[Truncated abstract] Knee osteoarthritis (OA) patients have high levels of pain, functional and strength deficits of the quadriceps, decreased proprioceptive acuity, and increased co-contraction and knee joint loading in gait, compared to age matched controls. The increased knee joint loading in this population occurs most commonly in the medial tibio-femoral compartment, due to increased external adduction moments, and with increasing disease severity there is a concomitant increase in the knee adduction moments. A key finding within the knee OA literature is that dynamic loading in gait, due to increased external adduction moments, strongly predicts pain and radiographic disease progression. Current research has shown that exercise interventions reduce pain and time to complete functional activities; however, the effect of these interventions on knee joint loading and muscular activation in gait is still unclear. In addition, the need for specific knee joint strengthening to cause these alterations has not been investigated and it remains unknown if improvements occur due to specific muscle strengthening or due to some general effect of exercise. Therefore, the primary aim of this research study was to examine the effects of general (upper body) and specific (lower body) resistance training interventions on self-perceived outcomes, neuromuscular function and kinematic, kinetic and muscle activation during gait of OA patients compared with asymptomatic controls. ... The examination of gait data following exercise (Study 4) showed trends for changes in the muscle co-contraction ratios. Specifically, the medial/lateral co-contraction ratio (MLCCR) displayed a trend in early stance where the upper body exercise group increased their lateral muscle activity and the lower body group reduced their lateral muscle activity, and the medial/lateral hamstring co-contraction ratio (HAMCCR) displayed this same trend during loading. The trend toward reduced lateral muscle activation, following lower body resistance training, suggests that specific muscle strengthening may have the ability to alter the load distribution. The kinematic and kinetic variables of gait were unchanged by the exercise interventions, highlighting the sensitivity of muscle activation pattern changes due to muscle strengthening. This thesis provides new insights into the co-contraction strategies utilised by knee OA patients. The directed co-contraction strategy employed by knee OA patients and its relationship to the external adduction moment in gait suggest an attempt to redistribute the loading within the knee joint, most likely in response to pain. Further, we have separated the effects of exercise and found differences in self-perceived outcomes based on exercise specificity. This first examination into muscle co-contraction following resistance training of knee OA patients has highlighted the possibility of alterations to the co-contraction patterns following lower body exercise. However, the implications of altering this muscle activation strategy and the consequent effect on distribution of load within the knee joint requires further consideration.

Thesis (M.Tech.:Chiropractic)-Dept. of Chiropractic, Durban Institute of Technology, 2006 18, xvii, 157, 14 leaves, Annexures A-K / The aim of this study was to assess the inter-examiner reliability of motion palpation of the patella, in both pathological (osteoarthritis) as well as functional (patellofemoral pain syndrome) conditions, in order to assess the validity of this assessment tool, which is commonly used as a method in identifying restricted patella motion.

Thesis (M.Tech.:Chiropractic) - Dept. of Chiropractic, Durban Institute of Technology, 2006 xvi, 82 leaves, Annexures A-L / To determine the efficacy of the Harpago and celery seed cream in mild to moderate degenerative joint disease of the knee in terms of subjective and objective clinical findings

Dissertation submitted in partial compliance with the requirements for the Master's Degree in Technology: Chiropractic, Durban Institute of Technology, 2006. / The aim of this study was to assess the inter-examiner reliability of motion palpation of the patella, in both pathological (osteoarthritis) as well as functional (patellofemoral pain syndrome) conditions, in order to assess the validity of this assessment tool, which is commonly used as a method in identifying restricted patella motion. / M

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

M.Tech. (Homoeopathy) / Osteoarthritis (OA) is a chronic and debilitating condition, characterized by irreversible damage to the joint space, most commonly affecting the knees, hips, hands and spine (Colledge et al., 2010). OA is the leading cause of joint pain and disability in middle-aged and elderly persons (Long et al., 2001). The prevalence of OA of the knee in adults living in the United Sates has grown from a reported 21 million in 1990 to a total estimate of 26.9 million in 2005 (CDC, 2011). By the age of 65 years, 80% of the total population has been reported as showing radiographic evidence of OA; while a 20-30% of the total population is symptomatic with radiographic evidence of OA (Doherty et al., 2006). Conventional treatment for OA of the knee is aimed at pain management by use of analgesics and non-steroidal anti-inflammatory drugs (NSAIDs). Some negative effects of these drugs include drug dependency, liver and kidney damage, cardiovascular pathologies, gastric upset and depression. Corticosteroid injections are also used to alleviate chronic inflammation and joint pain, but may lead to further joint destruction (Shamoon and Hochberg, 2000; Mayo Foundation for Medical Education and Research, 2011). OsteoEze Gold™ is a nutraceutical product that contains chondroitin sulphate, glucosamine sulphate, vitamin C and manganese. In combination, the constituents of OsteoEze Gold™ have been shown to be useful in the treatment for OA of the knee (Clegg et al., 2006). In addition, studies have shown that these ingredients prove effective in reducing moderate to severe pain in sufferers of OA of the knee (Vidyasagar et al., 2004). The aim of this study was to determine the effect of OsteoEze Gold™ on the inflammatory marker C-reactive protein (CRP) and quality of life in OA of the knee using blood tests and the Arthritic Impact Measurement Scales (AIMS2SF) respectively. This was a 16-week, double blind, placebo-controlled study using matched pairs according to age, gender and severity of symptoms, and formed part of a group study, with another researcher, who utilized the Intermittent and Constant Osteoarthritis Pain scale (ICOAP) Short Physical Performance Battery (SPPB) and the same sample...

