Biomedical subjects

E Roos

Publications and source records attributed to E Roos.

At least 19 recordsLinked to original sources

PubMed2006

Multiple socio-economic circumstances and healthy food habits.

OBJECTIVE: To examine associations between seven indicators of socio-economic circumstances and healthy food habits, while taking into account assumed temporal order between these socio-economic indicators. DESIGN AND SETTING: Data were derived from cross-sectional postal questionnaires in 2000-2002. Socio-economic circumstances were assessed by parental education, childhood economic difficulties, own education, occupational class, household income, home ownership and current economic difficulties. Healthy food habits were measured by an index consisting of consumption of fresh vegetables, fruit or berries, rye bread, fish and choosing vegetable fats on bread and oil in cooking. Sequential logistic regression models were used, adjusting for age and marital status. PARTICIPANTS: Employees of the City of Helsinki, Finland (n=8960, aged 40-60 years). RESULTS: Healthy food habits were reported by 28% of women and by 17% of men. Own education, occupational class, household income, home ownership and current economic difficulties were associated with healthy food habits. These associations were attenuated but mainly remained after mutual adjustments for the socio-economic indicators. Among women, a pathway was found suggesting that part of the effects of education on food habits were mediated through occupational class. CONCLUSIONS: Employees in higher and lower socio-economic positions differ in their food habits, and those in lower positions and economically disadvantaged are less likely to report healthy food habits. Health promotion programmes and food policies should encourage healthier food choices among those in lower socio-economic positions and among those with economic difficulties in particular.

Adult↗

PubMed2005

The association of employment status and family status with health among women and men in four Nordic countries.

AIMS: The Nordic countries have relatively equal employment participation between men and women, but some differences between countries exist in labour market participation. The aim was to examine the association between employment status and health among women and men in Denmark, Finland, Norway, and Sweden, and analyse whether this association is modified by marital status and parental status. METHODS: The data come from nationally representative cross-sectional surveys carried out in Denmark (n = 2,209), Finland (n = 4,604), Norway (n = 1,844) and Sweden (n = 5,360) in 1994-95. Women and men aged 25-49 were included. Employment status was categorized into full-time employed, part-time employed, unemployed, and housewives among women and into employed and unemployed among men. Health was measured by perceived health and limiting longstanding illness. Logistic regression analysis was used, adjusting for age and education. Marital status and parental status were analysed as modifying factors. RESULTS: The non-employed were more likely to report perceived health as below good and limiting longstanding illness than the employed among both women and men. The association between employment status and perceived health remained unchanged when marital status and parental status were adjusted for among all men and Finnish women, but the association was slightly strengthened among Danish and Swedish women, with the housewives becoming more likely to report ill health than employed women. The association between employment status and limiting longstanding illness was slightly strengthened among women, and slightly weakened among Norwegian men when marital and parental status were adjusted for. CONCLUSIONS: Non-employment was associated with poorer health in all countries, although there are differences in the employment patterns between the countries. Among women marital status and parental status showed a modest or no influence on the association between employment status and health. Among men there was no such influence.

Adult↗

PubMed2005

Gender differences in the association of age with physical workload and functioning.

AIMS: To test whether (1) physically demanding work is less frequent for older than younger employees, and whether (2) the association of physically demanding work with decline of physical functioning is stronger for older employees than their younger counterparts. The gender differences in these associations were examined. METHODS: Subjects of the study were 40-60 year old employees of the City of Helsinki. Data (n = 5802) were collected with mail questionnaires in 2000 and 2001. Functioning was measured with the Role Limitations due to Physical Health Problems scale of the SF36 health questionnaire. Logistic regression models were used to analyse the data. RESULTS: There was a linear trend of less physically demanding work in older than in younger age groups. This trend was more marked for men than women. Age and physically demanding work were associated with poor functioning. In women the association of physically demanding work with poor functioning tended to be stronger for older than for younger age groups, while the opposite was observed in men. CONCLUSIONS: Results suggest that physically demanding work causes more ailments in women of high age than men. It is possible that less men than women are still employed in physically demanding occupations at high age, even though direct evidence of exit from physically demanding work cannot be obtained from cross-sectional data. In these data the physically demanding occupations for men and women were largely different. High physical workload among women working in social and health care is likely to contribute to the gender differences.

