Conclusion: Shp and Npas2 crosstalk is essential to maintain hepatic lipid homeostasis. (Hepatology 2014) “
“Background:  To investigate pharmacokinetics and potency of antitumor activity of a novel 5-fluorouracil carrier erythrocyte (RBC-FU) in mice bearing malignant ascites. Methods:  RBC-FU was synthesized with a hyperosmotic technique. The entrapment efficiency of targeted

carrier erythrocytes was determined by reverse dialysis method with high-performance liquid chromatography (HPLC) for analyzing the quantity of 5-fluorouracil (5-FU). After a H22 hepatocarcinoma malignant ascites model was established in Kunming mice, 5-FU encapsulated by carrier erythrocytes (for Group A) and 5-FU solution (for Group B) at 20 mg per kg check details were injected into the peritoneal cavity of the mice, respectively. Blood and ascites samples were collected at different times to detect 5-FU quantity by HPLC. Body weight and survival time of mice were recorded in Group A, B and the Control Group in which mice were injected with normal saline only. Results:  5-FU was effectively encapsulated into erythrocytes, with an encapsulating effect as 55 ± 0.50%. In Group A, the maximum concentration (Cmax) and the area under

curve (AUC) in peritoneal exudates were significantly higher than those of Group B (P < 0.05). On the other hand, 5-FU level in serum was significantly LY294002 purchase lower than that in peritoneal exudates of Group A and B (P < 0.05). High drug levels in the abdominal cavity in Group A were maintained longer than those in Group B. Compared with that in Group B and the control, the quantity of malignant ascites in Group A had significant regression and the survival time was prolonged. Conclusion:  The hyperosmotic method described

here could be suitable for producing this novel RBC-FU as a liposomal drug of potential value for treating malignant 上海皓元 ascites by intraperitoneal administration. “
“Recently, we read with interest the article by van Bömmel et al.1 on tenofovir disoproxil fumarate (TDF) monotherapy for patients who failed to improve with other nucleoside/nucleotide analogues (NUC). Their findings showed that TDF monotherapy could induce a potent and long-lasting antiviral response in other NUC failure patients. However, we still have some questions to discuss. According to Asian Pacific Association for the Study of the Liver (APASL) and European Association for the Study of the Liver (EASL) guidelines,2, 3 primary nonresponse (PNR) is defined as a decrease in hepatitis B virus (HBV) DNA by <1 log10 IU/mL at week 12. But in the American Association for the Study of Liver Diseases (AASLD) guidelines,4 it is defined as a decrease in HBV DNA by <2 log10 IU/mL at week 24. Thus, we can see the time point at which determination of PNR in NUC treatment is still controversial. In this study, we thought it might not be good to define PNR at week 12 as treatment failure.

9 Sun et al.17 reported that some donor MHCII+ cells with dendritic morphology persist in the graft liver after preoperative lethal irradiation of the donor rat, suggesting the presence of radioresistant DCs. Surprisingly, the irradiated livers were acutely rejected when transplanted to allogeneic recipients, even when there were fewer DCs. The role of these remaining DCs, as well selleck products as other factors that are important in the rejection process, merits investigation. Here,

we show that rat liver conventional DCs contain at least two immunogenic subsets that have distinct trafficking patterns and radiosensitivities. We also found a novel migration pathway of passenger DCs that involves lymph-borne migration to the peritoneal cavity and then to regional LNs through diaphragmatic lymphatics. Even after DC depletion by graft irradiation, the remaining radioresistant DC subset induced an intense alloresponse in vitro that was probably responsible for the rejection. BrdU, 5-bromo-2′-deoxyuridine; DC,

dendritic NVP-BEZ235 cell; FACS, fluorescence-activated cell sorting; IL-2, interleukin-2; Irr(+)/Irr(−), irradiated/nonirradiated; LN, lymph node; LT, liver transplantation; MHCI, class I major histocompatibility complex; MHCII, class II major histocompatibility complex; PALS, periarterial lymphoid sheath; SIRP-α, signal-regulatory protein-alpha. Additional Materials and Methods information can be found in the online Supporting Information (Supporting Materials). Half of the donor DA rats received total-body sublethal split X-irradiation (filter: 0.5 mm aluminum + 0.1 mm copper, Hitachi MBR-1505R; Hitahci, Tokyo Japan). Animals were dosed twice at 3 Gy with a 4-hour intermission18 5 days before LT. We used a 5-day interval between irradiation and LT after conducting a

