No description available.

No description available.

It has been noticed that the need for total knee replacement surgery is increasing for Asian region. A total knee replacement is a permanent surgical solution for a patient having debilitating pain in knee joint suffering from arthritis. In this surgery, knee joint is replaced with components made up of bio-compatible materials after which the patient can resume the normal day to day activities. Western population has bigger build compared to Asian population. Most of the total knee replacement prosthesis are designed for western population. When these total knee prosthesis are used for Asian population, they cause a mismatch leading to various clinical complications such as reduced range of motion and pain. The studies have been limited to clinical complications caused by the mismatch. To address this limitation, current study is aimed to find the mechanical implications such as stress distribution, maximum stresses, maximum displacements etc., caused by mismatch of total knee replacement components with knee. A surgeon selects total knee components for a patient based on some critical dimensions of femur and tibia bone of knee. In addition, a method to accurately calculate these dimensions of the femur and tibia bone of a real knee was developed in the current study. This method calculated the points of curvature greater than a threshold (decided based on the radius of the curvature) found out using the formula of curvature. Further, the highest point was calculated based on maximum height from a line drawn between initial and final point within the captured points, also the extreme points were calculated based on the sign change in slope of points within the captured points, giving multiple points on the boundary of bones extracted in an MRI image of a patient. The distance between two selected farthest points, out of these points, in specific direction was the basis for selection of the TKR components. Total knee replacement components were modeled in Geomatics Studio 12 software, bones were modeled in Rhinoceros 5 software, assembly of bones and total knee replacements components was done in Solid works 2013 software, the finite element model of the assembly was developed in Hyper mesh 11 software and, the stress analysis and post processing was done in ABAQUS 6.13 software. A static, implicit non linear analysis was performed. Simulations were performed for two conditions: at standing (0o of flexion) and at hyper-flexed (120o of flexion). In order to figure out if there were any mechanical implications of mismatch, the full model of assembly consisting of femur, tibia and fibula bones assembled with total knee replacement components, and the reduced model consisting of only total knee replacement components were simulated separately, results of which have been discussed in the current thesis. In this work, the effect of change of length of ligaments at 120o of flexion in detail was also studied. This study brought out various outcomes of contact mechanics and kinematics between the components of total knee replacement prosthesis.

No description available.

Eine Methode zur Messung der Variabilität des Stabilitätsgrades von Knie-Endo-prothesen. In dieser Arbeit konnte ein valides Messverfahren für die zwangsfreie Messung der Qualität und Quantität der Stabilitätsgrade von Knieendoprothese anhand der AEQUOS-Knieendoprothese entwickelt werden. Dabei galt es, eine Messanordnung und Methodik zu schaffen, die die Messung der Gleichgewichts-lagen ohne Zwangsführung unter Freischaltung aller Freiheitsgrade ermöglicht. Besondere Berücksichtigung fanden in dieser Arbeit die labilen Zustände, da diese für die dynamischen Übergänge zwischen einzelnen Bewegungen nötig sind. Dazu wurde in der vorliegenden Arbeit die Hauptbewegungsrichtung in der Sagittalebene betrachtet. Um zu simulieren, wie der Roll-Gleitvorgang in der AEQUOS-Prothese durch die Inkongruenz der Gelenkflächen realisiert wird, wurden an der Apparatur kleine Flexionswinkel zwischen 15° und 25° eingestellt, wie sie in der Standphase beim Gehen und auch beim Stand auftreten. Größere Winkel zwischen 35° und 90° wurden den Alltagstätigkeiten wie Bücken, Treppensteigen und Hocken zugeordnet, bis hin zum Vorgang des Aufstehens vom Stuhl bei einem Winkel von 105°. Die Erzeugung von Gleichgewichtszuständen wurde erreicht, indem bei einem festen Flexionswinkel Messungen zu den resultierenden Kräften bei unterschiedlichen Kombinationen der Muskelkräfte durchgeführt wurden. Dabei wurden die Muskelgruppen der Extensorengruppe (M. quadriceps), der Flexoren- oder Hamstring-Gruppe, sowie der M. gastrocnemius und der M. popliteus bei jeder Änderung der Kraftvariante in unterschiedlichem Verhältnis zueinander belastet, um die Kraftvektoren zu variieren. Die Gesamtbelastung wurde dabei mit etwa 63 Kilogramm immer konstant gehalten. Die Einzelgewichte wurden für die entsprechende Muskelgruppe unterschiedlich verteilt. Die kleinen Auslenkungsschritte ermöglichten eine isotonische Messung. Eine Zielsetzung bestand darin, die Möglichkeiten der AEQUOS-Prothese zu simulieren und darzustellen, dass Gleichgewichte ohne äußere Einflussnahme nur durch Muskelaktivität unter der Bedingung des Kraftschlusses eingestellt werden. Es wurde erfolgreich gezeigt, dass der Gleichgewichtszustand und der Stabilitätsgrad im Kniegelenk muskulär geändert werden können wie von Nägerl und Kubein-Meesenburg 1993 postuliert.

