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Rats don't really like to swim, but they can be taught One well‐known way is “sink or swim.” The question is “What is the mechanism of learning?” and the follow‐up question: “How do we remember what we've learned?” Early researchers in the field demonstrated learning consolidation could be blocked by drugs that inhibited transcription or translation system wide. Monopoli et al. looked at the chronology of the learning consolidation using 2‐D DIGE and related proteomics techniques. Rats were taught a submerged platform water maze (with controls) and whole brain samples taken at 3, 12, and 24 h. Two waves of regulation were noted, confirming the previous work. A total of 42 proteins were involved in 6 major GO groups. Novel to this particular study was the observation of changes in Pea15 (astrocyte 15 kDa) at an early stage and changes in MAPK signaling‐control. pp. 4189–4201A pork belly in every pot or bovine fetuin in every tube Easy to promise early in the campaign, but making pork stomach mucin or bovine fetuin means someone has to wash the dishes in the end, no fun for these glycoproteins. Hence, Wang et al. tackled the problem head on, using some classical steps and some new steps to end up with a single tube procedure that produced solvent‐free glycans. They can be further analyzed by various chromatography and MS techniques. The glycans are released specifically and quantitatively and are simultaneously derivatized with 1‐phenyl‐3‐methyl‐5‐pyrazolone (PMP) under non‐oxidizing conditions. Samples can be easily centrifuged out of solvents such as ammonia or excess PMP for additional processing. While the procedure was developed on porcine mucin and bovine fetuin, it was also successful with human plasma. pp. 4229–4242Knock‐knock, who's there? Knock‐in and knock‐out mouse memory models The mouse brain is different than the human brain (Duh...), which makes it necessary to construct cell lines with “humanized” regions. In this work by Robinson et al., APP/PS‐1 cells retained human pharmacotoxic features (e.g. Alzheimers Aβ plaque formation at 4–9 months or characteristic oxidation damage to WT cells). Of special interest was the effect of N ‐acetyl‐cysteine (NAC), an antioxidant available over the counter. Proteomic analysis of the results of NAC treatment showed a broad spectrum of effects: increased levels of GSH, protection against peroxynitrite induced damage, and restored memory in aged senescence‐prone mice. Changes in expression were evaluated by 2‐D PAGE. NAC is registered for liver acetomenophen toxicity and heavy metal poisoning in the US. pp. 4243–4256