Objective To detect the PTEN gene mutation and loss of heterozygosity(LOH) on chromosome 10q in oligodendrogliomas. Methods The entire PTEN coding sequence of the 9 exons were screened by 9 different PCR reactions and followed by denaturing gradient gel electrophoresis(DGGE) and direct sequencing for detecte mutation.Microsatellite markers with fluorochrome on 10?q amplified by PCR were used to detecte LOH by PAGE on an automatic sequencer and analyzed with the Gene Scan program in 55 oligodendrogliomas and mixed oligodendrogliomas. Results The PTEN gene somatic mutations were detected in 2 tumors,one case that carried a PTEN mutation deletion T base in position 20 resulting stop codon moved to 347.Another case was a A to C transition at the codon 139 resulting in changeing from Leu to Phe.Twenty\|three of 55(42%) cases were observed the loss of heterozygosity(LOH) on chromosome 10?q.Fifteen of 55 cases allelic loss were detected on loci D10S 541 which located in the PTEN gene region at 10?q 23\^3 .Twelve of 55 cases were detected totaled LOH on 10?q.Conclusion\ The PTEN gene mutation is rare,loss of allelic 10?q is frequente in oligodendrogliomas,especially in high\|grade oligodendrogliomas.It could indicate that LOH on 10?q has an enhance effect in tumor progression,and chromosome 10?q harbors additional tumor suppressor genes in oligodendrogliomas.\;[

Objective To identify mutations in the OSMR gene in a pedigree with familial primary cutaneous amyloidosis (FPCA).Methods Clinical data were collected from a pedigree with FPCA.Peripheral blood samples were obtained from the proband,his 19 relatives,and 50 unrelated healthy human controls.Genomic DNA was extracted from these blood samples,and subjected to PCR for the amplification of 18 encoding exons and their flanking sequences of the OSMR gene followed by DNA sequencing.Results A heterozygous missense mutation c.2081C ＞ T,which leads to the substitution of proline by threonine at position 694,was detected in the OSMR gene of the proband and his affected relatives,but not in unaffected relatives or healthy controls.Conclusion The heterozygous mutation p.P694L in the OSMR gene may cause the clinical phenotype of FPCA in this family.

ViewRay magnetic resonance (MR) guided radiotherapy system not only solves the problem of imaging dose,but also can set up accurately,online adaptive radiotherapy and gated irradiation according to magnetic resonance imaging (MRI).The development of this system provides a new technical means of accurate radiotherapy.This review describes the main structure of the ViewRay system,and summarizes quality assurance (QA),dosimetric comparison,respiratory motion management,online adaptive radiotherapy,and preliminary treatment effect.

Objective : To investigate the inhibitory effect and molecular mechanism of ribosomal translation factor inhibitor Avilamycin on hepatitis B virus replication. Methods: Liver cancer Hep3B cells were treated with different concentrations of Avilamycin. Cell activity was detected by CCK⁃8 ; the apoptosis was detected by flow cytometry , and HBV⁃DNA、pgRNA、MTIF2、RPL10 gene expression level was detected by qPCR method. The HBsAg and HBeAg was detected by ELISA. The AFP was detected by chemiluminescence. Aspartate aminotransferase (AST) , alanine aminotransferase(ALT) , and alkaline phosphatase (ALP) proteins was detected by Biochemistry method. Results : Avilamycin had no inhibitory effect on Hep3B cell proliferation and apoptosis. However, it could promote cellular AST secretion , reduce AFP levels , and have less effect on ALP secretion. In Hep3B cells , Avilamycin promotes accumulation of pgRNA expression by intervening with MTIF2 and feedback upregulates mRNA expression of host RPL10 and MTIF2 genes. It can effectively reduce the HBsAg , HBeAg , and HBV - DNA levels. Conclusion Avilamycin can inhibit MTIF2 translation initiation , regulate the translation process of viral assembly protein by affecting translation initiation , and then inhibit hepatitis B virus replication.

ObjectiveTo investigate the role and mechanism of DNA repair regulation in the process of hepatocellular carcinoma （HCC） recurrence. MethodsHCC tissue samples were collected from the patients with recurrence within two years or the patients with a good prognosis after 5 years， and the Tandem Mass Tag-labeled quantification proteomic study was used to analyze the differentially expressed proteins enriched in the four pathways of DNA replication， mismatch repair， base excision repair， and nucleotide excision repair， and the regulatory pathways and targets that play a key role in the process of HCC recurrence were analyzed to predict the possible regulatory mechanisms. The independent samples t-test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsFor the eukaryotic replication complex pathway， there were significant reductions in the protein expression levels of MCM2 （P=0.018）， MCM3 （P=0.047）， MCM4 （P=0.014）， MCM5 （P=0.008）， MCM6 （P=0.006）， MCM7 （P=0.007）， PCNA （P=0.019）， RFC4 （P=0.002）， RFC5 （P<0.001）， and LIG1 （P=0.042）； for the nucleotide excision repair pathway， there were significant reductions in the protein expression levels of PCNA （P=0.019）， RFC4 （P=0.002）， RFC5 （P<0.001）， and LIG1 （P=0.042）； for the base excision repair pathway， there were significant reductions in the protein expression levels of PCNA （P=0.019） and LIG1 （P=0.042） in the HCC recurrence group； for the mismatch repair pathway， there were significant reductions in the protein expression levels of MSH2 （P=0.026）， MSH6 （P=0.006）， RFC4 （P=0.002）， RFC5 （P<0.001）， PCNA （P=0.019）， and LIG1 （P=0.042） in recurrent HCC tissue. The differentially expressed proteins were involved in the important components of MCM complex， DNA polymerase complex， ligase LIG1， long patch base shear repair complex （long patch BER）， and DNA mismatch repair protein complex. The clinical sample validation analysis of important differentially expressed proteins regulated by DNA repair showed that except for MCM6 with a trend of reduction， the recurrence group also had significant reductions in the relative protein expression levels of MCM5 （P=0.008）， MCM7 （P=0.007）， RCF4 （P=0.002）， RCF5 （P<0.001）， and MSH6 （P=0.006）. ConclusionThere are significant reductions or deletions of multiple complex protein components in the process of DNA repair during HCC recurrence.