Peptides 316-333 from E1 and 617-634 from E2 affect significantly the polymorphic phase behavior of DEPE, induce the presence of uncorrelated membranes, and present a high effect of membrane rupture and fusion. As suggested previously, the regions were these two peptides reside could hold a similar function in the corresponding proteins as that observed for other ones. Protein p7 is classified neither as a structural nor as a non-structural protein, is located in the cell ER, and forms a membrane pore. We have recently shown the presence of a highly membranotropic region in p7 presenting high leakage but low fusion. Microtiter plate-based PCR-enzyme linked amplification and hybridization assays for the detection of C. pneumoniae as well as other microorganisms have been described and are sensitive and robust methods suitable for the clinical laboratory. The PCR-EIA assay as described in this report is simple, user-friendly, and results can be obtained in the same day. An additional antigen-antibody reaction was included as a signal amplification step to enhance test sensitivity. A recent blinded proficiency study indicated the PCR-EIA system detects as few as 1 copy/reaction human herpesvirus-6 in spiked plasma specimens. The test sensitivity of the PCR-EIA in mock CSF samples is 25 C. pneumoniae organisms per ml of CSF. This is comparable to the sensitivity in mock CSF samples of the PCR assay described by Ikejima et al , which had a sensitivity of 100 organisms per ml of CSF. The nested-PCR assay used in this study has been shown previously to be as sensitive as the PCR assay described by Ikejima. A uracil-N-glycosylase-based inactivation system was adapted to control for possible amplicon carryover contamination. The general assumption is that tumor cells with intact p53 will stop proliferating after irradiation, whereas tumor cells with deficient p53 will proliferate continually post irradiation. Our results demonstrated that some tumor cells in the transgenic animals failed to initiate cell cycle arrest post irradiation, so that 0.93% lung tumor cells were Brdu positive. In comparison, there were no Brdu positive cells observed in the normal lung tissues collected from the same mouse post irradiation. Given that even one copy of intact p53 could cause a complete cell cycle arrest in mice lungs post irradiation, it follows that the Brdu positive cells observed in the lung tumors have lost p53 function completely. Several LY294002 potential mechanisms for p53 mutant induced tumorigenesis have been proposed. One possibility is that mutant p53 inhibits the sequence-specific DNA-binding and transactivation functions of wild-type p53 in a “dominant-negative” manner by forming hetero-oligomeric complexes with it. Alternatively, certain p53 mutants may possess intrinsic oncogenic potential, as their introduction into cells lacking endogenous p53 has been shown to enhance the tumorigenicity of these cells. Since human and murine p53 proteins are fully capable of forming hetero-oligomeric complexes.