The arthropathy of calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is distinctive and may affect lumbar spinal and sacroiliac joints, as well as appendicular joints. Subchondral pseudocysts that are a hallmark of the disease have a variable appearance, but often occur as a typical cluster of subchondral, coalescent lucencies with smudged, sclerotic margins. Structural joint collapse with fragmentation of cartilage and bone may occur and appear to be related, at least in some cases, to antecedent pseudocysts. Characteristic intra-articular osteochondral bodies are often extensive and may affect multiple joints; their pathogenesis is discussed. Articular synovial calcification is common and may be due to calcium hydroxyapatite, as well as CPPD, particularly if advanced degenerative changes are present. Recognition of the radiologic features may be encountered in CPPD crystal deposition disease is important for differential diagnosis.

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We can distinguish two classes of membrane transport changes in cultured cells: (a) growth-rate contingent changes are those which occur in coordination with the onset of density-dependent inhibition of growth; (b) transformation-specific changes are those which occur when cells become transformed, and which can be detected even when normal and transformed cells are growing at the same rate. Growth-rate contingent changes include the density-dependent changes in phosphate, nucleoside, glucose, amino acid, and potassium transport. Only one transformation-specific transport change has been found in Rous-transformed chicken embryo fibroblasts: an increased rate of hexose transport. The variation in potassium transport are associated with variations in the number of ouabain binding sites in the membrane. The molecular basis for changes in the rate of hexose transport is unknown, although gross changes in membrane bilayer composition and "fluidity" seem not to be involved. In analyzing the regulation of hexose transport activity, we find that decreased cAMP may play a role in the transformation-specific increase in hexose transport, but that fibrinolytic activity is not necessary.

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Two diagnostic schemes for detection of pulmonary embolism by ventilation-perfusion (V-P) scintigraphy were compared for relative accuracy by two groups of observers interpreting 70 V-P scintiscans. Observers in Group B, who used the criteria recently proposed by Biello et al., had a significantly smaller average number of "indeterminate" interpretations (41%) than did the observers in Group A (55%), who used a simpler scheme (p less than 0.05). In addition, Group B showed a slight improvement in positive predictive value without a deterioration in the negative predictive value compared with Group A. Along with this improvement in diagnostic performance, Group B achieved a significant reduction in interobserver variability compared with Group A for patients without pulmonary embolism (p less than 0.05). There was no significant difference in interobserver variability between the two groups for patients with pulmonary embolism. The diagnostic scheme introduced by Biello et al. represents a useful improvement for the diagnosis of pulmonary embolism by V-P imaging.