Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Willén Roger) ;srt2:(2005-2009)"

Sökning: WFRF:(Willén Roger) > (2005-2009)

  • Resultat 1-10 av 31
  • [1]234Nästa
Sortera/gruppera träfflistan
  • Lindahl, Bengt, et al. (författare)
  • Adjuvant tamoxifen in breast cancer patients affects the endometrium by time, an effect remaining years after end of treatment and results in an increased frequency of endometrial carcinoma.
  • 2008
  • Ingår i: Anticancer research. - International Institute of Cancer Research. - 1791-7530. ; 28:2B, s. 1259-1262
  • Tidskriftsartikel (refereegranskat)abstract
    • Tamoxifen is the most used adjuvant drug in breast cancer treatment. Its main action is as an anti-oestrogen, but in the endometrium of some patients it acts as an oestrogen. Some investigators have even reported an increased risk of developing endometrial carcinoma. The question of how to follow-up these patients and how to identify patients at risk of developing endometrial premalignant changes was investigated by the noninvasive ultrasound method. The follow-up of 292 patients from before the start of adjuvant treatment with tamoxifen and 94 without tamoxifen treatment was conducted at regular intervals. The changes in endometrial thickness as measured by ultrasound and histopathological changes are reported. A thicker endometrium was found in patients with receptor positive breast cancer even before the treatment with tamoxifen started. Cumulative increasing thickness was found during treatment and this thicker endometrium remained until almost 3 years after the end of treatment. If the endometrium was <3 mm after 3 months of treatment the probability that it would be thin after 5 years was high. An increased risk of developing endometrial carcinoma was found, however due to this regular follow-up the cancer was identified at an early stage.
  • Nilsson, Ingrid, et al. (författare)
  • Helicobacter ganmani infection associated with a spontaneous outbreak of inflammatory bowel-like disease in an IL-10-deficient mouse colony
  • 2008
  • Ingår i: Scandinavian Journal of Laboratory Animal Science. - Scandinavian Society for Laboratory Animal Science. - 0901-3393. ; 35:1, s. 13-24
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: A breeding colony of IL-10 deficient B6.129P2-Il10(tmICgn/J) mice, kept under conventional conditions, developed an inflammatory bowel-like disease (IBD) with rectal prolapse and blood tinged diarrhoea. No clinical signs of disease were observed at the time of arrival to our animal house. These animals were originally planned to serve as a negative control group in an experimental infection study with Helicobacter species to investigate colonization of the murine gut. Results: A spiral-shaped, Gram-negative bacterium was isolated from the breeding mice colony. In a first group of six animals, tissue specimens from the liver, small and large intestines, faeces and blood, were analysed by culture, PCR-denaturing gradient gel electrophoresis (PCR-DGGE), species-specific PCR assays and DNA-sequencing, histology and serology. Helicobacter ganmani, but no other Helicobacter species, was isolated from the liver, small bowel, caecum, colon and faeces. We found inflammation in caeca, colon and livers, most pronounced in the caecal areas of culture positive mice with a severe typhlitis with cystic dilatation of glandular structures and irregular crypt architecture. Some animals showed a pronounced colitis with mucosal and sub-mucosal inflammatory infiltrates. Other animals displayed large lymphoid infiltrates in the livers and hepatitis. Tissue samples and sera from 18 additional animals from the same breeding colony were analysed by the same methods, except for culture. H. ganmani was identified by PCR in most tissue samples of the 18 additional animals as well. Sero-conversion to H. ganmani correlated well with histopathological changes. Conclusions: Our findings emphasize the importance of using Helicobacter-free animals to develop murine models of chronic hepatitis and colitis.
  • Agnarsdóttir, Margrét, et al. (författare)
  • Malacoplakia and spermatic granuloma complicating vasectomy
  • 2006
  • Ingår i: Upsala Journal of Medical Sciences. - 0300-9734 .- 2000-1967. ; 111:2, s. 227-230
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Malacoplakia is a granulomatous disease with a histiocytic infiltrate containing calcified structures called Michaelis-Gutmann bodies. These structures are considered to represent an abnormal response to infection involving defective lysosomes and abnormal microbubular assembly. The disease most frequently involves urinary and genital tracts, but has also been described from most other organs. Here we present the first case of malacoplakia only involving the vas deferens.</p>
  • Agnarsdottir, Margret, et al. (författare)
  • Malacoplakia and spermatic granuloma complicating vasectomy
  • 2006
  • Ingår i: Uppsala Journal of Medical Sciences. - Taylor & Francis. - 0300-9734. ; 111:2, s. 227-230
  • Tidskriftsartikel (refereegranskat)abstract
    • Malacoplakia is a granulomatous disease with a histiocytic infiltrate containing calcified structures called Michaelis-Gutmann bodies. These structures are considered to represent an abnormal response to infection involving defective lysosomes and abnormal microbubular assembly. The disease most frequently involves urinary and genital tracts, but has also been described from most other organs. Here we present the first case of malacoplakia only involving the vas deferens.
