Thus, the current findings underscore the need to develop and implement effective smoking cessation treatments for agonist-treated pregnant patients in an effort to promote improved maternal and infant health outcomes. Future work to target pregnant agonist-treated women is of particular importance. Developing effective smoking cessation treatments has the free copy potential to reduce adverse health outcomes for both the mother and child. Also because pregnancy represents an opportunity to intervene and change problem behaviors, pregnant women engaged in drug treatment may be uniquely motivated for such interventions.

FUNDING MOTHER grants are from the National Institute on Drug Abuse (NIDA) unless noted otherwise: Brown University, R01 DA015778; Johns Hopkins University, R01 DA015764; Medical University of Vienna, R01 DA018417; Thomas Jefferson University, R01 DA015738; University of Toronto, R01 DA015741; University of Vermont, R01 DA018410 and M01 RR109; Vanderbilt University, R01 DA017513 and M01 RR00095, and Wayne State University, R01 DA15832. DECLARATION OF INTERESTS HJ discloses that she has received reimbursement for time and travel from Reckitt Benckiser. All other authors declare no competing financial interests. No contractual constraints on publishing have been imposed by any agency from which an author has received funding. The clinical trial was registered with ClinicalTrials.gov (Identifier: NCT00271219; Title: RCT Comparing Methadone and Buprenorphine in Pregnant Women).

The Family Smoking Protection and Tobacco Control Act requires that a new tobacco product, product standard, or modified risk tobacco product be evaluated based on its impact on public health. Public health impact is determined by the toxicity of the product, extent of uptake of the product, persistent use of the product, and the concurrent use with other tobacco products (Institute of Medicine, 2012). A conceptual model of tobacco product use holds that consumer response to a product, comprised both of product beliefs and subjective evaluations, relates to product uptake (Rees et al., 2009). Furthermore, a significant part of tobacco product evaluation involves determining its abuse liability (or potential for persistent use), which can include an individual��s subjective response to the product (Carter et al., 2009).

Although several types of scales have been used to assess different drugs on their use or abuse potential (e.g., Carter & Griffiths, 2009), few validated scales have been developed for tobacco products (Carter et al., 2009; Institute of Medicine, 2012; Hanson, O��Connor, & Hatsukami, 2009). Prior studies have used different methods to make these product assessments (Blank & Eissenberg, Dacomitinib 2010; Cobb, Weaver, & Eissenberg, 2010; Gray, Breland, Weaver, & Eissenberg, 2008; Kotlyar et al., 2011; Mendoza-Baumgart et al., 2007; O��Connor et al., 2011).

Limitations selleck chem and Future Directions These findings should be interpreted in the context of the study��s limitations. First, this is a laboratory study with adolescents who are not necessarily interested in quitting. Although findings demonstrate the acute effects of smoking abstinence, these laboratory assessments may not directly translate to the real-world experience of motivated quitters making a quit attempt. More naturalistic designs (i.e., the use of ecological momentary assessment of withdrawal effects) will be important for future research. In addition, the current design cannot disentangle the effects of abstinence from nicotine specifically versus withdrawal from the behavioral and psychological effects of smoking abstinence more generally.

Our findings should be followed up with studies that include additional comparison groups that decouple the effects of smoking and nicotine. For example, we recently found that sensorimotor replacement for smoking was more effective than nicotine replacement at reversing abstinence-induced craving, nicotine withdrawal symptoms, and usual-brand smoking among adult smokers with and without serious mental illness (Tidey, Rohsenow, Kaplan, Swift, & AhnAllen, 2012). Similar studies in adolescents could indicate whether temporary substitution of very low nicotine cigarettes for nicotine-containing cigarettes may provide a pathway toward reducing nicotine dependence in this population. Supplementary Material Supplementary Table 1 can be found online at http://www.ntr.oxfordjournals.org Funding This research was supported by grant R01 CA80255 awarded to Dr.

Colby from the National Cancer Institute. Declaration of interests None declared. Acknowledgment We thank Dr. Michael Sayette for his comments on earlier drafts of this manuscript.
Cigarette smoking is the number one preventable cause of death in the United States (Centers for Disease Control, 2009). Although considerable effort has been made to prevent smoking and promote cessation among current smokers (Piasecki, 2006; Shiffman, Pillitteri, Burton, & Marino, 2004), the central challenge is devising methods to combat smoking relapse (Piasecki, 2006). Relapse is the modal outcome for even the best smoking interventions (Piasecki, Fiore, McCarthy, & Baker, 2002; Shiffman et al., 1996), and there is no safe point beyond which relapse does not occur (Ockene et al.