preliminary kinetic study to determine how long it took to achieve a significant reduction of donor MHCII+ or CD103+ cells in the graft (not shown). Recipient Lewis rats that received LT with or without irradiation were designated as the irradiated 上海皓元医药股份有限公司 [Irr(+)] or nonirradiated [Irr(−)] groups. To investigate the recipient’s immune response, cryosections were triple-immunostained for CD8β, FoxP3, recipient class I MHC (MHCI) (I169.1+)(19), or donor MHCII (alkaline phosphatase-blue), type IV collagen (peroxidase brown), and 5-bromo-2′-deoxyuridine (BrdU) (alkaline phosphatase red). Graft tissues were divided into three anatomical compartments: the sinusoidal; portal; and hepatic vein areas.2 Because the loss of the sinusoidal area should be parallel to the loss of hepatocytes (i.e., liver function), we assumed that compression of the sinusoidal area by the expanding portal and hepatic vein areas reflected the degree of rejection of the graft liver. Accordingly, the percentage of the sinusoidal area relative to the total surface area of stained sections was estimated by image analysis.

28 These studies highlight the utility of perfusion decellularization to generate whole organ bioscaffolds with significant potential for organ bioengineering. Typically, neovascularization of bioengineered tissues was addressed by supplementing cells with angiogenic growth factors29, 30 or fabricating scaffolds from synthetic material that allowed micro-patterning of vascular tree-like structures.31 When growth factors are used alone, they tend to create only a microvasculature consisting

of small and fragile capillaries, and therefore this technique is only applicable for the engineering of smaller size tissues. An alternative fabrication method is using a micropatterning technique that can be scaled up to larger sizes by modular construction. However, selleck currently this method cannot replicate the progressive complexity and ECM composition of the native liver vascular tree.32 The bioscaffolds generated from whole livers produced via our decellularization method retain the complexity of multiple size vessels that can deliver

fluids from the larger vena cava or the portal vein and reach each individual liver lobule. An additional advantage of this method is the retention of important ECM molecules required for site-specific engraftment and/or differentiation of different cell types that are present in the liver. Prior research showed SB431542 nmr that liver-specific stem cells can be isolated18, 33 and differentiated to hepatic fate.34 We used hFLCs in combination with hUVECs to recellularize the bioscaffolds, compared with adult hepatocytes used in many previous studies, Adult hepatocytes are larger and susceptible to mechanical stresses, resulting in lower seeding medchemexpress and functional efficiencies. The advantage of seeding fetal liver cells is that they contain large numbers of hepatic progenitors18, 33 that can give rise to hepatocytes, biliary epithelial cells and EC. On the other hand, the progenitors require specific cues to direct them to their native niches in the tissue and to support their growth and differentiation.35, 36 Preservation of ECM molecules and

GAGs at their correct locations within the acellular bioscaffold provides these cues. Detection of CK19+/CK18−/ALB− tubular structures as well as clusters of ALB+/CK18+ cells in the parenchyma suggests that the bioscaffold is able to support the differentiation of the fetal hepatoblasts into biliary and hepatocytic lineages, respectively. Thus, the use of the decellularized liver bioscaffold provides not only a three-dimensional vascularized scaffold for nutrient delivery, but also retains the environmental cues necessary for progenitor hepatic and endothelial cells to grow, differentiate and maintain functionality.35-37 A major obstacle in producing large-volume tissues is the delivery of adequate numbers of cells to the entire thickness of the tissue.

4 Now joining this group of entry factors are RTKs, which Lupberger et al. have demonstrated in vitro and 5-Fluoracil in vivo to specifically cooperate with CD81 and CLDN1 to facilitate the intricate process of HCV entry. Using a large-scale short interfering RNA (siRNA) screen against 691 known human kinases, Lupberger et al. revealed 58 kinases that appear to have a role in the HCV life cycle. The investigators focused on two RTKs: epidermal

growth factor receptor (EGFR) and ephrin receptor A2 (EphA2). Focus was placed on these two RTKs because their functions have been extensively documented. Furthermore, they are highly expressed in the human liver, and protein kinase inhibitors (PKIs) specific for EGFR and EphA2 are approved U0126 clinically for use in the treatment of other conditions.5-7 RTKs are activated after growth factor(s) bind to their extracellular

