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Sökning: WFRF:(Henningsson A.)

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1.
  • Semb, G, et al. (författare)
  • Erratum
  • 2017
  • Ingår i: Journal of plastic surgery and hand surgery. - 2000-6764. ; 51:2, s. 158-158
  • Tidskriftsartikel (refereegranskat)
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2.
  • Sjöblom, A., et al. (författare)
  • Pre-oxygenation using high-flow nasal oxygen vs. tight facemask during rapid sequence induction
  • 2021
  • Ingår i: Anaesthesia. - : WILEY. - 0003-2409 .- 1365-2044. ; 76:9, s. 1176-1183
  • Tidskriftsartikel (refereegranskat)abstract
    • Pre-oxygenation using high-flow nasal oxygen can decrease the risk of desaturation during rapid sequence induction in patients undergoing emergency surgery. Previous studies were single-centre and often in limited settings. This randomised, international, multicentre trial compared high-flow nasal oxygen with standard facemask pre-oxygenation for rapid sequence induction in emergency surgery at all hours of the day and night. A total of 350 adult patients from six centres in Sweden and one in Switzerland undergoing emergency surgery where rapid sequence induction was required were included and randomly allocated to pre-oxygenation with 100% oxygen using high-flow nasal oxygen or a standard tight-fitting facemask. The primary outcome was the number of patients developing oxygen saturations <93% from the start of pre-oxygenation until 1 min after tracheal intubation. Data from 349 of 350 patients who entered the study were analysed (174 in the high-flow nasal oxygen group and 175 in the facemask group). No difference was detected in the number of patients desaturating <93%, five (2.9%) vs. six (3.4%) patients in the high-flow nasal oxygen and facemask group, respectively (p = 0.77). The risk of desaturation was not increased during on-call hours. No difference was seen in end-tidal carbon dioxide levels in the first breath after tracheal intubation or in the number of patients with signs of regurgitation between groups. These results confirm that high-flow nasal oxygen maintains adequate oxygen levels during pre-oxygenation for rapid sequence induction.
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3.
  • Wikell, A., et al. (författare)
  • The Impact of Borderline Quantiferon-TB Gold Plus Results for Latent Tuberculosis Screening under Routine Conditions in a Low-Endemicity Setting
  • 2021
  • Ingår i: Journal of Clinical Microbiology. - : AMER SOC MICROBIOLOGY. - 1098-660X .- 0095-1137. ; 59:12, s. 0137021-0137021
  • Tidskriftsartikel (refereegranskat)abstract
    • Quantiferon-TB Gold Plus (QFT-Plus) is an interferon gamma release assay used to diagnose latent tuberculosis (LTB). A borderline range (0.20 to 0.99 IU/ml) around the cutoff (0.35 IU/ml) has been suggested for the earlier QFT version. Our aims were to evaluate the borderline range for QFT-Plus and the contribution of the new TB2 antigen tube. QFT-Plus results were collected from clinical laboratories in Sweden and linked to incident active TB within 3 to 24 months using the national TB registry. Among QFT-Plus results from 58,539 patients, 83% were negative (<0.20 IU/ml), 2.4% were borderline negative (0.20 to 0.34 IU/ml), 3.4% were borderline positive (0.35 to 0.99 IU/ml), 9.6% were positive (≥1.0 IU/ml), and 1.6% were indeterminate. Follow-up tests after initial borderline results were negative (<0.20 IU/ml) in 38.3%, without any cases of incident active TB within 2 years. Applying the 0.35-IU/ml cutoff, 1.5% of TB1 and TB2 results were discrepant, of which 52% were within the borderline range. A TB2 result of ≥0.35 IU/ml with a TB1 result of <0.20 IU/ml was found in 0.4% (231/58,539) of all included baseline QFT-Plus test results, including 1.8% (1/55) of incident TB cases. A borderline range for QFT-Plus is clinically useful as more than one-third of those with borderline results are convincingly negative upon retesting, without developing incident active TB. The TB2 tube contribution to LTB diagnosis appears limited.
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5.
