Causality was established according to two of Bradford Hill’s criteria of medical causality, temporal and dose-response relationships.
Twenty-three patients with spinal fractures (group 1) of average
age 44 years were compared to 19 patients with self-reported back pain in the workplace pursuing claims for compensation (group 2) of average age 48 years. Both groups were comparable in terms of age and sex. The average ODI in group 1 was 28 % (SD 19) compared to 42 % (SD 19) in group 2 (P < 0.05). Similarly, LBOS was 39.7 versus 24.3 (P < 0.05), MSP 4.3 versus 9.3 (P < 0.05) and MZD 20.2 versus 34.8 (P < 0.05) in groups 1 and 2, respectively.
Despite high-energy trauma and significant structural damage to the spine, patients with the high energy 5-Fluoracil cell line injuries had better spinal outcome scores in all measures. There is no ‘dose-response’ relationship Selleck Adriamycin between
structural injury, low back pain and spinal disability. This is the reverse of what would be anticipated if structural injury was the cause of disability in workplace reported onset of low back pain.”
“Background: Data describing the inhibitory effects of nitric oxide synthase (NOS) on respiratory mechanics are conflicting, and no data are available concerning possible effects on the viscoelasticity of the respiratory system, on the inspiratory work of breathing (WOB) or on respiratory system hysteresis. Objectives: The aim of this study was to measure the effects of NOS inhibition by N-G-nitro-L-arginine methyl ester (L-NAME) on respiratory mechanics
in normal anesthetized rats. Methods: Using the end-inflation occlusion method, it was possible to quantify the ohmic and viscoelastic airway resistance and elastance of the respiratory system. Ohmic resistance is the normalized-to-flow pressure dissipation due to viscous forces opposing the airflow in the airways, as predicted by the Poiseuille law. Viscoelastic resistance is the normalized-to-flow pressure dissipation due to the resistance of respiratory system tissue to deformation during inflation, which is recovered after the arrest of the inspiratory flow (stress HDAC inhibitor relaxation). The inspiratory WOB, its elastic and resistive components, and hysteresis were also calculated. Results: L-NAME induced an increment in the ohmic airway resistance and in the resistive ohmic inspiratory WOB. The viscoelastic resistance due to stress relaxation and the elastic properties of the respiratory system were not modified, and no effect was detected on the related components of the inspiratory WOB and on hysteresis. Conclusions: NO acts in normal rats to reduce the ohmic component of airway resistance, decreasing the ohmic inspiratory WOB. The elastic and viscoelastic components are unaltered. Hysteresis is also unaltered, suggesting that NO has negligible effects on alveolar surfactant activity. Copyright (C) 2011 S.