Osteoarthritis is a degenerative disease of joints, which can be solved with implantation of total joints prosthesis. A high-quality proprioception of knee joint protects the joint against possible bending injury, it is also participating in stabilizing the knee in static position and it is important in the process of coordination of the motion system and precise flexibility of the knee joint. In this thesis are summed up the knowledge of osteoarthritis, total joints prosthesis and proprioception, all is taken in context of connection. The research includes comparison of proprioception of knee joint with arthrosis and total joints prosthesis. Also, the research compared mentioned knee joints with the healthy verification group. All monitored individuals absolved a medical examination of the quality of proprioception in the form of move sensitivity in position of 30ř, 50ř and 80ř. Amongst the knees with arthrosis and knees with total joints prosthesis there were not found a differences with static importance in each of the angle test. In the total comparison there was significantly better proprioception of the knees with the total joints prosthesis. The knee joints of the verification group unlike the joints with arthrosis and total prosthesis showed significantly better flexibility in position of...

Title: Knee - straining of modern gymnasts For the basic study of human movements we need to take into consideration geometry of moving units (bodies), kinematics and dynamics. The theoretical part generally describes all the subjects connected to the research project, especially information about functions of human musculoskeletal system, description of basic biomechanics of knee joint,walking and methods of acquiring and processing of data for kinematic analysis of walking. The experimental part focuses on straining on a knee joint of modern gymnasts. It is a methodical analysis of straining on a knee joint. The foundations for this diploma thesis are data recorded by the Kistler system which we used for measuring of the dynamical part of a jump. We also used the swedish Qualysis Motion Capture system for the kinematic analysis. All the data were processed by Qualysis Track Manager software. The results of the research is kinematical - dynamic analysis, which is further used for the result of full - year of legs - straining of selected type of sport movement. Key words: biomechanics of knee joint, walking, kinematic analysis, gymnastic jumps

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

Neuropeptides, such as substance P (SP) and bombesin/gastrin-releasing peptide (BN/GRP), and neurotrophins are involved in neuro-immunomodulatory processes and have marked trophic, growth-promoting and inflammation-modulating properties. The impact of these modulators in rheumatoid arthritis (RA) is, however, unclear. An involvement of the innervation, including the peptidergic innervation, is frequently proposed as an important factor for arthritic disease. Many patients with RA, but not all, benefit from treatment with anti-TNF medications. The studies presented here aimed to investigate the roles of neuropeptides, with an emphasis on BN/GRP and SP, and neurotrophins, especially with attention to brain-derived neurotrophic factor (BDNF), in human and murine knee joint tissue. The expression patterns of these substances and their receptors in synovial tissue from patients with either RA or osteoarthritis (OA) were studied in parallel with the levels of these factors in blood and synovial fluid from patients with RA and from healthy controls. Correlation studies were also performed comparing the levels of neuropeptides with those of pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)]. Furthermore, the impact of anti-TNF treatment on the levels of BDNF in blood was investigated. In a murine model of RA, the expression of these substances on articular chondrocytes along with their expression in synovial tissue was investigated. The expression of BN/GRP in human synovial tissue was confined to fibroblast-like and mononuclear-like cells whereas SP was detected in nerve-related structures. Receptors for these neuropeptides (GRP-R and NK-1R) were frequently present in blood vessel walls, and on fibroblast-like and mononuclear-like cells. The expression of BDNF and its receptors, p75 neurotrophin receptor and TrkB, was mainly confined to nerve structures. The levels of SP, and particularly those of BN/GRP, in synovial fluid and peripheral blood correlated with the levels of pro-inflammatory cytokines. There were clearly more correlations between SP-BN/GRP and inflammatory parameters than between BDNF and these factors. Plasma levels of BDNF were decreased following anti-TNF-treatment. In the joints of the murine model, there was a marked expression of neurotrophins, neurotrophin receptors and NK-1R/GRP-R in the articular chondrocytes. The expression was down-regulated in the arthritic animals. A neurotrophin system was found to develop in the inflammatory infiltrates of the synovium in the arthritic mice. The results presented suggest that there is a local, and not nerve-related, supply of BN/GRP in the human synovial tissue. Furthermore, BN/GRP and SP have marked effects in the synovial tissue of patients with RA, i.e., there were abundant receptor expressions, and these neuropeptides are, together with cytokines, likely to be involved in the neuro-immunomodulation that occurs in arthritis. The observations do on the whole suggest that the neuropeptides, rather than BDNF, are related to inflammatory processes in the human knee joint. A new effect of anti-TNF treatment; i.e., lowering plasma levels of BDNF, was observed. Severe arthritis, as in the murine model, lead to a decrease in the levels of neurotrophin, and neurotrophin and neuropeptide receptor expressions in the articular cartilage. This fact might be a drawback for the function of the chondrocytes. Certain differences between the expression patterns in the synovial tissue of the murine model and those of human arthritic synovial tissue were noted. It is obvious that local productions in the synovial tissue, nerve-related supply in this tissue and productions in chondrocytes to different extents occur for the investigated substances.

