Pretreatment with p-chlorophenylalanine for 2 days to reduced the synthesis of endogenous 5-HT diminished the effects of both CRF and soybean oil on gastric emptying. A 5-HT3 receptor agonist m-chlorophenylbiguanide suppressed gastric emptying of both phenol red and glass beads, and those effects were reversed by ramosetron. Conclusions:  These results suggest that CRF and soybean oil suppress

gastric emptying in rats by activating 5-HT3 receptors, and that by antagonizing these receptors, ramosetron may ameliorate symptoms of FD in clinical settings. “
“Aim:  With learn more the recent advances in medical or surgical treatments in chronic hepatic disorders, the indications for splenectomy in hepatic disorders have greatly expanded. We performed splenectomy for cirrhotic patients and investigated the effects of splenectomy on hepatic functional reserve and nutrition metabolism. Methods:  Eighteen patients (Child–Pugh B/C: 12/6; Child–Pugh PS341 A: excluded) who underwent splenectomy at our institute between 2005 and 2008 were enrolled. Twelve patients (67%) had hepatocellular carcinoma (HCC), eight of whom met the Milan criteria. Results:  Overall survival rate was 83.3% at 1 year and 62.7% at 2 years. The survival rate of six patients with liver

cirrhosis classified a Child–Pugh C was 80.0% at 1 year and 60.0% at 2 years. Three patients underwent hepatic resection and nine patients received ablation therapy against hepatocelluar carcinoma. Portal pressure decreased after splenectomy in most patients (mean decrease, 4.7 mmHg). Four weeks after MCE公司 the operation, the markers of hepatic functional reserve, indocyanine green retention rate at 15 min (ICGR15) and Technetium-99m-galactosyl human serum albumin value (99mTc-GSA), improved from 38.5% to 35.1%

and from 0.773 to 0.788 (LHL15), respectively. The non-protein respiratory quotient (npRQ) did not change in short period after the operation. Other outcomes, including liver function test in cirrhotic patients with long-term (1 year) follow-up after splenectomy (n = 7), did not improve significantly. Post-operative complications included portal thrombus (n = 2), ascites (n = 2) were observed in six patients (33%). Conclusion:  Splenectomy improved hepatic functional reserve and nutritional metabolism in some cases. However, the long-term outcomes should still be evaluated. “
“Hepatic innate immune cells, in particular, interstitial dendritic cells (DCs), regulate inflammatory responses and may promote inherent liver tolerogenicity. After tissue injury, adenosine triphosphate (ATP) is released and acts as a damage-associated molecular pattern that activates innate immune cells by pattern recognition receptors. CD39 (ectonucleoside triphosphate diphosphohydrolase-1) rapidly hydrolyzes extracellular ATP to maintain physiological levels. We hypothesized that CD39 expression on liver DCs might contribute to regulation of their innate immune functions.

In this study, we investigated the scale and bristle ultrastructure, along with sequences of three genes, for 19 isolates (18 species) of Mallomonas (18 isolates were from Korean EMD 1214063 order habitats). The isolates represented nine of the 19 sections. Sequences for both the nuclear SSU and LSU rDNA and plastid LSU of RUBISCO (rbcL) genes for each of the 19 Mallomonas isolates and four outgroups were determined. Bayesian and maximum-likelihood (ML) analyses

of the data revealed that Mallomonas consists of two strongly supported clades. Mallomonas bangladeshica (E. Takah. et T. Hayak.) Siver et A. P. Wolfe was at the base of the first clade that included taxa from the sections Planae and Heterospinae, both of which lack a V rib on the shield of the scales. Our results indicated that the sections Planae and Heterospinae should be combined. The second clade, with Mallomonas insignis Penard and Mallomonas punctifera Korshikov at the base, contained taxa from the sections Crizotinib Mallomonas, Striatae, Akrokomae, Annulatae, Torquatae, Punctiferae, and Insignes, all of which have V ribs or well-developed marginal ribs on the scales. Sister relationships between Mallomonas and Striatae were strongly supported, but