Hui, Pok Shun. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 274-293). / Abstracts in English and Chinese. / Abstract --- p.i / 摘要 --- p.iv / Acknowledgements --- p.vii / Publications Based on Work in this Thesis --- p.viii / Abbreviations --- p.ix / Table of Contents --- p.xi / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- The Mast Cell --- p.2 / Chapter 1.1.1 --- Origin and Development of Mast Cells --- p.3 / Chapter 1.1.2 --- Heterogeneity of Mast Cells --- p.5 / Chapter 1.1.2.1 --- Heterogeneity of Rodent Mast Cells --- p.5 / Chapter 1.1.2.2 --- Heterogeneity of Human Mast Cells --- p.6 / Chapter 1.1.3 --- Activation of Mast Cells --- p.8 / Chapter 1.1.3.1 --- IgE-dependent Activation of Mast Cells --- p.8 / Chapter 1.1.3.1.1 --- FceRI Aggregation and Tyrosine Residue Phosphorylation --- p.9 / Chapter 1.1.3.1.2 --- PLC Activation and Calcium Mobilization --- p.10 / Chapter 1.1.3.1.3 --- PKC and MAPK Activation --- p.11 / Chapter 1.1.3.2 --- IgE-independent Activation of Mast Cells --- p.14 / Chapter 1.1.3.2.1 --- Activation by IgG --- p.14 / Chapter 1.1.3.2.2 --- Activation by Basic Secretagogues --- p.14 / Chapter 1.1.3.2.3 --- Activation by Calcium Ionophores --- p.15 / Chapter 1.1.4 --- Mast Cell Mediators --- p.16 / Chapter 1.1.4.1 --- Preformed Mediators --- p.16 / Chapter 1.1.4.2 --- Newly Synthesized Lipid Mediators --- p.18 / Chapter 1.1.4.3 --- Cytokines and Chemokines --- p.19 / Chapter 1.1.5 --- Pathophysiological Roles of Mast Cells --- p.21 / Chapter 1.2 --- Arthritis --- p.23 / Chapter 1.2.1 --- Epidemiology of Arthritis --- p.23 / Chapter 1.2.2 --- Clinical Features of Arthritis --- p.25 / Chapter 1.2.2.1 --- Angiogenesis and Vasodilation --- p.25 / Chapter 1.2.2.2 --- Synovial Changes --- p.25 / Chapter 1.2.2.3 --- Cartilage Degradation and Bone Erosion --- p.26 / Chapter 1.2.3 --- Pathogenesis of Arthritis --- p.27 / Chapter 1.2.3.1 --- Roles of T Cells --- p.27 / Chapter 1.2.3.2 --- Roles of B Cells --- p.28 / Chapter 1.2.3.3 --- Roles of Mast Cells --- p.28 / Chapter 1.2.3.4 --- Roles of Cytokines --- p.31 / Chapter 1.2.4 --- Treatments of Arthritis --- p.32 / Chapter 1.2.4.1 --- NSAIDs --- p.33 / Chapter 1.2.4.2 --- Glucocorticoids --- p.34 / Chapter 1.2.4.3 --- DMARDs --- p.35 / Chapter 1.2.4.4 --- New Drugs --- p.36 / Chapter 1.3 --- Proteinase-Activated Receptor (PAR) --- p.38 / Chapter 1.3.1 --- Introduction to PARs --- p.38 / Chapter 1.3.2 --- Discovery of PARs --- p.39 / Chapter 1.3.2.1 --- PAR1 --- p.39 / Chapter 1.3.2.2 --- PAR2 --- p.39 / Chapter 1.3.2.3 --- PAR3 --- p.40 / Chapter 1.3.2.4 --- PAR4 --- p.41 / Chapter 1.3.3 --- Structure of PARs --- p.43 / Chapter 1.3.4 --- Activation of PARs --- p.43 / Chapter 1.3.4.1 --- Serine Proteinases --- p.44 / Chapter 1.3.4.1.1 --- Thrombin --- p.44 / Chapter 1.3.4.1.2 --- Trypsin --- p.46 / Chapter 1.3.4.1.3 --- Mast Cell Tryptase --- p.46 / Chapter 1.3.4.2 --- PAR Activating Peptides (PAR-APs) --- p.47 / Chapter 1.3.4.3 --- Proteinase Binding and the Tethered Ligand