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- Nettelbladt, C. G., et al.
(författare)
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Starvation increases the number of coliform bacteria in ceacum and induces bacterial adherence to caecal epithelium in rats
- 1997
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Ingår i: European Journal of Surgery. - Stockholm, Sweden : Taylor & Francis. - 1102-4151 .- 1741-9271. ; 163:2, s. 135-142
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To investigate the impact of starvation for 24 and 48 h on the number of coliform bacteria in the caecal contents, on the mucosal adherence of coliform bacteria, and on bacterial translocation in rats.Design: Open prospective study.Setting: University departments of surgery and microbiology, Sweden.Material: 46 adult male Sprague-Dawley rats.Interventions: 19 rats served as controls, and were fed until samples were taken. Six animals were starved for 24 h and another 15 for 48 h, with free access to water, and then anaesthetised before blood, mesenteric lymph nodes (MLN), caecum, and caecal contents were sampled. To verify bacterial translocation in this strain of rats, another six rats underwent controlled haemorrhage for 60 min to reduce the blood pressure to 55 mm Hg mean arterial pressure (MAP). These rats had free access to food and water before haemorrhage but were allowed only water until samples were taken 24 h after haemorrhage.Main Outcomes Measures: Presence and number of coliform bacteria in samples taken from caecal contents, caecal epithelium, MLN, and blood.Results: Starvation for 24 h increased the number of coliform bacteria (colony forming units (CFU)/g) in the caecal contents 25-fold (p < 0.05). Starvation for 48 h further increased the number by a factor of 100. The number of coliform bacteria that adhered to the caecal epithelium increased 3,000 times in rats that had been starved for 48 h (p < 0.001). There was no significant difference in translocation (as indicated by cultures from MLN) between rats that had been fed and those that had been starved for 48 h. In 4 of the 6 rats that were bled and then starved for 24 h there were signs of bacterial translocation, which was significantly more than the 1/19 in fed rats (p < 0.05).Conclusion: Starvation increases the number of bacteria in the caecal contents and increases bacterial adherence to the caecal epithelium. These changes may contribute to the previously reported increase in bacterial translocation in starved compared wit fed rats that were subjected to stress. The same changes in the gut were observed in animals subjected to haemorrhagic stress in addition to starvation, and in which bacterial translocation was evident.
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- Guan, Jikui, et al.
(författare)
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Clinical response of the novel activating ALK-I1171T mutation in neuroblastoma to the ALK inhibitor ceritinib.
- 2018
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Ingår i: Cold Spring Harbor molecular case studies. - : Cold Spring Harbor Laboratory. - 2373-2873. ; 4:4
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Tidskriftsartikel (refereegranskat)abstract
- Tumors with Anaplastic Lymphoma Kinase (ALK) fusion rearrangements, including non-small cell lung cancer and anaplastic large cell lymphoma, are highly sensitive to ALK tyrosine kinase inhibitors (TKIs), underscoring the notion that such cancers are addicted to ALK activity. While mutations in ALK are heavily implicated in childhood neuroblastoma, response to the ALK TKI crizotinib has been disappointing. Embryonal tumors in patients with DNA repair defects such as Fanconi anemia (FA) often have a poor prognosis, due to lack of therapeutic options. Here we report a child with underlying FA and ALK mutant high-risk neuroblastoma responding strongly to precision therapy with the ALK TKI ceritinib. Conventional chemotherapy treatment caused severe, life-threatening toxicity. Genomic analysis of the initial biopsy identified germ-line FANCA mutations as well as a novel ALK-I1171T variant. ALK-I1171T generates a potent gain-of-function mutant, as measured in PC12 cell neurite outgrowth and NIH3T3 transformation. Pharmacological inhibition profiling of ALK-I1171T in response to various ALK TKIs identified an 11-fold improved inhibition of ALK-I1171T with ceritinib when compared with crizotinib. Immunoaffinity-coupled LC-MS/MS phosphoproteomics analysis indicated a decrease in ALK signaling in response to ceritinib. Ceritinib was therefore selected for treatment in this child. Mono-therapy with ceritinib was well tolerated and resulted in normalized catecholamine markers and tumor shrinkage. After 7.5 months treatment, residual primary tumor was surgically removed and exhibited hallmarks of differentiation together with reduced Ki67 levels. Clinical follow-up after 21 months treatment revealed complete clinical remission including all metastatic sites. Therefore, ceritinib presents a viable therapeutic option for ALK-positive neuroblastoma.
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- HELLSTROM, PM, et al.
(författare)
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Role of bile in regulation of gut motility
- 1995
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Ingår i: Journal of internal medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 237:4, s. 395-402
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Tidskriftsartikel (refereegranskat)
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