A 51-year-old man presented with a 4-month history of upper abdominal distending pain and 1-month history of cutaneous nodules and plaques on the neck, trunk and bilateral thighs. The patient underwent many gastrointestinal tract examinations in several local hospitals, and symptomatic treatment did not work. The biopsy of nodules on the abdomen revealed medium- to large-sized atypical lymphoid cells within numerous small vessels in lower dermis and subcutaneous fat tissue. Additionally, the atypical cells were present exclusively within vascular lumina. Immunohistochemical labeling showed the reactivity of neoplastic cells to CD2, CD99, CD3ε, CD43, CD56, Epstein-Barr virus-encoded small nuclear RNAs (EBER), and cytotoxic proteins such as T-cell intracellular antigen-1 (TIA-1) and perforin, but not to CD4, CD8, CD20, CD79a,CD30, cytokeratin (CK), S100, or CD68. The endothelial cells lining the involved vessels exhibited the reactivity to CD31 and CD34. Based on the above findings, the patient was diagnosed with intravascular NK/T-cell lymphoma firstly manifesting as gastrointestinal tract symptom and complicated by skin lesions. Following combined chemotherapy with cyclophosphamide, daunorubicin, vincristine, prednisone and etoposide, the patient experienced a quick and satisfactory recovery and the follow-up still continued.

AIM: To study the influence of MG132 on the proliferation and cell cycle distribution of NK/T cell lymphoma cells, and to investigate the potential role of proteasome inhibitor on the treatment of NK/T cell lymphoma. METHODS: NK/T cell lymphoma cells HANK1 were treated with proteasome inhibitor MG132, and the proliferation was evaluated by MTT assay. The morphological changes were observed under inverse microscope. The cell cycle distribution and apoptosis were detected using flow cytometry. RESULTS: The growth inhibitory rate of HANK1 cells was(57.72±7.44)% after cultured for 24 h with 1 μmol/L MG132 and was just(3.98±0.07)% after cultured for 24 h with 0.1 μmol/L MG132. The positive relationship between the concentration of MG132 and growth inhibitory rate was observed. On the other hand, after cultured for 24 h with 1μmol/L MG132, the cells in G_1 and G_2 phases were(72.33±3.44)% and(12.86±1.29)%, respectively, much higher than those in control group(63.63%±2.29% and 7.94%±1.91%, respectively). The early and late apoptosis rates in MG132 group were 33.57%±2.10% and 16.66%±0.47%, respectively, much higher than that in control group (7.18%±0.82% and 3.81%±1.06%, respectively). CONCLUSION: MG132 inhibits cell proliferation and induces cell cycle arrested at G_1 and G_2 phases, and cell apoptosis in NK/T cell lymphoma cells in a concentration dependent manner. Proteasome inhibitor may be a good drug to treat patients with advanced NK/T cell lymphomas.

Objective To explore the clinical and endoscopy features of Mallory-Weiss Syndrome(MWS),and summarize the experience on the diagnosis and treatment of MWS. Methods We retrospectively analyzed the clinical data of cases of MWS. Results Including 11 cases homeostasis by endoscopy 31 cases received conservative treatment except 1 case by surgery. All cases were cured. Conclusion Endoscopy is the first choice of diagnosing MWS. It,s the effective homeostasis measure.

