In this issue

Abstract Renal rejection: your kidney don't love me no more pp. 32–47 Sometimes getting a new kidney installed is the easy part – it's getting it to stay there and not feel rejected by its new host that is the hard part. That and not coming down with some nasty disease due to enhanced levels of immunosuppressive therapy while trying to avoid rejection. That and suffering from the biopsy procedure when other things don't work. Transplants are no joke. Sigdel et al. took the shotgun approach to the problem, looking for urinary proteomic markers for rejection. Using a semi‐quantitative shotgun meant no labeled species, just counting the fragments of the desired size as they whizzed by. Three proteins have been further validated by ELISA performance. Likely candidates are UMOD, SERPINF1 and CD44.Adenoma: unique pattern midway to carcinoma pp. 60–70 It's a thoughtful cancer that gives the body a reasonable warning before it begins a frontal assault. But that, apparently, is what colorectal carcinoma (CRC) does. The early‐stage CRC begins life as an adenoma, which can be treated prospectively, before progressing. For those too young to have been subjected to the ignominy of a colonoscopic exam, a simple swab test would be greatly appreciated. Surely with such a kindness in mind, Lam et al. embarked on a 2‐D electrophoretic hunt for markers that could distinguish normal from adenoma tissue. Working with 20 paired sets of normal and adenoma tissue samples, they identified over 1000 proteins by 2‐DE and MALDI‐TOF/TOF. They found four proteins up‐regulated (Annexin A3, S100A11, eIF5A‐1, S100P) and three down‐regulated (S100A9, Galectin‐1, and FABPL) by at least twofold in both cases. Functionally, they made sense. Now for a business plan…Not so mighty mouse: plasma proteomics of mouse model of Duchenne Muscular Dystrophy pp. 71–83 The most common way to study Duchenne Muscular Dystrophy (DMD) is to work with a mouse model of the disease – it is convenient but current markers are not reliably applicable to larger animals. Colussi et al. needed markers for their studies of histone deacetylase inhibitors, drugs which restore some muscular strength in mdx (mutant) mice. In this article, they report their proteomic analysis of the effects of the drug SAHA on plasma protein levels. After establishing baseline levels for wt versus mdx, they then looked for differences between mdx and mdx+SAHA. At least eight differences were detected in wt versus mdx, three up‐ and five down‐regulated. For mdx versus mdx+SAHA, at least four changes were observed, including normalization of two proteins. Analysis was done by 2‐DE, in‐gel trypsin digestion and LC‐MS/MS.