As management of forests and parks intensifies, pruning of conifers becomes more common. Thus understanding the role of wounds as possible entry courts for decay fungi is vital. In order to study some aspects of this, three natural stands, one in New Brunswick and two in Nova Scotia, which had been pruned 4 to 7 years earlier by industrial or displaced workers, were examined. Five pruned and two unpruned balsam fir (Abies balsamea (L.) Mill.) trees from each stand were dissected; cultural isolations were taken from 207 knots where pruning had caused little or no apparent damage to the bole, and from 169 blazes resulting from less careful prunings. All 15 pruned trees, ranging in age from 23 to 42 years, had decay attributable to pruning which averaged 1.7% of the stem volume. This incidence and volume of decay exceeds that recorded in unpruned trees 40 to 60 years old in New Brunswick. Axe blazes were the major entry court for decay-causing fungis basidiomycetes were associated with 12% of the blazes and with 5% of the more carefully pruned knots. Neither stem nor butt decay was found in the unpruned trees. In a further study, 7 branches on each of 30 balsam fir trees near Fredericton, N. B. were experimentally axe pruned; some carefully, some carelessly; both during tree dormancy and during wet and dry periods of active growth. Thirty additional branches were saw pruned. At periods of 2 to 3 weeks, 5 to 7 months and 17 to 19 months after pruning, cultures were made in the field from 70 of the pruning wounds. Within 2 weeks of the latter period, the trees were dissected, measured and further cultures were made in the laboratory from the same 70 wounds. Eighteen months after pruning, 28 of 30 trees had decay averaging 3.9% of stem volume and basidiomycetes were isolated from 22 (31%) of 70 wounds. In the controls butt decay only occurred in 4 of 10 trees. These studies show: (l) that blazes into sapwood (careless pruning) were more frequently infected than those where little or no sapwood was exposed; (2) the incidence of infection was least in branches pruned during the dry period and about equal for those pruned in the wet-active and dormant periods; and (3) the successional pattern began with imperfect fungi and bacteria, and terminated with decay fungi. / Forestry, Faculty of / Graduate

No description available.

No description available.

No description available.

Doctor of Philosophy / The aim of the work presented in this thesis was to examine the associations between the kinematics of the knee characterised by the tibiofemoral contact pattern, and degenerative change, in the context of anterior cruciate ligament (ACL) injury. While the natural history of degenerative change following knee injury is well understood, the role of kinematics in these changes is unclear. Kinematics of the knee has been described in a variety of ways, most commonly by describing motion according to the six degrees of freedom of the knee. The advantage of mapping the tibiofemoral contact pattern is that it describes events at the articular surface, important to degenerative change. It was hypothesised that the tibiofemoral contact pattern would be affected by injury to the knee. A model of ACL injury was chosen because the kinematics of the knee have been shown to be affected by ACL injury, and because the majority of chronic ACL-deficient knees develop osteoarthritis, the associations between kinematics and degenerative change could be explored. A technique of tibiofemoral contact pattern mapping was established using MRI, as a quantifiable measure of knee kinematics. The tibiofemoral contact pattern was recorded from 0º to 90º knee flexion while subjects performed a leg-press against a 150N load, using sagittal magnetic resonance imaging (MRI) scans. The technique was tested and found to be reliable, allowing a description of the tibiofemoral contact pattern in 12 healthy subjects. The tibiofemoral contact patterns of knee pathology were then examined in a series of studies of subjects at a variety of stages of chronicity of ligament injury and osteoarthritis. Twenty subjects with recent ACL injury, 23 subjects with chronic ACL deficiency of at least 10 years standing, and 14 subjects with established osteoarthritis of the knee were recruited. The 20 subjects with recent ACL injury were examined again at 12 weeks and 2 years following knee reconstruction. The tibiofemoral contact patterns were examined for each group of subjects and the associations between changes in the contact patterns and evidence of joint damage explored. Evidence of joint damage and severity of osteoarthritis were recorded from xrays, diagnostic MRI, operation reports and bone densitometry at the tibial and femoral condyles of the knee. Each of the three groups with knee pathology exhibited different characteristics in the tibiofemoral contact pattern, and these differences were associated with severity of joint damage and osteoarthritis. The recently ACL-injured knees demonstrated a tibiofemoral contact pattern that was posterior on the tibial plateau, particularly in the lateral compartment. Those with chronic ACL deficiency demonstrated differences in the contact pattern in the medial compartment, associated with severity of damage to the knee joint. Osteoarthritic knees showed reduced femoral roll back and longitudinal rotation that normally occur during knee flexion. Two years following knee reconstruction there was no difference between the contact pattern of the reconstructed and healthy contralateral knees. This technique of tibiofemoral contact pattern mapping is sensitive to the abnormal characteristics of kinematics in ligament injury and osteoarthritis. This is the first time the tibiofemoral contact characteristics of chronic ACL-deficient and osteoarthritis knees have been described and links examined between tibiofemoral contact patterns and degenerative change.