ligand-binding domain, resulting in receptor dimerization and subsequent activation of intracellular signaling pathways.8 Perhaps, it is not surprising that RTKs are involved in the HCV life cycle, given that they are known to regulate a vast number of cellular processes, namely proliferation, differentiation, survival, metabolism, migration, and cell-cycle control.9 A number of elegant techniques were employed by the investigators to demonstrate that EGFR and EphA2 are necessary for HCV entry. Inhibition of EGFR and EphA2 with the PKIs, erlotinib or dasatinib, respectively, inhibited HCV entry into medchemexpress hepatoma cells and primary human hepatocytes without affecting HCV-RNA replication. Similarly, the blocking of these RTKs with specific antibodies and siRNA-mediated knockdown markedly decreased HCV entry. Mechanistically, the investigators showed that activation of EGFR and EphA2 promote an association between the HCV coreceptors, CD81 and CLDN1. This association and trafficking of these receptors is perturbed by treatment with PKIs erlotinib and dasatinib, and, in turn, HCV entry is blocked. Interestingly, PKI treatment did not appear to alter expression levels of CD81, CLDN1, or the other

HCV entry factors, SR-BI and OCLN. Furthermore, using cell-fusion assays it was shown that EGFR potentially plays a functional role in late steps of HCV entry, specifically via facilitating the fusion of the viral envelope to host cell membranes. To this end, treatment of the hepatocyte-derived cell lines, Huh-7.5.1, polarized HepG2 cells (expressing CD81), and primary human hepatocytes with EGF and transforming growth factor alpha (TGF-α), ligands of EGFR, appeared to increase the association between CD81 and CLDN1 and enhance the fusion of viral and host membranes, leading to increased uptake of HCV (Fig. 1). These extensive in vitro investigations were substantiated with the use of the well-characterized chimeric urokinase plasminogen activator/severe combined immunodeficiency (uPA-SCID) mouse model.

4 Now joining this group of entry factors are RTKs, which Lupberger et al. have demonstrated in vitro and www.selleckchem.com/products/azd-1208.html in vivo to specifically cooperate with CD81 and CLDN1 to facilitate the intricate process of HCV entry. Using a large-scale short interfering RNA (siRNA) screen against 691 known human kinases, Lupberger et al. revealed 58 kinases that appear to have a role in the HCV life cycle. The investigators focused on two RTKs: epidermal

growth factor receptor (EGFR) and ephrin receptor A2 (EphA2). Focus was placed on these two RTKs because their functions have been extensively documented. Furthermore, they are highly expressed in the human liver, and protein kinase inhibitors (PKIs) specific for EGFR and EphA2 are approved Erismodegib in vivo clinically for use in the treatment of other conditions.5-7 RTKs are activated after growth factor(s) bind to their extracellular

ligand-binding domain, resulting in receptor dimerization and subsequent activation of intracellular signaling pathways.8 Perhaps, it is not surprising that RTKs are involved in the HCV life cycle, given that they are known to regulate a vast number of cellular processes, namely proliferation, differentiation, survival, metabolism, migration, and cell-cycle control.9 A number of elegant techniques were employed by the investigators to demonstrate that EGFR and EphA2 are necessary for HCV entry. Inhibition of EGFR and EphA2 with the PKIs, erlotinib or dasatinib, respectively, inhibited HCV entry into MCE hepatoma cells and primary human hepatocytes without affecting HCV-RNA replication. Similarly, the blocking of these RTKs with specific antibodies and siRNA-mediated knockdown markedly decreased HCV entry. Mechanistically, the investigators showed that activation of EGFR and EphA2 promote an association between the HCV coreceptors, CD81 and CLDN1. This association and trafficking of these receptors is perturbed by treatment with PKIs erlotinib and dasatinib, and, in turn, HCV entry is blocked. Interestingly, PKI treatment did not appear to alter expression levels of CD81, CLDN1, or the other

HCV entry factors, SR-BI and OCLN. Furthermore, using cell-fusion assays it was shown that EGFR potentially plays a functional role in late steps of HCV entry, specifically via facilitating the fusion of the viral envelope to host cell membranes. To this end, treatment of the hepatocyte-derived cell lines, Huh-7.5.1, polarized HepG2 cells (expressing CD81), and primary human hepatocytes with EGF and transforming growth factor alpha (TGF-α), ligands of EGFR, appeared to increase the association between CD81 and CLDN1 and enhance the fusion of viral and host membranes, leading to increased uptake of HCV (Fig. 1). These extensive in vitro investigations were substantiated with the use of the well-characterized chimeric urokinase plasminogen activator/severe combined immunodeficiency (uPA-SCID) mouse model.

