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A companion to the tight, 17-track The Singles, this deluxe box set gathers up the 29 singles released between 1999 and 2009 -- including the new -written single '3,' the enticement for hardcore fans to buy The Singles -- presenting them as two-track CD-singles with one B-side per disc, adding a DVD containing almost all of the accompanying music videos. Naturally, this contains far more songs than the single-disc set, including lots of tracks from the start of the new millennium, an area that the 17-cut compilation downplays. Unlike that disc, this box isn't meant for casual listening -- it's an effort to listen to or rip all 29 discs -- but it's a collectors' item, one to be looked at as much as listened to. Those collectors may be irked that the singles contain just one B-side, instead of the legions of B-sides that appeared all over the world for each of these singles, but most of those flipsides were remixes anyway.
What mattered were the A-sides, and they're presented here quite attractively in a nice collectors-oriented package. [Jive released a box set version of the collection.].
Abstract Hyperplastic candidiasis is characterized by thickening of the mucosal epithelia with Candida albicans infection with occasional progression to squamous cell carcinoma (SCC). Albicans is a critical factor in tumor development; however, the oncogenic mechanism is unclear. We have previously produced an animal model for hyperplastic candidiasis in the rat forestomach.
In the present study, we investigate whether impaired DNA methylation and associated protein expression of tumor suppressor and DNA repair genes are involved in the SCC carcinogenesis process using this hyperplastic candidiasis model. Promoter methylation and protein expression were analyzed by methylation specific PCR and immunohistochemical staining, respectively, of 5 areas in the forestomachs of alloxan-induced diabetic rats with hyperplastic candidiasis: normal squamous epithelia, squamous hyperplasia, squamous hyperplasia adjacent to SCC, squamous hyperplasia transitioning to SCC, and SCC. We observed nuclear p16 overexpression despite increases in p16 gene promoter methylation during the carcinogenic process.