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Sökning: WFRF:(Thorlacius Henrik) > (2015-2019) > (2016)

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1.
  • Changhui, Yu, et al. (författare)
  • Platelet-Derived CCL5 Regulates CXC Chemokine Formation and Neutrophil Recruitment in Acute Experimental Colitis.
  • 2016
  • Ingår i: Journal of Cellular Physiology. - John Wiley and Sons Inc.. - 1097-4652. ; 231:2, s. 370-376
  • Tidskriftsartikel (refereegranskat)abstract
    • Accumulating data suggest that platelets not only regulate thrombosis and haemostasis but also inflammatory processes. Platelets contain numerous potent pro-inflammatory compounds, including the chemokines CCL5 and CXCL4 although their role in acute colitis remains elusive. The aim of this study was to examine the role of platelets and platelet-derived chemokines in acute colitis. Acute colitis was induced in female Balb/c mice by administration of 5% dextran sodium sulphate (DSS) for five days. Animals received a platelet-depleting, anti-CCL5, anti-CXCL4 or a control antibody prior to DSS challenge. Colonic tissue was collected for quantification of myeloperoxidase (MPO) activity, CXCL5, CXCL2, interleukin-6 (IL-6) and CCL5 levels as well as morphological analyses. Platelet depletion reduced tissue damage and clinical disease activity index in DSS-exposed animals. Platelet depletion not only reduced levels of CXCL2 and CXCL5 but also levels of CCL5 in the inflamed colon. Immunoneutralization of CCL5 but not CXCL4 reduced tissue damage, CXC chemokine expression and neutrophil recruitment in DSS-treated animals. These findings show that platelets play a key role in acute colitis by regulating CXC chemokine generation, neutrophil infiltration and tissue damage in the colon. Moreover, our results suggest that platelet-derived CCL5 is an important link between platelet activation and neutrophil recruitment in acute colitis. This article is protected by copyright. All rights reserved.
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2.
  • Koulaouzidis, Anastasios, et al. (författare)
  • Association Between Fecal Calprotectin Levels and Small-bowel Inflammation Score in Capsule Endoscopy : A Multicenter Retrospective Study
  • 2016
  • Ingår i: Digestive Diseases and Sciences. - Springer. - 1573-2568. ; 61:7, s. 2033-2040
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Accurate inflammation reporting in capsule endoscopy (CE) is important for diagnosis and monitoring of treatment of inflammatory bowel disease (IBD). Fecal calprotectin (FC) is a highly specific biomarker of gut inflammation. Lewis score (LS) was developed to standardize quantification of inflammation in small-bowel (SB) CE images.GOALS: Multicenter retrospective study aiming to investigate correlation between LS and FC in a large group of patients undergoing CE for suspected or known small-bowel IBD, and to develop a model for prediction of CE results (LS) based on FC levels.STUDY: Five academic centers and a district general hospital offering CE in UK, Finland, Sweden, Canada, and Israel. In total, 333 patients were recruited. They had small-bowel CE and FC done within 3 months.RESULTS: Overall, correlation between FC and LS was weak (r s: 0.232, P < 0.001). When two clinically significant FC thresholds (100 and 250 μg/g) were examined, the r s between FC and LS was 0.247 (weak) and 0.337 (moderate), respectively (P = 0.307). For clinically significant (LS ≥ 135) or negative (LS < 135) for SB inflammation, ROC curves gave an optimum cutoff point of FC 76 μg/g with sensitivity 0.59 and specificity 0.41.LIMITATIONS: Retrospective design.CONCLUSIONS: LS appears to show low correlation with FC as well as other serology markers of inflammation. FC does not appear to be a reliable biomarker for significant small-bowel inflammation. Nevertheless, FC level ≥ 76 μg/g may be associated with appreciable visual inflammation on small-bowel CE in patients with negative prior diagnostic workup.
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3.
  • Nilsson, Emelie, et al. (författare)
  • Use of Oral Contraceptives and Breast Cancer Survival
  • 2016
  • Ingår i: International Journal of Womens Health and Wellness. - 2474-1353. ; 2:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Oral contraceptives (OC) have been shown to give a transient increased breast cancer risk. However, studies on breast cancer survival after OC use are sparse and conflicting.Aim: The aim of this study was to examine previous use of OC in relation to survival after breast cancer diagnosis.Methods: Data was collected from Malmö Diet and Cancer Study, with baseline examinations between 1991 and 1996. Out of 17035 women who completed all study parts, 765 women with incident breast cancer were included in this study. Kaplan Meier and Cox Proportional Hazards analyses, with 95% confidence intervals (CI), were used to study OC in relation to breast cancer-specific and overall survival. All analyses were stratified on age at diagnosis.Results: Women who had ever used OC were younger and more often had grade III tumors than those who had never used OC. Breast cancer-specific survival in women who ever had used OC was better when adjusting for BMI, socioeconomic status as well as tumor characteristics. However, when adjusting for age at diagnosis, the results did not remain significant (0.68, CI 95% 0.39- 1.18). Stratified analyses on age at diagnosis (40-55, 56-70 and ≥ 71) showed no statistically significant associations.Conclusion: In this study we could not demonstrate a significant effect of OC use on breast cancer survival.