Mechanism --- p.49 / Chapter 1.3.5 --- Signaling of PARs --- p.50 / Chapter 1.3.5.1 --- Signaling of PAR1 --- p.51 / Chapter 1.3.5.2 --- Signaling of PAR2 --- p.52 / Chapter 1.3.5.3 --- Signaling of PAR 3 and PAR4 --- p.53 / Chapter 1.3.6 --- Termination of Signals and Antagonism of PARs --- p.53 / Chapter 1.3.6.1 --- Termination of Signals by Proteolysis --- p.53 / Chapter 1.3.6.2 --- Termination of Signals by Receptor Desensitization --- p.54 / Chapter 1.3.6.3 --- Antagonism of PARs --- p.55 / Chapter 1.3.7 --- Roles of PARs in Immune Responses --- p.56 / Chapter 1.3.7.1 --- PARs and Mast Cells --- p.57 / Chapter 1.3.7.2 --- PARs and A rthritis --- p.58 / Chapter 1.4 --- Aims of Study --- p.60 / Chapter Chapter 2 --- Materials and Methods --- p.62 / Chapter 2.1 --- Materials --- p.63 / Chapter 2.1.1 --- Materials for Study of PAR Gene Expression in Mast Cells by RT-PCR --- p.63 / Chapter 2.1.1.1 --- Materials for RNA Extraction --- p.63 / Chapter 2.1.1.2 --- Materials for cDNA Synthesis by Reverse Transcription --- p.63 / Chapter 2.1.1.3 --- Materials for Gene Amplification by PCR --- p.64 / Chapter 2.1.1.4 --- Materials for Agarose Gel Electrophoresis --- p.64 / Chapter 2.1.1.5 --- Miscellaneous --- p.64 / Chapter 2.1.2 --- Materials for Study of Histamine Release from RPMCs and LAD2 Cells --- p.65 / Chapter 2.1.2.1 --- Drugs --- p.65 / Chapter 2.1.2.1.1 --- Peptides --- p.65 / Chapter 2.1.2.1.2 --- Serine Proteinases --- p.65 / Chapter 2.1.2.1.3 --- Mast Cell Secretagogues --- p.66 / Chapter 2.1.2.1.4 --- Other Drugs --- p.66 / Chapter 2.1.2.2 --- Materials for Rat Sensitization --- p.66 / Chapter 2.1.2.3 --- Materials for LAD2 Cell Culture --- p.66 / Chapter 2.1.2.4 --- Materials for Buffers --- p.67 / Chapter 2.1.2.5 --- Materials for Spectrofluorometric Analysis of Histamine Contents --- p.67 / Chapter 2.1.2.6 --- Miscellaneous --- p.68 / Chapter 2.1.3 --- Materials for Histological Study of Synovial Mast Cells --- p.69 / Chapter 2.1.3.1 --- Drugs --- p.69 / Chapter 2.1.3.2 --- Chemicals --- p.69 / Chapter 2.1.3.3 --- Miscellaneous --- p.69 / Chapter 2.1.4 --- Materials for Study of Rat Knee Joint Inflammation --- p.70 / Chapter 2.1.4.1 --- Drugs --- p.70 / Chapter 2.1.4.1.1 --- Peptides --- p.70 / Chapter 2.1.4.1.2 --- Other Drugs --- p.70 / Chapter 2.1.4.2 --- Materials for Assessment of Vascular Permeability --- p.71 / Chapter 2.1.4.3 --- Miscellaneous --- p.71 / Chapter 2.2 --- Methods --- p.72 / Chapter 2.2.1 --- Study of PAR Gene Expression in Mast Cells by RT-PCR --- p.72 / Chapter 2.2.1.1 --- Animals --- p.72 / Chapter 2.2.1.2 --- LAD2 Cell Culture --- p.72 / Chapter 2.2.1.3 --- Preparation of Buffers --- p.73 / Chapter 2.2.1.4 --- RNA Extraction --- p.73 / Chapter 2.2.1.5 --- Heparinase and DNase Treatments --- p.74 / Chapter 2.2.1.6 --- cDNA Synthesis by Reverse Transcription --- p.75 / Chapter 2.2.1.7 --- Gene Amplification by PCR --- p.75 / Chapter 2.2.1.8 --- Agarose Gel Electrophoresis --- p.77 / Chapter 2.2.2 --- Study of Histamine Release