Psychophysics of reading--XIV. The page navigation problem in using magnifiers.

Most people with low vision require magnification to read. A magnifier's field of view often contains only a few letters at a time. Page navigation is the process by which the reader moves the magnifier from word to word, and from the end of one line to the beginning of the next line. Page navigation takes time and reduces reading speed. The major questions addressed in this paper are: (1) What role does page navigation play in limiting reading speed? and (2) Are the window width requirements for reading (number of characters in the field for a criterion performance level) increased by the need for page navigation? We measured the reading speeds of three normal-vision and seven low-vision subjects in two ways: with drifting-text requiring no page navigation, and with a closed-circuit TV (CCTV) magnifier which required page navigation. We built special hardware to record the location of the CCTV's magnified field in the text. These recordings were used to separate forward-reading time (left-to-right movement through the text) from retrace time (navigational movement). For normal-vision subjects, forward-reading and retrace times were about equal. For low-vision subjects, retrace times were shorter than forward-reading times, indicating that the forward-reading performance was limited by visual, not navigational, demands. The retrace time did have an impact, however, ranging from 17 to 50% of the overall time. The window requirements for reading with page navigation (CCTV) were larger than those for reading without page navigation (drifting-text). The difference was more than a factor of three for normal-vision subjects and close to a factor of two for low-vision subjects (10 characters for CCTV vs 5.2 characters for drifting-text for 85% of maximum reading speed.

Relationship between saliva and serum quinidine concentrations and suppression of ventricular premature beats.

Saliva and serum quinidine concentrations were determined in six cardiac patients after twice-daily dosing with 324 or 648 mg quinidine gluconate and the relationship of these concentrations to the degree of suppression of ventricular premature beats (VPB) was evaluated. Mixed saliva and corresponding serum samples were obtained at various times after the 1st, 9th, and 19th doses. With serum quinidine concentrations ranging from 0.05 to 0.83 micrograms/ml after the first dose, the average saliva/serum ratios for quinidine varied between 0.25 and 1.35 (0.54 +/- 0.43). At steady state with the serum quinidine concentrations ranging between 0.36 and 3.35 micrograms/ml, the average saliva/serum ratios ranged from 0.27 to 1.79 (0.81 +/- 0.72) and from 0.19 to 1.84 (0.90 +/- 0.85) for the 9th and 19th doses, respectively. The interpatient variations in the saliva/serum ratio were large for the three doses (approximately 90%). On the other hand, the intrapatient variations were smaller and diminished with each succeeding sampled dose (from 31 to 18 to 12% for the 1st, 9th, and 19th doses, respectively). Moreover, the value for the quinidine saliva/serum ratio for a given patient was similar for all three doses. No significant correlation between the extent of VPB suppression and the concentrations of quinidine in the saliva or serum was observed. The data suggest that salivary quinidine concentrations may be clinically useful to monitor serum drug concentrations in a given patient. However, the relationship between saliva and serum quinidine concentrations and suppression of VPB measured by Holter monitoring is not clear-cut.