No animal received any medical support (e.g., infusions, drugs) during the entire experimental period. The transplantation procedures were all performed by the same B-ultrasound expert with 5 years of extensive

experience. Animals were evaluated for up to 6 months after transplantation. As biochemical markers of liver metabolism, coagulation and hepatocyte damage, alanine aminotransferase (ALT), prothrombin time, total bilirubin, ammonia, blood urea nitrogen, and creatinine levels were analyzed Romidepsin cell line prior to hBMSC transplantation (baseline data) and then on days 1, 2, and 3 and weeks 1, 2, 3, 5, and 8 after transplantation. Survival was analyzed using a Kaplan-Meier plot and log-rank analysis. The data are expressed as the mean ± SD and were evaluated via Student t test and one-way analysis of variance with SPSS software version 16.0 (SPSS, Chicago, IL). The significance for all statistical analyses was defined as P < 0.05. To determine the effect of the transplanted hBMSCs on liver regeneration, hBMSC-derived hepatocytes engrafted in liver tissues were tracked using immunohistochemistry with the human hepatocyte-specific marker ALB (Bethyl, Montgomery, TX) and a hepatocyte-specific antigen antibody (HSA) (Abcam, Cambridge, UK). Liver tissues were harvested after the pigs died of FHF in the control and PVT groups. In

the IPT group, because many Selleckchem ONO-4538 unforeseen risks exist in FHF animals that undergo several partial hepatectomies and to ensure an adequate number of surviving animals for follow-up, liver tissue was

harvested from five animals. Three liver sections were harvested from each of the left, middle, and right lobes (10-20 g, each sample) via small partial hepatectomy under sterile conditions on weeks 2, 3, 上海皓元医药股份有限公司 5, 10, 15, and 20 after transplantation. Immunohistochemical analyses of ALB and HSA were performed using serial sections. The hepatectomy procedure was performed by a surgeon with 10 years of experience in liver transplantation. Each liver tissue specimen was analyzed by hematoxylin and eosin (H&E) staining. For H&E staining, each liver tissue section (4-μm-thick) was heat-fixed at 60°C for 1 hour and stained with H&E as described.16 For immunohistochemistry, serial tissue sections were applied to poly-L-lysine-coated slides. After the sections were dewaxed, rehydrated, and washed, endogenous peroxidases were inactivated with 3% H2O2 for 10 minutes at room temperature. The sections were incubated overnight with primary anti-human antibodies (ALB, 1:10,000, and HSA 1:1,000) with no cross-reactivity to pig tissues. The sections were washed with phosphate-buffered saline three times and incubated with the appropriate secondary antibodies at 37°C for 1 hour.

No animal received any medical support (e.g., infusions, drugs) during the entire experimental period. The transplantation procedures were all performed by the same B-ultrasound expert with 5 years of extensive

experience. Animals were evaluated for up to 6 months after transplantation. As biochemical markers of liver metabolism, coagulation and hepatocyte damage, alanine aminotransferase (ALT), prothrombin time, total bilirubin, ammonia, blood urea nitrogen, and creatinine levels were analyzed find more prior to hBMSC transplantation (baseline data) and then on days 1, 2, and 3 and weeks 1, 2, 3, 5, and 8 after transplantation. Survival was analyzed using a Kaplan-Meier plot and log-rank analysis. The data are expressed as the mean ± SD and were evaluated via Student t test and one-way analysis of variance with SPSS software version 16.0 (SPSS, Chicago, IL). The significance for all statistical analyses was defined as P < 0.05. To determine the effect of the transplanted hBMSCs on liver regeneration, hBMSC-derived hepatocytes engrafted in liver tissues were tracked using immunohistochemistry with the human hepatocyte-specific marker ALB (Bethyl, Montgomery, TX) and a hepatocyte-specific antigen antibody (HSA) (Abcam, Cambridge, UK). Liver tissues were harvested after the pigs died of FHF in the control and PVT groups. In

the IPT group, because many Erlotinib unforeseen risks exist in FHF animals that undergo several partial hepatectomies and to ensure an adequate number of surviving animals for follow-up, liver tissue was

