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Sökning: WFRF:(Willén Roger)

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  • Föregående 12[3]4567Nästa
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21.
  • Elgbratt, Kristina, 1969-, et al. (författare)
  • Aberrant T-cell ontogeny and defective thymocyte and colonic T-cell chemotactic migration in colitis-prone Galphai2-deficient mice.
  • 2007
  • Ingår i: Immunology. - 0019-2805. ; 122:2, s. 199-209
  • Tidskriftsartikel (refereegranskat)abstract
    • Galphai2-deficient mice, which spontaneously develop colitis, have previously been reported to have an increased frequency of mature, single positive thymocytes compared to wild-type mice. In this study we further characterized the intrathymic changes in these mice before and during overt colitis. Even before the onset of colitis, Galphai2(-/-) thymi weighed less and contained fewer thymocytes, and this was exacerbated with colitis development. Whereas precolitic Galphai2(-/-) mice had unchanged thymocyte density compared to Galphai2(+/-) mice of the same age, this was significantly decreased in mice with colitis. Thymic atrophy in Galphai2(-/-) mice involved mainly the cortex. Using a five-stage phenotypic characterization of thymocyte maturation based on expression of CD4, CD8, TCRalphabeta, CD69 and CD62L, we found that both precolitic and colitic Galphai2(-/-) mice had significantly increased frequencies of mature single-positive CD4(+) and CD8(+) medullary thymocytes, and significantly reduced frequencies and total numbers of immature CD4(+) CD8(+) double-positive thymocytes compared to Galphai2(+/-) mice. Furthermore, cortical and transitional precolitic Galphai2(-/-) thymocytes showed significantly reduced chemotactic migration towards CXCL12, and a trend towards reduced migration to CCL25, compared to wild-type thymocytes, a feature even more pronounced in colitic mice. This impaired chemotactic migration of Galphai2(-/-) thymocytes could not be reversed by increased chemokine concentrations. Galphai2(-/-) thymocytes also showed reduced expression of the CCL25 receptor CCR9, but not CXCR4, the receptor, for CXCL12. Finally, wild-type colonic lamina propria lymphocytes migrated in response to CXCL12, but not CCL25 and, as with thymocytes, the chemokine responsiveness was significantly reduced in Galphai2(-/-) mucosal lymphocytes.
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22.
  • Fredin, Maria Fritsch, 1970-, et al. (författare)
  • The application and relevance of ex vivo culture systems for assessment of IBD treatment in murine models of colitis
  • 2008
  • Ingår i: Pharmacological Research. - 1043-6618. ; 58:3-4, s. 222-231
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to investigate the relevance of mouse ex vivo cultures as a first screening model for new therapeutic agents of Inflammatory Bowel Disease (IBD). Two murine models (dextran sodium sulphate (DSS)-induced colitis and Gαi2-deficient mice) and two anti-inflammatory agents (methyl-prednisolone and the proteasome inhibitor MG132) were evaluated. The in vivo effects of methyl-prednisolone were assessed in both models. Ex vivo colonic tissue from both mouse models were cultured in the presence or absence of the drugs and TaqMan Low-Density arrays were used to assess the regulation of inflammatory genes before and after drug treatment. Colitis induced a similar inflammatory gene profile in both mouse models in in vivo studies and in ex vivo cultures. The differences encountered reflected the different phases of colitis in the models, e.g. innate cytokine/chemokine profile in the DSS model and T cell related markers in Gαi2-deficient mice. After steroid treatment, a similar pattern of genes was suppressed in the two mouse models. We confirmed the suppression of inflammatory gene expression for IL-1β, IL-6 and iNOS in ex vivo and in vivo colons from both mouse models by quantitative RT-PCR. Importantly, the inflammatory responses in the murine ex vivo culture system reflected the in vivo response in the inflamed colonic tissue as assessed by changes in inflammatory gene expression, suggesting that the murine culture system can be used for validation of future IBD therapies.
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23.
  • Friberg, Britt, et al. (författare)
  • Endometrial destruction by hyperthermia - A possible treatment of menorrhagia : An experimental study
  • 1996
  • Ingår i: Acta Obstetricia et Gynecologica Scandinavica. - Wiley-Blackwell. - 0001-6349. ; 75:4, s. 330-335
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Treatment of menorrhagia by heat-destruction of the endometrium, intended to be an alternative to hysterectomy, was investigated in an experimental study. Method. A specially designed catheter (Cavaterm™) with a silicone balloon containing a self-regulating heating element is inserted into the uterus, rilled with glycine to a pressure of around 180 mmHg and heated to about 75°C. We investigated the treatment effect in vitro in rive extirpated uteri (series A) and in vivo in three patients treated peroperatively just before hysterectomy, temperatures being monitored in the surrounding tissues (series B). In both series we monitored the following variables: heating-power, balloon-pressure, temperature of the heating element (around 85°C) and the temperatures at five locations from top to bottom of the balloon surface. Results. After 30 min in vitro treatment at 75°C, the endometrium was partly destructed, and condensed. Histological examination showed smooth muscle cells to be destroyed to a depth of 2-5 mm close to the endometrium. With in vivo treatment for 30 min at a heating power of about 20 W (resulting in balloon surface temperatures of 58-65°C). the increases in temperature of the surrounding tissue were too small to measure accurately (±1°C). Histological examination showed destruction of cells in the corpus uteri to a maximum depth of 8 mm. Conclusion. Findings in in vitro and in vivo experiments suggest that 30 min heating of the endometrium to 58-65°C with an intrauterine silicone balloon filled with a liquid to a pressure of 180 mmHg exerts therapeutic effects on both endometrium and uterine cavity smooth muscle cells without damage to surrounding tissues.
