ABSTRACT
A Fe-N conjugated organic polymer (SMP-Fr-Py) was prepared from ferrocene and pyrrole using a Scholl coupling reaction, which significantly improved the performance of Cr(VI) removal compared to the polymer (HCP-Fr-Py) prepared by adding the cross-linker formaldehyde dimethyl acetal (FDA). The results showed that at a pH of 2 and at 25 °C, the removal of Cr(VI) reached 90% for SMP-Fr-Py and only 58% for HCP-Fr-Py after 20 min of reaction. Subsequently, 99% and 78% were achieved after 120 min of reaction, respectively. The test results showed that the removal reaction followed a pseudo-second-order kinetic model. The removal efficiency decreased with increasing solution pH and initial Cr(VI) concentration, but increased with increasing SMP-Fr-Py dosage, reaching three cycles. The characterization of the reaction complexes and measurements of Cr species conversion revealed the near absence of Cr(VI) species in the solution. Approximately 38% of Cr(VI) was found to be adsorbed on the material surface, with another fraction present in solution (24%) and on the material surface (38%) in the form of Cr(III). The overall study showed that the direct connection of ferrocene and pyrrole in SMP-Fr-Py through C-C bonding increased the conjugated structure of the polymer backbone, which facilitated electron transfer and transport. Furthermore, the Fe-N elements worked synergistically with each other more easily, which improved the removal performance of Cr(VI) and provided a reference for the subsequent work.
ABSTRACT
OBJECTIVE: To investigate the role of chemokine receptor ACKR2 in cognitive impairment in young rats with traumatic brain injury. METHODS: Seventy-five young rats were randomly divided into TBI group, TBI+Negative control (NC) group, TBI+Sensory integration (SI) group, TBI+Atypical chemokine receptor 2 (ACKR2) group and TBI+SI+ACKR2 group. We employed several techniques, including the water maze test, transmission electron microscope, HE staining, enzyme-linked immunosorbent assay, RT-PCR, western blotting to elucidate the role of ACKR2 in young rats with traumatic brain injury. RESULTS: We observed that the ability of learning and memory were significantly decreased, the serum inflammatory factors CCL2, IL-1ß and TNF-α were increased, the expression of Tau and NG2 was increased, and the expression of ACKR2 was decreased in TBI rats. After ACKR2 overexpression combined with SI, the learning ability and memory ability of TBI rats were improved, the levels of CCL2, IL-1ß, TNF-α were decreased, the expressions of Tau and NG2 were decreased, which were better than those of SI and ACKR2 groups. CONCLUSION: ACKR2 may be an effective method for improving the results after TBI in young rats.
