This study evaluated the efficacy of different brief-exposure antibacterial washes (≤3 min) coupled with frozen storage against Listeria monocytogenes and Salmonella Typhimurium on blueberries. Inoculated berries where treated with sodium hypochlorite (NaOCl, 200 ppm), chlorine dioxide (15 ppm), ozone (3 and 5 ppm), or lactic acid (2%) for short exposure times (10 s, 1 min, or 3 min), and antibacterial effectiveness was determined with or without an additional freezing hurdle (−12°C, 1 week). Wash treatments alone resulted maximum log reductions from 1.0 to 2.8, while the additional freezing step increased this to a range from 3.7 to 6.6. The greatest reduction of L. monocytogenes (6.6 log) and Salmonella Typhimurium (5.3 log) was observed after freezing combined with 3 min of exposure to 2% lactic acid or 200 ppm of NaOCl, respectfully. After treatment, no residue was measured by the methodologies used. However, lactic acid treatment resulted in changes of color and aroma. In conclusion, wash treatments of blueberries using short exposure times had antimicrobial effectiveness (1.0 to 2.8 log reductions) and can be enhanced by coupling with freezing.
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Background: Innervation of adipose tissue is essential for the proper function of this critical metabolic organ. Numerous surgical and chemical denervation studies have demonstrated how maintenance of brain-adipose communication through both sympathetic efferent and sensory afferent nerves helps regulate adipocyte size, cell number, lipolysis, and ‘browning’ of white adipose tissue. Neurotrophic factors are growth factors that promote neuron survival, regeneration and plasticity, including neurite outgrowth and synapse formation. Peripheral blood immune cells have been shown to be a source of neurotrophic factors in humans and mice. Although a number of immune cells reside in the adipose stromal vascular fraction (SVF), it has remained unclear what roles they play in adipose innervation. We previously demonstrated that adipose immune cells secrete brain derived neurotrophic factor (BDNF). Methods: We now show that deletion of this neurotrophic factor from the myeloid lineage led to a ‘genetic denervation’ of inguinal subcutaneous white adipose tissue (scWAT), thereby causing decreased energy expenditure, increased adipose mass, and a blunted UCP1 response to cold stimulation. Results: We and others have previously shown that noradrenergic stimulation via cold exposure increases adipose innervation in the inguinal depot. Here we have identified a subset of myeloid cells that home to scWAT upon cold exposure and are Ly6C + CCR2 + Cx3CR1 + monocytes/macrophages that express noradrenergic receptors and BDNF. Conclusions: We propose that these cold induced neuroimmune cells (CINCs) are key players in maintaining adipose innervation as well as promoting adipose nerve remodeling under noradrenergic stimulation, such as cold exposure.
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