7% of the patient population with significantly elevated ALT valu

7% of the patient population with significantly elevated ALT values had similar levels of symptoms to the remainder of the population. One area of controversy in PBC is the role played by depression in the causation of fatigue. Whereas reports check details of depression are common in the clinical records of patients, detailed psychiatric evaluation has failed to demonstrate major depressive illness.12, 22 This issue is of real importance to patients both in terms of management and perceptions of their illness (both their own and those of others). In the UK population depression, assessed in terms of percentage of patients meeting criteria for “caseness”

using the HADS-D, a measure optimized for use in a chronic disease population, was rare as an isolated feature in both fatigued and nonfatigued patients (3% with severe fatigued and <1% with mild or

none). Depression was often seen in the context of a symptom complex, which included symptoms of autonomic dysfunction and daytime somnolence (two associations described previously and confirmed in this national patient cohort). Indeed, depressive symptoms were seen 10 times more often in fatigued patients with additional symptoms of autonomic dysfunction and/or sleep disturbance (30% of patients) than they were in isolation (3%). One interpretation would be that depression per se is not a cause of fatigue in PBC but may be a secondary, exacerbating feature in patients with click here a high cumulative burden of other symptoms. The presence of depression in this setting may contribute to the overall clinical expression of disease and impaired life quality, and is an important potential target for therapy. Such treatment should be prescribed with the realization that it may only improve the secondary depression and not the underlying mafosfamide fatigue or other symptoms. The importance of the complex of depressive symptoms, autonomic symptoms, and sleep disturbance with fatigue is indicated by the fact that 75% of patients with no fatigue or mild fatigue did not

have any of these additional underpinning symptoms. Only 11% of severely fatigued patients lacked additional symptoms. In contrast, 19% of severely fatigued patients had all three of these symptoms, a combination which was not seen in any patient with mild or no fatigue. In a cross-sectional study of this type it is difficult to draw conclusions about the hierarchy of symptoms linked to fatigue. A structured approach to management addressing each of these additional symptoms would be of interest, and would represent a potential approach to the treatment of fatigue. If any of these associated symptoms are causal in PBC, substantial gains in terms of fatigue reduction might be expected. Even if these symptoms are consequential upon fatigue in PBC they will exert a significant effect on life quality in their own right and QOL gains might be expected.

Designed human TaqMan assays (Applied Biosystems, Foster City, CA

Designed human TaqMan assays (Applied Biosystems, Foster City, CA) click here were used to quantify gene expression of osteocalcin (BGLAP), osteoprotegerin (TNFRSF11B), RANKL (TNFSF11), and Cbfa1 (RUNX2). Quantitative PCRs were carried out using ABI-Prism 7900 HT Fast Real-Time PCR System and a

TaqMan 5′-nuclease probe method (Applied Biosystems). Results were expressed as relative expression of each gene (versus β-actin gene expression), using arbitrary units according to the comparative CT (threshold cycle) method.20 All real-time PCR reactions for each sample were performed in triplicate. The primers used are listed in Table 1. Data are expressed as mean ± standard deviation (SD). All analyses were performed with the SPSS version 14.00 statistical package (SPSS Inc., selleck chemical Chicago, IL). Significant differences between any two groups were determined by Student t test or Mann-Whitney U test. When multiple groups were compared, analysis of variance was used, followed by a Tukey’s multiple contrast test, where applicable. A P value ≤0.05 was considered significant. Nonpassage human primary osteoblasts, after synchronization, displayed the characteristic pattern of gene expression and protein production of osteoblastic differentiation markers such as osteocalcin gene expression and alkaline phosphatase activity (data not shown). Increasing concentrations

of unconjugated bilirubin in the culture media resulted in a progressive decrease in cell viability, which was observed particularly at concentrations higher than 100 μM at 48 hours and higher than 50 μM at 72 hours (Table 2). The cell viability decrease was 36% and 56%, at 50 and 100 μM, respectively, compared with nontreated cells. Moreover, the presence of bilirubin (10 μM) resulted in significantly better cell viability Reverse transcriptase compared with no bilirubin in the experiments performed at 48 hours and in the plates without FBS. These effects on cell survival were partially prevented by the presence of 10% FBS, because the detrimental effect of bilirubin at 50 and 100 μM was completely abolished

in the experiments with FBS. Actually, in these latter experiments, the decreased cell viability was only observed with bilirubin at 1000 μM (Table 2). Serum samples from patients and healthy subjects were added at 2%, 10%, and 20% concentrations in culture medium. Cell viability significantly decreased in samples with increasing concentrations of sera from jaundiced patients at 72 hours (Table 3), with viability decreasing by 19%, 18%, and 33% at 2%, 10%, and 20% concentrations, respectively. No significant effect was observed at the other time points, although there was a trend in the experiments performed at 48 hours. Moreover, no effect on cell viability was observed in the experiments performed with samples from patients who had normal bilirubin levels.