harvested from five animals. Three liver sections were harvested from each of the left, middle, and right lobes (10-20 g, each sample) via small partial hepatectomy under sterile conditions on weeks 2, 3, MCE 5, 10, 15, and 20 after transplantation. Immunohistochemical analyses of ALB and HSA were performed using serial sections. The hepatectomy procedure was performed by a surgeon with 10 years of experience in liver transplantation. Each liver tissue specimen was analyzed by hematoxylin and eosin (H&E) staining. For H&E staining, each liver tissue section (4-μm-thick) was heat-fixed at 60°C for 1 hour and stained with H&E as described.16 For immunohistochemistry, serial tissue sections were applied to poly-L-lysine-coated slides. After the sections were dewaxed, rehydrated, and washed, endogenous peroxidases were inactivated with 3% H2O2 for 10 minutes at room temperature. The sections were incubated overnight with primary anti-human antibodies (ALB, 1:10,000, and HSA 1:1,000) with no cross-reactivity to pig tissues. The sections were washed with phosphate-buffered saline three times and incubated with the appropriate secondary antibodies at 37°C for 1 hour.

Further, treatment of CD133+ liver CSCs with the AKT1 inhibitor, along with doxorubicin or 5-fluorouracil, led to the complete inhibition of the preferential survival effect induced by CD133+ liver CSCs.30 Recently, Yamashita and colleagues have also identified a mechanism by which EpCAM+ liver CSCs are rendered sensitive to 5-fluorouracil chemotherapy. The receptor of oncostatin M (OSM), an interleukin 6-related cytokine that is known to induce the differentiation

of hepatoblasts into hepatocytes, was detected ALK inhibitor in the majority of EpCAM+ liver CSCs. Based on this finding, the authors investigated the effect of OSM on EpCAM+ liver CSCs. The treatment of these cells Ulixertinib with OSM enhanced the hepatocytic differentiation of EpCAM+ liver CSCs by inducing Stat3 activation, as determined by a decrease in the stem-cell related gene expression and a decrease in EpCAM, alpha fetoprotein and cytokeratin 19 protein expression, which was concomitant with an increase in albumin protein expression. Further, OSM-treated EpCAM+ liver CSCs showed enhanced cell proliferation with an expansion of the EpCAM- non-CSC population. The combination

of OSM treatment with 5-fluorouracil, which eradicated the EpCAM- non-CSCs, dramatically increased the number of apoptotic cells in vitro and suppressed tumor growth in vivo, when compared with either OSM or 5-fluorouracil treatment alone. Findings from the study suggest that OSM could be effectively used for the differentiation and active cell division of OSM receptor-positive EpCAM+ liver CSCs and that the combination of OSM and 5-fluorouracil can efficiently eliminate HCC by targeting both CSCs and non-CSCs subpopulations.31 Using chemotherapeutic drugs to select drug-resistant cancer cells in HCC, Wang et al. have demonstrated that chemoresistant cells display CSC-like features, including increased self-renewal ability, increased cell motility, medchemexpress resistance to multiple chemotherapeutic drugs, enhanced tumorigenic potential and elevated

expression of CD90+ cells. In addition, the expression of Oct4, a transcription factor essential in embryonic stem cells, was also strongly upregulated in the chemoresistant HCC cell subpopulation. The authors demonstrated that Oct4 plays a role in cancer cell chemoresistance through the following findings: (i) chemoresistant cancer cells displayed an enhanced expression of Oct4 through gene demethylation processes; (ii) the overexpression of Oct4 significantly increased, whereas the knockdown of Oct4 reduced the drug resistance of liver cancer cells in vitro and in vivo; and (iii) the overexpression of Oct4 induced the activation of TCL1, AKT and ABCG2 to mediate the chemoresistance.

The laboratory investigations Trichostatin A in vitro including CEA and CA19-9 were within normal limits. EUS showed a hypoechoic mass with mixed cystic and solid components in the pancreas (Figure

2a) and FNAB showed vascular architectures with pseudopapillary pattern (Figure 2b), numerous neoplastic cells with sheet-like arrangement, several multinucleated giant cells and hemosiderin-pigments. Immunohistochemical stain revealed that the tumor cells were positive for alpha 1-antitrypsin, vimentin, beta-catenin etc. These findings were consistent with SPT with marked degenerative change. A distal pancreatectomy and splenectomy were performed (Figure 2c) and histopathological analysis showed tumor cells consisting of atypical mononuclear cells admixed with abundant osteoclastic giant cells (OGCs)(Figure 2d). The Akt inhibitor OGCs were positive for CD68 (Figure 2e). Unlike the FNAB findings, the atypical mononuclear cells were positive for cytokeratin (Figure 2f).