Activities of Daily Living↗

PubMed2004

Tumour seeding in peritoneal wound sites in relation to growth-factor expression in early granulation tissue.

The purpose of these experiments was to identify growth factors produced during the formation of a peritoneal wound in relation to tumour cell seeding and stimulated growth in granulation tissue. Gelfoam(c) gelatin sponge was implanted in the mesenteric fan of nude mice to initiate the granulation process. Human HT29 colon carcinoma cells were inoculated intraperitoneally at various times after sponge implantation and tumour growth in granulation tissue was determined. RNA isolated from granulation tissue was used for polymerase chain reaction analysis of the expression of specific growth factors and receptors [vascular endothelial growth factor (VEGF), transforming growth factor-beta (TGF-beta) and lysophosphatic acid (LPA)], and for microarray analysis of differentially expressed genes in early vs. late granulation tissue. Inflammatory cells infiltrated the sponge within 1 day, followed by fibroblasts and the formation of an extracellular matrix. Tumour cell inoculation at 8 h to 3 days after sponge implantation resulted in extensive tumour formation in all cases. Inoculation at 10-28 days resulted in focal tumour growth in only 16-33% of the sponges. Low amounts of VEGF, TGF-beta(1-3), TGF-beta RIII and LPA receptors 1,2 were detected in early granulation tissue, with increased expression from day 10. Microarray analysis identified additional differentially expressed genes that may stimulate tumour take and growth in early granulation tissue.

Animals↗

PubMed2001

[Small changes in health differences in the Nordic countries during the 1980s and 1990s].

The study examined changes over time in health inequality in Denmark, Finland, Norway and Sweden. Data derive from comparable interview surveys carried out in 1986/87 and 1994/95. Limiting long-standing illness and perceived ill health were analysed regarding age, gender; educational attainment, and employment status. Age adjusted prevalence rates were calculated. Changes in differences in health were found in education and employment status groups. There was little or no change in the prevalence of ill health during the time period studied. Despite social and economic changes differences in health remained broadly stable in the examined countries.

Age Factors↗

PubMed2001

Stromal cell-derived factor-1-induced LFA-1 activation during in vivo migration of T cell hybridoma cells requires Gq/11, RhoA, and myosin, as well as Gi and Cdc42.

Dissemination of T cell hybridomas in mice, a model for in vivo migration of memory T cells and for T lymphoma metastasis, depends on the chemokine stromal cell-derived factor-1 (SDF-1) and the integrin LFA-1 and correlates well with invasion into fibroblast cultures. In addition to the known role of the pertussis toxin-sensitive heterotrimeric GTPase G(i), we show that also the pertussis toxin-insensitive GTPase G(q/11) is required for dissemination and invasion. Furthermore, we show that the small GTPases, Cdc42 and RhoA, are involved, and that invasion is blocked by inhibitors of actinomyosin contraction. G(q/11), RhoA, and contraction are specifically required for LFA-1 activation, since 1) they are essential for LFA-1-dependent migration toward low SDF-1 concentrations through ICAM-1-coated filters, but not for migration toward high SDF-1 levels, which is LFA-1 independent; 2) G protein (AlF(4)(-))-induced adhesion to ICAM-1 requires RhoA and contraction; 3) constitutively active G(q) induces aggregation, mediated by LFA-1. We previously reported that binding of this activated LFA-1 to ICAM-1 triggers a signal, transduced by the zeta-associated protein 70 tyrosine kinase, that activates additional LFA-1 molecules. This amplification of LFA-1 activation is essential for invasion. We show here that zeta-associated protein 70-induced LFA-1 activation requires neither Cdc42 and RhoA nor contraction and is thus quite different from that induced by SDF-1. We conclude that two modes of LFA-1 activation, with distinct underlying mechanisms, are required for the in vivo migration of T cell hybridomas.

