The bloodletting therapy or iron chelation therapy used before see more cirrhosis or diabetes can significantly improved the prognosis of the hemochromatosis patients. When

the patient with the following symptoms: Fatigue, right upper quadrant pain, joint pain, cartilage calcinosis disease, impotence, reduced libido, and heart failure or diabetes, whose diagnosis is not clear, detection of serum iron, transferrin saturation and ferritin is needed. Patients with abnormal detection results can underwent liver MRI, liver biopsy or the genetic testing of C28Y and H63D in order to diagnose the hemochromatosis CP-673451 concentration and be treated as early as possible. Key Word(s): 1. Hemochromatosis; 2. Clinical analysis; Presenting Author: HERYDJAGAT PURNOMO Additional Authors: HIRLAN HIRLAN, KASNO KASNO, EDI SUDIJANTO, DARMONO DARMONO, DALDIYONO DALDIYONO,

R. DJOKOMOELJANTO, SULTANAMH FARADZ Corresponding Author: HERYDJAGAT PURNOMO Affiliations: Dr Kariadi Hospital Diponegoro University, Disvison of gastroenterohepatology; Dr CiptoMangunkusumo; CEBIOR Diponegoro University Objective: NAFLD is considered as hepatic manifestation of metabolic syndrome (MS). Insulin resistance is a key component of metabolic syndrome. The aim of study was to determine correlation between severity of MS and histology of NAFLD. Methods: A total of 155 subjects (80 NAFLD cases and 75 healthy controls) were included. Liver biopsy was performed in all NAFLD cases. NAFLD severity was determined according to NAFLD Activity Score (NAS). NAFLD spectrum score was 1 to 5. Subject with NASH was grade as 5 and who without central obesity in control group was grade as 1. MS was defined by International Diabetes Federation criteria. Rucaparib in vitro Insulin resistance was assessed by the Homeostatic model Assessment-Insulin

Resistance (HOMA-IR) index. Results: The average of age was 44,9 ± 10,20 years, 85 (54.8%) male. Liver biopsies yield 29 non-alcoholic steatohepatisis (NASH), 40 possible NASH and 11 subjects were simple steatosis. In the cases group subjects had 4 components of MS 42%, 3 component 40% and 5 component 17%. Severity of Metabolic syndrome had a strong correlation with NAFLD spectrum score (r = 0.8; p < 0,001). The degree of HOMA-IR index had a moderate correlation with NAFLD spectrum score (r = 0,58; p < 0,001) Conclusion: Severity of metabolic syndrome has a strong correlation with histology of NAFLD spectrum score Key Word(s): 1. severity; 2. non alcoholic liver disease; 3. metabolic syndrome; 4.

Therefore, they could serve as ideal endogenous normalizers for circulating miRNAs. However, U6 and miR-16 expression was significantly different among the four groups (Fig. 1C), further supporting the previous notion that they are not reliable internal normalizers. Most important, U6 was differentially expressed between healthy

young and aging groups (Fig. 1D). Thus, cautious interpretation of the data reported by Starkey Lewis et al. is warranted. Different normalization methods should be further employed to make sure that findings are robust, irrespective of the way of standardization. We are convinced that these three miRNAs identified here are the best circulating endogenous controls reported thus far, although Epacadostat in vivo more validation in different conditions may still be needed. We recommend that suitable endogenous controls should be selected in light of the study design and research conditions, and that the use of two to three endogenous normalizers together resembling the mean expression value may additionally reduce bias and variation. Ruiqun Qi M.S.* † ‡, Matthew Weiland* †, Xing-Xua Gao M.D., Ph.D.‡, Li Zhou M.D.* † §, Qing-Sheng Mi M.D., Ph.D.* † §, * Henry Ford Immunology

