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Wayne Morrison

Publications and source records attributed to Wayne Morrison.

5 recordsLinked to original sources
PubMed2006

The influence of architecture on degradation and tissue ingrowth into three-dimensional poly(lactic-co-glycolic acid) scaffolds in vitro and in vivo.

The in vitro and in vivo degradation properties of poly(lactic-co-glycolic acid) (PLGA) scaffolds produced by two different technologies-thermally induced phase separation (TIPS), and solvent casting and particulate leaching (SCPL) were compared. Over 6 weeks, in vitro degradation produced changes in SCPL scaffold dimension, mass, internal architecture and mechanical properties. TIPS scaffolds produced far less changes in these parameters providing significant advantages over SCPL. In vivo results were based on a microsurgically created arteriovenous (AV) loop sandwiched between two TIPS scaffolds placed in a polycarbonate chamber under rat groin skin. Histologically, a predominant foreign body giant cell response and reduced vascularity was evident in tissue ingrowth between 2 and 8 weeks in TIPS scaffolds. Tissue death occurred at 8 weeks in the smallest pores. Morphometric comparison of TIPS and SCPL scaffolds indicated slightly better tissue ingrowth but greater loss of scaffold structure in SCPL scaffolds. Although advantageous in vitro, large surface area:volume ratios and varying pore sizes in PLGA TIPS scaffolds mean that effective in vivo (AV loop) utilization will only be achieved if the foreign body response can be significantly reduced so as to allow successful vascularisation, and hence sustained tissue growth, in pores less than 300 microm.

Animals↗
PubMed2004

Microvascular invasion during endochondral ossification in experimental fractures in rats.

In this study morphologic techniques have been used to detail the angiogenic response that accompanies endochondral fracture healing in a clinically relevant, reproducible rat model. In this displaced fracture, the gap fills with cartilage that later is replaced by bone, via endochondral ossification. A transient periosteal circulation, followed by a permanent medullary circulation accompany this progression. From 2 to 6 weeks, vessels grow out from the periosteal tissue and give rise to vascular buds, which abut directly onto the avascular zone corresponding to the fracture defect. From 3 weeks onwards, a second wave of vessels grows out from the marrow to the cartilage-filled fracture defect, terminating as vascular buds and loops lined by endothelial and perivascular cells. The loops and buds stain strongly for laminin but transmission electron microscopy does not demonstrate an identifiable basement membrane, pointing to a region of active extracellular matrix turnover. These vessels are intimately associated with osteoblasts and newly formed woven bone forming finger-like composite structures that protrude into the mineralized cartilage matrix with which they form a clearly demarcated interface. Invading vessels and woven bone successively replace the cartilage matrix to mediate repair. Both the vascular structures and progression of endochondral ossification observed, closely resemble those described in the normal epiphyseal growth plate, indicating that the fundamental processes are similar. However, there is a difference in the spatial orientation of cells such that the healing front in the fracture model is relatively disorganized, compared to the orderly linear array of cells at the epiphyseal growth plate.

Animals↗
PubMed2004

Early inducible nitric oxide synthase 2 (NOS 2) activity enhances ischaemic skin flap survival.

A functional skin-flap model of angiogenesis in the mouse was utilized to investigate ischaemic flap survival/angiogenesis whilst under pharmacological or genetic inhibition of nitric oxide synthase (NOS). In this model, the epigastric artery was cauterized. Following a five-day angiogenic period an abdominal skin-flap supplied by the pre-existing epigastric artery was raised and resutured. After a further six days the outcome was determined by measuring the area of living skin-flap that was sustained by new vessel growth around the cauterized artery. Both pharmacological [ S-methyl-isothiourea (SMT) given via i.p. injection for the five-day angiogenic period] and genetic inhibition of NOS 2 (using NOS 2-/- mice) caused a similar and significant fall in flap survival compared to saline-treated wild-type mice ( P < 0.05). Delaying pharmacological NOS 2 inhibition for two days post-arterial cauterization increased flap survival in wild-type mice to that of saline-treated controls, whilst treating wild-type mice with SMT for only the first three days of angiogenesis produced a significant decrease in flap survival, similar to that of five-day SMT-treated wild types. Immunoreactivity for NOS 2 in NOS 2-/- knockout mice was absent in both pedicles and skin-flaps, whilst mast cells from both the pedicle and the skin-flap stained positively for NOS 2 in wild-type mice. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF 2) immunoreactivity was also strongly evident in mast cells of both wild-type and NOS 2-/- mice at both sites. These results point to a significant role for NOS 2 in promoting wound healing/angiogenesis in its early stages.

Animals↗
PubMed2003

Too much vacuum-assisted closure.

There has been an explosion in the use of the vacuum-assisted closure device since 1997. Selectively and judiciously used, it is a valuable tool. However, we are concerned by the expanding list of 'indications' for its use. Prolonged applications, frequently several weeks, at the expense of early surgical reconstruction, might compromise the outcome in selected cases. We report four cases that illustrate this problem and stress the importance of timely surgical reconstruction utilizing the range of reconstructive techniques available as well as vacuum-assisted closure dressing.

Adult↗