  • Bengtsson, J., et al. (författare)
  • Can a failed ileal pouch anal anastomosis be left in situ?
  • 2007
  • Ingår i: Colorectal Disease. - 1462-8910 .- 1463-1318. ; 9:6, s. 503-508
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Objective: Failure after ileal pouch-anal anastomosis (IPAA) is reported with a frequency of 10-20%. The failed IPAA can be excised or defunctioned. Indications for excision and further management of an indefinitely diverted pouch are poorly described. The aim of the present investigation was to investigate pouch-related problems and the histopathological pattern of the pouch mucosa in this group of patients. Method: In a cohort of 620 patients having IPAA with a median follow-upof 14 years, 56 patients with failure were identified. The patients with defunctioned pouches were assessed with regard to pouch-related problems and endoscopy with biopsies was performed. Biopsies were stained with haematoxylin-eosin, PAS for neutral mucins and Alcian blue/high iron diamine for sialomucins/sulphomucins. Morphological changes were grouped into three types modified according to Veress and assessed for dysplasia. Results: Twenty-two patients withan indefinitely diverted pouch were found. The follow-up time after surgery for failure was 10 years. Thirteen patients completed the follow-up. Except for two patients with pelvic/perineal pain, there were no clinical problems. The majority of patients displayed mild to moderate macroscopic signs of inflammation. Morphologically, findings ranged from a preserved mucosal pattern to intense inflammatory reaction. No case of dysplasia or carcinoma was found. Conclusion: Most patients with an indefinitely diverted pouch had no complaints regarding the pouch. There was no case of dysplasia. Indefinite diversion may be preferable to pouch excision, especially given the associated morbidity.</p>
  • Bjursten, Malin, 1976-, et al. (författare)
  • Long-term treatment with anti-alpha 4 integrin antibodies aggravates colitis in G alpha i2-deficient mice.
  • 2005
  • Ingår i: European journal of immunology. - 0014-2980. ; 35:8, s. 2274-83
  • Tidskriftsartikel (refereegranskat)abstract
    • Targeted deletion of the heterotrimeric G protein, Galphai2, in mice induces lethal colitis closely resembling ulcerative colitis. In chronic colitis, migration of circulating leukocytes into the intestinal mucosa is partially dependent on alpha4 integrins. In previous studies, short-term administration of anti-alpha4 integrin antibodies has been shown to attenuate intestinal inflammation, and here we elucidate the effect of long-term administration of anti-alpha4 integrin antibodies on colitis in Galphai2(-/- )mice. Long-term blockade of alpha4 integrin significantly increased the severity of colitis in Galphai2(-/-) mice. The inflammation was confined to the colon, associated with increased cancer in situ, destruction of crypt architecture, and increased production of IL-1beta, TNF-alpha and IFN-gamma. Blockade of alpha4 integrin reduced the recruitment of activated T cells to the small intestine. In strong contrast, there were significantly higher numbers of activated T cells in the colonic lamina propria and epithelium, most probably due to in situ proliferation. Furthermore, treatment with alpha4 integrin antibodies induced decreased levels of total IgA and IgG in sera, whereas total IgM levels were unchanged. These new findings may have implications in the understanding of the progression of chronic intestinal inflammation.
  • Bjursten, Malin, 1976-, et al. (författare)
  • Transfer of colitis by Galphai2-deficient T lymphocytes: impact of subpopulations and tissue origin.