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24.
  • Friberg, Britt, et al. (författare)
  • Endometrial destruction by thermal coagulation : Evaluation of a new form of treatment for menorrhagia
  • 1998
  • Ingår i: Gynaecological Endoscopy. - 0962-1091. ; 7:2, s. 73-78
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. To report the first clinical evaluation of a new balloon endometrial, thermal destruction system Cavaterm®, for outpatient treatment of menorrhagia. Design. To elucidate possible technical problems during treatment, to evaluate how the patients tolerated the treatment and to judge which patients were suitable for this form of treatment. Main outcome measures. Measurements of bleeding volumes in pads and tampons before and after treatment were performed as well as subjective evaluation by bleeding charts. Patients also estimated their degree of satisfaction. Setting. Gynaecology department at a university hospital. Subjects. 36 patients under 52 pears of age with menorrhagia, without suspicion of intracavitary pathology including malignancy. Results. No procedure-related complications occurred. The patients tolerated the treatment well. There was a significant reduction in measured bleeding volumes in pads and tampons, collected during one menstruation, 2-7 months after treatment compared with measurements before treatment. Four patients subsequently underwent hysterectomy and should not have been included in the study (two with pedunculated myoma and one with a septum; the fourth showed premalignant endometrial changes in the curettage preceding the treatment). At 18-28-month follow up, 29 of the suitable patients (91%) reported a significant reduction in bleeding and another three patients reported reduced but still profuse bleeding compared with pretreatment; 88% (28/32) rated the treatment results as excellent, and a further 9% (3/32) as good. Conclusions. We found the Cavaterm® system for endometrial destruction to be safe, efficient and easy to use.
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25.
  • Fritsch Fredin, Maria, et al. (författare)
  • The application and relevance of ex vivo culture systems for assessment of IBD treatment in murine models of colitis
  • 2008
  • Ingår i: Pharmacological Research. - 1043-6618 .- 1096-1186. ; 58:3-4, s. 222-231
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The aim of this study was to investigate the relevance of mouse ex vivo cultures as a first screening model for new therapeutic agents of Inflammatory Bowel Disease (IBD). Two murine models (dextran sodium sulphate (DSS)-induced colitis and Galphai2-deficient mice) and two anti-inflammatory agents (methyl-prednisolone and the proteasome inhibitor MG132) were evaluated. The in vivo effects of methyl-prednisolone were assessed in both models. Ex vivo colonic tissue from both mouse models were cultured in the presence or absence of the drugs and TaqMan Low-Density arrays were used to assess the regulation of inflammatory genes before and after drug treatment. Colitis induced a similar inflammatory gene profile in both mouse models in in vivo studies and in ex vivo cultures. The differences encountered reflected the different phases of colitis in the models, e.g. innate cytokine/chemokine profile in the DSS model and T cell related markers in Galphai2-deficient mice. After steroid treatment, a similar pattern of genes was suppressed in the two mouse models. We confirmed the suppression of inflammatory gene expression for IL-1beta, IL-6 and iNOS in ex vivo and in vivo colons from both mouse models by quantitative RT-PCR. Importantly, the inflammatory responses in the murine ex vivo culture system reflected the in vivo response in the inflamed colonic tissue as assessed by changes in inflammatory gene expression, suggesting that the murine culture system can be used for validation of future IBD therapies.</p>
  •  
26.
  • Fritsch Fredin, Maria, et al. (författare)
  • The application and relevance of ex vivo culture systems for assessment of IBD treatment in murine models of colitis
  • 2008
  • Ingår i: Pharmacological Research. - 1043-6618 .- 1096-1186. ; 58:3-4, s. 222-231
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The aim of this study was to investigate the relevance of mouse ex vivo cultures as a first screening model for new therapeutic agents of Inflammatory Bowel Disease (IBD). Two murine models (dextran sodium sulphate (DSS)-induced colitis and Galphai2-deficient mice) and two anti-inflammatory agents (methyl-prednisolone and the proteasome inhibitor MG132) were evaluated. The in vivo effects of methyl-prednisolone were assessed in both models. Ex vivo colonic tissue from both mouse models were cultured in the presence or absence of the drugs and TaqMan Low-Density arrays were used to assess the regulation of inflammatory genes before and after drug treatment. Colitis induced a similar inflammatory gene profile in both mouse models in in vivo studies and in ex vivo cultures. The differences encountered reflected the different phases of colitis in the models, e.g. innate cytokine/chemokine profile in the DSS model and T cell related markers in Galphai2-deficient mice. After steroid treatment, a similar pattern of genes was suppressed in the two mouse models. We confirmed the suppression of inflammatory gene expression for IL-1beta, IL-6 and iNOS in ex vivo and in vivo colons from both mouse models by quantitative RT-PCR. Importantly, the inflammatory responses in the murine ex vivo culture system reflected the in vivo response in the inflamed colonic tissue as assessed by changes in inflammatory gene expression, suggesting that the murine culture system can be used for validation of future IBD therapies.</p>
  •  
27.
