Aim of this study was to develop and validate a Sinhala version of the CLDQ (sCLDQ) and to test its correlation with the degree of liver dysfunction in a cohort of Sri Lankan patients with cirrhosis. Methods: A standard translation method was used to develop the sCLDQ. Pilot testing was done with relevant cultural and language adaptations. The final version was self-administered to stable CLD patients, together with the WHO Quality of Life-BREF (WHOQOL-BREF) validated Sinhala version, for comparison. Epacadostat order sCLDQ was re-administered 4 weeks

later to test internal consistency and reliability. The validation was assessed by Cronabach’s alpha, intraclass correlation coefficient (ICC) and Pearson’s correlation coefficient. ANOVA and Pearson’s correlation were used to test correlation with the degree of liver dysfunction. Results: Validation was done with 214 subjects, mean age 55.6 (SD 10.4) years; male 77.6%. Overall Cronabach’s alpha was

0.926. Itra-class correlations varied from 0.431 to 0.912 and all were significant (p 0.000). Retesting was done on a sub-sample of 18 subjects. Test-retest correlation was 0.695 (p 0.008). WHO-BREF was applied on a sub-sample of 48 subjects. There was a significant correlation (Pearson’s r = 0.391; p = 0.004) between sCLDQ and WHOQOL BREF. sCLDQ was significantly Wnt tumor associated with MELD (r = −0.13; p = 0.038), MELD Sodium (r = −0.223; p = 0.002), Bilirubin (r = −0.124; p = 0.036), Serum Sodium (r = 0.172; p = 0.009), Serum Albumin (r = 0.201; p = 0.003) and Child grade (f = 3.687; p = 0.027). Conclusion: sCLDQ is a reliable and valid

tool to assess Glycogen branching enzyme QoL of Sri Lankan cirrhotics and correlates well with known indices of disease severity. Key Word(s): 1. Cirrhosis; 2. CLDQ; 3. Sinhala; 4. Quality of Life; Presenting Author: YINPENG JIN Additional Authors: GUANGFENG CHEN, QINGCHUN FU, XIAOQING LIU, CHENGWEI CHEN, HENG ZHOU Corresponding Author: QINGCHUN FU, XIAOQING LIU, CHENGWEI CHEN Affiliations: Shanghai Liver Diseases Research Center, the Nanjing Military Command; Tongji University Objective: Acute liver failure is a highly lethal disease with rare effective therapeutic methods. Allogeneic liver transplantation is a viable treatment for acute liver failure. However, there is a serious shortage of liver donors. Stem cell transplantation is a more promising alternative approach for acute liver failure. Here we show that the human adipose-derived stem cells (hADSCs) have promising therapeutic potential for rats with acute liver failure. Methods: HADSCs were isolated from fat tissue, purified by adherence screening method and cultured in serum-free medium.

87 patients discontinued LdT and were followed up over 1 year. The HBV DNA negative rate was 86.3% (201/233) after 24 weeks of LdT treatment. The HBeAg loss rates at year 1, 2 and 3 were 55.9%, 60.0% and 63.8%, respectively, Small molecule library cell line for the HBeAg seroconversion, the rates were 45.9%, 52.6% and 57.1%, respectively. The sustained HBeAg seroconversion rate was 73.6% (64/87) in patients who were followed at least 1 year after drug withdrawal. The recurrence rate of patients experiencing HBsAg<1000 IU/ml was significantly lower than that in patients experiencing HBsAg>1000

IU/ml (13.5% (5/37) vs. 32.0% (16/50)), with significant difference (χ2=3.97, P<0.05). Decline in HBV DNA, HBeAg and HBsAg was factor predicting HBeAg seroconversion. Conclusion: LDT as a monotherapy

or as a combination therapy with ADV shows good antiviral efficacy. Consolidation therapy for more than 2 years after achieving HBeAg seroconversion, total > 3 years of treatment, as well as decline in HBV DNA, HBeAg and HBsAg are associated with durability HBeAg sero-conversion. [Key words] chronic hepatitis B, HBeAg-positive, HBeAg seroconversion, telbivudine Disclosures: The following people have nothing to disclose: Yang Ding, Chong Acalabrutinib clinical trial Zhang, Qiuju Sheng, Mingxiang Zhang, Feng Wu, Baojun Song, Weili Zhu, Jingyan Wang, Lilan Shi, Xiaoguang Dou Background & Aims Entecavir (ETV) and tenofovir (TDF) have been established as the two most potent initial agents for chronic hepatitis B (CHB) patients. Since there is a lack of objective data on whether the two drugs are similar in antiviral efficacy,or one is superior to the other, we

