Portrayals of canine obesity in English-language newspapers and in leading veterinary journals, 2000-2009: Implications for animal welfare organizations and veterinarians as public educators

In industrialized societies, more than one in three dogs as well as people currently qualify as overweight or obese. Experts in public health expect both these figures to rise. While clinical treatment remains important, so are public perceptions and social norms. This article presents a thematic analysis of English-language mass media coverage on canine obesity from 2000 through 2009, and compares these results with a thematic analysis of articles on canine obesity in leading veterinary journals during the same time period. Drawing on Giddens’ theory of structuation, articles that emphasised individual agency, environmental structure or both as contributors to canine obesity were identified. Comparisons with weight-related health problems in human populations were virtually absent from the veterinary sample. While such comparisons were almost always present in the media sample, veterinarians and other animal welfare spokespeople were quoted in ways that emphasized the agency of individual owners over structural influences. Now that weight gain and obesity have been established as a pressing animal welfare problem, these results suggest a need for research and for interventions such as media advocacy that emphasizes intersections between animal-owner agency and socio-environmental determinants, and connections between animal welfare and human health

Mononuclear Cells From Human Lung Parenchyma Support Antigen‐Induced T Lymphocyte Proliferation

We have previously demonstrated that there is a subpopulation of loosely adherent pulmonary mononuclear cells that can be isolated from minced and enzyme‐digested lung tissue with a potent capacity to stimulate allogeneic T lymphocyte proliferation. We now demonstrate that these cells are also capable of stimulating an autologous mixed leukocyte reaction (AMLR) and presenting antigen to autologous T lymphocytes. These loosely adherent mononuclear cells (LAM) were more effective than either alveolar macrophages or monocytes as antigen‐presenting cells. Depletion of phagocytic or Fc receptor‐positive cells from the LAM population enhanced the stimulation of an reaction AMLR while preserving antigen‐induced T lymphocyte proliferation. These results indicate that there are nonphagocytic, Fc receptor‐negative accessory cells in human lung parenchyma capable of activating resting T cells in an AMLR and supporting antigen‐specific T lymphocyte proliferation. The identity of these cells is uncertain, but the data strongly suggest that the cell is not a classical monocyte‐derived macrophage. These antigen‐presenting cells may be critical in the initiation of immune responses within the lung.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141257/1/jlb0336.pd

Separation of Potent and Poorly Functional Human Lung Accessory Cells Based on Autofluorescence

Human alveolar macrophages obtained by bronchoalveolar lavage are usually poor accessory cells in in vitro lymphoprollferation assays. However, we recently described a subpopulation of pulmonary mononuclear cells, obtained from minced and enzyme‐digested lung, which were potent stimulators of allogeneic T‐lymphocyte proliferation. These cells were enriched in loosely adherent mononuclear cell (LAM) fractions, but further study of these accessory cells was hampered by the heterogeneous nature of LAM. It was observed that in the majority of lung tissue sections, most alveolar macrophages were autofluorescent, whereas most interstitial HLA‐DR positive cells were not. Therefore autofluorescence was utilized to fractionate LAM in an attempt to remove alveolar macrophages and selectively purify interstitial accessory cells. LAM were separated by flow cytometry using forward and side scatter to exclude lymphocytes, and red autofluorescence to obtain brightly autofluorescent (A pos) and relatively nonautofluorescent (A neg) mononuclear cells. Although both populations contained over 80% HLA‐DR positive cells, A pos cells were poor accessory cells, whereas A neg cells were extremely potent stimulators of a mixed leukocyte reaction at all stimulator ratios tested. When A pos cells were added to A neg cells, T‐cell proliferation was markedly suppressed in the majority of experiments. Morphologically, A pos cells appeared similar to classical alveolar macrophages with 95% of the cells being large and intensely nonspecific esterase positive. In contrast, the majority of A neg were smaller, B‐cell antigen‐negative, nonspecific esterase negative, and had a distinctive morphology on Wright‐stained smears. We conclude that fractionation of LAM based on autofluorescence is a powerful tool to isolate and characterize lung mononuclear cells that act either as stimulators or as suppressors of immune responses in the lung.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141667/1/jlb0458.pd

Host spatiotemporal overlap in a park with high endemicity of Echinococcus multilocularis