Program, Henry Ford Health System, Detroit, MI, high throughput screening compounds † Department of Dermatology, Henry Ford Health System, Detroit, MI, ‡ Department of Dermatology, No. 1 Hospital of China Medical University, Shenyang, China, § Department of Internal Medicine, Henry Ford Health System, Detroit, MI. “
“We aimed to evaluate hepatic vascular changes following lipiodol-based transarterial chemoembolization of hepatocellular carcinoma using epirubicin (EPI), miriplatin (MPT) and miriplatin plus low-dose epirubicin (MPT+EPI). A total of 185 arteries in 118 patients who underwent chemoembolization using EPI (67 arteries in 48 patients), MPT (64 arteries in

37 patients) and MPT+EPI (54 arteries in 33 patients) were retrospectively examined. The maximum dose limit of MPT was 140 mg and that of EPI was 50 and 20 mg for the EPI and MPT+EPI groups, respectively. Vascular changes and local recurrence were evaluated by Glycogen branching enzyme subsequent angiography. Factors affecting arterial damage were analyzed using multivariate logistic regression analysis. More severe arterial damage was observed in the EPI group (88.1%) than in the MPT+EPI (72.2%) and the MPT (18.7%) groups (P = 0.044 and P < 0.001, respectively). EPI usage (hazard ratio [HR] = 12.8, P < 0.001), selective chemoembolization (HR = 5.4, P < 0.001) and MPT usage (HR = 0.28, P = 0.020) were significant predictors for arterial damage induction. The local recurrence rate was lower for the lesions exhibiting arterial occlusion after chemoembolization (39.4%) than for the lesions exhibiting no vascular attenuation (73.9%) or wall irregularity (75.8%) (P = 0.001 and P = 0.005, respectively).

Therefore, they could serve as ideal endogenous normalizers for circulating miRNAs. However, U6 and miR-16 expression was significantly different among the four groups (Fig. 1C), further supporting the previous notion that they are not reliable internal normalizers. Most important, U6 was differentially expressed between healthy

young and aging groups (Fig. 1D). Thus, cautious interpretation of the data reported by Starkey Lewis et al. is warranted. Different normalization methods should be further employed to make sure that findings are robust, irrespective of the way of standardization. We are convinced that these three miRNAs identified here are the best circulating endogenous controls reported thus far, although Selleckchem Enzalutamide more validation in different conditions may still be needed. We recommend that suitable endogenous controls should be selected in light of the study design and research conditions, and that the use of two to three endogenous normalizers together resembling the mean expression value may additionally reduce bias and variation. Ruiqun Qi M.S.* † ‡, Matthew Weiland* †, Xing-Xua Gao M.D., Ph.D.‡, Li Zhou M.D.* † §, Qing-Sheng Mi M.D., Ph.D.* † §, * Henry Ford Immunology

Program, Henry Ford Health System, Detroit, MI, selleck inhibitor † Department of Dermatology, Henry Ford Health System, Detroit, MI, ‡ Department of Dermatology, No. 1 Hospital of China Medical University, Shenyang, China, § Department of Internal Medicine, Henry Ford Health System, Detroit, MI. “
“We aimed to evaluate hepatic vascular changes following lipiodol-based transarterial chemoembolization of hepatocellular carcinoma using epirubicin (EPI), miriplatin (MPT) and miriplatin plus low-dose epirubicin (MPT+EPI). A total of 185 arteries in 118 patients who underwent chemoembolization using EPI (67 arteries in 48 patients), MPT (64 arteries in

37 patients) and MPT+EPI (54 arteries in 33 patients) were retrospectively examined. The maximum dose limit of MPT was 140 mg and that of EPI was 50 and 20 mg for the EPI and MPT+EPI groups, respectively. Vascular changes and local recurrence were evaluated by MRIP subsequent angiography. Factors affecting arterial damage were analyzed using multivariate logistic regression analysis. More severe arterial damage was observed in the EPI group (88.1%) than in the MPT+EPI (72.2%) and the MPT (18.7%) groups (P = 0.044 and P < 0.001, respectively). EPI usage (hazard ratio [HR] = 12.8, P < 0.001), selective chemoembolization (HR = 5.4, P < 0.001) and MPT usage (HR = 0.28, P = 0.020) were significant predictors for arterial damage induction. The local recurrence rate was lower for the lesions exhibiting arterial occlusion after chemoembolization (39.4%) than for the lesions exhibiting no vascular attenuation (73.9%) or wall irregularity (75.8%) (P = 0.001 and P = 0.005, respectively).