We finally diagnosed as UCPOGC on histopathologic examination of surgical specimens. Conclusion: A undifferentiated carcinoma with osteoclast-like giant cells of the pancreas can be misconceived as a SPT on EUS and EUS-FNAB. Key Word(s): 1. pancreas; 2. undifferentiated carcinoma with osteoclast-like giant cells; 3. solid pseudopapillary tumor Presenting Author: HYUN JONG KIM Additional Authors: CHOONG YOUNG KIM, HEE JOON KIM, CHOL KYOON CHO, JIN SHICK SEOUNG Corresponding Author: HYUN JONG KIM Affiliations: Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School, Saint Carollo Hospital Objective: Acinar cell carcinoma is a rare pancreatic neoplasm. Because of its rarity, characteristics medchemexpress of this disease have not been fully investigated. Herein, we present two cases of acinar cell carcinoma of pancreas. Methods: Case 1. A 60-year-old woman was referred to our hospital for evaluation of pancreatic mass found on CT scan. Abdominal CT and MRI showed a about 3 cm sized well marginated non-enhancing round mass with internal bleeding

in pancreatic head. A preoperative diagnosis of solid pseudopapillary tumor was made, a pylorus preserving pancreaticoduodenectomy was performed. At laparotomy, a 3 x 3 cm sized brown soft mass was found in pancreatic head. Microscopic findings revealed invasive acinar cell carcinoma. The patient discharged 17 days following surgery without any complications. 2 months following the surgery, multiple hepatic metastases were found on follow up CT scan. Results: Case 2. A 51-year-old woman visited our hospital presenting epigastric pain and poor oral intake. Abdominal CT and pancreas MRI showed lobulated enhancing soft tissue mass and multiple conglomerated amorphic cystic lesions around main duct of pancreas in body and tail.

The laboratory investigations selleck kinase inhibitor including CEA and CA19-9 were within normal limits. EUS showed a hypoechoic mass with mixed cystic and solid components in the pancreas (Figure

2a) and FNAB showed vascular architectures with pseudopapillary pattern (Figure 2b), numerous neoplastic cells with sheet-like arrangement, several multinucleated giant cells and hemosiderin-pigments. Immunohistochemical stain revealed that the tumor cells were positive for alpha 1-antitrypsin, vimentin, beta-catenin etc. These findings were consistent with SPT with marked degenerative change. A distal pancreatectomy and splenectomy were performed (Figure 2c) and histopathological analysis showed tumor cells consisting of atypical mononuclear cells admixed with abundant osteoclastic giant cells (OGCs)(Figure 2d). The MI-503 cost OGCs were positive for CD68 (Figure 2e). Unlike the FNAB findings, the atypical mononuclear cells were positive for cytokeratin (Figure 2f).

We finally diagnosed as UCPOGC on histopathologic examination of surgical specimens. Conclusion: A undifferentiated carcinoma with osteoclast-like giant cells of the pancreas can be misconceived as a SPT on EUS and EUS-FNAB. Key Word(s): 1. pancreas; 2. undifferentiated carcinoma with osteoclast-like giant cells; 3. solid pseudopapillary tumor Presenting Author: HYUN JONG KIM Additional Authors: CHOONG YOUNG KIM, HEE JOON KIM, CHOL KYOON CHO, JIN SHICK SEOUNG Corresponding Author: HYUN JONG KIM Affiliations: Chonnam National University Medical School, Chonnam National University Medical School, Chonnam National University Medical School, Saint Carollo Hospital Objective: Acinar cell carcinoma is a rare pancreatic neoplasm. Because of its rarity, characteristics MCE公司 of this disease have not been fully investigated. Herein, we present two cases of acinar cell carcinoma of pancreas. Methods: Case 1. A 60-year-old woman was referred to our hospital for evaluation of pancreatic mass found on CT scan. Abdominal CT and MRI showed a about 3 cm sized well marginated non-enhancing round mass with internal bleeding

in pancreatic head. A preoperative diagnosis of solid pseudopapillary tumor was made, a pylorus preserving pancreaticoduodenectomy was performed. At laparotomy, a 3 x 3 cm sized brown soft mass was found in pancreatic head. Microscopic findings revealed invasive acinar cell carcinoma. The patient discharged 17 days following surgery without any complications. 2 months following the surgery, multiple hepatic metastases were found on follow up CT scan. Results: Case 2. A 51-year-old woman visited our hospital presenting epigastric pain and poor oral intake. Abdominal CT and pancreas MRI showed lobulated enhancing soft tissue mass and multiple conglomerated amorphic cystic lesions around main duct of pancreas in body and tail.