from RPMCs and LAD2 Cells --- p.77 / Chapter 2.2.2.1 --- Rat Sensitization --- p.77 / Chapter 2.2.2.2 --- Preparation of Buffers --- p.75 / Chapter 2.2.2.3 --- Preparation of Stock Solutions --- p.78 / Chapter 2.2.2.3.1 --- Stock Solutions of Peptides --- p.75 / Chapter 2.2.2.3.2 --- Stock Solutions of Serine Proteinases --- p.79 / Chapter 2.2.2.3.3 --- Stock Solutions of Mast Cell Secretagogues and Other Drugs --- p.79 / Chapter 2.2.2.4 --- Preparation of Mast Cells --- p.80 / Chapter 2.2.2.4.1 --- Isolation and Purification of RPMCs --- p.80 / Chapter 2.2.2.4.2 --- Preparation of LAD2 Cells --- p.81 / Chapter 2.2.2.4.3 --- Determination of Cell Number and Viability --- p.81 / Chapter 2.2.2.5 --- General Protocol for Histamine Release Assay --- p.82 / Chapter 2.2.2.5.1 --- RPMC Experiments --- p.52 / Chapter 2.2.2.5.2 --- LAD2 Cell Experiments --- p.53 / Chapter 2.2.2.6 --- Spectrofluorometric Analysis of Histamine Contents --- p.83 / Chapter 2.2.2.6.1 --- Manual Analysis --- p.85 / Chapter 2.2.2.6.2 --- Automated Analysis --- p.85 / Chapter 2.2.2.7 --- Data Analysis --- p.86 / Chapter 2.2.2.7.1 --- Calculation of Histamine Release --- p.86 / Chapter 2.2.2.7.2 --- Data Presentation and Statistical Analysis --- p.87 / Chapter 2.2.3 --- Histological Study of Synovial Mast Cells --- p.88 / Chapter 2.2.3.1 --- Preparation of Buffers and Chemicals --- p.88 / Chapter 2.2.3.2 --- Preparation of Drugs --- p.88 / Chapter 2.2.3.3 --- Intra-peritoneal Injections of Compound 48/80 --- p.88 / Chapter 2.2.3.4 --- Fixation --- p.89 / Chapter 2.2.3.5 --- Processing --- p.89 / Chapter 2.2.3.6 --- Embedding --- p.90 / Chapter 2.2.3 --- Sectioning --- p.90 / Chapter 2.2.3.8 --- Staining --- p.90 / Chapter 2.2.4 --- Study of Rat Knee Joint Inflammation --- p.91 / Chapter 2.2.4.1 --- Animals --- p.91 / Chapter 2.2.4.2 --- Preparation of Drugs --- p.92 / Chapter 2.2.4.3 --- Induction of Anaesthesia --- p.92 / Chapter 2.2.4.4 --- Intra-articular Injection of Drugs --- p.93 / Chapter 2.2.4.5 --- Topical Administration of Drugs --- p.93 / Chapter 2.2.4.6 --- Assessment of Mechanical Allodynia --- p.93 / Chapter 2.2.4.7 --- Assessment of Joint Oedema --- p.94 / Chapter 2.2.4.8 --- Assessment of Hyperaemia --- p.95 / Chapter 2.2.4.9 --- Assessment of Vascular Permeability --- p.95 / Chapter 2.2.4.10 --- Data Analysis --- p.96 / Chapter Chapter 3 --- Studies of Roles of PAR in Mast Cells --- p.97 / Chapter 3.1 --- Introduction --- p.98 / Chapter 3.2 --- Materials and Methods --- p.103 / Chapter 3.2.1 --- Study of PAR Gene Expression in Mast Cells by RT-PCR --- p.103 / Chapter 3.2.2 --- Study of Effects of PAR Agonists on Histamine Release from Mast Cells --- p.103 / Chapter 3.2.3 --- Study of Signaling Pathways Induced by PAR Agonists in Mast Cells --- p.104 / Chapter 3.3 --- Results --- p.105 / Chapter 3.3.1 --- Study of PAR Gene Expression in Mast Cells by RT-PCR --- p.105 / Chapter 3.3.1.1 --- PAR Gene Expression in RPMCs --- p.105 / Chapter 3.3.1.2 --- PAR Gene Expression in LAD2 