| 11. |
- Uedo, Noriya, et al.
(författare)
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Underwater endoscopic mucosal resection of large colorectal lesions.
- 2015
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Ingår i: Endoscopy. - : Georg Thieme Verlag KG. - 1438-8812 .- 0013-726X. ; 47:2, s. 172-174
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Tidskriftsartikel (refereegranskat)abstract
- In this prospective study, 11 consecutive patients with neoplastic colorectal lesions (median size 20 mm, range 15 - 25 mm) underwent endoscopic polyp removal by underwater endoscopic mucosal resection (EMR). Six lesions were removed en bloc and five lesions were removed by piecemeal resection. Pathological examination revealed seven R0 resections, and in four cases the pathology could not be determined. Two cases of procedure-related bleeding occurred but these were easily managed using hemostatic forceps and clip application. No perforations or delayed bleedings were observed. Underwater EMR is a relatively simple, safe, and useful method for the removal of large colorectal lesions.
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| 12. |
- Vilhjalmsson, Dadi, et al.
(författare)
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Compression anastomotic ring-locking procedure (CARP) is a safe and effective method for intestinal anastomoses following left-sided colonic resection.
- 2015
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Ingår i: International Journal of Colorectal Disease. - : Springer Science and Business Media LLC. - 1432-1262 .- 0179-1958. ; 30:7, s. 969-975
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Tidskriftsartikel (refereegranskat)abstract
- Compression anastomotic ring-locking procedure (CARP) is a novel procedure for creating colonic anastomoses. The surgical procedure allows perioperative quantification of the compression pressure between the intestinal ends within the anastomosis and postoperative monitoring of the anastomotic integrity. We have recently shown that CARP is a safe and effective method for colonic anastomoses in pigs, and the purpose of the present study was to evaluate CARP for colonic anastomoses in humans.
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| 13. |
- Vilhjalmsson, Dadi, et al.
(författare)
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The compression anastomotic ring-locking procedure : a novel technique for creating a sutureless colonic anastomosis
- 2015
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Ingår i: European Surgical Research. - : S. Karger AG. - 0014-312X .- 1421-9921. ; 54:3-4, s. 139-147
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND/AIM: Compression anastomoses might represent an improvement over traditional hand-sewn or stapled techniques. Herein, we describe a novel concept of sutureless colonic anastomosis named compression anastomotic ring-locking procedure (CARP).MATERIALS AND METHODS: The surgical device consists of two anastomotic rings and their associated helping tools, facilitating the placement of the rings into the intestinal ends. Furthermore, four catheters are connected to the surgical device, allowing the evaluation of the anastomosis during and after surgery. A total of 31 pigs underwent a low colocolic anastomosis using the anastomotic rings. The compression pressure was measured perioperatively and up to 96 h after surgery. Anastomotic integrity and morphology were analyzed by use of radiology and histology, respectively. A long-term follow-up was conducted in a subgroup of pigs up to 108 days after surgery when the bursting pressure and stricture formation were examined.RESULTS: All animals recovered uneventfully, and macroscopic examination revealed intact anastomoses without signs of pathological inflammation or adhesions. The perioperative compression pressure was inversely proportional to the gap size between the anastomotic rings. For example, an anastomotic gap of 1.5 mm created a colonic anastomosis with a perioperative compression pressure of 91 mbar, which remained constant for up to 48 h and resulted in a markedly increased compression pressure. Contrast infusion via the catheters effectively visualized the anastomoses, and no leakage was detected within the study. The surgical device was spontaneously evacuated from the intestines within 6 days after surgery. Histology showed collagen bridging of the anastomoses already 72 h after surgery. Long-term follow-up (54-108 days) revealed no stricture formation in the anastomoses, and the bursting pressure ranged from 120 to 235 mbar. The majority of bursts (10/12) occurred distant from the anastomoses.CONCLUSION: We conclude that the surgical device associated to CARP is safe and efficient for creating colonic anastomoses. Further studies in patients undergoing colorectal surgery are warranted.
