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Cystic renal cell carcinoma includes any malignant neoplasm of renal tubular epithelium which presents as a fluid-filled mass. Approximately 15 per cent of cases of renal cell carcinoma will be cystic on radiologic and pathologic examination. The clinical features of cystic renal cell carcinoma are similar to those which are solid. The radiographic and pathologic findings of cystic renal cell carcinoma are often more confusing and less specific than the findings of renal cell carcinoma which are predominantly solid. There are four basic pathologic mechanisms resulting in cystic renal cell carcinoma: intrinsic multiloculated growth; intrinsic unilocular growth (cystadenocarcinoma); cystic necrosis; and origin from the epithelial lining of a preexisting simple cyst. There are three basic radiologic patterns of cystic renal cell carcinoma: unilocular cystic mass, multiloculated cystic mass, and discrete mural nodule in a cystic mass. Cystic renal cell carcinoma is often extremely difficult to differentiate from non-neoplastic, benign neoplastic, and other malignant neoplastic masses utilizing radiologic studies alone. This review presents the clinical, pathologic, and radiographic features of cystic renal cell carcinoma and discusses its radiologic differential diagnosis.

Inpatient (n = 27) and outpatient (n = 22) cognitive-behavior therapy programs for bulimia nervosa were evaluated in an uncontrolled experiment. Both treatment conditions included exposure with response prevention and cognitive restructuring. Inpatient treatment had a mean length of stay of 5 weeks. Outpatient treatment lasted 15 weeks. Both groups were followed after the end of treatment. The results showed that both programs were effective in reducing problems associated with bulimia nervosa. The inpatient program led to very rapid progress, whereas the outpatient program led to more gradual improvement. There was, however, a trend toward relapse for inpatients. Other psychological disturbances, (e.g., depression) were improved after inpatient, but not outpatient, treatment. These data were discussed in terms of their implications for treatment planning for cases of bulimia nervosa.

Local cerebral glucose utilization was measured in parallel groups of conscious rats following intravenous injection of either 1 mg/kg 8-hydroxy-2-(di-N-propylamino)tetralin (a 5-hydroxytryptamine 1A binding site agonist), 3 mg/kg 5-methoxy 3-(1,2,3,6-tetrahydro-4-pyridinyl)1H indole, succinate (a 5-hydroxytryptamine1B agonist), or saline alone, using the 2-deoxyglucose quantitative autoradiographic techniques (n = 5 in each of the three groups). Following both drugs, local rates of glucose use in the majority of the 72 brain areas analysed remained unaltered, but in some other regions either increases or decreases were observed. In keeping with the observed behavioural response to 8-hydroxy-2-(di-N-propylamino)tetralin there were marked increases in cerebellum (+56%) and motor cortex where a columnar arrangement of increased metabolism (+34%) contrasted with adjacent columns of decrease (-26%). Hippocampal areas showed moderate decreases in glucose use (-13 to -21%). All areas which increased following 8-hydroxy-2-(di-N-propylamino)tetralin also increased following 5-methoxy 3-(1,2,3,6-tetrahydro-4-pyridinyl)1H indole, succinate, but in the latter case all elements of the basal ganglia were also increased, including globus pallidus (+105%) and the striatum where the changes (+54%) were limited to a discrete dorsal region of the nucleus. In the hippocampus only dorsal dentate gyrus was decreased (-24%) whilst a moderate increase (+16%) was observed in dorsal subiculum. The complexity of these results contrasts with previous 2-deoxyglucose investigations where less specific 5-hydroxytryptamine receptor ligands were used, and suggests that certain aspects of brain function may be selectively targeted by systemic pharmacological manipulation of endogenous serotonergic systems.