Doctor of Philosophy / The aim of the work presented in this thesis was to examine the associations between the kinematics of the knee characterised by the tibiofemoral contact pattern, and degenerative change, in the context of anterior cruciate ligament (ACL) injury. While the natural history of degenerative change following knee injury is well understood, the role of kinematics in these changes is unclear. Kinematics of the knee has been described in a variety of ways, most commonly by describing motion according to the six degrees of freedom of the knee. The advantage of mapping the tibiofemoral contact pattern is that it describes events at the articular surface, important to degenerative change. It was hypothesised that the tibiofemoral contact pattern would be affected by injury to the knee. A model of ACL injury was chosen because the kinematics of the knee have been shown to be affected by ACL injury, and because the majority of chronic ACL-deficient knees develop osteoarthritis, the associations between kinematics and degenerative change could be explored. A technique of tibiofemoral contact pattern mapping was established using MRI, as a quantifiable measure of knee kinematics. The tibiofemoral contact pattern was recorded from 0º to 90º knee flexion while subjects performed a leg-press against a 150N load, using sagittal magnetic resonance imaging (MRI) scans. The technique was tested and found to be reliable, allowing a description of the tibiofemoral contact pattern in 12 healthy subjects. The tibiofemoral contact patterns of knee pathology were then examined in a series of studies of subjects at a variety of stages of chronicity of ligament injury and osteoarthritis. Twenty subjects with recent ACL injury, 23 subjects with chronic ACL deficiency of at least 10 years standing, and 14 subjects with established osteoarthritis of the knee were recruited. The 20 subjects with recent ACL injury were examined again at 12 weeks and 2 years following knee reconstruction. The tibiofemoral contact patterns were examined for each group of subjects and the associations between changes in the contact patterns and evidence of joint damage explored. Evidence of joint damage and severity of osteoarthritis were recorded from xrays, diagnostic MRI, operation reports and bone densitometry at the tibial and femoral condyles of the knee. Each of the three groups with knee pathology exhibited different characteristics in the tibiofemoral contact pattern, and these differences were associated with severity of joint damage and osteoarthritis. The recently ACL-injured knees demonstrated a tibiofemoral contact pattern that was posterior on the tibial plateau, particularly in the lateral compartment. Those with chronic ACL deficiency demonstrated differences in the contact pattern in the medial compartment, associated with severity of damage to the knee joint. Osteoarthritic knees showed reduced femoral roll back and longitudinal rotation that normally occur during knee flexion. Two years following knee reconstruction there was no difference between the contact pattern of the reconstructed and healthy contralateral knees. This technique of tibiofemoral contact pattern mapping is sensitive to the abnormal characteristics of kinematics in ligament injury and osteoarthritis. This is the first time the tibiofemoral contact characteristics of chronic ACL-deficient and osteoarthritis knees have been described and links examined between tibiofemoral contact patterns and degenerative change.

Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 4 uppsatser.

The present study is part of a larger and ongoing research initiative investigating the cumulative cognitive effects of mild head injury in rugby union and focused specifically on high school rugby players. A comprehensive battery of neuropsychological tests was administered to top team high school rugby players (n = 47), and a non-contact sport control group of top team high school hockey players (n = 34). Direct comparisons of group mean scores and standard deviations across each neuropsychological test were carried out for the Total Rugby group versus the Total Hockey group as well as for the subgroups Rugby Forwards versus Rugby Backs. A correlational analysis was conducted to ascertain whether a relationship exists between the number of mild head injuries reported by the players and their cognitive test performance. Results of the group comparisons of means and variability on WMS Paired Associate Learning Hard Pairs - Delayed Recall provides tentative indications of the initial stages of diffuse damage associated with mild head injury in the rugby group and provides some evidence for impairment of verbal learning and memory in the Rugby Forwards group. The correlational analysis revealed no significant relationship between number of reported mild head injuries and cognitive performance. The findings and possible latent effects of the multiple mild head injuries reported by the rugby players are discussed in terms of brain reserve capacity theory and suggestions for future research are provided.

The purpose of this study was to examine the coping styles, beliefs, and symptoms of head-injured adults during long term recovery. Twenty-eight head-injured and thirty-two control subjects suffering from non-neurological illnesses or injuries participated. Subjects completed the Ways of Coping Questionnaire and two questionnaires developed for this study: the "Why Me?" Questionnaire assessed subjects' causal attributions and beliefs about responsibility and the Head-Injury Symptom List provided self-report of the severity of symptoms of head-injury. The coping and belief profiles of the two groups were compared. Head-injured subjects were more likely to place responsibility for their injury on others and to undertake personal efforts to effect their recovery. Various relations between injury attributions and coping styles were obtained. Among both head-injured and control subjects those who endorsed beliefs of retribution were more likely to cope by wishing they could change their situation. Responses to the Head-Injury Symptom List identified tiredness as the most pervasive symptom. Greater symptomatology was related both to a coping style characterized by lack of ability or willingness to engage in social activity or to seek social support and to beliefs that the injury had occurred to serve a meaningful purpose. Consistent with these quantitative results, interviews with head-injured subjects revealed themes of both loss and enhancement. A majority compared their recovery favorably with that of other individuals. In support of cognitive coping theory, this research demonstrates the feasibility of studying the coping capacities of head-injured individuals and shows that they have distinctive coping styles and beliefs which are related to each other. This knowledge should aid those trying to support the recovery of head-injured individuals by adding to the framework upon which interventions are based.

