Bladder pain syndrome (BPS) is a chronic disease characterized by urinary symptoms and pain in or around the bladder with uncertain reasons. The incidence of BPS is higher in the female and people in American and Europen countries. The BPS patients' quality of life has been damaged and a new disabled group has been formed. The pathogeneses of BPS include pathogens inducing inflammation, chronic ischemia and ischemia-reperfusion injury producing degeneration in bladder, lower urinary epithelium dysfunction, apoptosis in bladder tissue, epigenetic reprogramming, abnormal intracellular signaling pathway, pain regulating dysfunctioning, and autophagy inhibit-ed. There is no identified diagnosis for BPS. Cystoscopy, urodynamia, and biomarks in blood or urine are helpful in diagnosis. Diet, psycho-logical intervention, oral medicine, intravesical therapy, nerve blocking and nerve stimulation, and surgeries have been used for it, but the ef-ficacy remains unsatisfied.

Sepsis is one of the main cause of patients' death. Lung is the most vulnerable target organ during sepsis, and sepsis patients are often complicated with acute respiratory distress syndrome (ARDS), of which the main mechanism is vascular leakage caused by cytoskeleton rearrangement and cell-to-cell connection changes. IQ-guanosine triphosphatease-activating protein 1 (IQGAP1) has become the key component of cytoskeleton dynamics regulation in recent years. At present, the relationship between IQGAP1 and ARDS induced by sepsis is not yet clear. In this article, we will review the mechanism of the interaction between IQGAP1 and pathogenic microorganisms, changes of pulmonary micro vascular barrier function and cyto-skeleton at the molecular level.

The neurologic function and cerebral vascular anatomy of non-human primate are closely resemble to those of human, so non-human primate cerebral ischemic model is a particularly useful tool in studying the damage mechanism and therapy intervention of cerebrovascular disorder. The authors reviewed the establishment method and neurological behavioral assessmental method of non-human primate cerebral ischemic model.

Objective To evaluate the changes of reticulated platelets (RP)in diagnosis and treatment of idiopathic thrombocytopenic purpura (ITP). Methods RPs were measured by flow cytometry and the percentage and absolute counts of RPs were calcula- ted in ITP group,non-ITP group and control group.Results Compared with control group,ITP group had a significantly high percentage and low absolute counts of RPs (P

Objective To investigate the expression of C-MET in papillary thyroid carcinoma(PTC) with (cervical) lymph node metastases, PTC without cervical lymph node metastases,follicular thyroid carcinoma and benign thyroid disease and the clinical significance. Methods The expression level of C-MET was examined by immunohistochemical analysis with C-MET monoclonal antibody in 62 cases of PTC with cervical lymph node metastases, 50 cases of PTC without cervical lymph node mestastases, 10 cases of follicular (thyroid) (carcinoma) and 30 cases of benign thyroid disease. Results PTC with cervical lymph node metastases (expressed) significantly greater level of C-MET than the other forms of thyroid carcinoma and benign thyroid disease(P

Objective:To investigate the anti-proliferation and anti-metastasis effects and study the molecular mechanism of sinomenine in cell line(HepG2).Methods: HepG2 cells were cultured together with different treatment concentrations of sinomen-ine.The effect of sinomenine on inhibition of growth of HepG2 cells were determined by methyl thiazolyl tetrazolium(MTT) assay.The effect of sinomenine on inhibiting metastasis of HepG2 cells were determined by Transwell assay.The inhibitory effect of sinomenine on reverse transcriptase(RT) was studied using inhibitory kinetic method,on the basis,the reactive oxygen species(ROS) of HepG2 cells was monitored by indirect fluorescent labeling.The protein expressions of CASP3,CASP9,CAV1 and SOX2 were analyzed by Western blot experiment.Results: Sinomenine inhibited the proliferation and metastasis of HepG2 cells significantly.Sinomenine had a good inhibitory effect on the growth of HepG2 cells,half inhibitory concentration(IC50) was (15.35±2.43)μmol/L.Sinomenine was RT inhibitor,IC50 was (21.32±2.43)μmol/L.The Western blot showed that CASP3,CASP9 and CAV1 were up-regulated and SOX2 was down-regulated by the sinomenine treatment in HepG2 cells.Conclusion: The potential molecular mechanism of sinomenine suppresses proliferation and metastasis of HepG2 cells by up-regulation of CASP3,CASP9,CAV1 and down-regulation of SOX2.