Here, I examined whether species recognition may facilitate species isolation of Liolaemus lizards, for which up to seven closely related species with similar morphology and ecology may live in sympatry. I also tested whether coexistence with closely related species modulates species recognition. In three Liolaemus species

that differ in their current need for species recognition, I investigated their abilities to discriminate chemical stimuli from conspecifics and closely related congeners. For two of these focal species, tests included sympatric and allopatric congeners. The third species, which lives without congeners, was only tested with an allopatric congener. All three species chemo-discriminated between conspecifics and congeners, responding more vigorously to scents produced by their own species. Thus, chemical stimuli may help to maintain reproductive

BIBW2992 mw isolation. The existence of species recognition Selleck Neratinib in the allopatric species may be an ancestral trait or may have evolved as a side effect of a within-species recognition system. “
“Resting metabolic rate (RMR) is highly variable between individuals within a single species and the relationship between body mass and RMR does not wholly explain this variability. One factor that could account for a portion of the residual variation is animal personality or consistent individual differences (CIDs) in behaviour, but no study has examined this relationship in a free-living population of mammals. In this paper, we test for a relationship

between RMR and CIDs in activity in live-trapped meadow voles Microtus pennsylvanicus after controlling for the effect of body mass. We quantified Tangeritin the activity levels of voles both in an unfamiliar environment and for the first 2 min in the metabolic apparatus, and then measured RMR using open-flow respirometry. As expected, there was a linear relationship between RMR and body mass, and we found strong evidence for repeatable differences in activity levels between individuals. However, contrary to the hypothesis, we did not identify a significant correlation between CIDs in behaviour and RMR after controlling for body mass. Our results suggest that, at least within species, higher activity levels may not require a greater investment in energetically demanding tissues or increased capacity for processing of energy. Alternatively, if a relationship exists, our inability to detect it may reflect a weak behavioural signal in noisy RMR data that are influenced by many factors. Our results could also reflect an artefact of individual responses to stress or a sampling bias towards more exploratory individuals in animals captured by live-trapping. “
“The interaction between native and introduced predators can be an important determinant of the success of introduced species and of the magnitude of their effects.

5A-C). On western blot analysis, aP2 induction was evident in MED1fl/fl hepatocytes but not in MED1-deficient hepatocytes after Ad/PPARγ infection (Fig. 5D). These data clearly demonstrate the importance of MED1 in PPARγ-inducible adipogenic gene expression in liver under both in vivo and in vitro conditions. To ascertain the regulatory role of MED1 in PPARγ-stimulated adipogenic hepatic steatosis, we performed complementary DNA (cDNA) microarray analysis to check the global transcriptional profile in mouse liver 4 days after injection with Ad/LacZ or Ad/PPARγ.

When four-fold change is used as the cutoff, over 260 genes were up-regulated in Ad/PPARγ-stimulated MED1fl/fl mouse liver (Fig. 6A; Supporting Table 1). Most of these genes are involved in adipogenesis and lipid and glucose metabolism, suggesting a transdifferentiation trend AZD5363 datasheet of hepatocytes toward adipocytes or the development of adipogenic steatosis. In the absence of MED1 in liver the levels of expression ABT-888 in vitro of these genes were markedly subdued. These observations clearly establish that MED1 plays a key role in facilitating the transcriptional

regulation of PPARγ target genes (Fig. 6A). Data shown in the heat map reveal that the expression levels of 28 genes involved in PPARγ function are dramatically lower in MED1ΔLiv mouse liver when compared to MED1fl/fl mouse following Ad/PPARγ administration (Fig. 6B). These include adiponectin, Elovl4, caveolin-1, Fabp5, Psapl1, Cyp4a14, and

