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Träfflista för sökning "WFRF:(Benson L) srt2:(2005-2009)"

Sökning: WFRF:(Benson L) > (2005-2009)

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  • Anderson, R. B., et al. (författare)
  • Indigenous land rights in Canada : The foundation for development
  • 2005
  • Ingår i: International Journal of Entrepreneurship and Small Business. - : InderScience Publishers. - 1476-1297 .- 1741-8054. ; 2:2, s. 104-133
  • Tidskriftsartikel (refereegranskat)abstract
    • Throughout the middle decades of the 20th Century Indigenous people were the target of efforts to assist in economic development. In large part these externally developed, modernisation based efforts failed. In response, a second wave of Indigenous development has emerged; one in which Indigenous peoples are striving to rebuild their 'nations' and improve their lot through economic development 'on their own terms'. Key to this approach is the pursuit by Indigenous people of the recognition of their rights to their traditional lands and resources. This paper examines the emergence of this second wave of Indigenous development in Canada.
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  • Anderson, R. B., et al. (författare)
  • The Saskatchewan experience
  • 2007
  • Ingår i: International Handbook of Research on Indigenous Entrepreneurship. - Cheltenham : Edward Elgar Publishing. - 9781843768340 ; , s. 352-365
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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5.
  • Benson, Mikael, 1954, et al. (författare)
  • A haplotype in the inducible T-cell tyrosine kinase is a risk factor for seasonal allergic rhinitis.
  • 2009
  • Ingår i: Allergy. - : Wiley. - 1398-9995 .- 0105-4538. ; 64:9, s. 1286-91
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Identification of disease-associated single nucleotide polymorphisms (SNPs) in seasonal allergic rhinitis (SAR) may be facilitated by focusing on genes in a disease-associated pathway. OBJECTIVE: To search for SNPs in genes that belong to the T-cell receptor (TCR) pathway and that change in expression in allergen-challenged CD4+ cells from patients with SAR. METHODS: CD4+ cells from patients with SAR were analysed with gene expression microarrays. Allele, genotype and haplotype frequencies were compared in 251 patients and 386 healthy controls. RESULTS: Gene expression microarray analysis of allergen-challenged CD4+ cells from patients with SAR showed that 25 of 38 TCR pathway genes were differentially expressed. A total of 62 SNPs were analysed in eight of the 25 genes; ICOS, IL4, IL5, IL13, CSF2, CTLA4, the inducible T-cell tyrosine kinase (ITK) and CD3D. Significant chi-squared values were identified for several markers in the ITK kinase gene region. A total of five SNPs were nominally significant at the 5% level. Haplotype analysis of the five significant SNPs showed increased frequency of a haplotype that covered most of the coding part of ITK. The functional relevance of ITK was supported by analysis of an independent material, which showed increased expression of ITK in allergen-challenged CD4+ cells from patients, but not from controls. CONCLUSION: Analysis of SNPs in TCR pathway genes revealed that a haplotype that covers a major part of the coding sequence of ITK is a risk factor for SAR.
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6.
  • Benson, Mikael, 1954, et al. (författare)
  • Gene profiling reveals decreased expression of uteroglobin and other anti-inflammatory genes in nasal fluid cells from patients with intermittent allergic rhinitis
  • 2005
  • Ingår i: Clin Exp Allergy. - : Wiley. ; 35:4, s. 473-478
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Intermittent allergic rhinitis (IAR) results from interactions between a large number of pro- and anti-inflammatory mediators. Little is known about anti-inflammatory mediators in IAR. DNA microarrays allow simultaneous analysis of the whole transcriptome in a sample. OBJECTIVE: To identify anti-inflammatory transcripts in nasal fluid cells from patients with IAR during season and from healthy controls. METHODS: Nasal lavage fluids were obtained from 15 patients with symptomatic birch/and or grass pollen-induced IAR and 28 healthy controls. RNA was extracted from the nasal fluid cells and pooled into one patient- and one control pool. These were analysed with DNA microarrays containing more than 44,927 genes and variants. RESULTS: Seventeen thousand three hundred and fifty three genes were expressed in the controls and 17 928 in the patients. One thousand five hundred and seventy nine of the genes had higher expression in patients than in controls, and 1570 had lower expression in patients. Out of 189 up-regulated inflammatory genes, 187 were pro-inflammatory and two were anti-inflammatory. These genes regulated key steps of inflammation, ranging from influx of leukocytes to immunoglobulin production. By comparison, out of 49 down-regulated inflammatory genes, 36 were pro-inflammatory and 13 were anti-inflammatory. The anti-inflammatory gene that decreased most in expression in the patients was uteroglobin (also known as Clara Cell protein 16, CC16). The nasal fluid concentrations of uteroglobin protein were significantly lower in patients than in controls, 5.43+/-1.53 and 12.93+/-2.53 ng/mL, respectively (P<0.05). CONCLUSION: IAR is associated with decreased expression of uteroglobin and other anti-inflammatory genes.
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  • Veldtman, G R, et al. (författare)
  • Creation and enlargement of atrial defects in congenital heart disease.
  • 2005
  • Ingår i: Pediatric cardiology. - : Springer Science and Business Media LLC. - 0172-0643 .- 1432-1971. ; 26:2, s. 162-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Transcatheter creation and enlargement of interatrial defects (IAD) may improve hemodynamics; however, procedural outcomes have not been well defined. Hospital records were reviewed for children who underwent percutaneous procedures to create and enlarge an IAD and were grouped as follows: (1) right and (2) left heart obstructive lesions, (3) left atrial (LA) decompression during left heart assist, (4) failing Fontan circulation, and (5) miscellaneous. Forty-five children (mean age, 3.4 +/- 4.7 years; 30 (67%) male) were identified. In group 1 (n = 6), all achieved endpoints of right atrial (RA) decompression (n = 2), improved left ventricular filling (n = 3), or improved arterial saturations (n = 1). In group 2 (n = 18), mean LA pressure decreased (21 +/- 6 to 13 +/- 5 mmHg, p < 0.001) and arterial saturations increased (61 +/- 13% to 78 +/- 11%, p < 0.001). All except 2 patients achieved definitive repair, further palliation (n = 9), or heart transplantation (HTX) (n = 7). In group 3 (n = 5), the LA was decompressed (21 to 13 mmHg, p = 0.03) in all, and all except 1 patient survived to HTX (n = 2) or full recovery (n = 2). In group 4 (n = 11), of 7 patients with a low cardiac output syndrome after surgery, despite improved atrial shunting, 3 died and 1 required a HTX. In group 5 (n = 5), RA decompression (n = 1) or improved arterial saturation (n = 4) was achieved in all. Overall, 5-year HTX free survival was 75%. Mechanical ventilation before the procedure (p < 0.001), the need for a blade septostomy (p = 0.002), and higher LA pressures after the procedure (p = 0.04) independently predicted mortality or the requirement for HTX. Transcatheter optimization of an atrial communication can help optimize treatment strategies and has a low procedural risk.
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