Objective: To investigate the effect and mechanism of XTP4 gene in apoptotic hepatoblastoma HepG2 cell line. Methods: HepG2 cells were transiently transfected with small interfering RNA of XTP4 genes, plasmid pcDNA3.1/myc-His(-) A-XTP4, and hepatitis B virus X protein transactivated x gene 4 (HBX protein trans-activate gene4, XTP4) and their respective negative controls. After 48h, the overexpression and interference expression condition of XTP4 in HepG2 cells were detected by Western blot. HepG2 cells apoptosis was detected by flow cytometry. The expression levels of apoptosis-related proteins P53, Bcl-2, Bax and Caspase-3 in HepG2 cells were detected by Western blot, and Bcl-2/Bax ratio was calculated. The chemiluminescence assay was used to detect activity of caspase-3 in HepG2 cells. The measured data were presented as ( ± s), and independent sample t-test was used for comparison between the two groups. Results: HepG2 cells had successfully achieved the overexpression and interference expression of XTP4 protein. Compared with the control group, the overexpression of XTP4 in HepG2 cells had significantly decreased the number of apoptotic cells (P < 0.05), and increased Bcl-2/Bax (P < 0.05) ratio, but decreased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was decreased (P < 0.05). However, interference with XTP4 expression in HepG2 cells had significantly increased the number of apoptotic cells (P < 0.05) and decreased Bcl-2/Bax (P < 0.05) ratio, but increased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was increased (P<0.05). Conclusion In HepG2 apoptosis XTP4 has inhibitory effect, and its effect on inhibiting HepG2 apoptosis may be achieved by regulating the Bcl-2/Bax ratio, and the P53 protein may be involved.

Objective: To investigate the change in expression of anti-senescence marker protein calmodulin (RGN) in liver tissues of rats with immune hepatic fibrosis, and to observe the effect of compound glutathione inosine injection (CGII) on it. Methods: Rat liver fibrosis model was induced by intraperitoneal injection of porcine serum, and CGII intervention was administered at the appropriate time. Rat liver tissues were stained with HE and Masson. RGN and protein expression at mRNA in liver tissues was detected by fluorescence quantitative PCR and immunohistochemistry. One-way Anova was used for measurement data. LDS test was used for two-way comparison, and pathological semi-quantitative results were analyzed by rank-sum test. Results: The relative expression of RGN mRNA and protein in liver tissue of fibrotic rats was 82.23 ± 15.21 and 12.52 ± 3.23, respectively, which were significantly lower than that of normal rats 176.39 ± 11.35 and 59.23 ± 9.13 (P < 0.01). The degree of liver fibrosis in fibrotic rats after CGII intervention was significantly lower than fibrotic rats. The relative expression of RGN mRNA and protein in the intervention group was 168.78 ± 21.31 and 46.42 ± 4.71, respectively, which were significantly higher than fibrosis and spontaneous recovery group. The difference was statistically significant (P < 0.01). The relative expression of RGN mRNA and protein in the spontaneous recovery group was 86.23 ± 17.16 and 14.34 ± 5.16, which was higher than model group. The difference was not statistically significant (P > 0.05). Conclusion The expression of RGN in liver tissue of rats with hepatic fibrosis induced by porcine serum is decreased, while the expression of RGN increases with the decrease of fibrosis after CGII intervention, suggesting that the protein may play an important role in the development of liver fibrosis.

Objective: To investigate the differential expression of serum-and-glucocorticoid-inducible-kinase-2 (SGK2) in hepatocellular carcinoma (HCC) and normal liver tissues and the related mechanism mediating signal transduction of GSK-3 β / β catenin in HCC cells. Methods: Twenty pairs of matched HCC and normal tissues were collected and the situation of expression of SGK2 mRNA was detected by real-time fluorescence quantitative PCR. Western blot was used to detect the levels of SGK2 protein in human HCC cell lines (Huh-7, SMMC-7721) and normal human liver cell line (L02). SGK2 siRNA was used to transfect human HCC cell lines (SMMC-7721 and Huh-7), and then the protein expression levels of GSK-3 β/ β - catenin was successfully detected with the above-mentioned transfected cell line by western blot. Measurement data were expressed as mean ± standard deviation (±s), and the Student t -test was used as the statistical method. Results: SGK2 mRNA expression was up-regulated in all 20 HCC samples than that of the expression of matched normal liver tissues. SGK2 protein levels were significantly higher in Huh-7 and SMMC-7721 than normal human liver cell lines (P < 0.01). The downregulation of SGK2 expression in human HCC cell lines (SMMC-7721 and Huh-7) had inhibited the expression of unphosphorylated GSK-3 β. In addition, the downregulation of SGK2 expression in HCC cell lines had decreased the dephosphorylation of β - catenin to prevent degradation of the β - catenin proteasome. Conclusion SGK2 is overexpressed in HCC and mediates GSK-3β/β- catenin signaling in HCC cells.