A computer model for the dry, frictionless contact of real rough surfaces is presented. The model uses data directly recorded from a stylus measuring instrument and as a confirmation of the model it is shown to reproduce “smooth case” results with a high level of accuracy. Results are given for two important applications of the technique. The first considers the analysis of the contact pressure and displacements for a bearing surface including a debris induced dent in the contact zone. The results go someway to providing an explanation of early life failure often associated with debris contaminated oil. Secondly the relationship between load and real contact area is studied for a sample set of surface profiles. The results obtained are compared with random process theory. It is proposed that the numerical model represents a different approach to rough surface contact allowing certain assumptions about the nature of surface roughness to be relaxed.

This paper is the second in a series that examines grease lubrication mechanisms and failure in rolling element bearings. The aim of the work was to understand the grease condition changes during use and the relationship to lubrication performance and failure. R0F bearing tests were carried out with two lithium hydroxystearate greases and the effects of the temperature, the speed, and the additive package on lubrication life was studied. Post-test, one pair of bearings (fail and non-fail) was dismantled and grease distribution and condition assessed. IR spectroscopy was then used to determine the lubricant composition and the oxidation level of the grease remaining on the shields, the inner raceway, and the cage pockets.The additive package increased the grease life by 100-700% depending on the test condition. Most of the grease remaining in the bearing was found on the shields, with only trace amounts in the cage pockets or close to the rolling track. The IR analysis showed that the composition of the shield sample was similar to the fresh grease although the base oil oxidation was evident and this increased with the running time. The cage pocket and inner raceway films contained a number of chemical species; these included the base oil and the thickener and their oxidation products.The study concludes that after an initial running-in period the "active" lubricant is heavily degraded grease, which contains oxidized species from the base oil and the thickener. Different failure mechanisms are identified depending on the test condition. High-speed tests that fail relatively quickly are due to poor boundary lubrication performance or cage failure rather than the lubricant reaching its "oxidation" limit. Long-term tests at slower speeds suffer considerable base oil oxidation. Under these conditions, failure is due to a reduction in the amount and/or mobility of the raceway lubricant.

The response of rats to nicotine solutions was examined with the brief-exposure, taste reactivity test and a two-bottle, 24-hr preference test. In Experiment 1, naive nondeprived rats were administered intraoral infusions (0.8 ml infused during 1 min) of distilled water and 1 microgram/ml, 5 micrograms/ml, 10 micrograms/ml, 25 micrograms/ml, 50 micrograms/ml, and 100 micrograms/ml nicotine. The oral motor, taste reactivity (TR) responses of the rats were recorded during the infusion. Nicotine solutions up to a concentration of 50 micrograms/ml elicited a number of ingestive TR responses similar to that by water. Ingestive responses significantly decreased and aversive TR responses significantly increased in response to 100 micrograms/ml nicotine. On the basis of these results, two-bottle preferences for water versus 1 microgram/ml, 5 micrograms/ml, and 0 microgram/ml (water control group) nicotine were measured in three groups of naive rats. Rats initially showed an equal preference for 0 microgram/ml and 1 microgram/ml nicotine. After 16 days of exposure, however, rats developed a significant preference for 1 microgram/ml nicotine. The preference ratio for 5 micrograms/ml nicotine significantly increased during the experiment, but the preference ratio remained significantly less than that for 1 microgram/ml and 0 microgram/ml nicotine solutions. Last, TR responses elicited by intraoral infusions of 1 microgram/ml and 5 micrograms/ml nicotine were then measured in these rats having had the two-bottle experience. Rats showing a two-bottle preference for the 1 microgram/ml nicotine solution displayed significantly more ingestive TR responses to 1 microgram/ml and 5 micrograms/ml nicotine than did the control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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Regardless of the achievable remissions with first line hormone therapy in patients with prostate cancer (CaP), the disease escapes the hormone dependent stage to a more aggressive status where chemotherapy is the only effective treatment and no treatment is curative. This makes it very important to identify new targets that can improve the outcome of treatment. ATM and DNA-PK are the two kinases responsible for signalling and repairing double strand breaks (DSB). Thus, both kinases are pertinent targets in CaP treatment to enhance the activity of the numerous DNA DSB inducing agents used in CaP treatment such as ionizing radiation (IR). Colony formation assay was used to assess the sensitivity of hormone dependent, p53 wt (LNCaP) and hormone independent p53 mutant (PC3) CaP cell lines to the cytotoxic effect of IR and Doxorubicin in the presence or absence of Ku55933 and NU7441 which are small molecule inhibitors of ATM and DNA-PK, respectively. Flow cytometry based methods were used to assess the effect of the two inhibitors on cell cycle, apoptosis and H2AX foci formation. Neutral comet assay was used to assess the induction of DNA DSBs. Ku55933 or NU7441 alone increased the sensitivity of CaP cell lines to the DNA damaging agents, however combining both inhibitors together resulted in further enhancement of sensitivity. The cell cycle profile of both cell lines was altered with increased cell death, DNA DSBs and H2AX foci formation. This study justifies further evaluation of the ATM and DNA-PK inhibitors for clinical application in CaP patients. Additionally, the augmented effect resulting from combining both inhibitors may have a significant implication for the treatment of CaP patients who have a defect in one of the two DSB repair pathways.