Going belowground: burying anthropomorphic biases on gustation and olfaction

Chemical signaling underpins behavioral interactions among organisms in the soil. Understanding chemical communication in the soil requires a paradigm shift in methodology and perspectives compared to aboveground ecosystems because olfaction and gustation, accepted modalities of chemosensation aboveground, may not accurately represent chemical communication in the soil. To fully understand chemical communication in the soil, it is essential to consider how soil properties, such as moisture, pH, and adsorption, affect the transport and perception of semiochemicals. De-anthropomorphizing the study of chemosensation can avoid potential biases, particularly in soil systems, where distinctions between olfaction and gustation are confounded by the heterogeneity of the soil environment and its effects on the mobility of chemical signals. In this perspective, we first explore how soil heterogeneity confounds the dichotomy between olfaction and gustation with hypothetical but ecologically relevant examples. Then we examine how anthropomorphic biases in aboveground chemical ecology have influenced soil chemical ecology. Our examples and discussion are prepared primarily in reference to soil arthropods. We conclude by discussing seven future research directions and outstanding questions. The soil is a premier example of a system where investigators should avoid anthropomorphisms when studying behavioral and chemical ecology. Research in soil chemical ecology should further efforts towards developing a unified view of chemosensation that could apply to all environments where chemical communication occurs

Reducing Eating Disorder Risk Factors: A Controlled Investigation of a Blended Task-Shifting/Train-the-Trainer Approach to Dissemination and Implementation

Recent advances in psychological intervention research have led to an increase in evidence-based interventions (EBIs), yet there remains a lag in dissemination and implementation of EBIs. Task-shifting and the train-the-trainer (TTT) model offer two potential strategies for enhancing reach of EBIs. The Body Project, an EBI found to prevent onset of eating disorders, served as the vehicle for this dissemination/implementation study. The primary aim of this study was to determine if training of peer-leaders for the Body Project could be task-shifted to undergraduate students using a hybrid task-shifting/TTT model. Our secondary aim was to determine if subgroups of participants evidenced different trajectories of change through 14-month follow-up. Regarding the first aim, we found almost no evidence to suggest that a presence of a doctoral-level trainer yielded superior participant outcomes compared to training by undergraduates alone. Regarding Aim 2, almost all classes for all variables evidenced improvement or a benign response. Additionally, for three key risk factors (thin-ideal internalization, body dissatisfaction, and ED symptoms) virtually all trajectories showed improvement. This study provides initial support for the use of a blended task-shifting/TTT approach to dissemination and implementation within prevention generally, and further support for broad dissemination of the Body Project specifically

Reducing Eating Disorder Risk Factors: A Controlled Investigation of a Blended Task-Shifting/Train-the-Trainer Approach to Dissemination and Implementation

Recent advances in psychological intervention research have led to an increase in evidence-based interventions (EBIs), yet there remains a lag in dissemination and implementation of EBIs. Task-shifting and the train-the-trainer (TTT) model offer two potential strategies for enhancing reach of EBIs. The Body Project, an EBI found to prevent onset of eating disorders, served as the vehicle for this dissemination/implementation study. The primary aim of this study was to determine if training of peer-leaders for the Body Project could be task-shifted to undergraduate students using a hybrid task-shifting/TTT model. Our secondary aim was to determine if subgroups of participants evidenced different trajectories of change through 14-month follow-up. Regarding the first aim, we found almost no evidence to suggest that a presence of a doctoral-level trainer yielded superior participant outcomes compared to training by undergraduates alone. Regarding Aim 2, almost all classes for all variables evidenced improvement or a benign response. Additionally, for three key risk factors (thin-ideal internalization, body dissatisfaction, and ED symptoms) virtually all trajectories showed improvement. This study provides initial support for the use of a blended task-shifting/TTT approach to dissemination and implementation within prevention generally, and further support for broad dissemination of the Body Project specifically

Melanocortin 4 Receptors Reciprocally Regulate Sympathetic and Parasympathetic Preganglionic Neurons

Melanocortin 4 receptors (MC4Rs) in the central nervous system are key regulators of energy and glucose homeostasis. Notably, obese patients with MC4R mutations are hyperinsulinemic and resistant to obesity-induced hypertension. Although these effects are likely dependent upon the activity of the autonomic nervous system, the cellular effects of MC4Rs on parasympathetic and sympathetic neurons remain undefined. Here, we show that MC4R agonists inhibit parasympathetic preganglionic neurons in the brainstem. In contrast, MC4R agonists activate sympathetic preganglionic neurons in the spinal cord. Deletion of MC4Rs in cholinergic neurons resulted in elevated levels of insulin. Furthermore, re-expression of MC4Rs specifically in cholinergic neurons (including sympathetic preganglionic neurons) restores obesity-associated hypertension in MC4R null mice. These findings provide a cellular correlate of the autonomic side effects associated with MC4R agonists and demonstrate a role for MC4Rs expressed in cholinergic neurons in the regulation of insulin levels and in the development of obesity-induced hypertension

Leptin fails to blunt the lipopolysaccharide-induced activation of the hypothalamic-pituitary-adrenal axis in rats

