A terapia a laser de baixa potência vem sendo utilizada para minimizar os efeitos maléficos da inflamação, bem como para acelerar a cicatrização dos tecidos lesados. Este estudo, visa observar as alterações causadas pela irradiação do laser diodo arsenieto de gálio (904nm), no tendão calcâneo em ratos. Foram utilizados 30 ratos da linhagem Wistar, com peso médio de 235g, divididos em dois grupos, um com 20 e outro com 10 animais. Todos os animais foram submetidos a tenotomia do tendão calcâneo direito. O tratamento com laser foi iniciado após 24 horas em um dos grupos, com a dose de 4 J/cm 2 ; e o outro grupo foi usado como controle. Utilizamos o método pontual, com a caneta do aparelho em contato direto com a pele do animal. Os dois grupos foram divididos em subgrupos, e os animais destes, sacrificados em períodos distintos, sendo no 8º e 15º pós-operatório. O tendão foi excisado e submetido a análise histológica pela microscopia de luz, onde foi observado a presença de células inflamatórias, fibroblastos, vascularização e deposição de colágeno. Houve diferença estatisticamente significante (p<0.05), entre controle e tratamento na deposição de colágeno e presença de células inflamatórias. Este estudo, sugestiona que a terapia a laser, proporciona a aceleração da cicatrização na tenotomia calcâneana em ratos, pelo aumento da deposição de colágeno, tanto na fase inicial como na tardia do tratamento. / Low-potency laser therapy has been used as a means of minimizing the hazardous effects of inflammation and accelerating healing in damaged tissues. This paper aims at observeving the alterations caused by diode AsGa (904nm), laser in the calcaneal tendon of rats. Thirty 235g (average weight) Wistar rats were divided into 2 groups – one with 20 and other with 10 animals, all of which underwent right calcaneal tendon tenotomy. One group started laser treatment at a dosege of 4 J/cm 2 24hours after surgery, the other being used as control. The punctual method was employed and the appliance pen kept in direct contact with animal's skin. Both groups were divided into subgroups, the animals of which were sacrificed in different times – on the 8 th and 15 th postoperative day, respectively. The tendon was excised and submitted to histology analysis using light microscopy, which revealed the presence of inflammatory cells, fibroblasts, vascularization and collagen deposition. There was a statistically significant difference (p <0.05) between the control and the treatment as far as collagen deposition at the presence of inflammatory cells are concerned. This study suggests that laser therapy accelerates healing in calcanean tenotomy in rats by increase collagen deposition both in the early and late parts of the treatment.

Phosphate (Pi) is essential for healthy bone growth as well as normal fracture repair. Studies have shown that when animals are phosphate deficient normal fracture healing is interrupted. Although phosphate deficiency has been shown to impair fracture healing, it is unknown how different genetic factors interact with phosphate deficiency to disrupt healing. Furthermore, it is unknown if upon replenishing phosphate in the diet healing will be re-initiated or if the deficiencies will persist irreversibly to prolong the healing of the bones. To assess how genetic factors interact with phosphate deficiency, fractures were generated in three genetically distinct strains of mice that had previously been shown to have different patterns of endochondral bone formation. Phosphate deficiency was initiated two days prior to fracture and was then maintained for a 15 day period covering the normal duration of endochondral bone development. To assess if replenishing phosphate could rescue genetic expression of deficient healing, normal phosphate was re-introduced into the diet after 15 days of deficiency and bone healing was allowed to continue until 35 days post fracture. Messenger RNA expression for marker genes for cartilage and bone formation was assessed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) analysis over this time course of healing. Structural properties, callus mineralization and cartilage contents were assessed by micro-computed tomography and contrast agent enhanced micro- computed tomography (CECT). Torsional mechanical testing was used to measure bone strength. To assess if replenishing phosphate could rescue mineralization and biomechanical properties of deficient healing, normal phosphate was re-introduced after 15 days of deficiency and bone healing was allowed to continue until 21 days post fracture. The biological assessment of fracture healing showed that all three genetic strains had impaired expression of both cartilage and bone associated genes during the period of phosphate deficiency. Once phosphate was returned to the diet, however, the osteogenesis genes showed a burst of late expression in all three strains. Interestingly, torsional testing of the bones showed that phosphate deficient/replenished groups were all stronger but also more brittle than the bones of control mice. Micro-computed tomography demonstrated that bone mineral density was slightly higher in the phosphate deficient mice but the bone mineral density standard deviation in the calluses were also higher indicating that the mineralization within the healing calluses was unevenly distributed in the phosphate deficient/replenished group. Lastly, contrast agent enhanced computed tomography data showed that the overall callus tissue mineral density was lower in phosphate deficient/replenished calluses due to the greater cartilage in the phosphate deficient/replenished calluses. These results suggest that the increase strength in the phosphate deficient/replenished calluses is due to the burst of expression in osteogenesis genes that led to the rapid mineralization of the fracture gap in order to compensate for fracture instability due to the phosphate restriction. They also show that a gross metabolic alteration supersedes all other aspects of genetic variably in endochondral development. Finally, they show that even though fracture healing may be greatly delayed by phosphate deficiency, replacement of phosphate after deficiency leads to rapid regain in function. Future studies need to be carried out to determine if longer time lengths of phosphate deficiency can be rescued upon reintroduction of phosphate.

