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Träfflista för sökning "WFRF:(Johansson Anna 1972 ) srt2:(2000-2004)"

Sökning: WFRF:(Johansson Anna 1972 ) > (2000-2004)

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1.
  • Berggren, Vanja, 1972-, et al. (författare)
  • An explorative study of Sudanese midwives' motives, perceptions and experiences of re-infibulation after birth
  • 2004
  • Ingår i: Midwifery. - 0266-6138 .- 1532-3099. ; 20:4, s. 299-311
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: to explore Sudanese midwives' motives for and perceptions and experiences of re-infibulation after birth and to elucidate its context and determinants. DESIGN: triangulation of methods, using observational techniques and open-ended interviews. SETTING AND PARTICIPANTS: two government hospitals in Khartoum/Omdurman, Sudan, for the observations and in-depth interviews with 17 midwives. FINDINGS: midwives are among the major stakeholders in the performance of primary female genital cutting (FGC) as well as re-infibulation. Focusing on re-infibulation after birth, midwives were trying to satisfy differing, and sometimes contradictory, perspectives. The practice of re-infibulation (El Adel) represented a considerable source of income for the midwives. The midwives integrated the practice of re-infibulation into a greater whole of doing well for the woman, through an endeavour to increase her value by helping her to maintain her marriage as well as striving for beautification and completion. They were also trying to meet socio-cultural requests, dealing with pressure from the family while balancing on the edge of the law. KEY CONCLUSIONS AND IMPLICATIONS FOR PRACTICE: the findings confirm that midwives are important stakeholders in perpetuating re-infibulation, and indicate that the motives are more complex than being only economic. The constant balancing between demands from others puts the midwives in a difficult position. Midwives' potential role to influence views in the preventative work against FGC and re-infibulation should be acknowledged in further abolition efforts.
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2.
  • Johansson, Anna-Karin, 1974, et al. (författare)
  • Allergen-induced traffic of bone marrow eosinophils, neutrophils and lymphocytes to airways
  • 2004
  • Ingår i: Eur J Immunol. ; 34:11
  • Tidskriftsartikel (refereegranskat)abstract
    • We evaluated whether bone marrow (BM) inflammatory cells have capacity to traffic into the airways following allergen exposure in a mouse model of allergen-induced airway inflammation. We also evaluated the effect of IL-5 overexpression on (i) the production of eosinophils in BM, (ii) the accumulation of eosinophils, neutrophils and lymphocytes in blood and airways and (iii) the changes in CD34(+) cell numbers in BM, blood and airways. Bromodeoxyuridine (BrdU) was used to label cells produced during the exposure period. Furthermore, CD3 splenocytes were adoptively transferred to investigate the BM inflammatory response. Allergen exposure induced traffic of BM eosinophils, neutrophils and lymphocytes to the airways and increased the number of BrdU(+) eosinophils, neutrophils, lymphocytes and CD34(+) cells in BALf. IL-5 overexpression enhanced the eosinophilopoiesis and increased the presence of BrdU(+) eosinophils and CD34(+) cells in airways and enhanced the number of CD34(+) cells in BM and blood after allergen exposure. Adoptive transfer of CD3 lymphocytes overexpressing IL-5 caused increased BM eosinophilia. In conclusion, allergen exposure induces traffic of not only newly produced eosinophils but also newly produced neutrophils and lymphocytes into the airways.
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3.
  • Ladenvall, Per, 1972, et al. (författare)
  • Tissue-type plasminogen activator -7,351C/T enhancer polymorphism is associated with a first myocardial infarction.