Designed human TaqMan assays (Applied Biosystems, Foster City, CA

Designed human TaqMan assays (Applied Biosystems, Foster City, CA) selleck screening library were used to quantify gene expression of osteocalcin (BGLAP), osteoprotegerin (TNFRSF11B), RANKL (TNFSF11), and Cbfa1 (RUNX2). Quantitative PCRs were carried out using ABI-Prism 7900 HT Fast Real-Time PCR System and a

TaqMan 5′-nuclease probe method (Applied Biosystems). Results were expressed as relative expression of each gene (versus β-actin gene expression), using arbitrary units according to the comparative CT (threshold cycle) method.20 All real-time PCR reactions for each sample were performed in triplicate. The primers used are listed in Table 1. Data are expressed as mean ± standard deviation (SD). All analyses were performed with the SPSS version 14.00 statistical package (SPSS Inc., Palbociclib purchase Chicago, IL). Significant differences between any two groups were determined by Student t test or Mann-Whitney U test. When multiple groups were compared, analysis of variance was used, followed by a Tukey’s multiple contrast test, where applicable. A P value ≤0.05 was considered significant. Nonpassage human primary osteoblasts, after synchronization, displayed the characteristic pattern of gene expression and protein production of osteoblastic differentiation markers such as osteocalcin gene expression and alkaline phosphatase activity (data not shown). Increasing concentrations

of unconjugated bilirubin in the culture media resulted in a progressive decrease in cell viability, which was observed particularly at concentrations higher than 100 μM at 48 hours and higher than 50 μM at 72 hours (Table 2). The cell viability decrease was 36% and 56%, at 50 and 100 μM, respectively, compared with nontreated cells. Moreover, the presence of bilirubin (10 μM) resulted in significantly better cell viability Resveratrol compared with no bilirubin in the experiments performed at 48 hours and in the plates without FBS. These effects on cell survival were partially prevented by the presence of 10% FBS, because the detrimental effect of bilirubin at 50 and 100 μM was completely abolished

in the experiments with FBS. Actually, in these latter experiments, the decreased cell viability was only observed with bilirubin at 1000 μM (Table 2). Serum samples from patients and healthy subjects were added at 2%, 10%, and 20% concentrations in culture medium. Cell viability significantly decreased in samples with increasing concentrations of sera from jaundiced patients at 72 hours (Table 3), with viability decreasing by 19%, 18%, and 33% at 2%, 10%, and 20% concentrations, respectively. No significant effect was observed at the other time points, although there was a trend in the experiments performed at 48 hours. Moreover, no effect on cell viability was observed in the experiments performed with samples from patients who had normal bilirubin levels.

Designed human TaqMan assays (Applied Biosystems, Foster City, CA

Designed human TaqMan assays (Applied Biosystems, Foster City, CA) selleck kinase inhibitor were used to quantify gene expression of osteocalcin (BGLAP), osteoprotegerin (TNFRSF11B), RANKL (TNFSF11), and Cbfa1 (RUNX2). Quantitative PCRs were carried out using ABI-Prism 7900 HT Fast Real-Time PCR System and a

