RESUMO
TheR3TiSb5ternary compounds, withRa light rare earth (La to Sm) have been reported to crystallize with the anti-Hf5CuSn3-type hexagonal structure (Pearson's symbolhP18; space-groupP63/mcm, N. 193). An early article that reported possible superconductivity in some of these intermetallic phases (namely those withR= La, Ce, and Nd) caught our attention. In this work, we have now refined the crystal structure of theR3TiSb5compounds withR= Ce, Pr and Nd by Rietveld methods using high-resolution neutron powder diffraction data. The magnetic ground states of these intermetallics have been investigated by low-temperature magnetization and high-intensity neutron diffraction. We find two different magnetic transitions corresponding to two related magnetic structures atTN1= 4.8 K (k1= [0, 1/2, 1/8]) andTN2= 3.4 K (k2= [0, 0, 1/8]), respectively for Ce3TiSb5. However, the magnetic ordering appears to occur following a peculiar hysteresis: thek2-type magnetic structure develops only after thek1-type phase fraction has first slowly ordered with time and the size of the ordered Ce3+magnetic moment has become large enough to induce the second magnetic transition. AtT= 1.5 K the maximum amplitude of the Ce moment in the coexisting phases amounts toµCe= 2.15 µB. For Nd3TiSb5an antiferromagnetic ordering belowTN= 5.2 K into a relatively simpler commensurate magnetic structure with a magnetic moment ofµNd= 2.14(3)µBand magnetic propagation vector ofk= [0, 0, 0], was determined. No evidence of superconductivity has been found in Nd3TiSb5. Finally, Pr3TiSb5does not show any ordering down to 1.5 K in neutron diffraction while an antiferromagnetic ground state is detected in magnetization measurements. There is no sign of magnetic contribution from Ti atoms found in any of the studied compounds.
RESUMO
BACKGROUND: The accumulation of eosinophils is mediated by the chemokine receptor-3 (CCR3)-eotaxin axis. Increased expression of eotaxin and its receptor is associated with inflammatory bowel disease (IBD). Activation of eosinophils causes the release of cationic proteins that are neurotoxic such as eosinophil-derived neurotoxin (EDN). Damage to enteric neurons alters neurally controlled functions of the gut correlated with intestinal inflammation. We hypothesized that inhibition of the CCR3-eotaxin axis will prevent inflammation-induced functional changes to the gastrointestinal tract. METHODS: Hartley guinea pigs were administered with trinitrobenzene sulfonate (TNBS; 30 mg/kg in 30% ethanol) intrarectally to induce colitis. A CCR3 receptor antagonist (SB 328437 [SB3]) was injected intraperitoneally 1 hour postinduction of colitis. Animals were euthanized 7 days post-treatment and colon tissues were collected for ex vivo studies. The EDN-positive eosinophils in the colon, indicating eosinophil activation, were quantified by immunohistochemistry. Effects of SB3 treatment on gross morphological damage, enteric neuropathy, and colonic dysmotility were determined by histology, immunohistochemistry, and organ bath experiments. KEY RESULTS: The number of EDN-positive eosinophils was significantly increased in the lamina propria in close proximity to myenteric ganglia in inflamed colon. The TNBS-induced inflammation caused significant damage to colonic architecture and inhibition of colonic motility. Treatment with SB3 antagonist attenuated inflammation-associated morphological damage in the colon, reduced infiltration of EDN-positive eosinophils and restored colonic motility to levels comparable to control and sham-treated guinea pigs. CONCLUSION & INFERENCES: This is the first study demonstrating that inhibition of CCR3-eotaxin axis alleviates enteric neuropathy and restores functional changes in the gut associated with TNBS-induced colitis.