A framework for managing uncertain inputs: An axiomization of rewarding

The success postulate in belief revision ensures that new evidence (input) is always trusted. However, admitting uncertain input has been questioned by many researchers. Darwiche and Pearl argued that strengths of evidence should be introduced to determine the outcome of belief change, and provided a preliminary definition towards this thought. In this paper, we start with Darwiche and Pearl’s idea aiming to develop a framework that can capture the influence of the strengths of inputs with some rational assumptions. To achieve this, we first define epistemic states to represent beliefs attached with strength, and then present a set of postulates to describe the change process on epistemic states that is determined by the strengths of input and establish representation theorems to characterize these postulates. As a result, we obtain a unique rewarding operator which is proved to be a merging operator that is in line with many other works. We also investigate existing postulates on belief merging and compare them with our postulates. In addition, we show that from an epistemic state, a corresponding ordinal conditional function by Spohn can be derived and the result of combining two epistemic states is thus reduced to the result of combining two corresponding ordinal conditional functions proposed by Laverny and Lang. Furthermore, when reduced to the belief revision situation, we prove that our results induce all the Darwiche and Pearl’s postulates as well as the Recalcitrance postulate and the Independence postulate.

Testing bone substitutes in a small animal model of revision arthroplasty

This study evaluated a modification of the rat-pin model to enable testing of bone substitute materials. The model was characterized using the ceramic, beta-tricalcium phosphate (betaTCP) as a filler.

Correlation of synovial fluid cytokine levels with histological and clinical parameters of primary and revision total hip and total knee replacements

We retrieved synovial tissue and fluid samples from patients undergoing primary total hip replacement (THR) (n 15), revision of aseptically loose THR (n 12), primary total knee replacement (TKR) (n 13) and revision of aseptically loose TKR (n 6). Several histological parameters were assessed on a relative scale of 1-4. Primary TJRs were clinically evaluated for degree of osteoarthrosis. Revision TJRs were assessed for migration of the implant, gross loosening and the degree of radiolucency. Cytokine levels in synovial fluid were determined with ELISA.

Cells deficient in the base excision repair protein, DNA polymerase beta, are hypersensitive to oxaliplatin chemotherapy

A significant proportion of human cancers overexpress DNA polymerase beta (Pol beta), the major DNA polymerase involved in base excision repair. The underlying mechanism and biological consequences of overexpression of this protein are unknown. We examined whether Pol beta, expressed at levels found in tumor cells, is involved in the repair of DNA damage induced by oxaliplatin treatment and whether the expression status of this protein alters the sensitivity of cells to oxaliplatin. DNA damage induced by oxaliplatin treatment of HCT116 and HT29 colon cancer cells was observed to be associated with the stabilization of Pol beta protein on chromatin. In comparison with HCT116 colon cancer cells, isogenic oxaliplatin-resistant (HCT-OR) cells were found to have higher constitutive levels of Pol beta protein, faster in vitro repair of a DNA substrate containing a single nucleotide gap and faster repair of 1,2-GG oxaliplatin adduct levels in cells. In HCT-OR cells, small interfering RNA knockdown of Pol beta delayed the repair of oxaliplatin-induced DNA damage. In a different model system, Pol beta-deficient fibroblasts were less able to repair 1,2-GG oxaliplatin adducts and were hypersensitive to oxaliplatin treatment compared with isogenic Pol beta-expressing cells. Consistent with previous studies, Pol beta-deficient mouse fibroblasts were not hypersensitive to cisplatin treatment. These data provide the first link between oxaliplatin sensitivity and DNA repair involving Pol beta. They demonstrate that Pol beta modulates the sensitivity of cells to oxaliplatin treatment. Oncogene (2010) 29, 463-468; doi:10.1038/onc.2009.327; published online 19 October 2009