Putting ourselves in another’s skin: using the plasticity of self-perception to enhance empathy and decrease prejudice

The self is one the most important concepts in social cognition and plays a crucial role in determining questions such as which social groups we view ourselves as belonging to and how we relate to others. In the past decade, the self has also become an important topic within cognitive neuroscience with an explosion in the number of studies seeking to understand how different aspects of the self are represented within the brain. In this paper, we first outline the recent research on the neurocognitive basis of the self and highlight a key distinction between two forms of self-representation. The first is the “bodily” self, which is thought to be the basis of subjective experience and is grounded in the processing of sensorimotor signals. The second is the “conceptual” self, which develops through our interactions of other and is formed of a rich network of associative and semantic information. We then investigate how both the bodily and conceptual self are related to social cognition with an emphasis on how self-representations are involved in the processing and creation of prejudice. We then highlight new research demonstrating that the bodily and conceptual self are both malleable and that this malleability can be harnessed in order to achieve a reduction in social prejudice. In particular, we will outline strong evidence that modulating people’s perceptions of the bodily self can lead to changes in attitudes at the conceptual level. We will highlight a series of studies demonstrating that social attitudes towards various social out-groups (e.g. racial groups) can lead to a reduction in prejudice towards that group. Finally, we seek to place these findings in a broader social context by considering how innovations in virtual reality technology can allow experiences of taking on another’s identity are likely to become both more commonplace and more convincing in the future and the various opportunities and risks associated with using such technology to reduce prejudice

Endocrine and Other Influences on the Trafficking of Immune Cells

This dissertation examines endocrine and other influences on the trafficking of immune cells. This work aimed to increase the understanding of underlying mechanisms pertaining to immune cell entry into breast milk, and prolactin’s involvement in this important physiological phenomenon. Because of observations made during this study, the work also examined various aspects of sexual dimorphism in lymph nodes and thymus. Luminal mammary epithelial cell secretions act as chemoattractants, inducing migration of a variety of lymphocytes, phagocytes, and granulocytes. Prolactin treatment of mammary epithelial cells increases production of chemoattractants and migration of most of these cell types. This supports a role for luminal mammary epithelial cells in immune cell concentration into milk. CCL2 and CXCL1 were two chemoattractants identified responsible for a significant degree of migration of monocytes and neutrophils, respectively. In-vivo prolactin treatment increased immune cell flux through the mammary tissue and increased expression of CCL2 and CXCL1 in a mammary cell line in vitro. Female mice have more T-cells in their popliteal lymph nodes than males, while males have a greater proportion of T-cells that are suppressive in function. This combination supports a rationale for females having a higher delayed-type hypersensitivity response in a region drained by this lymph node. The sex difference in T-cells is present prior to puberty and is to some extent dependent on Sry expression as males overexpressing Sry have even fewer T-cells. In addition, male gonadal secretions amplified the sex difference as mice aged. Adult female mice with two X chromosomes exhibit a greater delayed-type hypersensitivity response to Candida albicans at proestrus than at metestrus or diestrus, while females with an X and a Y chromosome, the latter minus the Sry gene, did not exhibit different responses across these stages of the estrous cycle. There is therefore a combined effect of the sex chromosomal complement and hormonal changes occurring at proestrus that permits maximal response. These results demonstrate significant interactions between the endocrine and immune systems both in regions where one might expect (the mammary gland during lactation) and in regions (the popliteal lymph node) where gene and endocrine sex effects were not anticipated

Endocrine and Other Influences on the Trafficking of Immune Cells

This dissertation examines endocrine and other influences on the trafficking of immune cells. This work aimed to increase the understanding of underlying mechanisms pertaining to immune cell entry into breast milk, and prolactin’s involvement in this important physiological phenomenon. Because of observations made during this study, the work also examined various aspects of sexual dimorphism in lymph nodes and thymus. Luminal mammary epithelial cell secretions act as chemoattractants, inducing migration of a variety of lymphocytes, phagocytes, and granulocytes. Prolactin treatment of mammary epithelial cells increases production of chemoattractants and migration of most of these cell types. This supports a role for luminal mammary epithelial cells in immune cell concentration into milk. CCL2 and CXCL1 were two chemoattractants identified responsible for a significant degree of migration of monocytes and neutrophils, respectively. In-vivo prolactin treatment increased immune cell flux through the mammary tissue and increased expression of CCL2 and CXCL1 in a mammary cell line in vitro. Female mice have more T-cells in their popliteal lymph nodes than males, while males have a greater proportion of T-cells that are suppressive in function. This combination supports a rationale for females having a higher delayed-type hypersensitivity response in a region drained by this lymph node. The sex difference in T-cells is present prior to puberty and is to some extent dependent on Sry expression as males overexpressing Sry have even fewer T-cells. In addition, male gonadal secretions amplified the sex difference as mice aged. Adult female mice with two X chromosomes exhibit a greater delayed-type hypersensitivity response to Candida albicans at proestrus than at metestrus or diestrus, while females with an X and a Y chromosome, the latter minus the Sry gene, did not exhibit different responses across these stages of the estrous cycle. There is therefore a combined effect of the sex chromosomal complement and hormonal changes occurring at proestrus that permits maximal response. These results demonstrate significant interactions between the endocrine and immune systems both in regions where one might expect (the mammary gland during lactation) and in regions (the popliteal lymph node) where gene and endocrine sex effects were not anticipated

Subcutaneous administration of leptin normalizes fasting plasma glucose in obese type 2 diabetic UCD-T2DM rats.

