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Sökning: WFRF:(Lindh Emma)

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  • Askerlund, Therese, et al. (författare)
  • Småbarnsföräldrars konsumentbeteende : En kvantitativ studie om engagemang, säkerhetstänkande, värderingar och omgivningens påverkan på köpbeslut
  • 2008
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • Den här boken är resultat av åtta studenters arbete under en uppsatsperiod på tio veckor. Vi började träffas i mars 2008 och i april satte arbetet igång på allvar. Under perioden gjorde studenterna en enkät, samlade in data och analyserade för att komma fram till hur småbarnsföräldrar funderar kring inköp av artiklar åt sina barn. I slutet av maj var arbetet klart! Det har varit ett nöje att få handleda arbetet och jag känner mig stolt att som handledare få presentera den här boken, vars innehåll är väldigt rikt med tanke på under vilken kort period den skapats. Jag hoppas att den kommer att läsas av studenter i marknadsföring som vill ha inspiration till hur undersökningar om konsumentbeteende kan genomföras, eller som helt enkelt bara vill läsa sig mer om ämnet. Vi vill alla tacka några personer som engagerat sig i att hjälpa till med arbetet, genom att låta sig intervjuas, släppa in oss i sällskap av konsumerande föräldrar eller givit synpunkter på arbetet som helhet. Tack till Linn Söderlund, Nicolaus Eberhardt och Maria Hedlund. Cecilia Lindh, Maj 2008
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  • Eberhardson, Michael, et al. (författare)
  • Randomised, Double-blind, Placebo-controlled Trial of CCR9-targeted Leukapheresis Treatment of Ulcerative Colitis Patients.
  • 2017
  • Ingår i: Journal of Crohn's & colitis. - : Oxford University Press (OUP). - 1876-4479 .- 1873-9946. ; 11:5, s. 534-542
  • Tidskriftsartikel (refereegranskat)abstract
    • Ulcerative colitis patients display increased numbers of circulating pro-inflammatory monocyte human leukocyte antigen-DR [HLA-DRhi] monocytes expressing high levels of the gut-homing C-C chemokine receptor 9 [CCR9] and tumour necrosis factor [TNF]-α. The aim of this first-in-human, double-blind, randomised, placebo-controlled trial was to evaluate selective removal of circulating CCR9-expressing monocytes by leukapheresis in patients with moderate to severe ulcerative colitis, with regards to safety, tolerability, and immunological response.Patients with ulcerative colitis were treated every second day with leukapheresis during five sessions with a C-C chemokine ligand 25 [CCL25; CCR9 ligand] column or a placebo column.No major safety concerns were raised and the procedure was well tolerated. Pro-inflammatory HLA-DRhi cells decreased significantly in the active treatment group [p = 0.0391] whereas no statistically significant change was seen in the placebo group [p = 0.4688]. There was a significant decrease of HLA-DRhi monocytes in the active group compared with the placebo group when corrected for the imbalance in weight between the groups [p = 0.0105]. Mayo score decreased in the active group [p = 0.0156] whereas the change in the placebo group was not significant [p = 0.1250]. Mayo score ≤ 3 was observed in five out of 14 patients [35.7%] in the active group compared with one out of eight [12.5%] receiving placebo. The number of responders in the active treatment group was eight out of 14 patients [57.1%], whereas in the corresponding placebo group three out of eight patients [37.5%] responded to placebo. A dose-response correlation was observed between the blood volume processed and clinical outcome.This clinical induction trial using CCL25-tailored leukapheresis demonstrates a safe and effective removal of activated monocytes with a clinical effect in patients with ulcerative colitis.
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  • Gonzalez Lindh, Margareta, 1965-, et al. (författare)
  • Swallowing difficulties in adolescents : A case report and suggestion of treatment model
  • 2022
  • Ingår i: Clinical Case Reports. - : John Wiley & Sons. - 2050-0904. ; 10:8
  • Tidskriftsartikel (refereegranskat)abstract
    • Dysphagia or difficulty swallowing in childhood necessitates multi-disciplinary evaluation and management. This case report highlights the teamwork required for diagnostic work-up to distinguish functional dysphagia from organic and psychiatric conditions in an adolescent girl. Treatment model based on cognitive behavioral therapy is also presented.
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  • Gonzalez Lindh, Margareta, 1965-, et al. (författare)
  • Swallowing dysfunction in patients hospitalised due to a COPD exacerbation
  • 2021
  • Ingår i: ERJ Open Research. - : European Respiratory Society. - 2312-0541. ; 7:2, s. 00173-2021-
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: This cross-sectional study aimed to investigate the prevalence of self-reported and clinically screened swallowing dysfunction (dysphagia) in COPD patients with severe exacerbations and to identify any associated factors. Findings were then compared to a control group.Methods: Participants included 30 patients hospitalised due to a COPD exacerbation. The control group consisted of 30 adults hospitalised with acute cardiac symptoms. Data were derived from spirometry, the 150 mL timed water swallow test, a cookie swallow test and a dyspnoea questionnaire (modified Medical Research Council (mMRC)). Scores from the 10-item Eating Assessment Tool (EAT-10) were calculated to assess patient perception of swallowing dysfunction.Results: Self-reported swallowing dysfunction and clinical signs thereof were more common in COPD patients than in the control group (67% versus 23% and 80% versus 37%, respectively; p <= 0.001). Clinical signs of swallowing dysfunction in the group with acute exacerbation of COPD were associated with self-reported swallowing dysfunction (p=0.02) and xerostomia (p=0.04). Dyspnoea (mMRC >= 2) was more common among the COPD patients (90% versus 47%, p<0.001). There was a significant negative correlation between lung function and self-reported dysphagia (r=-0.39, p=0.03), but not between lung function and clinically screened dysphagia (r=-0.23, p=0.21).Conclusion: COPD patients hospitalised with an acute exacerbation experienced significantly more self-reported and clinically screened swallowing dysfunction compared to a control group of patients with cardiac symptoms. Both patient groups experienced dyspnoea, but it was twice as common in the group with acute exacerbation of COPD. Both groups also experienced xerostomia.
