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- Papadopoulos, Konstantinos I., et al.
(författare)
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Autoimmunity in sarcoidosis : the tip of the Iceberg
- 2023
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Ingår i: Clinical and Experimental Medicine. - : Springer Science and Business Media LLC. - 1591-8890 .- 1591-9528. ; 23, s. 951-953
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Tidskriftsartikel (refereegranskat)abstract
- Sarcoidosis is a mysterious condition with an etiology that has to date eluded explanation. Innumerable clinical and serological organ- and non-organ-specific autoimmune associations have been reported. Many of the associated conditions are life-threatening but easily manageable if diagnosed early. Due to the long latency that precedes the clinical onset of autoimmune diseases, it is prudent to ensure a long follow-up and a broad viewing perspective while maintaining a high index of suspicion when viewing the autoimmunity iceberg in sarcoidosis.
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- Zhang, Wei, et al.
(författare)
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Knockdown of MMP-7 inhibits cell proliferation and enhances sensitivity to 5-fluorouracil and X-ray irradiation in colon cancer cells
- 2014
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Ingår i: Clinical and Experimental Medicine (Testo stampato). - : Springer Verlag (Germany). - 1591-8890 .- 1591-9528. ; 14:1, s. 99-106
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Tidskriftsartikel (refereegranskat)abstract
- The role of matrix metalloproteinase-7 (MMP-7) in the pathogenesis of colon cancer is not understood thoroughly. Previous studies from our group have shown that the expression levels of MMP-7 were highly elevated in colorectal cancer patient specimens and were correlated with Dukes Staging, histological differentiation grade and CEA level. The goal of this study was to investigate the cellular impact of MMP-7 in colon cancer. In this study, we used the SW480 colon cancer cell lines of MMP-7 knockdown by lentivirus-mediated RNA interference as a model system to investigate the impact of MMP-7 on cell proliferation and sensitivity to 5-Fluorouracil (5-FU) and X-ray irradiation (IR). Cell proliferation and sensitivity to 5-FU and IR were measured by MTT assay and colony formation assay. Cell cycle was evaluated by flow cytometry. We showed that the down regulation of MMP-7 inhibits colon cancer cell proliferation and sensitizes tumour cells to 5-FU and IR (P less than 0.05). Decreased MMP-7 expression in SW480 cells by RNA interference triggered cell cycle arrest at G1 phase (P less than 0.05). Down regulation of MMP-7 may inhibit the cell proliferation of colon cancer cells and increase tumour cells sensitivity to radiotherapy and chemotherapy. RNAi-mediated silencing of MMP-7 may represent a powerful therapeutic approach for controlling human colorectal cancer growth.
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- Boija, Per Olov, et al.
(författare)
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Hypovolaemic stress induced glycogenolysis, isolated liver perfusion study
- 1987
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Ingår i: Research in experimental medicine. - : Springer. - 0300-9130 .- 1433-8580. ; 187:5, s. 315-322
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Tidskriftsartikel (refereegranskat)abstract
- Intrinsic hepatic glycogenolysis was examined after hypovolemic stress. Hemorrhagic hypotension of 70 (P70) and 40 mm Hg (P40) for 60 min was inflicted for two postprandial groups and of 70 mm Hg (S70) in a 24-h starved group. The results were compared with three control groups; one postprandial (Pc), one 24-h starved (Sc), and one starved for 9 h (Sc: 9) to mimic the glycogen depletion produced by 70 mm Hg hemorrhagic hypotension. Glucose output was studied in vitro using av recirculating isolated liver perfusion system with a perfusate free of glucose and endocrine stimulation. Liver glycogen determination was made before perfusion start. Although the glycogen stores were decreased after hemorrhage glucose yield was increased (P70) and unchanged (P40) as compared to controls (Pc and Sc: 9). Both starved groups delivered small amounts of glucose, but the released fraction of the S70 group was more than twice that from the Sc group. These data suggest a liver enzyme activation with increased velocity of the enzymesubstrate reactions responsible for glycogen degradation, induced during in vivo hemorrhage and persisting for at least 30 min in vitro perfusion.
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- Håkansson, Åsa, et al.
(författare)
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Immunological alteration and changes of gut microbiota after dextran sulfate sodium (DSS) administration in mice
- 2015
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Ingår i: Clinical and Experimental Medicine. - : Springer Science and Business Media LLC. - 1591-9528. ; 15:1, s. 107-120
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Tidskriftsartikel (refereegranskat)abstract
- Ulcerative colitis (UC) is characterized bychronic inflammation of the colonic mucosa. Administrationof dextran sulfate sodium (DSS) to animals is a frequentlyused model to mimic human colitis. Deregulationof the immune response to the enteric microflora orpathogens as well as increased intestinal permeability havebeen proposed as disease-driving mechanisms. To enlargethe understanding of the pathogenesis, we have studied theeffect of DSS on the immune system and gut microbiota inmice. Intestinal inflammation was verified through histologicalevaluation and myeloperoxidase activity. Immunologicalchanges were assessed by flow cytometry inspleen, Peyer0s patches and mesenteric lymph nodes andthrough multiplex cytokine profiling. In addition, quantificationof the total amount of bacteria on colonic mucosaas well as the total amount of lactobacilli, Akkermansia,Desulfovibrio and Enterobacteriaceae was performed bythe use of quantitative PCR. Diversity and communitystructure were analysed by terminal restriction fragmentlength polymorphism (T-RFLP) patterns, and principalcomponent analysis was utilized on immunological andT-RFLP patterns. DSS-induced colitis show clinical andhistological similarities to UC. The composition of thecolonic microflora was profoundly changed and correlatedwith several alterations of the immune system. The resultsdemonstrate a relationship between multiple immunologicalchanges and alterations of the gut microbiota after DSSadministration. These data highlight and improve the definitionof the immunological basis of the disease andsuggest a role for dysregulation of the gut microbiota in thepathogenesis of colitis.
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- Schoenberg, M H, et al.
(författare)
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Hemorrhagic shock in the dog. I. Correlation between survival and severity of shock.
- 1985
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Ingår i: Research in experimental medicine. - 0300-9130 .- 1433-8580. ; 185:1, s. 21-33
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Tidskriftsartikel (refereegranskat)abstract
- A prerequisite elucidating the pathomechanism of hemorrhagic shock are reproducible experimental models, leading to a predictable outcome. Two concepts have been reported to be a good predictor for the outcome both employing a fixed hypotension level: total oxygen deficit and shed blood volume uptake. To correlate these two models we subjected 31 dogs to a standardized hemorrhagic shock procedure. Besides determination of acid-base status, hematocrit, mean arterial pressure, and cardiac output, these two parameters were measured continuously. Seventeen dogs survived the shock procedure, 14 died within 24 h. During shock, neither oxygen deficit nor any other parameter mentioned above correlated with the final outcome of the shock state. The only significant difference between surviving and non-surviving animals during this period was the amount of uptake. The non-surviving dogs exhibited a higher uptake volume, indicating an incipient collapse of the microcirculation. Terminating the duration of hypotension at an uptake volume of 5% of the maximum shed blood, all animals survived, while after an uptake volume of 15% about 50% of the dogs died. Using uptake volumes of various degrees in a hemorrhagic shock model as the endpoint of the hypotensive stress, it seems possible to produce reliable survival rates.
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