Intestinal lesions in dogs with acute hemorrhagic diarrhea syndrome associated with netF-positive Clostridium perfringens type A

Acute hemorrhagic diarrhea syndrome (AHDS), formerly named canine hemorrhagic gastroenteritis, is one of the most common causes of acute hemorrhagic diarrhea in dogs, and is characterized by acute onset of diarrhea, vomiting, and hemoconcentration. To date, histologic examinations have been limited to postmortem specimens of only a few dogs with AHDS. Thus, the aim of our study was to describe in detail the distribution, character, and grade of microscopic lesions, and to investigate the etiology of AHDS. Our study comprised 10 dogs with AHDS and 9 control dogs of various breeds, age, and sex. Endoscopic biopsies of the gastrointestinal tract were taken and examined histologically (H&E, Giemsa), immunohistochemically (Clostridium spp., parvovirus), and bacteriologically. The main findings were acute necrotizing and neutrophilic enterocolitis (9 of 10) with histologic detection of clostridia-like, gram-positive bacteria on the necrotic mucosal surface (9 of 10). Clostridium perfringens isolated from the duodenum was identified as type A (5 of 5) by multiplex PCR (5 of 5). In addition, each of the 5 genotyped isolates encoded the pore-forming toxin netF. Clostridium spp. (not C. perfringens) were cultured from duodenal biopsies in 2 of 9 control dogs. These findings suggest that the pore-forming netF toxin is responsible for the necrotizing lesions in the intestines of a significant proportion of dogs with AHDS. Given that the stomach was not involved in the process, the term acute hemorrhagic diarrhea syndrome seems more appropriate than the frequently used term hemorrhagic gastroenteritis

Harnessing the Creative Potential of Consumers: Money, Participation and Creativity in Idea Crowdsourcing

Given the growing importance of innovation and consumer engagement, many firms are strongly interested in finding ways to encourage their consumers to generate creative new product ideas for them in their crowdsourcing initiatives. To that end, managers often use monetary rewards – one of the most commonly used managerial tools to stimulate desired behaviors. A critical question in this respect is whether the use of monetary rewards is effective in stimulating creativity and, if so, how large those rewards should be. This study aims to answer these questions. The results of an experiment suggest that introducing monetary rewards does not contribute to the number of new product ideas generated by a single consumer or the novelty of his/her ideas, and when the reward is relatively small it can even be harmful. Monetary rewards, however, are effective in encouraging widespread participation in crowdsourcing initiatives and improving the appropriateness of the new product ideas. As a whole, these findings take us a step further toward better understanding the motivational mechanisms of consumer creativity in new product ideation

Polymorphisms in the Tlr4 and Tlr5 Gene Are Significantly Associated with Inflammatory Bowel Disease in German Shepherd Dogs

Inflammatory bowel disease (IBD) is considered to be the most common cause of vomiting and diarrhoea in dogs, and the German shepherd dog (GSD) is particularly susceptible. The exact aetiology of IBD is unknown, however associations have been identified between specific single-nucleotide polymorphisms (SNPs) in Toll-like receptors (TLRs) and human IBD. However, to date, no genetic studies have been undertaken in canine IBD. The aim of this study was to investigate whether polymorphisms in canine TLR 2, 4 and 5 genes are associated with IBD in GSDs. Mutational analysis of TLR2, TLR4 and TLR5 was performed in 10 unrelated GSDs with IBD. Four non-synonymous SNPs (T23C, G1039A, A1571T and G1807A) were identified in the TLR4 gene, and three non-synonymous SNPs (G22A, C100T and T1844C) were identified in the TLR5 gene. The non-synonymous SNPs identified in TLR4 and TLR5 were evaluated further in a case-control study using a SNaPSHOT multiplex reaction. Sequencing information from 55 unrelated GSDs with IBD were compared to a control group consisting of 61 unrelated GSDs. The G22A SNP in TLR5 was significantly associated with IBD in GSDs, whereas the remaining two SNPs were found to be significantly protective for IBD. Furthermore, the two SNPs in TLR4 (A1571T and G1807A) were in complete linkage disequilibrium, and were also significantly associated with IBD. The TLR5 risk haplotype (ACC) without the two associated TLR4 SNP alleles was significantly associated with IBD, however the presence of the two TLR4 SNP risk alleles without the TLR5 risk haplotype was not statistically associated with IBD. Our study suggests that the three TLR5 SNPs and two TLR4 SNPs; A1571T and G1807A could play a role in the pathogenesis of IBD in GSDs. Further studies are required to confirm the functional importance of these polymorphisms in the pathogenesis of this disease

Obesity Takes Its Toll on Visceral Pain: High-Fat Diet Induces Toll-Like Receptor 4- Dependent Visceral Hypersensitivity

