Localized Malignant Myxoid Anaplastic Mesothelioma of the Pericardium

Primary malignant mesothelioma of the pericardium is a rare cardiac neoplasm. Most are diffuse and have poor prognosis with median survival of six months. In the paper, we describe a young male patient having no exposure history of asbestos with localized malignant myxoid mesothelioma of the pericardium. The tumor displayed significant myxoid change in stroma, and anaplastic cytology, including pleomorphy, poor cohesion, prominent nuclei, with high mitoses, which led to difficulty in diagnosis. The tumor showed typical immunohistochemical phenotypes of mesothelioma, positive for WT-1, calretinin and CK5/6. Ki-67 labeling index was about 50% in general and nearly 80% in the most active areas. The patient showed better outcome. The report suggests the diagnosis of myxoid mesothelioma is supposed to rely on clinical data, and immunohistochemistry is assumed to be for differentiation

Rigid vortices in MgB2

Magnetic relaxation of high-pressure synthesized MgB$_2$ bulks with different thickness is investigated. It is found that the superconducting dia-magnetic moment depends on time in a logarithmic way; the flux-creep activation energy decreases linearly with the current density (as expected by Kim-Anderson model); and the activation energy increases linearly with the thickness of sample when it is thinner than about 1 mm. These features suggest that the vortices in the MgB$_2$ are rather rigid, and the pinning and creep can be well described by Kim-Anderson model.Comment: Typo corrected & reference adde

Dichlorido(4,5-diaza­fluoren-9-one-κ2 N,N′)palladium(II)

The structure of the title compound, [PdCl2(C11H6N2O)], shows a nearly square-planar geometry for the PdII atom within a Cl2N2 donor set

Original Article 5-Aza-CdR can reverse gefitinib resistance caused by DAPK gene promoter methylation in lung adenocarcinoma cells

Abstract: To explore the relationship between death associated protein kinase (DAPK) gene promoter methylation and gefitinib resistance in Lung adenocarcinoma cell lines. EGFR-mutation lung adenocarcinoma cell lines PC9 and the gefitinib-resistant with T790M Mutation cell lines PC9/GR were chosen as cell models, and PC9/GR were treated with 5-aza-CdR (1 μmol/L). The experiments were divided into three groups: PC9 group, PC9/GR group and PC9/GR with 5-Aza-CdR pretreatment group. Treat three groups cell with different concentrations gefitinib, the cell proliferation was determined by MTT assay. The apoptotic rates were detected by flow cytometry. The methylation of DAPK gene promoter region was examined by methylation-specific PCR (MSP). The expressions of DAPK protein were detected by Western blot. MTT results showed that the half maximal inhibitory concentration (IC50) of PC9 and PC9/GR cell lines increase from 0.12 μmol/L to 8.52 μmol/L. But after treated with 5-aza-CdR, the IC50 of PC9/GR cell lines decrease to 4.35 μmol/L, and the resistance index (RI) decrease from 71 to 36 (P<0.05). Flow cytometry results showed that the apoptosis rate were 24.80%±0.28%, 12.70%±0.31%, 19.8%±0.15% respectively. MSP results showed that DAPK gene promoter region was un-methylated in PC9 cells and methylated in PC9/GR cells, when treated with 5-aza-CdR, DAPK gene promoter region was partly methylated in PC9/GR cells (P<0.05). Western blot results showed that the levels of DAPK protein were reduced significantly in PC9/GR cell lines compared with PC9, and after treated with 5-aza-CdR, the expression levels of DAPK protein in PC9/GR were increased (P<0.05). In conclusion, DAPK gene promoter methylation may contribute to the downregulation of DAPK gene and protein, and consequently affect the sensitivity of gefitinib in lung adenocarcinoma lines, induced gefitinib resistance. But 5-Aza-CdR can reverse gefitinib resistance by demethylation of DAPK gene promoter