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- Jeppsson, Bengt, et al.
(författare)
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Evidence-based medicine in HBP surgery: Is there any?
- 2005
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Ingår i: HPB. - : Elsevier BV. - 1477-2574 .- 1365-182X. ; 7:3, s. 197-200
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Tidskriftsartikel (refereegranskat)abstract
- Background. Evidence-based medicine (EBM) has become widely accepted as a basis for clinical decision in many fields of medicine. This review examines the specific role of EBM in hepato-biliary and pancreatic (HBP) surgery. EBM relies on four main sources, including clinical guidelines, meta-analyses, primary information and clinical experience. Randomized controlled trials (RCTs) constitute the cornerstone of EBM and a recent study reported that there are relatively few RCTs evaluating the effectiveness of surgical therapies and procedures (1,530 out of 45,342 or 3.4% in five leading surgical journals) and only a few in HBP surgery. Although the effort must be to implement EBM as far as possible in HBP surgery, there are several obstacles to conducting RCTs in HBP surgery, including problems associated with standardization of surgical skills, sham-operations often impossible to perform, and the general applicability of specific findings may be uncertain.Discussion. This paper will provide two relevant examples of EBM in HBP surgery in patients with hepatic metastases and pancreatic adenocarcinoma, illustrating some problems but also the potential of introducing EBM in HBP surgery. In the future, our effort must be devoted to implementing EBM in applicable areas of HBP surgery but also remembering that in certain areas accumulated knowledge from observational studies, including drainage of abscesses and surgical treatment of intestinal obstruction, may have similar or even higher clinical value than RCTs.
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| 2. |
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| 3. |
- Laschke, MW, et al.
(författare)
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New experimental approach to study host tissue response to surgical mesh materials in vivo
- 2005
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Ingår i: Journal of Biomedical Materials Research. Part A. - : Wiley. - 1552-4965 .- 1549-3296. ; 74A:4, s. 696-704
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Tidskriftsartikel (refereegranskat)abstract
- Implantation of surgical meshes is a common procedure to increase abdominal wall stability in hernia repair. To improve biocompatibility of the implants, sophisticated in vivo animal models are needed to study inflammation and incorporation of biomaterials. Herein, we have established a new model that allows for the quantitative analysis of host tissue response and vascular ingrowth into surgical mesh materials in vivo. Ultrapro meshes were implanted into dorsal skinfold chambers of Syrian golden hamsters. Angiogenesis, microhemodynamics, microvascular permeability, and leukocyte-endothelial cell interaction of the host tissue were analyzed in response to material implantation over a 2-week period using intravital fluorescence microscopy. Mesh implantation resulted in a short-term activation of leukocytes, reflected by leukocyte accumulation and adherence in postcapillary venules. This cellular inflammatory response was accompanied by an increase of mac-romolecular leakage, indicating loss of integrity of venular endothelial cells. Angiogenesis started at day 3 after implantation by protrusion of capillary sprouts, originating from the host microvasculature. Until day 10, these sprouts interconnected with each other to form a new microvascular network. At day 14, the inflammatory response had disappeared and the vascular ingrowth was completed. Histology confirmed the formation of granulation tissue with adequate incorporation of the mesh filaments within the host tissue. We conclude that this novel model of surgical mesh implantation is a useful experimental approach to analyze host tissue response and vascular ingrowth of newly devised materials for hernia repair.
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| 4. |
- Wang, Yusheng, et al.
(författare)
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Mast cell-derived tumour necrosis factor-alpha mediates macrophage inflammatory protein-2-induced recruitment of neutrophils in mice.
- 2005
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Ingår i: British Journal of Pharmacology. - : Wiley. - 1476-5381 .- 0007-1188. ; 145:8, s. 1062-1068
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Tidskriftsartikel (refereegranskat)abstract
- 1 Recent studies have indicated that mast cells play an intermediate role in chemokine-induced neutrophil recruitment in vivo. 2 The aim of the present investigation was to determine the role of tumour necrosis factor-alpha (TNF-alpha) in neutrophil recruitment provoked by the CXC chemokine macrophage inflammatory protein-2 (MIP-2). For this purpose, we used mast cell- and TNF-alpha-deficient mice and studied neutrophil adhesion to endothelial cells in vitro and neutrophil recruitment in the mouse cremaster muscle in vivo. 3 In contrast to the classical chemoattractant formyl-methionine-leucine-phenylalanin ( fMLP), MIP-2 dose dependently increased neutrophil accumulation in vivo. This MIP-2-regulated neutrophil recruitment was abolished in mast cell- deficient mice. 4 TNF-alpha increased E-selectin mRNA expression in both wild-type (WT) and mast cell-deficient mice. In contrast, MIP-2 challenge increased gene expression of E-selectin in WT but not in mast cell-deficient animals. Moreover, MIP-2-provoked extravascular accumulation of neutrophils was reduced by 78% in mice lacking TNF-alpha. 5 In order to better define the role of mast cell-derived TNF-alpha in neutrophil responses to MIP-2, we used an in vitro endothelial cell adhesion assay with and without mast cells. Interestingly, MIP-2-induced neutrophil adhesion to endothelial cells was decreased by 58% using TNF-alpha-deficient compared to WT mast cells. Moreover, mast cell secretion of TNF-alpha increased by more than 71% in response to challenge with MIP-2. 6 Taken together, our results suggest that MIP-2-induced neutrophil recruitment is mediated by TNF-alpha released from local mast cells. These findings help to explain the complex molecular interactions between chemokines, mast cell activation and neutrophil infiltration in vivo.
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