Objective To investigate the influence of the aberrant protein expression and mRNA transcription of transforming growth factor ? 1(TGF? 1) on the biological behavior of human bladder transitional cell carcinomas. Methods The expression of TGF? 1 was investigated in 74 specimens of TCCs by SP immunohistochemistry staining, and the level of TGF? 1 mRNA were determined in 43 cases of TCCs by the method of quantitative RT PCR. Results The positives expression rate of TGF? 1 was 89.2%. Superficial tumors had lower overexpressive rate of TGF? 1(33.3%) than the invasive TCCs(83.8%), P

Purpose:To investigate the relationships between the biological behavior of human transitional cell carcinomas(TCCs) and the protein expression of transforming growth factor ?1(TGF?1) as well as its'related receptors.Methods:The expression of TGF?1 ,T?RⅠ,T?RⅡ and PCNA were examined in 74 specimens of TCCs by S P immunohistochemistry staining.Results:The positive expression rate of TGF?1 , T?RⅠ and T?R Ⅱ were 89.2%,70.3% and 48.6%,respectively. Superficial tumors had lower overexpression rate of TGF?1 (33.3%) than muscle invasive TCCs (83.8%) ( P

Objective To investigate the expression of c-kit and analyze its relationship with proliferating cell nuclear antigen (PCNA) in RCC subtypes and its clinical progression. Methods Expression of c-kit protein was retrospectively studied with immunohistochemistry in paraffin sections from 137 cases of clear renal cell carcinoma (CCRCC), 82 papillary renal cell carcinoma (PRCC), 51 chromophobe renal cell carcinoma (ChRCC). Results The positive rate of c-kit in ChRCC was 94.1%(48/51), it was statistically higher than that in CCRCC (16. 1%, 22/137) and PRCC (28.1 %, 23/82)(P=0. 001 ). In ChRCC, the positive expression of c-kit was related with TNM stages. The positive expression of PCNA was related with the grade in CCRCC and PRCC. But there was no relationship between PCNA expression and grade of ChRCC. It also had the relationship with the metastasis in CCRCC. Conclusions The expression of c-kit in ChRCC is higher than in other subtype of RCC, and associated with tumor local progression. That makes c-kit as a helpful marker to discriminate different subtypes of kidney cancer.

OBJECTIVE: To investigate the effect of down-regulation of pannexin 2 (Panx-2) channels on cisplatin-induced apoptosis in I-10 cells. METHODS: The expression of Panx-2 protein in testicular cancer cells was detected with Western blotting. The testicular cancer cell line I-10 was transfected with two short hairpin RNA (shRNA1 and shRNA2) Lipofectamine, the empty vector (NC group) or Lipofectamine2000 (blank control group), and the changes in the expression of Panx-2 was detected with Western blotting. The effects of transfection with a Panx-2 inhibitor on surviving fraction of the cells treated with cisplatin (16 μmol/L) for 24 h, 48 h and 72 h was assessed with MTT assay, and the clonogenic capacity of the cells was evaluated with colony-forming assay. At 8 h after incubation with 16 μmol/L cisplatin, AnnexinV/PI double staining was used to detect the early apoptosis of the cells. After 24 h of treatment with 16 μmol/L cisplatin, the cells were examined for expressions of caspase-3, Bcl-2 and Bax using Western blotting. RESULTS: The expression of Panx-2 was significantly increased in cisplatin-resistant I-10/DDP ( < 0.001) cells and Tcam-2/DDP ( < 0.01) cells as compared with I-10 cells and Tcam-2 cells. Transfection of I-10 cells with shRNA1 and shRNA2 resulted in significantly decreased Panx-2 expression ( < 0.05) and significantly reduced cell surviving fraction ( < 0.001). In the presence of cisplatin, the cells in NC group showed a higher clonogenic efficiency than those in shRNA1 and shRNA2 groups ( < 0.001). The early-stage apoptosis rate of the cells in shRNA1 and shRNA2 groups were significantly higher than that in NC group ( < 0.01). Panx-2 knockdown in I-10 cells significantly increased caspase-3 and Bax expressions ( < 0.05) and significantly decreased the expression of Bcl-2 ( < 0.01). CONCLUSIONS Down-regulation of Panx-2 channel enhances cisplatin-induced apoptosis in cultured testicular cancer cells.
Antineoplastic Agents ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cisplatin ; Connexins ; Down-Regulation ; Drug Resistance, Neoplasm ; Humans ; Male ; Testicular Neoplasms

OBJECTIVE: To investigate the effect of connexin43 (Cx43) protein on autophagy in cisplatin (DDP)-resistant testicular cancer I-10 cells. METHODS: The expression of Cx43 proteins in testicular cancer I-10 cells and I-10/DDP cells were detected with Western blotting. I-10/DDP cells were transfected with a full- length mouse Cx43 vector (mCx43) Lipofectamine, the empty vector or Lipofectamine (blank control group), and the changes in the expressions of LC3 and p62 proteins were determined with Western blotting. mCherry-GFP-LC3B transfection and transmission electron microscopy were used to analyze the changes in autophagy of the cells with Cx43 overexpression. RESULTS: Cx43 was significantly decreased in I-10/DDP cells compared with I-10 cells ( < 0.01). Transfection of the I-10/DDP cells with mCx43 vector resulted in significantly increased Cx43 expression in the cells ( < 0.01) and caused significantly decreased expression of LC3-Ⅱ ( < 0.01) and increased expression of p62 ( < 0.05) as compared with the negative control cells. Both transmission electron microscopy and mCherry-GFP-LC3B transfection showed that the number of autophagosomes was obviously reduced in mCx43-transfected cells as compared with the negative control cells. CONCLUSIONS Cx43 inhibits autophagy in cisplatin-resistant testicular cancer I-10 /DDP cells.
Animals ; Autophagy ; Cell Line, Tumor ; Cisplatin ; Connexin 43 ; metabolism ; Drug Resistance, Neoplasm ; Male ; Mice ; Testicular Neoplasms ; metabolism ; pathology

This paper summarized clinical experience of Professor Peng Qinghua in the staged treatment of autoimmune uveitis （AU）. The pathogenesis of AU is always based on root-cause deficiency and manifestation excess， with weakness of healthy qi as the root， and accumulation of wind， dampness and blood stasis as the minifestation. Syndrome differentiation and treatment is usually carried out according to different stages of disease. During the acute stage， deficiency of healthy qi and stagnation of wind-dampness are the key pathomechanisms， so the treatment is to replenish qi and activate blood， dispel wind and remove dampness， and self-made Yiqi Huoxue Qufeng Chushi Decoction （益气活血祛风除湿方） can be used. During remission stage， deficiency of spleen and kidney is the key mechanism， so the treatment is to tonify the spleen and kidney， replenish the essence and brighten the eyes， and self-made Yijing Mingmu Decoction （益精明目汤） can be used. Meanwhile， it was recommened to treat early， prevent and interrupt the disease， commonly combine with Chinese patent medicine Zhengqing Fengtongning tablets （正清风痛宁缓释片）， and promote regulation of living to prevent recurrence.