, 2000). One Entinostat line of research on antismoking appeals has investigated how visual smoking cues and strength of antismoking arguments influence various outcomes, finding unintended negative effects of such cues��specifically that exposure to ads with smoking cues and weak arguments can increase smoking urges in smokers (Kang, Cappella, Strasser, & Lerman, 2009). Relapse must be avoided if smoking cessation programs are to be successful (Warner, 2002).

, 2007). The former study reported 35 SNPs with suggestive evidence of association with nicotine dependence (p<.0001), found strong evidence for small effects being played by a number of cholinergic genes, and nominated Neurexin 1 and CHRNB3 as genes having a potentially critical role in nicotine dependence. The latter study identified more than 20 genes with significant Nilotinib Bcr-Abl inhibitor evidence of association with a substantial portion of those genes coding for nicotinic receptors. We attempted to confirm and extend the most significant of these findings into an epidemiologically sound population using the Iowa Adoption Studies, the largest case�Ccontrol adoption study of substance abuse in the United States (Cadoret, Troughton, O��Gorman, & Heywood, 1986; Cadoret, Yates, Troughton, Woodworth, & Stewart, 1995; Yates, Cadoret, & Troughton, 1998), for the most significantly associated SNPs from the NICSNP Consortium’s high-density association study and for every SNP from their genotyping of nicotinic receptors that were analyzed in the candidate gene analysis.

Methods The methods and procedures of the Iowa Adoption Studies have been described extensively elsewhere (Yates et al., 1998). All procedures described here were approved by the University of Iowa Institutional Review Board for Human Subjects. The behavioral data for this study were derived from interviews conducted during the past two waves of the study (1999�C2004 and 2004�Ccurrent) using an adapted version of the Semi-Structured Assessment for the Genetics of Alcoholism, Version II (Bucholz et al.

, 1994), a robust, widely used instrument that allows assessment of DSM-IV substance use dependence and a variety of other common behavioral illnesses. Using these data, we derived symptom counts for nicotine dependence (maximum score of 7) in this population using criteria from DSM-IV (American Psychiatric Association, 1994). Similarly, total scores for the Fagerstr?m Test for Nicotine Dependence (FTND) Scale (maximum score of 10; Heatherton, Kozlowski, Frecker, & Fagerstr?m, 1991) were determined using these data. The first set of SNPs (see Supplementary Table 1) contained 33 of the 35 most significantly associated SNP variants from the 2006 high-density association analysis (Bierut et al., 2007). The second set of SNPs (see Supplementary Table 1) contained 129 polymorphisms from 21 candidate genes for nicotine dependence, including 15 nicotinic genes, from the candidate gene (Saccone et al.

, 2007) and high-density association analyses. Genotyping for the present study was performed by Sequenom Inc. (San Diego, CA) using DNA prepared in our laboratory from whole blood using cold protein precipitation (Lahiri & Nurnberger, Entinostat 1991) or from lymphoblast DNA provided from the National Institutes of Health Rutgers Repository.

Each analysis included only participants with complete data for the five primary variables. SS was missing for 4.2% of participants, compared with 3.6% for negative affect, 5% for risk perceptions, 0.3% for past 30-day smoking, and 0.2% for lifetime smoking. All five variables were present for 90.3% (n = 1,524) of participants, nevertheless excluding those who endorsed use of a fictitious substance or provided inconsistent data. To estimate an overall response rate (i.e., proportion of potential participants who provided usable data), we multiplied this figure by the 92% nonrefusal rate for all versions of the survey, yielding an estimated total response rate of 83.1%. All hypothesis tests used an alpha level of .05. Results Preliminary Analyses We first examined relationships between smoking outcomes and demographic variables.

