Student Assistant for Learning from Text (SALT): a hypermedia reading aid.

Student Assistant for Learning from Text (SALT) is a software system for developing hypermedia versions of textbooks designed to help students with learning disabilities and other low-achieving students to compensate for their reading difficulties. In the present study, 10 students with learning disabilities (3 young women and 7 young men ages 15 to 17) in Grades 9 and 10 read passages from a science textbook using a basic computer version and an enhanced computer version. The basic version included the components found in the printed textbook (text, graphics, outline, and questions) and a notebook. The enhanced version added speech synthesis, an on-line glossary, links between questions and text, highlighting of main ideas, and supplementary explanations that summarized important ideas. Students received significantly higher comprehension scores using the enhanced version. Furthermore, students preferred the enhanced version and thought it helped them learn the material better.

Blastomyces dermatitidis and the adult respiratory distress syndrome. Case reports and review of the literature.

The adult respiratory distress syndrome (ARDS) developed in 2 patients with blastomycosis. In one, ARDS apparently followed the rupture of an infected subcarinal lymph node into a bronchus. Extensive involvement of alveoli with Blastomyces dermatitidis was noted at autopsy in both patients. Four additional cases of blastomycosis with definite or presumed ARDS are reviewed. The clinical course of these 6 patients was characterized by a prolonged prodrome (median, 36 days), consistent with pulmonary blastomycosis, and a rapid demise (median, 5 days) associated with ARDS.

Elevated fibrin(ogen) degradation products in the adult respiratory distress syndrome.

During a 60-h period after the onset of either the adult respiratory distress syndrome (ARDS) in 14 patients, or similar predisposing conditions without respiratory insufficiency (non-ARDS) in 12 patients, blood was obtained 3 times for assessment of coagulation, fibrinolysis, and complement. Platelet counts decreased progressively in both groups, and a platelet release protein, Beta-thromboglobulin, was similarly increased in both groups. Fibrinopeptide A concentrations were similarly increased in both groups. Hemolytic activity of complement components C3 and C5 was within the normal range in both groups. In contrast, the fibrin/fibrinogen degradation product, D-antigen, was significantly increased in the ARDS group over all time periods (p < 0.01). These findings suggested that higher concentrations of circulating fibrin/fibrinogen degradation products are associated with ARDS itself, either as a marker or more extensive microvascular injury or as a possible mediator of injury.

Positive end-expiratory pressure shifts left ventricular diastolic pressure-area curves.

Positive end-expiratory pressure (PEEP) ventilation is frequently associated with reduction in cardiac output despite unchanged transmural left ventricular (LV) end-diastolic pressure. These findings have been interpreted to indicate decreased contractility, but could also be explained by altered LV diastolic pressure-volume characteristics. To study this possibility, radiopaque markers were inserted into a plane of the LV in nine dogs. Transmural pressure (LV-pericardial) was synchronized with LV area during ventilation with zero end-expiratory pressure and with 15 cmH2O PEEP. Mean polynomial curves derived from the diastolic pressure-area data demonstrated that PEEP shifted the curves upward so that a given diastolic area was associated with a higher transmural LV pressure (P less than 0.0001). PEEP decreased end-diastolic area and stroke area, both of which were normalized with dextran volume expansion. Restoration of stroke area by normalizing end-diastolic area with volume expansion suggests the initial changes with PEEP were due to a decrease in preload rather than in contractility.

T4 toxicosis.

We have described a 25-year-old man with hyperthyroidism and normal levels of serum T3 and reverse T3, but with abnormalities in serum T4I, T3U, FTI, FT4, and T3 suppression and TRH stimulation tests consistent with the diagnosis of T4 toxicosis. Serum total iodine was elevated several-fold, and the observed response to iodine depletion and loading suggested that the T4 toxicosis in this patient probably resulted from an increased iodine load, with production of T4 preferentially to T3. There appeared to be no evidence of a defect in peripheral conversion of T4 to T3.