Search

An automated method for determining whether dairy cows with subclinical mammary infections recover after antibiotic treatment would be a useful tool in dairy production. For that purpose, inline L-lactate dehydrogenase (LDH) measurements was modeled using a dynamic linear model; the variance parameters were estimated using the expectation-maximization algorithm. The method used to classify cows as infected or uninfected was based on a multiprocess Kalman filter. Two learning data sets were created: infected and uninfected. The infected data set consisted of records from 48 cows with subclinical Staphylococcus aureus infection from 4 herds collected in 2010. The uninfected data set came from 35 uninfected cows collected during 2013 from 2 herds. Bacteriological culturing was used as gold standard. To test the model, we collected data from the 48 infected cows 50 d after antibiotic treatment. As a result of the treatment, this test data set consisted of 25 cows that still had a subclinical infection and 23 cows that were recovered. Model sensitivity was 36.0% and specificity was 82.6%. To a large extent, L-lactate dehydrogenase reflected the cow's immune response to the presence of pathogens in the udder. However, cows that were classified correctly before treatment had a better chance of correct classification after treatment. This indicated a variation between cows in immune response to subclinical mammary infection that may complicate the detection of subclinically infected cows and determination of recovery.

Members of the epidermal growth factor (EGF) receptor family are known to be specifically involved in mammary carcinogenesis. As a nuclear target of activated receptors, we examined c-Jun in mammary epithelial cells. For this, we used a c-JunER fusion protein which was tightly controlled by estrogen. Activation of the JunER by hormone resulted in the transcriptional regulation of a variety of AP-1 target genes. Hormone-activated JunER induced the loss of epithelial polarity, a disruption of intercellular junctions and normal barrier function and the formation of irregular multilayers. These changes were completely reversible upon hormone withdrawal. Loss of epithelial polarity involved redistribution of both apical and basolateral proteins to the entire plasma membrane. The redistribution of E-cadherin and beta-catenin was accompanied by a destabilization of complexes formed between these two proteins, leading to an enrichment of beta-catenin in the detergent-soluble fraction. Uninduced cells were able to form three-dimensional tubular structures in collagen I gels which were disrupted upon JunER activation, leading to irregular cell aggregates. The JunER-induced disruption of tubular structures was dependent on active signaling by growth factors. Moreover, the effects of JunER could be mimicked in normal cells by the addition of acidic fibroblast growth factor (aFGF). These data suggest that a possible function of c-Jun in epithelial cells is to modulate epithelial polarity and regulate tissue organization, processes which may be equally important for both normal breast development and as initiating steps in carcinogenesis.