Objective To analyze the clinical and genetic features of a Chinese family with nonsyndromic hearing loss ,and to find deafness‐causing mutations in the GJB2 gene .Methods After a detailed history and clinical examination ,genomic DNA was ex‐tracted from peripheral blood for the proband and their family members .Two exons of the GJB2 gene was amplified by polymerase chain reaction ,and the PCR products were subjected to automatic DNA sequencing .Finally ,the mutation analysis was performed by SeqMan software of DNASTAR to compare BLAST .Results All patients in this family had late‐onset and progressive hearing loss and ultimately involved all frequencies .Six SNP polymorphisms were found in this pedigree ,which were previously reported world‐wide ,c .79G > A(p .Val27Ile) ,c .341G > A(p .Glu114Gly) ,were also identified in this family .Four single nucleotide polymorphisms (SNPs) were firstly identified in the GJB2 3′‐UTR ,including g .4159T > C ,g .5142G/T ,g .5227G/A ,g .5352T /C .Two SNPs .Con‐clusion Mutation in exons of GJB2 gene was excluded as a pathogenic cause for nonsyndromic hearing loss in this family .

Aim To study the mechanism of anti-tumor effect of PHⅡ-7 to K562 and K562/A02 cells.Methods The effects of individual and combined doxorubicin on K562 and K562/A02 cells were observed by MTT assay.The coefficient of drug interaction was used to analyse the synergistic effect of PHⅡ-7,obtaining the RNA from the cells stimulated by PHⅡ-7 with different doses to analyse the MDR1 gene expression level.Finally,the cumulation of doxorubicin was observed in K562 and K562/A02 cells after being coped with PHⅡ-7.Results PH Ⅱ-7 had anti-tumor effect with IC50 of (1.37?0.37) ?mol?L-1;(1.48?0.34) ?mol?L-1 for K562 and K562/A02,respectively.It could potentiate the anti-tumor effect of dororubicin with CDI of 0.22 and 0.09 for K562 and K562/A02,respectively.PHⅡ-7 could synergistically inhibit the proliferation of K562 and K562/A02 cells.The decrease of MDR1 expression level depended on the increase of dose of PHⅡ-7 acting on cells.PHⅡ-7 could also develop the cumulation of doxorubicin in cells.Conclusion PHⅡ-7 is not only a Cytotoxinic drug but also can synergistically inhibit the proliferation of K562 and K562/A02 cells with the decrease of MDR1 expression level,especially in K562/A02 cells.

This study examined the role of regulated upon activation normal T cell expressed and secreted (RANTES) and its receptor C-C chemokine receptor type 5 (CCR5) in gastric cancer metastasis and the associated mechanism. The expression of RANTES and CCR5 was detected by using immunohistochemical staining and Western blotting in the gastric cancer tissues obtained from 60 gastric cancer patients with or without lymph node metastasis (n=30 in each). The results showed that the expression levels of RANTES and CCR5 were higher in gastric cancer with lymph node metastasis than in that without metastasis (P<0.05). The expression levels of RANTES in 30 lymph nodes with cancerous invasion were higher than in 30 normal lymph nodes (P<0.05). Chemotactic test revealed that the number of migrating gastric cancer cells (n=295.0±54.6) induced by the protein of cancer-invading lymph nodes was greater than that by the protein mixture from cancer-invading lymph nodes and RANTES antibody (n=42.5±11.6) (P<0.05). RT-PCR showed that the expression levels of the main Th1 cytokines (IL-2, Γ-IFN) were lower in gastric cancer with lymph node metastasis (2.22±0.90, 3.26±1.15 respectively) than in that without metastasis (3.07±1.67, 4.77±1.52 respectively) (P<0.05), but the expression level of the main Th 2 cytokine (IL-10) was higher in gastric cancer with lymph nodes metastasis (6.06±2.04) than in that without metastasis (4.88±1.87) (P<0.05). It was concluded that RANTES and its receptor CCR5 may contribute to gastric cancer metastasis through influencing the balance of Th1/Th2. RANTES and CCR5 may become a marker of gastric cancer metastasis.

This study examined the role of regulated upon activation normal T cell expressed and secreted (RANTES) and its receptor C-C chemokine receptor type 5 (CCR5) in gastric cancer metastasis and the associated mechanism.The expression of RANTES and CCR5 was detected by using immunohistochemical staining and Western blotting in the gastric cancer tissues obtained from 60 gastric cancer patients with or without lymph node metastasis (n=30 in each).The results showed that the expression levels of RANTES and CCR5 were higher in gastric cancer with lymph node metastasis than in that without metastasis (P＜0.05).The expression levels of RANTES in 30 lymph nodes with cancerous invasion were higher than in 30 normal lymph nodes (P＜0.05).Chemotactic test revealed that the number of migrating gastric cancer cells (n=295.0±54.6) induced by the protein of cancer-invading lymph nodes was greater than that by the protein mixture from cancer-invading lymph nodes and RANTES antibody (n=42.5+11.6) (P＜0.05).RT-PCR showed that the expression levels of the main Th1 cytokines (IL-2,γ-IFN) were lower in gastric cancer with lymph node metastasis (2.22±0.90,3.26±1.15 respectively)than in that without metastasis (3.07±1.67,4.77±1.52 respectively) (P＜0.05),but the expression level of the main Th 2 cytokine (IL-10) was higher in gastric cancer with lymph nodes metastasis (6.06±2.04)than in that without metastasis (4.88±1.87) (P＜0.05).It was concluded that RANTES and its receptor CCR5 may contribute to gastric cancer metastasis through influencing the balance of Th1/Th2.RANTES and CCR5 may become a marker of gastric cancer metastasis.