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Träfflista för sökning "WFRF:(Nordlander Sofia 1981) "

Sökning: WFRF:(Nordlander Sofia 1981)

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1.
  • Björk, Sofia, 1979, et al. (författare)
  • FutureFit SWEDEN
  • 2020
  • Annan publikation (övrigt vetenskapligt/konstnärligt)
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2.
  • Delbro, Dick, et al. (författare)
  • Nuclear expression of mu-opioid receptors in a human mesothelial cell line
  • 2009
  • Ingår i: Autonomic & Autacoid Pharmacology. - : Wiley. - 1474-8665 .- 1474-8673. ; 29:4, s. 165-170
  • Tidskriftsartikel (refereegranskat)abstract
    • 1 Possibly acting via mu-opioid receptors (MORs), morphine inhibits the formation ofexperimentally induced postoperative abdominal adhesions in rats. Mesothelial cells mayparticipate in adhesion formation by secreting mediators that interfere negatively withfibrinolysis. Morphine may prevent adhesions by inhibiting the release of pro-adhesionmediators from mesothelial cells. This study aimed to investigate whether human mesothelialcells express MOR-1; if so, such could constitute a site of action for morphine in adhesionprevention.2 Cells from Met-5A, a human mesothelial cell line were seeded and prepared forimmunocytochemistry and Western blotting.3 Immunocytochemistry showed MOR-1 expression in mesothelial cells, predominantly in thenuclei. Western blotting showed two bands (c. 35 and 50 kDa) which correspond to thoseobtained with a control lysate from cells known to express MORs. In addition, we foundMOR-1 expression with nuclear and cytoplasmatic localization in biopsies from humanabdominal adhesions.4 The current findings may suggest that morphine could interact directly with mesothelial cellsvia MOR-1 receptors, and thereby modulate adhesion formation, possibly by interfering withthe release of pro-adhesion factors from these cells
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3.
  • Iribarren, Cristina, 1993, et al. (författare)
  • Fecal luminal factors from patients with irritable bowel syndrome induce distinct gene expression of colonoids
  • 2022
  • Ingår i: Neurogastroenterology and Motility. - : Wiley. - 1350-1925 .- 1365-2982. ; 34:10
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Alteration of the host-microbiota cross talk at the intestinal barrier may participate in the pathophysiology of irritable bowel syndrome (IBS). Therefore, we aimed to determine effects of fecal luminal factors from IBS patients on the colonic epithelium using colonoids. Methods: Colon-derived organoid monolayers, colonoids, generated from a healthy subject, underwent stimulation with fecal supernatants from healthy subjects and IBS patients with predominant diarrhea, phosphate-buffered saline (PBS), or lipopolysaccharide (LPS). Cytokines in cell cultures and fecal LPS were measured by ELISA and mRNA gene expression of monolayers was analyzed using Qiagen RT2 Profiler PCR Arrays. The fecal microbiota profile was determined by the GA-map (TM) dysbiosis test and the fecal metabolite profile was analyzed by untargeted liquid chromatography/mass spectrometry. Key results: Colonoid monolayers stimulated with fecal supernatants from healthy subjects (n = 7), PBS (n = 4) or LPS (n = 3) presented distinct gene expression profiles, with some overlap ((RY)-Y-2 = 0.70, Q(2) = 0.43). Addition of fecal supernatants from healthy subjects and IBS patients (n = 9) gave rise to different gene expression profiles of the colonoid monolayers ((RY)-Y-2 = 0.79, Q(2) = 0.64). Genes (n = 22) related to immune response (CD1D, TLR5) and barrier integrity (CLDN15, DSC2) contributed to the separation. Levels of proinflammatory cytokines in colonoid monolayer cultures were comparable when stimulated with fecal supernatants from either donor types. Fecal microbiota and metabolite profiles, but not LPS content, differed between the study groups. Conclusions: Fecal luminal factors from IBS patients induce a distinct colonic epithelial gene expression, potentially reflecting the disease pathophysiology. The culture of colonoids from healthy subjects with fecal supernatants from IBS patients may facilitate the exploration of IBS related intestinal micro-environmental and barrier interactions.
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4.
  • Pettersson, Ann, 1982-, et al. (författare)
  • Expression of the endogenous, nicotinic acetylcholine receptor ligand, SLURP-1, in human colon cancer.