Hkdc1, among others.6 Interestingly, several genes, including fibroblast growth factor 21 (FGF21),25, 26 Fads2, Fads6, Elovl2, Apoa4, and Acot1, showed increased expression in MED1ΔLiv mouse with PPARγ overexpression (Fig. 6B). We validated microarray results by quantitative polymerase chain reaction (Q-PCR), which showed remarkably Clomifene lower expression of S3-12, promethin, Fabp5, Hkdc1, Insig2, Nfatc4, Apob48r, caveolin-1, and Hsd17b2 in MED1ΔLiv mouse liver compared to MED1fl/fl mouse after injection with Ad/PPARγ (Fig. 6C; see Supporting Table 2 for primers used for Q-PCR). These data clearly establish that the loss of hepatic MED1 results in an abrogation of induction of lipogenesis-related genes but MED1 is not required for the induction of CD36 and FSP27 (Fig. 4). To further confirm the role of MED1 in PPARγ-stimulated hepatic steatosis in vivo, MED1 was re-expressed in MED1ΔLiv mouse liver using adenovirally-driven MED1 (Ad/MED1) (Fig. 7A-F). As expected, re-expression of MED1 in MED1ΔLiv mouse liver restored the PPARγ-stimulated steatotic response (Fig. 7B,D,F). The relative liver weight of MED1ΔLiv mouse injected with both Ad/MED1 and Ad/PPARγ increased as compared to MED1ΔLiv mouse treated with Ad/MED1 and Ad/LacZ (Fig. 7G). Re-expression of MED1 in MED1ΔLiv mouse liver also restored the expression of adipogenesis-related genes in response to PPARγ (Fig. 7H,I). These data clearly establish the critical role for MED1 in PPARγ-stimulated hepatic steatosis.

OPN-c, for example, has been associated with a more aggressive tumor phenotype click here in breast and ovarian cancers. Studies of OPN isoforms in liver cancers however, have been limited to OPN-a (total OPN). We therefore hypothesized that OPN isoforms are overexpressed in cholangiocarcinoma, and the pattern of isoform overexpres-sion is associated with tumor phenotype. TGF-p is a classical promoter of fibrosis and cancer, and also interacts with OPN. Therefore, we further evaluated if OPN isoforms could modulate TGF-b signaling. Methods: Three human cholangiocarcinoma cell lines were used: HUCCT1, SG231 and CCLP1. Specific plasmids for each isoform were used for overexpression. Gene expression for OPN-a, b,

c, and epithelial-mesenchymal transition (EMT) markers (vimentin, aSMA, E-cadherin, PPARg were evaluated by qRT-PCR. The ectopic overexpression of OPN isoforms and their effects on the components of TGF-p signalling pathway were evaluated by WB. Results: CCLP1 cells expressed the highest levels of OPN mRNA for the 3 isoforms and exhibited the most mesenchymal phenotype (high vimentin and low E-cadherin). By contrast, HuCCT1 expressed

the least OPN-a, b, c, and were most epithelial (high E-cadherin and low vimentin). In all three cell lines, mRNA levels for OPN-a, and b were more abundant than OPN-c (∼10 fold). All 3 OPN isoforms exhibited similar mRNA stability. The ectopic overex-pression of OPN-c in SG231 cells downregulated mesenchy-mal genes (vimentin and aSMA) by

