Using performance Petri Nets modelling and analysis of communication protocol implementation

This thesis reports from an investigation of the adequacy of performance Petri nets (PPNs) for modelling communication protocols and evaluating their performance. The report describes PPNs and their tools. It shows how an abstract specification of an existing communication protocol, the Trivial File Transfer Protocol (TFTP), can be modeled and how implemenmtation details can be added while preserving correctness. We use the tools to predict the performance of TFTP. The performance parameters of the model are obtained from an existing UNIX implementation of TFTP. The predicted performance is compared with measured performance of TFTP on a Sun workstation. From the results we evaluate PPNs with respect to modelling limitations, complexity, expressivity and accuracy

Abstract 2826: Carbohydrate intake, glycemic load, and glycemic index and prostate cancer risk

Abstract Background: The typical U.S. diet is characterized by high carbohydrate intake, and dietary carbohydrates can modulate insulin sensitivity depending on their glycemic effect. Glycemic load and glycemic index, which represent the quality and quantity of carbohydrate foods, and prostate cancer risk are poorly characterized. Objective: To examine the association between dietary carbohydrate intake, glycemic load, and glycemic index and risk of prostate cancer, and determine if these associations differ between Whites and Blacks. Methods: We analyzed data from an ongoing case-control study of White (N=109) and Black (N=143) veterans at the Durham VA Medical Center. Cases were 65 men with biopsy-confirmed prostate cancer. There were two groups of controls: biopsy-negative controls (N=89) and healthy (i.e. no biopsy indication) controls (N=98). All men had a PSA test done in the year prior to enrolling in the study. Demographic and lifestyle risk factors were collected using self-administered questionnaires. Diet information was obtained using the Harvard food frequency questionnaire. Odds ratios (OR) and corresponding 95% confidence intervals (95% CI) for prostate cancer risk were obtained using logistic regression analyses adjusted for age, race, and total energy. Results: Mean carbohydrate intake, glycemic load, and glycemic index were similar among cases and both groups of controls (all p-values &amp;gt;0.05). We did not observe any statistically significant risk estimates for high (≥median) carbohydrate intake, glycemic load, or glycemic index. Compared to healthy controls, the ORs for prostate cancer risk associated with high carbohydrate intake, glycemic load, and glycemic index were 0.66 (95% CI 0.34-1.30), 0.57 (95% CI 0.22-1.49), and 1.18 (95% CI 0.61-2.02) respectively. Corresponding ORs when compared to biopsy-negative controls were 0.88 (95% CI 0.46-1.70), 0.69 (95% CI 0.29-1.64), and 0.83 (95% CI 0.43-1.59), respectively. The associations between carbohydrate intake, glycemic load, or glycemic index and risk of low-grade (gleason score &amp;lt;7) as well as high-grade (gleason score ≥7) prostate cancer relative to healthy controls were null for all analyses. There was no evidence of effect modification by race in our analyses. Additional adjustment for fiber intake did not appreciably alter any of the ORs. Conclusion: Our findings in a small case-control study do not suggest that a high carbohydrate intake and/or high glycemic load increase the risk of prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2826.</jats:p

Abstract B110: Dietary polyunsaturated fatty acids and risk of prostate cancer

Abstract Background: Prostate cancer is the most commonly diagnosed cancer among men in the United States, and disproportionately affects African-American men. It has been suggested that diet plays a role in prostate cancer development and progression. Evidence regarding the effect of polyunsaturated fatty acids (PUFA) indicate that n-3 PUFAs may suppress prostate cancer development while n-6 PUFAs may enhance prostate cancer carcinogenesis. Epidemiologic studies, however, have been inconsistent and the association between PUFAs and prostate cancer has not been adequately studied in racially diverse samples. Objectives: The objectives of this work were to 1) examine the association between dietary intake of PUFAs [n-3 (ALA, EPA, DHA); n-6(AA, LA)] and risk of prostate cancer, and 2) determine if these associations differ between Whites and African-Americans. Methods: Data are from an ongoing case-control study among veterans at the Durham VA Medical Center that includes biopsy-positive cases (N=66), biopsy-negative controls (N=91), and healthy controls (N=101). All men had a PSA test done in the year prior to study enrollment. Data were collected on various demographic, lifestyle, and other risk factors for prostate cancer using self-administered questionnaires. Diet was assessed using a food frequency questionnaire that asked participants to recall their diet in the past 12 months. Logistic regression analyses were used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) among Whites (N=111) and African-Americans (N=146). Results: The median percent of energy from total n-6 PUFAs was higher in cases compared to healthy controls (6.2% vs 5.7%, p=0.05). The ORs for cases relative to healthy controls were greater than one for high (i.e. ≥median) intakes of total n-6 PUFAs (OR: 1.79, 95% CI 0.92–3.48), yet close to null for total n-3 PUFAs (OR: 1.02, 95% CI 0.53–1.96). There were non-statistically significant inverse associations for specific PUFAs such as EPA, DHA, and LA (ORs 0.77, 0.68, and 0.62, respectively; all p-values &amp;gt;0.05). A higher n-3:n-6 ratio was suggestive of lower prostate cancer risk (OR: 0.80, 95% CI 0.42–1.54). These findings were relatively unchanged in analyses comparing cases to biopsy-negative controls. In race-specific analyses comparing cases to biopsy-negative controls, there was evidence of effect modification by race for the relationship between LA intake and prostate cancer risk (OR: 0.78, 95% CI 0.30–2.04 in Whites; OR: 3.23, 95% CI 1.24–8.40 in African-Americans; Pinteraction=0.04). We did not observe any other statistically significant differences in prostate cancer risk between Whites and African-Americans. Conclusion: Our overall findings do not suggest a strong role for n-3 or n-6 PUFAs in prostate cancer development, although racial differences in risk should be investigated in larger racially diverse samples. Citation Information: Cancer Prev Res 2010;3(1 Suppl):B110.</jats:p