  • 2008
  • Ingår i: Autonomic & Autacoid Pharmacology. - : Wiley. - 1474-8665 .- 1474-8673. ; 28:4, s. 109-116
  • Tidskriftsartikel (refereegranskat)abstract
    • 1. Secreted mammalian Ly-6/urokinase plasminogen activator receptor-related protein-1 (SLURP-1) is a recently discovered endogenous ligand at the alpha7 subunit of the nicotinic acetylcholine receptors. Previous reports have shown that SLURP-1 is expressed in normal human keratinocytes seemingly with a pro-apoptotic function. Conversely, such expression was markedly attenuated in transformed cells and it was suggested that the molecule could convey protection against malignant transformation. 2. In this study, we demonstrated the mRNA expression (by RT-PCR) and protein expression (by Western blotting and immunocytochemistry) of SLURP-1 in the human colon cancer cell line, HT-29. 3. Furthermore, we demonstrated the expression of SLURP-1 (by immunohistochemistry) in tumour cells of human colon cancer tissue, and, to a greater extent, in immune and smooth muscle cells of adjacent, macroscopically tumour-free colon tissue. 4. The current findings suggest that SLURP-1 participates in the regulation of gut immune functions and motility, as well as possibly playing a role in colon carcinogenesis/cancer progression.
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5.
  • Sundin, Johanna, et al. (författare)
  • Colonic mast cell numbers, symptom profile, and mucosal expression of elements of the epithelial barrier in irritable bowel syndrome
  • 2019
  • Ingår i: Neurogastroenterology and Motility. - : Wiley. - 1350-1925 .- 1365-2982. ; 31:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Background This study aimed to determine whether patients with IBS displayed altered mucosal mast cell (MC) numbers and proportions of MCs co-localizing with nerves compared with healthy subjects (HS) and whether these MC characteristics correlated with IBS symptoms, elements of the epithelial barrier, or visceral sensitivity. Methods Mucosal MC characteristics were determined using immunoassay. IBS symptoms, gene expression of elements of the epithelial barrier, fecal serine protease activity, and visceral sensitivity were assessed. Key Results The MC numbers per mm(2) were 2.0 (0.0-6.0) in patients with IBS (n = 43) and 3.5 (1.1-9.1) in HS (n = 20, P = .26). Of these, MCs were 0.0 (0.0-20) % vs 3.1 (0.0-18) % (P = .76) in IBS and HS, respectively, in co-localization with nerve fibers. MC characteristics were equivalent in the different IBS subtypes. Hierarchical cluster analysis identified two distinct groups among patients with IBS: MC high (higher MC numbers and proportions of MCs co-localizing with nerves) and MC low (lower MC numbers and proportions of MCs co-localizing with nerves). The MC high and MC low groups could not be discriminated with regard to IBS symptoms, parameters of visceral sensitivity, gene expression of elements of the epithelial barrier, and fecal protease activity. Conclusion and Inferences There was no evidence of increased infiltration or altered localization of MCs in the colonic mucosa of patients with IBS. These MC characteristics were not linked to global IBS symptoms or mucosal expression of elements of the epithelial barrier. These findings indicate that quantity and location of mucosal MCs are factors not involved in the pathophysiology of IBS.
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6.
  • Sundin, Johanna, et al. (författare)
  • Evidence of altered mucosa-associated and fecal microbiota composition in patients with Irritable Bowel Syndrome
  • 2020
  • Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 10:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Altered bacterial composition and small intestinal bacterial overgrowth (SIBO) may be associated with irritable bowel syndrome (IBS). This study aimed to determine the fecal and mucosa-associated bacterial composition along the gastrointestinal (GI) tract and to assess SIBO in IBS. Bacterial composition of feces, and mucosa of the duodenum and sigmoid colon was determined by 16S rRNA-amplicon-sequencing. SIBO was evaluated by bacterial culture of duodenal aspirate, glucose and lactulose breath tests. Mucosal antibacterial gene expression was assessed by PCR Array. The bacterial profiles of feces and the mucosa of sigmoid colon, but not duodenum, differed between IBS patients (n = 17) and HS (n = 20). The IBS specific bacterial profiles were linked to the colonic antibacterial gene expression. Fecal bacterial profile differed between IBS subtypes, while the mucosa-associated bacterial profile was associated with IBS symptom severity and breath tests results at baseline (H-2 and/or CH4 >= 15 ppm). The prevalence of SIBO was similar between IBS patients and HS. This study demonstrates that alterations in the bacterial composition of the sigmoid colon of IBS patients were linked to symptoms and immune activation. While breath tests reflected the mucosa-associated bacterial composition, there was no evidence for high prevalence of SIBO or small intestinal bacterial alterations in IBS.
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