Long-term followup data will be needed to determine whether there will be a lower incidence of biochemical relapse as determined by prostate specific antigen, local recurrence or metastasis, with an improvement in patient survival.

Road traffic injuries could become the fifth leading cause of death globally by 2030 unless appropriate countermeasures are taken. Reliable reconstruction of collisions is essential for understanding and hence reducing the injuries sustained by pedestrians. The significant influence of vehicle speed, pedestrian speed and pedestrian gait on pedestrian transverse motion and rotation about the longitudinal axis has been qualitatively noted in the literature, but there has been no quantitative approach to this problem. The MADYMO multibody pedestrian model is widely used for collision reconstruction, but its validation to date mostly remains limited to body segment trajectories in the vertical plane along the direction of vehicle travel. In this article, the MADYMO pedestrian model is compared to staged tests and a real collision in terms of head trajectory, longitudinal and transverse head translations relative to the primary contact location of the pedestrian on the vehicle, impact location on the head (and hence longitudinal rotation of the body), head impact time and head impact velocity. It is shown that the model can reproduce staged cadaver and dummy tests in terms of head trajectory (mostly within 10%), longitudinal head translation (within 17%), transverse translation (two cases: errors of 0% and 19%), impact location on the head (within 45 in the majority of cases), head impact time (mean difference of 8.7 ms) and head impact velocity (mean difference of 1.8 m/s). A sensitivity analysis showed that the model is largely unaffected by changes in vehicle stiffness and vehicle-pedestrian friction, while variations in the pedestrian stance and the height of the vehicle front have a considerable effect on the kinematics of a collision. This is the first time that the MADYMO pedestrian model has been evaluated with regard to transverse motion and longitudinal rotation of the pedestrian. The results presented here mean that the MADYMO model is appropriate for further analysis of the influence of gait on pedestrian post-impact kinematics.

Overexpression of the nm23H1 gene has been associated with the suppression of metastasis in several solid tumors. However, in colorectal carcinoma and neuroblastoma, increased levels of nm23 H1 nucleoside diphosphate kinase A (NDPKA) mRNA are associated with tumorigenesis. To determine the role of rim23 H1/ NDPKA in the prostate, normal and/or malignant tissue samples from 29 consecutive patients were studied. Levels of rim23 H1/NDPKA mRNA and nm23 H1/NDPKA mRNA protein were determined in tissue from 18 and 27 patients, respectively. In all, 16 of the 18 tumor samples expressed increased levels of nm23 H1/NDPKA mRNA as compared with those measured in normal tissue. The level of rim23 H1/NDPKA mRNA was > 10-fold higher in a metastatic lymph node than in normal prostate tissue. All cancer specimens and areas of prostatic intraepithelial neoplasia showed immunoreactivity with the nm23 H1/ NDPKA antibody; however, normal prostatic tissue was unreactive. These findings suggest that overexpression of the rim23 H1/NDPKA gene occurs frequently in adenocarcinomas of the prostate and may be an early event in prostate cancer tumorigenesis.Over the last 15 years, adenocarcinoma of the prostate has become the most common cancer of men in the United States, with the estimated incidence being 23% [2]. Prostate cancer accounts for more than 12% of cancer deaths among men, and the mortality associated with this malignancy in men is second only to that of lung cancer. This high death rate occurs despite the observation that prostate cancer is being identified at an earlier clinical stage through aggressive screening studies [3]. Therefore, biological events rather than clinical stage alone are important in the formation of metastases.Correspondence to: D. P. Wood, Jr.; Fax: +1 (606) Tumorigenicity and metastatic potential are related to a series of complex independent and linked sequential events [5]. The formation of metastases required cellular transformation, invasion through the basement membrane, cell motility, penetration of the vascular and/or lymphatic beds, angiogenesis, and proliferation at distant sites [6,15]. Altering the ability of a cell to perform any of these activities would suppress the metastatic potential of that cell. Steeg et al. [20], in an attempt to identify the genes involved in suppressing or promoting metastasis, performed differential colony hybridization of mRNA between melanoma cell lines with low and high metastatic potentials. These experiments resulted in the discovery of a potential metastatic suppressor gene, rim23 H1, with low levels of nm23 H1 mRNA expression being found in highly metastatic melanoma cell lines and higher levels occurring in cell lines with low metastatic potential [20]. Additional experiments determined that rim23 H1 is part of a gene family, and two nm23 genes have been identified: rim23 H1 and nm23 H2. The gene product of nm23 H1 is nucleoside diphosphate kinase A (NDPKA) [7], whereas that of nm23 H2 is nucleoside diphosphate kinase B [7,19].Various human tumor tissues ha...

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