Biomedical subjects
A J Farrell
Publications and source records attributed to A J Farrell.
Inactivation of synovial fluid alpha 1-antitrypsin by exercise of the inflamed rheumatoid joint.
alpha 1-Antitrypsin (alpha 1AT) is known to be oxidised by reactive oxygen species both in vitro and in vivo, leading to its inactivation. We report here that synovial fluid (SF) alpha 1AT is inactivated during exercise of the knee-joints of rheumatoid arthritis (RA) patients. Sequential SF sampling from exercised RA patients showed a marked decrease in the mean activity of alpha 1AT after exercise with no change in the molecular forms of alpha 1AT. No such inactivation was found in the control (continuously resting) RA patients. We suggest that oxidation may contribute to alpha 1AT inactivation as a consequence of 'hypoxic-reperfusion' injury after exercise of the inflamed joint.
Exercise induced release of von Willebrand factor: evidence for hypoxic reperfusion microvascular injury in rheumatoid arthritis.
Experimental evidence suggests that rheumatoid synovitis may be perpetuated by the generation of reactive oxygen species during hypoxic reperfusion injury. The latter occurs because increased intra-articular pressure during exercise exceeds synovial capillary perfusion pressure, impairing blood flow. The object of this study was to establish a marker for and the mechanism of synovial hypoxic reperfusion injury. Von Willebrand factor (vWF) is only released from endothelial cells and platelets and is an in vivo and in vitro marker of endothelial injury. In vivo exercise induced changes in plasma vWF were therefore investigated in patients with rheumatoid arthritis (RA) compared with controls and in vitro vWF release by human umbilical vein endothelial cells subjected to hypoxia reperfusion. Pre-exercise plasma vWF levels were 1001 and 817 IU/l, increasing after exercise to 1658 and 845 IU/l in patients with RA and controls respectively. Von Willebrand factor release from human umbilical vein endothelial cells followed a biphasic pattern, occurring during both hypoxia and reperfusion. Hypoxia reperfusion induced vWF release by human umbilical vein endothelial cells in vitro suggests that exercise induced vWF release in patients with RA is best explained by synovial hypoxic reperfusion injury. This study supports evidence that generation of reactive oxygen species plays a principal part in synovial hypoxic reperfusion injury and suggests vWF as a useful marker of this phenomenon.
von Willebrand factor antigen in giant cell arteritis.
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Increased concentrations of nitrite in synovial fluid and serum samples suggest increased nitric oxide synthesis in rheumatic diseases.
Cytokines induce nitric oxide synthesis by endothelial cells, macrophages and polymorphonuclear leucocytes, indicating a role for nitric oxide in inflammatory processes. Nitric oxide production was therefore measured indirectly as nitrite in serum and synovial fluid samples from patients with rheumatoid arthritis (RA) and osteoarthritis (OA) together with serum samples from healthy volunteers matched for age and sex. Serum nitrite concentrations in patients with RA and OA were significantly higher than in controls. In both disease groups synovial fluid nitrite was significantly higher than serum nitrite, implying nitric oxide synthesis by the synovium. Serum and synovial fluid nitrite concentrations in RA were also significantly higher than those in OA. These data show increased nitric oxide production in RA and OA and suggest a role for nitric oxide as an inflammatory mediator in rheumatic diseases.
Inactivation of the elastase inhibitory activity of alpha 1 antitrypsin in fresh samples of synovial fluid from patients with rheumatoid arthritis.
The proteinase inhibitory ability of alpha 1 antitrypsin was measured in 23 samples of rheumatoid arthritis synovial fluid, eight osteoarthritic synovial fluids and nine normal control serum samples. For each sample a detailed kinetic analysis was performed with porcine pancreatic elastase as the target proteinase. Samples were stored for less than 24 hours at 4 degrees C before analysis, which does not significantly alter the proportion of inactive alpha 1 antitrypsin. In rheumatoid synovial fluid the elastase inhibitory ability was disproportionately depressed relative to the immunochemically determined concentrations of alpha 1 antitrypsin.
Hypoxia and inflammatory synovitis: observations and speculation.
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First attack of rheumatic fever in an adult: the case for greater awareness.
A 40 year old white woman presenting with rash, fever, and migratory polyarthralgia developed a symmetrical polyarthropathy and remained unwell for 10 weeks. Fulfilment of the revised Jones criteria reinforced the clinical diagnosis of rheumatic fever. Antistreptococcal antibodies peaked four to six weeks into the illness and declined thereafter.
Low power laser therapy of shoulder tendonitis.
30 patients with supraspinatus or bicipital tendonitis were randomly allocated to active infrared laser therapy at 904 nm three times weekly for 2 weeks, dummy laser or drug treatment for 2 weeks. Objectively maximum active extension, flexion and abduction of the shoulder, and subjectively pain stiffness movement and function were measured at 0 and 2 weeks. Significant improvement of active over dummy laser was noted for all seven assessments. Active laser therapy produced significant improvement over drug therapy for all three objective measures and pain. Naproxen sodium significantly improved only movement and function compared to dummy laser. These results demonstrate the effectiveness of laser therapy in tendonitis of the shoulder.
Resistogram method for differentiation of strains of Candida albicans.
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