TaqMan 5′-nuclease probe method (Applied Biosystems). Results were expressed as relative expression of each gene (versus β-actin gene expression), using arbitrary units according to the comparative CT (threshold cycle) method.20 All real-time PCR reactions for each sample were performed in triplicate. The primers used are listed in Table 1. Data are expressed as mean ± standard deviation (SD). All analyses were performed with the SPSS version 14.00 statistical package (SPSS Inc., MAPK Inhibitor Library Chicago, IL). Significant differences between any two groups were determined by Student t test or Mann-Whitney U test. When multiple groups were compared, analysis of variance was used, followed by a Tukey’s multiple contrast test, where applicable. A P value ≤0.05 was considered significant. Nonpassage human primary osteoblasts, after synchronization, displayed the characteristic pattern of gene expression and protein production of osteoblastic differentiation markers such as osteocalcin gene expression and alkaline phosphatase activity (data not shown). Increasing concentrations

of unconjugated bilirubin in the culture media resulted in a progressive decrease in cell viability, which was observed particularly at concentrations higher than 100 μM at 48 hours and higher than 50 μM at 72 hours (Table 2). The cell viability decrease was 36% and 56%, at 50 and 100 μM, respectively, compared with nontreated cells. Moreover, the presence of bilirubin (10 μM) resulted in significantly better cell viability Teicoplanin compared with no bilirubin in the experiments performed at 48 hours and in the plates without FBS. These effects on cell survival were partially prevented by the presence of 10% FBS, because the detrimental effect of bilirubin at 50 and 100 μM was completely abolished

in the experiments with FBS. Actually, in these latter experiments, the decreased cell viability was only observed with bilirubin at 1000 μM (Table 2). Serum samples from patients and healthy subjects were added at 2%, 10%, and 20% concentrations in culture medium. Cell viability significantly decreased in samples with increasing concentrations of sera from jaundiced patients at 72 hours (Table 3), with viability decreasing by 19%, 18%, and 33% at 2%, 10%, and 20% concentrations, respectively. No significant effect was observed at the other time points, although there was a trend in the experiments performed at 48 hours. Moreover, no effect on cell viability was observed in the experiments performed with samples from patients who had normal bilirubin levels.

In addition, to date,

no study has specifically investiga

In addition, to date,

no study has specifically investigated the potential interaction between BMI and BFP as related to FL risk. By focusing our attention on the fact that FL occurs among both under and over-weight Japanese, we investigated the factors related to FL by using existing anthropometric data from health checkups, including height, weight, and body fat percentage, which are easily measurable at checkups. Then, we discussed the possibility of interaction between BMI and BFP in FL. We performed a cross-sectional study using data obtained from health checkups at Nishinarachuo Hospital Health Care Center, Nara Prefecture (Japan). Subjects included 3139 persons (1871 male, 1268 female) aged 30 years and over, who visited the Alisertib nmr center from January 2008 to March 2011, and who underwent a medical checkup, including abdominal ultrasonography. For those who underwent multiple checkups during the

study period, we used the first data for the analysis. In the biochemical workup, subjects who were found to be positive for hepatitis C virus antibody or HBs antigen were excluded. Of the 3139 patients, usable data were obtained MAPK inhibitor from

3110 patients (1851 male, 1259 female). This study was approved by the Ethics Committee of Nara (Japan) and Nishinarachuo Hospital, Mannose-binding protein-associated serine protease and conforms to the Declaration of Helsinki (as revised in Tokyo in 2004). Data obtained during the health checkup included anthropometrical measurements, biochemical tests, and ultrasonography findings. Height and weight were measured while wearing lightweight clothing and no shoes. BMI (kg/m2) was computed by dividing body weight (kg) by the square of the height (m). BFP was measured by a device using the body impedance method, with subjects holding a grip with both hands. BFP (%) was calculated as: mass of fat (kg)/body weight (kg) × 100. Systolic and diastolic blood pressures were measured in the seated position by an automatic blood pressure recorder at the center, using the subject’s right or left arm. Using a self-administered questionnaire, subjects provided information about their disease history and various lifestyle habits, including drinking habits, smoking status, regular exercise, and weight gain ≥10 kg since the age of 20.

17 Future studies in our laboratory are under way to target hsp90

17 Future studies in our laboratory are under way to target hsp90 in liver diseases regulated by proinflammatory responses, such as ALD, NAFLD, and liver fibrosis. The authors thank Karen Kodys for labeling oligonucleotides for EMSA analysis. Additional Supporting Information may be

found in the online version of this article. “
“Aim:  Current medical transplantation methods focus on solutions for major problems such as the shortage of donors. To overcome these issues, expanding organ preservation time has become a major concern. A new refrigerating chamber has been recently developed, which can cool the inside of a material to the required temperature by frequently sensing the temperature of both inside and surface of the materials. this website The purpose of this study is to evaluate the usefulness of a