interrelations among the remaining sections were not resolved, probably due to inclusion of too few species. Our results suggest that the current classification of the genus Mallomonas at the section level will require some revision. Additional species will need to be added in future analyses. “
“Mesophyllum sphaericum sp. nov. is described based on spherical maërl individuals (up to 10 cm) collected in a shallow subtidal maërl bed in Galicia (NW Spain). MCE The thalli of these specimens are radially organized, composed of arching tiers of compact medullary filaments. Epithallial cells have flattened to rounded outermost walls, and they occur in a single layer. Subepithallial initials are as long as, or longer than the daughter cells that subtend them. Cell fusions are abundant. Multiporate

asexual conceptacles are protruding, mound-like with a flattened pore plate, lacking a peripheral raised rim. Filaments lining the pore canal and the conceptacle roof are composed of five to six cells with straight elongate and narrow cells at their base. Carposporangial conceptacles are uniporate, protruding, and conical. Spermatangial conceptacles were not observed. Molecular results placed M. sphaericum near to M. erubescens, but M. sphaericum is anatomically close to M. canariense. The examination of the holotype and herbarium specimens of M. canariense indicated that both species have pore canal filaments with elongate basal cells, but they differ in number of cells (five to six in M. sphaericum vs. four in M. canariense). Based on the character of pore canal filaments, M. canariense shows similarities with M. erubescens (three to five celled). The outermost walls of epithallial cells of M.

In this study, we investigated the scale and bristle ultrastructure, along with sequences of three genes, for 19 isolates (18 species) of Mallomonas (18 isolates were from Korean selleck habitats). The isolates represented nine of the 19 sections. Sequences for both the nuclear SSU and LSU rDNA and plastid LSU of RUBISCO (rbcL) genes for each of the 19 Mallomonas isolates and four outgroups were determined. Bayesian and maximum-likelihood (ML) analyses

of the data revealed that Mallomonas consists of two strongly supported clades. Mallomonas bangladeshica (E. Takah. et T. Hayak.) Siver et A. P. Wolfe was at the base of the first clade that included taxa from the sections Planae and Heterospinae, both of which lack a V rib on the shield of the scales. Our results indicated that the sections Planae and Heterospinae should be combined. The second clade, with Mallomonas insignis Penard and Mallomonas punctifera Korshikov at the base, contained taxa from the sections BMS-354825 manufacturer Mallomonas, Striatae, Akrokomae, Annulatae, Torquatae, Punctiferae, and Insignes, all of which have V ribs or well-developed marginal ribs on the scales. Sister relationships between Mallomonas and Striatae were strongly supported, but

interrelations among the remaining sections were not resolved, probably due to inclusion of too few species. Our results suggest that the current classification of the genus Mallomonas at the section level will require some revision. Additional species will need to be added in future analyses. “
“Mesophyllum sphaericum sp. nov. is described based on spherical maërl individuals (up to 10 cm) collected in a shallow subtidal maërl bed in Galicia (NW Spain). medchemexpress The thalli of these specimens are radially organized, composed of arching tiers of compact medullary filaments. Epithallial cells have flattened to rounded outermost walls, and they occur in a single layer. Subepithallial initials are as long as, or longer than the daughter cells that subtend them. Cell fusions are abundant. Multiporate

asexual conceptacles are protruding, mound-like with a flattened pore plate, lacking a peripheral raised rim. Filaments lining the pore canal and the conceptacle roof are composed of five to six cells with straight elongate and narrow cells at their base. Carposporangial conceptacles are uniporate, protruding, and conical. Spermatangial conceptacles were not observed. Molecular results placed M. sphaericum near to M. erubescens, but M. sphaericum is anatomically close to M. canariense. The examination of the holotype and herbarium specimens of M. canariense indicated that both species have pore canal filaments with elongate basal cells, but they differ in number of cells (five to six in M. sphaericum vs. four in M. canariense). Based on the character of pore canal filaments, M. canariense shows similarities with M. erubescens (three to five celled). The outermost walls of epithallial cells of M.

