The prevention of pain from sickle cell disease by trandolapril

A 48-year-old African-American woman with both sickle cell anemia and chronic pain was treated with a hydrophobic angiotensin I-converting enzyme (ACE) inhibitor. This resulted in the complete resolution of her pain. When the ACE inhibitor was deliberately stopped, her pain recurred, only to cease again after the ACE inhibitor was deliberately resumed. The activation of ACE may be an early step in the arterial vaso-occlusion typical of sickle cell disease.     

Effect of myoelectric signal processing on the relationship between muscle force and processed EMG

The relationship between the force generated by an isometrically contracting muscle and the associated myoelectric signal has been the subject of extensive investigation in the past and conflicting results were reported regarding this relationship. The objective of the present study was to investigate some of the sources that may lead to such conflicting results. Two possible sources were examined. The first was the variability in the force-EMG relationship resulting from processing the EMG signal with different EMG signal processing techniques and the second was the variability in the force-EMG relation obtained from repeated muscle contractions. The results of the study indicate that slight variations in the force-EMG relationships can be attributed to the selection of different processing techniques. However, the variability in the force-EMG relation, obtained by using different EMG signal processors, was found to be significantly smaller than the variability in this relationship obtained from repeated muscle contractions.     

Deriving a risk-adjustment model for pressure ulcer development using the Minimum Data Set

OBJECTIVE: To use the Minimum Data Set (MDS) to derive a risk-adjustment model for pressure ulcer development that may be used in assessing the quality of nursing home care. DESIGN: Perspective observational study using MDS data from 1997. SETTING: A large, for-profit, nursing home chain. PARTICIPANTS: Our unit of analysis was 39,649 observations made on 14,607 nursing home residents who were without a stage 2 or larger pressure ulcer on an index assessment. MEASUREMENTS: Pressure ulcer status was determined at an outcome assessment approximately 90 days after an index assessment. Potential predictors of pressure ulcer development were examined for bivariate associations, contributing to the development of a multivariate logistic regression model. RESULTS: A stage 2 or larger pressure ulcer developed in 2.3% of the observations. Seventeen resident characteristics were found to be associated with pressure ulcer development. These included dependence in mobility and transferring, diabetes mellitus, peripheral vascular disease, urinary incontinence, lower body mass index, and end-stage disease. A risk-adjustment model based on these characteristics was well calibrated and able to discriminate among residents with different levels of risk for ulcer development (model c-statistic = 0.73). CONCLUSION: A clinically credible risk-adjustment model with good performance properties can be developed using the MDS. This model may be useful in profiling nursing homes on their rate of pressure ulcer development.     

The neurotoxic effect of gold sodium thiomalate on the peripheral nerves of the rat: Insights into the antiinflammatory actions of gold therapy

Although gold is one of the few therapeutic agents that has been proven effective in producing remission in patients with rheumatoid arthritis, its mechanism of action is unknown. Since nociceptive afferent and sympathetic efferent fibers of the peripheral nervous system contribute to the pathophysiology of inflammation, and since a known side effect of gold therapy is a polyneuropathy, we tested the hypothesis that gold is toxic to small-diameter peripheral nerve fibers in the rat. We found that prolonged treatment with gold, at the same dosage reported to be effective against adjuvant-induced arthritis in the rat, produced a significant decrease in the numbers of unmyelinated, but not of myelinated, axons. Gold treatment also elevated nociceptive thresholds in both articular and nonarticular structures. These results suggest that gold produces an antiinflammatory effect on arthritis by a neurotoxic effect on the peripheral nerves involved in neurogenic inflammation.