Aktualumas. Kelio sąnario skausmas yra dažna aktyviai gyvenančių vyrų ir moterų problema. Neretai skausmo priežasties nepavyksta nustatyti, tačiau dėl raumenų silpnumo ir kojų asimetrijos biomechanikos pokyčių skausmai yra dažnesni. Todėl šiame darbe iškėlėme hipotezę, kad po kineziterapijos padidės blauzdos lenkiamųjų ir tiesiamųjų raumenų jėga, sumažės kojų raumenų asimetrija bei išnyks kelio sąnario skausmas. Darbo tikslas — nustatyti blauzdos tiesiamųjų ir lenkiamųjų raumenų jėgos pokyčius taikant KT sportuojantiesiems ir nesportuojantiesiems. Buvo atliktas tyrimas, kuriame dalyvavo 29 tiriamieji: 15 sportuojančių asmenų (3 vyrai ir 12 moterų, amžiaus vidurkis 24,1±3,7 metai) ir 14 nesportuojančių asmenų (4 vyrai ir 10 moterų, amžiaus vidurkis 26,5±6,5 metai). Kineziterapija buvo atliekama Lietuvos Olimpiniame Sporto Centre (LOSC) masažo kabinete. Biodex Medikai System (Biodex Medikai System 3 PRO Sertifikuota ISO 9001 EN 46001) aparatūra buvo registruojama raumenų jėga, kai kampinis greitis buvo 60 l/s, 180 l/s ir 360 l/s. Buvo vertinta kairės ir dešinės blauzdos lenkiamujų ir tiesiamųjų raumenų maksimali jėga, galingumas ir maksimali jėga atitinkanti kūno masę. Gauti duomenys parodė, kad didžiausia raumenų jėga pasiekiama tada, kai sportuojančiųjų ir nesportuojančiųjų kampinis greitis yra mažiausias — 60 l/s. Sportuojančiųjų ir nesportuojančiųjų blauzdos tiesiamieji raumenys yra stipresni už lenkiamuosius esant visiems trims kampiniams greičiams. Kineziterapija labiau... [toliau žr. visą tekstą] / Actuality. The problem of the knee joint pain is frequent among women as well as men who lead an active way of life. Unfortunately, causative factors are difficult to state although muscle weaknesses, asymmetry, biomechanical changes with leg pain are frequent. The hypothesis of this work is that due to physical therapy the power of shin flexion and extension increases while their asymmetry decreases and the knee joint pain disappears. The aim of the work is to define the shin flexion and extension muscle power changes while put up into physical therapy among those who are both sport active and sport passive ones. The research work with 29 participants was done; 15 of them were sport active (3 men and 12 women, the average age of them was 24, 1=3,7years old) the rest 14 sport passive ones (4 men and 10 women, the average age of them was 26, 5= 6, 5 years old). Physical therapy exercises took place at Lithuanian Sport Centre in the massage room. The Biodex Medical System (Biodex Medical System 3PRO Certificated ISO 9001 EN 46001) was registered under the power of 60 l/s, 180 l/s and 360 l/s corner speed. The left and the right shin flexion and extension maximal power of participants were evaluated in comparison with their maximal body mass power. The final results reveal that the strongest power is reached under the low 60 l/s corner speed among people who are sport active as well as sport passive. Physical therapy strengthens more shin flexion muscles among sport active... [to full text]