| 1. |
- Buchwald, Pamela, et al.
(författare)
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ABC om divertikulit
- 2009
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Ingår i: Läkartidningen. - 0023-7205. ; 106:9, s. 594-597
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Tidskriftsartikel (refereegranskat)
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| 2. |
- Halvarsson, Britta, et al.
(författare)
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Phenotypic heterogeneity in hereditary nonpolyposis colorectal cancer: identical germline mutations associated with variable tumor morphology and immunohistochemical expression.
- 2007
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Ingår i: Journal of Clinical Pathology. - : BMJ. - 1472-4146 .- 0021-9746. ; 60:7, s. 781-786
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Hereditary non-polyposis colorectal cancer (HNPCC) is associated with high risks for colorectal and endometrial cancer, young age at onset and an increased risk of multiple primary tumours. Colorectal cancer in HNPCC is characterised by poor tumour differentiation, an expanding growth pattern, and a pronounced lymphocytic reaction with tumour-infiltrating lymphocytes. Aims and METHODS: The mutation spectrum in HNPCC is diverse and in order to clarify whether the HNPCC tumour phenotype is influenced by the underlying genetic alteration, 29 colorectal cancers and 12 adenomas from 24 individuals in two HNPCC families were morphologically and immunohistochemically characterised. RESULTS: The tumour morphology as well as the immunohistochemical expression of beta-catenin varied extensively within the families as well as between synchronous/metachronous colorectal cancers from the same individual. Poor tumour differentiation, an expanding growth pattern, and tumour-infiltrating lymphocytes occurred at higher frequencies in proximal tumours, whereas distal colorectal cancers often lacked distinct HNPCC-associated morphological features. CONCLUSIONS: The clinical, morphological and immunohistochemical variability observed within these families indicates that other mechanisms than the underlying germline mutation influence the HNPCC phenotype. Since morphological features linked to HNPCC are less frequent in distal cancers, it may be particularly relevant to obtain family history and age of onset in these tumours in order to identify individuals with HNPCC.
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| 3. |
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| 4. |
- Mangell, Peter, et al.
(författare)
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Critical role of P-selectin-dependent leukocyte recruitment in endotoxin-induced intestinal barrier dysfunction in mice.
- 2007
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Ingår i: Inflammation Research. - : Springer Science and Business Media LLC. - 1420-908X .- 1023-3830. ; 56:5, s. 189-194
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To define the importance of leukocyte recruitment in endotoxin-induced gut permeability. Materials and methods: 31 male C57BL/6 mice were challenged with lipopolysaccharide (LPS). Ileal permeability was measured in Ussing chambers and leukocyte-endothelium interactions studied with intravital fluorescence microscopy after 18 h. Results: LPS caused a clear-cut increase in leukocyte accumulation and intestinal permeability. Immunoneutralisation of P-selectin not only reduced leukocyte recruitment significantly (54% reduction) but also abolished endotoxin-induced intestinal leakage. Intestinal levels of pro-inflammatory chemokines increased markedly in response to LPS but were not influenced by inhibition of P-selectin in vivo. Conclusion: The present study shows not only that endotoxin-induced leukocyte recruitment is mediated by P-selectin but also that sepsis-associated intestinal leakage in the gut is largely regulated by leukocyte accumulation. Thus, our novel data demonstrate a critical link between P-selectin-dependent leukocyte recruitment and gut barrier failure in endotoxemia.
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| 5. |
- Mangell, Peter
(författare)
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On Lactobacillus plantarum 299v, bacterial translocation and intestinal permeability.
- 2007
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The gastrointestinal tract harbours a huge load of bacteria which exerts important biological functions to maintain health. In certain conditions the relation between commensal bacteria and pathogens may be set off balance, with an increase in number of pathogens and risk of bacterial translocation (BT). Disease and trauma may also render the intestinal barrier dysfunctional, inducing BT and increased permeability. Probiotic bacteria, i.e. living bacteria which, when ingested, exerts beneficial effects on the host, have been found to stabilize the intestinal mucosa and affect the intestinal microflora. The aim of this thesis was to study the effects of Lactobacillus plantarum 299v in relation to intestinal permeability and BT. In study I L. plantarum 299v normalized E. coli-induced permeability in distal ileum of rats. This effect was achieved with a more continuous supply of L. plantarum 299v, rather than intermittent or acute pretreatment. Study II showed that pretreatment with L. plantarum 299v prevented BT in rats rendered septic with LPS. The protective effect seemed to be dependent on the ability of L. plantarum 299v to adhere to intestinal mucosa, indicating competitive inhibition as a possible mechanism behind prevention of translocation. Moreover, treatment with prebiotics, without a probioticum, did not prevent translocation. In study III LPS-induced intestinal barrier dysfunction on rats was found to be regulated by P-selectin-dependent leukocyte recruitment. With anti-P-selectin antibody intestinal permeability was attenuated, as well as leukocyte rolling and adhesion. This indicates anti-P-selectin treatment as a mean of ameliorating barrier dysfunction in sepsis. Finally, in study IV, it was found that high doses of L. plantarum 299v given to patients undergoing colon surgery were not able to reduce translocation of selected enteric bacteria but seemed to have a stimulatory effect on bacterial load in the colon. Further, L. plantarum 299v could be given to patients with malignancy without risk of tumour proliferation. Taken together, the findings herein indicates a potential of L. plantarum 299v pretreatment in reducing BT and intestinal permeability and warrants further studies in the clinical setting.
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| 6. |
- Nilbert, Mef, et al.
(författare)
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Broad phenotypic spectrum in familial adenomatous polyposis; from early onset and severe phenotypes to late onset of attenuated polyposis with the first manifestation at age 72
- 2008
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Ingår i: BMC Medical Genetics. - : Springer Science and Business Media LLC. - 1471-2350. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Background: Familial adenomatous polyposis (FAP) is typically characterized by multiple colonic polyps and frequent extracolonic features. Whereas the number of colonic polyps has been linked to the APC gene mutation, possible genotype-phenotype correlations largely remain to be defined for the extracolonic manifestations. Methods: Full genomic sequencing combined with multiplex ligation-dependent probe amplification was used to identify APC gene mutations, which were correlated to the clinical presentations. Results: 10 novel APC gene mutations were identified in 11 families. A broad spectrum of extracolonic manifestations was identified in most of these individuals. Two sisters with an insertion in codon 528 (c.1582_1583insGC) both showed severe phenotypes with classical polyposis, upper gastrointestinal polyps and thyroid cancer. A woman with a 3'APC mutation (c.5030_5031 insAA) developed colon cancer at age 72 as the first manifestation of attenuated FAP. Conclusion: With an increasing number of FAP families diagnosed, a broad and variable tumor spectrum and a high frequency of extracolonic manifestations are gradually recognized. We report novel APC mutations and present two FAP cases that suggest familial aggregation of thyroid cancer and demonstrate the need to consider attenuated FAP also among elderly patients with colon cancer.
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