| 1. |
- Ragnarson Tennvall, Gunnel, et al.
(författare)
-
Annual costs of treatment for venous leg ulcers in Sweden and the United Kingdom
- 2005
-
Ingår i: Wound Repair and Regeneration. - : Wiley. - 1524-475X .- 1067-1927. ; 13:1, s. 13-18
-
Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to estimate costs of treating venous leg ulcers in Sweden and the United Kingdom during 1 year and to quantify costs in different health states, The costs of treating four different types of venous leg ulcers were estimated for 52 weeks by a stochastic health economic model, which simulated resource use data obtained from prospectively collected patient data, expert panels in the two countries, and published scientific. literature, The average cost of treating an ulcer varied between E 1332 and E2585 in Sweden and from E814 to E1994 in the United Kingdom. Cost of treating large ulcers (greater than or equal to10 cm(2)) of long duration (greater than or equal to6 months) was highest in both countries. Frequency of dressing changes and duration of time for each dressing change were higher in Sweden than in the United Kingdom, resulting in higher total cost per patient in Sweden. An important factor for the total costs was time to heal. Other important variables influencing treatment costs were frequency and duration of dressing changes, Actions to reduce time used for dressing changes and the total time to healing are thus very important in reducing costs spent on treatment of venous leg ulcers in both countries.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Koskela, Anita, 1979-, et al.
(författare)
-
Regulation of fibroblast gene expression by keratinocytes in organotypic skin culture provides possible mechanisms for the antifibrotic effect of reepithelialization
- 2010
-
Ingår i: Wound Repair and Regeneration. - : The Wound Healing Society. - 1067-1927 .- 1524-475X. ; 18:5, s. 452-459
-
Tidskriftsartikel (refereegranskat)abstract
- To investigate the mechanisms behind the antifibrotic effect associated with epidermal regeneration, the expression of 12 fibroblast genes important for the modulation of the extracellular matrix (ECM), as well as alpha-smooth muscle actin, was studied in a keratinocyte-fibroblast organotypic skin culture model. The study was performed over time during epidermal generation and in the presence or absence of the profibrotic factor transforming growth factor-beta. the Presence of epidermal differentiation markers in the model was essentially coherent with that of native skin. Fibroblast gene expression was analyzed with real-time polymerase chain reaction after removal of the epidermal layer. After 2 days of air-exposed culture, 11 out of the 13 genes studied were significantly regulated by keratinocytes in the absence or presence of transforming growth factor-beta. The regulation of connective tissue growth factor, collagen I and III, fibronectin, plasmin system regulators, matrix metalloproteinases and their inhibitors as well as alpha-smooth muscle actin was consistent with a suppression of ECM formation or contraction. Overall, the results support a view that keratinocytes regulate fibroblasts to act catabolically on the ECM in epithelialization processes. This provides possible mechanisms for the clinical observations that reepithelialization and epidermal wound coverage counteract excessive scar formation.
|
|
| 7. |
- Liu, Yawei, 1967-, et al.
(författare)
-
Fibroblast proliferation due to exposure to a platelet concentrate in vitro is pH dependent
- 2002
-
Ingår i: Wound Repair and Regeneration. - 1067-1927 .- 1524-475X. ; 10:5, s. 336-340
-
Tidskriftsartikel (refereegranskat)abstract
- The influence of platelet-rich plasma lysates on fibroblast proliferation was studied in culture. Cells were exposed to platelet lysates that had been preincubated at different pHs (5.0, 7.1, and 7.6). Proliferation was evaluated with the MTT assay and incorporation of [3H]thymidine into macromolecules, while type I collagen production was assayed by Western blotting. Enzyme-linked immunosorbent assays were used to determine platelet-derived growth factor and transforming growth factor-β concentrations. Platelets preincubated in an acidic environment (pH 5.0) induced the highest degree of fibroblast proliferation, and the concentration of platelet-derived growth factor in the different treated lysates was the highest at that particular pH. The concentration of transforming growth factor-β, however, was lower after incubation at pH 5.0 than at either pH 7.1 or 7.6. These findings may be relevant to normal wound healing in vivo and useful in the treatment of wounds and delayed healing processes.
|
|
| 8. |
- Seifert (Bock), Oliver, et al.
(författare)
-
Identification of unique gene expression patterns within different lesional sites of keloids
- 2008
-
Ingår i: Wound Repair and Regeneration. - 1067-1927 .- 1524-475X. ; 16:2, s. 254-265
-
Tidskriftsartikel (refereegranskat)abstract
- Keloid disease is a significant clinical problem, especially in black populations, with an estimated incidence of 4–16%. Keloids are fibroproliferative dermal tumors developing as a result of deregulated wound healing. The dynamic nature of keloids is illustrated by clinical regression in the center, while the margin remains active growing into the surrounding healthy skin. Therefore, the gene expression profiles of fibroblasts from different sites of the keloids were characterized using Affymetrix microarrays covering the whole human genome. This study revealed 105 genes that were differentially regulated (79 genes were up-regulated and 26 down-regulated) in a unique gene expression profile in different sites of keloids where progression or regression of the process was in progress. The apoptosis inhibitor AVEN was found to be up-regulated at the active margin of keloids, while apoptosis-inducing genes such as ADAM12 and genes inducing extracellular matrix (ECM) degradation such as matrix metalloproteinase-19 were up-regulated in the regressing keloid center. We identified genes previously not described in the development of keloids. Activating proapoptotic genes or inhibiting ECM-inducing genes as INHBA or monocyte chemoattractant protein-1 might be possible target genes for new treatment strategies for keloid disease.
|
|
| 9. |
|
|
| 10. |
|
|
