FUNGAL AND MICOTOXIN CONTAMINATION IN MIXED FEEDS: EVALUATING RISK IN CATTLE INTENSIVE REARING OPERATIONS (FEEDLOTS)

Argentina is the fourth global beef producer. Exposure to mycotoxins through contaminated feed is a major hazard for ruminants. In the present study we assess mycobiota, aflatoxin B1 (AFB1), fumonisin B1 (FB1), deoxynivalenol (DON) and zearalenone (ZEA) levels in total mixed rations (TMRs) during two consecutive years. Total fungal counts were evaluated and fungal species were identified. Also, ability of A. flavus isolates to produce AFB1 in vitro was tested. Natural contamination with AFB1 and FB1 was quantified by HPLC. Deoxynivalenol and zearalenone were analysed by immunochromatography and thinlayer chromatogra- phy (TLC), respectively. Fungal counts varied from not detectable (ND) to 2.10 x 108 CFU g-1. The prevalent genera were Aspergillus spp (60 %) and Fusarium spp (66.7 %), respectively The prevalent species was Aspergillus fumigatus. 50 % of A. flavus strains produced 75 to 112.5 μg g-1 AFB1. 46 % of 2007 samples were contaminated with 4 to 10 μg kg-1 AFB1. Deoxynivalenol was detected in 33.3 % of the samples (≥ 1. 25 μg g-1). Fumonisin B1 and ZEA were not detected. This study can be useful to estimate the mycotoxicological risk of cattle TMRs in this region and to compare results with studies from other beef-producing countries

Modification of Collagen by 3-Deoxyglucosone Alters Wound Healing through Differential Regulation of p38 MAP Kinase

Background: Wound healing is a highly dynamic process that requires signaling from the extracellular matrix to the fibroblasts for migration and proliferation, and closure of the wound. This rate of wound closure is impaired in diabetes, which may be due to the increased levels of the precursor for advanced glycation end products, 3-deoxyglucosone (3DG). Previous studies suggest a differential role for p38 mitogen-activated kinase (MAPK) during wound healing; whereby, p38 MAPK acts as a growth kinase during normal wound healing, but acts as a stress kinase during diabetic wound repair. Therefore, we investigated the signaling cross-talk by which p38 MAPK mediates wound healing in fibroblasts cultured on native collagen and 3DG-collagen. Methodology/Principal Findings: Using human dermal fibroblasts cultured on 3DG-collagen as a model of diabetic wounds, we demonstrated that p38 MAPK can promote either cell growth or cell death, and this was dependent on the activation of AKT and ERK1/2. Wound closure on native collagen was dependent on p38 MAPK phosphorylation of AKT and ERK1/2. Furthermore, proliferation and collagen production in fibroblasts cultured on native collagen was dependent on p38 MAPK regulation of AKT and ERK1/2. In contrast, 3DG-collagen decreased fibroblast migration, proliferation, and collagen expression through ERK1/2 and AKT downregulation via p38 MAPK. Conclusions/Significance: Taken together, the present study shows that p38 MAPK is a key signaling molecule that plays

Wnt signaling in triple-negative breast cancer

Wnt signaling regulates a variety of cellular processes, including cell fate, differentiation, proliferation and stem cell pluripotency. Aberrant Wnt signaling is a hallmark of many cancers. An aggressive subtype of breast cancer, known as triple-negative breast cancer (TNBC), demonstrates dysregulation in canonical and non-canonical Wnt signaling. In this review, we summarize regulators of canonical and non-canonical Wnt signaling, as well as Wnt signaling dysfunction that mediates the progression of TNBC. We review the complex molecular nature of TNBC and the emerging therapies that are currently under investigation for the treatment of this disease