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A Mäenpää

Publications and source records attributed to A Mäenpää.

8 recordsLinked to original sources
PubMed2005

Heavy metals (Cr, Zn, Ni, V, Pb, Cd) in lingonberries (Vaccinium vitis-idaea L.) and assessment of human exposure in two industrial areas in the Kemi-Tornio region, Northern Finland.

The concentration of Cr, Zn, Ni, V, Pb, and Cd were measured in lingonberries (Vaccinium vitis-idaea L.) sampled at 23 sampling sites around a ferrochrome and stainless steel works and opencast chromium mine in the Kemi-Tornio region, Northern Finland. Two different microwave-assisted digestion procedures were used for sample digestion, i.e., a mixture of HNO3 + H2O2 and a mixture of HNO3 + H2O2 + HCl + HF + H3BO3. According to the results, the digestion procedure with the mixture of HNO3 + H2O2 underestimated especially the Cr concentrations in plant material. The maximum concentrations of Cr (1.3 mg kg(-1), wet weight), Ni (358 microg kg(-1); ww), V (36 microg kg(-1); ww), and Cd (2.4 microg kg(-1); ww) in the immediate vicinity of the point sources were 33, 6, 4, and 8 times higher than the background levels, respectively. The dietary intakes of Cd and Pb were assessed and compared to the health criteria recommendations set by the joint Food and Agriculture Organization and World Health Organization Expert Committee on Food Additives (JECFA). The results showed that, depending on the consumption of lingonberries, human exposure based on the mean concentrations for Pb and Cd varied between 0.04% and 0.07% for Pb and between 0.04% and 0.09% for Cd compared to the tolerable total quantities of 25 microg kg(-1) for Pb and 7 microg kg(-1) for Cd per body weight per week set by JECFA.

Air Pollutants↗
PubMed1997

Lymphocyte adhesion molecule ligands and extracellular matrix proteins in gliomas and normal brain: expression of VCAM-1 in gliomas.

To identify antigenic differences between gliomas and normal brain, we have immunohistochemically studied the expression of lymphocyte adhesion molecules (ICAM-1, ICAM-2, ICAM-3, VCAM-1, E-selectin and CD58), epidermal growth factor receptor (EGFR) and extracellular matrix proteins (collagen IV, fibronectin, laminin, merosin, tenascin and vitronectin) in these tissues. Gliomas expressed high levels of ICAM-1, CD58 (LFA-3), EGFR, tenascin and vitronectin, whereas only very low levels were detected in normal brain. VCAM-1 expression was detected in 15 out of 25 gliomas but not in normal brain. The presence of VCAM-1 in gliomas was verified by immunoblotting and RNase protection assay, and in glioma cell lines by Northern blotting. Expression of VCAM-1 in gliomas may partially explain lymphocytic infiltration, and anti-VCAM-1 antibodies may be of potential in antibody mixtures for targeted therapy of gliomas.

Adult↗
PubMed1996

Different expression of adhesion molecules on stromal cells and endothelial cells of capillary hemangioblastoma.

Cell-cell and cell-matrix interactions are essential for many basic functions, including differentiation and development. In pathological conditions such as inflammation and tumorigenesis adhesive events also play a major role. Cellular adhesion is mediated by specific molecules expressed by both normal and neoplastic tissues. Capillary hemangioblastoma is a tumor of controversial origin, characterized by two major components, vacuolated stromal cells and a capillary network. In order to shed light on the differentiation of the stromal cells and the interactions between the two major components of hemangioblastoma we studied the expression of several adhesion molecules by immunocytochemistry. The endothelium-associated adhesion molecules (ICAM-1, ICAM-2, VCAM-1, PECAM-1 and ELAM-1) were expressed by endothelial cells within the tumors, but not by stromal cells. In contrast, the stromal cells showed strong neuronal cell adhesion molecule (NCAM/CD56) expression, further distinguishing them from endothelial cells. In addition, the stromal cells expressed CD44, which is of interest, as this membrane protein is linked to ezrin, a cytoskeleton-associated protein also expressed by stromal cells. We conclude that the stromal cells and endothelial cells of capillary hemangioblastoma exhibit quite divergent expression patterns of adhesion molecules. The NCAM expression in stromal cells suggests neuroectodermal or mesenchymal differentiation of this tumor. In addition, the NCAM expression could contribute to the sometimes problematic differential diagnosis between capillary hemangioblastoma and metastatic renal cell carcinoma of the central nervous system.

Capillaries↗
PubMed1996

Expression of complement membrane regulators membrane cofactor protein (CD46), decay accelerating factor (CD55), and protectin (CD59) in human malignant gliomas.

