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Träfflista för sökning "WFRF:(Ekholm A.) srt2:(2005-2009)"

Sökning: WFRF:(Ekholm A.) > (2005-2009)

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  • Chamberlain, M A, et al. (författare)
  • Vocational rehabilitation : An educational review
  • 2009
  • Ingår i: Journal of rehabilitation. - : Medical Journals Sweden AB. - 0022-4154 .- 1650-1977 .- 1651-2081. ; 41:11, s. 856-869
  • Forskningsöversikt (refereegranskat)abstract
    • The aim of this review is to describe aspects of vocational rehabilitation relevant for a physician aiming to become a specialist in physical and rehabilitation medicine (PRM). The review discusses the epidemiology of incapacity for work, the major patient groups in vocational rehabilitation (musculoskeletal and psychiatric diagnoses comprise approximately 50-70% of the patients), the influence of different kinds of environmental and individual risk factors on work resumption (such as the legal framework, application of the law, resources for rehabilitation and its effectiveness, the degree of co-operation between vocational rehabilitation agencies, economic factors/labour market situation, medical and personal factors). The review describes different models of vocational rehabilitation, the effectiveness of various vocational rehabilitation programmes on work resumption or sick leave (where strong evidence is reported for multimodal rehabilitation programmes for patients with long-lasting musculoskeletal pain). Finally, there are sections about the PRM physician's history-taking in vocational rehabilitation (using the International Classification of Functioning, Disability and Health (ICF)), and report writing with a Structure where ICF body functions and activity limitations are reported separately.
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  • Vaziri-Sani, Fariba, et al. (författare)
  • Phenotypic expression of factor H mutations in patients with atypical hemolytic uremic syndrome
  • 2006
  • Ingår i: Kidney International. - : Nature Publishing Group. - 0085-2538 .- 1523-1755. ; 69:6, s. 981-988
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated the phenotypic expression of factor H mutations in two patients with atypical hemolytic uremic syndrome (HUS). Factor H in serum was assayed by rocket immunoelectrophoresis, immunoblotting, and double immunodiffusion and in tissue by immunohistochemistry. Functional activity was analyzed by hemolysis of sheep erythrocytes and binding to endothelial cells. A homozygous mutation in complement control protein (CCP) domain 10 of factor H was identified in an adult man who first developed membranoproliferative glomerulonephritis and later HUS. C3 levels were very low. The patient had undetectable factor H levels in serum and a weak factor H 150 kDa band. Double immunodiffusion showed partial antigenic identity with factor H in normal serum owing to the presence of factor H-like protein 1. Strong specific labeling for factor H was detected in glomerular endothelium, mesangium and in glomerular and tubular epithelium as well as in bone marrow cells. A heterozygous mutation in CCP 20 of factor H was found in a girl with HUS. C3 levels were moderately decreased at onset. Factor H levels were normal and a normal 150 kDa band was present. Double immunodiffusion showed antigenic identity with normal factor H. Factor H labeling was minimal in the renal cortex. Factor H dysfunction was demonstrated by increased sheep erythrocyte hemolysis and decreased binding to endothelial cells. In summary, two different factor H mutations associated with HUS were examined: in one, factor H accumulated in cells, and in the other, membrane binding was reduced.
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  • Ammoun, Sylwia, et al. (författare)
  • OX1 orexin receptors activate extracellular signal-regulated kinase in Chinese hamster ovary cells via multiple mechanisms : the role of Ca2+ influx in OX1 receptor signaling
  • 2006
  • Ingår i: Molecular Endocrinology. - : The Endocrine Society. - 0888-8809 .- 1944-9917. ; 20:1, s. 80-99
  • Tidskriftsartikel (refereegranskat)abstract
    • Activation of OX1 orexin receptors heterologously expressedin Chinese hamster ovary (CHO) cells led to a rapid, strong,and long-lasting increase in ERK phosphorylation (activation).Dissection of the signal pathways to ERK using multiple inhibitorsand dominant-negative constructs indicated involvement of Ras,protein kinase C, phosphoinositide-3-kinase, and Src. Most interestingly,Ca2+ influx appeared central for the ERK response in CHO cells,and the same was indicated in recombinant neuro-2a cells andcultured rat striatal neurons. Detailed investigations in CHOcells showed that inhibition of the receptor- and store-operatedCa2+ influx pathways could fully attenuate the response, whereasinhibition of the store-operated Ca2+ influx pathway alone orthe Ca2+ release was ineffective. If the receptor-operated pathwaywas blocked, an exogenously activated store-operated pathwaycould take its place and restore the coupling of OX1 receptorsto ERK. Further experiments suggested that Ca2+ influx, as such,may not be required for ERK phosphorylation, but that Ca2+,elevated via influx, acts as a switch enabling OX1 receptorsto couple to cascades leading to ERK phosphorylation, cAMP elevation,and phospholipase C activation. In conclusion, the data suggestthat the primary coupling of orexin receptors to Ca2+ influxallows them to couple to other signal pathways; in the absenceof coupling to Ca2+ influx, orexin receptors can act as signalintegrators by taking advantage of other Ca2+ influx pathways.
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  • Hellden, A, et al. (författare)
  • Death delusion
  • 2007
  • Ingår i: BMJ (Clinical research ed.). - 1756-1833. ; 335:7633, s. 1305-1305
  • Tidskriftsartikel (refereegranskat)
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