There has been a spate of recent cases of human alveolar echinococcosis (AE) in Alberta, Canada. Alveolar echinococcosis is caused by Echinococcus multilocularis, which is prevalent among coyote populations and present in domestic dogs in Alberta. Using qPCR, we estimated the seasonal fecal prevalence of E. multilocularis in coyotes and dogs in a multiuse recreation area close to Edmonton, Alberta, where we also setup remote cameras to model seasonal changes in the overlap in temporal activity and the spatial intensity of use among coyotes, humans, and dogs, as a proxy of potential transmission. We detected E. multilocularis in 18 of 137 wild canid feces and none in 44 dog feces. After correcting for the qPCR test’s sensitivity and specificity, we estimated at 15.7% (9.7-22.7%, 95% CrI) the true fecal prevalence for coyotes. Temporal overlap between coyotes and both humans and dogs increased in the fall and winter relative to the spring and summer. Coyote intensity of use showed seasonal variations and was higher on maintained trails and locations closer to visitor parking and at sites with high intensity of dog use. Our results reinforce the need of an integrated approach, typical of both One-Health and Eco-Health, to park management for minimizing the likelihood of transmission where human and dog activity results in significant overlap with the one of the natural definitive hosts of zoonotic parasites

Hydrogen peroxide is a diffusible paracrine signal for the induction of epithelial cell death by activated myofibroblasts

Cell‐cell signaling roles for reactive oxygen species (ROS) generated in response to growth factors/cytokines in nonphagocytic cells are not well defined. In this study, we show that fibroblasts isolated from lungs of patients with idiopathic pulmonary fibrosis (IPF) generate extracellular hydrogen peroxide (H2O2) in response to the multifunctional cytokine, transforming growth factor‐β1 (TGF‐β1). In contrast, TGF‐β1 stimulation of small airway epithelial cells (SAECs) does not result in detectable levels of extracellular H2O2. IPF fibroblasts independently stimulated with TGF‐β1 induce loss of viability and death of overlying SAECs when cocultured in a compartmentalized Transwell system. These effects on SAECs are inhibited by the addition of catalase to the coculture system or by the selective enzymatic blockade of H2O2 production by IPF fibroblasts. IPF fibroblasts heterogeneously express α‐smooth muscle actin stress fibers, a marker of myofibroblast differentiation. Cellular localization of H2O2 by a fluorescent‐labeling strategy demonstrated that extracellular secretion of H2O2 is specific to the myofibroblast phenotype. Thus, myofibroblast secretion of H2O2 functions as a diffusible death signal for lung epithelial cells. This novel mechanism for intercellular ROS signaling may be important in physiological/pathophysiological processes characterized by regenerating epithelial cells and activated myofibroblasts.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154383/1/fsb2fj042882fje.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154383/2/fsb2fj042882fje-sup-0001.pd

Characterization and comparison of recombinant full-length ursine and human sex hormone-binding globulin

Sex hormone‐binding globulin (SHBG) regulates the bioavailability of sex steroid hormones in the blood. Levels of SHBG increase markedly in brown bears (Ursus arctos) during hibernation, suggesting that a key regulatory role of this protein is to quench sex steroid bioavailability in hibernation physiology. To enable characterization of ursine SHBG and a cross species comparison, we established an insect cell‐based expression system for recombinant full‐length ursine and human SHBG. Compared with human SHBG, we observed markedly lower secretion levels of ursine SHBG, resulting in a 10‐fold difference in purified protein yield. Both human and ursine recombinant SHBG appeared as dimeric proteins in solution, with a single unfolding temperature of ~ 58 °C. The thermal stability of ursine and human SHBG increased 5.4 and 9.5 °C, respectively, in the presence of dihydrotestosterone (DHT), suggesting a difference in affinity. The dissociation constants for [(3)H]DHT were determined to 0.21 ± 0.04 nm for human and 1.32 ± 0.10 nm for ursine SHBG, confirming a lower affinity of ursine SHBG. A similarly reduced affinity, determined from competitive steroid binding, was observed for most steroids. Overall, we found that ursine SHBG had similar characteristics to human SHBG, specifically, being a homodimeric glycoprotein capable of binding steroids with high affinity. Therefore, ursine SHBG likely has similar biological functions to those known for human SHBG. The determined properties of ursine SHBG will contribute to elucidating its potential regulatory role in hibernation physiology

Diurnal and dietary-induced changes in cholesterol synthesis correlate with levels of mRNA for HMG-CoA reductase

We determined the extent to which diurnal variation in cholesterol synthesis in liver is controlled by steady-state mRNA levels for the rate-limiting enzyme in the pathway, hydroxymethylglutaryl (HMG)-CoA reductase. Rats 30 days of age and maintained on a low-cholesterol diet since weaning were injected intraperitoneally wit