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Among the various consequence arising from lung injury, hepatic fibrosis is the most severe. Decreasing the effects of hepatic fibrosis remains one of the primary therapeutic challenges in hepatology. Dysfunction of hepatic sinusoidal endothelial cells is considered to be one of the initial events that occur in liver injury. Vascular endothelial growth factor signaling is involved in the progression of genotype changes. The aim of the present study was to determine the effect of the tyrosine kinase inhibitor, vatalanib, on hepatic fibrosis and hepatic sinusoidal capillarization in a carbon tetrachloride (CCl4)-induced mouse model of liver fibrosis. Liver fibrosis was induced in BALB/c mice using CCl4 by intraperitoneal injection for 6 weeks. The four experimental groups included a control, and three experimental groups involving administration of CCl4, vatalanib and a combination of the two. Histopathological staining and measuring live hydroxyproline content evaluated the extent of liver fibrosis. The expression of α-smooth muscle actin (SMA) and cluster of differentiation (CD) 34 was detected by immunohistochemistry. Collagen type I, α-SMA, transforming growth factor (TGF)-β1 and vascular endothelial growth factor receptor (VEGFR) expression levels were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The average number of fenestrae per hepatic sinusoid was determined using transmission electron microscopy. Liver fibrosis scores and hydroxyproline content were decreased in both vatalanib groups. In addition, both doses of vatalanib decreased mRNA expression levels of hepatic α-SMA, TGF-β1, collagen-1, VEGFR1, and VEGFR2. Levels of α-SMA and CD34 protein were decreased in the vatalanib group compared with the CCl4 group. There were significant differences in the number of fenestrae per sinusoid between the groups. The present study identified that administration of vatalanib was associated with decreased liver fibrosis and hepatic sinusoidal capillarization in CCl4-induced mouse models, and is a potential compound for counteracting liver fibrosis.

Diagnostic peritoneoscopy is typically performed by using a rigid laparoscope. Inspired by gastric submucosal tunneling for peritoneal natural orifice transluminal endoscopic surgery access and peroral endoscopic myotomy for the treatment of achalasia, we developed a novel esophago-cardial-gastric tunneling (ECGT) peritoneoscopy technique with a flexible endoscope. This study aims to evaluate its feasibility and safety.The study comprised 10 Beagle dogs. A longitudinal mucosal incision was made on the esophageal wall, and a submucosal tunnel was created through the cardia into the stomach. An incision was made in the muscular layer of the stomach, and then the endoscope was advanced into the peritoneal cavity. Peritoneoscopy with the flexible endoscope was performed. After intraperitoneal exploration, the esophageal mucosal entry was closed with endoclips. All dogs resumed food intake 12 hours after the procedures. Diets, behavior, and body temperature of all of the dogs were observed. Endoscopic examinations were performed 4 weeks after the procedure, and then the animals were sacrificed for necropsy.The ECGT peritoneoscopy was successfully done in all dogs. Diets, behavior, and body temperature were normal in all dogs. The entry of the esophagus was healed well in 9 dogs; the mucosa of the entry was torn in 1 dog, but the submucosal tunnel was healed well at the cardia. Necropsy showed complete closure of the gastric serosal exit, and no intraperitoneal abscess was found. Histopathological examinations showed submucosal tunnels healed well.The ECGT peritoneoscopy is feasible and safe for peritoneal exploration. It should be a good choice for the clinical application of diagnostic peritoneoscopy.

The aim of the present study was to detect the effect of the recombinant human endostatin Endostar on hepatic sinusoidal capillarization in CCl4‑induced murine models of liver fibrosis. The liver fibrosis model was induced in BALB/c mice using intraperitoneal injection of CCl4 for 6 weeks. Animals were divided into the following six treatment groups: Group 1, normal animals; group 2, CCl4‑induced liver fibrosis; group 3, CCl4+Endostar 20 mg/kg/day for 6 weeks; group 4, CCl4+Endostar 10 mg/kg/day for 6 weeks; group 5, CCl4+Endostar 20 mg/kg/day for 4 weeks; and group 6, CCl4+Endostar 10 mg/kg/day for 4 weeks. The average number of fenestrae per hepatic sinusoid was determined using transmission electron microscopy. Vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR) 1 and 2 expression was detected by western blot analysis. There were significant differences in the number of fenestrae per sinusoid between the normal control and untreated model fibrotic mice (P

Ro60/SSA is a vital auto antigen that is targeted in Sjogren's syndrome and systemic lupus erythematosus (SLE). However, its role in solid cancers has rarely been reported. The present study investigated the expression and function of Ro60/SSA in the development of pancreatic ductal adenocarcinoma (PDAC) both in vitro and in vivo. Immunohistochemistry was used to examine the expression of Ro60/SSA in PDAC and normal pancreatic tissues by using tissue microarray chips. The results showed that Ro60/SSA expression was increased in PDAC tissues compared with normal pancreatic tissues. Knockdown of Ro60/SSA by siRNA transfection significantly decreased cell proliferation and invasion in vitro. Furthermore, knockdown of Ro60/SSA inhibited the growth of subcutaneous tumors in vivo. Taken together, the current study provides evidence of new function of Ro60/SSA in the development of cancer. It facilitates pancreatic cancer proliferation, migration and invasion. Therefore, it may represent a novel molecular target for the management of pancreatic cancer.

NOTES cholecystectomy has become one of the hottest areas of research. But most of the cases need the assistance of the laparoscope. This study is conducted to evaluate the feasibility and safety of a newly proposed operative method-functional cholecystectomy by pure NOTES.The functional cholecystectomy was performed on eight female miniature pigs. An incision was made on the vaginal wall, and an endoscope was inserted into the peritoneal cavity to create a pneumoperitoneum to expose the intra-abdominal viscera, gallbladder, and cystic duct. The cystic duct was isolated and closed with a clip. Then, an injection needle was inserted into the gallbladder to suck up the bile. After the gallbladder was washed with saline, an incision was made on the wall of the gallbladder, and the tip of the endoscope was inserted into the gallbladder cavity. After the endoscope was withdrawn, the gallbladder incision was closed with clips in four pigs and was suspended in the other four pigs. The vaginal incision was closed with clips. All the animals were closely monitored and euthanized 28 days after the procedure. Necropsy was performed.The functional cholecystectomy was successfully completed in all eight pigs. No severe intraoperative complications occurred. The animals recovered well postoperatively. At necropsy, no macroscopic signs of intraperitoneal infection or bile leakage in the peritoneal cavity were observed, and the clips were still present on the cystic duct in a good position in all cases. The gallbladder incision healed, with no sign of bile leakage or injury to the adjacent organs.We successfully performed the functional cholecystectomy by transvaginal approach on pigs, which appears to be feasible, safe, and convenient. Functional cholecystectomy provides a new fitting path to pure NOTES.