Exposure to high-fat diet induces both, peripheral and central alterations in TLR4 expression. Moreover, functional TLR4 is required for the development of high-fat diet-induced obesity. Recently, central alterations in TLR4 expression have been associated with the modulation of visceral pain. However, it remains unknown whether there is a functional interaction between the role of TLR4 in diet-induced obesity and in visceral pain. In the present study we investigated the impact of long-term exposure to high-fat diet on visceral pain perception and on the levels of TLR4 and Cd11b (a microglial cell marker) protein expression in the prefrontal cortex (PFC) and hippocampus. Peripheral alterations in TLR4 were assessed following the stimulation of spleenocytes with the TLR4-agonist LPS. Finally, we evaluated the effect of blocking TLR4 on visceral nociception, by administering TAK-242, a selective TLR4-antagonist. Our results demonstrated that exposure to high-fat diet induced visceral hypersensitivity. In parallel, enhanced TLR4 expression and microglia activation were found in brain areas related to visceral pain, the PFC and the hippocampus. Likewise, peripheral TLR4 activity was increased following long-term exposure to high-fat diet, resulting in an increased level of pro-inflammatory cytokines. Finally, TLR4 blockage counteracted the hyperalgesic phenotype present in mice fed on high-fat diet. Our data reveal a role for TLR4 in visceral pain modulation in a model of diet-induced obesity, and point to TLR4 as a potential therapeutic target for the development of drugs to treat visceral hypersensitivity present in pathologies associated to fat diet consumption

Personality psychology: Lexical approaches, assessment methods, and trait concepts reveal only half of the story—Why it is time for a paradigm shift

This article develops a comprehensive philosophy-of-science for personality psychology that goes far beyond the scope of the lexical approaches, assessment methods, and trait concepts that currently prevail. One of the field’s most important guiding scientific assumptions, the lexical hypothesis, is analysed from meta-theoretical viewpoints to reveal that it explicitly describes two sets of phenomena that must be clearly differentiated: 1) lexical repertoires and the representations that they encode and 2) the kinds of phenomena that are represented. Thus far, personality psychologists largely explored only the former, but have seriously neglected studying the latter. Meta-theoretical analyses of these different kinds of phenomena and their distinct natures, commonalities, differences, and interrelations reveal that personality psychology’s focus on lexical approaches, assessment methods, and trait concepts entails a) erroneous meta-theoretical assumptions about what the phenomena being studied actually are, and thus how they can be analysed and interpreted, b) that contemporary personality psychology is largely based on everyday psychological knowledge, and c) a fundamental circularity in the scientific explanations used in trait psychology. These findings seriously challenge the widespread assumptions about the causal and universal status of the phenomena described by prominent personality models. The current state of knowledge about the lexical hypothesis is reviewed, and implications for personality psychology are discussed. Ten desiderata for future research are outlined to overcome the current paradigmatic fixations that are substantially hampering intellectual innovation and progress in the field

THE EFFECTS OF A HIGH-FAT DIET ON NEURONAL INFLAMMATION

David S. Umbaugh, Jane C. Maciejewski, & Brianne L. Guilford Southern Illinois University Edwardsville, Edwardsville, Illinois; e-mail: [email protected] Diabetic neuropathy is a common complication of diabetes that reduces the quality of life for millions of Americans. Overweight humans with dyslipidemia develop neuropathy before developing overt diabetes. In addition, recent evidence indicates a high-fat diet induces signs of neuropathy in rodents and may contribute to the development of neuropathy in pre-diabetic and/or diabetic humans, but mechanisms underlying high-fat diet induced neuropathy have not been elucidated. PURPOSE: The overall aim was to identify neuronal inflammation as a potential mechanism underlying the pathogenesis of high-fat diet-induced neuropathy. These experiments tested the hypothesis that a HF diet induces neuronal inflammation. METHODS: Male C57Bl/6 mice were randomized to two groups and fed a standard (Std) or high-fat diet (HF) for 8 weeks. The lumbar dorsal root ganglia were harvested and inflammatory mediators (IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-17, MCP-1, IFN-γ, TNF-γ, MIP-1α, GMCSF, and RANTES) were analyzed using a Multiplex ELISA. Neuropathy was characterized using the von Frey test for hindpaw mechanical sensitivity at baseline and every other week thereafter. RESULTS: At the end of the 8 wk intervention, the HF fed mice had significantly higher bodyweight and fasting blood glucose levels. Hindpaw mechanical sensitivity was not significantly different between groups at any timepoint. However, hindpaw mechanical sensitivity trended toward an increase from baseline (56.3 ± 0.05%) to wk 8 (70.8 ± 0.06%) in HF (p = 0.055) compared to Std (baseline: 56.9 ± 0.05% ; wk 8 : 61.4 ± 0.07%). MCP-1 was significantly higher in HF compared to Std after the 8 wk intervention. There were no other significant differences in inflammatory mediators between the groups. CONCLUSION: Although hindpaw mechanical hypersensitivity is characteristic of HF feeding in mice, the mild increase in hindpaw mechanical sensitivity did not reach statistical significance in this cohort. The HF fed mice exhibited elevated MCP-1 levels compared to Std fed mice which is suggestive of diet-induced inflammation. MCP-1 is understood to play a crucial role in the recruitment of inflammatory mediators, which suggests diet-induced inflammation may play a role in establishing neuropathy. Funding provided by Southern Illinois University Edwardsville Seed Grants for Transitional and Exploratory Projects