Conclusion: Chest CT scan for achalasia patients undergoing a POEM procedure can be used to detect early signs of postoperative bleeding, but routine

application is probably not warranted. The role in guiding the management of post-POEM pneumothorax who need intervention has to be studied further. Key Word(s): 1. POEM; 2. esophageal achalasia; 3. chest CT scan; Presenting Author: AKRAM POURSHAMS Additional Authors: ELHAM JAFARI Corresponding Author: AKRAM POURSHAMS Affiliations: Tehran University of Medical Sciences; Tehran University of Medical Sciences Objective: The incidence of esophageal squamous cell carcinoma (ESCC) shows geographic variation. Northeastern Iran (Golestan province) GDC-0973 purchase has one of the highest incidences of ESCC in the world, over 50 per 100,000 person-years. Aim: to identify host and environmental risk factors associated with ESCC in northeastern Iran. Methods: we included published data of all ecologic, case-control studies, and the Golestan Cohort Study, (50,000 members) that conducted by the Digestive Disease Research Center of Tehran University of Medical Sciences (with collaboration of national CYC202 and international cancer research centers) in the area during the last 13 years. Results: Socio-economic status was inversely

related to ESCC. The strongest inverse association was found with education. Poor oral health was also correlated to ESCC. A total of 16.7%, 13.7% and 0.7% of cohort members were current tobacco, opium and alcohol consumers respectively. Tobacco and opium use was strongly associated with ESCC in the case-control study but alcohol consumption was not. About 98% of the cohort participants drank black tea regularly, (mean volume >1 L/d), 39.0% drank their tea at temperatures less than 60°C, 38.9% at 60–64°C, and 22.0% at 65°C or higher. Drinking very hot tea was associated with increased risk of ESCC (OR: 8.16, 3.93–16.9). Fresh vegetable, fruit and Vitamin A intake were low especially in ESCC cases and rural dwellers.

Two cross sectional studies have confirmed high exposure of the general population to polycyclic aromatic hydrocarbons (PAHs). An ecologic study suggests that certain foods and cooking methods increase exposure to PAHs. In addition, levels MCE of PAH DNA adducts was significantly higher in ESCC tissues than in normal tissues of cases and healthy controls. The highest rate of TP53 mutations ever reported in any cancer was observed. Also a high rate of p16 hyper methylation was reported in ESCC tissues. A nonsense variant of BRCA2 was associated with higher ESCC risk with a frequency of 4.6% among cases and 0.8% among controls. No selenium deficiency was observed among cohort members. Contamination with carcinogenic mycotoxins was not found in raw rice, sorghum and wheat samples. The prevalence of the gluten-sensitive enteropathy was about 1%, so this disease is unlikely to be a risk for ESCC in the area.

HCC occurs in the context of these two divergent responses, leading to distinctive pathways of carcinogenesis. In this review we highlight pathways of liver tumorigenesis that

depend on, or are enhanced by, fibrosis. Activated hepatic stellate cells drive fibrogenesis, changing the composition of the extracellular matrix. Matrix quantity and stiffness also increase, providing a reservoir for bound growth factors. In addition to promoting angiogenesis, these factors may enhance the survival of both preneoplastic hepatocytes and activated hepatic stellate cells. Fibrotic changes also modulate the activity of inflammatory cells in the liver, reducing the activity of natural killer and natural this website killer T cells that normally contribute to tumor surveillance. These pathways synergize with inflammatory signals, including telomerase reactivation and reactive oxygen species release, ultimately resulting in cancer. Clarifying fibrosis-dependent tumorigenic mechanisms will help rationalize antifibrotic therapies as a strategy to prevent and treat HCC. (HEPATOLOGY 2012) Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world and the third most common cause of cancer mortality.1 In the United States the incidence of HCC is rising precipitously, primarily as a result of the increasing prevalence of advanced chronic

hepatitis C2 and fatty liver disease.3 The incidence of HCC varies by etiology, race, ethnicity, gender, age, and geographic region,

but the presence of fibrosis is a common link among each CHIR-99021 mouse of these risks.4, 5 Liver fibrosis is strongly associated MCE公司 with HCC, with 90% of HCC cases arising in cirrhotic livers.6 For hepatitis B infection, the presence of cirrhosis, along with age, gender, viral DNA load, and viral core promoter mutations, is a risk factor for HCC.7 Fibrosis has also been identified as a risk factor in hepatitis C infection, where cancer risk is directly related to fibrosis severity.8 Overall, ≈80% of hepatitis B and C patients presenting with HCC are already cirrhotic.9 Similarly, HCC development is also linked to alcoholic cirrhosis,10 nonalcoholic steatohepatitis (NASH),11 and hemochromatosis,12 with a yearly HCC incidence of 1.7% in alcoholic cirrhosis10 and 2.6% in NASH cirrhosis.11 Despite these associations, the mechanisms linking fibrosis and HCC remain largely unsettled—does fibrogenesis or the presence of fibrosis actively promote HCC, or is fibrosis merely a byproduct of chronic liver damage and inflammation, with no direct impact on tumor formation (Fig. 1)? The contribution of inflammation to HCC has been reviewed extensively, and is not the focus of this article; we direct the reader to outstanding articles on nuclear factor kappa B signaling,13 reactive oxygen species,6, 14 and telomere shortening.15, 16 Here we focus specifically on potential links between fibrosis and HCC.