Gliomas are malignant brain tumors, which, despite recent progress in surgical and radiological treatment, still have a poor prognosis. Since gliomas apparently resist immunological clearance mechanisms, we became interested in examining bow gliomas resist killing by the human complement system. The resistance of human cells to complement-mediated damage is, in large part, mediated by specific inhibitors of complement:membrane cofactor protein (CD46), decay-accelerating factor (CD55), and protectin (CD59). In the present study we examined the expression of complement regulators in 14 human glioma tumors and in 7 glioma cell lines (U251, U87, HS683, U373, U138, U118, and H2). Protectin was found to be strongly expressed by all glioma tumors and cell lines. Northern blotting analysis demonstrated the typical pattern of four to five protectin mRNAs in the glioma cells. Except for blood vessels, the expression of decay-accelerating factor was weak or absent in the tumors in situ, whereas in the cell lines its expression varied, ranging from negative to intermediate. Membrane cofactor protein was moderately expressed by all the cell lines but only weakly in the tumors. Cell-killing experiments demonstrated that the glioma cell lines were exceptionally resistant to C-mediated lysis. Five of the seven cell lines (U373, HS683, U118, U138, and H2) resisted complement lysis under conditions where most other cell lines were sensitive to killing. Neutralization experiments using specific monoclonal antibodies indicated that protectin was functionally the most important complement regulator in the glioma cells. The killing of the U87 and U251 cells could be significantly increased by a blocking anti-protectin monoclonal antibody, whereas for the other cell lines only moderate or no response was observed. The H2 cell line resisted killing by all antibodies and by complement. These results show that protectin is the most important complement regulator on human glioma cells. The exceptional complement resistance of some glioma cell lines suggests that they may utilize other, hitherto less well characterized, mechanisms to resist complement killing.

Adult↗
PubMed1993

Expression of integrins and other adhesion molecules on NK cells; impact of IL-2 on short- and long-term cultures.

We have investigated, using flow cytometry, the expression of 19 adhesion molecules on fresh and IL-2-activated NK cells. The study included beta 1, beta 2 and beta 3 integrins, CD2, CD54 and CD58 (belonging to the immunoglobulin superfamily), and CD44 and L-selectin (homing receptors). alpha 1 and alpha 2 of the beta 1 integrins were non-existent and alpha 3 was weak on freshly isolated NK cells, but their expression increased after 4 weeks in culture with IL-2. On the other hand, some down-regulation of alpha 4 and alpha 5 and disappearance of alpha 6 was detected. CD 11a/CD18 was upregulated by IL-2, whereas CD11b-c/CD18 were down-regulated. As a novel finding we detected beta 3 on IL-2-activated T and NK cells. CD2, CD44, CD54 and CD58 were increased by IL-2 but L-selectin was strongly down-regulated on the long-term-activated NK cells. Although IL-2-activated lymphocytes are potent tumor-lysing killer cells in vitro and therefore a potential modality in cancer treatment, the IL-2 induced changes in lymphocyte adhesion molecule expression may also lead to undesired effects, such as altered untargeted distribution and compromised migratory capacity.

Cell Adhesion Molecules↗
PubMed1992

Migration of recombinant IL-2-activated T and natural killer cells in the intercellular space of human H-2 glioma spheroids in vitro. A study on adhesion molecules involved.

The migration of rIL-2-activated T and NK cells into the intercellular space of glioma tissue was studied using multicellular spheroids grown from the human H-2 glioblastoma cell line as targets. Lymphocytes of all analyzed subtypes migrated into the spheroids, but CD56+ cells were particularly migratory. Lymphocytes and the H-2 tissue expressed adhesion molecule subunits for the following potential cell-cell or cell-matrix interactions: alpha 3 beta 1 (VLA-3) to fibronectin, laminin, and collagen; alpha 4 beta 1 (VLA-4) and alpha 5 beta 1 (VLA-5) to fibronectin; alpha 6 beta 1 (VLA-6) to laminin; alpha 4 beta 1 to VCAM-1; alpha L beta 2 (Leu-CAMa/LFA-1) to CD54 (ICAM-1); CD44 to fibronectin, collagen, laminin, hyaluronate; CD2 to CD58 (LFA-3); and CD56 (N-CAM) to CD56. In the H-2 tissue, CD54 and VCAM-1 were expressed as a gradient. The expression of CD54 was weak in the peripheral zone and the expression was stronger in the quiescent deeper zone, whereas the distribution of VCAM-1 showed an inversed pattern. The low expression of CD54 was up-regulated along the frontier of migrating lymphocytes. The migration was almost totally prevented by the anti-CD18 (beta 2) mAb IB4 and TS1/18, and also strongly inhibited by the anti-CD54 mAb LB-2. Instead, mAb known to inhibit the binding of beta 1 integrins to fibronectin were not significantly inhibitory. However, a combination of the GPEILDVPST and GRGDS peptides, which compete for the binding of alpha 4 beta 1 and alpha 5 beta 1 to fibronectin and may also affect other adhesion systems, partially prevented migration.

Amino Acid Sequence↗
PubMed1991

Frequencies of HLA-DR3, -DR4, -B8 and -Bw62 in diabetic children diagnosed between 1960 and 1990.

An analysis of the HLA-types of 351 children in whom a diagnosis of insulin dependent diabetes mellitus (IDDM) had been made between 1960 and 1990 revealed that although the frequencies of HLA-DR3, -DR4, -DR3/4, -B8 and -Bw62 were increased there was, depending on the year of diagnosis, a marked fluctuation in the frequencies of these HLA-antigens and in the frequency with which -B8 was associated with -DR3 and -Bw62 with -DR4 suggesting heterogeneity/variation in agents initiating/triggering IDDM.

Chickenpox↗