Assessment of argyrophilic nucleolar organizer region quantification in benign and malignant bone tumors.

Quantification of argyrophilic nucleolar organizer regions has been proposed as a technique that may aid in diagnosing and predicting the biologic behavior of a variety of neoplasms. A 1-step silver staining technique was used to identify and quantify argyrophilic nuclear organizer regions in a series of 96 bone tumor specimens. Malignant bone tumors had a higher mean argyrophilic nuclear organizer region count (3.05 +/- 0.82) than giant cell tumors (1.39 +/- 0.14, p < 0.001) and benign bone tumors (1.51 +/- 0.42, p < 0.001). Despite these differences in mean counts, an overlap of argyrophilic nuclear organizer region scores was observed in some benign and malignant cases. The argyrophilic nuclear organizer region counts of the osteosarcomas were analyzed to determine whether they correlated with tumor behavior. The mean argyrophilic nuclear organizer region count of specimens from patients in whom metastatic disease developed was not significantly different than that of patients who remained disease free.

Urinary excretion of 3-methylhistidine: an assessment of muscle protein catabolism in adult normal subjects and during malnutrition, sepsis, and skeletal trauma.

The urinary excretion of 3-methylhistidine (3 MEH) has been shown to be a reliable index of muscle protein breakdown. It is decreased in protein-calorie malnutrition and increased during the hypercatabolic phase of sepsis and thermal trauma. Losses of 3 MEH after moderate to severe skeletal trauma in man and animals are reported as increased or unchanged. To clarify this response, 24 male and 6 female skeletal trauma patients were evaluated for 24 hr urinary losses of 3 MEH, nitrogen and creatinine. Eight of the 24 males also received a catabolic steroid for treatment of a head injury. In addition, 3 male and 1 female septic patients were similarly evaluated. Controls consisted of 10 volunteers on a meat free diet for 4 days and of 8 volunteers who were given only intravenous 5% dextrose in water for 3 days. The 3 MEH excretion for all control males was 3.6 mumole/Kg/day and for females was 2.8 Skeletal trauma produced a 280% increase for the males and a 225% increase for the females. Trauma with steroids caused a 325% increase. Sepsis induced a 227% increase in 3 MEH losses for males and 292% for females during the febrile episode. Creatinine excretion also increased significantly in response to trauma and sepsis but the magnitude of the increase was less than for 3 MEH. This was reflected in the 3 MEH to creatinine molar ratio increase from 0.018 for controls to 0.030-0.040 in sepsis and trauma. Patients with extensive body weight loss showed decreases in 3 MEH and creatinine excretion and a molar ratio similar to controls. The calculated contribution of muscle protein to whole body protein breakdown in the trauma and septic groups showed a twofold increase compared to the control group. The data indicate that the increased muscle protein catabolic response following stress of skeletal trauma and sepsis provides an insight on the origin of the large urinary nitrogen losses following such insults.