Logistic regression showed that males were more likely to endorse past 30-day (odds ratio [OR] = 1.46 [95% CI 1.13, 1.89], p = .004) and lifetime smoking (OR = 1.37 [1.10, 1.70], p = .004), and that both 30-day (OR = 1.48 [1.31, 1.67], p < .001) and lifetime smoking (OR = 1.42 [1.28, 1.57], p < .001) increased with grade. Race/ethnicity was not associated with 30-day smoking but was related to lifetime smoking (OR = 1.09 [1.00, 1.20], p = .049), such that Asian Americans were less likely than others to endorse ever having smoked. Descriptive statistics for SS, risk perceptions, and negative affect are shown in Table 1. Male participants reported higher levels of SS but lower levels of both risk perceptions and negative affect.

Freshmen had lower levels of SS compared with juniors and seniors and lower levels of negative affect compared with sophomores and juniors. There were no grade differences in risk perceptions. Asian Americans reported lower levels of SS compared with other participants, whereas Hispanic students perceived smoking as least dangerous. There was no association between race/ethnicity and negative affect. Because of the associations between demographic variables and our primary variables, hypothesis tests using the full sample included interactions between SS and sex, grade, and race-ethnicity. Nonsignificant interactions were removed and the model was re-fit. Table 1. Associations Between Demographic Factors, Sensation Seeking, Mediators, and Outcomes SS and Smoking Logistic regression indicated that the interactions between SS and grade and race/ethnicity were not significant.

However, the sensation seeking �� sex interaction was significant for both 30-day (OR = 0.89 [0.82, 0.97], p = .008] and lifetime (OR = 0.92 [0.86, 0.99], p = .027) smoking. After stratifying Brefeldin_A the sample by sex to interpret these interactions, we found that SS was significantly associated with smoking for both sexes and that the association tended to be stronger for males (30 day: OR = 1.39 [1.30, 1.49], p < .001; lifetime: OR = 1.36 [1.28, 1.44], p < .

g., current depression, current use of antidepressant medications), and whether gender or race was covaried for or included as an interaction term in the analyses of depression and smoking outcomes. In addition kinase inhibitor Bosutinib to frequency and descriptive statistics, differences by type of study and whether studies found a significant impact of depression on smoking cessation outcomes were examined using t-tests for continuous variables and chi-squares for categorical variables. Statistical analyses were conducted using SPSS v.16.0 software for PC (SPSS, Inc.). Statistical tests were two-tailed and differences were considered significant when p < .05. RESULTS Study Characteristics General Study Characteristics A total of 190 articles published between 1990 and 2010 were identified through the literature search and individually examined.

Of the 190 articles, 68 (36%) met all the criteria to be included in the review. Table 1 shows a summary of characteristics for studies that examined smoking cessation outcomes for adults with depression as compared with adults without depression (DEP/CON, n = 57) and Table 2 shows a summary of characteristics for studies that examined smoking cessation outcomes within samples were restricted to only adults with depression (DEP/DEP, n = 11). An increasing number of articles examined smoking cessation treatment and depression over time (1990�C1994, n = 3; 1995�C1999, n = 13; 2000�C2004, n = 19; 2005�C2010, n = 33). Sixty-five percent of studies included a general sample of smokers while 35% of studies examined a subgroup of smokers (e.g.

, smokers with medical illnesses, adolescent smokers; see Tables 1 and and2).2). Table 1. Study Characteristics for Studies That Compared Smoking Treatment Outcomes for Smokers With and Without Depression Table 2. Study Characteristics for Studies That Examined Smoking Treatment Outcomes for Samples With Depression Funding Agency Nearly two-third of studies (64.7%; n = 44) reported a single source of funding while 25% reported multiple sources and 10.3% did not report a funding source. Government agencies were the most common source of funding (n = 52, 85.2% of studies that listed at least one source of funding) Additional sources of funding were pharmaceutical companies (n = 12), private foundations (n = 9), and university sources (n = 5). The majority of the research was conducted in the United States (88.

2%) with additional research conducted in the Netherlands, Germany, France, Turkey, and Iceland. Two studies, led by researchers located Anacetrapib in the United States, collected data in multiple countries. Sample Size (Tables 1 and and22) The sample sizes of the reviewed studies ranged from 25 to 3,056 with a mean sample size of 402 (SD = 497) and a median sample size of 250. Mean Age of Participants Forty-nine studies reported the average age of their participant sample (range = 16�C59 years old) and three-quarter of the mean ages fell between 40 and 49 years.