HCC occurs in the context of these two divergent responses, leading to distinctive pathways of carcinogenesis. In this review we highlight pathways of liver tumorigenesis that

depend on, or are enhanced by, fibrosis. Activated hepatic stellate cells drive fibrogenesis, changing the composition of the extracellular matrix. Matrix quantity and stiffness also increase, providing a reservoir for bound growth factors. In addition to promoting angiogenesis, these factors may enhance the survival of both preneoplastic hepatocytes and activated hepatic stellate cells. Fibrotic changes also modulate the activity of inflammatory cells in the liver, reducing the activity of natural killer and natural LY2835219 killer T cells that normally contribute to tumor surveillance. These pathways synergize with inflammatory signals, including telomerase reactivation and reactive oxygen species release, ultimately resulting in cancer. Clarifying fibrosis-dependent tumorigenic mechanisms will help rationalize antifibrotic therapies as a strategy to prevent and treat HCC. (HEPATOLOGY 2012) Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world and the third most common cause of cancer mortality.1 In the United States the incidence of HCC is rising precipitously, primarily as a result of the increasing prevalence of advanced chronic

hepatitis C2 and fatty liver disease.3 The incidence of HCC varies by etiology, race, ethnicity, gender, age, and geographic region,

but the presence of fibrosis is a common link among each Rapamycin research buy of these risks.4, 5 Liver fibrosis is strongly associated MCE with HCC, with 90% of HCC cases arising in cirrhotic livers.6 For hepatitis B infection, the presence of cirrhosis, along with age, gender, viral DNA load, and viral core promoter mutations, is a risk factor for HCC.7 Fibrosis has also been identified as a risk factor in hepatitis C infection, where cancer risk is directly related to fibrosis severity.8 Overall, ≈80% of hepatitis B and C patients presenting with HCC are already cirrhotic.9 Similarly, HCC development is also linked to alcoholic cirrhosis,10 nonalcoholic steatohepatitis (NASH),11 and hemochromatosis,12 with a yearly HCC incidence of 1.7% in alcoholic cirrhosis10 and 2.6% in NASH cirrhosis.11 Despite these associations, the mechanisms linking fibrosis and HCC remain largely unsettled—does fibrogenesis or the presence of fibrosis actively promote HCC, or is fibrosis merely a byproduct of chronic liver damage and inflammation, with no direct impact on tumor formation (Fig. 1)? The contribution of inflammation to HCC has been reviewed extensively, and is not the focus of this article; we direct the reader to outstanding articles on nuclear factor kappa B signaling,13 reactive oxygen species,6, 14 and telomere shortening.15, 16 Here we focus specifically on potential links between fibrosis and HCC.

Indications for antiviral therapies for persistent HBV infection

are based on the need for treatment, related to a range of factors such as age, disease stage, degree of liver disease (inflammation and fibrosis), and risk of further progression to liver cirrhosis and/or HCC. The three key criteria that are currently used in determining whether to treat are histological progression, ALT levels and HBV DNA levels. In numerous reports on factors linked to antiviral therapeutic effects, ALT and HBV DNA levels have been shown to influence the progression of the disease, and are also noted as common factors associated with therapeutic effects for both IFN and NAs. Guidelines from the American Association for the Study of selleck chemicals llc Liver learn more Diseases (AASLD),[27] the European Association for the Study of the Liver (EASL),[6] the Asia Pacific Association for the Study of the Liver (APASL),[7] and the Japanese Ministry of Health, Labour and Welfare (MHLW) research group[28] all nominate these

