Colonic interposition between the liver and left diaphragm - management of Chilaiditi syndrome: A case report and literature review.

Chilaiditi syndrome refers to a medical condition that is indicated by the presence of Chilaiditi sign, the radiological observation of a colonic interposition between the liver and the diaphragm, and is associated with other clinical symptoms. Chilaiditi syndrome is a rare entity and therefore, is often misdiagnosed in clinical practice, however, it may be accompanied by a series of severe complications, such as bowel obstruction and perforation. The current study describes a 47-year-old male who presented with repeated abdominal pain and acute intestinal obstruction. The patient was diagnosed with Chilaiditi syndrome via radiological observation and was cured by conservative treatment. The clinical data of seven additional patients with Chilaiditi syndrome, which was reported in the Chinese literature between January 1990 and January 2013, were also collected. The pathogenesis, clinical manifestation, diagnosis and treatment of this syndrome have been reviewed and analyzed. The current study may be useful to familiarize clinical practitioners with Chilaiditi syndrome, in order to avoid a misdiagnosis during clinical treatment.

Identification of metastasis-associated proteins involved in gallbladder carcinoma metastasis by proteomic analysis and functional exploration of chloride intracellular channel 1.

Advanced gallbladder cancer has an extremely poor prognosis because of metastasis. Identification of metastasis-related biomarkers is essential to improve patient survival. In the present study, metastasis-associated proteins were identified by comparative proteomic analysis and the metastasis-related function of the candidate protein, chloride intracellular channel 1 (CLIC1), was further elucidated. Two cell lines with high or low metastatic potential (termed GBC-SD18H and GBC-SD18L, respectively), originating from the same parental gallbladder carcinoma GBC-SD cell line, were identified by spontaneous metastasis in vivo and characterized by metastatic phenotypes analysis in vitro. Subsequently, a proteomic approach comprised of two-dimensional gel electrophoresis analysis and mass spectroscopy was used to identify and compare the protein expression patterns between GBC-SD18L and GBC-SD18H. Twenty-six proteins were identified and further verified by one-dimensional Western blotting and semiquantitative reverse transcriptase polymerase chain reaction analysis. It was determined that CLIC1, ezrin, vimentin, annexin A3, WD repeat domain 1, triosephosphate isomerase, C1-tetrahydrofolate synthase, Rho GDP-dissociation inhibitor 1, T-complex protein 1, heterogeneous nuclear ribonucleoprotein K, glutamate dehydrogenase 1, proteasome activator complex subunit 3 and Rab GDP-dissociation inhibitor beta were significantly up-regulated in the highly metastatic GBC-SD18H cell line compared to the poorly metastatic GBC-SD18L cell line. However, phosphoglycerate kinase 1 and programmed cell death protein 8 were significantly down-regulated in the highly metastatic GBC-SD18H cell line compared to GBC-SD18L. Considering that CLIC1 was profuse in highly metastatic GBC-SD18H but scarce in poorly metastatic GBC-SD18L, the association of CLIC1 with metastasis was further elucidated by the overexpression and RNA interference of CLIC1 in GBC-SD18L cells and GBC-SD18H cells, respectively. The results demonstrated that the overexpression of CLIC1 promoted cell motility and invasion of GBC-SD18L in vitro, while RNA interference of CLIC1 remarkably decreased cell motility and invasive potency of GBC-SD18H in vitro, indicating that CLIC1 might play an important role in metastasis of gallbladder carcinoma.

Role of dissection of secondary branches of splenic pedicle in portal hypertension cases undergoing splenectomy.