The original experiments of Emlen, which established stars as a compass cue, actually provided some suggestion of time compensation, although only with three birds (Emlen, 1967). However, subsequent investigation provided no evidence of time compensation (Mouritsen & Larsen, 2001), without which longitude

is not discernible. Additionally, there is no evidence for a clock mechanism playing a role in detecting displacements per se, which would preclude both star and sun navigation as a mechanism for longitude (Kishkinev, small molecule library screening Chernetsov & Mouritsen, 2010). However, a meta-analysis of displacement experiments of juvenile migratory birds in orientation cages suggests that they are more likely to correct under starry skies than overcast skies, suggesting a role for celestial cues in this behaviour (Thorup & Rabøl, 2007). Indeed, many studies of the role of sun and stars in migratory navigation test only juvenile birds (e.g. Mouritsen & Larsen, 2001, Muheim & Akesson, 2002), or the age is not reported (e.g. Able & Dillon, CCR antagonist 1977, Able & Cherry, 1986). Rejection of celestial navigation thus relies to some extent on the assumption that the cues used by homing pigeons and migratory birds are the same.

It is however difficult to reconcile the global availability of celestial navigation with the apparent limits on true navigation in some migrating songbirds (see earlier). Sounds in the range of 0.1–10 Hz are known to spread over hundreds if not thousands of miles. If stable, these have the potential

MCE to act as a gradient for navigation. Evidence has been presented that pigeon homing performance is disrupted by infrasound disturbance, such as disturbance of pigeon races by sonic booms of aircraft (Hagstrum, 2000, 2001), or fluctuations in orientation performance that correlate with atmospheric fluctuations (Hagstrum, 2013). The data, while in many cases compelling, are correlational, however, making it difficult to currently assess whether this is a result of disruption of infrasound navigation cues, co-correlation with other factors propagated by atmospheric means, or disturbance in motivation to home. An experiment, which removed the cochlea of homing pigeons did not produce any deficits in homing performance (Wallraff, 1972), which, although not precluding that infrasound is part of a multifactorial map, does not support the argument made by (Hagstrum, 2013) that infrasonic cues are the sole solution to the navigational map question in pigeons. No experiment has yet demonstrated any effects of infrasound on bird migration.

The original experiments of Emlen, which established stars as a compass cue, actually provided some suggestion of time compensation, although only with three birds (Emlen, 1967). However, subsequent investigation provided no evidence of time compensation (Mouritsen & Larsen, 2001), without which longitude

is not discernible. Additionally, there is no evidence for a clock mechanism playing a role in detecting displacements per se, which would preclude both star and sun navigation as a mechanism for longitude (Kishkinev, Napabucasin cell line Chernetsov & Mouritsen, 2010). However, a meta-analysis of displacement experiments of juvenile migratory birds in orientation cages suggests that they are more likely to correct under starry skies than overcast skies, suggesting a role for celestial cues in this behaviour (Thorup & Rabøl, 2007). Indeed, many studies of the role of sun and stars in migratory navigation test only juvenile birds (e.g. Mouritsen & Larsen, 2001, Muheim & Akesson, 2002), or the age is not reported (e.g. Able & Dillon, ZD1839 mw 1977, Able & Cherry, 1986). Rejection of celestial navigation thus relies to some extent on the assumption that the cues used by homing pigeons and migratory birds are the same.