factors as patient selection criteria, as shown in Table 7. ALT and HBV DNA levels change over the natural course of the disease, and this must be taken into account when deciding when to initiate treatment. 2) 1–2 × ULN >40 years Family history of HCC liver biopsy 2) <1 × ULN liver biopsy 2) ≤2 × ULN >40 years liver biopsy 2) 1–2 × ULN >40 years Family history of HCC liver biopsy 2) <1 × ULN liver biopsy 2) ≤2 × ULN >40 years liver biopsy 4 (<4a) >1 × ULN (>2 × ULNa) Recently a link has been posited between HBsAg levels and carcinogenesis, with some reports claiming that patients with high HBsAg levels (even when the HBV DNA level is less than 4 log copies/mL following HBeAg seroconversion) have higher rates of further progression and cancinogenesis.[29] However there is still insufficient evidence on the link between HBsAg MCE levels and long term outcomes, and further studies are required before HBsAg levels can be incorporated into the patient

selection criteria. Recommendations The three key criteria currently used to determine whether to treat persistent HBV infection are histological progression, ALT levels and HBV DNA levels. The question of whether HBsAg levels should be added to these criteria requires further studies. Indications for treatment for chronic hepatitis include abnormal ALT levels, high HBV DNA levels, and presence of histological liver disease. Treatment is therefore not indicated when ALT levels are within the normal range and histological disease is mild or absent altogether – in other words, for HBeAg positive asymptomatic carriers during the immune tolerance phase and inactive carriers following HBeAg seroconversion. Note that in cases of HBeAg-positive chronic hepatitis with elevated ALT levels, there is a 7–16% probability (in annual terms) of the HBeAg seroconversion over the natural course of the disease.

e., fitness) of the variants. Conclusion: Although resistance emerged during monotherapy with BMS-790052, the substantial anti-HCV effect of this compound makes it an excellent candidate for effective combination

therapy. (HEPATOLOGY 2011) The hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is a multifunctional protein with key roles in HCV replication. NS5A has also been implicated in the modulation of cellular signaling pathways.1, 2 Because it is required in vivo and in vitro for viral replication and has no known human homologs, NS5A provides an attractive selleck screening library target for therapeutic intervention.3 BMS-790052 is a potent HCV

NS5A replication complex inhibitor, with 50% effective concentration (EC50) values of 9 and 50 pM against genotype 1b and 1a replicons, respectively.4, 5 It is also potent against live virus (genotype 2a, JFH-1), with an EC50 of ∼28 pM.4 BMS-790052 has broad genotype coverage, with EC50 values ranging from pM to low nM for replicons with NS5A sequences derived this website from genotype 2a, 3a, 4a, and 5a.4 Proof of concept for BMS-790052 has been achieved clinically, where its exceptional in vitro potency translated to an in vivo effect in a single-ascending dose study.4 In this study, marked HCV RNA decline (∼2.9 log10) was needed for detection of resistant variants, suggesting that the variants were likely present as preexisting minor quasi species and were uncovered by the efficient suppression of wild-type

virus.4 However, the ability of BMS-790052 to further suppress viral replication with continuous dosing could not be assessed in the single-ascending 上海皓元医药股份有限公司 dose study. In addition, analysis of specimens from the single-ascending dose study did not reveal whether the resistance detected clinically correlates with resistance observed in the in vitro replicon system. In the multiple-ascending dose (MAD) study reported here, a total of 24 chronically infected patients (4 active patients per cohort) were treated with BMS-790052 at 1, 10, 30, 60, and 100 mg once-daily or 30 mg twice-daily for 14 days. The treated patients generally experienced rapid, marked viral load declines. However, HCV RNA remained detectable in all genotype 1a–infected patients, and viral breakthrough was observed during the course of treatment in the majority of these patients. In contrast, viral breakthrough was observed less often in patients infected with HCV genotype 1b, and, in several patients, HCV RNA dropped below the level of quantitation (<25 IU/mL).

e., fitness) of the variants. Conclusion: Although resistance emerged during monotherapy with BMS-790052, the substantial anti-HCV effect of this compound makes it an excellent candidate for effective combination

therapy. (HEPATOLOGY 2011) The hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is a multifunctional protein with key roles in HCV replication. NS5A has also been implicated in the modulation of cellular signaling pathways.1, 2 Because it is required in vivo and in vitro for viral replication and has no known human homologs, NS5A provides an attractive Palbociclib in vivo target for therapeutic intervention.3 BMS-790052 is a potent HCV