compared therapeutic outcomes between ETV- and TDF-treated CHB patients without prior therapy, specifically in the early phase. Methods This retrospective study included CHB patients with and without cirrhosis who were initially treated with 300mg/day TDF (n=99) or 0.5mg/day ETV (n=1,226). All patients had baseline HBV DNA levels >2,000 IU/mL and Child-Pugh class A liver function. We compared virological, serological, and biochemical responses between the TDF and ETV groups at week 48. Results Although proportion of cirrhosis (54.5% vs 41.6%) and mean serum alanine aminotransferase (ALT) level (119.4 vs 193.5 Clomifene IU/L) at baseline differed between the TDF and ETV groups (Ps<0.05), there was no significant difference in mean serum HBV DNA level (6.8 log10 vs. 6.9 log10 IU/ml) and percentage of HBeAg positivity (57.6% vs 55.4%; Ps=NS). At week 48, ALT normalization rate for all patients and HBeAg loss/seroconversion rate for HBeAg-positive patients were similar between the two groups (82.6% and 83.4%, and 19.3% and 16.8 % respectively; Ps=NS). The mean reductions in HBV DNA level at week 48 were -6.7 and – 6.5 log10 IU/mL, respectively, for the HBeAg-positive patients in the TDF and ETV groups (P=NS); and – 6.2 and – 6.0 log10 IU/mL, respectively for the HBeAg-negative patients (P=NS).

“
“Overdose of acetaminophen (APAP), the active ingredient of Tylenol, is the leading cause of drug-induced acute liver failure in the United States. As such, it is necessary

to develop novel strategies to prevent or manage APAP toxicity. In this report, we reveal a novel function of the liver X BGJ398 ic50 receptor (LXR) in preventing APAP-induced hepatotoxicity. Activation of LXR in transgenic (Tg) mice or by an LXR agonist conferred resistance to the hepatotoxicity of APAP, whereas the effect of LXR agonist on APAP toxicity was abolished in LXR-deficient mice. The increased APAP resistance in LXR Tg mice was associated with increased APAP clearance, increased APAP sulfation, and decreased formation of toxic APAP metabolites. The hepatoprotective effect of LXR may have resulted from the induction of antitoxic phase II conjugating enzymes, such as Gst and Sult2a1, as well as the suppression of protoxic phase I P450 enzymes, such as Cyp3a11 and Cyp2e1. Promoter analysis suggested the mouse Gst isoforms as novel transcriptional targets of LXR. The suppression of Cyp3a11 may be accounted for by the inhibitory effect of LXR on the PXR-responsive I-BET-762 supplier transactivation of Cyp3a11. The protective effect of LXR in preventing APAP toxicity is opposite to the sensitizing effect of pregnane X receptor, constitutive androstane receptor, and retinoid X receptor alpha. Conclusion: We conclude that LXR represents

a potential therapeutic target for the prevention and treatment of Tylenol toxicity. (HEPATOLOGY 2011) Overdose of the analgesic and antipyretic, acetaminophen (APAP), is the leading cause of drug-induced acute liver failure.1 APAP usually is well tolerated at recommended therapeutic doses, and the majority

of APAP is rapidly metabolized by the phase II conjugating enzymes, UDP-glucuronosyltransferase (UGT) and sulfotransferase (SULT), in the liver to nontoxic compounds,2 which is followed by renal Fluorometholone Acetate and biliary excretion. Another metabolic pathway is bioactivation by phase I cytochrome P450 (CYP) enzymes to the highly reactive intermediate metabolite, N-acetyl-p-benzoquinone-imine (NAPQI).3 NAPQI has a short half-life under normal conditions and is eliminated by conjugation with glutathione (GSH), a reaction carried out by glutathione S-transferase (GST), and then further metabolized to a mercapturic acid and excreted into the urine.4 In the event of APAP overdose, the glucuronidation and sulfation pathways become saturated, and increasing amounts of APAP undergo P450-mediated formation of NAPQI, as well as depletion of GSH.5 Accumulated NAPQI then binds to cellular macromolecules, leading to structural and metabolic disarray of the cells.6 Furthermore, depletion of intracellular GSH renders the hepatocytes highly susceptible to oxidative stress and apoptosis. CYP1A2, 2E1, and 3A are the most active P450s that convert APAP to NAPQI.7 Treatment with Cyp1a2 inducers increased APAP hepatotoxicity in rodents.8 Cyp2e1 was found to activate APAP to NAPQI.