No description available.

Tendon injury is painful and often debilitating, and is a one of the most prevalent soft tissue injuries encountered in the clinic. While common, the underlying molecular and genetic processes of tendon damage and repair remain poorly understood. The work described herein used genome-wide expression analyses to investigate tendon injury and healing from three perspectives. The first identified novel gene expression in tendon fibroblasts following their stimulation with nitric oxide (NO). Of particular relevance to tendon healing was the observation that stimulated fibroblasts express a number of extracellular matrix (ECM) genes in response to NO in a dose-dependent manner, and that NO significantly affects cellular adhesion, a critical process during tendon repair. These findings will be of use when optimising dosages of NO delivery in future work investigating NO as potential treatment for tendon injuries. The second study examined gene expression in an acute tendon injury model in the rat at 1, 7, and 21 days post injury, roughly representing the inflammation, proliferation, and remodelling phase of wound repair. Several novel genes and pathways were found to be differentially expressed at each stage of healing. Of particular interest were the presence of a significant number of genes related to glutamate signaling, a method of cellular communication that has not previously been shown to exist in tendon. Also upregulated were a number of genes which have previously only been associated with embryonic development. Finally, gene expression in a supraspinatus tendinopathy model in the rat was investigated. Several genetic pathways were identified in tendinopathic tendons which have not previously been associated with the disease, and, analogous to the acute injury model study, glutamate signaling gene overexpression was also prevalent. Further in vitro studies showed that the expression of these genes in tendon fibroblasts were stimulated by glutamate treatment, which in turn upregulated pro-apoptotic pathways causing cell death. This may prove to be an important causative factor in the tendon degeneration seen in tendinopathy, in which apoptosis has been identified as playing a significant role. The results of these studies contribute to a better understanding of the aetiology of several extremely common pathologies of this soft tissue, and may help to develop more targeted therapies for increasing the efficacy of tendon healing in future.