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| 14. |
- Wang, Yongzhi, et al.
(författare)
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Monocytes regulate systemic coagulation and inflammation in abdominal sepsis.
- 2015
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Ingår i: American Journal of Physiology: Heart and Circulatory Physiology. - : American Physiological Society. - 1522-1539 .- 0363-6135. ; 308:5, s. 540-547
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Tidskriftsartikel (refereegranskat)abstract
- Abdominal sepsis is associated with significant changes in systemic inflammation and coagulation. The purpose of this study was to examine the role of peripheral blood monocytes for systemic coagulation, including thrombin generation and consumption of coagulation factors. Abdominal sepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice. Plasma and lung levels of interleukin-6 (IL-6), CXC chemokines (CXCL1, CXCL2 and CXCL5) as well as pulmonary activity of myeloperoxidase (MPO), thrombin generation and coagulation factors were determined 6h after CLP induction. Administration of clodronate liposomes decreased circulating levels of monocytes by 96%. Time to peak thrombin formation was increased and peak and total thrombin generation was decreased in plasma from CLP animals. Monocyte depletion decreased time to peak formation of thrombin and increased peak and total generation of thrombin in septic animals. In addition, monocyte depletion decreased the CLP-induced increase in the levels of thrombin-antithrombin complexes in plasma. Depletion of monocytes increased plasma levels of prothrombin, factor V, factor X, protein C and in septic mice. Moreover, depletion of monocytes decreased CLP-induced levels of IL-6 and CXC chemokines in plasma and lung by more than 59% and 20%, respectively. CLP-induced MPO activity in the lung was attenuated by 44% in animals depleted of monocytes. Taken together, our findings show for the first time that peripheral blood monocytes regulates systemic coagulation and improve our understanding of the pathophysiology of sepsis and encourage further attempts to target innate immune cell functions in abdominal sepsis.
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| 15. |
- Wang, Yongzhi, et al.
(författare)
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Thrombin generation in abdominal sepsis is Rho-kinase-dependent.
- 2015
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Ingår i: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 460:3, s. 691-696
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Tidskriftsartikel (refereegranskat)abstract
- Sepsis causes severe derangements of the coagulation system. However, the signaling mechanisms regulating sepsis-induced thrombin generation remain elusive. Herein, we hypothesized that Rho-kinase might be an important regulator of thrombin generation in abdominal sepsis. Abdominal sepsis was induced by cecal ligation and puncture (CLP) in C57Bl/6 mice. Thrombin generation, coagulation factors, lung histology and myeloperoxidase (MPO) activity were determined 6 h and 24 h after induction of CLP. Induction of CLP triggered a systemic inflammatory response characterized by neutrophil accumulation and tissue injury in the lung as well as thrombocytopenia and leukocytopenia. Administration of Y-27632, a Rho-kinase inhibitor, attenuated these markers of systemic inflammation in CLP animals. Moreover, peak thrombin formation was decreased by 77% and 81% in plasma from mice 6 h and 24 h after induction of CLP. Total thrombin generation was reduced by 64% and 67% 6 h and 24 h after CLP induction, respectively. Notably, administration of Y-27632 increased peak formation by 99% and total thrombin generation by 66% in plasma from septic animals. In addition, CLP markedly decreased plasma levels of prothrombin, factor V and factor X at 6 h and 24 h. Interestingly, Rho-kinase inhibition significantly enhanced levels of prothrombin, factor V and factor X in plasma from septic mice. In addition, inhibition of Rho-kinase decreased CLP-induced elevations of CXCL2 by 36%and interleukin-6 by 38%. These novel findings suggest that sepsis-induced thrombin generation is regulated by Rho-kinase. Moreover, inhibition of Rho-kinase reverses sepsis-evoked consumption of coagulation factors. Thus, our results show that targeting Rho-kinase signaling might protect against coagulation dysfunction in abdominal sepsis.
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| 16. |
- Zhang, Songen, et al.