Idasanutlin datasheet new refrigerating system in hepatic preservation. Methods:  The liver grafts were harvested from rats and divided into two groups. Group A consisted of grafts preserved in chilled University of Wisconsin solution (UW) solution (on ice) for 24, 72 and 168 h. Group B consisted of grafts preserved in the UW solution in a new refrigerator at 4°C. Results:  In group B, aspartate aminotransferase released into effluent after cold storage for 72 h showed a marked decrease compared to group A (P < 0.05). The levels of ammonia and lactate decreased significantly in group B (P < 0.05). In group B, the levels of adenosine triphosphate were significantly preserved after cold storage for 24 h and 72 h compared to group A (P < 0.05). Immunohistochemistry showed positive cells for heme oxygenase-1 were significantly increased in group B after cold storage. Conclusion:  This new refrigerator can improve preservation injury of hepatic grafts and may provide an innovative technique for liver transplantation. "
“Background and Aim:  Inflammatory bowel disease (IBD) is a multi-factorial disease with an unknown etiology characterized by oxidative stress, leukocyte infiltration and a rise in inflammatory cytokines. This study was

conducted to investigate lithium in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced chronic model of experimental IBD, and the contribution of potassium channels as a possible underlying mechanism. Methods:  Experimental IBD was induced in rats Glycogen branching enzyme by a single colonic administration of 10 mg of TNBS. Lithium, Glibenclamide (a potassium channel blocker), Lithium + Glibenclamide, Cromakalim or Lithium + Glibenclamide + Cromakalim were given twice daily for 7 successive days. At the end of the experiment, macroscopic and histopathologic scores, colonic malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) level, and myeloperoxidase (MPO) activity as well as plasma lithium level were assessed. Results:  Both macroscopic and histological features of colonic injury were markedly ameliorated by lithium. Likewise, the elevated amounts of MPO and MDA were diminished as well as those of TNF-α (P < 0.05).

All patients except one (955%) were initially diagnosed by upper

All patients except one (95.5%) were initially diagnosed by upper endoscopy and biopsy. The tumor location was the 1st or 2nd portion in the great majority of patients (20/22, 90.9%): 2nd portion 11, bulb 6, superior duodenal angle 3, 3rd portion 1, 4th portion 1. The most Peptide 17 patients (81.8%)

had advanced diseases (stage III 9 and IV 9). Pancreatic invasion was observed in 6 (27.3%) and 9 (40.9%) had distant metastasis. Twelve patients (54.5%) underwent surgery, 12 (54.5%) took anticancer chemotherapy including 8 cases of adjuvant therapy, and 7 (31.8%) radiotherapy. The median survival time was 24.3 months (95% CI 14.6–34.0). One year and 3 years survival rates were 55% and 22%., The advanced disease at the time of diagnosis was an independent prognostic factor for survival on multivariate analysis (hazard ratio 5.811, 95% CI 1.954–17.288, p = 0.002). Conclusion: Primary duodenal adenocarcinoma is prevalent among the elderly male. It developed mostly in the upper portion and could be diagnosed endoscopically. The

majority of the patients were diagnosed at the advanced stage which was an independent prognostic FXR agonist factor. These suggest that early diagnosis by through endoscopic examination beyond the bulb would be required for improving prognosis of primary duodenal adenocarcinoma. Key Word(s): 1. duodenum; 2. neoplasm; 3. non-ampullary; 4. adenocarcinoma; Presenting Author: PING-I HSU Corresponding Author: PING-I HSU Affiliations: Kaohsiung Veterans General Hospital Objective: Platelet ADP-receptor antagonists impair the healing of peptic ulcers, and 9% of patients with a history of peptic ulcer bleeding who take clopidogrel have recurrent ulcer bleeding

within one year. The aim of this randomized controlled trial was to investigate whether histamine-2 receptor antagonist can prevent recurrent peptic ulcer in atherosclerotic patients with long-term use of thienopyridine. We also investigated the effects of histamine-2 receptor antagonist on the antiplatelet action of thienopyridine. Methods: Long-term thienopyridine (clopidogrel or ticlopidine) users with peptic ulcer history who did not have peptic ulcers on enrollment Ponatinib were randomly assigned to receive either famotidine (20 mg b.i.d.) or placebo for 6 months. Eradication therapy was administered if endoscopy on enrollment revealed H. pylori infection. Follow-up endoscopy was carried out at the end of the 6th month and whenever severe epigastric discomfort, hematemesis or melena occurred. Platelet aggregation tests were performed on days 1 and 28 for patients who participated in the pharmacodynamic study. Results: The cumulative incidence of recurrent peptic ulcer during the 6-month period was 8.8% among patients given famotidine (n = 91) and 7.8% among patients given placebo (n = 90) (difference, 1.0%; 95% confidence interval, −7.0%–9.0%; P = 0.805).

