are not understood. Studies so far have been retrospective, and there is a lack of population-based prospective studies. The possibility identifying children at type 1 diabetes risk among first-degree relatives has resulted in prospective studies aimed at identifying postnatal events associated with the appearance of autoantibody markers for type 1 diabetes and a possible later onset of diabetes. However, the majority (85%) of new onset type 1 diabetes children do not have a first-degree relative with the disease. Population-based studies are therefore designed to prospectively analyse pregnant mothers and their offspring. One such study is DiPiS (Diabetes Prediction in Skane), which is examining a total of about 10 000 pregnancies expected every year in the Skane (Scania) region of Sweden that has 1.1 million inhabitants. Blood samples from all mothers in this region are obtained during pregnancy and at the time of delivery. Cord blood is analysed for HLA high-risk alleles and for autoantibodies against the 65 kD isoform of glutamic acid decarboxylase (GADA), the protein tyrosine phosphatase-related IA-2 antigen (IA-2A) and insulin (IAA) as a measure of prenatal autoimmune exposure. Identifying high-risk children by genetic, autoimmune and gestational risk factors followed by prospective analyses will make it possible to test the hypothesis that gestational events may trigger beta cell autoimmunity as a prerequisite for childhood type 1 diabetes. Copyright (C) 2004 John Wiley Sons, Ltd.
|
|
| 2. |
- Larsson, Mårten, et al.
(författare)
-
Selective interaction of megalin with postsynaptic density-95 (PSD-95)-like membrane-associated guanylate kinase (MAGUK) proteins
- 2003
-
Ingår i: Biochemical Journal. - 0264-6021 .- 1470-8728. ; 373:2, s. 381-391
-
Tidskriftsartikel (refereegranskat)abstract
- Megalin is an integral membrane receptor belonging to the low-density lipoprotein receptor family. In addition to its role as an endocytotic receptor, megalin has also been proposed to have signalling functions. Using interaction cloning in yeast, we identified the membrane-associated guanylate kinase family member postsynaptic density-95 (PSD-95) as an interaction partner for megalin. PSD-95 and a truncated version of megalin were co-immunoprecipitated from HEK-293 cell lysates overexpressing the two proteins, which confirmed the interaction. The two proteins were found to be co-localized in these cells by confocal microscopy. Immunocytochemical studies showed that cells in the parathyroid, proximal tubuli of the kidney and placenta express both megalin and PSD-95. We found that the interaction between the two proteins is mediated by the binding of the C-terminus of megalin, which has a type I PSD-95/ Drosophila discs-large/zona occludens 1 (PDZ)-binding motif, to the PDZ2 domain of PSD-95. The PSD-95-like membrane-associated guanylate kinase ('MAGUK') family contains three additional members: PSD-93, synapse-associated protein 97 (SAP97) and SAP102. We detected these proteins, apart from SAP102, in parathyroid chief cells, a cell type having a marked expression of megalin. The PDZ2 domains of PSD-93 and SAP102 were also shown to interact with megalin, whereas no interaction was detected for SAP97. The SAP97 PDZ2 domain differed at four positions from the other members of the PSD-95 subfamily. One of these residues was Thr(389), located in the alphaB-helix and part of the hydrophobic pocket of the PDZ2 domain. Surface plasmon resonance experiments revealed that mutation of SAP97 Thr(389) to alanine, as with the other PSD-95-like membrane-associated guanylate kinases, induced binding to megalin.
|
|
| 3. |
- Lundmark, Martin, et al.
(författare)
-
Increased levels of electrical fields in buildings
- 2002
-
Ingår i: Biological effects of EMFs : proceedings, Rhodes, Greece, 7 - 11 October 2002. - Rhodes : University of Ioannina. - 960867333X
-
Konferensbidrag (refereegranskat)abstract
- In order to save energy and improve the performance, various electrical apparatus are equipped with power electronics. Normally power electronic equipment produce harmonics and high frequency noise. To handle noise emission, power electronic equipment uses EMC filters and are tested according to EMC standards. But the question is whether these tests are enough to avoid noise emissions in buildings? It has been shown, that electrical equipment distributes electrical fields inside a building using the PE wire. In order to avoid or limit electrical field it is necessary to find the sources and stop the distribution. The levels of electrical fields in the frequency range between 10 kHz and 30 MHz in office buildings and homes are rather unknown. One reason is lack of civil standards, another is lack of and difficulties in measurements.In this paper results from measurements of electrical fields in the frequency range between 10 kHz and 30 MHz at different locations is shown. An interesting result from these measurements is that the level of the electrical fields from a HF-fittings are approximately 10 times the level from video display units (VDU). This paper also shows a method to analyze sources of electrical fields.
|
|
| 4. |
- Lundmark, Martin, et al.
(författare)
-
The use of protective earth as a distributor of fields and radiation
- 2000
-
Ingår i: Biological effects of EMFs. - Heraklio : Workshop on Biological Effects of Electromagnetic Fields. - 9608673305
-
Konferensbidrag (refereegranskat)abstract
- Apart from being a safety arrangement, the protective earth, PE, is also defined as an equipotential plane which serves as a reference voltage for a circuit. Interest in the PE for EMC reasons is focused on an equipotential point. Still, most PE installation on site is carried out as a safety arrangement. In order to fulfill EMC standards regarding low emission, equipment is shielded and the shield is connected to the PE wire.The purpose of this paper is to show that electrical equipment distributes its electrical fields using the PE wire. Measurements have been taken on light fittings.
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Dixelius, Johan, et al.
(författare)
-
Endostatin-induced tyrosine kinase signaling through the Shb adaptor protein regulates endothelial cell apoptosis
- 2000
-
Ingår i: Blood. - 0006-4971 .- 1528-0020. ; 95:11, s. 3403-3411
-
Tidskriftsartikel (refereegranskat)abstract
- Endostatin, which corresponds to the C-terminal fragment of collagen XVIII, is a potent inhibitor of angiogenesis. Fibroblast growth factor-2 (FGF-2)-induced angiogenesis in the chicken chorioallantoic membrane was inhibited by endostatin, but not by an endostatin mutant R158/270A, lacking heparin-binding ability. Endostatin was internalized by endothelial cells, but not by mouse fibroblasts. Treatment of murine brain endothelial (IBE) cells with endostatin reduced the proportion of cells in S phase, whereas growth-arrested IBE cells in collagen gels treated with endostatin displayed enhanced tubular morphogenesis. IBE cells overexpressing Shb, an adaptor protein implicated in angiostatin-induced apoptosis, displayed elevated apoptosis and decreased tubular morphogenesis in collagen gels in response to endostatin when added together with FGF-2. Induction of apoptosis was dependent on the heparin-binding ability of endostatin and the expression of Shb with a functional Src homology 2 (SH2)-domain. Endostatin treatment for 10 minutes or 24 hours induced tyrosine phosphorylation of Shb and formation of multiprotein complexes. An Shb SH2 domain fusion protein precipitated a 125-kd phosphotyrosyl protein in endostatin-treated cells. The 125-kd component either contained intrinsic tyrosine kinase activity or occurred in complex with a tyrosine kinase. In conclusion, our data show that endostatin induces tyrosine kinase activity and enhanced apoptosis in FGF-treated endothelial cells.
|
|
