Synthesis and properties of graphene and graphene/carbon nanotube-reinforced soft magnetic FeCo alloy composites by spark plasma sintering

The effect of the addition of graphene nanoplatelets (GNP) and graphene nanoplatelet/carbon nanotube (GNT) mixtures on the mechanical and magnetic properties of spark plasma sintered soft magnetic FeCo alloys was studied. Three different volume fractions (0.5, 1 and 2 vol%) of GNPs and GNTs were investigated. Ball milling was used to disperse the GNPs in monolithic FeCo powder, while magnetic stirring and ultrasonic agitation were used to prepare hybrid GNT prior to ball milling. The highest saturation induction (B sat) of 2.39 T was observed in the 1 vol% GNP composite. An increase in the volume fraction of the ordered nanocrystalline structure was found to reduce the coercivity (H c) of the composites. The addition of CNTs to the GNP composite prevented grain growth, leading to grain refinement. An 18 % increase in hardness was observed in the 1 vol% GNP composite as compared to the as-received FeCo alloy. A reduction in tensile strength was observed in all of the composite materials, except for the 0.5 vol% GNT composite, for which a value of 643 MPa was observed. Raman spectroscopy indicated a reduction in the defect density of the GNPs after adding CNTs

The atypical chemokine receptor ACKR2 suppresses Th17 responses to protein autoantigens

Chemokine-directed leukocyte migration is a critical component of all innate and adaptive immune responses. The atypical chemokine receptor ACKR2 is expressed by lymphatic endothelial cells and scavenges pro-inflammatory CC chemokines to indirectly subdue leukocyte migration. This contributes to the resolution of acute inflammatory responses <i>in vivo</i>. ACKR2 is also universally expressed by innate-like B cells, suppressing their responsiveness to the non-ACKR2 ligand CXCL13, and controlling their distribution <i>in vivo</i>. The role of ACKR2 in autoimmunity remains relatively unexplored, although <i>Ackr2</i> deficiency reportedly lessens the clinical symptoms of experimental autoimmune encephalomyelitis induced by immunization with encephalogenic peptide (MOG<sub>35–55</sub>). This was attributed to poor T-cell priming stemming from the defective departure of dendritic cells from the site of immunization. However, we report here that <i>Ackr2</i>-deficient mice, on two separate genetic backgrounds, are not less susceptible to autoimmunity induced by immunization, and in some cases develop enhanced clinical symptoms. Moreover, ACKR2 deficiency does not suppress T-cell priming in response to encephalogenic peptide (MOG<sub>35–55</sub>), and responses to protein antigen (collagen or MOG<sub>1–125</sub>) are characterized by elevated interleukin-17 production. Interestingly, after immunization with protein, but not peptide, antigen, <i>Ackr2</i> deficiency was also associated with an increase in lymph node B cells expressing granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that enhances T helper type 17 (Th17) cell development and survival. Thus, <i>Ackr2</i> deficiency does not suppress autoreactive T-cell priming and autoimmune pathology, but can enhance T-cell polarization toward Th17 cells and increase the abundance of GM-CSF<sup>+</sup> B cells in lymph nodes draining the site of immunization

The atypical chemokine receptor ACKR2 suppresses Th17 responses to protein autoantigens

Chemokine-directed leukocyte migration is a critical component of all innate and adaptive immune responses. The atypical chemokine receptor ACKR2 is expressed by lymphatic endothelial cells and scavenges pro-inflammatory CC chemokines to indirectly subdue leukocyte migration. This contributes to the resolution of acute inflammatory responses <i>in vivo</i>. ACKR2 is also universally expressed by innate-like B cells, suppressing their responsiveness to the non-ACKR2 ligand CXCL13, and controlling their distribution <i>in vivo</i>. The role of ACKR2 in autoimmunity remains relatively unexplored, although <i>Ackr2</i> deficiency reportedly lessens the clinical symptoms of experimental autoimmune encephalomyelitis induced by immunization with encephalogenic peptide (MOG<sub>35–55</sub>). This was attributed to poor T-cell priming stemming from the defective departure of dendritic cells from the site of immunization. However, we report here that <i>Ackr2</i>-deficient mice, on two separate genetic backgrounds, are not less susceptible to autoimmunity induced by immunization, and in some cases develop enhanced clinical symptoms. Moreover, ACKR2 deficiency does not suppress T-cell priming in response to encephalogenic peptide (MOG<sub>35–55</sub>), and responses to protein antigen (collagen or MOG<sub>1–125</sub>) are characterized by elevated interleukin-17 production. Interestingly, after immunization with protein, but not peptide, antigen, <i>Ackr2</i> deficiency was also associated with an increase in lymph node B cells expressing granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that enhances T helper type 17 (Th17) cell development and survival. Thus, <i>Ackr2</i> deficiency does not suppress autoreactive T-cell priming and autoimmune pathology, but can enhance T-cell polarization toward Th17 cells and increase the abundance of GM-CSF<sup>+</sup> B cells in lymph nodes draining the site of immunization

Teaching Bioeconomics

Bioeconomics is a relatively young field that uses an expanded microeconomics to examine animal behavior, human behavior, and animal and human social institutions. A voluminous literature is rapidly accumulating. There are as yet no standard textbooks, but there are several excellent books and/or articles that can be used in combination with videos and other aids to make a course that students will enjoy and that teachers can use to advance the frontiers of scholarship in economics and biology. Copyright Springer 2005altruism, conflict, cooperation, evolution, game theory, institutions, rationality,