3a). No amplification signal was observed at the lowest concentration of 10−3 ng−1 PCR. To estimate the sensitivity of S. pyogenes detection, serial dilutions of S. pyogenes cells were prepared in saline and 5-μL

aliquots from each dilution series were added directly to the PCR mixture containing primer pair 212F/212R for PCR reaction. Simultaneously, the aliquots (100 μL) were plated on tryptose MI-503 cost agar plates up to 10−6 dilution. A PCR amplicon of 212 bp was observed up to 10−5 dilution (Fig. 3b). The numbers of CFU observed for 100-μL aliquots of different dilutions are presented in Supporting Information, Table S1. The specificity of SCAR primers 212F/212R was evaluated against the DNA extracted from 270 clinical throat swabs of pharyngitis patients. Twenty-three samples were positive for the SCAR primers, which indicated the presence of S. pyogenes in these throat swabs. In contrast to this, only eight samples were found to be positive Metformin for S. pyogenes in the standard

bacteriological analysis. Hence the SCAR primers are found to be an efficient tool in the identification of S. pyogenes from the throat metagenome. It is important to identify S. pyogenes accurately from clinical samples as this bacterium remains a significant human pathogen among Gram-positive organisms and is responsible for a wide array of infections. For the past two decades several methods have been tried for the identification of S. pyogenes, such as the DAI test (Venezia et al., 1985), fluorescent antibody (Facklam & Carey, 1985), latex agglutination test (Gerber et al., 1984), Baricitinib enzyme immunoassay (Schwabe et al., 1991), rapid optical immunoassay technique (Harbeck et al., 1993) and DNA probe (Steed et al., 1993). Due to lack of sensitivity and

specificity, these methods are no longer used, and clinicians have switched over to molecular tools such as ribotyping (Bruneau et al., 1994; Shundi et al., 2000), RFLP analysis (Cleary et al., 1988) and REA (Bingen et al., 1992) for the identification of S. pyogenes. However, these methods usually need sequence determination and are not economical for clinical use. RAPD profiling is a molecular typing method that makes it possible to identify natural polymorphisms using a single, short oligonucleotide primer. This method is faster, technically less demanding and more economical (Seppala et al., 1994). In addition, this method produces a high range of profiling with a very low stringency (Wang et al., 1993). This agrees with our RAPD profile, where the 33 isolates were classified into eight groups (A–H). Profiles A, F and G were observed in 42%, 30% and 9% of isolates, respectively. The H2 primer generated two to eight bands of varying sizes and eight different strains were observed within the 33 S. pyogenes isolates.

There were more mild PEP rates recorded in 5Fr group (93% vs 56% P = 0.0549) that was not statistically significant. There appears to be no relationship

between stent characteristics and the risk or severity of PEP in patients with manometrically proven SOD. “
“Information on the find more long-term prognosis of nonalcoholic fatty liver disease (NAFLD) is limited. We sought to describe the long-term morbidity and mortality of patients with NAFLD with advanced fibrosis or cirrhosis by prospectively studying 247 such patients from four international centers (in Australia, USA, UK and Italy). Their natural history was then compared with 264 patients with HCV infection who were either naïve or non-responders to treatment. Both cohorts were Child-Pugh class A and had advanced fibrosis (stage 3) or cirrhosis (stage 4) confirmed by liver biopsy at enrollment. In the NAFLD cohort, followed up for a

mean of 85.6 months (range, 6-297), there were 48 (19.4%) liver-related complications and 33 (13.4%) deaths or liver transplants. In the HCV cohort, followed up for 74.9 months (mean; range, 6-238), there were 47 (16.7%) liver-related complications and 25 (9.4%) deaths or liver transplants. When adjusting for baseline differences in age and gender, the cumulative incidence of liver-related complications was lower in the NAFLD than the HCV cohort (P = 0.03), including incident hepatocellular cancer (6 versus 18; P = 0.03), but that of cardiovascular events (P = 0.17) and overall mortality (P = 0.6) were similar in both groups. In the NAFLD cohort, platelet count, stage 4 fibrosis, lowered platelet 4-Aminobutyrate aminotransferase count, and lowered serum cholesterol and alanine aminotrasferase ABT-737 molecular weight (ALT) levels were associated with liver-related complications; an aspartate aminotransferase/ALT ratio >1 and older age were associated with overall mortality, and higher serum bilirubin levels and stage 4 fibrosis were associated with liver-related mortality. Conclusions: Patients with NAFLD with advanced fibrosis or cirrhosis have lower rates of liver-related complications and hepatocellular cancer than corresponding patients

with HCV infection, but similar overall mortality. Some clinical and laboratory features predict liver-related complications and other outcomes in patients with NAFLD. (HEPATOLOGY 2011;54:1208–1216) Nonalcoholic fatty liver disease (NAFLD) has become the most prevalent cause of chronic liver disease worldwide.1-3 Regarded as the hepatic manifestation of the metabolic syndrome, NAFLD represents a histological spectrum of disease that extends from simple steatosis to steatohepatitis (NASH).1-5 NAFLD may be associated with advanced fibrosis or cirrhosis, which is a concern, as many of the liver-related complications and mortality (e.g., liver failure, varices, etc.) occur in these patients.6 In addition to an increasing need for transplantation,7 patients with NAFLD with and without cirrhosis may also develop hepatocellular cancer (HCC).

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 Veliparib purchase 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 MAPK Inhibitor Library manufacturer 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 IKBKE 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.

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) 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) 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) 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.