Our study indicates that all patients with ALS have the potential to suffer from pain, the intensity of which increases with decreased functional status.

The pathogenesis of bronchial asthma is not yet fully understood. Recently much attention has been given to the hypothesis that intracellular free calcium ([Ca2+]i) metabolism is abnormal in various diseases. In this study weinvestigated whether [Ca2+]i exists abnormally in subjects with bronchial asthma. The [Ca2+]i in 32 treated or untreated subjects with bronchial asthma were compared with 63 normal subjects. Resting levels of [Ca2+]i were estimated by loading the fluorescent indicator Fura-2 in washed platelets. The [Ca2+]i level in the control subjects was 129.7+18.0 nM(mean±SD). However, in that of the bronchial asthma patients was 152.7+44.1 nM, significantly higher than that of the control subjects (p<0.05). It is well recognized that an increase of [Ca2+]i in vascular smoothmuscle involves contraction. The findings suggest that the same phenomenon is quite possible in the tracheal smooth muscle and that it plays an important role in the pathogenesis of bronchial asthma. (Internal Medicine 34: 722-727, 1995)

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