Home About us Contact
|
Home About us Contact | ||
|
|
||
Wound Bed. (wound + bed)
Selected AbstractsIn Vivo Perfusion of Human Skin Substitutes With Microvessels Formed by Adult Circulating Endothelial Progenitor CellsDERMATOLOGIC SURGERY, Issue 2 2008ELAINE F. KUNG MD BACKGROUND At present, tissue-engineered human skin substitutes (HSSs) mainly function as temporary bioactive dressings due to inadequate perfusion. Failure to form functional vascular networks within the initial posttransplantation period compromises cell survival of the graft and its long-term viability in the wound bed. OBJECTIVES Our goal was to demonstrate that adult circulating endothelial progenitor cells (EPCs) seeded onto HSS can form functional microvessels capable of graft neovascularization and perfusion. MATERIALS AND METHODS Adult peripheral blood mononuclear cells (PBMCs) underwent CD34 selection and endothelial cell (EC) culture conditions. After in vitro expansion, flow cytometry verified EC phenotype before their incorporation into HSS. After 2 weeks in vivo, immunohistochemical analysis, immunofluorescent microscopy, and microfil polymer perfusion were performed. RESULTS CD34+ PBMCs differentiated into EPC demonstrating characteristic EC morphology and expression of CD31, Tie-2, and E-selectin after TNF,-induction. Numerous human CD31 and Ulex europaeus agglutinin-1 (UEA-1) microvessels within the engineered grafts (HSS/EPCs) inosculated with recipient murine circulation. Limitation of murine CD31 immunoreactivity to HSS margins showed angiogenesis was attributable to human EPC at 2 weeks posttransplantation. Delivery of intravenous rhodamine-conjugated UEA-1 and microfil polymer to HSS/EPCs demonstrated enhanced perfusion by functional microvessels compared to HSS control without EPCs. CONCLUSION We successfully engineered functional microvessels in HSS by incorporating adult circulating EPCs. This autologous EC source can form vascular conduits enabling perfusion and survival of human bioengineered tissues. [source] OASIS® wound matrix versus Hyaloskin® in the treatment of difficult-to-heal wounds of mixed arterial/venous aetiologyINTERNATIONAL WOUND JOURNAL, Issue 1 2007Marco Romanelli Abstract Mixed arterial/venous (A/V) ulcers are difficult to treat and slow to heal likely as a result of deficiencies in molecular and cellular elements in the wound bed. Recently, biomaterials have been developed that replace extracellular matrix (ECM) molecules and growth factors critical to the normal healing process. In this study, the effects of OASIS® and Hyaloskin® were evaluated to compare the effectiveness of these two ECM-based products in their ability to achieve complete wound healing of mixed A/V ulcers. After 16 weeks of treatment, patients in each group were evaluated on four criteria: complete wound healing, time to dressing change, pain and comfort. Complete wound closure was achieved in 82·6% of OASIS® -treated ulcers compared with 46·2% of Hyaloskin® -treated ulcers (P < 0·001). Statistically significant differences favouring the OASIS® treatment group were also reported for time to dressing change (P < 0·05), pain (P < 0·05) and patient comfort (P < 0·01). Overall, OASIS® was superior to Hyaloskin® for the treatment of patients with mixed A/V ulcers, a population in which standard treatment options largely consist of moist wound dressings and compression therapy is typically not an option. OASIS® is a useful and well-tolerated treatment for mixed A/V ulcers that has the potential to improve quality of life and reduce costs associated with standard of care. [source] Upregulation of gamma-2 laminin-332 in the mouse ear vesicant wound model,JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2009Yoke-Chen Chang Abstract Epithelial cell migration during wound healing is regulated in part by enzymatic processing of laminin-332 (formerly LN-5), a heterodimer formed from ,, ,, and , polypeptide chains. Under static conditions, laminin-332 is secreted into the extracellular matrix as a proform and has two chains processed to smaller forms, allowing it to anchor epithelial cells to the basement membrane of the dermis. During incisional wounding, laminin ,2 chains in particular are processed to smaller sizes and function to promote epithelial sheet migration over the wound bed. The present study examines whether this same function occurs following chemical injury. The mouse ear vesicant model (MEVM) was used to follow the pathology in the ear and test whether processed laminin-332 enhances epithelial cell migration. Skin biopsies of sulfur mustard (SM) exposed ears for several time points were analyzed by histology, immunohistochemistry, real-time PCR, and Western blot analysis. SM exposure greatly increased mRNA levels for laminin-,2 in comparison to the other two chains. Protein production of laminin-,2 was upregulated, and there was an increase in the processed forms. Protein production was in excess of the amount required to form heterotrimeric laminin-332 and was associated with the migrating epithelial sheet, suggesting a potential role in wound healing for monomeric laminin-,2. