The total effective rate for clinical symptomstreated with oral decoction with Weiweikang(benefit-ting atrophic stomach)granules and Huoli(vitality)Bolus guided by the principle of invigorating Qi,warming the interior,activating circulation and elimi-nating blood stasis,was 91.8%,while that for thechronic atrophic gastritis with metaplasia and atypicalhyperplasia of intestinal epithelium was 87.5% and74.4% respectively.After treatment,the volume ofblood flowing was markedly increased(P

Objective The study aimed to explore the main forms of double minute chromosomes(DMs)in the cell cycle of colorectal cancer at different phases,and to clarify the replication and separation phases of DMs.Methods After using serum-free starvation to block the progression of cell cycle in colorectal cancer COLO 320DM cells,Calyculin-A was used to induce interphase cells to prepare karyotype samples through advanced chromatin condensation.COLO 320DM cells were treated with colchicine to ob-tain mitosis(M)phase cells for karyotype analysis.The karyotypes of cells at the early stage of DNA synthesis(G1 phase),the late stage of DNA synthesis(G2 phase),metaphase(M-mid),anaphase(M-late),and telophase(M-ter)of mitosis were observed and photographed under a regular optical microscope,and counted the number of DMs.Results DMs mainly existed in monotypic form at the G1 phase,M-late phase and M-ter phase of cells.In the G2 and M-mid phases of cells,DMs mainly existed in a diploid form.Conclusion Monomeric DMs undergo replication in the S phase and transform from monomers to diploids,while diploid DMs in the M-late phase complete separation and transition from diploids to monomers.

Objective:To identify the genetic variation in a mucopolysaccharidosis type Ⅱ(MPS Ⅱ)family, and conduct a functional study of iduronate-2-sulfatase(IDS): c.323A>C.Methods:A five-generation MPS Ⅱ family of 83 individuals including 4 patients from northern China was collected. Urine mucopolysaccharide and Alder-Reilly body were tested to assist the clinical diagnosis of MPS Ⅱ. IDS enzyme activity was detected on core family members. By the whole exome sequencing of a MPS Ⅱ patient in this family and bioinformatics analysis, the variant was screened and further identified by PCR-Sanger sequencing. Finally, to validate the function of the variant in vitro, the wild-type IDS overexpression plasmid(pCMV-hIDS-WT)and the IDS overexpression plasmid carrying the mutation site(pCMV-hIDS-c.323A>C)were transfected into COS-7 cells and the IDS activity was detected. Results:The proband(Ⅳ3)and Ⅳ4 were diagnosed as MPS Ⅱ by urine mucopolysaccharide, Alder-Reilly body, and IDS enzyme activity tests. Ⅳ3, Ⅳ4, Ⅲ19, and Ⅲ32 were determined to carry IDS: c.323A>C missense variant through the whole-exome sequencing, and diagnosed as MPS Ⅱ. Meanwhile, Ⅱ2, Ⅱ4, Ⅱ8, Ⅱ12, Ⅱ14, Ⅲ5, Ⅲ7, Ⅳ14 in the MPS Ⅱ family carried IDS: c.323A>C missense variant, and were excluded as MPS Ⅱ. The in vitro experiment in COS-7 cells showed that the missense mutation led to a significant decrease in IDS enzyme activity. Conclusion:The variant IDS: c.323A>C: p.Y108S significantly decreases the activity of IDS enzyme in vivo and in vitro, and it is identified as a pathogenic variant for MPS Ⅱ.