  • 2005
  • Ingår i: Inflammatory bowel diseases. - 1078-0998. ; 11:11, s. 997-1005
  • Tidskriftsartikel (refereegranskat)abstract
    • To elucidate the potential cell population(s) involved in the induction of colitis in inhibitory G protein Galphai2(-/-) mice, Galphai2-deficient or competent bone marrow or splenic and mesenteric lymph node (MLN) T cells were transferred into immunodeficient mice. The mice were followed up to 23 weeks after transfer, recording changes in body weight. Colitis was graded on hematoxylin and eosin-stained colonic tissue, and production of serum interleukin-18 and colon-derived interferon-gamma was measured using ELISA. After adoptive transfer of Galphai2(-/-) bone marrow, severe colitis developed in irradiated wild type recipients, whereas irradiated Galphai2(-/-) mice increased their life span more than 3 times after transfer of wild type bone marrow, accompanied by significant amelioration of colitis. Neither purified Galphai2(-/-) CD4(+), nor CD8(+) splenic or MLN-derived T cells could induce colitis in recombination-activating gene V(RAG) 2(-/-) recipient mice, whereas transfer of splenic Galphai2(-/-) CD3(+) T cells induced severe colitis. In contrast, transfer of Galphai2(-/-) CD3(+) T cells from the MLN caused only minor histopathological changes in the intestinal mucosa. Finally, serum levels of interleukin-18 and interferon-gamma production from colonic tissue cultures correlated well with disease severity. Our results show that bone marrow transplantation can prolong the life of Galphai2(-/-) mice and ameliorate intestinal inflammation. Splenic CD4(+) or CD8(+) T cells on their own were poor inducers of colitis, whereas the combination of both was highly involved in the induction of intestinal inflammation. Furthermore, we show that the tissue origin of CD3(+) T cells is critical for their potency to induce colitis.
  • Dahlgren, Eva, et al. (författare)
  • Sertoli-Leydig cell tumour in a postmenopausal woman showing all facets of the insulin resistance syndrome (IRS)
  • 2005
  • Ingår i: Ups J Med Sci. ; 110:3, s. 233-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Sertoli-Leydig cell tumours are rare sex stromal tumours with an incidence of < 0.5% of all ovarian tumours. Most frequently this tumour occurs in young women with a history of amenorrhoea, hirsutism and lowered pitch. Here, we report on a woman with IRS, postmenopausal virilization and increased testosterone levels due to a Sertoli-Leydig cell tumour. This is the first case to suggest an association between IRS and Sertoli-Leydig cell tumours. Furthermore, we highlight the difficulties in detecting this ovarian tumour with sonography.
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 31
  • [1]234Nästa
fritt online (2)
Typ av publikation
tidskriftsartikel (29)
bokkapitel (1)
forskningsöversikt (1)
Typ av innehåll
refereegranskat (30)
övrigt vetenskapligt (1)
Willén, Roger, (26)
Hultgren Hörnquist, ... (5)
Agnarsdóttir, Margré ... (3)
Carlén, Birgitta (3)
Ranstam, Jonas, (3)
Lindahl, Bengt, (3)
visa fler...
Walther, Bruno, (2)
Johansson, Jan (2)
Abu Al-Soud, Waleed, (2)
Nilsson, Hans-Olof, (2)
Wadström, Torkel, (2)
Nilsson, Ingrid, (2)
Gustavsson, Bengt, 1 ... (2)
Andolf, Ellika (2)
Lindahl, B (2)
Sturegård, Erik, (2)
Carlsson, Göran, 195 ... (2)
Gustavsson, Bengt (2)
Ingvar, Christian, (2)
Willen, R. (2)
Bland, Paul William, ... (2)
Persson, Jan, (1)
Hammarstrom, L, (1)
Nilsson, Staffan, 19 ... (1)
Engstrand, Lars, (1)
Nilsson, I, (1)
Saalman, Robert (1)
Nilsson, Staffan, (1)
Jansson, Per-Anders, ... (1)
Börjesson, L. (1)
Sundler, Frank, (1)
Jansson, Per-Anders (1)
Saksena, Pushpa (1)
Andolf, E, (1)
Wanders, Alkwin, (1)
Bengtsson, J (1)
Hultberg, A (1)
Månsson, Wiking, (1)
Lucas, Steven (1)
Ingvar, C (1)
Sturegard, E (1)
Falk, Peter, 1962-, (1)
Ivarsson, Marie-Loui ... (1)
Palmgren, Ingrid, 19 ... (1)
Måsbäck, Anna, (1)
Wadstrom, T (1)
Davidsson, Thomas (1)
Øresland, T, (1)
Rosen, T., (1)
Hultén, L. (1)
visa färre...
Uppsala universitet (17)
Göteborgs universitet (8)
Lunds universitet (5)
Karolinska Institutet (2)
Örebro universitet (1)
Chalmers tekniska högskola (1)
Engelska (30)
Svenska (1)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (26)


pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy