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Sökning: WFRF:(Sandgren S)

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  • van der Meer, PF, et al. (författare)
  • Aggregates in platelet concentrates
  • 2015
  • Ingår i: Vox sanguinis. - : Wiley. - 1423-0410 .- 0042-9007. ; 108:1, s. 96-125
  • Tidskriftsartikel (refereegranskat)
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  • Getahun, H, et al. (författare)
  • Management of latent Mycobacterium tuberculosis infection: WHO guidelines for low tuberculosis burden countries
  • 2015
  • Ingår i: The European respiratory journal. - : European Respiratory Society (ERS). - 1399-3003 .- 0903-1936. ; 46:6, s. 1563-1576
  • Tidskriftsartikel (refereegranskat)abstract
    • Latent tuberculosis infection (LTBI) is characterised by the presence of immune responses to previously acquired Mycobacterium tuberculosis infection without clinical evidence of active tuberculosis (TB). Here we report evidence-based guidelines from the World Health Organization for a public health approach to the management of LTBI in high risk individuals in countries with high or middle upper income and TB incidence of <100 per 100 000 per year. The guidelines strongly recommend systematic testing and treatment of LTBI in people living with HIV, adult and child contacts of pulmonary TB cases, patients initiating anti-tumour necrosis factor treatment, patients receiving dialysis, patients preparing for organ or haematological transplantation, and patients with silicosis. In prisoners, healthcare workers, immigrants from high TB burden countries, homeless persons and illicit drug users, systematic testing and treatment of LTBI is conditionally recommended, according to TB epidemiology and resource availability. Either commercial interferon-gamma release assays or Mantoux tuberculin skin testing could be used to test for LTBI. Chest radiography should be performed before LTBI treatment to rule out active TB disease. Recommended treatment regimens for LTBI include: 6 or 9 month isoniazid; 12 week rifapentine plus isoniazid; 3–4 month isoniazid plus rifampicin; or 3–4 month rifampicin alone.
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  • Hjelmfors, A-L, et al. (författare)
  • Patient perspectives of prognosis communication
  • 2017
  • Ingår i: European Journal of Cardiovascular Nursing. - : Sage Publications. - 1474-5151 .- 1873-1953. ; 16:Suppl. 1, s. S65-S66
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Several studies describe that patients with heart failure (HF) find it important to discuss prognosis and that they want to be informed about the expectations about the illness progression. However, little is known about their actual preferences for professional communication about prognosis.Purpose: to explore patient’s perspectives regarding communication with health care professionals about the HF prognosis.Methods: 15 patients participated in focus group interviews and a further 9 patients completed individual semi-structured interviews. The patients (75% men, 52-87 years of age) were in NYHA I-III, and were not diagnosed with any other major life threatening disease. Data was analysed using thematic analysis to identify and interpret patterns in the data.Results: One overarching theme was identified: “The tension between hoping for the best and preparing for the worst” with three sub-themes. Ignorance is bliss. Describes how patients preferred to avoid thinking about the HF prognosis because they did not want to lose hope for the future. They lived one day at the time, focusing on here and now, wanting to forget about the illness altogether. Patients also preferred to decide themselves whether they wanted to talk about the prognosis with professionals or not. Nothing but the truth. Describes how patients wanted to know the objective and absolute truth about their illness and its’ prognosis and were afraid to live under false expectations. The truth about their prognosis was that they might die because of their illness. Even though the truth may hurt, they believed that knowing the truth was necessary to live as good as possible. Good news only. Patients described that they knew that HF was a chronic illness but they were ambivalent in their approach towards discussing prognosis. They wanted to know the truth about their prognosis, but at the same time they did not want to know anything since they fear they might hear something they do not want to, as this may hurt. They only wanted to receive “good” and positive information from the professionals, since they perceived such information to be something that they can benefit from.Conclusions: This study shows that patients have different preferences for communication about prognosis and uses different approaches in order to cope living with a serious condition such as heart failure. Professionals need to respect the strategies a patient uses, and be ready to support the patient according to their needs, preferences and life situation.
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  • Köhn, Linda, et al. (författare)
  • Breakpoint characterization of a novel approximately 59 kb genomic deletion on 19q13.42 in autosomal-dominant retinitis pigmentosa with incomplete penetrance.
  • 2009
  • Ingår i: European Journal of Human Genetics. - : Springer Science and Business Media LLC. - 1018-4813 .- 1476-5438. ; 17:5, s. 651-655
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to identify and characterize the underlying molecular mechanisms in autosomal-dominant retinitis pigmentosa (adRP) with incomplete penetrance in two Swedish families. An extended genealogical study and haplotype analysis indicated a common origin. Mutation identification was carried out by multiplex ligation-dependent probe amplification (MLPA) and sequencing. Clinical examinations of adRP families including electroretinography revealed obligate gene carriers without abnormalities, which indicated incomplete penetrance. Linkage analysis resulted in mapping of the disease locus to 19q13.42 (RP11). Sequence analyses did not reveal any mutations segregating with the disease in eight genes including PRPF31. Subsequent MLPA detected a large genomic deletion of 11 exons in the PRPF31 gene and, additionally, three genes upstream of the PRPF31. Breakpoints occurred in intron 11 of PRPF31 and in LOC441864, 'similar to osteoclast-associated receptor isoform 5.' An almost 59 kb deletion segregated with the disease in all affected individuals and was present in several asymptomatic family members but not in 20 simplex RP cases or 94 healthy controls tested by allele-specific PCR. A large genomic deletion resulting in almost entire loss of PRPF31 and three additional genes identified as the cause of adRP in two Swedish families provide an additional evidence that mechanism of the disease evolvement is haploinsufficiency. Identification of the deletion breakpoints allowed development of a simple tool for molecular testing of this genetic subtype of adRP.
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