@misc{gookin_hanrahan_levy_2017, title={The conundrum of feline trichomonosis: The more we learn the "trickier' it gets}, volume={19}, ISSN={["1532-2750"]}, DOI={10.1177/1098612x17693499}, abstractNote={Practical relevance: Trichomonosis of the large intestine of the cat was described as a cause of chronic diarrhea over 20 years ago. The trichomonad was identified as Tritrichomonas foetus, with a genotype that is distinct from venereal T foetus of cattle. Clinical challenges: Despite multiple means for diagnosis of the infection, including light microscopy, protozoal culture and PCR amplification using species-specific primers, tests with even greater sensitivity are needed. Feline trichomonosis is resistant to all commonly used antiprotozoal drugs. Ronidazole is currently the only drug demonstrated to be effective in eliminating the infection from cats; however, this drug has a narrow safety margin and clinical resistance is increasingly recognized. The more we learn about trichomonosis in cats, the more complicated and controversial the infection has become, ranging from what we should call the organism to whether we should even bother trying to treat it. Global importance: Feline trichomonosis is recognized to occur worldwide and is regarded as one of the most common infectious causes of colitis in the domestic cat. The infection is widespread in catteries and shelters; and, while remission of diarrhea may occur over time, persistence of the infection is common. Evidence base: This review provides a comprehensive examination of what is currently known about feline trichomonosis and pinpoints areas, based on the authors’ opinion, where further research is needed. }, number={3}, journal={JOURNAL OF FELINE MEDICINE AND SURGERY}, author={Gookin, Jody L. and Hanrahan, Katherine and Levy, Michael G.}, year={2017}, month={Mar}, pages={261–274} }
 @article{newman_sills_hanrahan_ziegler_tidd_cook_sannes_2015, title={Expression of WNT5A in Idiopathic Pulmonary Fibrosis and Its Control by TGF-β and WNT7B in Human Lung Fibroblasts}, volume={64}, ISSN={0022-1554 1551-5044}, url={http://dx.doi.org/10.1369/0022155415617988}, DOI={10.1369/0022155415617988}, abstractNote={ The wingless (Wnt) family of signaling ligands contributes significantly to lung development and is highly expressed in patients with usual interstitial pneumonia (UIP). We sought to define the cellular distribution of Wnt5A in the lung tissue of patients with idiopathic pulmonary fibrosis (IPF) and the signaling ligands that control its expression in human lung fibroblasts and IPF myofibroblasts. Tissue sections from 40 patients diagnosed with IPF or UIP were probed for the immunolocalization of Wnt5A. Further, isolated lung fibroblasts from normal or IPF human lungs, adenovirally transduced for the overexpression or silencing of Wnt7B or treated with TGF-β1 or its inhibitor, were analyzed for Wnt5A protein expression. Wnt5A was expressed in IPF lungs by airway and alveolar epithelium, smooth muscle cells, endothelium, and myofibroblasts of fibroblastic foci and throughout the interstitium. Forced overexpression of Wnt7B with or without TGF-β1 treatment significantly increased Wnt5A protein expression in normal human smooth muscle cells and fibroblasts but not in IPF myofibroblasts where Wnt5A was already highly expressed. The results demonstrate a wide distribution of Wnt5A expression in cells of the IPF lung and reveal that it is significantly increased by Wnt7B and TGF-β1, which, in combination, could represent key signaling pathways that modulate the pathogenesis of IPF. }, number={2}, journal={Journal of Histochemistry & Cytochemistry}, publisher={SAGE Publications}, author={Newman, Donna R. and Sills, W. Shane and Hanrahan, Katherine and Ziegler, Amanda and Tidd, Kathleen McGinnis and Cook, Elizabeth and Sannes, Philip L.}, year={2015}, month={Nov}, pages={99–111} }