Animals↗

PubMed2001

The GATA factor Serpent is required for the onset of the humoral immune response in Drosophila embryos.

Innate immunity in Drosophila is characterized by the inducible expression of antimicrobial peptides. We have investigated the development and regulation of immune responsiveness in Drosophila embryos after infection. Immune competence, as monitored by the induction of Cecropin A1-lacZ constructs, was observed first in the embryonic yolk. This observation suggests that the yolk plays an important role in the humoral immune response of the developing embryo by synthesizing antimicrobial peptides. Around midembryogenesis, the response in the yolk was diminished. Simultaneously, Cecropin expression became inducible in a large number of cells in the epidermis, demonstrating that late-stage embryos can synthesize their own antibiotics in the epidermis. This production likely serves to provide the hatching larva with an active antimicrobial barrier and protection against systemic infections. Cecropin expression in the yolk required the presence of a GATA site in the promoter as well as the involvement of the GATA-binding transcription factor Serpent (dGATAb). In contrast, neither the GATA site nor Serpent were necessary for Cecropin expression in the epidermis. Thus, the inducible immune responses in the yolk and in the epidermis can be uncoupled and call for distinct sets of transcription factors. Our data suggest that Serpent is involved in the distinction between a systemic response in the yolk/fat body and a local immune response in epithelial cells. In addition, the present study shows that signal transduction pathways controlling innate and epithelial defense reactions can be dissected genetically in Drosophila embryos.

Animals↗

PubMed2001

The imd gene is required for local Cecropin expression in Drosophila barrier epithelia.

Surfaces of higher eukaryotes are normally covered with microorganisms but are usually not infected by them. Innate immunity and the expression of gene-encoded antimicrobial peptides play important roles in the first line of defence in higher animals. The immune response in Drosophila promotes systemic expression of antimicrobial peptides in response to microbial infection. We now demonstrate that the epidermal cells underlying the cuticle of larvae respond to infected wounds by local expression of the genes for the antimicrobial peptide cecropin A. Thus, the Drosophila epidermis plays an active role in the innate defence against microorganisms. The immune deficiency (imd) gene was found to be a crucial component of the signal-induced epidermal expression in both embryos and larvae. In contrast, melanization, which is part of the wound healing process, is not dependent on the imd gene, indicating that the signalling pathways promoting melanization and antimicrobial peptide gene expression can be uncoupled.

Animals↗

PubMed2001

Retention of CXCR4 in the endoplasmic reticulum blocks dissemination of a T cell hybridoma.

The dissemination of T cell hybridomas to multiple nonhematopoietic tissues is blocked by pertussis toxin, suggesting the involvement of a chemokine. To study whether this chemokine is SDF-1, we employed a strategy proposed previously for gene therapy of AIDS, whereby the SDF-1 receptor CXCR4 (also a coreceptor for HIV) is retained in the endoplasmic reticulum (ER) and fails to reach the cell surface. We transfected SDF-1, carrying an ER retention sequence, into a T cell hybridoma. This altered chemokine is retained in the ER, where it binds CXCR4 and prevents the latter protein from reaching the surface. These cells failed to migrate toward SDF-1 or to invade fibroblast monolayers, although they could still migrate toward thymus and activation-regulated chemokine (TARC) and invade TARC-treated monolayers. Furthermore, the ability of the transfected cells to disseminate to multiple organs upon intravenous injection into mice was abolished. This dissemination reflects the in vivo migration patterns of activated and memory T cells into nonhematopoietic tissues, which is thus likely to depend on CXCR4. Attempts to block CXCR4 function as a therapy for AIDS may affect this migration with consequences for T cell function. Our results also suggest a decisive role for CXCR4 in the dissemination of hematopoietic malignancies expressing this receptor.

Animals↗

PubMed2001

Changing health inequalities in the Nordic countries?