Leptin has been shown to reduce hyperglycemia in rodent models of type 1 diabetes. We investigated the effects of leptin administration in University of California, Davis, type 2 diabetes mellitus (UCD-T2DM) rats, which develop adult-onset polygenic obesity and type 2 diabetes. Animals that had been diabetic for 2 mo were treated with s.c. injections of saline (control) or murine leptin (0.5 mg/kg) twice daily for 1 mo. Control rats were pair-fed to leptin-treated animals. Treatment with leptin normalized fasting plasma glucose and was accompanied by lowered HbA1c, plasma glucagon, and triglyceride concentrations and expression of hepatic gluconeogenic enzymes compared with vehicle (P < 0.05), independent of any effects on body weight and food intake. In addition, leptin-treated animals exhibited marked improvement of insulin sensitivity and glucose homeostasis compared with controls, whereas pancreatic insulin content was 50% higher in leptin-treated animals (P < 0.05). These effects coincided with activation of leptin and insulin signaling pathways and down-regulation of the PKR-like endoplasmic reticulum (ER) kinase/eukaryotic translation inhibition factor 2α (PERK-eIF2α) arm of ER stress in liver, skeletal muscle, and adipose tissue as well as increased pro-opiomelanocortin and decreased agouti-related peptide in the hypothalamus. In contrast, several markers of inflammation/immune function were elevated with leptin treatment in the same tissues (P < 0.05), suggesting that the leptin-mediated increase of insulin sensitivity was not attributable to decreased inflammation. Thus, leptin administration improves insulin sensitivity and normalizes fasting plasma glucose in diabetic UCD-T2DM rats, independent of energy intake, via peripheral and possibly centrally mediated actions, in part by decreasing circulating glucagon and ER stress

Consensus on media violence effects : comment on Bushman, Gollwitzer, and Cruz (2015)

We summarize the main findings of Bushman, Gollwitzer, and Cruz (2015), highlight its empirical contributions, and note interesting patterns and implications for future research. The results demonstrate that consensus exists among experts on the reality of harmful media violence effects on children and adolescents. We note likely differences in the makeup of the different samples and how these might have affected the results. This comment also presents a new breakdown of the Bushman et al. findings, highlighting the high consensus for causal screen media violence effects on aggression, which fairly closely mirrors findings from that voluminous research literature, and compares this to the lack of consensus on the harmful effects of print media violence, which corresponds to a quite small research literature. We conclude with a call for research on how to overcome resistance to unpopular scientific findings.7 page(s

Modelling of the pharmacodynamic interaction between phenytoin and sodium valproate

1. Treatment of epilepsy with a combination of antiepileptic drugs remains the therapeutic choice when monotherapy fails. In this study, we apply pharmacokinetic-pharmacodynamic modelling to characterize the interaction between phenytoin (PHT) and sodium valproate (VPA). 2. Male Wistar rats received a 40 mg kg(−1) intravenous dose of PHT over 5 min either alone or in combination with an infusion of VPA resulting in a steady-state concentration of 115.5±4.9 μg ml(−1). A control group received only the infusion of VPA. The increase in the threshold for generalized seizure activity (ΔTGS) was used as measure of the anticonvulsant effect. 3. PHT pharmacokinetics was described by a pharmacokinetic model with Michaelis-Menten elimination. The concentration-time course and plasma protein binding of PHT were not altered by VPA. The pharmacokinetic parameters V(max) and K(m) were, respectively, 294±63 μg min(−1) and 7.8±2.4 μg ml(−1) in the absence of VPA and 562±40 μg min(−1) and 15.6±0.9 μg ml(−1) upon administration in combination with VPA. 4. A delay of the onset of the effect relative to plasma concentrations of PHT was observed. The assessment of PHT concentrations at the effect site was based on the effect-compartment model, yielding mean k(e0) values of 0.128 and 0.107 min(−1) in the presence and absence of VPA, respectively. 5. A nonlinear relationship between effect-site concentration and the increase in the TGS was observed. The concentration that causes an increase of 50% in the baseline TGS (EC(50%TGS)) was used to compare drug potency. A shift of EC(50%TGS) from 13.27±3.55 to 4.32±0.52 μg ml(−1) was observed upon combination with VPA (P<0.01). 6. It is concluded that there is a synergistic pharmacodynamic interaction between PHT and VPA in vivo