Lymphoplasmacyte-rich meningioma with atypical cystic-solid feature:A case report

BACKGROUND Lymphoplasmacyte-rich meningioma(LPRM)is one of the rarest variants of meningioma and is classified as grade I(benign)tumor.It is characterized by abundant infiltrates of lymphocytes and plasma cells.Here,we report an extremely rare case of LPRM with an atypical imaging finding of multiple cysts around a solid mass.CASE SUMMARY The patient was a 36-year-old man with intermittent headache,dizziness,and vomiting for 2 years.Computed tomography and magnetic resonance imaging presented a cystic solid mass in the right frontal lobe with heavy peritumoral edema and obvious contrast enhancement.The patient was treated with right frontotemporal craniotomy,and gross total resection of the tumor was achieved without adjuvant therapy.There was no clinical or neuroradiological evidence of recurrent or residual tumor for 3 years after initial surgery.CONCLUSION LPRM is one of the rarest variants of meningioma.Although,the mass of this case had common features,multiple cysts with nonuniform size and thin wall around the solid part are uncommon imaging finding,increasing the rate of misdiagnosis.The definitive diagnosis of LPRM relies on histopathological findings.

The Effect of Interleukin-18 on Airway Inflammation in Asthmatic Murine Models and Its Mechanisms

In order to investigate the effect of interleukin-18 （IL-18） on airway inflammation in asthmatic murine models and its mechanisms, BALB/C mice were randomly divided into three groups （n=10 in each group）： group A （control group）; group B （asthmatic model group）; group C （IL-18-treated group）. The asthmatic model was established in groups B and C by respiratory syncytial virus （RSV） killed by ultraviolet. Saline solution （0.1 mL） and IL-18 （0.1 mL, 1μg） were intraperitoneally injected respectively in groups B and C at 7 time points （day 1, 2, 7, 8, 9, 21, 22）. The number of eosinophils （EOS） and plasmacytes in the airway was observed. The levels of interferon gamma （IFN-γ） in bronchoalveolar lavage fluid （BALF） were measured by ELISA. The results showed that symptoms of asthma in group C were more severe than in groups A and B. In group A, there were no EOS and plasmacytes in the airway submucosa. The number of EOS [ 15±3 （average cell counts per microscopic visual field, the same below）] and plasmacytes （10±2） in group B were increased significantly. However, the number of EOS and plasmacytes in group C （6±2 and 2±1, respectively） was decreased significantly as compared with group B （both P〈0.05）. The levels of IFN-γ in groups A, B and C were 31±3, 40±5 and 63±5 μg/mL respectively, and those in group C were significantly higher than in groups A and B （both p〈0.05）. It was suggested that the mechanism by which IL-18 inhibited the airway inflammation in asthmatic mice might be contributed to the fact that IL-18 could induce the induction of IFN-γ.

Effects of interleukin-18 on asthmatic airway inflammation and nuclear factor kappa-B in murine models

Objective To investigate the effects of Interleukin-18 (IL-18) on asthmatic airway inflammation and nuclear factor kappa-B (NF-κB) in a murine asthmatic model. Methods BALB/C mice were randomly divided into three groups: group A(control group,n=10); group B (asthmatic model group, n=10); group C (IL-18 injection group, n=10). The asthmatic model was established in group B and C by respiratory syncytial virus (RSV) killed by ultraviolet light. Saline solution (0.1 ml) and IL-18 (0.1 ml, 1 μg) was injected in groups B and C at seven time points (1, 2, 7, 8, 9, 21, 22 d). The symptoms and the numbers of eosinophils and plasmacytes in the airways were observed and the expression of NF-κB activation in the lung was analyzed by Immohistochemistry (IHC) and Western blot. Results The symtoms of group C were more severe than in groups A and B. Group A did not have EOS and plasmacytes in the airway submucosal while the numbers of eosinophils [15±3 (average cell counts per microscopic visual field, the same below)] and plasmacytes (10±2) in group B were found to have increased significantly. But the numbers of eosinophils and plasmacytes in group C were decreased significantly when compared with group B (6±2 and 2±1, respectively, both P<0.05). ISH showed that the expression of NF-κB activation in group B was stronger than that in groups A and C. The amount of NF-κB inhibitor (IκB) in group A and group C were 3.5 times and 2.5 times more than that of group B respectively via Western blot. Conclusion IL-18 can inhibit asthmatic airway inflammation in mice and its mechamism may be due to the fact that IL-18 can inhibit the activation of NF-κB in the murine asthmatic model.