Cells --- p.105 / Chapter 3.3.2 --- Study of Effects of PAR Agonists on Histamine Release from Mast Cells --- p.106 / Chapter 3.3.2.1 --- Effects of Serine Proteinases on Histamine Release from RPMCs --- p.106 / Chapter 3.3.2.1.1 --- Thrombin --- p.106 / Chapter 3.3.2.1.2 --- Trypsin --- p.106 / Chapter 3.3.2.1.3 --- Tryptase --- p.107 / Chapter 3.3.2.2 --- Effects of PAR-APs on Histamine Release from RPMCs --- p.107 / Chapter 3.3.2.2.1 --- TFLLR-NH2 (PAR1-AP) --- p.107 / Chapter 3.3.2.2.2 --- SLIGRL-NH2 (PAR2-AP) --- p.108 / Chapter 3.3.2.2.3 --- 2-Furoyl-LIGRLO-NH2 (PAR2-AP) --- p.108 / Chapter 3.3.2.2.4 --- SFNGGP-NH2 (PAR3-AP) --- p.109 / Chapter 3.3.2.2.5 --- AYPGKF-NH2 (PARrAP) --- p.110 / Chapter 3.3.2.3 --- Effects of PAR Control Peptides on Histamine Release from RPMCs --- p.111 / Chapter 3.3.2.4 --- Effects of PAR-APs on Histamine Release from LAD2 Cells --- p.111 / Chapter 3.3.3 --- Study of Signaling Pathways Induced by PAR Agonists in Mast Cells --- p.112 / Chapter 3.3.3.1 --- Effect of PTX on PAR-AP-induced Histamine Release from RPMCs --- p.112 / Chapter 3.3.3.2 --- Effect of BAC on PAR-AP-induced Histamine Release from RPMCs --- p.113 / Chapter 3.4 --- Discussion --- p.115 / Chapter 3.5 --- Figures and Tables --- p.132 / Chapter Chapter 4 --- Studies of Roles of PAR in Rat Knee Joint Inflammation --- p.175 / Chapter 4.1 --- Introduction --- p.176 / Chapter 4.2 --- Materials and Methods --- p.181 / Chapter 4.2.1 --- Histological Study of Synovial Mast Cells --- p.181 / Chapter 4.2.2 --- Study of Rat Knee Joint Inflammation Induced by Intra-articular Injections of PAR-APs --- p.181 / Chapter 4.2.3 --- Study of Rat Knee Joint Blood Flow Changes Induced by Topical Administration of PAR-APs --- p.182 / Chapter 4.2.4 --- Study of the Involvement of Bradykinin B2 Receptors in Rat Knee Joint Inflammation Induced by PAR-APs --- p.183 / Chapter 4.3 --- Results --- p.184 / Chapter 4.3.1 --- Histological Study of Synovial Mast Cells --- p.184 / Chapter 4.3.2 --- Study of Rat Knee Joint Inflammation Induced by Intra-articular Injections of PAR-APs --- p.185 / Chapter 4.3.2.1 --- Intra-articular Injections of Carrageenan and Ovalbumin --- p.185 / Chapter 4.3.2.2 --- Intra-articular Injections of PAR-APs --- p.187 / Chapter 4.3.2.2.1 --- TFLLR-NH2 (PARrAP) --- p.187 / Chapter 4.3.2.2.2 --- 2-Furoyl-LIGRLO-NH2 (PAR2AP) --- p.187 / Chapter 4.3.2.2.3 --- SFNGGP-NH2 (PARrAP) --- p.189 / Chapter 4.3.2.2.4 --- AYPGKF-NH2 (PAR4-AP) --- p.190 / Chapter 4.3.2.3 --- Intra-articular Injections of PAR Control Peptides --- p.191 / Chapter 4.3.3 --- Study of Rat Knee Joint Blood Flow Changes Induced by Topical Administration of PAR-APs --- p.191 / Chapter 4.3.3.1 --- Topical Administration of 2-Furoyl-LIGRLO-NH2 (PAR2-AP) --- p.191 / Chapter 4.3.3.2 --- Topical Administration of A YPGKF-NH2 (PAR4-AP) --- p.192 / Chapter 4.3.4 --- Study of the Involvement of Bradykinin B2 Receptors in Rat Knee Joint Inflammation Induced by PAR-APs --- p.193 / Chapter 4.3.4.1 --- Effect of