4; P = .04). (2) After adjusting for typical migraine aura, comparison of 17 “visual snow” patients with 17 age and gender matched controls showed brain hypermetabolism

in the right lingual gyrus (Montreal Neurological Institute coordinates 16-78-5; kE = 101; ZE = 3.41; P < .001) and the left cerebellar anterior lobe adjacent to the left lingual gyrus (Montreal Neurological Institute coordinates -12-62-9; kE = 152; ZE = 3.28; P = .001). Comorbid migraine aggravates the clinical phenotype of the “visual snow” syndrome by worsening some of the additional visual symptoms and tinnitus. This might bias studies on “visual snow” by migraineurs offering study participation more likely than non-migraineurs due to a more severe clinical presentation. The independence of entoptic phenomena from comorbid migraine indicates “visual www.selleckchem.com/products/Cilomilast(SB-207499).html snow” is the main determinant. The hypermetabolic lingual gyrus confirms a brain dysfunction in patients with “visual snow.” The metabolic pattern differs from interictal migraine with some similarities

to migrainous photophobia. The findings support the view that “visual snow,” migraine, and typical migraine aura are distinct syndromes with shared pathophysiological mechanisms that need to be addressed in order to develop rational treatment strategies for this disabling condition. selleck screening library Patients with “visual snow” (VS) describe a visual disturbance that consists of tiny dynamically flickering dots in the entire visual field resembling the “static” or “snow” of a badly tuned analogue television. The symptoms are continuous and can persist over years. Persistent visual disturbance is mentioned sporadically in the literature without larger systematic studies.1-3 Patients are often diagnosed as having persistent migraine aura, malingering, or psychogenic disorder because objective measures for the condition are not available to date. A recent study of a substantial cohort of subjects with VS confirmed that the visual disturbance is often associated with migraine

and migraine aura. However, not every patient with VS has a history of migraine. Further, VS starts only rarely with migraine aura, and the phenotypical description as well as the clinical course of VS by no means resembles typical migraine aura, which is in general homonymous, often presents with MCE公司 moving zigzag lines, and typically lasts less than 60 minutes. This suggests that VS is a unique condition different from migraine aura.4-6 Importantly, VS should be seen as a syndrome since it is almost always associated with additional visual complaints including palinopsia, entoptic phenomena that arise from the optic apparatus itself (ie, floaters, blue field entoptic phenomenon, self-light of the eye and photopsia),[7] poor night vision (nyctalopia), and photophobia. A large proportion of VS patients has bilateral continuous tinnitus.

Only five SNPs showed a consistent significant association (P < 0.05). In another case-control population (507 cases and 215 controls), these SNPs were tested for association with HCC. However, only one SNP (rs17401966) was confirmed in this replication sample (P =

Vismodegib 3.9 × 10−5). Again, this finding could be replicated in another independent case-control population (751 cases and 509 controls) as well as by evaluation of the rs17401966 transmission status in 159 family trios (cases and their unaffected parents) with HBV-related HCC, which allows a family-based association test robust against population stratification (transmission disequilibrium test) for the presence of genetic linkage between a marker locus and a disease susceptibility locus. The combined analysis of the three independent case-control populations (1962 cases and 1430 controls) from different Chinese regions as well as the combination of these and the genome-wide association data (2310 cases and 1789 controls) provided evidence for a highly significant association of rs17401966 at a genome-wide level (P = 5.1 × 10−15 and P = 3.4 × 10−19, respectively). HCC risk was significantly reduced in the presence of the mutant [G] allele of the

rs17401966 SNP (odds ratio = 0.61; confidence interval = 0.55-0.67). Risk-allele frequencies were 19.3% in patients with HCC (n = 2310), 27.7% in non-HCC controls (n = 1,789), selleck products and 31.4% in non-HBV carriers (n = 185). Pairwise linkage disequilibrium analysis (measured by r2) revealed a linkage disequilibrium block of about 244 kilobases mapping to chromosome 1p36.22,