4.
  • Rönnow, Carl-Fredrik, et al. (författare)
  • Frimand Needle Holder Reduces Suturing Time and Surgical Stress When Suturing in Palm Grip.
  • 2016
  • Ingår i: Surgical Innovation. - SAGE Publications. - 1553-3506. ; 23:3, s. 235-241
  • Tidskriftsartikel (refereegranskat)abstract
    • The Frimand needle holder (FNH) was developed to facilitate palm grip suturing. In the present study, we wanted to examine the impact of the FNH compared with a conventional Hegar-styled needle holder (HSNH) on suture time and surgical stress.
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5.
  • Sternby, Hanna, et al. (författare)
  • Predictive Capacity of Biomarkers for Severe Acute Pancreatitis.
  • 2016
  • Ingår i: European Surgical Research. - Karger. - 0014-312X. ; 56:3-4, s. 154-163
  • Tidskriftsartikel (refereegranskat)abstract
    • Early prediction of severe acute pancreatitis (SAP) substantially improves treatment of patients. A large amount of biomarkers have been studied with this objective. The aim of this work was to study predictive biomarkers using preset cut-off levels in an unselected population of patients with acute pancreatitis (AP).
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6.
  • Wang, Yongzhi, et al. (författare)
  • Rac1 regulates bacterial toxin-induced thrombin generation.
  • 2016
  • Ingår i: Inflammation Research. - Birkhäuser Verlag. - 1420-908X.
  • Tidskriftsartikel (refereegranskat)abstract
    • Systemic inflammatory response syndrome is associated with severe coagulopathy. The purpose of this study was to examine thrombin generation in systemic inflammation triggered by the endotoxin lipopolysaccharide (LPS) and the exotoxin streptococcal M1 protein.
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7.
  • Wetterholm, Erik, et al. (författare)
  • Platelet-derived CXCL4 regulates neutrophil infiltration and tissue damage in severe acute pancreatitis
  • 2016
  • Ingår i: Translational Research. - Elsevier. - 1931-5244. ; 176, s. 105-118
  • Tidskriftsartikel (refereegranskat)abstract
    • Platelets are known to play an important role in acute pancreatitis (AP) via promotion of neutrophil accumulation, although mechanisms behind platelet-dependent accumulation of neutrophils in the pancreas remain elusive. Platelets contain a wide spectrum of different pro-inflammatory compounds, such as chemokines. CXCL4 (platelet factor 4) is one of the most abundant chemokine in platelets, and we hypothesized that CXCL4 might be involved in platelet-dependent accumulation of neutrophils in the inflamed pancreas. The aim of this study was to examine the role of CXCL4 in severe AP. Pancreatitis was provoked by infusion of taurocholate into the pancreatic duct or by intraperitoneal administration of L-arginine in C57BL/6 mice. Animals were treated with an antibody against platelets or CXCL4 before induction of pancreatitis. Plasma and lung levels of CXCL2, CXCL4, and interleukin (IL)-6 were determined by use of enzyme-linked immunosorbent assay. Flow cytometry was used to examine surface expression of macrophage-1 (Mac-1) on neutrophils. Plasma was obtained from healthy individuals (controls) and patients with AP. Challenge with taurocholate increased plasma levels of CXCL4, and depletion of platelets markedly reduced plasma levels of CXCL4 indicating that circulating levels of CXCL4 are mainly derived from platelets in AP. Inhibition of CXCL4 reduced taurocholate-induced neutrophil recruitment, IL-6 secretion, edema formation, amylase release, and tissue damage in the pancreas. However, immunoneutralization of CXCL4 had no effect on CXCL2-evoked neutrophil expression of Mac-1 or chemotaxis in vitro, suggesting an indirect effect of CXCL4 on neutrophil recruitment in AP. Targeting CXCL4 significantly attenuated plasma and lung levels of CXCL2, which is a potent neutrophil chemoattractant, and inhibition of the CXCL2 receptor attenuated neutrophil infiltration and tissue damage in the inflamed pancreas. A significant role of CXCL4 was confirmed in an alternate model of AP induced by L-arginine challenge. Moreover, patients with AP had significantly increased plasma levels of CXCL4 compared with healthy controls. These findings’ results suggest that platelet-derived CXCL4 is a potent stimulator of neutrophil accumulation in AP and that this is mediated via generation of CXCL2 in the inflamed pancreas. We conclude that CXCL4 plays an important role in pancreatic inflammation and that targeting CXCL4 might be a useful way to ameliorate tissue damage in AP.
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