  • Gotlind, Yu-Yuan, et al. (författare)
  • Interplay between T(h)1 and T(h)17 effector T-cell pathways in the pathogenesis of spontaneous colitis and colon cancer in the Gi2-deficient mouse
  • 2013
  • Ingår i: International Immunology. - 0953-8178 .- 1460-2377. ; 25:1, s. 35-44
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Colitis induced by Gi2-knockout features both T(h)1 and T(h)17 responses.Gi2-deficient mice spontaneously develop colitis. Using xMAP technology and RTPCR, we investigated cytokine/chemokine profiles during histologically defined phases of disease: (i) no/mild, (ii) moderate, (iii) severe colitis without dysplasia/cancer and (iv) severe colitis with dysplasia/cancer, compared with age-matched wild-type (WT) littermates. Colonic dysplasia was observed in 4/11 mice and cancer in 1/11 mice with severe colitis. The histology correlated with progressive increases in colon weight/cm and spleen weight, and decreased thymus weight, all more advanced in mice with dysplasia/cancer. IL-1, IL-6, IL-12p40, IL-17, TNF-, CCL2 and CXCL1 protein levels in colons, but not small intestines increased with colitis progression and were significantly increased in mice with moderate and severe colitis compared with WT mice, irrespective of the absence/presence of dysplasia/cancer. CCL5 did not change during colitis progression. Colonic IL-17 transcription increased 40- to 70-fold in all stages of colitis, whereas IFN- mRNA was gradually up-regulated 12- to 55-fold with colitis progression, and further to 62-fold in mice with dysplasia/cancer. IL-27 mRNA increased 4- to 15-fold during the course of colitis, and colonic IL-21 transcription increased 3-fold in mice with severe colitis, both irrespective of the absence/presence of dysplasia/cancer. FoxP3 transcription was significantly enhanced (3.5-fold) in mice with moderate and severe colitis, but not in mice with dysplasia/cancer, compared with WT mice. Constrained correspondence analysis demonstrated an association between increased protein levels of TNF-, CCL2, IL-1, IL-6 and CXCL1 and dysplasia/cancer. In conclusion, colonic responses are dominated by a mixed T(h)1/T(h)17 phenotype, with increasing T(h)1 cytokine transcription with progression of colitis in Gi2(/) mice.</p>
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28.
  • Holgersson, Georg, et al. (författare)
  • The prognostic value of pre-treatment thrombocytosis in two cohorts of patients with non-small cell lung cancer treated with curatively intended chemoradiotherapy
  • 2017
  • Ingår i: Neoplasma (Bratislava). - Bratislava : AEPress. - 0028-2685 .- 1338-4317. ; 64:6, s. 909-915
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Chemoradiotherapy is the standard of care for inoperable stage III non-small cell lung cancer (NSCLC). This treatment, however, offers only a small chance of cure and is associated with many side effects. Little research has been made concerning which patients benefit most/least from the treatment. The present study evaluates the prognostic value of anemia, leukocytosis and thrombocytosis at diagnosis in this treatment setting. In the present study, data were collected retrospectively for 222 patients from two different phase II studies conducted between 2002-2007 in Sweden with patients treated with chemoradiotherapy for stage IIIA-IIIB NSCLC. Clinical data and the serum values of hemoglobin (Hgb), White blood cells (WBC) and Platelets (Plt) at enrollment were collected for all patients and studied in relation to overall survival using Kaplan-Meier product-limit estimates and a multivariate Cox proportional hazards regression model. The results showed that patients with thrombocytosis (Plt &gt; 350 x 109 /L) had a shorter median overall survival (14.5 months) than patients with normal Plt at baseline (23.7 months). Patients with leukocytosis (WBC &gt; 9 x 109 /L) had a shorter median survival (14.9 months) than patients with a normal WBC at baseline (22.5 months). However, in a multivariate model including all lab parameters and clinical factors, only thrombocytosis and performance status displayed a prognostic significance. In Conclusion, thrombocytosis showed to be an independent prognostic marker associated with shorter overall survival in stage III NSCLC treated with curatively intended chemoradiotherapy. This knowledge can potentially be used together with established prognostic factors, such as performance status when choosing the optimal therapy for the individual patient in this clinical setting</p>
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