DMEM and fetal bovine serum (FBS) was obtained from Gibco Life Technologies, Inc. (Hercules, CA, USA). The chromatin immunoprecipitation (ChIP) assay kit was purchased from Millipore (Billerica, MA, USA). The M-PER mammalian protein extraction reagent, BCA, and Bradford protein assay kits were from Pierce Biotechnology Inc. (Rockford, IL, USA). ECL or enhanced kinase inhibitor Ixazomib ECL chemiluminescence reagents were obtained from either Pierce Biotechnology or Pharmacia (Erlangen, Germany). Antibodies anti-SR-BI (H-180), anti-ISX (C-16), and anti-RAR (M-454) were from Santa Cruz Biotechnologies (Santa Cruz, CA, USA), and anti-RAN was from Abcam (Cambridge, MA, USA). The anti-mouse-HRP and anti-rabbit-HRP conjugated secondary antibodies were purchased from Promega (Madison, WI, USA).

Oligonucleotides were purchased from Integrated DNA Technologies (Coralville, IA, USA). Animals, diets, and experimental procedures Mice were maintained in accordance with the Swiss and American animal protection laws throughout these experimental studies. B6;129S6-Bcmo1tm1dnp-knockout (Cmo1?/?) and control (B6;129S6) mice were housed individually under environmentally controlled conditions (24��C, 12-h light-dark cycle) with ad libitum access to feed and water. Powdered ��vitamin A-free�� diet Ssniff?EF 1/51, containing a residual amount of 0.15 IU vitamin A/g (Ssniff GmbH, Soest, Germany) was used as the basal diet. This was supplemented with control beadlets (DSM Ltd, Sisseln, Switzerland) in group 1 or with ��,��-carotene-containing beadlets (10% CWS; DSM Ltd) in groups 2 and 3 to provide 150 ��g/g ��,��-carotene.

Mice of group 3 also received 300 IU vitamin A in the form of retinyl palmitate (Dr. Ehrenstorfer GmbH, Augsburg, Germany) by weekly oral gavage in Miglyol 812 (Sasol, Witten, Germany). Lrat?/? mice used in this study have been described previously (23). For determination of the effects of vitamin A deficiency (VAD) and vitamin A sufficiency (VAS) on ISX expression in the duodenum and jejunum of these mice, they were fed AIN-93 formulation diets supplemented with 10 IU vitamin A (VAS diet) and without vitamin A supplementation (VAD diet). Diets were purchased from ResearchDiets (New Brunswick, NJ, USA). For determination of the effect of RA on intestinal ISX mRNA expression, 8 wk old Lrat?/? mice were subjected to a vitamin A-deficient diet for 10 d (AIN-93G Growing Rodent Diet Without Added Vitamin A; Research Diets, New Brunswick, NJ, USA). Animals (n=3 each) were gavaged twice, 24 h apart, with 0.5 mg RA (Sigma) dissolved in 100 ��l of corn oil or with vehicle alone. After 24 h, animals were sacrificed, and the small intestine and liver were removed and snap-frozen in liquid Entinostat nitrogen until further analyses.

Originally, the new technique was proposed new product in clinical practice as a non-invasive, surrogate marker of fibrosis and many studies demonstrated good reproducibility and a high correlation between LS and liver fibrosis at histology. However, liver elasticity is influenced not only by fibrosis, but also by the presence and extent of liquid, lipid and inflammatory infiltrates within the liver. The evidence that Fibroscan (FS) is significantly influenced by major variations of liver inflammation (as we previously showed), in addition to variations of staging, prompted the new frontier of testing FS values in the management of patients with chronic hepatitis.

Research frontiers The course of liver disease in a significant proportion of chronic hepatitis B (CHB) patients is characterized by hepatitis exacerbations, intervened by prolonged remissions whose biochemical and virologic patterns can be mistaken with those of chronic inactive carriers. Thus, measuring LS might be useful to distinguish active from inactive HBV carriers. We addressed this question and present here the results of the cross-sectional and prospective studies of a large cohort of pedigreed hepatitis B virus (HBV) carriers (68 inactive carriers, 200 CHB and nine acute hepatitis B patients). Innovations and breakthroughs FS correlates with fibrosis in CHB patients and FS provides a reliable method to assess the overall status of liver disease in the carrier with chronic HBV infection. The mean FS values of HBV-inactive carriers were comparable to those of normal controls and significantly lower than those of CHB patients.