It is however difficult to reconcile the global availability of celestial navigation with the apparent limits on true navigation in some migrating songbirds (see earlier). Sounds in the range of 0.1–10 Hz are known to spread over hundreds if not thousands of miles. If stable, these have the potential

上海皓元医药股份有限公司 to act as a gradient for navigation. Evidence has been presented that pigeon homing performance is disrupted by infrasound disturbance, such as disturbance of pigeon races by sonic booms of aircraft (Hagstrum, 2000, 2001), or fluctuations in orientation performance that correlate with atmospheric fluctuations (Hagstrum, 2013). The data, while in many cases compelling, are correlational, however, making it difficult to currently assess whether this is a result of disruption of infrasound navigation cues, co-correlation with other factors propagated by atmospheric means, or disturbance in motivation to home. An experiment, which removed the cochlea of homing pigeons did not produce any deficits in homing performance (Wallraff, 1972), which, although not precluding that infrasound is part of a multifactorial map, does not support the argument made by (Hagstrum, 2013) that infrasonic cues are the sole solution to the navigational map question in pigeons. No experiment has yet demonstrated any effects of infrasound on bird migration.

Botanical therapy can be divided into 3 categories: oral, topical, and “aromatherapy.” In this article,

the options in these categories and the evidence supporting their use are discussed. Unfortunately, evidence is sparse for most herbal treatments, in large part due to a paucity SCH772984 solubility dmso of funding for the type of studies needed to assess their efficacy. Butterbur and feverfew are the 2 herbal oral preparations best studied, and they seem to have real potential to help many patients with migraine and perhaps other headache types. Patients most appropriate for trials of herbal therapy include those who have been refractory to pharmaceutical and other modes of therapy, patients who have had intolerable side effects from pharmaceutical medications, and patients willing to participate in controlled comparative studies. As for mechanisms behind botanical treatments, the lack of funding selleckchem for studying these agents will continue to retard progress in this area as well, but hopefully the future will bring more concentrated efforts in this field. “
“Objective.— To explore the efficacy and tolerability of levetiracetam in medical treatment of trigeminal

neuralgia. Background.— Antiepileptic drugs (AEDs) are considered as first-line treatment for trigeminal neuralgia, although their use is often limited due to incomplete efficacy and tolerability. Newer AEDs with improved safety profile may be useful in this disorder. Methods.— Patients suffering from trigeminal neuralgia (either primary or secondary) refractory to previous treatments were recruited to be treated with levetiracetam (3-4 g/day) for 16 weeks as add-on therapy, after a 2-week baseline period. Rescue

medication was allowed in both the baseline and treatment phases. The primary efficacy measure was the number of attacks per day. The medchemexpress patients’ efficacy evaluation, the patients’ global evaluation for both safety and efficacy, changes in the Hamilton Depression Scale, the Hamilton Anxiety Scale, and the Quality of Life Measure Short Form-36 were secondary parameters. Results.— Twenty-three patients were included in the analysis. After treatment and compared to the baseline phase, the number of daily attacks decreased by 62.4%. All secondary parameters changed significantly with the exception of the Quality of Life Measure Short Form-36 score. Seven patients withdrew from the study. Five patients (21.7%) reported side effects and 2 withdrew. Conclusions.— Levetiracetam may be effective and safe in trigeminal neuralgia treatment. Confirmation in a randomized controlled study is needed. (Headache 2010;50:1371-1377) “
“(Headache 2012;52:808-819) Aim.— Spontaneous intracranial hypotension (SIH) is caused by spontaneous cerebrospinal fluid (CSF) leaks and is known to cause orthostatic headaches. Phase-contrast magnetic resonance imaging (PC-MRI) is a non-invasive technique that can be used to quantify variation in CSF flow.

Botanical therapy can be divided into 3 categories: oral, topical, and “aromatherapy.” In this article,

the options in these categories and the evidence supporting their use are discussed. Unfortunately, evidence is sparse for most herbal treatments, in large part due to a paucity PF-01367338 mouse of funding for the type of studies needed to assess their efficacy. Butterbur and feverfew are the 2 herbal oral preparations best studied, and they seem to have real potential to help many patients with migraine and perhaps other headache types. Patients most appropriate for trials of herbal therapy include those who have been refractory to pharmaceutical and other modes of therapy, patients who have had intolerable side effects from pharmaceutical medications, and patients willing to participate in controlled comparative studies. As for mechanisms behind botanical treatments, the lack of funding PD0325901 supplier for studying these agents will continue to retard progress in this area as well, but hopefully the future will bring more concentrated efforts in this field. “
“Objective.— To explore the efficacy and tolerability of levetiracetam in medical treatment of trigeminal