∼30%, but upregulated the epithelial marker PPARg compared with OPN-a. Overexpres-sion of OPN-a, however, reduced levels of SnoN, a repressor of TGF-p pathway (i.e. GSI-IX mouse leads to unopposed TGF-p signaling), whereas OPN-c overexpression has no effect. Conclusions: The levels of OPN correlate with degrees of EMT (marker of aggressiveness) in cholangiocarcinoma. OPN-c is associated with the most epithelial oxyclozanide phenotype (i.e. most differentiated and least aggressive). These differences in tumor behavior may be related to the changes in the levels of TGF-p repressor, SnoN. Future studies are needed to ascertain the clinical significance in patients with cholangiocarcinoma. Disclosures: The following people have nothing to disclose: Marco A. Briones-Orta, Jason D. Coombes, Naoto Kitamura, Paul P. Manka, Roger Williams, Ali Canbay, Salvatore Papa, Wing-Kin Syn Background: We have previously shown that hyperammonemia is a mediator of the liver muscle axis in cirrhosis. However the molecular mechanisms responsible for this have not been well understood. We examined the ERK-c-myc axis as a mediator of skeletal muscle protein synthesis during cirrhosis. Methods: Time course studies were performed on differentiated C2C12 murine myotubes during hyperammonemia. Rate of protein synthesis was quantified by the puromycin incorporation assay. Ribosomal biogenesis was examined by expression levels of c-myc and RNA translational capacity.

By the end of the study, recurrence was documented in 51 patients (44%) (mean HIF inhibitor time to recurrence: 23 ± 3 months, mean survival time after recurrence: 12 ± 2 months). Surgical margins (R-Sit-uation) and performance of locoregional lymphadenectomy were the only independent variables to improve overall

survival in a multivariate regression analysis. An abnormal CA 19-9 (≥ 37 u/mL), AJCC/UICC T3-4 vs. T1-2, and R1-2 vs. R0 were the independent predictors of recurrence. Neoadjuvant or adjuvant therapies did not yield a survival benefit in patients undergoing liver resection. Conclusion: Surgery remains the only curative treatment for patients with CCA. Extended resection in order to achieve histologically free margins and the performance of locoregional lymphadenectomy improve survival. Additive therapeutic strategies selleckchem to prolong disease-free survival are still ineffective. Disclosures: The following people have nothing to disclose: Arash Nickkholgh, Arianeb Meh-rabi, Thomas Bruckner, Benjamin Goeppert, Peter Schemmer Background/Aim: Novel, non-invasive biomarkers to assess liver function and predict

clinical outcomes are urgently needed. Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide and often occurs in cirrhosis. Surgical resection of HCC is a potentially curative treatment option, however it has the capacity to cause hepatic decompensation. No single test currently in clinical use offers reliable risk stratification. This study aims to assess the clinical utility of the 13C methacetin breath test (13CMBT, measure of hepatocyte mic-rosomal function), transient elastography using FibroScan and indocyanine green (ICG) clearance (measure of liver perfusion and excretory function) in

predicting hepatic decompensation in patients undergoing liver resection. Methods: 13CMBT, FibroScan and ICG clearance were prospectively measured in 105 patients being assessed for liver resection. Patient demographics, clinical and laboratory data were recorded including Child-Pugh-Turcotte selleck products (CPT) and Model for End-Stage Liver Disease (MELD) scores. 23 patients had surgery. Post-operative hepatic decompensation was determined by biochemical (elevation in bilirubin or INR) and clinical (ascites, encephalopa-thy) parameters. 2 tailed P values <0.05* or <0.01** were considered statistically significant. Results: There was significant correlation of 13CMBT, FibroScan and ICG clearance with serum bilirubin (R=-0.43**, 0.21*, 0.42**) and albumin levels (R=0.37**,-0.41**, -0.72**), respectively. Only ICG clearance was associated with INR (R=0.26*). Both CPT (R=-0.44**, 0.46**, 0.68**) and MELD scores (R=-0.2 [p=0.08], 0.28*, 0.38**) correlated with these biomarkers. ICG clearance correlated with FibroScan (R=0.5**) and 13CMBT (R=-0.55**) as did FibroScan with 13CMBT (R=-0.38**).