Interestingly, in HBV inactive carriers with metabolic liver disease FS values were significantly higher than in HBV-inactive carriers without liver AV-951 disease. All factors stemming for activity of liver disease, namely the phase of infection (active or inactive), HBV-DNA and ALT levels influenced LS at multivariate analysis. Accordingly, in untreated patients without cirrhosis, histological necrosis and inflammation and ALT were the only factors influencing FS in addition to fibrosis. Thus both necrosis and inflammation influence LS that qualifies as a very promising tool for the non-invasive diagnostic assessment of the liver in the HBV carrier. The best cut-off values for fibrosis and cirrhosis were significantly lower than in chronic hepatitis C (CHC) patients, studied in identical conditions (same center, instrument, operators and test timing), suggesting that FS is influenced also by the different histopathology features of CHB and CHC. This prospective study on patients with hepatitis B exacerbations confirmed 1.2 to 4.4-fold increases of FS values at the time of ALT flares. Similarly, LS paralleled ALT fluctuations in patients with acute hepatitis B.

DISCUSSION This study aimed to alter smoking behavior and attitudes Crenolanib side effects toward smoking in order to reduce ETS exposure for nonsmokers, specifically women and children since most smokers in Egypt are adult males. Our results showed that the study��s community-based intervention had an overall positive impact in both aspects of tobacco control. The results also support findings from previous research that community-based education and enforced smoking bans in public areas are effective measures for reducing ETS exposure. One of the most widely known and successful programs for reducing ETS exposure has been the California Tobacco Program (Bal, Lloyd, Roeseler, & Shimizu, 2001; Rohrbach et al., 2002). The program had multiple components, including the reduction of ETS through local policies and public education programs.

Campaigns that focused on encouraging families to restrict smoking in their homes and cars resulted in a significant decrease in the proportion of 10th grade youths who reported being exposed to ETS in the previous week over a 2-year period. In 10 studies reviewed in the U.S. Department of Health and Human Services Community Guide (Hopkins et al., 2001 ; Zaza, Briss and Harris, 2005), all demonstrated a positive effect of clean indoor air regulations, at both the local and state levels, on reduced consumption, lower prevalence of smoking, and increased cessation. Our intervention demonstrated success in educating respondents about the hazards of smoking and ETS and how to respond.

For example, we saw an increase in knowledge: in the questions asking whether participants had received information on the common effects of smoking on children, adults, and pregnant women, the intervention group reported significantly higher rates of affirmative responses than the control group. Our results also showed a greater increase from pre- to postintervention in the number of respondents, particularly those in the intervention group, who recognized that smoking shisha is not a safer alternative to cigarettes. This is in alignment with two reports released by the World Health Organization (Mohamed, Loffredo, & Israel, 2006; World Health Organization, 2005). The greatest behavior change was seen in both groups demonstrating a greater ability to ask smokers to stop smoking and to implement total or partial smoking bans in the home.

Regarding smokers, the results of our Brefeldin_A study support the evidence (Fiore et al., 2008; Lancaster, Stead, Silagy, & Sowden, 2000) that changes in smokers�� behaviors are difficult to achieve, as these behaviors become entrenched through the addictive components in tobacco and the social rituals surrounding the act of smoking. This study found that neither the control nor intervention group showed any changes in the number of current smokers or in rates for quitting during the study��s time period. This might be attributed to the lack of smoking cessation clinics offering professional help to smokers who wanted to quit.

These experiments www.selleckchem.com/products/MLN-2238.html were designed to specifically focus on insulin-induced glucose metabolism in skeletal muscles and adipose tissue by infusing insulin at a rate known to suppress hepatic glucose production in all groups (Terrettaz et al., 1986). Following an overnight fast, glycaemia and insulinaemia were higher in Sirolimus- than in vehicle-treated rats (Table 1). Glycaemia was similar in both groups at the end of the clamps, while the hyperinsulinaemia reached was higher in the Sirolimus- than in the vehicle-treated group (Table 1). This resulted from the higher basal values brought about by the Sirolimus treatment, together with the fact that the same rate of insulin was infused in both groups.