HOE 140 on Rat Knee Joint Inflammation Induced by Bradykinin --- p.193 / Chapter 4.3.4.2 --- Effect of HOE 140 on Rat Knee Joint Inflammation Induced by 2-Furoyl-LIGRLO-NH2 (PAR2-AP) --- p.194 / Chapter 4.3.4.3 --- Effect of HOE 140 on Rat Knee Joint Inflammation Induced by AYPGKF-NH2 (PARrAP) --- p.195 / Chapter 4.4 --- Discussion --- p.196 / Chapter 4.5 --- Figures and Tables --- p.209 / Chapter Chapter 5 --- General Discussions and Concluding Remarks --- p.261 / Chapter 5.1 --- General Discussions --- p.262 / Chapter 5.2 --- Further Studies --- p.267 / Chapter 5.3 --- Conclusion --- p.271 / References --- p.274

M.Tech. (Homoeopathy) / Osteoarthritis (OA) is a musculoskeletal condition affecting the synovial joints of the body, most commonly the knee and hip (Colledge et al., 2010). OA is the most prevalent joint disorder worldwide (Ickinger & Tikly, 2010). The prevalence of OA of the knee in developing countries, including South Africa, is expected to increase due to the increase in obesity and life-expectancy (Woolf & Pfleger, 2003). OA not only impacts negatively on many areas of the patient’s personal life, but it also has a considerable impact on health care systems and cost to the patient (Lapsley et al., 2001; Majani et al., 2005). The two main complaints in patients suffering from OA of the knee are knee pain and decreased daily functionality, such as walking (Samson et al., 2007). The main aim of conventional treatment is pain reduction. This treatment does not prevent progression of the OA, and may have negative side-effects (Day & Graham, 2005). Treatments for OA, such as OsteoEze GoldTM, may provide an effective and safer alternative. The aim of this study is to determine the effect of OsteoEze GoldTM on pain and functional ability in osteoarthritis of the knee using the Intermittent and Constant Osteoarthritis Pain (ICOAP) scale: knee version (Appendix D) and the Short Physical Performance Battery (SPPB) test (Appendix E). This was a 16-week study, conducted at the Homoeopathic Health Centre, Doornfontein campus (DFC), University of Johannesburg (UJ). The study was randomised, double blind placebo controlled, and matched pairs were utilised. Sixty-seven participants, who satisfied the inclusion and exclusion criteria, were recruited, and 48 of the participants completed the study. Participants were recruited by advertisements, placed in and around the UJ Homoeopathy Health Centre (with relevant permission given) and by word of mouth. The participants were split into two groups using matched pairs according to age, gender and severity of symptoms (Appendix H). The participants in group A received the OsteoEze GoldTM capsules, and the participants in group B received the placebo capsules. Each capsule of OsteoEze GoldTM contained 500mg glucosamine sulphate, 267mg of chondroitin sulphate, 50mg of vitamin C and 1mg of manganese. The OsteoEze GoldTM or the placebo capsules were distributed at the initial (week-0) and second (week-8) consultations.