neuralgia. Background.— Antiepileptic drugs (AEDs) are considered as first-line treatment for trigeminal neuralgia, although their use is often limited due to incomplete efficacy and tolerability. Newer AEDs with improved safety profile may be useful in this disorder. Methods.— Patients suffering from trigeminal neuralgia (either primary or secondary) refractory to previous treatments were recruited to be treated with levetiracetam (3-4 g/day) for 16 weeks as add-on therapy, after a 2-week baseline period. Rescue

medication was allowed in both the baseline and treatment phases. The primary efficacy measure was the number of attacks per day. The 上海皓元 patients’ efficacy evaluation, the patients’ global evaluation for both safety and efficacy, changes in the Hamilton Depression Scale, the Hamilton Anxiety Scale, and the Quality of Life Measure Short Form-36 were secondary parameters. Results.— Twenty-three patients were included in the analysis. After treatment and compared to the baseline phase, the number of daily attacks decreased by 62.4%. All secondary parameters changed significantly with the exception of the Quality of Life Measure Short Form-36 score. Seven patients withdrew from the study. Five patients (21.7%) reported side effects and 2 withdrew. Conclusions.— Levetiracetam may be effective and safe in trigeminal neuralgia treatment. Confirmation in a randomized controlled study is needed. (Headache 2010;50:1371-1377) “
“(Headache 2012;52:808-819) Aim.— Spontaneous intracranial hypotension (SIH) is caused by spontaneous cerebrospinal fluid (CSF) leaks and is known to cause orthostatic headaches. Phase-contrast magnetic resonance imaging (PC-MRI) is a non-invasive technique that can be used to quantify variation in CSF flow.

MAIN OUTCOME MEASURE: Mortality from all causes, cardiovascular disease, cancer, and liver disease (up to 18 years of follow-up). RESULTS: The prevalence of non-alcoholic fatty liver disease with and without increased levels of liver

enzymes in the population was 3.1% and 16.4%, respectively. Compared with participants without steatosis, www.selleckchem.com/products/ldk378.html those with non-alcoholic fatty liver disease but normal liver enzyme levels had multivariate adjusted hazard ratios for deaths from all causes of 0.92 (95% confidence interval 0.78 to 1.09), from cardiovascular disease of 0.86 (0.67 to 1.12), from cancer of 0.92 (0.67 to 1.27), and from liver disease of 0.64 (0.12 to 3.59). Compared with participants without steatosis, those with non-alcoholic fatty liver disease and increased liver enzyme levels had adjusted hazard ratios for deaths from all causes of 0.80 (0.52 to 1.22), from cardiovascular disease of 0.59 (0.29 to 1.20), from cancer of 0.53 (0.26 to 1.10), and from liver disease of 1.17 (0.15 to 8.93). CONCLUSIONS: Non-alcoholic fatty liver disease was not associated with an increased risk of death from all causes, cardiovascular selleck chemicals llc disease, cancer, or liver disease. Charlton MR, Burns JM, Pedersen RA, Watt KD, Heimbach JK, Dierkhising RA. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United

States. Gastroenterology 2011;141:1249-1253. (Reprinted with permission.) BACKGROUND & AIMS: The relative frequency of nonalcoholic steatohepatitis (NASH) as an indication for liver transplantation and comparative outcomes following transplantation are poorly 上海皓元 understood. METHODS: We analyzed the Scientific Registry of Transplant Recipients for primary adult liver transplant recipients from 2001 to 2009. RESULTS: From 2001 to 2009, 35,781 patients underwent a primary liver transplant, including 1959 for who NASH was the primary or secondary indication. The percentage of patients undergoing a liver transplant for NASH increased from 1.2% in 2001 to 9.7% in 2009.

NASH is now the third most common indication for liver transplantation in the United States. No other indication for liver transplantation increased in frequency during the study period. Compared with other indications for liver transplantation, recipients with NASH are older (58.5±8.0 vs 53.0±8.9 years; P<.001), have a larger body mass index (>30 kg/m2) (63% vs 32%; P<.001), are more likely to be female (47% vs 29%; P<.001), and have a lower frequency of hepatocellular carcinoma (12% vs 19%; P<.001). Survival at 1 and 3 years after liver transplantation for NASH was 84% and 78%, respectively, compared with 87% and 78% for other indications (P=.67). Patient and graft survival for liver recipients with NASH were similar to values for other indications after adjusting for level of creatinine, sex, age, and body mass index.