flanking rs17401966, and spanning the genes KIF1B (encodes a kinesin superfamily member involved in the transport of organelles and vesicles), PDG (protein involved in the pentose phosphate metabolism), and the 3′-end of UBE4B (encodes ubiquitin 上海皓元 conjugation factor E4 involved in multiubiquitin chain assembly). Multiple logistic regression analysis and haplotype analysis suggested that there might be a single susceptibility locus in this region, which was only attributable to rs17401966 (NM_015074.3: c.2537+518A>G), which is located in intron 24 of KIF1B. Regardless of the fact that the only common nonsynonymous SNP at this region (rs2297881) showed no disease association, it remains unclear whether rs17401966 is in linkage disequilibrium with a disease-causing mutation or whether the SNP itself has a direct influence on HCC development. The identified susceptibility locus on chromosome 1p36.22 lies in a region that has been identified to be commonly affected by chromosomal losses or gains in several malignancies such as colorectal cancer, breast cancer, neuroblastoma, and also in HCC.

Only five SNPs showed a consistent significant association (P < 0.05). In another case-control population (507 cases and 215 controls), these SNPs were tested for association with HCC. However, only one SNP (rs17401966) was confirmed in this replication sample (P =

Bafilomycin A1 ic50 3.9 × 10−5). Again, this finding could be replicated in another independent case-control population (751 cases and 509 controls) as well as by evaluation of the rs17401966 transmission status in 159 family trios (cases and their unaffected parents) with HBV-related HCC, which allows a family-based association test robust against population stratification (transmission disequilibrium test) for the presence of genetic linkage between a marker locus and a disease susceptibility locus. The combined analysis of the three independent case-control populations (1962 cases and 1430 controls) from different Chinese regions as well as the combination of these and the genome-wide association data (2310 cases and 1789 controls) provided evidence for a highly significant association of rs17401966 at a genome-wide level (P = 5.1 × 10−15 and P = 3.4 × 10−19, respectively). HCC risk was significantly reduced in the presence of the mutant [G] allele of the

rs17401966 SNP (odds ratio = 0.61; confidence interval = 0.55-0.67). Risk-allele frequencies were 19.3% in patients with HCC (n = 2310), 27.7% in non-HCC controls (n = 1,789), selleck chemicals llc and 31.4% in non-HBV carriers (n = 185). Pairwise linkage disequilibrium analysis (measured by r2) revealed a linkage disequilibrium block of about 244 kilobases mapping to chromosome 1p36.22,

flanking rs17401966, and spanning the genes KIF1B (encodes a kinesin superfamily member involved in the transport of organelles and vesicles), PDG (protein involved in the pentose phosphate metabolism), and the 3′-end of UBE4B (encodes ubiquitin 上海皓元 conjugation factor E4 involved in multiubiquitin chain assembly). Multiple logistic regression analysis and haplotype analysis suggested that there might be a single susceptibility locus in this region, which was only attributable to rs17401966 (NM_015074.3: c.2537+518A>G), which is located in intron 24 of KIF1B. Regardless of the fact that the only common nonsynonymous SNP at this region (rs2297881) showed no disease association, it remains unclear whether rs17401966 is in linkage disequilibrium with a disease-causing mutation or whether the SNP itself has a direct influence on HCC development. The identified susceptibility locus on chromosome 1p36.22 lies in a region that has been identified to be commonly affected by chromosomal losses or gains in several malignancies such as colorectal cancer, breast cancer, neuroblastoma, and also in HCC.

Only five SNPs showed a consistent significant association (P < 0.05). In another case-control population (507 cases and 215 controls), these SNPs were tested for association with HCC. However, only one SNP (rs17401966) was confirmed in this replication sample (P =

