Clinical utility and tolerability of JSPH-1 wireless esophageal pH monitoring system.

BACKGROUND: Wireless esophageal pH monitoring system is an important approach for diagnosis of gastroesophageal reflux disease (GERD), the aim of this study is to test the tolerability and utility of the first wireless esophageal pH monitoring system made in China, and evaluate whether it is feasible for clinical application to diagnose GERD. METHODS: Thirty patients from Department of Gastroenterology of The First Affiliated Hospital of Chongqing Medical University who were suspected GERD underwent JSPH-1 pH capsule. The capsule was placed 5 cm proximal to the squamocolumnar junction (SCJ) by endoscopic determination, the data was recorded consecutively for 48 hours. Then all pH data was downloaded to a computer for analysis. The discomforts reported by patients were recorded. RESULTS: 30 patients were placed JSPH-1 pH capsule successfully and completed 24-hour data recording, 29 patients completed 48-hour data recording. One patient complained of chest pain and required endoscopic removal. No complications and interference of daily activities were reported during data monitoring or follow-up period. 48-hour pH monitoring detected 15 patients of abnormal acid exposure, on day1 detected 9 patients, the difference had statistical significance (P<0.01). Positive symptom index (SI) was identified in 3 patients with normal pH data in both 24-hours. In total, 48-hour monitoring increased diagnosis of GERD in 9 patients. CONCLUSION: 48-hour esophageal pH monitoring with JSPH-1 wireless pH monitoring system is safe, well tolerated and effective. It can be feasible for clinical application to diagnose GERD.

[Effects of rofecoxib on angiogenesis of pancreatic cancer xenograft in nude mice].

BACKGROUND & OBJECTIVE: Angiogenesis plays a crucial role in invasive tumor growth. Overexpressed cyclooxygenases-2 (COX-2) may be related to increased angiogenesis in the rapidly progressed tumor. The purpose of the present study was to investigate the effects of the highly selective COX-2 inhibitor,rofecoxib on the growth of pancreatic cancer xenografts in nude mice in vivo as well as on tumor-associated angiogenesis. METHODS: BXPC-3 human pancreatic cancer cells overexpressing COX-2 was inoculated subcutaneously into nude mice. Rofecoxib (30 mg/kg) was administered orally to animals every day for eight weeks. The microvessel density was immunostained with factor VIII antibody. The expression of VEGF on BXPC-3 pancreatic cancer cell line was measured by immunocytochemistry in vitro. Gelatin zymography and RT-PCR technology were used to determine MMP-2 progelatinase and expression of MMP-2 mRNA. RESULTS: Rofecoxib significantly reduced the tumor volume with an inhibition rate of 87.7% as well as tumor weight with an inhibition rate of 73.64% for xenografts in nude mice. The density of microvessel was notably lower in xenografts treated with rofecoxib than in those without treatment (1.5+/-0.2 vs 4.7+/-1.5/200x; P< 0.05). Expression of VEGF protein, MMP-2 progelatinase and MMP-2 mRNA levels in the xenografts treated with rofecoxib were lower than those of control group. CONCLUSION: Antiangiogenesis is one of the mechanisms by which Rofecoxib suppresses pancreatic cancer proliferation.

Inhibitory effect of octreotide on gastric cancer growth via MAPK pathway.

AIM: Somatostatin and its analogues may suppress the growth of various tumor cells. However, the effect of octreotide on growth of gastric adenocarcinoma is still largely unknown. This study was to explore if octreotide could inhibit the growth of gastric adenocarcinoma and its probable mechanisms. METHODS: Proliferation of gastric cancer cell line affected by octreotide was determined by (3)H-thymidine incorporation. After xenografts of human gastric cancer were implanted orthotopically in stomach, nude mice were administrated octreotide for 8 weeks. The mRNA of somatostatin receptor in the SGC-7901 cells was detected by reverse transcription polymerase chain reaction technique. Extracellular signal-regulated protein kinase and c-Fos in gastric cancer tissues were measured by immunohistochemistry and Western blot. Activator protein-1 binding activity was examined by electrophoretic mobility sift assay. RESULTS: (3)H-thymidine incorporation into SGC-7901 cells was significantly decreased by octreotide in a concentration dependent manner. Either size or weight of tumors treated with octreotide was significantly reduced in vivo. The inhibition rate for tumor was 62.3 % in octreotide group. The genes of somatostatin receptors 2 and 3 were expressed in SGC-7901 gastric cancer cell lines. Extracellular signal-regulated protein kinase and c-Fos protein level were decreased in gastric adenocarcinoma treated with octreotide. Moreover, fetal calf serum stimulated activator protein-1 binding activity could be suppressed by octreotide potentially. CONCLUSION: Inhibition of sequential molecular events in MAPK pathway may interpret the mechanisms underlying the effect of octreotide on the growth of gastric adenocarcinoma.

[The combination of octreotide to rofecoxib enhanced the inhibitory effect on growth of human hepatocellular carcinoma].

OBJECTIVE: To know whether octreotide combined with rofecoxib would enhance the inhibitory effect on proliferation of hepatocellular carcinoma (HCC) in vitro and in vivo. METHODS: The proliferation of HCC SMMC 7721 cells were measured by incorporating (3)H-thymidine ribotide ((3)H-TdR) into DNA. The effect of octreotide combined with rofecoxib on proliferation of HCC cells was evaluated according to the median-response principle. SMMC-7721 cells were implanted orthotopically in the liver of nude mice. Nude mice were treated with either octreotide (100 micro g x kg(-1) x d(-1)) combined with rofecoxib (30 mg x kg(-1) x d(-1)) or rofecoxib (30 mg x kg(-1) x d(-1)) alone for 8 weeks. The volumes of implanted tumors were measured. RESULTS: The combination of octreotide and rofecoxib significantly inhibited (3)H-TdR incorporation of HCC cell line in culture in a dose-dependent manner (r = -0.997, P < 0.01). The combination indexes of octreotide and rofecoxib in the majority of effect range were less than 1. The inhibitory rate of xenograft in situ in the combined group (97.1%) was significantly higher than that in the rofecoxib group (73.2%). In addition, increased amount of fibroplasia was observed in the combined group as compared with that in control group. No severe side effect was observed in all the treatment groups. CONCLUSIONS: The inhibitory effect of octreotide combined with rofecoxib on HCC cell line was significantly greater than that of octreotide or rofecoxib alone in vitro. Octreotide combined with rofecoxib greatly enhanced the anti-growth effects on HCC in vivo when compared with rofecoxib alone. These synergic results may be of potential therapeutic benefit to those patients with non-resectable HCC.