NS5A replication complex inhibitor, with 50% effective concentration (EC50) values of 9 and 50 pM against genotype 1b and 1a replicons, respectively.4, 5 It is also potent against live virus (genotype 2a, JFH-1), with an EC50 of ∼28 pM.4 BMS-790052 has broad genotype coverage, with EC50 values ranging from pM to low nM for replicons with NS5A sequences derived selleck kinase inhibitor from genotype 2a, 3a, 4a, and 5a.4 Proof of concept for BMS-790052 has been achieved clinically, where its exceptional in vitro potency translated to an in vivo effect in a single-ascending dose study.4 In this study, marked HCV RNA decline (∼2.9 log10) was needed for detection of resistant variants, suggesting that the variants were likely present as preexisting minor quasi species and were uncovered by the efficient suppression of wild-type

virus.4 However, the ability of BMS-790052 to further suppress viral replication with continuous dosing could not be assessed in the single-ascending MCE dose study. In addition, analysis of specimens from the single-ascending dose study did not reveal whether the resistance detected clinically correlates with resistance observed in the in vitro replicon system. In the multiple-ascending dose (MAD) study reported here, a total of 24 chronically infected patients (4 active patients per cohort) were treated with BMS-790052 at 1, 10, 30, 60, and 100 mg once-daily or 30 mg twice-daily for 14 days. The treated patients generally experienced rapid, marked viral load declines. However, HCV RNA remained detectable in all genotype 1a–infected patients, and viral breakthrough was observed during the course of treatment in the majority of these patients. In contrast, viral breakthrough was observed less often in patients infected with HCV genotype 1b, and, in several patients, HCV RNA dropped below the level of quantitation (<25 IU/mL).

In our population, it also seems to have a greater influence on treatment response. IL28B’s mechanism of action is likely effected through ISG expression. These results indicate that patient’s native IL28B genotype has a greater influence than donor genotype on relevant ISG expression, and consequently on treatment response. Disclosures: Richard Gilroy – Advisory Committees

or Review Panels: FDA GIDAC; Speaking and Teaching: Salix, Vertex, Gilead The following people have nothing to disclose: Zoe Raglow, Chuanghong Wu, Winston Transferase inhibitor Dunn, Yu-Jui Y. Wan BACKGROUND & AIMS MicroRNAs (miRNAs) are an important class of small non-coding RNA molecules that bind to their complementary sequence on their target mRNAs, resulting in translational repression. MiRNAs play major

roles in development, metabolism, infection, and cancer. The diagnosis of cholangiocarcinoma is sometimes difficult due to the lack of a specific tumor marker and limited sampling for histological evaluation. In this study, we analyzed miRNA expression in bile to identify predictive miRNAs for hepatobiliary malignancy. METHODS MiRNAs were obtained from bile samples taken from 25 patients with benign hepatobiliary disease and 34 patients with malignant hepatobiliary disease, including cholangiocarcinoma and gallbladder cancer. Expression of 328 miRNAs was determined with the TaqMan real-time PCR detection system using a MicroRNA Assays Human Panel. MiRNAs were functionally Ensartinib nmr evaluated in cholangiocarcinoma cell lines (Huh28, Hucct1, and KMBC) following the overexpression or knocking down of specific miRNAs using mimic-miRNA or anti-miRNA. RESULTS Among the 328 miRNAs tested, 16 were differentially expressed between the bile of patients with malignant hepatobiliary disease and those

with benign hepatobiliary MCE disease (p<0. 05). From these 16 miRNAs, we focused on the two—miR-451 and miR-486—that were most significantly increased in malignant hepatobiliary disease. The area under the curve of the receiver operating characteristic curve for the prediction of malignant hepatobiliary disease using these miRNAs was 0. 85, which was equivalent to that of the tumor marker CA19-9. Univariate analysis using multiple clinical parameters, including tumor markers (CEA and CA19-9) and a liver function test, revealed serum ALT and T-Bil, miR-451, and miR-486 as significant variables. Multivariate analysis identified CEA, CA19-9, and miR-486 as significant variables. Functional analysis of these miRNAs showed that miR-451 had tumor suppressive and anti-inflammatory properties by decreasing the expression of PDGFRα, KRT7, IL1, and IL6, while miR486 was tumorigenic by increasing the expression of PDGFRα, N-cadherin, and p38MAPK. CONCLUSIONS We identified two predictive miRNAs, miR-451 and −486, in bile for the diagnosis of malignant hepatobiliary disease.