Active viral activity of HCV was considered if there was either d

Active viral activity of HCV was considered if there was either detectable HCV RNA or grade 2 or higher HCV inflammation on corresponding histopathology.[14, 15] Active HBV activity was considered if there was presence of HBV DNA ≥ 104 copies/mL.[16] In cases with co-infection by HCV and HBV, either active HCV or HBV was considered active viral activity. In non-viral-related liver diseases, the Child-Pugh classification

was used to assess liver status between abnormal ALT and normal ALT cases. The non-viral-related liver BGB324 order diseases in this study included alcoholic liver disease, non-alcoholic steatohepatitis, primary biliary cirrhosis, autoimmune hepatitis, and glycogen storage disease. After applying an AFP cutoff of ≥ 20 ng/mL for both AFP-producing HCC and positive HCC recurrence, there were a number of false positive and false negative results. The majority of false positive AFP was within 100 ng/mL and most of these cases were associated with abnormal ALT. Therefore, we propose two sets of modified AFP criteria

for both AFP-producing HCC and recurrent HCC which have been adjusted for patients with elevated ALT (≥ 40 U/L) to eliminate LY2606368 false interpretations from liver inflammation. Increased inflammatory activity independent of HCC could miscategorize non-AFP-producing tumors as AFP-producing HCC and thus produce false positive recurrences after RFA. The details of the two modified criteria are shown in Table 1. The diagnostic performance of AFP using the modified cutoff levels were calculated and compared.

Baseline characteristics of all patients were analyzed by descriptive statistics. Skewed variables including AFP, ALT, and AST were estimated using median and interquartile range (IQR). Continuous variables were compared using the Mann–Whitney U-test or the Student’s t-test, and by using the Chi-square or Fisher’s exact test for categorical Branched chain aminotransferase variables. The performance of AFP in the detection of HCC recurrence was evaluated by sensitivity, specificity, positive predictive value, negative predictive value, and accuracy. Analyses were conducted using SPSS software (version 20 IBM, New York, NY, USA) with a two-sided P value < 0.05 set as the level of significance. In multiple comparison analysis, an adjusted P value was applied using Bonferroni correction. There were 146 RFA treatment courses for solitary HCC in 131 patients eligible for the study. Of these patients, a majority of the patients were male (73.3%) with a mean age of 64.1 ± 10.6 (standard deviation) years. The mean baseline and recurrent tumor sizes were 2.4 cm and 2.6 cm, respectively. The median follow-up time after the first RFA was 8.2 months. The gender, age, pretreatment serum AFP level, liver function tests, underlying liver diseases, Child-Pugh classification, and diagnostic criteria for recurrence are shown in Table 2. Of 146 treated HCCs, 103 demonstrated no tumor recurrence at last follow-up while 43 HCC had local recurrences.

We enrolled all patients

with chronic hepatitis B (CHB) a

We enrolled all patients

with chronic hepatitis B (CHB) at Severance Hospital (Seoul, South Korea) or CHA Bundang Medical Center (Seongnam-Si, South Korea) who were started on ETV (0.5 mg once a day) between January 2007 and June 2008 and for whom stored serum was available. The inclusion criteria were the presence of serum HBsAg for 6 or more months, HBV genotype C, an age greater than 16 years, and a Afatinib mouse previous lack of treatment with a subsequent ETV treatment period of at least 24 months. ETV was commenced when the HBV DNA level was more than 10,000 copies/mL and when either the alanine aminotransferase (ALT) level was greater than 2 times the upper limit of normal or biopsy showed significant fibrosis/cirrhosis.25 The exclusion criteria were a coinfection with hepatitis C virus