(författare)
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STAT3-dependent CXC chemokine formation and neutrophil migration in Streptococcal M1 protein-induced acute lung inflammation.
- 2015
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Ingår i: American Journal of Physiology: Lung Cellular and Molecular Physiology. - : American Physiological Society. - 1522-1504 .- 1040-0605. ; 308:11, s. 1159-1167
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Tidskriftsartikel (refereegranskat)abstract
- Streptococcus pyogenes cause infections ranging from mild pharyngitis to severe streptococcal toxic shock syndrome (STSS). The M1 serotype of Streptococcus pyogenes is most frequently associated with STSS. Herein, it was hypothesized that STAT3 signaling might be involved in M1 protein-evoked lung inflammation. The STAT3 inhibitor, S3I-201, was administered to male C57Bl/6 mice before i.v. challenge with M1 protein. Bronchoalveolar fluid and lung tissue were harvested for quantification of STAT3 activity, neutrophil recruitment, edema and CXC chemokine formation. Neutrophil expression of Mac-1 was quantified by use of flow cytometry. Levels of IL-6 and HMGB1 were determined in plasma. CXCL2-induced neutrophil chemotaxis was studied in vitro. Administration of S3I-201 markedly reduced M1 protein-provoked STAT3 activity, neutrophil recruitment, edema formation and inflammatory changes in the lung. In addition, M1 protein significantly increased Mac-1 expression on neutrophils and CXC chemokine levels in the lung. Treatment with S3I-201 had no effect on M1 protein-induced expression of Mac-1 on neutrophils. In contrast, inhibition of STAT3 activity greatly reduced M1 protein-induced formation of CXC chemokines in the lung. Interestingly, STAT3 inhibition markedly decreased plasma levels of IL-6 and HMGB1 in animals exposed to M1 protein. Moreover, we found that S3I-201 abolished CXCL2-induced neutrophil migration in vitro. In conclusion, these novel findings indicate that STAT3 signaling plays a key role in mediating CXC chemokine production and neutrophil infiltration in M1 protein-induced acute lung inflammation.
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| 17. |
- Zhang, Songen, et al.
(författare)
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Streptococcal M1 protein triggers chemokine formation, neutrophil infiltration, and lung injury in an NFAT-dependent manner.
- 2015
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Ingår i: Journal of Leukocyte Biology. - 1938-3673. ; 97:6, s. 1003-1010
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Tidskriftsartikel (refereegranskat)abstract
- Streptococcus pyogenes of the M1 serotype can cause STSS, which is associated with significant morbidity and mortality. The purpose of the present study was to examine the role of NFAT signaling in M1 protein-induced lung injury. NFAT-luc mice were treated with the NFAT inhibitor A-285222 before administration of the M1 protein. Neutrophil infiltration, edema, and CXC chemokines were quantified in the lung, 4 h after challenge with the M1 protein. Flow cytometry was used to determine Mac-1 expression. Challenge with the M1 protein increased NFAT-dependent transcriptional activity in the lung, spleen, and liver in NFAT-luc mice. Administration of the NFAT inhibitor A-285222 abolished M1 protein-evoked NFAT activation in the lung, spleen, and liver. M1 protein challenge induced neutrophil recruitment, edema, and CXC chemokine production in the lung, as well as up-regulation of Mac-1 on circulating neutrophils. Inhibition of NFAT activity attenuated M1 protein-induced neutrophil infiltration by 77% and edema formation by 50% in the lung. Moreover, administration of A-285222 reduced M1 protein-evoked pulmonary formation of CXC chemokine >80%. In addition, NFAT inhibition decreased M1 protein-triggered Mac-1 up-regulation on neutrophils. These findings indicate that NFAT signaling controls pulmonary infiltration of neutrophils in response to streptococcal M1 protein via formation of CXC chemokines and neutrophil expression of Mac-1. Thus, the targeting of NFAT activity might be a useful way to ameliorate lung injury in streptococcal infections.
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