Post-traumatic osteoarthritis (PTOA) of the knee is a complication resulting from direct injury to the joint, such as anterior cruciate ligament and meniscus tears, and accounts for approximately 12% of all OA cases. The economic and clinical impact of PTOA is also greater than idiopathic OA, as patients are younger and often more active, requiring treatments for symptomatic OA over a greater fraction of their lifetime. A common strategy to manage pain and inflammation associated with PTOA is the intraarticular administration of corticosteroids. However, these injections are limited due to the requirement of high-doses imposed by synovial joint clearance rates and their resulting systemic side effects. In addition, currently used broad-spectrum corticosteroids are palliative and not curative, stemming from incomplete knowledge of specific mechanisms that drive cartilage degeneration and other joint pathologies. Thus, most patients with PTOA eventually undergo surgical procedures such as osteochondral graft transplantation for focal defects and in more severe cases, total knee arthroplasty. As such, the studies presented in this dissertation (i) offer specific insights into mechanisms by which traumatic injury can drive joint degeneration and (ii) present novel strategies to modulate joint responses to pathological factors by leveraging sustained drug-delivery platforms. In Part I, mechanistic assessments of human cartilage and synovium responses to insults are conducted to identify novel pathways that may lead to impaired joint homeostasis. First, a direct consequence of traumatic injury, hemarthrosis, is explored as a potential contributor to the development of PTOA specifically through contributions by red blood cells. We demonstrate for the first time the differential roles of erythrocytes in their intact and lysed states through measures of oxidative stress and changes to metabolomic profiles in the context of ferroptosis. Furthermore, we demonstrate the therapeutic potential of Ferrostatin-1, a lipophilic radical scavenger in inhibiting pathological changes to cartilage and its crosstalk with the neighboring synovium in an in vitro model of hemophilic arthropathy. Second, a strategy to prevent an indirect consequence of traumatic injury, arthrofibrosis, is presented in an in vitro model of joint contraction. Fibrosis and the presence of hyperplastic synovium are implicated in the progression of OA through pathological shifts in tissue composition as well as secreted factors that promote cartilage degeneration and the maintenance of a pro-inflammatory joint environment. A type I transforming growth factor beta-1 receptor inhibitor, SB-431542, is encapsulated in polymeric microspheres for the prophylactic treatment of arthrofibrosis through sustained low-dose drug delivery to circumvent the challenges associated with resident joint clearance rates. Utilizing human-based in vitro models of cartilage and synovium pathology, we present novel mechanisms and therapeutic strategies to prevent pathological changes following traumatic joint injury that may contribute to the development of PTOA. In Part II, the sustained delivery platform introduced in Part I is extended to the treatment of PTOA. Osteochondral graft transplantation is currently the clinical gold standard for large focal cartilage lesions. However, allograft procedures are limited due to the lack of available donor tissues and autografts are associated with complications due to donor-site morbidity. In both cases, grafts are subject to failure, potentially in part due to the continual presence of pro-inflammatory factors following surgical procedure. In this section, we present cellular agarose hydrogels embedded with dexamethasone-releasing microspheres that are integrated with a titanium base as a functional tissue-engineered alternative to native osteochondral allografts. These allogenic tissue-engineered grafts were assessed in an in vivo preclinical canine model in their ability to maintain clinical function and to modulate the inflammatory response over the course of 12 months. We successfully demonstrated the feasibility of using engineered grafts by comparing clinical measures of range of motion, function, lameness, and pain, as well as modified cartilage graft scores, against native osteochondral allograft controls. In addition, improvements in the histopathological scoring of neighboring synovial and meniscal tissues indicate the therapeutic capacity of dexamethasone released from within the joint to modulate the inflammatory response up to one-year post-implantation. Taken together, the studies presented in this dissertation identify novel mechanisms behind pathological changes to the cartilage and synovium that may contribute to the development of PTOA following injury. Potential therapeutic targets, inhibitory compounds, and delivery strategies are also assessed using human-based in vitro models of disease and further validated in an in vivo canine model through a clinically relevant timeframe. Ultimately, we demonstrate for the first time, the use of dual-function tissue-engineered grafts in a weight-bearing region of the knee joint to circumvent limitations associated with the clinical gold standard for the treatment of large focal cartilage defects.