Wound healing is a dynamic process that ultimately leads to restoration of tissue integrity and function. The pineal gland hormone melatonin is known for its anti-oncotic, anti- inflammatory and immuno-modulatory effects. However, its role in wound healing has not been established. Since melatonin is synthesised endogenously, we primarily sought to investigate whether the melatonin receptors played a role in the wound healing process. Using immunohistochemical methods and Western blot analysis we observed that MT₁ was normally absent in the rat skin but was strongly expressed on day 1 to day 3 post wounding in the epidermis adjacent to the wound edge. MT₁ expression was restricted to the stratum granulosum and stratum spinosum layers of the epidermis in the rat wounds. MT₁ expression declined thereafter and became nonexistent by day 21 when the wound had completely healed. In contrast, MT₂ was constitutively expressed in all the layers of the normal rat epidermis. MT₂ expression gradually decreased at the injury site following wounding but returned to the normal profile by day 21. Aged rat epidermis showed similar MT₁ and MT₂ expression as adult rats. The profile of tissue distribution of MT₁ and MT₂ in the human epidermis was comparable to the rat epidermis. In the CVUs MT₁ and MT₂ localisation profiles resembled that of a healing wound, akin to a day 1 or day 3 rat dermal wound, during the inflammatory phase. Surprisingly, in contrast to all the tissues investigated, MT₁ was also localised in the stratum basale layer of the keloid epidermis. MT₂ localisation in the same keloid tissues however resembled normal human skin profiles. Secondly, we determined the effects of exogenously administered melatonin, on scarring and wound healing, using a full thickness incisional model of wound healing in rats. Melatonin treatment significantly improved the quality of scarring by day 21. However, our findings would have been strengthened by a more explicit wound closure analysis, measurement of granulation tissue weight, tensile strength, hydroxyl proline content and immunohistochemical assessments of neutrophil infiltration, macrophages, fibroblasts, myofibroblasts and reepithelialization. The treatment also accelerated the angiogenic process and enhanced the VEGF protein profile. Arginase generates proline, the building block for collagen synthesis. Melatonin treatment increased arginase activity and consequently would increase collagen synthesis from day 1. An increase in NOS activity and therefore NO production is known to be detrimental during inflammation. However, various studies have also shown that the NO is essential for granulation tissue formation. Melatonin treatment significantly decreased iNOS activity during the acute inflammatory phase in this study, but significantly increased iNOS activity during the resolving phase. Other markers of inflammatory response and repair were also examined in this study. COX-2 has been shown to play an anti-inflammatory role and melatonin increased COX-2 activity and protein following wounding. SOD (the antioxidant enzyme) activity was also significantly increased during the chronic inflammatory phase on melatonin administration. HO-1 and HO-2 isoforms have also been previously demonstrated to participate in the repair process. Melatonin treatment increased up-regulation of both HO-1 and HO-2 protein expression in the wounded skin. A significant decrease in all the mitochondrial enzyme activities (except complex-II-III), was observed post wounding. Melatonin treatment restored the complex activities to near normal levels. Melatonin also protected mitochondrial membrane integrity and reduced oxidative stress as evidenced by the maintained level of aconitase and citrate synthase activities at near normal levels. In vitro experiments using macrophage and fibroblast cell lines illustrated that melatonin may decrease NOS activity and protein profiles indirectly by stimulating arginase activity and thereby depleting the availability of arginine. This study is the first to fully demonstrate the distribution of melatonin receptors in normal and abnormal wounds. Improvement in the quality of scarring in a rat model of wound healing on melatonin administration is promising but much more quantitative work and preclinical studies are required before melatonin advances into clinical assessment.

I am a Latje Latje man born and raised in Mildura. I am a contemporary artist, a dancer and a father. I began dancing with the Latje Latje dance group when I was four. I come from river country. I spent the first six years of my life on the banks of the Murray River. The river runs right through my work. During the course of my Masters, I have been spending time in the north of Victoria, in central Victoria and in South Gippsland by the sea in Boonerwrung country. I a man of the river, but since the birth of my son, I have been developing a relationship with the sea. My relationship to the sea changed when my son moved to the sea. My spiritual connection to the sea has grown the more time I have spent there and the more spiritual knowledge I have gained of my ancestral country of the Boonerwrung. Within this research project, I explore the question: How can art-making generate a process of recovery, healing and celebration? In my Masters I have developed two series of paintings, one from the river and one from the sea. The first group of paintings were shown in a nine-month solo exhibition, 'City Style - Country Youth' at Bunjilaka, the Aboriginal Section of the Melbourne Museum. The second group were shown at another solo exhibition called 'Mungo Stories' held at the Australia Dreaming Art gallery in Fitzroy, Melbourne. Artefacts My Master of Arts includes the following artefacts: • An Exhibition of Paintings selected from the 63 artworks I have undertaken during the course of my Masters • An Exegesis in which I tell the story of my paintings and my research and in which I give an overview of the paintings I have done during my research degree • A Digital Story which combines didgeridoo music with a selection of my images • Two Audio Tracks, 'Paintings Talk' and 'Grinding the Ochre' • A Short Film in which I describe my experience as a contemporary Indigenous artist.

Thesis (D. Min.)--Ashland Theological Seminary, 2005. / Abstract. Includes bibliographical references (leaves 152-161).

