Sas software v9

This study was designed to address its primary objectives to determine the toxicity and tolerability of Melanoma GVAX administered in the adjuvant setting, with or without low dose CPM. Thus, the trial was designed to include at least 19 patients in 3 sequentially enrolled cohorts (3 in Cohort A, 8 in Cohort B, and 8 in Cohort C). Changes in pharmacodynamic variables were evaluated using the Wilcoxon paired-sample signed rank test, and comparisons between cohorts were performed using the Mann–Whitney U test. Analyses of peripheral blood leukocyte subsets over time on treatment and among cohorts were performed using linear mixed effect models. Potential correlations between IFN-g serum concentrations and monocyte characteristics were subjected to a 2-sided Spearman correlation analysis. All statistical analyses were 2-sided, and p values <0.05 were considered significant (SAS software v.9.3, Cary, NC; R version 2.15.1; or GraphPad Prism v.5, San Diego, CA, USA). Secondary endpoints were considered exploratory and included changes in anti-melanoma immune responses. A positive immune response was defined as a two-fold increase in melanoma-specific reactivity compared to background assay values, comparing pre- to post-treatment levels.

Descriptive analyses of sociodemographic and clinical characteristics were conducted for case and control patients. These included matching variables (gender and, at index date, age, income level, WOMAC pain, and KL grade), the aforementioned covariates, and exposure to the different classes of oral OA therapies in the 3 years prior to KR. Proportions were calculated for categorical variables, and median and interquartile range (IQR) for continuous variables.
The association between the occurrence of KR and sociodemographic/clinical characteristics (not those used in the matching between cases and controls) was measured using crude conditional logistic regression. An adjusted regression model including significant covariates and pertinent clinical variables was employed to determine the association between exposure to oral OA therapies and occurrence of KR. Odds ratios (OR) and 95% confidence interval (CI) were calculated. Only data with sufficient patient number (n > 10) per time exposure were analyzed and presented. A two-tailed p value <0.05 was considered significant. All statistical analyses were performed using SAS software, V.9.3 (SAS Institute, Cary, NC, USA).

The obtained data were statistically processed using the SAS software, v. 9.3. (24 ). Statistical analysis included descriptive statistics (average, minimum and maximum value), analysis of variance (one-way ANOVA) and comparison of mean values (Duncan’s multiple-range test). Principal component analysis (PCA) was constructed using Python library Scikit-learn v. 0.20.3 (25 ) was used for both classifiers.

Data are reported as mean (SD) or median (interquartile range, IQR) unless otherwise indicated. Proportions were compared using chi-square test or Fisher's exact test. The accordance with a normal distribution was tested by Shapiro-Wilk and Kolmogorov-Smirnov tests. For intergroup comparisons between control subjects and RA patients, Student's t-test or Mann-Whitney test was used where appropriate. General Linear Models (GLM) procedure was used for age-sex adjusted comparisons between the controls and RA subjects. Homogeneity of variances was verified by Levene's test and in appropriate cases,Welch correction was applied.
GLM were used to test unadjusted and age-sex adjusted differences between the three groups: non-RA and RA subjects with low and high activity of disease-type III sum of square was used. The Bonferroni test was performed for post hoc comparisons. Spearman rank correlations were applied to test associations between systemic inflammatory markers (ESR, hsCRP, TNF-α, and IL-6) and biochemical measures of endothelial activation (vWf, MCP-1, ADMA, sVCAM-1, sE-selectin, OPG, and PTX3) in either non-RA and or RA subjects.
Two-tailed P values of less than 0.05 were considered statistically significant. Statistical analysis was performed by SAS software v. 9.3 (SAS Institute, Cary, NC, USA).