The purpose of this study is to explore the neuroprotection mechanism of levetiracetam (LEV) with acute focal cerebral ischemia-reperfusion (I/P) mouse. The cerebral artery I/P animal model was prepared with a middle artery cerebral occlusion method. For drug intervention, mice were intraperitoneally injected with LEV with a dose of either 15 or 150 mg/kg. Neuronal injury was evaluated by measuring the infarct area, apoptosis ratio, and observation of blood-brain barrier ultrastructure with transmission electron microscope. CD8(+) antibody and perforin antibody were used to make cross-reference screen through flow cytometry to determine a perforin-positive rate in CD8(+) T lymphocytes (PFN + %). Injection of LEV can reduce infarct area, apoptosis ratio, and blood-brain barrier damage 24 h later after acute I/P in WT mice. In vitro, perforin can lower hippocampal neuron viability. In vivo, removing perforin can relieve neuronal injury. High dose injection of LEV (150 mg/kg) can inhibit perforin secreting from CD8(+)T lymphocytes. In addition, LEV can still protect neurons with perforin knockout mice. Therefore, our results suggested that LEV may contribute to neuron protection after cerebral ischemia reperfusion. The possible mechanism may be related with perforin release. However, we cannot roll out other mechanisms.

Psoriasis is a chronic inflammatory disease characterized by erythematous scaly plaques, accompanied by systemic damage that leads to the development of multiple comorbidities. In particular, the association between psoriasis and cardiometabolic comorbidities, including cardiovascular diseases (CVDs), obesity, diabetes mellitus, and metabolic syndrome, has been verified in a considerable number of clinical trials. Moreover, the increased risk of cardiometabolic comorbidities positively correlates with psoriasis severity. Biologic therapy targeting inflammatory pathways or cytokines substantially improves the life quality of psoriasis patients and may affect cardiometabolic comorbidities by reducing their incidences. In this review, we focus on exploring the association between cardiometabolic comorbidities and psoriasis, and emphasize the benefits and precautions of biologic therapy in the management of psoriasis with cardiometabolic comorbidities. The pathogenic mechanisms of cardiometabolic comorbidities in psoriasis patients involve common genetic factors, lipid metabolism, insulin resistance, and shared inflammatory pathways such as tumor necrosis factor-α and interleukin-23/Th-17 pathways.

In this paper, Eu3+ beta-diketone Complexes with the two ligands 1-(2-naphthoyl)-3, 3, 3-trifluoroacetonate (TFNB) and 2'2-bipyridine (bpy) have been synthesized. Furthermore, we reported a systematical study of the co-fluorescence effect of Eu(TFNB)3bpy doped with inert rare earth ions (La3+, Gd3+ and Y3+) and luminescence ion Tb3+. The co-luminescence effect can be found by studying the luminescence spectra of the doped complexes, which means that the existence of the other rare earth ions (La3+, Y3+, Gd3+ and Tb3+) can enhance the luminescence intensity of the central Eu3+, which may be due to the intramolecular energy transfer between rare earth ions and Eu3+. The efficient intramolecular energy transfer in all the complexes mainly occurs between the ligand TFNB and the central Eu3+. Full characterization and detail studies of luminescence properties of all these synthesized materials were investigated in relation to co-fluorescence effect between the central Eu3+ and other inert ions. Further investigation into the luminescence properties of all the complexes show that the characteristic luminescence of the corresponding Eu3+ through the intramolecular energy transfers from the ligand to the central Eu3+. Meantime, the differences in luminescence intensity of the 5D0-->7F2 transition, in the 5D0 lifetimes and in the 5D0 luminescence quantum efficiency among all the synthesized materials confirm that the doped complex Eu(0.5)Tb(0.5)(TFNB)3bpy exhibits higher 5D0 luminescence quantum efficiency and longer lifetime than the pure Eu(TFNB)3bpy complex and other materials.