  • 2002
  • Ingår i: Thrombosis and haemostasis. - 0340-6245. ; 87:1, s. 105-9
  • Tidskriftsartikel (refereegranskat)abstract
    • We recently identified a polymorphic Sp1 binding site in an enhancer at the tissue-type plasminogen activator (tPA) locus (tPA -7,351C/T), which was associated with vascular tPA release. Subjects homozygous for the -7,351C allele had twice the tPA release rate compared to subjects carrying the -7,351T allele. In this study we tested the hypothesis that the tPA -7,351C/T polymorphism is associated with myocardial infarction (MI). In a population-based prospective nested case-control study within northern Sweden, genotypes were determined among 61 MI cases and 120 controls. In a multivariate model, the tPA -7,351C/T polymorphism (OR 2.68 for T allele carriers; 95% CI 1.31-5.50), tPA antigen (OR 1.16; 95% CI 1.07-1.25) and apo A-I (OR, 0.997; 95% CI 0.995-0.999) were independently associated with a first MI. These findings suggest that genetic markers of local tPA release and circulating steady-state tPA levels carry independent prognostic information.
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4.
  • Sergejeva, Svetlana, 1972, et al. (författare)
  • Allergen exposure-induced differences in CD34+ cell phenotype: relationship to eosinophilopoietic responses in different compartments
  • 2004
  • Ingår i: Blood. ; 103:4, s. 1270-7
  • Tidskriftsartikel (refereegranskat)abstract
    • We hypothesized that the allergen-induced increased number of airway eosinophils results from increased recruitment of eosinophils from bone marrow (BM) and local development of CD34(+) cells into eosinophils. We also assumed that the phenotype of airway eosinophils depends on whether these cells have differentiated within BM or airway. C57BL/6 mice were sensitized and subsequently exposed to ovalbumin (OVA) on 5 consecutive days. Newly produced cells were labeled with a thymidine analog. Clonogenic activity and interleukin 5 (IL-5) release from bronchoalveolar lavage fluid (BALf) CD34(+) cells were evaluated by using cell-culture techniques. Allergen exposure induces increase in CD135(+) primitive myeloid progenitors within the BM CD34(+) cell population, without significant changes in total number of CD34(+) cells or newly produced CD34(+) cells. CD34(+)/IL-5Ralpha(+) cells in the first stage of cell differentiation were found only in BM, arguing that early commitment of CD34(+) cells into the eosinophil lineage is restricted to the BM compartment. Allergen exposure induces a shift in differentiation of BM, blood, and BALf eosinophillineage-committed CD34(+) cells toward mature eosinophils and recruitment of these cells via blood into airway. We further demonstrate in vitro that ability to multiply persists in BALf CD34(+) cells but not CD34(-) cells, likely via autocrine IL-5 release and IL-5-induced up-regulation of IL-5Ralpha.
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5.
  • Sitkauskiene, Brigita, et al. (författare)
  • Regulation of Bone Marrow and Airway CD34+ Eosinophils by Interleukin-5
  • 2004
  • Ingår i: Am J Respir Cell Mol Biol. ; 30:3
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to evaluate the effect of a neutralizing anti-interleukin (IL)-5 monoclonal antibody (TRFK-5) on bone marrow and airway CD34(+) and immature eosinophils. A focus was to determine the effect of the timing of treatment. Balb/c mice were ovalbumin-sensitized and subsequently exposed to ovalbumin for 5-10 d via airway route. Animals were treated intraperitoneally with TRFK-5 or its isotype control (50 microg) once at different time points. Newly produced eosinophils were labeled using 5-bromo-2'-deoxyuridine (BrdU). BrdU(+) and CD34(+) eosinophil numbers were examined by immunocytochemistry. TRFK-5 reduced bone marrow immature eosinophils within 3 d. This effect was closely related to a reduction of BrdU(+) and CD34(+) bone marrow eosinophils, and reduced numbers of blood eosinophils. However, bronchoalveolar lavage (BAL) eosinophilia was not attenuated to the same degree. The effect of TRFK-5 was most prominent in the extended allergen-exposure protocol, where the treatment was given in the middle of the exposure, with strongly reduced bone marrow CD34(+) and immature bone marrow eosinophils, blood eosinophils as well as BAL BrdU(+) eosinophils, and BAL CD34(+) eosinophils. These data argue that anti-IL-5 downregulates eosinophilopoiesis within 3 d by action in the bone marrow, by inhibition of the early stages of eosinophil maturation from CD34(+) cells.
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