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  • Lindh, Emma, et al. (författare)
  • Autoimmunity and cystatin SA1 deficiency behind chronic mucocutaneous candidiasis in autoimmune polyendocrine syndrome type 1
  • 2013
  • Ingår i: Journal of Autoimmunity. - : Elsevier BV. - 0896-8411 .- 1095-9157. ; 42, s. 1-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Patients with the monogenic disease autoimmune polyendocrine syndrome type I (APSI) develop autoimmunity against multiple endocrine organs and suffer from chronic mucocutaneous candidiasis (CMC), a paradoxical complication with an unknown mechanism. We report here that saliva from APSI patients with CMC is defective in inhibiting growth of Candida albicans in vitro and show reduced levels of a salivary protein identified as cystatin SA1. In contrast, APSI patients without CMC express salivary cystatin SA1 and can inhibit C. albicans to the same extent as healthy controls. We evaluated the anti-fungal activity of cystatin SA1 and found that synthesized full length cystatin SA1 efficiently inhibits growth of C. albicans in vitro. Moreover, APSI patients exhibit salivary IgA autoantibodies recognizing myosin-9, a protein expressed in the salivary glands, thus linking autoimmunity to cystatin SA1 deficiency and CMC. This data suggests an autoimmune mechanism behind CMC in APSI and provides rationale for evaluating cystatin SA1 in antifungal therapy.
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  • Lindh, Emma (författare)
  • The autoimmune regulator : studies of immunological tolerance in mouse and man
  • 2009
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The aim of the work presented in this thesis was to investigate how failure in the mechanisms that regulate self-tolerance can lead to autoimmune disease. In particular, I have studied a key player in immunological tolerance, the autoimmune regulator gene (AIRE). Mutations in this gene lead to a severe autoimmune disorder called autoimmune polyendocrine syndrome type I (APS I). APS I patients suffer from a combination of diseases caused by the immunological destruction of various tissues and organs, mainly the endocrine organs. The most common disease components are hypoparathyroidism, adrenocortical insufficiency and chronic mucocutaneous candidiasis (CMC). It has been clearly shown that AIRE is involved in the negative selection of autoreactive thymocytes. The suggested mechanism is that AIRE induce expression of tissue-specific antigens (TSAs) in the thymus that are needed for the deletion of autoreactive thymocytes, but the exact molecular events and relative importance of this are controversial. The first publication on which this thesis is based, reports that AIRE is involved in the regulation of T cell-independent B cell-responses, and that B cells in Aire-/- mice have an increased activation status. This finding was thought to be connected to the increased serum levels of B cell activating factor of the TNF family (BAFF) found in both Aire-/- mice and APS I patients. The excessive BAFF was produced by AIRE-deficient dendritic cells upon IFN-gamma stimulation, which was independent of the presence of autoreactive T cells. It was suggested that AIRE regulates peripheral tolerance by inhibiting STAT1 signaling downstream of the IFN-gamma receptor. The second paper describes how AIRE deficiency results in impaired development of iNKT cells, which may contribute to the pathogenesis of APS I. This finding suggests that AIRE has other functions apart from inducing TSAs in the thymus, given that iNKT cells recognize lipid antigens and are not dependent on ectopic peptide expression in the thymus for their development. In the third paper, the mechanisms behind CMC in APS I are described. It is shown that APS I patients have defects in innate immune mechanisms, i.e. the anti-fungal activity of the saliva. The patients exhibit IgA autoantibodies recognizing salivary glands as an indication of ongoing immunological destruction. Furthermore, they lack expression of salivary cystatin SA1, a protein with potent anti-fungal activity. The final paper describes investigations into possible mechanisms governing thymocyte development in the absence of AIRE. This was performed in a system independent of TSA expression where endogenous superantigens mediate selection and activation of transgenic T cells specific for an ovalbumin peptide presented by H2-IAb (OT-II T cells). It was found that the OT-II T cells were reduced in Aire-/- mice compared to wild type littermates, and showed an immature phenotype. It was also found that the OT-II Aire-/- mice had increased TCR revision after activation in peripheral organs. The findings in Aire-/- mice and APS I patients presented in this thesis are not explained by reduced TSA expression in the thymus. They show that AIRE has additional functions in both central and peripheral tolerance.
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