The Nordic countries, referring here to Denmark, Finland, Norway, and Sweden, have often been viewed as a group of countries with many features in common, such as geographical location, history, culture, religion, language, and economic and political structures. It has also been habitual to refer to a "Nordic model" of welfare states comprising a large public sector, active labour market policies, high costs for social welfare as well as high taxes, and a general commitment to social equality. Recent research suggests that much of this "Nordicness" appears to remain despite the fact that the Nordic countries have experienced quite different changes during the 1980s and 1990s. How this relates to changes in health inequalities is in the focus of this supplement.

Finland↗

PubMed2000

Gi and Gq/11 proteins are involved in dissemination of myeloid leukemia cells to the liver and spleen, whereas bone marrow colonization involves Gq/11 but not Gi.

The migration of leukocytes into tissues is regulated by chemokines and other chemotactic factors that act on receptors that signal through Gi proteins. It seems likely that the colonization of tissues during dissemination of hematopoietic tumor cells is similarly regulated. In fact, dissemination of a T-cell hybridoma, a model for T lymphoma, was blocked when Gi proteins were inactivated by the S1 catalytic subunit of pertussis toxin that had been transfected into those cells. Pertussis toxin S1 blocked dissemination of MDAY-D2 murine myeloid leukemia cells to the liver and spleen, as in T-cell hybridoma cells, but it did not prevent bone marrow colonization. In contrast, overexpression of a function-defective mutant of the Gq/11 protein blocked dissemination to the bone marrow and also prevented Gq/11 dissemination to the liver and spleen. This indicates that the influx of these myeloid cells into all tissues requires the Gq/11 protein in addition to the Gi protein in the liver and spleen. (Blood. 2000;96:691-698)

Animals↗

PubMed2000

Cytoplasmic domain mutants of beta1 integrin, expressed in beta 1-knockout lymphoma cells, have distinct effects on adhesion, invasion and metastasis.

Structural requirements for beta 1 integrin cytoplasmic domain functions in adhesion, migration and signaling have been studied mainly for fibroblasts in vitro. The relevance for beta 1-dependent in vivo migration of lymphoid cells has not been assessed. To study this, we transfected beta 1 mutants into beta 1-deficient double knockout (DKO) ESb lymphoma cells, and tested the capacity of the cells to metastasize to liver and spleen. This was compared to alpha 4 beta 1-dependent invasion into cell monolayers in vitro and Mn2+-induced adhesion to fibronectin. Deletion of the five C-terminal residues or mutation of both threonines T788 and T789 to alanines blocked invasion and metastasis and greatly reduced adhesion, in line with known in vitro effects. However, mutations of the NPXY motif tyrosines had unexpected consequences. A Y783F mutation had no effect at all, but a Y783,795F double mutation strongly reduced Mn2+-induced adhesion, whereas it had limited effects on invasion and metastasis. Furthermore, cells expressing a beta 1 beta 2 chimeric subunit, which contains phenylalanines in the NPXY/F motifs, adhered poorly but invasion and metastasis was fully restored to the same levels as for cells expressing wild-type beta 1. We conclude that part of the functions of the beta 1 cytoplasmic domain that are required for adhesion are not essential for beta 1-dependent invasion and metastasis.

Adaptor Proteins, Signal Transducing↗

PubMed2000

Encapsulation matrices for neurotrophic factor-secreting myoblast cells.

Encapsulated-cell therapy is an emerging technology that entails implantation of cell-containing devices that secrete therapeutic factors. One potential application of this technology is the delivery of neurotrophic factors to treat neurodegenerative disease. These devices typically use an internal matrix to serve as a cell scaffold. This study compares collagen-coated polyethylene terephthalate (PET) yarn scaffold versus collagen as a matrix for engineered C2C12 myoblasts. C2C12 cells transfected to secrete ciliary neurotrophic factor (CNTF) were immobilized in matrices and encapsulated into hollow fiber membrane devices. Encapsulated cells were monitored in vitro for viability, morphology, and factor secretion. Two independent methods (histology assessment and metabolic assay) were used to estimate viable cell density; a high correlation between the methods was found. After 4 weeks, encapsulated devices with PET scaffold had an almost nine-fold greater number of viable cells compared to collagen. PET matrix devices contained a thick annulus of compact, highly oriented cells. Collagen matrix devices contained sparse viable cells in a thin rim. Secretion assays showed cells in PET matrix released approximately four-fold the amount of CNTF versus cells in collagen (averaging 542 and 129 ng/day per device for PET and collagen matrix, respectively). The choice of encapsulation matrix was found to have a profound effect on cell morphology, level of secreted factor, and viability of encapsulated C2C12 cells.