Antiinfection Compound Library manufacturer 3.9 × 10−5). Again, this finding could be replicated in another independent case-control population (751 cases and 509 controls) as well as by evaluation of the rs17401966 transmission status in 159 family trios (cases and their unaffected parents) with HBV-related HCC, which allows a family-based association test robust against population stratification (transmission disequilibrium test) for the presence of genetic linkage between a marker locus and a disease susceptibility locus. The combined analysis of the three independent case-control populations (1962 cases and 1430 controls) from different Chinese regions as well as the combination of these and the genome-wide association data (2310 cases and 1789 controls) provided evidence for a highly significant association of rs17401966 at a genome-wide level (P = 5.1 × 10−15 and P = 3.4 × 10−19, respectively). HCC risk was significantly reduced in the presence of the mutant [G] allele of the

rs17401966 SNP (odds ratio = 0.61; confidence interval = 0.55-0.67). Risk-allele frequencies were 19.3% in patients with HCC (n = 2310), 27.7% in non-HCC controls (n = 1,789), Buparlisib chemical structure and 31.4% in non-HBV carriers (n = 185). Pairwise linkage disequilibrium analysis (measured by r2) revealed a linkage disequilibrium block of about 244 kilobases mapping to chromosome 1p36.22,

flanking rs17401966, and spanning the genes KIF1B (encodes a kinesin superfamily member involved in the transport of organelles and vesicles), PDG (protein involved in the pentose phosphate metabolism), and the 3′-end of UBE4B (encodes ubiquitin 上海皓元 conjugation factor E4 involved in multiubiquitin chain assembly). Multiple logistic regression analysis and haplotype analysis suggested that there might be a single susceptibility locus in this region, which was only attributable to rs17401966 (NM_015074.3: c.2537+518A>G), which is located in intron 24 of KIF1B. Regardless of the fact that the only common nonsynonymous SNP at this region (rs2297881) showed no disease association, it remains unclear whether rs17401966 is in linkage disequilibrium with a disease-causing mutation or whether the SNP itself has a direct influence on HCC development. The identified susceptibility locus on chromosome 1p36.22 lies in a region that has been identified to be commonly affected by chromosomal losses or gains in several malignancies such as colorectal cancer, breast cancer, neuroblastoma, and also in HCC.

In the univariate analysis, fulminant hepatic failure (odds ratio [OR] 5.714, 95% confidence interval [CI] 1.045–31.245, p = 0.027), life expectancy less than 7 days according to UNOS liver status GSK126 concentration classification (status 1 and 2a) (OR 2.97, 95% CI 0.883–8.242, p = 0.074), history of recent hemodialysis (OR 3.129, 95% CI 2.340–4.183, p = 0.043), recipient

bile duct opening number of more than 2 (OR 5.208, 95% CI 1.721–15.761, p = 0.002) were significant (p < 0.1). In the multivariate analysis, recipient bile duct opening number of more than 2 was statistically significant risk factor (OR 5.208, 95% CI 1.721–15.761, p = 0.003). Conclusion: Recipient bile duct opening number was associated with spontaneous hemobilia after LT. Further studies are required in order to clarify the role of recipient bile duct opening number in spontaneous hemobilia in LT patients. Key Word(s): 1. liver transplantation; 2. biliary complication; 3. spontaneous hemobilia; 4. risk factor Presenting Author: SOO KYUNG PARK Additional Authors: JONG HO MOON, HYUN JONG CHOI, YUN NAH LEE, TAE HOON LEE, SANG WOO CHA, YOUNG DEOK CHO, SANG HEUM PARK, SUN JOO KIM Corresponding Author: SOO-KYUNG PARK

Affiliations: Selleckchem Pexidartinib Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, Soonchunhyang University School of Medicine, SoonChunHyang University School of Medicine, Soonchunhyang University School of Medicine Objective: Covered

self-expandable metallic stent (SEMS) may improve stent patency but have the risk of migration in comparison with uncovered stent in patients with distal malignant biliary obstruction. Intraductal placement above the papillary orifice of SEMS may MCE公司 prevent duodeno-biliary reflux after stenting. This study was performed to evaluate the efficacy of modified fully covered SEMS in patients with distal malignant biliary obstruction. Methods: Total 55 patients with distal malignant biliary obstruction and obstructive jaundice were enrolled in this study. The modified fully covered SEMS (12 mm in diameter) has center portion of smaller diameter (8 mm) and long lasso without flare in both ends. Results: Causes of biliary obstruction were 27 common bile duct cancers, 21 pancreatic cancers, 5 gallbladder cancers and 2 metastatic cancers. Intraductal stenting above the papillary orifice was performed in 83.6% (46/55). Early complication rate was 5.5% (3/55, 3 mild pancreatitis). Clinical improvement of obstructive jaundice was achieved in all enrolled patients. 11 patients with operability underwent surgical resection after stenting.