TTP as a primary endpoint in such studies seems to have some advantages but, as discussed above, the evaluation of response and progression shows particular difficulties in HCC after locoregional therapy. An additional necessity corroborated by our data are

new dosimetry conceptions that incorporate the intrahepatic distribution of microspheres in the calculation of the applied dose aiming at lower exposure of normal liver tissue and, equally important, higher intratumoral radioactive doses. This may result in a further enhancement of local response, which should translate into a further improvement of overall survival. “
“Background and Aims:  The American Association for the Study of Liver Disease issued guidelines that proposed that SAHA HDAC hepatocellular carcinoma (HCC) can be diagnosed if a mass is larger than 2 cm in a cirrhotic liver and Selleck LY2606368 shows typical features of HCC at triphasic liver computed tomography (CT) or dynamic magnetic resonance

imaging (MRI). In non-cirrhotic livers, the criteria were not applicable. The aim of the present study was to retrospectively analyze the sensitivity of imaging by samples of definite HCC postoperatively and test their application to diagnose HCC in non-cirrhotic livers. Methods:  From January 2006 to November 2008, a total of 343 pathologically-diagnosed HCC patients via surgical resection were reviewed. Among the 343 patients, 204 patients had undergone liver CT examination, and 80 patients underwent MRI examination; serum α-fetoprotein had been checked for all 343 patients prior to operation. The diagnostic sensitivity of HCC by imaging was evaluated and compared in patients with/without cirrhosis by ultrasound and histology. Results:  The diagnostic sensitivity of HCC by single imaging was approximately 65–80% (liver CT or MRI). A higher sensitivity of HCC diagnosis was found in patients with ultrasound-diagnosed cirrhosis than non-cirrhosis, but the difference in sensitivity disappeared very after histologically-cirrhotic validation. The results indicated that regardless of the presence or absence

of cirrhosis (histology), a typical vascular pattern could diagnose HCC with equally high sensitivity. Conclusions:  We provide evidence that the sensitivity of HCC diagnosis by imaging is not influenced by the cirrhotic background. Further study is needed to validate the specificity and accuracy. “
“The epidemiology and natural history of pediatric primary sclerosing cholangitis (PSC), autoimmune sclerosing cholangitis (ASC), and autoimmune hepatitis (AIH) are not well characterized. Using multiple, overlapping search strategies followed by a detailed records review, we identified all cases of pediatric PSC, ASC, AIH, and inflammatory bowel disease (IBD) in a geographically isolated region of the United States.

In 2006, we reported the first case of UC exacerbation induced by combination therapy of PEG-IFN and RIB for chronic hepatitis C.10,13 Use of this combination therapy is common in Japan and increasing; therefore, additional cases of development or exacerbation of UC associated with this treatment have been reported. Here, we describe the results of a literature review of cases in which the development or exacerbation of UC was coincident with IFN and/or RIB treatment for chronic hepatitis C. We ACP-196 chemical structure also summarize the results of studies that evaluated the effectiveness of IFN for UC or Crohn’s disease, which were carried out primarily in Europe and the USA.18–24 IFN is an antiviral agent that belongs

to a class of proteins known as cytokines. IFN exerts many effects on the immune system, such as: (i) activating macrophages; (ii) upregulating natural killer cell activity; (iii) stimulating antibody-dependent cellular cytotoxicity; (iv) enhancing the effects of killer T cells; and (v) modulating antibody production.25 Common adverse effects of IFN include: (i) flu-like symptoms, fever, ague, general fatigue, headache, and arthralgia; (ii) gastrointestinal symptoms, such as appetite loss, nausea, vomiting, abdominal pain, diarrhea, and constipation; and (iii) skin eruptions or itching.26 Although the incidence is low, several autoimmune diseases can occur as adverse reactions to IFN. These include:

(i) UC and Crohn’s disease/inflammatory bowel disease (IBD); (ii) interstitial pneumonia; (iii) thyroid function abnormalities;27 (iv) autoimmune hemolytic anemia; (v) systemic lupus erythematosus; and (vi) rheumatoid arthritis. In the reported Proteasome inhibitor nine cases of UC exacerbation induced by IFN therapy in Japan (Table 1), seven were associated with IFN-α,2–8 one with IFN-α2b plus RIB,10 and the other with IFN-β;9 thus cases associated with IFN-α were more common. Many more cases of UC exacerbation induced by

PEG-IFN-α2a or 2b plus RIB are expected to be reported in the future as the use of combination therapy becomes more widespread. However, the number of reported cases of UC induced by IFN and RIB has not increased to date. One case of UC exacerbation induced by IFN-β has been reported in Japan,9 and Rodrigues et al. reported four cases of UC exacerbation induced by IFN-β therapy for multiple sclerosis (MS) in 2010.17 IFN-β has been evaluated as a treatment Paclitaxel research buy for UC in Europe and the USA; however, because IFN-β may cause or exacerbate UC, caution is needed in the design of future studies. The period between the development or exacerbation of UC from the start of IFN treatment ranges from only 1 day to 4.5 years, varying very widely among the nine cases reported in Japan2–10 and seven cases found through a MEDLINE search11–17 (one was a publication also found through a search of Japana Centra Revuo Medicina). The reports have assumed a cause-and-effect correlation between IFN treatment and UC development (Tables 1 and 2).

This finding has not been reported in Phase II-III clinical trials and suggests the need for close monitoring of TPV, especially in at risk patients. “
“Ursodeoxycholic acid (UDCA) Selleckchem SB525334 treatment is an effective medical therapy for patients with primary biliary cirrhosis (PBC); however, 40% of PBC patients show an incomplete response to the UDCA therapy. This study aimed to investigate the safety and efficacy of umbilical cord-derived mesenchymal stem cell (UC-MSC) transfusion in PBC patients with an incomplete response to UDCA. We conducted a single-arm trial

that included seven PBC patients with a suboptimal response to UDCA treatment. UC-MSCs were first cultured, and then 0.5 × 106 cells/kg body weights were infused through a peripheral vein. UC-MSCs were Selleck MAPK Inhibitor Library given three times at 4-week intervals, and patients were followed up for 48 weeks. Primary outcomes were to evaluate the safety and feasibility of UC-MSC treatment, and secondary outcomes were to evaluate liver functions and patient’s quality of life. No obvious side-effects were found in the patients treated with UC-MSCs. Symptoms such as fatigue and pruritus were obviously alleviated in most patients after

UC-MSC treatment. There was a significant decrease in serum alkaline phosphatase and γ-glutamyltransferase levels at the end of the follow-up period as compared with baseline. No significant changes were observed in serum alanine aminotransferase, aspartate aminotransferase, total bilirubin, albumin, prothrombin time activity,

international normalized ratio, or immunoglobulin TCL M levels. The Mayo risk score, a prognostic index, was also stable during the treatment and follow-up period. UC-MSC transfusion is feasible and well tolerated in patients with PBC who respond only partially to UDCA treatment, thus representing a novel therapeutic approach for patients in this subgroup. A larger, randomized controlled cohort study is warranted to confirm the clinical efficacy of UC-MSC transfusion. Primary biliary cirrhosis (PBC) is a progressive autoimmune liver disease that causes substantial loss of intrahepatic bile ducts, ultimately resulting in cholestasis, advanced fibrosis, cirrhosis, liver failure, and even hepatocellular carcinoma. Ursodeoxycholic acid (UDCA) is currently the only drug specifically approved for the treatment of PBC.[1] Patients who respond to UDCA treatment have a life expectancy comparable with the general population;[2] however, more than 40% of patients have an incomplete response to UDCA, resulting in progressive disease necessitating liver transplantation or death from liver-related causes.[3] Currently, no efficient treatment is clinically available for this population of UDCA-resistant patients.