Animals↗

PubMed1999

LFA-1 to LFA-1 signals involve zeta-associated protein-70 (ZAP-70) tyrosine kinase: relevance for invasion and migration of a T cell hybridoma.

We previously showed that LFA-1-dependent in vitro invasion and in vivo migration of a T cell hybridoma was blocked in cells overexpressing a truncated dominant-negative zeta-associated protein (ZAP)-70. The truncated ZAP-70 also blocked LFA-1-dependent chemotaxis through ICAM-1-coated filters induced by 1 ng/ml stromal cell-derived factor-1, but not LFA-1-independent chemotaxis induced by 100 ng/ml stromal cell-derived factor-1. This suggested that LFA-1 engagement triggers a signal that amplifies a weak chemokine signal and that dominant-negative ZAP-70 blocks this LFA-1 signal. Here we show that cross-linking of part of the LFA-1 molecules with Abs causes activation of free LFA-1 molecules (not occupied by the Ab) on the same cell, which then bind to ICAM-2 on other cells. This causes cell aggregation that was also blocked by dominant-negative ZAP-70. Thus, an LFA-1 signal involving ZAP-70 activates other LFA-1 molecules, suggesting that the chemokine signal can be amplified by multiple cycles of LFA-1 activation. The chemokine and the LFA-1 signal were both blocked by a phospholipase C inhibitor and a calpain inhibitor, suggesting that one of the amplified signals is the phospholipase C-dependent activation of calpain. Finally, we show that both Src-homology 2 domains are required for inhibition of invasion, chemotaxis, and aggregation by the truncated ZAP-70, suggesting that ZAP-70 interacts with a phosphorylated immunoreceptor tyrosine-based activation motif (ITAM) sequence. Remarkably, this is not an ITAM in the TCR/CD3 complex because this is not expressed by this T cell hybridoma.

Animals↗

PubMed1999

From regional ethnographies to interdisciplinary approaches-research on meals in Finland.

The paper reviews Finnish research on meals and meal patterns since the turn of the century. The main research traditions and cases representing various methodological approaches-qualitative interview, health behaviour questionnaire and dietary survey-are discussed. In line with studies undertaken in other industrialized countries, the Finnish studies show that meal patterns are related to socio-economic structure, work schedules, lifecourse, living conditions and food availability. Meal patterns vary by individual energy needs, and the nutrient contents of meals can be different from those of snacks. It is difficult to account for all determinants and characteristics of meals in a single study. The three cases shed light on the various aspects of the meal. When planning an empirical study on meals the researcher should ask herself/himself at least four questions: (1) who defines the meal?; (2) are meal patterns assumed to vary by time and between subgroups of the study population?; (3) is information on nutrient content of various eating occasions relevant to the study?; and (4) could information on meals be obtained from existing data sources?

Cultural Characteristics↗

PubMed1999

The effect of breakfast cereal on diet and serum cholesterol: a randomized trial in North Karelia, Finland.