Knee osteoarthritis (KOA) is the primary cause of chronic immobility in populations over the age of 65. It is a joint degenerative disease in which the articular cartilage in the knee joint wears down over time, leading to symptoms of pain, instability, joint stiffness, and misalignment of the lower extremities. Without intervention, these symptoms gradually worsen over time, decreasing the overall knee range of motion (ROM) and ability to walk. Current clinical interventions include offloading braces, which mechanically realign the lower extremities to alleviate the pain experienced in the medial compartment of the knee joint. Though these braces have proven effective in pain management, studies have shown a significant decrease in knee ROM while using the brace. Concurrently, development of active exoskeletons for rehabilitative gait has increased within recent years in efforts to provide patients with a more effective intervention for dealing with KOA. Though some developed exoskeletons are promising in their efficacy of fostering gait therapy, these devices are heavy, tethered, difficult to control, unavailable to patients, or costly due to the number of complicated components used to manufacture the device. However, the idea that an active component can improve gait therapy for patients motivates this study. This study proposes the design of an adjustable lower extremity exoskeleton which features a single linear actuator adapted onto a commercially available offloading brace. This design hopes to provide patients with pain alleviation from the brace, while also actively driving the knee through flexion and extension. The design and execution of this exoskeleton was accomplished by 3D computer simulation, 3D CAD modeling, and rapid prototyping techniques. The exoskeleton features 3D printed, ABS plastic struts and supports to achieve successful adaptation of the linear actuator to the brace and an electromechanical system with a rechargeable operating capacity of 7 hours. Design validation was completed by running preliminary gait trials of neutral gait (without brace or exoskeleton), offloading brace, and exoskeleton to observe changes between the different gait scenarios. Results from this testing on a single subject show that there was an observed, significant decrease in average knee ROM in the offloading brace trials from the neutral trials and an observed, significant increase in average knee ROM in the exoskeleton trials when compared to the brace trials as hypothesized. Further evaluation must be completed on the clinical efficacy of this device with a larger, and clinically relevant sample size to assess knee ROM, pain while using the device, and overall comfort level. Further development of this design could focus on material assessment, cost analysis, and risk mitigation through failure mode analysis.

Είναι ενδιαφέρουσα αλλά συνάμα δύσκολη η ανάλυση ιατρικών εικόνων, επειδή υπάρχουν πολύ μικρές διακυμάνσεις και μεγάλος όγκος δεδομένων για επεξεργασία. Είναι αρκετά δύσκολο να αναπτυχθεί ένα αυτοματοποιημένο σύστημα αναγνώρισης, το οποίο θα μπορούσε να επεξεργάζεται μεγάλο όγκο πληροφοριών των ασθενών και να παρέχει μια σωστή εκτίμηση. Στην ιατρική, η συμβατική διαγνωστική μέθοδος για εικόνες MR γονάτου για αναγνώριση ανωμαλιών, είναι από την επίβλεψη έμπειρων ιατρών. Η τεχνική της ασαφούς λογικής είναι πιο ακριβής, αλλά αυτό εξαρτάται πλήρως από τη γνώση των εμπειρογνωμόνων, η οποία μπορεί να μην είναι πάντα διαθέσιμη. Στη παρούσα εργασία, τμηματοποιούμε την MR εικόνα του γονάτου με την τεχνική Mean Shift, αναγνωρίζουμε τα κύρια μέρη με τη βοήθεια των ΗΜRF και τέλος εκπαιδεύουμε ταξινομητή ANFIS. Η απόδοση του ταξινομητή ANFIS αξιολογήθηκε όσον αφορά την απόδοση της εκαπαίδευσης και της ακρίβειας ταξινόμησης. Επιβεβαιώθηκε ότι ο ταξινομητής είχε μεγάλη ακρίβεια στην ανίχνευση ανωμαλιών στις ακτινογραφίες Στην εργασία αυτή περιγράφεται η προτεινόμενη στρατηγική για την διάγνωση ανωμαλιών στις εικόνες μαγνητικής τομογραφίας γόνατος. / It is a challenging task to analyze medical images because there are very minute variations & larger data set for analysis. It is a quite difficult to develop an automated recognition system which could process on a large information of patient and provide a correct estimation. The conventional method in medicine for knee MR images classification and diseases detection is by human inspection. Fuzzy logic technique is more accurate but it fully depends on expert knowledge, which may not always available. Here we extract the feature using Mean Shift segmentation and region recognition with HMRF and after that training using the ANFIS tool. The performance of the ANFIS classifier was evaluated in terms of training performance and classification accuracy. Here the result confirmed that the proposed ANFIS classifier with high accuracy in detecting the knee diseases. This work describes the proposed strategy to medical image classification of patient’s MRI scan images of the knee.