  • Henningsson, A. J., et al. (författare)
  • Rapid diagnosis of acute norovirus-associated gastroenteritis: evaluation of the Xpert Norovirus assay and its implementation as a 24/7 service in three hospitals in Jonkoping County, Sweden
  • 2017
  • Ingår i: European Journal of Clinical Microbiology and Infectious Diseases. - : SPRINGER. - 0934-9723 .- 1435-4373. ; 36:10, s. 1867-1871
  • Tidskriftsartikel (refereegranskat)abstract
    • Noroviruses are a leading cause of epidemic and sporadic cases of acute gastroenteritis worldwide. The rapid diagnosis of norovirus infection is important for prompt infection control measures and may reduce the need for additional diagnostic testing. Here we evaluated the performance of the rapid Xpert Norovirus assay, and assessed the turn-around time (TAT) before and after the implementation of the analysis as a 24/7 service at all the three hospitals in Jonkoping County, Sweden. We describe the implementation process which was performed in two steps during 2014. A total number of 276 clinical samples (stool and vomitus) from patients with symptoms of acute gastroenteritis were included in 2014-2015. The samples were analysed with the Xpert Norovirus assay and the already existing routine method: an in-house reverse transcription real-time PCR. Samples showing discrepant results with the two assays were further analysed by a third PCR method. The Xpert Norovirus assay performed well with a sensitivity of 100% and a specificity of 93% compared to the gold standard (defined as the result obtained by at least two of the three PCR methods). The median TAT decreased from 22 hours in 2013 to 2.4 hours in 2015 (p amp;lt; 0.001). We conclude that the performance of the Xpert Norovirus assay was excellent, and that the implementation of the analysis as a 24/7 service at all three hospitals in the county has greatly reduced the time to diagnosis which is beneficial for both patients and healthcare providers.
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9.
  • Silverpil, Elin, 1978, et al. (författare)
  • Negative feedback on IL-23 exerted by IL-17A during pulmonary inflammation
  • 2013
  • Ingår i: Innate Immunity. - : SAGE Publications. - 1753-4259 .- 1753-4267. ; 19:5, s. 479-492
  • Tidskriftsartikel (refereegranskat)abstract
    • It is now established that IL-17 has a broad pro-inflammatory potential in mammalian host defense, in inflammatory disease and in autoimmunity, whereas little is known about its anti-inflammatory potential and inhibitory feedback mechanisms. Here, we examined whether IL-17A can inhibit the extracellular release of IL-23 protein, the upstream regulator of IL-17A producing lymphocyte subsets, that is released from macrophages during pulmonary inflammation. We characterized the effect of IL-17A on IL-23 release in several models of pulmonary inflammation, evaluated the presence of IL-17 receptor A (RA) and C (RC) on human alveolar macrophages and assessed the role of the Rho family GTPase Rac1 as a mediator of the effect of IL-17A on the release of IL-23 protein. In a model of sepsis-induced pneumonia, intravenous exposure to Staphylococcus aureus caused higher IL-23 protein concentrations in cell-free bronchoalveolar lavage (BAL) samples from IL-17A knockout (KO) mice, compared with wild type (WT) control mice. In a model of Gram-negative airway infection, pre-treatment with a neutralizing anti-IL-17A Ab and subsequent intranasal (i.n.) exposure to LPS caused higher IL-23 and IL-17A protein concentrations in BAL samples compared with mice exposed to LPS, but pre-treated with an isotype control Ab. Moreover, i.n. exposure with IL-17A protein per se decreased IL- 23 protein concentrations in BAL samples. We detected IL-17RA and IL-17RC on human alveolar macrophages, and found that invitro stimulation of these cells with IL-17A protein, after exposure to LPS, decreased IL-23 protein in conditioned medium, but not IL-23 p19 or p40 mRNA. This study indicates that IL-17A can partially inhibit the release of IL-23 protein during pulmonary inflammation, presumably by stimulating the here demonstrated receptor units IL-17RA and IL-17RC on alveolar macrophages. Hypothetically, the demonstrated mechanism may serve as negative feedback to protect from excessive IL-17A signaling and to control antibacterial host defense once it is activated.
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