Despite this higher insulinaemia, Sirolimus-treated animals displayed a marked decrease in the glucose infusion rate (GIR) compared with the vehicle-infused controls during the euglycaemic hyperinsulinaemic clamps (Figure 2C). In keeping with such a decreased GIR in Sirolimus-treated animals, the glucose utilization index measured in both red and white skeletal muscles was strongly reduced by the treatment (Figure 2D). Although the low amount of fat mass is unlikely to significantly contribute to the observed overall insulin resistance, Sirolimus treatment also significantly decreased the glucose utilization index of the epididymal and mesenteric, but not the inguinal fat depot (Figure 2E). Chronic mTOR inhibition by Sirolimus impairs Akt signalling and glucose transporter expression in skeletal muscle To gain insight into the molecular mechanisms by which Sirolimus triggers muscle insulin resistance, we analysed the expression and phosphorylation of critical insulin signalling effectors in skeletal muscle.

As muscles were collected from animals immediately at the end of the 2-DG procedure during euglycaemic hyperinsulinaemic clamps, they were stimulated with insulin before ex vivo tissue analyses. As shown in Figure 3A, the mTOR pathway was effectively blocked by Sirolimus, as evidenced by the lack of phosphorylation of S6, a substrate of the S6K, which is directly activated by mTORC1. Although phosphorylation of the insulin receptor and of Akt on Thr308 was unaffected, Akt phosphorylation on Ser473, which depends on the mTORC2 complex, was completely inhibited in Sirolimus-treated animals, in contrast to what has previously been observed in the liver of rapamycin-treated animals (Houde et al., 2010). This impaired Akt activation was further reflected by a decreased phosphorylation of AS160/TBCD4 and the glycogen synthase kinase 3 (GSK3) (Figure 3A), two important substrates of Akt controlling translocation of glucose transporters to Cilengitide the plasma membrane and glycogen synthesis.

The averages of cell replacement by Fah-positive hepatocytes were 2.8% at 6 weeks (6.4% at utmost) and 6.8% at 12 weeks (13.2% at utmost), respectively (Figure 3G). Therefore, human fetal liver cells could xeno-engraft into liver of Fah?/?Rag2?/? mice for liver xeno-repopulation. Figure 3 Human fetal liver cells selleck chem inhibitor have capacity for xeno-engraftment. A: Percentage of E-Cad+ cells in isolated human fetal liver cells by FACS. B: Percentage of E-Cad+ cells after enrichment by FACS; FAH (C; original magnification, ��100) … Livers of primary recipients with high level of repopulation (>10% FAH+ hepatocyte on sections) were perfused to isolate hepatocytes. The level of FAH+ hepatocytes in total isolated hepatocytes was detected by FAH antibody immuno-staining on cytospin slides.

Results indicated that two values about FAH+ hepatocytes were 12.43 �� 2.23% and 11.22 �� 3.12%. Based on this information, we transplanted 3 �� 105 FAH+ hepatocytes into each secondary Fah?/?Rag2?/? recipients. Treatments of anti-asialo GM1 and FK506 were performed as before. At 6 and 12 weeks, liver samples of recipients were harvested and analyzed. The average levels of FAH+ hepatocytes were 8.6% (14.6% at utmost) at 6 weeks and 26.4% (46.7% at utmost) at 12 weeks (Figure 3, E and G). These levels were similar to the levels achieved using adult human hepatocytes. We further confirmed liver xeno-repopulation from human hepatocytes using immunohistochemical analysis with antibody against human albumin.

The levels of human albumin-positive hepatocytes were found to be similar to the levels of FAH+ hepatocytes in both primary (Figure 3, C and D) and secondary Fah?/?Rag2?/? recipients (Figure 3, E and F). Thus the FAH+ hepatocytes were proven to be human hepatocytes. Hepatic Function of Human Hepatocytes after Liver Xeno-Repopulation The recovery of hepatic and metabolic function could be reflected by body weight as a parameter of health status.11 We have found that Fah?/?Rag2?/? recipients with high levels of repopulation gradually gained normal weight by 5 weeks after human hepatocyte transplantation (Figure 4C). By serial staining for hAlb and hAAT with a specific antibody we confirmed the human origin of engrafted hepatocytes and the synthetic function of human hepatocytes (Figure 4, A and B). Figure 4 Engraftment and hepatic function of human hepatocytes after liver xeno-repopulation. Serial staining of human specific Alb Ab (A; original magnification, ��200), and AAT Ab (B; original magnification, ��200) on liver specimen of chimeric … Metabolic parameters were used to analyze the AV-951 recovery of metabolic functions from the replaced human hepatocytes in mouse recipients.