THE EFFECTS OF A HIGH-FAT DIET AND EXERCISE ON THE PGC-1α-FNDC5/IRISIN PATHWAY IN C57BL/6 MICE

Jake C. Parson1, Stephanie N. Vick1, Caleb W. Grote2, Janelle M. Ryals2, Douglas E. Wright2, & Brianne L. Guilford1. 1Southern Illinois University Edwardsville, Edwardsville, Illinois, 2University of Kansas Medical Center, Kansas City, Kansas; e-mail: [email protected] Recent research has identified irisin as a novel protein that stimulates the “browning” of white adipose by inducing thermogenesis in white adipose via increased uncoupling protein 1 (UCP1) levels. Exercise, in a peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) dependent manner, increases the release of the irisin precursor, fibronectin type III domain-containing protein 5 (FNDC5), from muscle. Irisin holds potential as a novel pharmacotherapeutic that could be used in the treatment of obesity. Prior studies have assessed the effects of exercise on irisin and proteins upstream and downstream of its activation, but the effects of diet on irisin have not been investigated. PURPOSE: The aim of this study was to evaluate the effects of diet and exercise on FNDC5 and associated proteins. METHODS: C57BL/6 mice were randomized into three groups for the 4 week intervention: Mice were fed a standard diet (Std), a high-fat diet (HF), or fed a high-fat diet and housed individually with free access to a running wheel (HFEX). At the end of the 4 week intervention, mice were sacrificed, tissues were harvested, and protein levels were measured in the gastrocnemius muscle using western blots. RESULTS: Body weight, fasting glucose and insulin, and homeostatic model of insulin resistance (HOMA-IR) were significantly higher in HF compared to Std and HFEX after the 4 week intervention. There was a trend (p = 0.09) toward increased FNDC5 levels in HF compared to HFEX. UCP-1 levels were significantly lower in the HFEX compared to both Std and HF. There were no significant differences among groups in PGC-1α. CONCLUSION: Although there were no statistically significant differences in FNDC5 levels, the trend toward increased FNDC5 in HF compared to HFEX suggests increased FNDC5 may be a compensatory mechanism to offset HF diet-induced weight gain by increasing energy expenditure. Exercise prevented excess weight gain and metabolic derangements in HF fed mice, but these effects do not appear to be mediated by increased FNDC5 levels. Further investigation, including assessment of FNDC5, PGC1-α, and UCP1 levels in adipose from these mice is needed to confirm the effects of HF feeding on the FNDC5/irisin pathway. Funding provided by Southern Illinois University Edwardsville Seed Grants for Transitional and Exploratory Projects

Effects of age and reproductive status on individual foraging site fidelity in a long-lived marine predator.

Individual foraging specialisations, where individuals use a small component of the population niche width, are widespread in nature with important ecological and evolutionary implications. In long-lived animals, foraging ability develops with age, but we know little about the ontogeny of individuality in foraging. Here we use precision global positioning system (GPS) loggers to examine how individual foraging site fidelity (IFSF), a common component of foraging specialisation, varies between breeders, failed breeders and immatures in a long-lived marine predator – the northern gannet Morus bassanus. Breeders (aged 5+) showed strong IFSF: they had similar routes and were faithful to distal points during successive trips. However, centrally placed immatures (aged 2-3) were far more exploratory and lacked route or foraging site fidelity. Failed breeders were intermediate: some with strong fidelity, others being more exploratory. Individual foraging specialisations were previously thought to arise as a function of heritable phenotypic differences or via social transmission. Our results instead suggest a third alternative - in long-lived species foraging sites are learned during exploratory behaviours early in life, which become canalised with age and experience, and refined where possible – the exploration-refinement foraging hypothesis. We speculate similar patterns may be present in other long-lived species and moreover that long periods of immaturity may be a consequence of such memory-based individual foraging strategies