or human immunodeficiency virus, a history of organ transplantation, decompensated liver cirrhosis (ascites, varices, encephalopathy, albumin level < 3 mg/dL, total bilirubin level > 2.5 mg/dL, or prothrombin time > 3 seconds longer than normal), and a concurrent use of immunomodulatory drugs or corticosteroids. Written, informed consent was obtained from all participating patients. This study Selleckchem Metformin was approved by the local institutional review board and was conducted in accordance with the principles set forth in the Declaration of Helsinki. Routine biochemical tests, including ALT, albumin, total bilirubin, and creatinine levels, were performed with a sequential multiple autoanalyzer. The Architect HBsAg QT immunoassay (Abbott Diagnostic, very Wiesbaden, Germany) was used to quantify qHBsAg according to the manufacturer’s instructions.5, 13

Briefly, the assay was carried out in two steps: HBsAg present in the sample was bound to antibody to hepatitis B surface antigen (anti-HBs)–coated microparticles, and an acridinium-labeled anti-HBs conjugate was added together with pretrigger and trigger solutions. The products of the resulting chemiluminescent reaction were measured in relative light units. The qHBsAg calibration curve ranged from 0.05 to 250 IU/mL, and the samples were diluted with a diluent (1:20 or 1:250) as needed to expand the detection range. The Architect platform (Abbott Diagnostic) was also used to quantify qHBeAg. Briefly, qHBeAg was measured with an automated microparticle chemiluminescent immunoassay based on a previously described method.

6A and Supporting Information) Substitutions pL127P and pG1040

6A and Supporting Information). Substitutions p.L127P and p.G1040R are predicted to result in structural changes within the transmembrane domains of ATP8B1 (Fig. 6B,F). The p.G308V mutation causes a destabilizing rearrangement in the ATP8B1 Actuator domain (Fig. 6C), which likely influences the association between the Actuator selleck chemicals llc and Phosphorylation domains (indicated by A and P in Fig. 6A), two ATP8B1 structural domains that are highly conserved in all P-type ATPases. The residues D454 and D554 are close together in the cytosolic core of the protein, and are critical for the catalytic cycle of P-type ATPases (Fig. 6D). I661

is a fully exposed residue, located in the Nucleotide-binding domain (N-domain) (Fig. 6E). The I661T mutation does not seem to result in major structural changes within ATP8B1, CH5424802 in line with the relatively mild clinical consequences of this mutation.11 ATP8B1 R1164X lacks three helical turns

of the last transmembrane helix (shown green in Fig. 6A) and 80 C-terminal residues, whose structure could not be reliably predicted. Together, these modeling data support the hypothesis that most of the studied mutations result in significant structural alterations. We investigated whether treatment with the pharmacological chaperone 4-PBA ameliorated the low expression of ATP8B1 mutants. ATP8B1 G308V protein expression was significantly increased by 4-PBA treatment in a dose-dependent manner (Fig. 7A). Total cellular expression of ATP8B1 G308V, D454G, D554N, and R1164X was induced two-fold to five-fold by 4-PBA treatment (Fig. 7B). Interestingly, protein expression of ATP8B1 I661T and G1040R showing

only mildly reduced expression levels in control conditions, also poorly responded to 4-PBA treatment. ATP8B1 WT expression was not stimulated by 4-PBA, suggesting specific up-regulation selleck inhibitor of otherwise misfolded proteins. Subsequently, cell surface biotinylation was performed to determine whether 4-PBA stimulated the trafficking of ATP8B1 mutants to the cell surface. Neither ATP8B1 nor the transferrin receptor (used as a loading control) was detected when biotin was omitted, indicating the specificity of the signal for cell surface resident proteins. ATP8B1 G308V, D454G, and D554N showed a 1.5-fold to 2-fold increase in plasma membrane expression upon 4-PBA treatment (Fig. 8B). Despite increased protein expression upon 4-PBA treatment, no ATP8B1 R1164X signal was detectable at the cell surface in either condition. Interestingly, ATP8B1 I661T abundance in the biotinylated fraction was strongly enhanced (5-fold to 10-fold) upon 4-PBA treatment, suggesting markedly improved trafficking to the plasma membrane (Fig. 8A,B). The reverse occurred when cells were cultured at 40°C. This temperature increase resulted in a significant decrease in the amount of ATP8B1 I661T, but not WT protein at the cell surface (Fig. 8C).