Objective: To study the inhibition effects of thalidomide on the growth and metastasis of gastric cancer in vivo in nude mice. Methods: Metastatic model simulating human gastric cancer was established by orthotopic implantation of histologically intact human tumor tissue into gastric wall of nude mice. Mice were randomly divided into 4 groups: control group (saline solution 0.5 ml, ip), 5 FU group (fluorouracil 30 mg?kg -1 ?d -1 , ip), thalidomide group (thalidomide 250 mg?kg -1 ?d -1 ,ip), combined treatment group (both 5 FU and thalidomide, ip). Six weeks after implantation, the tumor weight, inhibition rates, intratumoral microvessel density (MVD), apoptotic index (AI) and the metastasis were evaluated after the mice were sacrificed. Results: Compared with the control group, growth of tumor was significantly reduced in mice treated with 5 FU, thalidomide and combined treatment (inhibition rate 39.8%, 48.1% and 74.1%). The incidences of liver metastases was also significantly inhibited in the 5 FU group, thalidomide group and combined treatment group than in control group(8/11 vs 4/12, 3/12 and 0/12). The incidences of peritoneal metastases was also significantly inhibited in the 5 FU group, thalidomide group and combined treatment group than in control group(7/11 vs 3/12, 3/12 and 0/12). The MVD decreased significantly in thalidomide group and combined treatment group. AI increased significantly in the treated mice. Conclusion: Thalidomide can induce apoptosis in gastric cancer by inhibiting tumor angiogenesis and has inhibitory effect on growth and metastasis of human gastric cancer implanted in nude mice. Combination of thalidomide with cytotoxic agents is more effective.

ObjectiveTo study the effects of angiogenesis inhibitor SU6668 on the growth and metastasis of colon cancer in vivo. MethodsMetastatic model of human colon cancer was established by orthotopic implantation of human tumor tissue into colon wall of nude mice. Mice were randomly divided into control, 5 Fu, SU6668, and combined treatment group (both 5 Fu and SU6668 i.p.) respectively. After six weeks tumor weight, inhibition rates, intratumoral microvessel density (MVD), apoptotic index (AI) and metastasis were evaluated. ResultsCompared with control, tumor growth was significantly inhibited in mice treated respectively with 5 Fu, SU6668 and 5Fu plus SU 6668 with an inhibition rate of 0%, 42 6%, 80 9% and 87 2% respectively. MVD decreased significantly in treated groups \[(13 8?5 2)?(12 3?4 5), (2 4?1 5) and (0 9?0 5)\]. AI increased significantly in treated groups \[(3 6?2 4)%? (7 1?5 7)%, (11 9?3 9)% and (19 9?8 6)%\]. The incidences of peritoneal and liver metastases was significantly inhibited in 5 Fu, SU6668 and combined treatment group (100%? 45 5%, 16 7% and 0; 75 0%? 36 4%, 16 7% and 0). The growth and metastasis of human colon cancer implanted in nude mice were significantly inhibited in the SU6668 group and combined group than that in control group and 5 Fu group ( P

Objective To study the effects of angiogenesis inhibitor SU5416 on the growth and metastasis to the liver of gastric cancer and to investigate its effect on the apoptosis of gastric cancer cells. Methods Metastatic model simulating human gastric cancer was established by orthotopic implantation of histologically intact human tumor tissue into gastric wall of nude mice. Mice were randomly divided into 4 groups: control group (saline solution), 5 FU group (fluorouracil 30 mg?kg -1 ?d -1 i.p.), SU5416 group (SU5416 15 mg?kg -1 ?d -1 i.p.), and combined treatment of both 5 FU and SU5416 group. Eight weeks after implantation, the tumor weight, inhibition rates, intratumoral microvessel density (MVD), apoptotic index (AI), and the presence of metastasis were evaluated respectively after the mice were sacrificed. Results Compared with the control group, the growth of the orthotopically implanted tumor was significantly inhibited due to the reduced weight and the inhibition rate of tumor was 44.5%, 79.3%, and 84.4% respectively in mice treated with 5 FU, SU5416 and both. The incidences of liver metastases were also significantly decreased in the 5 FU group, SU5416 group, and combined group compared with those in control group (36.4%, 25.0%, and 0% vs 90.0%). The MVD was decreased significantly in the treated mice ( 14.6 ? 5.8 vs 13.1?4.7, 3.9? 1.8 , and 2.1?1.5). The AI was increased significantly in the treated mice [(3.76?2.25)% vs (6.81? 4.92 )%, (9.82?3.76)% and (17.65?9.85)%]. The growth and liver metastasis of human gastric cancer implanted in nude mice were more significantly inhibited in the SU5416 group and combined group than in control group and 5 FU group ( P

Objective To establish an orthotopic implantation and metastasis model of human colon cancer in nude mice. Methods Tumor cell line SW1116 of human colon adenocarcinoma was inoculated subcutaneously into nude mice to develop implantation tumor.Histologically intact tumor tissue was then harvested and implanted to the colon wall of nude mice to set up a model similar to human colon cancer.The formation of implanted tumor rate, local tumor growth characteristics,and metastasis rates were examined. Results A 100% lymphatic metastasis rate was obtained in this model. The incidences of local lymphatic metastasis, peritoneal and liver metastases were 100%, 91.7% and 75.0% respectively.Emacication and exhaustion of the nude mice were presented in late stage of the experimentation. The median survival time of the tumor-bearing nude mice was 10 weeks. Conclusions The orthotopic implantation tumor and metastasis model provide useful tools for the study of mechanism of metastasis and its treatment of human colon cancer.