<p>Sår är ett stort problem som medför lidande för patienten, är tidskrävande och medför stora kostnader för sjukvården. Nutrition är livsnödvändigt och en rätt sammansatt kost är viktig för att kroppen ska må bra och fungera väl. Sår och nutrition ligger inom sjuksköterskans ansvarsområde och därför är det av stor vikt att beskriva näringsämnens och nutritionssupplements inverkan på sårläkning. Syftet med denna studie var att beskriva nutritionens betydelse för sårläkning. Studien genomfördes som en deskriptiv litteraturstudie där vetenskapliga artiklar sökts i tidskrifter. Dessa tidskrifter har haft orden nutrition, wound eller nursing i tidskriftens namn. Resultatet, baserat på 13 vetenskapliga artiklar, visar att nutrition har betydelse för sårläkning. I alla studier har en signifikant förbättrad sårläkning påvisats genom nutrition utom i en studie där ett signifikant samband inte fanns men där en trend sågs som antydde på samband. I alla studier som använt sig av nutritionssupplement har en förbättrad sårläkning påvisats, men då flertalet studier innefattar många olika näringsämnen är det svårt att avgöra vilka av dessa som enskilt påverkar sårläkningen.</p>

Epithelial wound healing is a common occurrence in many organisms. In spite of a long history of study in this field, we do not have a complete understanding of the molecular and cellular mechanisms of wound healing, which is a key element to appreciate in order to modulate this process for better clinical outcomes. Optimal outcomes are especially critical in the cornea as a failure to regenerate can result in blindness and a huge decline in quality of life. Matrix Metalloproteinases (MMPs) are a family of zinc dependent proteases that have been shown to be both regulators and effectors of the corneal wound healing process. Strict regulation of MMP-9, the most extensively studied member of the MMP family, has been shown to be critical for efficient wound regeneration. While we now know that MMP-9 is important, and we even have evidence defining some of the roles it plays in the corneal wound healing process, the mechanism by which MMP-9 is regulated is still under debate. Possible extracellular regulatory mechanisms range from cell-cell interactions to cell-matrix interactions to secreted factors. However, the detailed mechanism of events that takes place on the extracellular surface and the downstream signals that mediate MMP-9 are unknown. Therefore, one of the objectives of the presented work is to define the external mechanisms which mediate MMP-9 expression in resurfacing epithelial cells and to link these external signals to internal signaling pathways in vitro. Furthermore, while MMP-9 acts to slow the resurfacing phase of wound healing, other MMPs seem to cause opposing effects. The second objective of the presented work is to provide the first global spatial and temporal MMP expression profile for an in vivo epithelial wound healing scenario and to define possible macroscopic roles of these heretofore unknown MMPs. Finally, this thesis will look at the expression of many MMP family members in a penetrating model which is an increasingly more common wound scenario due to the increase in corrective surgery. The final objective is to examine human post-LASIK corneas and correlate MMP expression with age, post-operative time, or histopathological abnormalities. The knowledge obtained from all aspects of these studies will contribute to the current understanding and knowledge about the roles and regulatory mechanisms of MMPs in the corneal wound healing process.

Sår är ett stort problem som medför lidande för patienten, är tidskrävande och medför stora kostnader för sjukvården. Nutrition är livsnödvändigt och en rätt sammansatt kost är viktig för att kroppen ska må bra och fungera väl. Sår och nutrition ligger inom sjuksköterskans ansvarsområde och därför är det av stor vikt att beskriva näringsämnens och nutritionssupplements inverkan på sårläkning. Syftet med denna studie var att beskriva nutritionens betydelse för sårläkning. Studien genomfördes som en deskriptiv litteraturstudie där vetenskapliga artiklar sökts i tidskrifter. Dessa tidskrifter har haft orden nutrition, wound eller nursing i tidskriftens namn. Resultatet, baserat på 13 vetenskapliga artiklar, visar att nutrition har betydelse för sårläkning. I alla studier har en signifikant förbättrad sårläkning påvisats genom nutrition utom i en studie där ett signifikant samband inte fanns men där en trend sågs som antydde på samband. I alla studier som använt sig av nutritionssupplement har en förbättrad sårläkning påvisats, men då flertalet studier innefattar många olika näringsämnen är det svårt att avgöra vilka av dessa som enskilt påverkar sårläkningen.