BACKGROUND: It is well known that conventional splenectomy, which requires careful handling and ligation of tissue of the splenic hilum, can easily cause complications such as splenic fever and pancreatic fistula. Here, we use the technique of dissection of the secondary branches of the splenic pedicle to handle the hilum in the portal hypertension patients who are subjected to splenectomy. METHODS: We retrospectively compared and analyzed the complications, postoperative hospital stay, operative time, and occurrence of hemorrhage in 121 patients with portal hypertension undergoing splenectomy and devascularization of the gastric cardia from January 1999 to December 2007. The selected cases consisted of 51 patients undergoing conventional splenectomy and 70 patients undergoing dissection of secondary branches of the splenic pedicle. In addition, we analyzed the relationship between size of the spleen and occurrence of complications. RESULTS: The incidence of pancreatic fistula and splenic fever (0/70 and 9/70) was lower in patients undergoing dissection of secondary branches of the splenic pedicle as compared with that of the conventional group (5/51 and 18/51 respectively). In addition, there was no significant difference in operative time and volume of blood loss between two groups. The spleen thickness of those patients who had pancreatic fistula and splenic fever was significantly greater than those without complications. CONCLUSIONS: These results indicate that dissection of secondary branches of the splenic pedicle in portal hypertension patients undergoing splenectomy can decrease the incidence of splenic fever and pancreatic fistula, and shorten the postoperative hospital stay, especially in the patients with a large spleen. So dissection of secondary branches of the splenic pedicle is a valuable technique for splenectomy.

[Mesenchymal stem cells inhibit the expression of CD25 on phytohaemagglutinin-activated lymphocytes].

OBJECTIVE: To investigate the regulatory effects of rat mesenchymal stem cell (MSC) on T lymphocyte proliferation by examining the early activated markers such as CD25 and CD69. METHODS: MSC had been isolated and expanded in vitro. Then it was identified by cell morphology, membrane phenotype, and differentiation potential. Nylon wool column was applied to purify T-lymphocytes. MSCs and T-lymphocytes were cultured together and were stimulated by phytohaemagglutinin (PHA), and then the expressions of CD25 and CD69 were assessed. The levels of TGF-beta1 and IL-10 in the supernatants of MSC cultures were detected by using ELISA. RESULTS: (1) The expression of CD25 is suppressed in a dose-dependent manner when the T-lymphocytes are co-cultured with 10,000 MSCs or more, while 100 MSCs have no detectable effect; (2) The suppression of CD25 can be lasted more than 96 hrs; (3) The down regulation of CD25 is mediated by some soluble factors; (4) The reduced expression of CD25 caused by MSC inhibition is not mediated by TGF-beta1 and IL-10. CONCLUSION: MSCs have significant immune regulatory effects on PHA-stimulated T-lymphocyte culture. It might provide a remarkable immune suppression in organ-transplantation to achieve better outcome in the near future.

[Effects of vascular endothelial growth factor (VEGF) antisense oligodeoxynucleotide on mRNA and expression of VEGF, flt-1, and kinase insert domain containing receptor and VEGF excretion in human gallbladder carcinoma cells].

OBJECTIVE: To investigate the effects of vascular endothelial growth factor (VEGF) antisense oligodeoxynucleotide (ASODN) on the mRNA and protein expression of VEGF, Flt-1, and kinase insert domain containing receptor (KDR) and VEGF excretion in human gallbladder carcinoma cells. METHODS: Human gallbladder carcinoma cells of the line GBC-SD were cultured and transfected with VEGF ASODN and sense oligodeoxynucleotide (SODN) mediated by Oligofectamine. The toxicity of SODN and Oligofectamine to the GBC-SD cells was examined by MTT method. RT-PCR was used to detect the mRNA and expression of VEGF, Flt-1, and KDR, and ELISA was used to detect the protein expression of VEGF. RESULTS: MTT method showed that SODN and Oligofectamine were not toxic to the GBC-SD cells. The mRNA expression levels of VEGF, Flt-1, and KDR of the ASODN and ASODN + Oligofectamine groups were all significantly lower than those of the control group (all P < 0.05), and were the lowest 72 hours after transfection, and then gradually increased. ELISA showed that there were not significant differences in the VEGF protein concentration in the supernatant of the GBC-SD cells among the SODN, SODN + Oligofectamine, and control groups (all P < 0.05), however, the VEGF protein concentration in the supernatant of the GBC-SD cells of the ASDN and ASDN + Oligofectamine groups were significantly lower than that of the control group (both P < 0.05). CONCLUSION: VEGF ASODN inhibits the mRNA and protein expression of VEGF, Flt-1, and KDR and VEGF excretion in human gallbladder carcinoma cells. Oligofectamine strengthens the effect of ASODN.