OBJECTIVE: To test the hypothesis that a high carbohydrate breakfast with breakfast cereal leads to a meaningful reduction in dietary energy intake from fat, especially from saturated fat, and thus lower serum cholesterol levels. DESIGN: An open randomized controlled cross-over trial. The subjects were randomized into intervention breakfast cereal or usual breakfast (control) groups. SETTING: Free-living subjects aged 29-71 y in Eastern Finland SUBJECTS: 224 enrolled, 209 completed the study. The subjects were recruited from a survey of a random population sample and from other sources, and their serum cholesterol was not lower than 5.0 mmol/l. Recruited persons did not have any chronic disease or very low saturated fat intake. INTERVENTION: The cereal group consumed 80 g (men) or 60 g (women) cereal at breakfast and the control group continued their usual dietary habits for six weeks. After a wash out of six weeks, a cross-over with another six week trial period took place. Measurements (including serum samples and a 3 d food record) took place before and after the two trial periods. RESULTS: The intervention period led to 2.5 en% (energy percent units) reduction in saturated fatty acids intake. The reduction in total fat intake was 5.5 en%. This was compensated for by increased intake of carbohydrates. The reduction in saturated fatty acids intake led to modest (but in group 1 significant) 0.15 mmol/l (2.5%) reduction in total serum cholesterol level. CONCLUSIONS: The trial showed that regular cereal breakfast can lead to reduced intake of total and saturated fatty acids of the daily diet and consequently to reduction in serum cholesterol level.

Adult↗

PubMed1999

Dif and cactus are colocalized in the larval nervous system of Drosophila melanogaster.

The Rel protein Dif is a transcription factor suggested to control part of the immune response in the fruit fly Drosophila melanogaster. In uninfected animals, Dif is normally located in the cytoplasm, most likely in a complex with an IkappaB molecule such as Cactus. Upon infection, Dif is enriched in the nucleus of immunoresponsive tissues such as fat body and blood cells. Rel proteins in mammals not only participate in the control of the immune response, but are also thought to play important roles in the function of the nervous system. Here, we demonstrate that both Dif and Cactus are expressed in the central nervous system (CNS) of Drosophila. Interestingly, Dif and Cactus colocalize in their distribution, suggesting a functional link between these proteins in the CNS. In the larval CNS, both Dif and Cactus are expressed at relatively low levels in most cells and at high levels in the mushroom bodies and in small subsets of neurosecretory cells. The cytoplasmic localization of Dif and Cactus in the CNS cells is not affected by bacterial challenge. Instead, we observed changes in nuclear versus cytoplasmic localization of Cactus (but not Dif) along the dark-light cycle, with a strong nuclear localization in perineurial glia toward the end of the dark period. In the CNS of the prepupa, the intensity of the immunostaining for both Dif and Cactus is higher than in the larva. Interestingly, in fat body of uninfected prepupae, the Dif localization was mainly nuclear, suggesting a function for Dif during the process of pupariation.

Animals↗

PubMed1998

ZAP-70 tyrosine kinase is required for LFA-1-dependent T cell migration.

The ZAP-70 tyrosine kinase is essential for T cell activation by the T cell receptor. We show that ZAP-70 is also required for migration of T cells that is dependent on the integrin LFA-1. Invasion of TAM2D2 T cell hybridoma cells into fibroblast monolayers, which is LFA-1-dependent, was blocked by overexpression of dominant-negative ZAP-70 and by piceatannol but not by herbimycin A. The Syk inhibitor piceatannol blocks the Syk homologue ZAP-70, which is expressed by TAM2D2 cells, with the same dose dependence as the inhibition of invasion. Dominant-negative ZAP-70 completely inhibited the extensive metastasis formation of TAM2D2 cells to multiple organs upon i.v. injection into mice. Migration of TAM2D2 cells through filters coated with the LFA-1 ligand ICAM-1, induced by 1 ng/ml of the chemokine SDF-1, was blocked by anti-LFA-1 mAb and also abrogated by dominant-negative ZAP-70 and piceatannol. In contrast, migration induced by 100 ng/ml SDF-1 was independent of both LFA-1 and ZAP-70. LFA-1 cross-linking induced tyrosine phosphorylation, which was blocked by dominant-negative ZAP-70 and piceatannol. We conclude that LFA-1 engagement triggers ZAP-70 activity that is essential for LFA-1-dependent migration.

Animals↗