Copyright @ 2013 The authors. This work is licensed under a Creative Commons Attribution 3.0 Unported License.Obesity is a risk factor for sepsis morbidity and mortality, whereas the hypothalamic-pituitary-adrenal (HPA) axis plays a protective role in the body's defence against sepsis. Sepsis induces a profound systemic immune response and cytokines serve as excellent markers for sepsis as they act as mediators of the immune response. Evidence suggests that the adipokine leptin may play a pathogenic role in sepsis. Mouse endotoxaemic models present with elevated leptin levels and exogenously added leptin increased mortality whereas human septic patients have elevated circulating levels of the soluble leptin receptor (Ob-Re). Evidence suggests that leptin can inhibit the regulation of the HPA axis. Thus, leptin may suppress the HPA axis, impairing its protective role in sepsis.We hypothesised that leptin would attenuate the HPA axis response to sepsis.We investigated the direct effects of an i.p. injection of 2 mg/kg leptin on the HPA axis response to intraperitoneally injected 25 μg/kg lipopolysaccharide (LPS) in the male Wistar rat. We found that LPS potently activated the HPA axis, as shown by significantly increased plasma stress hormones, ACTH and corticosterone, and increased plasma interleukin 1β (IL1β) levels, 2 h after administration. Pre-treatment with leptin, 2 h before LPS administration, did not influence the HPA axis response to LPS. In turn, LPS did not affect plasma leptin levels. Our findings suggest that leptin does not influence HPA function or IL1b secretion in a rat model of LPS-induced sepsis, and thus that leptin is unlikely to be involved in the acute-phase endocrine response to bacterial infection in rats.The section is funded by grants from the MRC, BBSRC, NIHR and an Integrative Mammalian Biology (IMB) Capacity Building Award, and by a FP7-HEALTH-2009-241592 EuroCHIP grant and is supported by the NIHR Imperial Biomedical Research Centre Funding Scheme. This work is supported by a BBSRC Doctoral Training-Strategic Skills Award grant (BB/F017340/1)

Postnatal Growth after Intrauterine Growth Restriction Alters Central Leptin Signal and Energy Homeostasis

Intrauterine growth restriction (IUGR) is closely linked with metabolic diseases, appetite disorders and obesity at adulthood. Leptin, a major adipokine secreted by adipose tissue, circulates in direct proportion to body fat stores, enters the brain and regulates food intake and energy expenditure. Deficient leptin neuronal signalling favours weight gain by affecting central homeostatic circuitry. The aim of this study was to determine if leptin resistance was programmed by perinatal nutritional environment and to decipher potential cellular mechanisms underneath

10 Years of C-K Theory: A Survey on the Academic and Industrial Impacts of a Design Theory.

The goal of our research1 was to understand what is expected today from a design theory and what types of impact such type of scientific proposition may reach. To answer these questions with a grounded approach we chosed to study the developement of C-K theory as phenomenon per se that can inform our research work. C-K theory is clearly recognized as a design theory and it is a good representative of the level of generality and abstraction of contemporary design theory. Indeed, the validity of the theory as such has already been documented (e.g. Hatchuel & Weil 2002, 2003, 2008, 2009; Kazakçi 2009; Reich et al 2010; Le Masson et al 2010; Ullah et al 2012). Instead the current work sets out to understand the dissemination and the impact of the theory in both academic and industrial fields. The data collection overlooks the literature on C-K theory in English and in French, and includes interviews and feedbacks of students and industrial partners who applied C-K methodologies and tools. This research confirms the rapid diffusion and multiples impact of C-K theory. Beyond, such study signals that there are important expectations and potential impacts of a Design Theory within the field of knowledge at large. However there are strong conditions to meet these expectations: generality, generativity, and relatedness to contemporary sciences. A similar research could be done on Nam Suh's axiomatic approach to further test these conditions. It is impossible to say what will be the next generations of Design theory but it is sure that they should progress on these directions

Melanocortin 4 receptors in autonomic neurons regulate thermogenesis and glycemia

SUMMARY Melanocortin 4 receptors (Mc4rs) are expressed by extra-hypothalamic neurons including cholinergic autonomic pre-ganglionic neurons. However, whether Mc4rs in these neurons are required to control energy and glucose homeostasis is unclear. Here we report that Mc4rs in sympathetic, but not parasympathetic, pre-ganglionic neurons are required to regulate energy expenditure and body weight including brown and white adipose tissue thermogenic responses to diet and cold exposure. In addition, deletion of Mc4rs in both sympathetic and parasympathetic cholinergic neurons impairs glucose homeostasis

Novel delivery system enhances efficacy of antiretroviral therapy in animal model for HIV-1 encephalitis

Most potent antiretroviral drugs (e.g., HIV-1 protease inhibitors) poorly penetrate the blood-brain barrier. Brain distribution can be limited by the efflux transporter, P-glycoprotein (P-gp). The ability of a novel drug delivery system (block co-polymer P85) that inhibits P-gp, to increase the efficacy of antiretroviral drugs in brain was examined using a severe combined immunodeficiency (SCID) mouse model of HIV-1 encephalitis (HIVE). Severe combined immunodeficiency mice inoculated with HIV-1 infected human monocyte-derived macrophages (MDM) into the basal ganglia were treated with P85, antiretroviral therapy (ART) (zidovudine, lamivudine and nelfinavir (NEL)), or P85 and ART. Mice were killed on days 7 and 14, and brains were evaluated for levels of viral infection. Antiviral effects of NEL, P85, or their combination were evaluated in vitro using HIV-1 infected MDM and showed antiretroviral effects of P85 alone. In SCID mice injected with virus-infected MDM, the combination of ART-P85 and ART alone showed a significant decrease of HIV-1 p24 expressing MDM (25% and 33% of controls, respectively) at day 7 while P85 alone group was not different from control. At day 14, all treatment groups showed a significant decrease in percentage of HIV-1 infected MDM as compared with control. P85 alone and combined ART-P85 groups showed the most significant reduction in percentage of HIV-1 p24 expressing MDM (8% to 22% of control) that were superior to the ART alone group (38% of control). Our findings indicate major antiretroviral effects of P85 and enhanced in vivo efficacy of antiretroviral drugs when combined with P85 in a SCID mouse model of HIVE