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Milk is one of the most important food items consumed by humans worldwide. In addition to its nutritional importance, milk is an excellent culture medium for microorganisms, which may include pathogens such as Listeria monocytogenes (L. monocytogenes). Traditional processing of milk for direct consumption is based on thermal treatments that efficiently eliminate pathogens, including pasteurization or sterilization. However, the occurrence of L. monocytogenes in milk as a consequence of failures in the pasteurization process or postpasteurization contamination is still a matter of concern. In recent years, consumer demand for minimally processed milk has increased due to the perception of better sensory and nutritional qualities of the products. This review deals with the occurrence of L. monocytogenes in milk in the last 10 years, including regulatory aspects, and recent advances in technologies for the inactivation of this pathogen in milk. The results from studies on nonthermal technologies, such as high hydrostatic pressure, pulsed electric fields, ultrasounds, and ultraviolet irradiation, are discussed, considering their potential application in milk processing plants.

A region on mouse distal chromosome 1 (Chr. 1) that is highly enriched in quantitative trait loci (QTLs) controlling neural and behavioral phenotypes overlaps with the peak region of a major obesity QTL (Nob3.38), which we identified in an intercross of New Zealand Obese (NZO) mice with C57BL/6J (B6). By positional cloning we recently identified a microdeletion within this locus causing the disruption of Ifi202b that protects from adiposity by suppressing expression of 11β-Hsd1. Here we show that the Nob3.38 segment also corresponds with the QTL rich region (Qrr1) on Chr. 1 and associates with increased voluntary running wheel activity, Rota-rod performance, decreased grip strength, and anxiety-related traits. The characterization of a subcongenic line carrying 14.2 Mbp of Nob3.38 with a polymorphic region of 4.4 Mbp indicates that the microdeletion and/or other polymorphisms in its proximity alter body weight, voluntary activity, and exploration. Since 27 out of 32 QTL were identified in crosses with B6, we hypothesized that the microdeletion and or adjacent SNPs are unique for B6 mice and responsible for some of the complex Qrr1-mediated effects. Indeed, a phylogenic study of 28 mouse strains revealed a NZO-like genotype for 22 and a B6-like genotype for NZW/LacJ and 4 other C57BL strains. Thus, we suggest that a Nob3.38 interval (173.0-177.4 Mbp) does not only modify adiposity but also neurobehavioral traits by a haplotype segregating with C57BL strains.