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:172,184, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20275 [source] A coordinated approach to cutaneous wound healing: vibrational microscopy and molecular biologyJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 5b 2008K. L. Andrew Chan Abstract The repair of cutaneous wounds in the adult body involves a complex series of spatially and temporally organized processes to prevent infection and restore homeostasis. Three characteristic phases of wound repair (inflammation, proliferation including re-epithelialization and remodelling) overlap in time and space. We have utilized a human skin wound-healing model to correlate changes in genotype and pheno-type with infrared (IR) and confocal Raman spectroscopic images during the re-epithelialization of excisional wounds. The experimental protocols validated as IR images clearly delineate the keratin-rich migrating epithelial tongue from the collagen-rich wound bed. Multivariate statistical analysis of IR datasets acquired 6 days post-wounding reveal subtle spectral differences that map to distinct spatial distributions, which are correlated with immunofluorescent staining patterns of different keratin types. Images computed within collagen-rich regions expose complementary spatial patterns and identify elastin in the wound bed. The temporal sequence of events is explored through a comparison of gene array analysis with confocal Raman microscopy. Our approach demonstrates the feasibility of acquiring detailed molecular structure information from the various proteins and their subclasses involved in the wound-healing process. [source] Prostaglandin E2 is activated by airway injury and regulates fibroblast cytoskeletal dynamics,THE LARYNGOSCOPE, Issue 7 2009Vlad C. Sandulache MD Abstract Objectives/Hypothesis: To characterize the activation of cyclooxygenase (COX)-2/prostaglandin (PG) E2 signaling during airway mucosal repair and its subsequent role during the wound healing process. Study Design: Prospective animal study. Methods: The subglottis was approached via cricothyroidotomy. Sham airways were closed, and wounded airways were subjected to laser injury and closed. Subglottic tissue was harvested at 12 hours, 24 hours, 48 hours, and 72 hours postinjury. Secretions were collected preoperatively and at time of sacrifice. Inflammatory gene expression was analyzed using quantitative reverse transcriptase polymerase chain reaction. Subglottic/tracheal explants were exposed to exogenous IL-1, in the presence or absence of COX inhibitors. Explant-produced PGE2 levels were assayed using enzyme linked immunoassays. Human airway fibroblast migration and collagen contraction were assayed in the presence or absence of prostaglandin E2. Results: Laser injury triggers a rapid, dose-dependent increase in mucosal IL-1, and COX-2 gene expression, with an anatomical distribution proportional to the distance from the site of injury. Gene upregulation correlates with dose-dependent increases in PGE2 mucosal secretion levels. Ex vivo analysis indicates IL-1, is responsible for the activation of the COX-2 / PGE2 pathway. Prostaglandin E2 differentially inhibits airway fibroblast migration and contraction in a specific, dose-dependent manner. Conclusions: PGE2 is activated during mucosal inflammation and acts to decrease fibroplastic activity in the mucosal wound bed. During subglottic stenosis (SGS) development, the levels of PGE2 generated in response to injury may be insufficient to blunt the intrinsically fibroplastic phenotype of SGS fibroblasts, resulting in excessive scarring. Laryngoscope, 2009 [source] Effects of Tisseel and FloSeal on Primary Ischemic Time in a Rat Fasciocutaneous Free Flap Model,THE LARYNGOSCOPE, Issue 2 2004Aaron W. Partsafas BS Abstract Objectives: Free flaps are the technique of choice for reconstruction of defects resulting from extirpation of tumors of the head and neck. Advances in microsurgical technique have resulted in success rates of greater than 95%. Numerous intraoperative factors, ranging from technical issues to topically applied agents, can complicate the outcome of microsurgical free tissue transfer. Synthetic tissue adhesives and hemostatic agents are playing an ever-increasing role in reconstructive surgery. The safety of these factors in free flap surgery has not been ascertained. Study Design: Animal Care Committee live rat model. Methods: Male Sprague-Dawley rats were divided into three groups: group I, Control; group 2, FloSeal; group 3, Tisseel. In each group, a 3 × 6 cm ventral fasciocutaneous groin flap based on the left superficial epigastric artery was elevated and the experimental material applied beneath the flap and around the flap pedicle prior to suturing of the flap back to the wound bed. The experimental materials consisted of 0.2 mL saline in the control group, 0.5 mL FloSeal, and 0.2 mL Tisseel. In phase I of this study, the effect of each treatment on flap survival was assessed by survival at postoperative day 4. In phase II of the study, the effects of these agents on ischemic tolerance was investigated. Five rats in each treatment group were exposed to ischemic times of 6, 8, 10, and 12 hours. Survival of the flap was assessed 7 days after reversal of the ischemia. Probit curves and the critical ischemic time (CIT50) were calculated. Results: All flaps survived the 2-hour period of ischemia and were viable at postoperative day 4. Flap survival from group 1 (Control), group 2 (FloSeal), and group 3 (Tisseel) at the various ischemic times was as follows: at 6 hours, 80%, 80%, and 80%, respectively; at 8 hours, 80%, 80%, 60%; at 10 hours, 60%, 33%, 40%; at 12 hours, 20%, 20%, 0%. The CIT50 for the Control, FloSeal, and Tisseel groups was 9.4, 9.0, and 7.0 hours, respectively. Conclusions: FloSeal, a thrombin-based hemostatic agent, and Tisseel, a fibrin glue, displayed no adverse effect on flap survival in this model. [source] | ||||||||||