OBJECTIVES To modify the Prostate Cancer Prevention Trial Risk Calculator (PCPTRC) to predict low- versus high-grade (Gleason grade ≥ 7) prostate cancer and incorporate percent free PSA. METHODS Data from 6664 PCPT placebo arm biopsies [5826 individuals] where prostate-specific antigen (PSA) and digital rectal examination (DRE) results were available within one year prior to the biopsy and PSA was ≤ 10 ng/mL were used to develop a nominal logistic regression model to predict the risk of no versus low-grade (Gleason grade < 7) versus high-grade (Gleason grade ≥ 7) cancer. Percent free PSA was incorporated into the model based on likelihood ratio (LR) analysis of a San Antonio Biomarkers of Risk cohort. Models were externally validated on ten Prostate Biopsy Collaborative Group cohorts and one Early Detection Research Network (EDRN) reference set. RESULTS 5468 (82.1%) of the PCPT biopsies were negative for prostate cancer, 942 (14.1%) detected low-grade and 254 (3.8%) high-grade disease. Significant predictors were (log-base-2) PSA (OR for low-grade versus no cancer: 1.29*, high-grade versus no cancer: 2.02*, high-grade versus low-grade cancer: 1.57*), DRE (0.96, 1.49*, 1.55*, respectively), age (1.02*, 1.05*, 1.03*), African American race (1.13, 2.83*, 2.51*), prior biopsy (0.63*, 0.81, 1.27), and family history (1.31*, 1.25, 0.95), where * indicates p-value < 0.05. The new PCPTRC 2.0 either with or without percent free PSA (also significant by the LR method) validated well externally. CONCLUSIONS By differentiating risk of low- versus high-grade disease on biopsy, PCPTRC 2.0 better enables physician-patient counseling concerning whether to proceed to biopsy.

Anti-AT1R and -ETAR Abs are more frequent in SSc-PAH/connective tissue disease-PAH compared with other forms of pulmonary hypertension, and serve as predictive and prognostic biomarkers in SSc-PAH. Both antibodies may contribute to SSc-PAH via increased vascular endothelial reactivity and induction of pulmonary vasculopathy.

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In a group of 15 male Wistar rats overfed with cafeteria foods (delivering a mean fat percentage of 60%) during 5 months from the age of 8 weeks and in a control group of 15 rats fed with a standard chow for the same period, serum leptin, insulin and corticosterone were measured by RIA and body composition was determined by dual-energy X-ray absorptiometry. Significantly higher fasting serum concentrations of leptin, insulin and corticosterone were found in the cafeteria-diet group. Fasting leptin concentrations were significantly higher in rats with a body fat percentage of more than 25% compared to the others, irrespective of the type of feeding. The log serum leptin correlated positively with body fat percentage and fasting insulin concentration but not with corticosterone concentration. Leptin concentration corrected for body fat mass was, however, comparable between the two diet groups, while the leptin/insulin ratio was lower in the cafeteria-diet group. In conclusion, chronic overfeeding resulting in an increased body fat percentage in rats is associated with hyperleptinemia, hyperinsulinemia and hypercorticism. Serum leptin levels appear to primarily track total body fat percentage and are unaffected by dietary fat manipulation in cafeteria-diet-induced obese rats.

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